20

2006
WORLD
CONGRESS
October 11 - 14, 2006
Prague, Czech Republic
(Prague Congress Centre)
Hosted by Czech Small Animal Veterinary Association

31 st
World Small Animal Veterinary Congress WSAVA

12 th
European Congress FECAVA

14 th
Czech Small Animal Veterinary Association Congress CSAVA

PROCEEDINGS
 COMMITTEES
Local Organizing Committee

Congress President Jiří Beránek (Czech Republic)

President of Scientific Committee Miroslav Svoboda (Czech Republic)
Treasurer Pavel Štellar (Czech Republic)
Travel and Social Programme Coordinator Pavla Kněžourová (Czech Republic)
Coordinators Z. Hanzálek (Czech Republic)
J. Aragones (Spain)
Peter J. Vit (Switzerland)
International Organizing Committee

WSAVA Representative Gabriel Varga (Slovak Republic)

WSAVA Advisors Raul Carranca (Mexico)
Diane Sheehan (Australia)
WSAVA Scientific Committee Coordinator Robert Washabau (USA)
FECAVA Representative & Ellen Bjerkås (Norway)
FECAVA Scientific Committee Advisor

Scientific Committee Coordinators

Lowell Ackerman David Lloyd

Collin Burrows Sjeng Lumeij
Ray Butcher Alois Nečas
Christine B. Chambreau Gregory Ogilvie
Richard A. le Couteur Zlatko Pavlica
Theresa W. Fossum Alan Rebar
Philip R. Fox Stefano Romagnoli
Alex German Jan Rothuizen
Moisés Heiblum David F. Senior
Hans Kooistra Andrew Sparkes
Terry Lake Luis Tello
Chris Lamb Miroslav Toman
Michael R. Lappin Anjop Venker van Haagen
2006 World Congress WSAVA/FECAVA/CSAVA

ISBN
978-80-902595-4-6

Editor: Miroslav Svoboda

Whilst every effort has been made by the editor to see that no inaccurate or misleading data, opinion, or statement appears in
these proceedings, he wishes to make clear that the data and opinions appearing in the abstracts herein are the sole responsibili-
ty of the contributors concerned. Accordingly, the editor of this proceedings and the members of the WSAVA/FECAVA/CSAVA
Committees and their employees accept no responsibility or liability whatsoever for the consequences of any such inaccurate
or misleading data, opinion or statement.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system or transmitted in any form or
by means without the written permission of the copyright holder or in accordance with the provisions of the copyright holder.
Any person who does unauthorized act in relation to this publication may be liable to criminal prosecution and civil claims for
damages.

© World Congress WSAVA/FECAVA/CSAVA – Prague 2006

2
Back to contents
WELCOME MESSAGE

Dear Colleagues and Friends,

First of all, let us welcome you at the World Congress of WSAVA/FECAVA/

CSAVA in the Czech Republic. We are honored to be part of this outstanding
event with participants from more than 80 countries all over the world. We
feel rewarded for selecting us as organizers and we take it as an appreciation
of a scientific level that veterinary medicine has reached in the region of
central European during recent years.

We paid a special attention to preparation of high level clinical and scientific

meetings. Therefore, we invited 95 speakers, all of them experts in their fields,
to share with you their knowledge, experience, and most recent scientific
information.
Apart of scientific program, the hosting city of Prague offers you a unique
opportunity to get closer to its culture, as well as to get in touch with its long
and eventful history.

Ladies and gentlemen, our precious guests, we strongly believe that this
Congress Proceedings will meet all your expectations and we hope you will
enjoy it, as you certainly will enjoy hospitality of our country and our friendly
people.

Dr. Miroslav Svoboda Dr. Jiří Beránek

Scientific Committee Chairman Congress President

2006 World Congress WSAVA/FECAVA/CSAVA

Pavel Stellar (LOC), Zdenek Hanzalek (LOC), Pavla Knezourova (LOC),

Jiri Beranek (LOC), Milan Svoboda (PCO), Miroslav Svoboda (LOC),
Renata Somolova (PCO), Karel Suchy (PCO), Barbora Vinsova (PCO),
Alena Fullsackova (PCO)
3
Back to contents
 2006
WORLD
CONGRESS
2006 World Congress WSAVA/FECAVA/CSAVA

WSAVA/FECAVA/CSAVA

4
Back to contents
TABLE OF CONTENTS

STATE OF THE ART LECTURES 9

/Lectures are listed in alphabetical order of the surname of the first author/

INVITED LECTURES - FULL PAPERS 31

/Streams are listed in alphabetical order/

A Standards of Care 31
Al Controversies in Alternative Medicine 113
B Behaviour 129
C Cardiology and Pulmonology 165
Cr Critical Care & Anaesthesiology 187
D Dermatology 211
De Dentistry 247
Di Diagnostic Imagine 267
E Endocrinology 293
Ex Exotics 321
Fe Feline Medicine 343
G Gastroenterology 377
H Hepatology 419
He Hereditary & Genetic Diseases - FECAVA Symposium 439
I Clinical Immunology 451
Ip Infectious & Parasitic Diseases 465
M Veterinary Management 491
N Nursing 507
Ne Neurology 521
O Oncology 549
Op Ophthalmology 585
Or Orthopaedics 619
P Cytology, Haematology & Clinical Pathology 647
R Reproduction 673 2006 World Congress WSAVA/FECAVA/CSAVA
S Soft Tissue Surgery 727
T Ear - Nose - Throat 763
U Nephrology & Urology 783
W Animal Welfare 811
POSTERS – ABSTRACTS 829
/Abstracts are listed in alphabetical order of the surname of the first author/

AUTHOR INDEX – POSTERS 895

AUTHOR INDEX – STATE OF THE ART LECTURES 903

AND INVITED LECTURES

5
Back to contents
 6
2006 World Congress WSAVA/FECAVA/CSAVA

Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

STATE STATE
OF
F THE
T OF THE
ART LECTUR
LECTURES

ART LEC
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

STATE STATE
OF THE OF THE
ART LECTURES

ART LEC

STATE OF THE ART LECTURE
THE IMPORTANCE OF PROTEINURIA AND MICROALBUMINURIA
Scott Brown, VMD,
PhD, DACVIM
Associate Dean for Academic
Affairs
Josiah Meigs Distinguished
Professor and Head
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
sbrown@vet.uga.edu
Cathy Brown, VDN,
PhD, DACVP
Professor
Department of Pathology
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
cabrown@vet.uga.edu
E
We now recognize that proteinuria is associated
with increased risk of developing end-stage
renal failure in cats and with an increased risk
of mortality even in nonazotemic animals.
Further, studies have shown that therapies that
reduce the magnitude of proteinuria are often
renoprotective.
Recent findings have suggested that renal
protein leak is not only a marker of severity
of renal disease but also potentially could be
a cause of renal injury. While the role of this
protein leak in producing renal damage has
not been clearly established in cats, findings in
cell culture studies and investigations of rodent
models of renal failure raise our con cerns for the
importance of separately evaluating our patients
for the presence or absence of proteinuria and for
CTU-
monitoring patients with proteinuria to determine
its magnitude, location, persistence. We should
investigate proteinuria in those cases where it
is present and institute appropriate therapy, if
indicated. It is critical, however, that veterinary
clinicians develop an enlightened approach to the
diagnosis and management of proteinuria.
Proper management of proteinuria mandates
two initial steps. First, a finding of proteinuria
should lead to characterization (confirmation by
sulfosalicylic acid or Robert’s reagent or urine
protein/creatinine ratio; quantification by the
urine protein/creatinine ratio) and if confirmed, it
should be categorized.
Back to contents
SOTAL
Katie Surdyk, DVM
Internal Medicine Resident
Department of Small Animal
Medicine and Surgery
College of Veterinary
Medicine
University of Georgia
Athens, GA 30602 USA
ksurdyk@vet.uga.edu
Categorizing Proteinuria - Prerenal Proteinuria
Prerenal proteinuria is caused by the presence
of proteins in the plasma that are filtered through
a normal glomerulus with normal permeability
to macromolecules (i.e., permselectivity).
These proteins may be normal proteins (e.g.,
hemoglobin) or abnormal proteins such as
immunoglobulin light chains (e.g., Bence-Jones
proteins)
Categorization of Proteinuria - Postrenal
Postrenal proteinuria is due to plasma proteins
from hemorrhage or inflammation in the urinary
tract (kidneys, ureters, bladder, urethra, and/or 2006 World Congress WSAVA/FECAVA/CSAVA
accessory sex glands). Many would also include
extra-urinary losses such as from the accessory
glands or genital tract as a postrenal cause of
proteinuria.
Categorization of Proteinuria – Three Types of
Renal Proteinuria
Most, but not all, causes of renal proteinuria
are abnormal. There are some functional causes
of proteinuria (e.g., fever or exercise) that are
transient, mild, and reversible and considered
variants of normal.
Pathological renal proteinuria is due to a renal
abnormality in protein handling. It may occur
from increased leakage of protein across the
glomerulus (permselectivity defect causing
glomerular proteinuria) or abnormal tubular
9
SOTAL
handling of filtered protein (tubular proteinuria),
or both. Tubular proteinuria occurs because small
plasma proteins (<15,000 molecular weight)
freely traverse the glomerular barrier. There are
also small amounts of larger molecular weight
proteins (e.g., albumin = 69,000 gm/mole) that
are filtered through the normal filtration barrier. In
a normal kidney, the tubules reabsorb practically
all of this filtered protein. In some diseases (e.g.,
gentamicin nephrotoxicosis) the glomerulus
is normal and permits filtering of only small
molecular weight proteins and a minor amount
of albumin. However, the diseased tubules are
unable to metabolize these proteins and tubular
proteinuria ensues.
Protein may also enter the tubular fluid from
interstitial inflammation (e.g., pyelonephritis
or renal neoplasia) and this is referred to as
interstitial proteinuria.
Proteinuria in cats
Once proteinuria is identified and categorized, it is
critical to ascertain whether or not it is persistent.
Generally, this means assessing the urine protein/
creatinine ratio on 3 occasions at 2 week intervals.
In cats with chronic kidney disease, urine protein/
creatinine values ≥ 0.4 in cats are associated
with an increased risk of mortality. A benefit of
angiotensin converting enzyme inhibitor therapy
has been shown for cats with a ratio of 1.0 or
greater. Anti-proteinuric, renoprotective therapy
is generally taken to be indicated in cats with
kidney disease and a persistently elevated ratio
which exceeds 0.5. In cats, this will initially be
an angiotensin converting enzyme inhibitor (e.g.,
benazepril at 0.5 mg/kg once daily).
Results of recent studies suggest have heightened
our concern about the importance of proteinuria
in dogs and cats, as evidence suggests that
persistent proteinuria is associated with
2006 World Congress WSAVA/FECAVA/CSAVA
progression of chronic kidney disease (CKD) and
worsened mortality rates, perhaps even in animals
without CKD. In veterinary medicine, we have
traditionally relied upon the urine dipstick and
more recently, the urine protein-to-creatinine
ratio, to identify and characterize proteinuria.
Now there is a renewed focus on proteinuria
and more specifically on microalbuminuria as
a screening test for our patients. It is altogether
fitting and proper that we should do this.
It has long been known that in diabetic
people, proteinuria is a hallmark of impending
nephropathy. Studies to quantify protein in the
urine of diabetic people demonstrated that even
small quantities of albuminuria were predictive
of subsequent renal disease. This small amount
of albuminuria (30-300 mg albumin in a 24-hour
urine collection) was less than that observed
10
Back to contents
in overt proteinuria (>300 mg/24 hrs) and it
became known as microalbuminuria because it
was a comparatively smaller (“micro”) amount
of albumin observed in the urine. A 24-hour
urine collection test to detect for the presence
microalbuminuria test has been used for decades as
a screen in diabetic people. In this nomenclature,
< 30mg albumin/day is normal in people,
30-300 mg/day is defined as microalbuminuria,
and >300mg/day is proteinuria.
While we often think of proteinuria originating
from the glomerulus as a sign of kidney disease,
recently it has been shown that in people with
endothelial dysfunction small amounts of albumin
can leak through the glomeruli of an otherwise
normal kidney, producing microalbuminuria.
This led to a new hypothesis: generalized
endothelial dysfunction is manifest in the
renal microcirculation as glomerular capillary
albumin leak, which the clinician (veterinarian
and physician) can detect as the presence of
microaobuminuria. These consequent small
amounts of albumin may be detected only by
sensitive tests, which may confirm the presence
of microalbuminuria. Traditionally this would
require a 24-hour urine collection as a screening
test.
Tests for microalbuminuria became a focus
in human medicine where microalbuminuria
is an independent risk factor for death from
cardiovascular disease and for the development
of myocardial infarction and stroke in people
with CKD. Indeed, these cardiovascular
complications are more common end-points
than uremic mortality for people with CKD. In
the past decade it has become apparent that that
microalbuminuria is a marker for fairly common
renal and cardiovascular problems, including
systemic hypertension, neoplasia, and generalized
inflammatory conditions in people. As the need
for a more clinically useful microalbuminuria
test arose, measurement of the urine albumin/
creatinine ratio (> 30 mg/gm is abnormal) or the
use of albumin dipsticks became commonplace
in people as a screening test for the presence of
microalbuminuria.
Veterinary medicine has historically utilized the
routine (traditional) urine dipstick as a screening
tool for identifying proteinuria and employed the
urine protein-to-creatinine ratio to provide semi-
quantitative information about the magnitude of
proteinuria in positive cases. This back-up test is
required because the dipstick is only qualitative
and is fraught with problems, particularly in
specificity. There is now a commercially available
albumin-detecting dipstick test (E.R.D.-Screen™
Urine Test, Heska, Ft. Collins, CO) which is
more sensitive and specific than the routine urine

dipstick and that could be used to confirm the
presence of proteinuria in the face of a positive
dipstick result. It is altogether fitting and proper
that we should do this.
Critically, the traditional dipstick will generally
detect urine albumin present at a concentration
of >30 mg/dL, whereas the new albumin-specific
dipstick can reportedly detect > 1 mg/dL. Because
this microalbuminuria is thus reportedly more
sensitive than the traditional urine dipstick, it has
been become possible to use this new dipstick as a
test for the presence of microalbuminuria in dogs
and cats. It can thus be employed as a screening
test in dogs and cats, similar to the approach
in people. By one method of classification
in veterinary medicine, microalbuminuria is
defined as a positive albumin-specific dipstick
in the absence of a positive routine (traditional)
urine dipstick. We could use this test to screen
all dogs and cats for the presence of CKD or for
the presence of endothelial dysfunction. Based on
what we know today, we need to act cautiously in
this regard as it is probably not altogether fitting
and proper that we should do this.
First, transient microalbuminuria may be
observed in a variety of transient conditions,
some of which remain to be identified in dogs and
cats. Persistent microalbuminuria is an important
clinical finding. In dogs and cats, persistent
microalbuminuria is defined by the ACVIM
Proteinuria Consensus Panel as microalbuminuria
found repeatedly in ≥ 3 specimens obtained
≥ 2 weeks apart which cannot be attributed to a
postrenal cause. Persistent microalbuminuria is
often due to altered glomerular permselectivity
(CKD or endothelial dysfunction); but impaired
tubular handling of the small amounts of albumin
that traverses the normal glomerular filtration
barrier can also cause microalbuminuria. There is
no clinically applicable way to reliably determine
the source of microalbuminuria (glomerular vs.
tubular). Nonetheless, progressive increases in
magnitude of microalbuminuria are likely to
indicate significant renal injury.
Since persistent microalbuminuria may be a
marker of either CKD or endothelial dysfunction
in dogs and cats, a microalbuminuria screening
test may lead to discovery of a treatable underlying
CKD or an inflammatory, metabolic, or neoplastic
condition in an apparently healthy animal.
Urine testing that for the presence of
microalbuminuria should be considered for the
following circumstances: animals with chronic
illnesses that may be complicated by proteinuric
nephropathies (e.g., systemic lupus), screening
apparently healthy dogs that are ≥ 6 years old
and cats that are ≥ 8 years old, animals with
confirmed or suspected systemic hypertension,
Back to contents
SOTAL
screening dogs or cats to detect possible onset of
a hereditary nephropathy as early as possible.
Much remains to be learned about this exciting
and novel approach that utilizes of the presence
of small amounts of protein in the urine as a
potentially valuable early marker of CKD and
other conditions of clinical importance in dogs
and cats. As veterinarians, we should be open to
adopting this approach as we carefully scrutinize
the literature for developing new information. It
is altogether fitting and proper that we should do
this.
References
1. Brown SA, Finco DR, Brown CA, et al.
Evaluation of the effects of inhibition of
angiotensin converting enzyme with enalapril in
dogs with induced chronic renal insufficiency.
Am J Vet Res 64: 321, 2003.
2. Brown SA, Brown CA, Crowell WA, et al.
Beneficial effects of chronic administration of
dietary omega-3 polyunsaturated fatty acids in
dogs with renal insufficiency. J Lab Clin Med 13:
447, 1998.
3. Brown SA, Brown CA, Crowell WA, et al.
Effects of dietary polyunsaturated fatty acid
supplementation in early renal insufficiency in
dogs. J Lab Clin Med 135: 275, 2000.
4. Grauer GF, Greco DS, Getzy DM, et al. Effects
of enalapril versus placebo as a treatment for
canine idiopathic glomerulonephritis. J Vet Intern
Med 14: 526, 2000.
5. Lees G, Brown S, Elliott J, Grauer G, and Vaden
S. ACVIM Proteinuria Consensus Statement,
2004.
6. Jacob F, Polzin D, Osborne C, et al. Association
of initial proteinuria with morbidity and mortality
in dogs with spontaneous chronic renal failure
(abst). J Vet Intern Med 18: 417, 2004.
7. Syme HM, Elliott J. Relation of survival time 2006 World Congress WSAVA/FECAVA/CSAVA
and urinary protein excretion in cats with renal
failure and/or hypertension (abst). J Vet Intern
Med 17: 405, 2004.
11
SOTAL
STATE OF THE ART LECTURE
CARDIAC DISEASE IN HUMANS AND ANIMALS:
MERGING RESEARCH AND CLINICS TO BENEFIT BOTH
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery Texas A&M
University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu
Cardiac surgery includes procedures performed
on the pericardium, cardiac ventricles, atria,
venae cavae, aorta, and main pulmonary artery.
Closed cardiac procedures (i.e., those that do not
require opening major cardiac structures) are most
commonly performed; however, some conditions
require open cardiac surgery (i.e., a major cardiac
structure must be opened to accomplish the
repair). Open cardiac surgery necessitates that
circulation be arrested during the procedure by
inflow occlusion or cardiopulmonary bypass
Inflow Occlusion
Inflow occlusion is a technique used for open
heart surgery where all venous flow to the heart is
temporarily interrupted. Because inflow occlusion
results in complete circulatory arrest, it allows
limited time to perform cardiac procedures.
Ideally, circulatory arrest in a normothermic
patient should be less than 2 minutes, but can be
extended to 4 minutes if necessary. Circulatory
2006 World Congress WSAVA/FECAVA/CSAVA
arrest time can be extended up to 6 minutes with
mild, whole-body hypothermia (32˚ to 34˚ C).
Temperatures below 32˚ C may predispose to
fibrillation and should be avoided. The advantage
of inflow occlusion is that it does not require
specialized equipment; however, the limited
time available to perform the surgery requires
that the procedure be well planned and executed
with speed and expertise. We have used this
technique primarily for right atrial tumors and
cor-triatriatum dexter.
Cardiopulmonary Bypass
Cardiopulmonary bypass is a procedure whereby
an extracorporeal system provides flow of
oxygenated blood to the patient while blood is
diverted away from the heart and lungs. This
greatly extends the time available for open cardiac
12
Back to contents
surgery. Several advances (i.e., development of
membrane oxygenators, improved methods of
myocardial protection, increased availability of
monitoring technologies, and improved veterinary
critical care) have made cardiopulmonary bypass
increasingly feasible in dogs. Cardiopulmonary
bypass can be used to treat dogs with congenital
or acquired cardiac defects. Readers are referred
to a cardiovascular surgery text for details of
performing cardiopulmonary bypass.
SUB-AORTIC STENOSIS
Surgical treatment of sub-aortic stenosis (SAS)
in dogs has been successful in the short term in
reducing the systolic pressure gradient across
the aortic valve, but has not been shown to
decrease the incidence of sudden death in this
population. Reports of closed transventricular
dilation showed marked post-operative decreases
in pressure gradients, but restenosis is common,
usually within three months. This restenosis is
consistent with reports in the human literature
following transventricular dilation. The most
promising results thus far are found in techniques
investigating the use of cardiopulmonary bypass
and open surgical correction.
To date, 3 dogs with subaortic stenosis has
undergone cardiopulmonary bypass and open-
heart correction of this defect at Texas A&M
University. These patients had severe SAS with
a Doppler-derived gradient in excess of 200 mmHg
and moderate to severe left ventricular hypertrophy
without significant ventricular ectopy or mitral
regurgitation. Through a median sternotomy, a
right ventriculotomy was performed in 2. An
initial incision into the hypertrophied septum
allowed exploration of the left ventricular outflow
tract (LVOT). An aortotomy was also performed
to improve visualization of the LVOT and aortic

valve. A large portion (1.5 x 2 cm) of the dorsal
septum was removed and the subvalvular fibrous
tissue resected without damage to the mitral
valve. The septal defect was repaired with
autologous pericardium harvested at surgery
and treated with glutaraldehyde to improve its
handling characteristics. Full thickness resection
was performed in an attempt to alleviate the late
restenosis noted with alternate partial thickness
resection techniques. One dog survived long-
term
PULMONIC STENOSIS
Although supra and subvalvular lesions have
been seen, the most common cause of pulmonic
stenosis in dogs is valvular dysplasia. Dogs with
moderate to severe stenosis may experience
syncope or changes leading to congestive heart
failure and are at risk for sudden death. Surgery
or balloon valvuloplasty should be considered
if the pressure gradient is above 80 mmHg.
Valvuloplasty may be beneficial for primarily
valvular lesions, but it efficacy may be reduced in
those cases with significant subvalvular muscular
hypertrophy. Restenosis, presumably due to
scarring, has been reported.
Alternatively a patch graft technique, using
PTFE or Gortex material, may be more likely to
provide a greater and longer standing reduction
in the pressure gradient, although survival
data have not been previously evaluated. Patch
grafting techniques may be performed under
inflow occlusion and mild hypothermia; however,
the use of cardiopulmonary bypass affords the
surgeon more time for precise placement of the
graft and thus may allow for improved post-
operative outcomes.
Dogs with an aberrant coronary artery contributing
to their pulmonic stenosis are not considered
candidates for balloon valvuloplasty or patch
grafting techniques due to the risk of disturbance
of that coronary vessel. Surgery in these animals
would generally require cardiopulmonary bypass
and placement of a conduit from the right
ventricle to the pulmonary artery to circumvent
the stenosis.
MITRAL VALVE DISEASE
Despite mitral valve disease (MVD) being the
most common cause of heart failure in dogs, no
medical therapy has yet been identified that will
delay or alter the progression of this disease.
Valve repair or replacement has become the
standard of care in human patients with chronic
degenerative valve disease. If possible, valve
repair is considered preferable to replacement as
it eliminates the need for anti-coagulative therapy
post-operatively and is less expensive. Depending
Back to contents
SOTAL
on the stage of disease, a variety of repair
techniques are available to improve the dynamics
of the valve. Ruptured chordae may be repaired
with synthetic (Gortex) sutures to re-establish
normal motion of the valve leaflets; an Alferari
procedure (“bow-tie” or procedure in which a
suture is placed between the anterior and posterior
valve leaflets) can decrease the regurgitant area
and provide support for leaflets and chordae. An
annuloplasty is generally required and involves
placement of a synthetic ring or sutures to reduce
the size of the dilated mitral annulus. Once
systolic function has deteriorated to the point that
continued inotrope support (other than digoxin)
is essential, mitral valve repair bypass surgery
becomes substantially more risky.
Other congenital defects that may be amenable
to definitive surgical repair
Ventricular septal defect (VSD) is the second
most common congenital heart defect in cats
and accounts for 5% to 10% of congenital heart
defects seen in dogs. Most ventricular septal
defects in small animals occur in the membranous
septum. Perimembranous defects are located
in the membranous septum, medial to the
septal tricuspid leaflet, and inferior to the crista
supraventricularis. Infundibular or supracristal
defects are located in the right outflow tract
superior to the crista supraventricularis. The
pathophysiology of VSD depends on the size of the
defect and on pulmonary vascular resistance. VSD
typically causes a left-to-right shunt. A typical
VSD overloads the left heart and, depending on
its size and location, may overload the right heart
as well. A large VSD can progress to left-sided
congestive heart failure. Chronic overcirculation
of the lungs can cause progressive pulmonary
vascular remodeling leading to severe pulmonary
hypertension and right-to-left shunting of blood
(Eisenmenger’s physiology). Aortic insufficiency 2006 World Congress WSAVA/FECAVA/CSAVA
is a fairly common secondary abnormality
associated with VSD, particularly infundibular
VSD. Aortic insufficiency results from prolapse
of an aortic leaflet into the defect. This prolapse
is due to the Venturi effect associated with VSD
flow and loss of support of the aortic annulus.
Aortic insufficiency adds to the left ventricular
volume overload and is usually progressive.
Definitive patch closure of VSD can be
accomplished with the aid of cardiopulmonary
bypass in dogs over 4 kg in body weight. A
perimembranous VSD is corrected from the
right side via a right atriotomy approach.
An infundibular VSD is corrected via a right
ventriculotomy from a left thoracotomy or median
sternotomy approach.
Tetralogy of Fallot (T of F) is the most common
13
SOTAL
congenital heart defect that causes cyanosis in small
animals. It occurs in cats and a variety of canine
breeds. Tetralogy of Fallot can be simplified into
two physiologically significant defects: pulmonic
stenosis and ventricular septal defect (VSD).
The pathophysiologic consequences of tetralogy
depend on the relative magnitude of these two
defects. If a large VSD and hemodynamically
insignificant pulmonic stenosis are present,
the functional result is a left-to-right shunt and
volume overload of the left heart similar to an
isolated, large VSD. If severe pulmonic stenosis,
suprasystemic right heart pressures, and right-
to-left shunt are present, the result is moderate
to severe cyanosis, exercise intolerance, and
progressive polycythemia. A shortened life span
is expected in these animals due to complications
of hyperviscosity-induced thromboembolism
or sudden death. Animals that have pulmonic
stenosis and VSD that are somewhat balanced are
functionally similar to those that have a VSD and
pulmonary artery banding performed. Animals
with predominantly left-to-right shunt are termed
acyanotic tetralogy and may function reasonably
2006 World Congress WSAVA/FECAVA/CSAVA
14
Back to contents
well as long as the shunt flow is insufficient to
cause left heart failure. Progression of pulmonic
stenosis due to infundibular hypertrophy is
possible and may cause acyanotic animals to
become cyanotic as they age. Surgery should
be considered for severely cyanotic animals to
lessen clinical signs and prolong life. Animals
with a resting arterial oxygen saturation less than
70% should be considered candidates for surgery.
Palliative surgeries for tetralogy include isolated
correction of the pulmonic stenosis or creation
of a systemic-to-pulmonary shunt (e.g., Blalock-
Taussig shunt). Correction of the pulmonic
stenosis risks overcorrection of the stenosis and an
overwhelming left-to-right shunt. For this reason,
valve dilation, either surgically or by balloon
dilation, is preferred over a more definitive
procedure such as a patch-graft. Definitive repair
of tetralogy can be undertaken in medium- to
large-breed dogs with cardiopulmonary bypass.
Patch closure of the VSD and patch-grafting
of the pulmonary outflow tract are undertaken
through a right ventriculotomy approach.

STATE OF THE ART LECTURE
UPDATE ON INFLAMMATORY BOWEL DISEASE
Dr. Alex German
Department of Veterinary Clinical
Science
University of Liverpool
Small Animal Hospitál
Crown Street
Liverpool
L7 7EX
United Kingdom
ajgerman@liv.ac.uk
INTRODUCTION
Inflammatory bowel disease (IBD) is a collective
term describing a group of disorders characterized
by persistent or recurrent GI signs, with
histological evidence of intestinal inflammation
on biopsy material. Variations in the histologic
appearance of the inflammation suggest that
idiopathic IBD is not a single disease entity, and
nomenclature reflects the predominant cell type
present. Lymphocytic-plasmacytic enteritis (LPE)
is the most common form reported, eosinophilic
(gastro-) enteritis (EGE) is less common, and
granulomatous enteritis is rare. Histiocytic
ulcerative colitis (HUC) is a rare form, most
commonly seen in boxer dogs.
It is a controversial, enigmatic, condition and much
remains to be understood of its aetiopathogenesis,
diagnosis and optimal treatment. Numerous
studies have now been published on companion
animal IBD, and our understanding is undoubtedly
increasing. However, despite a growing
knowledge base much remains to be determined
and understood. This presentation will review the
current understanding and current controversies
in canine and feline IBD.
AETIOPATHOGENESIS OF IBD
The gastrointestinal associated lymphoid
tissue (GALT) is the largest and most complex
immunological organ of the body, and must
be capable of mounting protective immune
responses to pathogens, whilst maintaining
tolerance to harmless environmental antigens
such as commensal bacteria and food. A delicate
balance exists at the level of the intestinal mucosa
with the ‘mucosal barrier’ separating the cells of
the GALT from the endogenous bacterial flora,
which represents an enormous and potentially
overwhelming antigenic challenge.
Whilst a number of recognized diseases are
associated with chronic intestinal inflammation,
Back to contents
SOTAL
the cause of idiopathic IBD is, by definition,
unknown. Rodent models of chronic intestinal
inflammation have demonstrated that
abnormalities in the mucosal barrier, the bacterial
flora and/or the GALT itself can lead to the
development of chronic mucosal inflammation.
Firstly, disruption of the mucosal barrier
allows increased passage of antigens across the
mucosa and can lead to inflammation. Second,
a dysregulated immune response, especially
involving CD4+ T cells, could underlie the
development of uncontrolled inflammation.
Finally, in certain circumstances, the presence of
certain luminal antigens (e.g. dietary components
and more importantly the endogenous bacterial
flora), can also influence the development and
severity of mucosal inflammation. Studies of
human IBD suggest that similar mechanisms may
be involved in both Crohn’s disease and ulcerative
colitis. Whilst these mechanisms are also said to
underlie IBD in companion animals, convincing
data are limited. Most notably, a recent study of
mucosal cytokine gene expression in dogs with
chronic enteropathies, failed to demonstrate
upregulation. Nonetheless, studies do suggest 2006 World Congress WSAVA/FECAVA/CSAVA
alterations in immune cell populations (although
variable and inconsistent amongst studies) and
a favourable response to anti-inflammatory and
immunosuppressive medications. More work is,
therefore, required to clarify the pathogenesis in
both cats and dogs.
CLINICAL PRESENTATION
Idiopathic IBD is a common cause of chronic
vomiting and diarrhoea in dogs and cats but its
true incidence is unknown. IBD is most common
in middle-age animals, and there is no apparent
gender predisposition. Although IBD can
potentially occur in any dog or cat breed, some
breeds are predisposed e.g. GSDs, soft coated
wheaten terriers, Shar peis and Siamese cats. In
15
SOTAL
cats, an association (termed ‘triaditis’) has been
reported between IBD, lymphocytic cholangitis
and pancreatitis.
Vomiting and diarrhoea are the most common
clinical signs. The nature of signs approximately
correlates with the region of the GI tract affected:
gastric signs are more common if gastric or upper
SI inflammation is present; LI-type diarrhoea
may be the result of colonic inflammation, or may
result from prolonged SI diarrhoea. The presence
of blood in the vomit or diarrhoea is associated
with more severe disease and, especially,
eosinophilic inflammatory infiltrates. Severe
disease is associated with weight loss and PLE,
with consequent hypoproteinaemia and ascites.
DIAGNOSIS
Intestinal biopsy is necessary for a definitive
diagnosis of IBD, although the clinical signs and
physical findings may be suggestive. Further, a
diagnosis of idiopathic IBD requires that all other
aetiologies be excluded, including infectious,
diet-responsive and antibacterial-responsive
conditions. Therefore, a complete diagnostic work-
up additionally involves preliminary laboratory
evaluation (haematology, serum biochemistry
and urinalysis, faecal analysis) and diagnostic
imaging (radiography and ultrasonography).
These tests eliminate the possibility of systemic
disorders, anatomic intestinal disease (e.g.
tumour, intussusception), extra-intestinal disease
(e.g. pancreatitis) and known causes of intestinal
inflammation. Further, by determining whether
focal or diffuse intestinal disease is present, the
most appropriate method of intestinal biopsy can
be chosen.
Faecal examination is most important in
eliminating other reasons for mucosal
inflammation, e.g. nematodes (e.g. Trichuris,
Uncinaria, Ancylostoma, Strongyloides), Giardia
2006 World Congress WSAVA/FECAVA/CSAVA
and bacterial infections (e.g. Salmonella or
Campylobacter, Clostridia).
Other tests. An assay for canine α1-protease
inhibitor has recently been developed and validated
for use on faecal extracts. In preliminary studies
it has proven to be a promising as a marker of
early intestinal protein loss. Therefore, increased
faecal α1-protease inhibitor concentrations would
be expected in dogs with IBD.
Serum concentrations of folate and cobalamin
are affected by intestinal absorption, and hence
proximal, distal or diffuse inflammation can
result in subnormal folate concentrations,
cobalamin concentrations, or both, respectively.
Although such alterations are not pathognomonic
for IBD, they may provide supportive evidence
and highlight the need for therapeutic
supplementation. Anecdotal evidence suggests
16
Back to contents
that such deficiencies can be a reason for failure
to respond optimally to immunosuppressive
therapy.
Intestinal biopsy. Intestinal biopsy is necessary to
document intestinal inflammation. Endoscopy is
the less invasive, but is limited by the fact that
samples are superficial and can only be collected
from the proximal SI in most cases. Alternatively,
full-thickness biopsies can be collected at
exploratory coeliotomy, and such samples are
superior for diagnosis. However, this technique is
more invasive and can be problematic if severe
hypoproteinaemia is present. Nevertheless,
exploratory coeliotomy is, perhaps, most suitable
for cats, given the tendency for multi-organ
involvement (e.g. concurrent intestinal, hepatic
and pancreatic inflammation).
Histopathological assessment of biopsy material
remains the gold standard for IBD diagnosis,
and the pattern of histopathological changes
depends upon the type of IBD present. However,
interpretation is subjective, and agreement
between pathologists is often poor. Further, it can be
difficult to differentiate severe IBD changes from
those of alimentary lymphoma. An international
working party is currently attempting to
standardize diagnostic criteria for IBD.
TREATMENT OF IBD
Treatment usually involves a combination
of dietary modification, antibacterials and
immunosuppressive therapy. Unfortunately,
objective information of efficacy is lacking
and most recommendations are based upon
individual experience. If possible, a staged
approach to therapy should be used. Initially,
anti-parasiticides (e.g. fenbendazole, Panacur @
50 mg/kg q24h for 3 days) should be administered
to eliminate the possibility of occult endoparasite
infestation such as Giardia intestinalis. Thereafter,
sequential treatment trials with an exclusion
diet and antibacterials are pursued, and
immunosuppressive medication is used only as a
last resort. If clinical signs are intermittent, the
owners should be instructed to keep a diary; this
will provide objective information as to whether
an improvement as actually occurred.
Dietary modification. The first therapeutic trial
usually involves the use of dietary modification.
Use of an exclusion diet trial will eliminate the
possibility of should an adverse food reaction,
although cases with idiopathic IBD may also
improve with dietary modification. This may
either be because a secondary dietary allergy
has developed, because other beneficial dietary
characteristics (improved digestibility, reduced
fat content, reduced fiber content, altered fatty
acid composition etc), or because of a change in

feeding pattern (e.g. smaller volume per meal,
increased frequency). An easily digestible diet
decreases intestinal antigenic load, and thus
decrease mucosal inflammation.
A variety of commercially available antigen-
limited diets are available which combine single
protein and carbohydrate sources. Recently,
hydrolyzed protein diets have also been
introduced, and initial experience of their use
is promising. Supplementation with oral folate
and parenteral cobalamin is indicated if serum
concentrations are subnormal.
Antibacterial therapy. Treatment with antimicrobials
can be justified in IBD, in part to treat secondary
SIBO, and partly due to the importance of bacterial
antigens in IBD pathogenesis. Ciprofloxacin and
metronidazole are most commonly used in human
IBD, but metronidazole is the preferred drug for
small animals. The efficacy of metronidazole may
not just be related to its antibacterial activity, since
there may be immunomodulatory effects on cell-
mediated immunity. Further, other antibacterials
such as tylosin may also have immunomodulatory
effects, and empirically this drug has proved useful
in many cases. In fact, a recent study in a rodent
model of intestinal inflammation has shown that
both metronidazole and tylosin are effective in
decreasing inflammation. Finally, cases of HUC
have recently been show to antibacterials such
as enrofloxacin, suggesting a possible infectious
agent underlies this condition. In fact, a recent
study has confirmed the presence of invasive E.
coli in HUC lesions.
Immunosuppressive drugs. If cases do not respond
adequately to dietary modification, with or without
antibacterials, immunosuppressive therapy is
indicated. In dogs and cats glucocorticoids are used
most frequently, and prednisone or prednisolone
are the drugs of first choice. In severe IBD,
prednisolone can be administered parenterally,
since oral absorption may be poor. Budesonide,
an enteric-coated, locally active steroid that is
destroyed 90% first-pass through the liver, has
been successful in maintaining remission in
human IBD with minimal hypothalamo-pituitary-
adrenal suppression. A preliminary study showed
apparent efficacy in dogs, but limited information
on the use of this drug is available.
In dogs azathioprine is commonly used in
combination with glucocorticoids, when initial
response is poor or steroid side effects are marked.
However, its activity may be delayed in onset
(up to 3 weeks) and, given its myelosuppressive
potential, regular haematological monitoring is
necessary. Azathioprine is not recommended for
cats and chlorambucil (2-6 mg/m2 PO q24h until
remission, then tapering) is a suitable alternative.
Other immunosuppressive drugs include
Back to contents
SOTAL
methotrexate and ciclosporin. Methotrexate is
effective in the treatment of human Crohn’s
disease, and a recent case report has suggested
efficacy in canine IBD. Ciclosporin has recently
been adopted by many as a treatment for
refractory IBD and a recent study has confirmed
its effectiveness in such cases. The main limitation
to its use is its cost.
Novel therapies for IBD. Novel therapies are
increasingly used for human IBD, attempting
to target more accurately the underlying
pathogenetic mechanisms. They include new
immunosuppressive drugs, monoclonal antibody
therapy, cytokines and transcription factors and
dietary manipulation. In the future such therapies
may be adopted for small animal IBD. Finally,
modulation of the enteric flora, with probiotics
or prebiotics, may have benefits in targeting the
pathogenesis of IBD.
PROGNOSIS AND PROGNOSTIC
INDICATORS
A recent study examining prognosis in canine IBD
has suggested that success of therapy is variable.
Although many cases reportedly respond only
a quarter achieve complete remission; a further
half still have intermittent signs, whilst response
is poor in the remaining cases and many are
euthanased.
In humans, activity indices are used to quantify
IBD disease severity, aiding the assessment of
the response to treatment and the prognosis. An
activity index has recently been suggested for
clinical signs of GI disease in dogs (the canine
IBD activity index; CIBDAI) and response to
treatment has been shown to correlate with
improvement in CIBDAI score. Its use in future
studies of canine IBD is recommended since
severity and response can be compared. In fact,
many of the most recent studies have incorporated
the scheme.
Other potential markers for IBD prognosis include
serum acute phase proteins, such as C-reactive 2006 World Congress WSAVA/FECAVA/CSAVA
protein, which has been shown to be increased in
canine IBD and decline upon successful therapy.
Mucosal pANCA expression has recently been
shown to be increased (prior to therapy) in cases
that ultimately respond to dietary management,
and expression of this marker increases post-
therapy in steroid-responsive cases. Finally, low
pre-treatment mucosal lymphocyte P-glycoprotein
expression has recently been shown to predict a
favourable response to therapy, suggesting that it.
REFERENCES
References are available on request.
17
SOTAL
STATE OF THE ART LECTURE
GROWTH HORMONE DISORDERS IN DOGS
Dr. Hans S. Kooistra,
Dipl ECVIM-CA
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
Yalelaan 108
3584 CM UTRECHT
THE NETHERLANDS
H.S.Kooistra@vet.uu.nl
INTRODUCTION
Pituitary growth hormone (GH) secretion is
pulsatile in nature. Pituitary GH secretion is
regulated predominantly by the opposing actions
of the stimulatory hypothalamic peptide GH-
releasing hormone (GHRH) and the inhibitory
hypothalamic peptide somatostatin. Each GH
secretory episode seems to be initiated by a burst
of GHRH into the hypophyseal portal system,
preceded by a reduction of somatostatinergic
input to the pituitary. This regulatory system is
influenced by negative feedback from peripherally
formed growth factors, particularly insulin-like
growth factor-1 (IGF-1). The amplitude and
frequency of GH secretory pulses are regulated
by a complex array of external and internal
stimuli including age, gender, estrous cycle
phase, genetic background, nutritional status,
disease status and body composition. In addition,
hormones such as progesterone, glucocorticoids
and thyroid hormones influence the pulsatile
secretion pattern of GH. GH release can also
be elicited by synthetic GH secretagogues, that
exert their effect on GH release by acting through
receptors different from those for GHRH. In
2006 World Congress WSAVA/FECAVA/CSAVA
1999, Kojima et al. characterized the endogenous
ligand for these receptors, i.e., ghrelin.1 The main
source of circulating ghrelin appears to be the
stomach. Also in the dog ghrelin stimulates GH
secretion.2
In the dog, GH is not only produced in the
pituitary gland but also in the mammary gland,
under the influence of endogenous or exogenous
progestins.3,4 These progestin-stimulated plasma
GH levels do not have a pulsatile secretion pattern,
are not sensitive to stimulation with GHRH or
the α-adrenergic agonist clonidine, and are not
inhibited by somatostatin. Mammary-derived GH
is biochemically identical to pituitary GH.
The pulsatile secretion pattern of GH also changes
during the luteal phase of healthy bitches, with
higher basal GH secretion and less GH secreted
in pulses during stages with a high plasma
18
Back to contents
progesterone concentration.5 It is likely that this
is caused by a partial suppression of pituitary GH
release by progesterone-induced GH production
in the mammary gland, indicating that progestin-
induced mammary GH production is not just
an aberration, but a normal physiological event
during the luteal phase of the estrous cycle in
healthy cyclic bitches. Ovariectomy of bitches
in the mid-luteal phase lowers basal plasma GH
levels and restores GH pulsatility.6
Changes in the release of other hormones may also
affect GH release. For example, canine primary
hypothyroidism is associated with elevated basal
GH release and less GH secreted in pulses.7
Pituitary-dependent hyperadrenocorticism in
dogs leads to a decrease in pulsatile GH release,
while basal GH release remains unaltered low.8
ACROMEGALY
The pathogenesis of acromegaly is completely
different in dogs compared with other species.
In middle-aged and elderly female dogs, either
endogenous progesterone (luteal phase of the
estrous cycle) or exogenous progestins (used
for estrus prevention) may give rise to GH
hypersecretion of mammary origin. GH excess
due to a pituitary tumor is extremely rare in
dogs.
Signs and symptoms of GH hypersecretion tend
to develop slowly and are characterized initially
(particularly in the dog) by soft tissue swelling of
the face and the abdomen. In some acromegalic
dogs severe hypertrophy of soft tissues of the
mouth, tongue, and pharynx causes snoring and
even dyspnea. Usually the dogs are also presented
with polyuria (and sometimes polyphagia).
The polyuria is usually without glucosuria, but
manifest diabetes mellitus can develop due to
insulin resistance. Physical examination may
reveal thick skin folds, especially in the neck,
and prognathism and wide interdental spaces.
Prolonged GH excess also leads to generalized
visceromegaly resulting in abdominal enlargement.

The diagnosis of GH excess can generally be
established by measuring basal plasma GH
levels. The basal plasma GH level in acromegalic
animals often exceeds the upper limit of the
reference range. However, if the disease is mild
or just beginning, the basal plasma GH levels
may be only slightly elevated. Conversely, a high
value may be the result of a secretory pulse in
a normal subject. Nonresponsiveness of normal
or elevated GH levels to stimulation may further
support the diagnosis.
Measurement of elevated plasma IGF-I levels
may also contribute to the diagnosis. Being
bound largely to proteins, the IGF-I level is much
less subject to fluctuation than is GH. However,
there is some overlap in plasma IGF-I levels
between healthy animals and individuals with
acromegaly.
Canine acromegaly can be treated easily
and effectively by withdrawal of exogenous
progestagens and/or ovario(hyster)ectomy. The
animal may then change dramatically, owing
to the reversal of the soft tissue changes. In
cases in which the GH excess did not lead to
complete exhaustion of the pancreatic beta cells,
the elimination of the progesterone source may
prevent persistent diabetes mellitus. Progesterone-
receptor blockers may also be useful.
PITUITARY DWARFISM OR CONGENITAL
GH DEFICIENCY
Congenital growth hormone deficiency is
primarily known to occur in German shepherd
dogs as an autosomal recessive inherited
condition,9 which is characterized by profound
dwarfism with retention of puppy hairs and lack of
primary guard hairs. Basal plasma concentrations
of GH and IGF-I, prolactin, thyrotropin, and
luteinizing hormone are low. In a combined
anterior pituitary function test, employing four
releasing hormones, there is very consistently no
response of GH, TSH, and prolactin, while there
is a minor response of LH and FSH. The response
of ACTH is not impaired.10
Pituitary dwarfs are usually presented to the
veterinarian at the age of 2-5 months because
of proportionate growth retardation and an
abnormally soft and woolly hair coat. The latter
is due to retention of secondary hairs and lack
of guard hairs. The hairs are easily epilated and
there is gradual development of truncal alopecia,
beginning at the points of wear and sparing the
head and the extremities. The skin becomes
progressively hyperpigmented and scaly.
Secondary bacterial infections of the skin are
quite common.
There does not appear to be a gender predilection
for pituitary dwarfism. In male dwarfs unilateral
Back to contents
SOTAL
or bilateral cryptorchidism is a common finding,
whereas in female dwarfs persistent oestrus is
quite common. Persistent oestrus in these female
dwarfs is characterized by swelling of the vulva,
attractiveness to male dogs, and bloody vaginal
discharge of more than four weeks duration.
The plasma progesterone concentration in these
bitches remains low, often below 3 nmol/l,
indicating that ovulation does not occur. Physical
examination may also reveal a continuous heart
murmer due to a patent ductus arteriosus.10
Initially, pituitary dwarfs are usually lively and
alert. With time the animals develop inappetence
and become less active. This situation is usually
reached at the age of two or three years and has
been ascribed to secondary hypothyroidism and
impaired renal function.
Routine laboratory examination usually does
not reveal abnormalities, except for an elevated
plasma creatinine concentration. Because
pituitary dwarfism is often the result of combined
pituitary hormone deficiency, in most pituitary
dwarfs there is also secondary hypothyroidism.
Plasma IGF-I concentrations are low in pituitary
dwarfs, even when age and body size are taken
into account. Nevertheless, IGF-I measurements
do not provide such a definitive diagnosis as
do the measurements of GH before and after
stimulation.
Since basal plasma GH values may also be
low in healthy animals, the definitive diagnosis
GH deficiency is based upon the results of a
stimulation test. For this purpose GHRH or
ghrelin (1-2 µg/kg bodyweight) or a-adrenergic
drugs, such as clonidine (10 µg/kg bodyweight)
or xylazine (100 µg/kg bodyweight), can be
used. The plasma GH concentration should be
determined at least immediately before and 20-
30 minutes after intravenous administration of
the stimulant. In the normal dog, plasma GH
concentrations should increase at least two- to 2006 World Congress WSAVA/FECAVA/CSAVA
four-fold after administration of the stimulant. In
dogs with pituitary dwarfism there is no significant
rise in circulating GH levels. Administration of
xylazine or clonidine may give rise to sedation,
bradycardia, hypotension, and vomiting.
Porcine growth hormone, which is identical to
canine growth hormone,11 can be used for treatment
in subcutaneous doses of thrice weekly 0.1 – 0.3
IU per kg body weight. Use of heterologous
GH such as bovine and human GH cannot be
recommended because of the development of
antibodies.12 Treatment with porcine GH may
result in GH excess and consequently side effects
such as diabetes mellitus may develop. Monitoring
of the plasma concentrations of GH, IGF-I
and glucose is therefore of utmost importance.
Subsequent treatment with heterologous GH
19
SOTAL
(dosage and interval) after this induction
period should also depend on measurements
of the plasma concentrations of GH and IGF-I.
Treatment often does not result in a significant
increase in body size, because the growth plates
in most dwarfs have already closed or are about
to close at the time GH treatment is initiated.
The hairs that grow back is mainly primary hair;
growth of guard hairs is variable.
The demonstration of the ability of progestagens
to induce the expression of the GH gene in the
canine mammary gland and the subsequent
secretion of this GH into the systemic circulation
has raised the possibility of treatment of dogs
with congenital GH deficiency with progestagens.
Treatment of young German shepherd dwarfs with
subcutaneous injections of medroxyprogesterone
acetate in doses of 2.5-5.0 mg per kg body weight,
initially at 3-week intervals and subsequently at
6-week intervals, has resulted in some increase
in body size and the development of a complete
adult hair coat. Parallel with the physical
improvements, plasma IGF-I concentrations
rose sharply, whereas plasma GH concentrations
did rise but never exceeded the upper limit of
the reference range.13 Treatment of dogs with
congenital GH deficiency with progestagens
may give rise to several side effects, such as
recurrent periods of pruritic pyoderma, skeletal
maldevelopment, development of mammary
tumours, acromegaly, diabetes mellitus and cystic
endometrial hyperplasia. As with the treatment
using porcine GH, monitoring of the plasma
concentrations of GH, and especially, IGF-I and
glucose are important to prevent side effects.
Bitches should be ovariohysterectomized before
2006 World Congress WSAVA/FECAVA/CSAVA
20
Back to contents
the start of the progestagen treatment. Despite
the possible side-effects, long-term treatment
with progestagens can be used as an alternative
for porcine GH in the treatment of dogs with
congenital GH deficiency. Thyroid hormone
replacement should be started as soon is there is
evidence of secondary hypothyroidism.
REFERENCES
1. Kojima M, et al. Nature 1999;402:656.
2. Bhatti SFM, et al. Mol Cell Endocrinol
2002;197:97.
3. Selman PJ, et al. Endocrinology
1994;134:287.
4. Mol JA, et al. J Clin Invest 1995;95:2028.
5. Kooistra HS, et al. J Reprod Fertil
2000;119:217.
6. Lee WM, et al. Thesis Lee WM, Utrecht
University, 2004:59.
7. Lee WM, et al. J Endocr 2001;168:59.
8. Lee WM, et al. Domest Anim Endocrinol
2003;24:59.
9. Andresen E and Willeberg P. Nord Vet Med
1976;28:481.
10. Kooistra HS, et al. Domest Anim Endocrinol
2000;19:177.
11. Ascacio-Martinez JA and Barrera Saldana
HA. Gene 1994;143:277.
12. Van Herpen H et al. Veterinary Record
1994;134:171.
13. Kooistra HS, et al. Domest Anim Endocrinol
1998;15:93.

STATE OF THE ART LECTURE
HOW TO LOOK AT RADIOGRAPHS
Christopher R. Lamb MA,
VetMB, DipACVR,
DipECVDI, ILTM, MRCVS
Department of Veterinary Clinical
Science
The Royal Veterinary College,
Hawkshead Lane,
North Mymms,
Herts AL9 7TA
U.K.
clamb@rvc.ac.uk
In an ideal world, the results of diagnostic tests
would always be true. Ideal diagnostic tests
would always give a positive result in patients
with the disease, and would always be negative
in unaffected patients. Unfortunately, the practice
of medicine is not perfect and false test results are
encountered frequently.
Test result
Subjects + -
diseased TP FN
healthy FP TN
Diagnostic imaging is not immune from the
problem of imperfect results!
•false negative results may occur when a lesion
is not visualized because it is small or in an
inaccessible anatomic location
•false positive results may occur if a normal
structure is misinterpreted as abnormal or if a
measurement of a normal organ is outside the
reference range.
Avoiding radiographic errors
False negative
•Make good quality radiographs
•Include all relevant anatomy
•Search the film carefully
False positive
•Make good quality radiographs
•Know normal anatomical variations
Once good quality radiographs have been made,
they must be searched carefully for signs of
disease. How to look at a radiograph is not as
obvious as you might think. They are major
differences of opinion between radiologists
about how to search films for abnormalities. Two
methods are described:
Back to contents
SOTAL
•directed search pattern, i.e. look at the various
structures on the radiographs according to a
preconceived sequence in an attempt to avoid
concentrating on a central or obvious abnormality
at the expense of peripheral or unexpected lesions.
Periphery first is a common search pattern.
•hypothesis-driven search, i.e. form a hypothesis
about possible diagnosis from the history or from
the initial observation of a suspected abnormality,
then use this to guide further examination of the
radiograph.
It is common practice to teach undergraduates and
radiology residents to use a directed search pattern
for examining radiographs despite evidence
that higher performing students and expert
diagnosticians search radiographs according to
hypotheses they generate about the patient rather
than using a directed search pattern.
This approach reflects the fact that clinical
radiographs must always be considered in the
context of a specific patient. There are assessments
that present candidates with radiographs without
any accompanying patient information or history, 2006 World Congress WSAVA/FECAVA/CSAVA
but this is an artificial situation. In practice, I
suggest that we should always know why we
have made radiographs, hence the history is very
important. Without the history it is not possible to
answer these key questions:
•what is the aim of this study?
•is the study adequate?
•what is the prior probability (prevalence) of
disease?
- does the history suggest a diagnosis?
- affects vigilance
- helps interpret a negative result
Even though the history may be incomplete, there
is usually some information available that prompts
examination of specific parts of the film. With
increasing experience, we become more familiar
21
SOTAL
with the usual location and appearance of all the
common veterinary conditions, which means we
are more likely to check specific locations on the
film, chosen because of our suspicions about that
patient, rather than use a traditional “periphery
first” directed search pattern. Even if there is no
history, our initial observation of the film may
reveal a sign that we analyse first and then use
to prompt examination of the other parts of the
film. There is abundant evidence that experienced
radiologists begin to form hypotheses almost
immediately they start the information-gathering
process, and these hypotheses influence the
direction of further searches for information.
To take a simple example: the first observation
made by an experienced radiologist when
examining thoracic radiographs of a cat with
a history of regurgitation might be a thick soft
tissue band on the dorsal aspect of the tracheal
lumen, i.e. a tracheal stripe sign, which occurs
because of air in the oesophagus. This finding
will rapidly prompt a search of specific areas of
the film for other signs of oesophageal dilatation,
oesophageal foreign material, hiatus hernia, and
then signs of aspiration pneumonia, a common
sequel to regurgitation. The expert may go further,
looking for evidence of a mediastinal mass that
might be present if thymoma and concurrent
myasthenia gravis are the conditions underlying
a megaoesophagus. All this is done in the time it
takes a novice following a directed search pattern
to examine the ribs.
A recent study at The RVC compared the
performance in a film-reading quiz of students
taught a directed search pattern and students
encouraged to use a hypothesis-driven search.
There was a trend suggesting a better performance
by students taught a hypothesis-driven search, and
students taught a hypothesis-driven search were
less likely to record a false positive observation
2006 World Congress WSAVA/FECAVA/CSAVA
than students taught a directed search.
These results are compatible with the results of
an earlier study of chiropractic students, which
concluded that those who are most skilled at film
reading examination:
•are better able to identify key radiographic signs
•are better able to recognise the relationship
between multiple abnormalities
22
Back to contents
•think of possible diagnoses early in their
examination of the films
•make a complete examination of the film.
It is known that medical students taught a highly
structured, step-wise approach to examining
radiographs performed no better than students
who did not receive such coaching. So why does
the directed search pattern persist? The rationale
that underpins the directed search is based
largely on the assumption that it maximises the
completeness of scrutiny of the radiograph while
minimising the potential to miss an unsuspected
or subtle abnormality in a patient with an obvious
abnormality - the error known as satisfaction of
search.
Satisfaction of search occurs because obvious
abnormalities capture visual attention and
decrease vigilance for more subtle abnormalities,
which may be fixated but are not recognised,
either because of decreased search time or other
mechanisms. It is not clear that use of a directed
search pattern reduces satisfaction of search. In
a study in which radiologists were interviewed
during film interpretation, satisfaction of
search was reduced, possibly because the act
of describing their focus of attention may have
prompted observers to inspect the radiographs
in a more deliberate, systematic way; however,
there is also evidence that it is difficult to perform
a directed search: studies of eye movements in
radiologists trained to use a directed search found
that most used a free search, including those who
believed they were following a directed search.
Many radiologists scan the entire radiograph
with short excursions to examine in more detail
regions that they suspect might be abnormal.
This is precisely the approach that the classic
description of a directed search advises against.
It is my belief that a hypothesis-based search
pattern is more efficient, more accurate and
easier to learn that a directed search. Students
of radiology should consider adopting it and
teachers (and examiners) should be tolerant of
this approach.
There will always be radiographic abnormalities that
defy diagnosis because they are unexpected and/or
subtle. All we can do is try to remain vigilant.

STATE OF THE ART LECTURES
THERAPY OF CONGESTIVE HEART FAILURE IN DOGS WITH
INODILATORS
Christophe W. Lombard,
Prof. DACVIM (Cardiology),
DECVIM-CA
Dept. of clinical veterinary
medicine
Vetsuisse Faculty, University of
Berne
Länggass-Strasse 124, PO Box
CH-1201 Bern/Switzerland
christophe.lombard@kkh.unibe.ch
The recent two decades have seen revolutionary
changes in the concept of treating congestive
heart failure in man and animals. The recognition
of overshooting neuroendocrine mechanisms,
in particular excessive activation of the renin-
angiotensin-aldosterone system (RAAS) with
increased angiotensin-II levels elevating afterload
and stimulating excessive myocardial hypertrophy
(cardiac remodelling), is now well established,
Increased afterload damages an already failing
heart even further. Inhibitors of the angiotensin-
converting enzyme (ACE-inhibitors) have been
developed to counteract these adaptations and
have proven their efficacy for treating congestive
heart failure in man and in dogs. They have
also demonstrated efficacy in combination
with digoxin and diuretics. Additionally, ACE-
inhibitors have shown to prolong survival in man,
and in dogs with endocardiosis with mitral and/
or tricuspid insufficiency compared to placebo-
controls on conventional therapy. Efficacy- and
improved survival data have been published for
enalapril (the COVE trial 1995, the LIVE trial
1998) and for benazepril (the BENCH trial 1999).
Increasing contractile function of the failing heart
in cardiomyopathy continues to be a goal for
therapeutic intervention (Endoh 2001). Attention
has focused on drugs using other than direct
stimulation via adrenergic receptors and the
adenylate cyclase pathway. Phosphodiesterase
III-inhibitors such as milrinone are potent
positive inotropes, but their regrettable side
effect of increasing mortality in humans through
arrhythmogenesis (the “PROMISE” trial, Packer
et al 1991) prevented their successful registration
and release for treatment.
The recent development of inodilator drugs
has addressed this problem in an elegant and
successful way. These substances utilise a new
Back to contents
SOTAL
mode of action, the sensitisation of cardiac
troponin C to calcium, to improve contractility.
Such compounds are referred to as “Calcium
– Sensitizers” and have been described to have
a positive impact on myocardial energetics
(Hasenfuss et al 1989, Remme et al 1994). The
ideal positive inotropic drug should have some
negative chronotropic effects, should be mediated
by other than increases in calcium transients,
and should decelerate cross-bridge kinetics
(Holubarsch 1997). Mixtures of the d- and l-
isomers of Pimobendan were shown to cause
stereospecific increases of the calcium sensitivity
of cardiac myofilaments, specifically at the
regulatory calcium binding sites of troponin C
(Solaro et al 1989), besides having vasodilatatory
properties mediated by the phosphodiesterase III-
effects on vascular smooth muscle. The inodilator
drug Pimobendan has been used successfully
for the treatment of heart failure in humans in
Japan (Kato, 1997). A recent study revealed
significantly less adverse cardiac events, defined 2006 World Congress WSAVA/FECAVA/CSAVA
as death or hospitalisation due to heart failure,
in human patients under Pimobendan therapy
(EPOCH Study Group, 2002). Clinical studies
performed in dogs revealed an efficacy at doses
between 0.2 to 0.6 mg/kg/day (Kleemann and
others 1998a), as well as clearly superior clinical
benefits over digoxin (Kleemann et al 1998b,
Poulsen Nautrup et al 1998). In these studies,
dogs with chronic valvular disease (endocardiosis
with mitral and/or tricuspid regurgitation) as
well as dilated cardiomyopathy in advanced
stages of heart failure were included. They
improved their clinical condition under therapy.
Furthermore, Pimobendan was shown to clearly
and highly significantly prolong the survival time
in a small number of Dobermans with dilated
cardiomyopathy, increasing the median survival
23
SOTAL
time from 50 days to 329 days (Luis Fuentes et
al 2002).
We are going to review the major blinded,
placebo-controlled multicenter studies of the last
few years that have investigated the efficacy of
Pimobendan for the treatment of congestive heart
failure in dogs. Some of the above-mentioned
investigations and data led to the licensing of
Pimobendan for the therapy of canine CHF in
the majority of European countries over last few
years, an achievement that no other veterinary
drug can claim so far.
The PiTCH-Study is a multicenter randomised
positive-controlled study that was conceived
in the late 90ies and tested the concept that
dogs in congestive heart failure due to mitral
regurgitation or dilated cardiomyopathy could
be treated with either Pimobendan, Benazepril or
both drugs together with the additional diuretic
Furosemide where needed due to pulmonary
congestion. 105 Dogs with moderately to severe
CHF were included and blindly randomised to
one of the 3 treatment groups. The initial efficacy
study period over 28 days revealed a significantly
higher drop-out rate of 34% for the Benazepril
group vs. 11% for the Pimobendan group and 9%
for the combination group. On a clinical scoring
system based on signs such as dyspnea/cough,
nocturnal restlessness, appetite, general activity
etc. both groups with Pimobendan outperformed
the Benazepril group. The combination of
Pimobendan with Benazepril did not provide
significant better results than Pimobendan alone.
A voluntary longevity study followed, during
which the dogs could receive, upon request of
the owner when their dogs deteriorated, the drug
that they hadn’t gotten before as an addition to
their therapy. The survival time was determined
until such addition of drug or death or euthanasia
occurred and compared Benazepril-treated
2006 World Congress WSAVA/FECAVA/CSAVA
dogs against dogs receiving Pimobendan alone
or both drugs. A significantly longer survival
time resulted for the dogs on Pimobendan. This
study contained several weaknesses, namely an
(unnecessary) combination-TX group and an
unfortunately small number of dogs with mitral
regurgitation that lead to small group numbers
preventing meaningful statistical evaluation and
power of the study.
The Vetscope study is a multicenter doubleblinded
trial which sought to compare the advantages of
Pimobendan against Benazepril in dogs with
moderately to severe congestive heart failure
(ISACHC-classes 2 and 3) due to valvular
disease/mitral regurgitation. A total of 76 dogs
were enrolled. The study parameters and the set-
up were similar to the PiTCH-study. Furosemide
was allowed and used equally (ca. 2/3 of the
cases) in both treatment groups.
24
Back to contents
Overall efficacy was rated as very good or good
in 85% of the Pimobendan cases versus 41% of
the Benazepril cases (P<0.0001). In the 56-Day
study period, 2 dogs in the Pimobendan group
and 7 in the Benazepril group died or were
euthanised due to cardiac reasons. The group
mean of radiographically determined heart size
diminished in the Pimobendan group, while it
increased slightly in the Benazepril group (p =
0.0329). Survival analysis according to Kaplan-
Meier for the 56-day period revealed significant
differences in favour of Pimobendan (P=0.0386).
Median survival time for Pimobendan treated
dogs was 430 days versus 228 days for dogs
receiving no Pimobendan. Again, survival
analysis according to Kaplan-Meier revealed
significant differences in favour of pimobendan
(P=0.002). The complete study report will appear
in the Journal of the American Animal Hospital
Association in the summer of this year 2006.
Another study by Smith et al 2005 evaluated 43
dogs suffering from mitral regurgitation and mild
to moderately severe congestive heart failure in
a prospective randomised, single-blind parallel-
group trial against Ramipril over a study period
of 6 months. All dogs received variable dosages
of Furosemide. Study endpoints were were
completion of the entire study period, and the
need for hospitalisation and therapy adjustment
in case of worsening. Pimobendan treated
dogs completed the study in higher numbers
(68%) than Ramipril-treated dogs (43%), and
Pimobendan-treated dogs also had a significantly
lower adverse HF-outcome (18%) than Ramipril-
treated dogs (48%, p= 0.046 calculated as an odds
ratio). Tolerance, i.e. drug-related sideeffects, of
Pimobendan was low and comparable to Ramipril,
as it had been in comparison to Benazepril in the
studies above.
All 3 studies did not reveal any tendency to
increased tachyarrhythmias or heart rate elevation,
although ECGs had only been measured over max.
5 minutes, rather than by Holter electrocardio-
graphy for convincing proof of the absence of
arrhythmogenesis of this drug.
General remarks and conclusions
The new inodilator or calcium-sensitiser drug
Pimobendan has shown convincing evidence of
good tolerability, safety and clinical efficacy in
randomised, blinded multicenter clinical trials; it
proved statistically superior to the ACE-inhibitors
Benazepril and Ramipril when analysing clinical
parameters, and prolonged survival significantly.
The drug showed these desired effects in both of
the most common canine cardiac diseases dilated
cardiomyopathy and mitral regurgitation due to
chronic valvular disease, in moderate to severe

stages of congestive heart failure. It appears
therefore that this new drug represents a new
pillar in the heart failure therapy of dogs. What
remains to be tested are its safety and efficacy
when applied in less severe stages of heart failure,
convincing evidence of non-arrhythmogenesis,
and elucidation of its influence on pathologic
remodelling of the heart during these diseases.
References
Pouchelon, Jean-Louis for the BENCH group
(1999): The effects of Benazepril on survival
times and clinical signs of dogs with congestive
heart failure: Results of a multicenter, prospective,
randomized, double-blinded, placebo-controlled,
long-term clinical trial. J Vet Cardiol 1: 7-18
The COVE study group (1995): Controlled
clinical evaluation of Enalapril in dogs with
heart failure: results of the cooperative veterinary
Enalapril study group. J Vet Intern Med 9: 243-
252
The EPOCH Study Group (2002): Effects of
pimobendan on adverse cardiac events and
physical activities in patients with mild to
moderate chronic heart failure. Circulation 66;
(2): 149-157
Endoh M (2001): Mechanism of action of Ca2+
sensitizers--update 2001. Cardiovasc Drugs Ther.
15;(5):397-403
Fujino K, Sperelakis N, Solaro RJ. Sensitization
of dog and guinea pig heart myofilaments to Ca2+
activation and the inotropic effect of pimobendan:
comparision with milrinone. Circ Res 1988; 63:
911-922.
Holubarsch C (1997): New inotropic concepts:
Rationale for and differences between calcium
sensitizers and phosphodiesterase inhibitors.
Cardiology 88 (suppl 2): 12-20
Kato K (1997): Clinical efficacy and safety
of Pimobendan in treatment of heart failure
– Experience in Japan. Cardiology 88 (suppl 2):
28-36
Back to contents
SOTAL
Kleemann R, Le Bobinnec G, Bruyère D, Baatz
G, Justus C, Schmidt H (1998a): Clinical efficacy
of the novel inodilator pimobendan in dogs
suffering from congestive heart failure. Proc. 41st
BSAVA Cong.Birmingham, 274
Kleemann R, LeBobinnec G, Bruyère D, Justus C,
Schmidt H (1998b): Clinical efficacy of the new
inodilator pimobendan, in comparison to digoxin
for the treatment of congestive heart failure in
dogs. Proc. 4th FECAVA SCIVAC Congress,
Bologna, 513
The LIVE study group (1998): Effects of enalapril
maleate on survival of dogs with naturally
acquired heart failure. JAVMA 213: 1573-1577
Luis-Fuentes V, Corcoran B, French A, Schober
KE, Kleemann R, Justus C (2002): A double-
blind, randomised, placebo-controlled study of
pimobendan in dogs with dilated cardiomyopathy.
J Vet Intern Med 16 (3), 255-261
Packer M, Carver JR, Rodeheffer RJ and others
(1991): Effect of oral Milrinone on mortality in
severe chronic heart failure. N Engl J Med 325:
1468-1475
Poulsen Nautrup, Barbara, Justus, Claus,
Kleemann, Rainer (1998): Pimobendan – a new
positive inotropic and vasodilatatory substance
for the treatment of canine congestive heart
failure, in comparison with digoxin (in German)
Kleintierpraxis 43: 509-526
Smith PJ, French AT, van Israel N et al 2005:
Efficacy and safety of Pimobendan in canine
heart failure caused by myxomatous mitral valve
disease. J sm An Pract 46; 121-130
Solaro RJ, Fujino K, Sperelakis N (1989): The
positive inotropic effect of pimobendan involves
stereospecific increases in the calcium sensitivity
of cardiac myofilaments. J cardiovasc pharm 14
(suppl 2): S27-S12
2006 World Congress WSAVA/FECAVA/CSAVA
25
 2006 World Congress WSAVA/FECAVA/CSAVA

26
SOTAL

Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

INVIT INVITED
LECTURE LECTURES -
FULL PAPERS

FULL PA
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

INVIT INVITED
LECTURE LECTURES -
FULL PAPERS

FULL PA
TED
S
APERS
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

AA of Care
Standards
andar
(How I Treat)

INVITED LECTURES - FULL PAPERS
A - Standards of Care (How I Treat)
CANINE GENERALIZED DEMODICOSIS
Didier-Noël CARLOTTI,
Dip ECVD
Aquivet clinique vétérinaire
F-33320 Bordeaux-Eysines
France (EU)
dncvetderm@aol.com
Generalized demodicosis and other forms of
demodicosis requiring therapy
Once the diagnosis of generalized demodicosis is
made, treatment is mandatory both in the juvenile
and the adult form. Arbitrarily, generalized
demodicosis is clinically characterized by the
involvement of either many (at least five) distinct
areas or one/several large and diffuse areas.
Otodemodecosis and above all pododemodicosis
(usually multiple) are also considered severe and
must be treated as a generalized form. Without
treatment, bacterial cellulitis, which may be fatal,
is likely to occur in generalized demodicosis and
pododemodicosis
Clipping and cleansing of the lesions are essential
at the beginning of the treatment. Benzoyl
peroxide shampoos are particularly recommended
for their follicular flushing effect.
Amitraz applied topically (concentration: 0.025%)
was the first effective topical treatment. Due
to insufficient activity and potential secondary
effects in both the patient and the person applying
the product we no longer use amitraz and prefer
systemic macrocyclic lactones.
Milbemycin oxime was the first product
administered orally and used to treat generalized
demodicosis. It is very effective if the dose is at
least 1 mg kg-1 per day (ideally close to 2 mg
kg-1). It is licensed in some countries for this
use. The rate of clinical and parasitological cure
is 60 to 96% but there are 10 to 75% of relapses,
particularly at the lowest dosage. We use it but
its current price makes it unacceptable for many
owners.
Ivermectin is used at the daily dose of 400 to
600 μg kg-1 of the injectable form administered
orally. In predisposed breeds in which there is a
frequent mutation of the gene mdr 1 (multiple drug
resistance1) such as Collies, Shetland Sheepdogs,
Back to contents
A
Border Collies, and Old English Sheep Dogs, a
potentially fatal idiosyncrasic reaction is possible
and the product should not be used.
Moxidectin is our drug of choice at the moment.
We use the injectable form which we give orally
at the dose of 400 μg kg-1 daily. Tolerance is good
and efficacy seems to be as good as milbemycin
oxime if not better: 96% of the patients are
cured in 2 to 6 months with a negative parasite
evaluation in 2 to 7 months. The recently launched
2.5% spot-on has been relatively ineffective in
our hands so far despite its license for generalized
demodicosis.
The follow–up of the patients is essential. The
treatment should be continued until multiple
scrapings are negative, twice one month apart.
These must be done in the same body locations
(at least five) every month. This procedure is
time-consuming; it must be explained to the
owner. A control should be done 3 and 12 months
after cessation of therapy. Obviously, antibiotic
treatment of the associated deep pyoderma is
essential. It should be continued beyond its 2006 World Congress WSAVA/FECAVA/CSAVA
clinical cure and as long as the scrapings show
numerous mites. Glucocorticoid therapy, even
topically (e.g. auricular formulations) is absolutely
contraindicated in generalized demodicosis. In
the adult-onset form of the disease, an underlying
cause, such as Cushing’s disease, must be treated
appropriately.
In conclusion, generalized demodicosis is difficult
to treat but its cure is achievable with the help
of systemic macrocyclic lactones. A thorough
follow-up is mandatory.
References can be provided upon request.
31
A
A - Standards of Care (How I Treat)
FLEA ALLERGY DERMATITIS
Peter J. Ihrke, VMD,
Diplomate ACVD
Professor of Dermatology, Chief
- Dermatology Service, VMTH
Department of Medicine &
Epidemiology
School of Veterinary Medicine
University of Kalifornia
One Shields Avenue
Davis, California 95616-8737,
U.S.A.
A. Introduction
1. Flea allergy dermatitis is not only the most
common skin disease seen in general small animal
practice in most countries in the world; it most
likely is the most common disease of any organ
system seen in small animal practice worldwide.
2. Somewhat surprisingly, flea allergy dermatitis
still is seen relatively commonly in University
dermatology clinics and dermatology specialty
practice worldwide. This occurs despite modern
advances in flea control plus the fact that most
small animal clinicians are quite cognizant of flea
allergy dermatitis and routinely manage dogs and
cats with flea allergy dermatitis.
3. Self-referral by the owner (second opinion)
or veterinary referral of dogs and cats with flea
allergy dermatitis occurs for multiple reasons.
4. Surprisingly, when you suspect flea allergy,
your most important task is convincing the owner
that you are making the correct diagnosis.
B. Reasons Flea Allergy Dermatitis is seen in
Dermatology Specialty Practice
1. Owner disbelief that flea allergy is the correct
diagnosis.
2006 World Congress WSAVA/FECAVA/CSAVA
2. Owner skepticism that flea allergy is the correct
diagnosis based on management failure.
3. Veterinary practitioner skepticism that flea
allergy is the correct diagnosis based on perceived
management failure or lack of visualization of
fleas.
C. Owner Disbelief in the Diagnosis of FAD
1. Failures in the management of flea allergy
dermatitis correlate strongly with owner disbelief
that fleas are the underlying problem. (“My
veterinarian believes that the problem is due to
fleas but I know that it is not!”)
2. Reasons for disbelief
a. Fleas not seen by owner
b. Cultural biases against having ectoparasites
32
Back to contents
– “It is not acceptable for me to have
ectoparasites! - Therefore it is not acceptable
for my dog to have ectoparasites!”
c. “How can fleas cause this much trouble?
d. “All dogs have fleas.”
D. Owner or Veterinary Skepticism Based on Past
Management Failure
1. Owner - “I am already doing everything that I
can to kill fleas!”
2. We are already using the latest “wonder
drugs”.
E. Reasons for Flea Allergy Dermatitis Treatment
Failure
1. Failure to treat all in-contact animals (The
squeaky wheel gets the oil...) In-and-out cats are a
frequent cause of treatment failure in households
with multiple animals. Consider regular animal
visitors that are not receiving flea control.
2. Failure to maintain consistency in treatment
3. Failure to deal with environmental issues in
severe cases
4. Substitution of prescription spot-ons with less
expensive, but less effective and less safe spot-on
products from pet stores
F. Clinical Features of FAD that may be useful in
convincing the owner
1. Pruritus predominantly localized to the caudal
one-half of the dog
2. Characteristic distribution pattern - Partially
bilaterally symmetric pattern, involve the dorsal
lumbosacral region, tail-base, perineum, medial,
caudal thighs
3. Crusted papules in the umbilical fold -
(especially in male dogs), an under-appreciated
clinical marker for flea allergy dermatitis
4. Lesions - Crusted papules, secondary lesions
associated with chronicity

5. Fibropruritic nodules - Highly characteristic
clinical marker of flea allergy dermatitis in
susceptible dogs
G. Techniques for Convincing Owners that Flea
Allergy Dermatitis is the appropriate diagnosis -
(“Backing into” the diagnosis as FAD)
1. How a diagnosis is made - (Lesions, distribution
pattern, frequency of occurrence, ruling out other
diseases)
2. Defining allergy - (Atopic dermatitis, food
allergy, flea allergy)
3. Flea allergy - (Flea saliva, at least 4 different
types of allergic reaction, severity of the allergic
response - “Your dog is special…”)
4. Drawing an imaginary line around the middle
of a dog - (Does your dog itch more in front of
or behind this line? Flea allergy dermatitis is
the only known canine pruritic skin disease seen
consistently with a markedly caudal distribution
pattern)
5. Diffusing hostility (cultural biases) - “Fleas are
a way of life in _____ ., “My own dogs get fleas
if I don’t practice flea control consistently.”
6. Owner alternatives - Expensive additional
testing or trying 6 weeks of concerted flea control
based on our recommendations.
7. Final gambit – Not, “Trust me.” Instead -
“Prove me wrong”!
H. Modern Flea Control
1. New, considerably less toxic prescription
products that also are much easier to use are
available that kill adult fleas and disrupt the flea
life-cycle. Most insecticides can effectively kill
fleas; preventing reinfestation is the problem.
Insuring long-term pet owner compliance
is required for on-going flea control. The
comparatively recent development of both
insecticides and insect growth regulators with
novel and convenient dosage forms (such as
spot-ons, collars, and oral products) coupled
with prolonged residual activity has dramatically
improved pet owner compliance and hence
prevented reinfestations. Although insecticidal
resistance most often is suspected when flea
control measures have failed, lack of control
more often results from lack of understanding of
flea biology, poor application technique, and too
infrequent reapplication of the products.
2. The goals of flea control should be elimination
of existing fleas on affected animals, continued
elimination of fleas acquired from infested
premises, and the prevention of reinfestation. In
order to accomplish these goals, an integrated
flea control plan must be instituted. Effective
Back to contents
A
residual adulticides must be used to kill fleas plus
provide residual killing activity and insect growth
regulators must be use to used to disrupt flea
reproduction. In addition, mechanical control
procedures such as cleaning pet’s blankets, beds,
pet carriers, and throw rugs and vacuuming or
removing furniture that can house pre-adult fleas
must be instituted. Preventions of pests that can
carry fleas (rats, opossums, squirrels, raccoons,
skunks, feral cats) from entering crawl spaces,
foundation vents, porches and garages also is
important.
I. Modern Flea Control Products
1. New spot-on prescription products are
excellent products with superior efficacy, safety,
and residual activity. These products need
to be applied directly to the skin, not to the
haircoat. Our very strong clinical impression at
UC Davis is that dogs and cats with severe flea
hypersensitivity experience much better efficacy
with these products applied every 3 weeks instead
of monthly. Our clinical impression remains that
either bathing or swimming degrades the efficacy
of all of these products. Over-the-counter (OTC)
competing products commonly are advertised
as ‘just as good as what you can get from your
veterinarian’ but ‘less expensive’. In general,
these products contain concentrated permethrin
or other synthetic pyrethroids. All indications are
that these OTC products do not have either the
efficacy, residual activity, or the safety profile of
the spot-on prescription products
2. Imidacloprid (Advantage®, Bayer)
a. Advantages – larvicidal on the animal and
kills/debilitates adult fleas on contact, ease of
application
b. Disadvantages – does not have repellent
action, diminished efficacy after bathing or
swimming, does not have activity against
ticks, occasional application site reactions 2006 World Congress WSAVA/FECAVA/CSAVA
c. Bottom-line – Good narrow-spectrum
product for fleas
(Canada – Imidacloprid & Moxidectin -
Advantage Multi®, Bayer)
(Europe – Imidacloprid & Moxidectin -
Advocate®, Bayer)
3. Fipronil & S-Methoprene (Frontline® Plus,
Merial), Fipronil (Frontline® Spray, Merial)
a. Advantages – kills adult fleas, disrupts flea
life cycle, ease of application, kills ticks, spray
– rapid dispersion and coverage,
b. Disadvantages – does not have repellent
action, some diminished efficacy after bathing
or swimming, occasional application site
33
A
reactions, spray is labor-intensive
c. Bottom-line – Good broader spectrum product
4. Imidacloprid & 44% permethrin (Advantix®,
Bayer)
a. Advantages – larvicidal on the animal
and kills/debilitates adult fleas on contact,
interrupts flea life cycle, repellant ‘flushing’
activity of permethrin, ease of application,
also kills ticks and mosquitoes
b. Disadvantages – dog only product, do not
use on cats, diminished efficacy after bathing
or swimming, occasional application site
reactions?
c. Bottom-line – Good broader spectrum
product, dog only product
5. Selamectin (Revolution® [USA]; Stronghold®
[Europe], Pfizer)
a. Advantages – broad spectrum against many
internal and external parasites, kills adult fleas
plus larvae and eggs, kills ticks, kills some
ectoparasitic mites (Sarcoptes, Notoedres,
Cheyletiella, Otodectes), ease of application,
b. Disadvantages – does not have repellent
action, diminished efficacy after bathing or
swimming, slower efficacy?, application site
reactions?
c. Bottom-line – Good broader spectrum
product
6. Nitenpyram (Capstar™, Novartis)
a. Advantages – very rapid response with
visual results, kills 100% of adult fleas within 6
hours, short-acting, ease of oral administration,
give every 24-72 hours (half-life in dogs is 2.8
hours, half-life in cats is 7.7 hours) very safe
product, adverse reactions not seen yet
b. Disadvantages – does not have repellent
2006 World Congress WSAVA/FECAVA/CSAVA
action, does not disrupt flea life cycle, short-
acting, does not have activity against ticks
c. Bottom-line – Good narrow spectrum
product, use with spot-ons initially for rapid
response, not for use as sole therapy, use
in dogs requiring frequent shampooing,
compliance problems?
7. Lufenuron (Program®, Novartis; Sentinel®
[lufeneron + milbemycin oxime])
a. Advantages – oral product, very safe
product without known mammalian toxicity,
adverse reactions not seen yet,
b. Disadvantages – does not kill adult fleas or
pupa, time lag – 60-90 days required to disrupt
flea life cycle, does not have repellent action,
adult flea must feed on animal to ingest, does
34
Back to contents
not have activity against ticks, must give with
food
c. Bottom-line – use with spot-ons for long-
term control, not for use as sole therapy unless
very closed environment, treat all animals,
use in dogs requiring frequent shampooing,
compliance problems?
8. Pyriproxifen (Nylar®) containing collars –
Pyriproxifen & amitraz collars (Preventic PLUS®,
Virbac), dogs only!, no longer available in the
USA
Pyriproxifen & 2% permethrin (KnockOut®
Collar for Dogs, Virbac), no longer available in
the USA
Pyriproxifen (KnockOut® Cat & Kitten Collar for
Dogs, Virbac), no longer available in the USA
a. Advantages – ovicidal and larvicidal for
fleas, UV stable juvenile hormone analogue,
translocates to bedding, IGR efficacy for 3
months, Preventic Plus® adds tick protection
b. Disadvantages – long-term residual status
may affect beneficial insects
c. Bottom-line – very useful adjunct to spot-
ons or spray products, useful in dogs requiring
frequent shampooing
9. Synthetic pyrethroid containing pump sprays
(variety of manufacturers
a. Advantages – daily use in dogs requiring
frequent shampooing
b. Disadvantages – frequency of application,
compliance, poor residual activity
c. Bottom-line – rarely used as sole therapy
unless very closed environment, use in dogs
requiring frequent shampooing, compliance
problems?
J. Personal Recommendations
1. Flea control must be regionalized and often
personalized based on severity of possible
infestation in your locale, number of dogs and
cats in the environment, indoor/outdoor/run
free status, infested pests and strays in the
environment, finances of the owner, and severity
of disease vs. magnitude of the infestation
2. ‘The average dog or cat’ will respond to fipronil
and S-methoprene, imidacloprid with or without
lufenuron, or selamectin as sole therapy.
3. Severely flea allergic dogs will require
fipronil and S-methoprene or imidacloprid plus
permethrin, plus either nitenpyram, with or
without lufenuron.
4. (Severely flea allergic cats will require spot-
on preparations plus nitenpyram with or without

lufenuron. Pump-sprays also may be beneficial.)
5. Animals with tick exposure benefit from fipronil
and S-methoprene, imidacloprid plus permethrin
(dogs only!), and pyriproxifen & amitraz collars
(dogs only!)
K. Suggested Readings
Rust MK. Advances in the control of
Ctenocephalides felis (cat flea) on cats and dogs.
Trends Parasitol. 2005; 21:232-236.
Rust MK, Dryden M. The biology, ecology, and
management of the cat flea. Ann Rev Entomol.
1997; 42:451-473.
Back to contents
A
Scott DW, Miller WH & Griffin CE. (2001)
Muller & Kirk’s Small Animal Dermatology, 6th
edn. pp. 476-484, WB Saunders Co, Philadelphia:
WB Saunders Co, 2001; 476-484.
Carlotti DN, Jacobs DE. Therapy, control and
prevention of flea allergy dermatitis in dogs and
cats. Vet Dermatol. 2000; 83-98.
Ihrke PJ: Flea allergy dermatitis: Convincing the
owner! Proceedings of the 15th Annual George
H. Muller Veterinary Dermatology Seminar in
Hawaii, Kohala, Hawaii, Kauai, 1999.
2006 World Congress WSAVA/FECAVA/CSAVA
35
A
A - Standards of Care (How I Treat)
FELINE DIABETES MELLITUS
Professor David Church
Department of Veterinary Clinical
Science
The Royal Veterinary College
Hawkshead Lane
North Myjme
Hatfield
Hertfordshire, AL9 7TA.
dchurch@rvc.ac.uk
Introduction
The majority of cats with diabetes mellitus have
a form of the disease characterised by both
subnormal insulin secreting capacity resulting in
either a relative or absolute insulin deficiency and
variable degrees of insulin resistance. Although
non-diabetic cats can have a wide range of insulin
sensitivities, most diabetic cats are roughly six
times less sensitive to insulin than healthy cats.
Insulin insensitivity
Decreased insulin sensitivity can be a result
of many factors including obesity, various
primary endocrinopathies that inhibit insulin’s
peripheral action, virtually any systemic disease,
pregnancy, drugs such as glucocorticoids and
various progestins as well as, most frustratingly,
hyperglycaemia itself.
Additionally other hormones may have a role
in the pathogenesis of insulin resistance and the
development of diabetes. Leptin has recently been
shown to be important for fatty acid homeostasis
and leptin resistance may lead to fat deposits in
non-adipose tissue causing dysfunction. Plasma
leptin concentrations increase in obese cats that
are insulin resistant correlating highly with the
2006 World Congress WSAVA/FECAVA/CSAVA
degree of obesity. It is assumed that these obese
cats have leptin resistance since the increase in
leptin is not associated with a decrease in food
intake.
Hyperglucagonaemia is also a well known feature
of obesity and type-2 diabetes in other species
and is thought to be secondary to the reduction
of insulin action on alpha cell activity. Glucagon
concentrations are significantly higher in obese
than in lean cats and may be important in the
progression from obesity and insulin resistance to
diabetes, as glucagon increases insulin resistance
and may hasten beta cell exhaustion.
Insulin sensitivity varies dramatically in healthy
cats and those animals with lower insulin
sensitivities have been shown to be at increased
risk of developing impaired glucose intolerance
36
Back to contents
if other factors (such as obesity) exacerbate their
insulin insensitivity.
Insulin secretory capacity – ‘functional’ and
‘structural’ disorders
While the cause of the reduced insulin secreting
capacity found in diabetic cats remains unclear,
it is almost certainly multifactorial and includes
impairment of insulin secretion because of
functional abnormalities as well as possible
but poorly defined alterations in the beta cells
themselves. In other words there is both a
‘functional’ defect in beta cell activity and a
‘structural’ one.
Functional islet disorders This so-called functional
defect is clearly demonstrated by the alteration in
insulin secreting capacity seen in some diabetic
cats where a subnormal insulin secretory profile
to various insulinogenic stimuli can normalise
as a result of periods where insulin demand is
substantially reduced through the administration
of exogenous insulin and/or a reduction in the
level of insulin resistance. Diabetic cats with
no insulin secreting capacity in response to a
glucagon stimulation responded normally once
they were no longer diabetic. It is worth noting
that this apparently ‘reversible’ lack of insulin
secretory capacity means ‘insulin stimulation
tests’ are of questionable value in assessing the
presence or absence of the underlying insulin
secreting capacity of feline diabetics in the
clinical setting.
At least part of this reversible or ‘functional’
impaired islet capacity is due to so called
glucose toxicity–the name given to the
impaired capacity of beta cells exposed to
chronic (greater than 3-10 days) hyperglycaemia
to produce insulin.
There is also evidence that fatty acids and
triglycerides may play a role in the deterioration
of beta cell function and may be involved in the
progression from insulin resistant to diabetic
states. Glucose inhibits fatty acid oxidation and

fatty acids inhibit glucose oxidation. Glucose
must be metabolised in order to cause insulin
secretion, therefore decreased glucose metabolism
due to increased fatty acid concentrations might
explain the lowering of the early phase insulin
secretion in insulin resistant patients.
Although most diabetic cats have minimal insulin
secreting capacity at the time of diagnosis, many
will recover substantial levels of insulin output
with appropriate treatment aimed at reducing
insulin demand. This is generally best achieved
through a combination of exogenous insulin and
reduction in the dietary glucose load. Remission
can occur in anywhere from 30 to 80% of diabetic
cats depending upon the sample of diabetics cats
examined and the method or methods used to
‘unload the endocrine pancreas’.
Structural islet disorders Over the last five years
various researchers have suggested islet amyloid
may have a role in the development of impaired
insulin secreting capacity in diabetic cats. While
islet amyloid can be found in the pancreatic
tissue of many diabetic cats, over 50% of non-
diabetic aged cats have islet amyloid as well.
Not all glucose-intolerant cats have islet amyloid
and various studies have failed to demonstrate
any relationship between the severity of islet
dysfunction and amyloid deposition.
Additionally, the demonstration of a lack of any
difference between endocrine cell volume in
diabetic and non-diabetic cats suggests the initial
defect in insulin secretion, essential for the clinical
expression of diabetes, occurs independently of
alterations in beta cell mass.
It is of course possible that the most appropriate
response to insulin resistance would be beta
cell hyperplasia and could be argued that the
unremarkable beta cell mass in diabetic cats is
actually ‘inappropriately normal’.
Some studies have found evidence of structural
damage in islets during the progression from
glucose-intolerance to overt diabetes, suggesting
the hypersecretion that occurs in response
to insulin resistance leads to exhaustion and
apoptosis of beta cells over time. However,
histological evidence for this is difficult to
interpret as at least one study demonstrated one
or more combinations of amyloidosis, vacuolar
degeneration, reduced islet number or reduced
islet cell mass in cats with transient diabetes.
Despite all these beta cell abnormalities, the cats
still returned to euglycaemia with no need of
exogenous insulin.
Regardless of the microscopic appearance of
‘stressed islets’ and the relative importance of
functional verses structural changes on islet
endocrine activity, chronic hypersecretion
of insulin from beta cells occurs in response
Back to contents
A
to insulin resistance and can be substantially
amplified if this inherent insulin insensitivity is
exacerbated by diets high in readily available
carbohydrates.
The carnivore connection and predisposition to
diabetes mellitus
While the level of insulin resistance is certainly
greater in cats with glucose intolerance or
diabetes mellitus than it is in normal cats, it has
been suggested that as a strict carnivore, the cat
is inherently more insensitive to insulin and less
able to cope with carbohydrate loads than other
more omnivorous species.
It has been proposed that during its evolutionary
development the cat’s natural diet of food of
animal origin only has resulted in it becoming
markedly adapted to a diet high in protein
(approximately 54% of dry matter) and low
in carbohydrates (approximately 8% of dry
matter). This adaptation is reflected by the cat’s
unique metabolism of various nutrients, making
it a true and strict carnivore. When comparing
carbohydrate metabolism of the cat with those
of other, more omnivorous species, there are a
number of specific adaptations evident. These
include altered levels of enzymes responsible for
digestion and uptake of both starches and sugars in
the intestine, an altered capacity to handle glucose
loads including both a slower incorporation rate
of glucose to glycogen and elongation of glucose
elimination times with standard glucose tolerance
tests, the effective absence of hepatic fructokinase
and, perhaps most tellingly, the minimal hepatic
glucokinase activity present in the cat. This low
level of glucokinase activity limits the cat’s ability
to metabolise large glucose loads, as glucokinase
has a far lower Km than hepatic hexokinase and
hence is more readily able to respond to changes
in blood glucose.
According to the carnivore connection theory
propagated by Brand Miller and Colagiuri,
2006 World Congress WSAVA/FECAVA/CSAVA
chronic ingestion of a low carbohydrate-high
protein diet results in selection pressure favouring
animals with a tendency for increased hepatic
glucose production and decreased peripheral
glucose utilisation, i.e. insulin resistance. Both
the ability of insulin to inhibit hepatic glucose
production and to augment tissue glucose disposal
are therefore impaired.
The increased hepatic glucose production is the
result of the high protein intake and is mediated
through an increased carbon flux through the
gluconeogenic pathways. This increased carbon
flux may be mediated by a number of different
mechanisms including a mass action affect
of increased concentrations of gluconeogenic
substrates, an increase in glucagon levels that
37
A
stimulate gluconeogenesis and/or the activation
of a number of key enzymes in the gluconeogenic
pathway.
The decreased insulin stimulated glucose disposal
by peripheral tissues is largely due to the decrease
in carbohydrate intake and the consequent
hypoinsulinaemia and/or reduced insulin efficacy
peripherally, i.e. peripheral insulin resistance.
In other words a predominantly carnivorous
diet (or expressed another way a high protein-
low carbohydrate diet) may produce metabolic
adaptation which is effectively expressed as
insulin resistance, both in the liver and peripheral
tissues.
As previously mentioned, insulin resistance in
man is now recognised as the earliest metabolic
defect in those destined to develop non-insulin
dependent diabetes mellitus and enhanced insulin
resistance is a feature of many diabetic cats. It has
been proposed by the devotees of the carnivore
connection theory that insulin resistance was
the normal phenotype for an obligate or strict
carnivore and this very insulin resistance
increases the likelihood of the development of
diabetes in strict carnivores fed a diet high in
carbohydrate for any protracted period of time.
Such diets, through evoking higher post prandial
insulin responses, might lead to over stimulation
of the pancreatic beta cells and ultimately result
in their ‘exhaustion’ as well as of course reducing
their functional capacity through such processes
as glucose toxicity.
When allowed to graze ad libitum, cats do not
exhibit a post-prandial rise in blood glucose and
hepatic glucokinase activity does not increase
in response to increased carbohydrate feeding.
Additional support for the cat’s adaptation
to a carnivorous diet is found with the levels
of gluconeogenic enzymes present in feline
hepatocytes.
2006 World Congress WSAVA/FECAVA/CSAVA
38
Back to contents
When a diet contains low amounts of glucose,
hepatic gluconeogenesis is predicted to be the
major pathway for maintaining blood glucose.
Consistent with this latter expectation, the
activities of key gluconeogenic enzymes, (glucose-
6- phosphatase, fructose-1,6 biphosphatase and
pyruvate carboxylase) are increased in the liver
of normal cats. Additionally, unlike the situation
in rodents and man, the gluconeogenic capacity
of the feline liver is not inhibited by glucose.
The recently reported finding that in cats,
stress hyperglycaemia is caused by enhanced
hepatic glucose output rather than, as previously
postulated, insulin resistance underscores the
gluconeogenic potential of the feline liver
and suggests its possible role in the genesis of
pathological hyperglycaemia such as is observed
in diabetes mellitus.
Interestingly the low carbohydrate of the
carnivore’s diet may not be the only important
factor in the development of impaired insulin
secreting capacity. A recent study evaluating
the effect of a high fat diet on glucose tolerance
in intact male cats demonstrated a reduction in
the acute insulin response to a glucose tolerance
test suggesting diminished pancreatic insulin
secretion and/or beta cell responsiveness to
glucose as a result of high fat diets.
Consequently the very adaptive processes that
have favoured selection for the obligate carnivore
also favour the development of hyperinsulinaemia
and a chronic state of increased demand for
insulin production being placed upon the beta
cells of the pancreatic islets. While in its most
overt form this may manifest itself as progressive
islet destruction, in the cat, beta cell dysfunction
appears to precede any obvious evidence for
structural islet changes that can be correlated
with this impaired function.

A - Standards of Care (How I Treat)
HYPERADRENOCORTICISM
Professor David Church
Department of Veterinary Clinical
Science
The Royal Veterinary College
Hawkshead Lane
North Myjme
Hatfield
Hertfordshire, AL9 7TA.
dchurch@rvc.ac.uk
Adrenal tumors
Generally an adrenal tumor (AT) is most effectively
treated via surgical removal. This results in
the removal of the animal’s principle source of
cortisol, as the glucocorticoid (GC) secreting
sections of the contralateral adrenal gland are
invariably atrophic and at least temporarily non-
functional. Consequently, GC replacement intra-
and post-operatively is essential for a successful
recovery. Use of hydrocortisone sodium succinate
as a continuous infusion (0.5 mg/kg/hr for 12-24
hours then 0.2 mg/kg/hr for 24 hours) provides
adequate GC replacement in the short term post-
operative period. Once the animal is eating, oral
replacement therapy using cortisone acetate
(1mg/kg/12hr, decreasing over two weeks) is
usually satisfactory. Cortisone is preferable
in this situation as its shorter half life should
reduce the time for the contralateral gland to
regain GC secreting capacity.
Obviously not all cases of adrenal neoplasia
will be appropriate surgical candidates. In those
patients were surgery is not an option it may
be worth considering palliative therapy with
ketoconazole, mitotane or possibly deprenyl.
Pituitary dependent hyperadrenocorticism
Although patients with PDH may be treated
with bilateral adrenalectomy and a similar
replacement regime, the most common method
has been long term mitotane (o, pDDD)
administration. The essence of this regime is to
destroy most of the hyperplastic adrenal cortex.
The remaining tissue provides normal plasma
cortisol concentrations despite being subjected to
almost supraphysiological levels of ACTH.
In other words the animal no longer has the
capacity to raise its plasma cortisol level
above 20-50 nmol/l. This magnitude of adrenal
destruction is essential to achieve significant
clinical improvement.
This “chemical adrenalectomy” can be
achieved using two different protocols, one
aimed at achieving complete and permanent
Back to contents
A
adrenocorticolysis and the other at reducing
adrenocortical activity to normal levels through
partial adrenocorticolysis. The second protocol
has been generally accepted as the favoured
method and involves administration of mitotane
(25 mg/kg/12hr with food) for five to seven
days. During this period water consumption,
appetite and general demeanour are CLOSELY
monitored. If any of these parameters change
for more than 12 hours the mitotane therapy
is stopped. Animals are evaluated with an
ACTH response test 48 hours after the last dose
of mitotane. Adrena l destruction is deemed
satisfactory when both pre and post ACTH
cortisols are similar and below the MID-
RANGE for the laboratory’s normal basal
cortisol concentration. In approximately 15% of
cases this may require a second or more courses
of daily mitotane.
Once satisfactory adrenal destruction has been
achieved it can be maintained by once or twice
weekly mitotane administration (25 mg/kg/12hr
with food on one or two days per week). Patients
can be rechecked with an ACTH response test
once every 8-12 weeks to ensure adequate control
is being maintained.
Animals treated in this way cannot mount an 2006 World Congress WSAVA/FECAVA/CSAVA
appropriate stress response to trauma or illness.
Consequently, from the start of mitotane therapy
prednisolone should always be available and
the owners instructed to administer 1-2 mg/kg
orally in an emergency while awaiting veterinary
attention.
The alternative protocol involves using mitotane
on a daily basis for a longer period and attempting
to bring about irreversible adrenocorticolysis
and subsequently managing patients with
glucocorticoid supplementation.
Both protocols have disadvantages. With
complete chemical adrenalectomy approximately
30% of patients have sufficiently severe side-
effects to justify suspending treatment and the
reported relapse rate can be as high as 39%. With
the more widely used method of creating and
39
A
maintaining induction and remission by inducing
a selective degree of adrenocorticolysis, the
continuous requirement for ACTH stimulation
tests along with similar relapse rates makes
this regime complicated, involved and often
expensive.
As both mitotane protocols could be considered
less than ideal, a number of alternative methods
of safely and consistently reducing adrenocortical
activity in canine PDH have been explored.
These have included using different inhibitors of
steroidogenisis or ACTH release. However, to
date, with ONE exception, these alternative drugs
have been either only inconsistently effective
or produced side-effects in an unacceptable
proportion of patients.
Traditionally the main alternative treatment
to mitotane for PDH in the dog has been
ketoconazole. More recently three other
drugs have been investigated for canine PDH:
aminoglutethimide, L-deprenyl (selegiline) and
trilostane.
Ketoconazole
This is an imidazole derivative that interferes
with steroid synthesis by inhibiting cytochrome
P-450-dependent enzymes. Although it is
potentially hepatotoxic, ketoconazole has been
effective in a variable proportion of dogs with
hyperadrenocorticism. Ketoconazole seems to
be better tolerated when the dose is increased
gradually. The usual treatment regime starts with
a dose of 5mg/kg/12hr for 5-7days and if there
are no side-effects (generally GIT related), the
dose is increased to 10mg/kg/12hr for 10 to 14
days and an ACTH stimulation test performed at
this time.
Satisfactory resolution of clinical signs requires
sufficient inhibition of steroidogenesis to
insure relatively normal plasma cortisol levels
despite the adrenal cortex being subjected to
2006 World Congress WSAVA/FECAVA/CSAVA
supraphysiological levels of ACTH. In other
words the animal no longer has the capacity to
raise its plasma cortisol level above 0.7-1.8ug/
dl. This level of inhibition of cortisol secretion
appears to be essential to achieve significant
clinical improvement. Unfortunately over 25% of
PDH cases do not respond to ketoconazole and
many of the cases that do respond need doses of
between 15 and 20mg/kg/12hr.
Furthermore many endocrinologists provide
anecdotal evidence of unacceptably high
occurrences of side-effects. Consequently the
difficulties with unpredictable efficacy along
with the inconvenience of twice daily dosing and
the substantial cost have limited its widespread
use as a satisfactory alternative to mitotane in the
treatment of canine PDH.
40
Back to contents
Aminoglutethimide
Aminoglutethimide prevents the conversion
of cholesterol to pregnenolone by blocking
cholesterol side-chain cleavage. At higher doses
it inhibits 11-ß-hydroxylase thereby reducing
cortisol, aldosterone and adrenal androgens. Two
studies using aminoglutethimide in dogs with
PDH had conflicting results. While one showed
clinical remission and a tendency towards
normalization of several laboratory values, a more
recent study demonstrated marked hepatotoxicity
with little effect. At least in the author’s opinion
there is insufficient evidence to justify the use of
this drug in the treatment of canine PDH.
Selegiline, l-deprenyl (anipryl)
Selegiline (or L-deprenyl) is a centrally acting
selective and irreversible inhibitor of the enzyme
monoaminooxidase B. The drug theoretically
results in increased levels of CNS dopamine.
Its main use in humans is in the treatment of
Parkinson’s disease while in dogs it has been used
for the treatment of geriatric cognitive disorders.
The use of L-deprenyl for treating canine PDH is
premised on the hypothesis that CNS dopamine
levels will reduce adenohypophyseal ACTH
secretion.
Although two studies in the late 1990s
suggested a proportion of dogs with pituitary
dependent hyperadrenocorticism may show
some improvement in clinical signs, there was
no clinicopathological or endocrine evidence
to suggest significant changes in these dog’s
hyperadrenocorticoid status. Subsequently two
independent studies investigating the efficacy of
L-deprenyl in a total of 21 dogs with pituitary
dependent hyperadrenocorticism demonstrated
minimal and non-sustainable improvements
in clinical signs. This apparent lack of efficacy
was supported by no change in both basal and
post-ACTH plasma cortisol levels, continuing
elevations in the plasma ACTH concentration
and persistently elevated urinary corticoid:
creatinine ratios in PDH dogs receiving selegiline
over a 30 - 90 day period. 8,9 Both investigations
concluded the drug couldn’t be recommended for
the treatment of PDH.
Trilostane is a synthetic, orally active
steroid analogue that competitively inhibits
3ß hydroxysteroid dehydrogenase and hence
synthesis of several steroids, including cortisol
and aldosterone. This competitive inhibition is
reversible and seems to be dose-related.
In dogs peak trilostane concentrations are seen
within 1.5 hours of dosing and decrease to baseline
values in about 18 hours. Trilostane is variably
absorbed after oral administration, at least partly
due to its poor water solubility. Absorption may

be enhanced by administering the drug with
food although this phenomenon has not been
investigated in dogs with hyperadrencocorticism.
Trilostane’s safety as well as both short and long
term efficacy in controlling hyperadrenalism
in dogs has been documented in a number of
abstracts and four controlled studies utilising a
total of 180 dogs with a follow-up period of 180
days or more.
In the four studies 36 of 180 patients were
euthanased or died, in 6 trilostane was withdrawn
due to perceived adverse effects and 3 cases
were lost to follow-up. The mean survival of all
trilostane treated dogs in one long-term study was
661 days (Neiger et al 2002). Additionally dogs
on trilostane have similar long-term survival to
those on mitotane. A preliminary study showed
that 58 dogs with PDH on trilostane survived a
median of 310 days while 26 dogs on mitotane
survived 476 days.
In all four studies the trilostane starting dose
was approximately 6 mg/kg/24hr. During
the first 180 days, over 50% of all dogs had a
change in dose, mostly an increase, resulting in
a final dose of between 6.1 and 11.4 mg/kg/24hr
in three studies. In one study with a markedly
lower post ACTH cortisol concentration as a
target, understandably the final trilostane dose
was substantially higher at a mean of 18.1 mg/kg
(range 5.3 to 48.7 mg/kg).
Trilostane was found to be effective in resolving
the signs of PDH in most dogs. In three studies
polyuria/polydipsia resolved in 116 of 127 dogs
(91%) while polyphagia resolved in 68 of 84
dogs (81%). The time frame for the resolution
was variable although marked improvement was
noted within 2 months in the majority of cases.
Reduction in these clinical signs continued as
long as the dogs were maintained on adequate
doses of trilostane.
Trilostane resulted in a significant reduction in
cholesterol, ALP and ALT although 28 dogs still
had an ALP level above the reference range after
six months of treatment. A significant decrease
in sodium and increase in potassium was also
documented with hyperkalaemia recorded
in 34 dogs at some time during the period of
observation.
Trilostane caused a significant reduction in
both the mean basal and post-ACTH cortisol
concentrations after 10 days of treatment in all
four studies. In one study the post ACTH cortisol
concentration decreased to less than 250 nmol/l
within one month in 81% of dogs and in another
15% at some time whilst on treatment. These
improvements were maintained in the study
population for the duration of the trial. In the
study targeting lower post ACTH cortisol values
Back to contents
A
all dogs were well or acceptably controlled (post
ACTH cortisol ≤ 75 nmol/l and ≤125 nmol/l
respectively) although as mentioned previously,
in some dogs these goals were only obtained by
marked increases in the daily dose.
It should be noted that in all four studies the
“effective” dose of trilostane was, to varying
degrees, determined by the demonstration of a
significant reduction in the post-ACTH cortisol
concentration although the time between
dosing and ACTH stimulation testing was not
standardised. Recent reports now suggest the
duration of trilostane’s inhibition of steroid
synthesis is relatively short-lived and certainly
less than 20 hours. Consequently, as all four
studies determined the “effective” trilostane dose
on the basis of “acceptable” suppression of post-
ACTH cortisol levels sampled upto 24 hours after
trilostane’s administration, in each investigation
there has been some potential for over-estimation
of the “appropriate trilostane dose”. Some
preliminary evidence suggesting, at least in the
dog, trilostane also may reduce tissue sensitivity
to cortisol, supports this possibility.
Trilostane seems to be well tolerated by most
dogs, although mild, self-limiting side effects
such as diarrhoea, vomiting and lethargy were
noted by 63% of owners in one study. More
significantly however in another study acute
death was described in two dogs two and four
days after starting therapy and another two
developed signs and biochemical evidence of
hypoadrenocorticism. One of these dogs recovered
with appropriate therapy. The other died despite
withdrawal of trilostane and administration of
appropriate therapy.
The question of how a drug with the capacity
to suppress cortisol levels for no more than
20 hours could create clinically significant
hypoadrenocorticism remains unanswered.
Interestingly anecdotal incidents of acute
death shortly after starting trilostane have been 2006 World Congress WSAVA/FECAVA/CSAVA
noted while a recent report documented the
development of bilateral adrenal necrosis in two
dogs on trilostane. The likelihood of long-term
trilostane treatment leading to increased risk of
adrenal necrosis through as a result of ACTH
hypersecretion and/or direct effects of trilostane
or its metabolites needs to be looked at further.
In summary both trilostane and mitotane seem
to be effective in correcting clinical signs and
hormonal abnormalities associated with pituitary
dependent hyperadrenocorticism in approximately
80 - 85% of cases. Unfortunately this means a
substantial number of affected affected dogs may
not respond to standard medical therapy and in
these cases a practical alternative needs to be
considered sooner rather than later.
41
A
SURGICAL ALTERNATIVES TO MITOTANE/
TRILOSTANE
Investigators at the University of Utrecht have
had considerable success using hypophysectomy,
however, this is a specialised surgical procedure
and not widely available. Additionally,
despite apparently complete removal of the
adenohyphysis, relapses have been common.
Another therapeutic alternative is bilateral
adrenalectomy.
Bilateral adrenalectomy
Although this procedure has been proposed
as a possible treatment some time, reported
difficulties in the post-operative management
of the adrenalectomised patient has resulted
in the technique not achieving widespread
2006 World Congress WSAVA/FECAVA/CSAVA
42
Back to contents
acceptance as a feasible alternative to chemical
adrenalectomy. However the surgery itself
is relatively simple and management of the
surgically-induced “panhypoadrenocorticism”
is inexpensive and uncomplicated by potential
hyperadrenocorticoid relapses. In the author’s
opinion the reported difficulties with this
procedure can be largely overcome by reducing
the potential for perioperative glucocorticoid
and mineralocorticoid deficiencies with a
continuous hydrocortisone infusion at an initial
rate of 0.5mg/kg/hr until the animal is taking
food and water orally and then changing to a
combination of cortisone acetate with or without
fludrocortisone for long term replacement therapy.
This procedure may be a practical alternative for
the treatment of PDH in the dog.

A - Standards of Care (How I Treat)
CHRONIC HEPATITIS
Sharon A. Center, DVM, Dipl
ACVIM
College of Veterinary Medicine
Cornell University
Ithaca
New York
USA
14853
Sac6@cornell.edu
The First Step: Defining Disease Characteristics
Definitive histomorphologic characterization
of hepatobiliary disease (routine and special
stains for fibrosis, metals, infectious agents),
combined with tissue culture (aerobic and
anaerobic bacterial), cytologic imprints of biopsy
specimens (may disclose infectious agents not
recognized on histology), and quantitative metal
analyses (copper [Cu], iron [Fe], zinc [Zn]) are
essential for selection of interventional therapies.
It is important to recognize that there are no
controlled trials or even long retrospective studies
on response to specific interventional approaches
to most disorders in dogs and cats.
The Second Step: Consider Pathomechanisms of
Liver Injury
Oxidative Injury: This is complex involving
cellular and molecular mechanisms that initiate
and perpetuate damage that leads to liver injury
and fibrosis. Oxidative injury and production
of reactive oxygen species [ROS] are central
pathomechanisms in most forms of acquired liver
injury.
Toxins, Endotoxins, Infectious Agents: The central
role of the liver in intermediary metabolism
and detoxification processes, its large resident
macrophage population (Kupffer cells = 80%
of the fixed macrophages in the body) and its
sentinel position between the splanchnic and
systemic circulatory systems puts the liver at
high risk for toxic, infectious, endotoxin, and
oxidant mediated injuries. Receiving 75% of its
blood flow directly from the alimentary canal
(the richest source of oxidants, invading bacteria,
and toxins), both acute and chronic enteritis are
thought to substantially contribute to liver injury.
Pancreatic inflammation (involving parenchyma
or ducts) imposes risk for obstructive cholestasis
and hepatobiliary inflammation. A variety of
toxins have been identified that specifically
impose liver injury, including certain drugs:
NSAIDs, acetaminophen, phenobarbital,
Back to contents
A
primidone, diazepam (cat), bacteria, enterotoxins,
endotoxins (LPS), toxins derived from molds,
fungi, algae, spoiled or contaminated food, or
effects of consumed transition metals.
Cholestatic Liver Disease: a heterogeneous
group of disorders associated with impaired bile
flow. In severe hepatic insufficiency (associated
with acquired portosystemic shunting [PSS]
secondary to intrahepatic fibrosis and portal
hypertension), and in patients with other forms of
cholestasis, accumulation of membranocytolytic
bile acids (BA) (hydrophobic BA) contributes
to ongoing hepatocellular injury. Noxious BA
damage cell and organelle membranes, induce
intracellular structural and functional change,
inflammation, and compromise bile flow. Free
radicals also contribute to cholestatic injury;
a central mechanism of BA hepatotoxicity is
reduction of mitochondrial glutathione (GSH)
resulting in reduced production of cell energy.
Polymorphonuclear leukocytes (neutrophils)
contribute to tissue injury in many cholestatic
conditions, also contributing to oxidtant injury.
Likewise, hepatocellular copper (Cu) retention
(due to impaired Cu egress in bile) and iron (Fe)
accumulation (in macrophages secondary to 2006 World Congress WSAVA/FECAVA/CSAVA
inflammation) also contribute to ROS generation.
Sulfation of membranocytolytic BA reduces their
toxicity and facilitates BA renal elimination. This
occurs extensively cats but not dogs. Taurine
conjugation enhances physiologic digestive
functions of BA and slows their passive intestinal
absorption (small bowel). Taurine is thought to
attenuate (to some degree) hepatocellular BA
toxicity, for a variety of reasons and may be
helpful when ursodeoxycholic acid is chronically
administered to patients with impaired bile acid
elimination.
Immune- Mediated Mechanisms: are thought
to perpetuate chronic necroinflammatory /
cholestatic liver injury and to augment injury
instigated by infection, endotoxins, or obstructed
bile flow. A variety of pathologic immunologic
43
A
responses perpetuate inflammation that
ultimately impose oxidative insult. Phenomena
thought to unite infection and “auto”immune
responses include molecular mimicry (antigens
of the infectious agent closesly mimicking self-
antigens) or innocent bystander effects (exposure
or mobilized self-antigens). These responses
may culminate in a learned immune repertoire
involving T-cells and B-cells ultimately targeting
foci on normal cells. Infectious agents may initiate
or aggravate responses through an adjuvant effect,
providing co-stimulatory inflammatory signals
or by functioning as superantigens capable of
broadly activating T cells. Environmental factors
and toxins also have been implicated in induction
of chronic immune responses in humans that
demonstrate “auto”immune behavior.
Transition Metals: Copper (Cu) & Iron (Fe):
While these metals function as important catalysts
for enzymes and reactions essential to health,
pathologic hepatic accumulation imposes oxidant
injury. Mitochondria are a primary site of injury
where impaired GSH concentrations disrupt cell
energy production.
Hepatic Iron: Fe accumulates in macrophages
in many necroinflammatory disorders (80%
biopsies). While older theories proposed that
such sequestered Fe is unable to catalyze free
radical reactions, recent data refutes this dogma.
Fe is constantly in flux within and between cells
and even the minute hepatocellular pool of free
Fe participates in free radical reactions. Excess
Fe also initiates/ promotes fibrogenesis. In the
presence of toxins, Fe hepatotoxicity is enhanced
(e.g. endotoxin imposes a “priming” effect on
Kupffer cells).
Hepatic Copper (Cu): while increased liver
Cu concentrations may derive from genetic
(transport/storage) disorders, it is more common
secondary to cholestasis in dogs. Normally,
Cu absorbed from the gut circulates bound
2006 World Congress WSAVA/FECAVA/CSAVA
to transport proteins. After hepatic uptake
and binding to cytosolic proteins, Cu is used
in enzyme pathways and ultimately stored
affiliated with metallothionein an important thiol
bearing protein. Normally, Cu excretion into
canalicular bile and enterohepatic circulation
of Cu regulates a neutral Cu balance. However,
cholestasis from any cause, impedes biliary Cu
excretion causing eventual lysosomal loading.
This leads to organelle damage secondary to cell
membrane oxidation. Rupture of lysosomes leads
to hepatocyte death. Accumulation of Cu storage
“granules” (Cu-binding protein) can be identified
on routine H&E histology. Such identification
is commonly “over-interpreted” as Cu storage
disease (genetic) prompting recommendation of
chelation therapy.
44
Back to contents
How to Define Transition Metal Associated
Liver Injury? Special stains (Prussian blue for
Fe; Rhodanine or Rubeanic acid for Cu) must
be reconciled with quantitative metal analysis
(ug/gm dry weight tissue) and histologic
interpretation of a biopsy. Histology defines the
acinar distribution of Cu or Fe (macrophage,
hepatocyte). Very small liver biopsies can yield
erroneous measured metal values and histologic
interpretations; e.g. biopsy of only a regenerative
nodule may misrepresent tissue activity engaged
in the disease process (regenerated tissue has
low metal relative to actively diseased tissue).
Quantitative tissue Cu measurements reconciled
with histology define the need for chelation
therapy or Zn supplementation and antioxidants
(high Cu or Fe liver concentrations indicate a
need for Vit. E and a thiol donor).
The Third Step: Categorizing Disorders
(common): Pathomechanisms Linked to
Interventional Rx
Necroinflammatory: chronic hepatitis (CH,
canine); cholangiohepatitis (CCHS, cat);
extrahepatic bile duct occlusion (EHBDO);
lobular dissecting hepatitis; repeated toxin
induced injury.
Rx: immunomodulation, antioxidants, UDCA,
+antifibrotics (based on histology).
Cholestatic: parenchymal disorders with
hyperbilirubinemia or high BA, bile duct
focused disorders: CCHS, cholangitis, EHBDO,
biliary mucocele, hepatocellular dysfunction /
canalicular collapse: hepatic lipidosis (HL, cats),
severe vacuolar hepatopathy (VH, dogs)
Rx: correct mechanical obstruction, rectify
mucocele, Rx: UDCA, SAMe (antioxidant, other
effects), antioxidants, + taurine (esp. cat).
Metal Associated: inflammatory / cholestatic
disease with high Cu or Fe concentrations, +/- Zn
depletion
Rx: If high Cu (> 1,500 ug/gm dry wt liver):
chelation, restrict Cu intake in food & water, anti-
oxidants, Zn supplementation NOT concurrent
with chelation; if Zn depletion (< 120 ug/gm dry
liver): supplemental Zn (common if PSS, feeding
protein restricted diets).
Fibrogenesis: non-inflammatory: juvenile
fibrosing hepatitis inflammatory: CH, chronic
CCHS, chronic EHBDO
Rx: Polymodal therapy recommended:
immunomodulation, antioxidant, Vitamin E,
Silibinin, polyunsaturated phosphatidylcholine
or colchicine. Colchicine inhibits neutrophil

function & collagen deposition and can impose
important side effects if dosed too high.
Hepatotoxicity: multiple toxins / drug toxicities
described. Rule out: infection (serum titers tissue
cultures), Environmental toxins: food, garbage,
contaminated water (e.g. cyanobacteria/algae)
Rx: Suspend toxin exposure, appropriate enteric
removal (emesis, colonic lavage, activated
charcoal avoiding repeated dosing with sorbital),
discontinue suspected toxin, research toxic
mechanisms (internet, PubMed), give appropriate
antidote(s). Do not give prednisone, rather remove
toxin and facilitate toxin excretion / removal (e.g.
acetaminophen: administer cimetidine to slow
biotransformation to toxic adduct. Generally,
use hepatoprotectants and antioxidants: n-
acetylcysteine (NAC), SAMe, silibinin, and
Vit. E. For mushroom toxicity (amanita, death
cap) give silibinin, penicillin (impairs cell toxin
uptake), and antioxidants.
Portosystemic Vascular Anomaly (PSVA):
congenital macroscopic portal shunting
“around” the liver; congenital microvascular
intrahepatic shunting (microvascular dysplasia,
MVD). no necroinflammatory or cholestatic
pathomechanisms involved.
Rx: PSVA: surgical ligation or medical
management of hepatic encephalopathy, Zn
supplementation. MVD: usually requires no
therapy. UDCA NOT indicated in most patients,
antioxidant NOT indicated in most patients.
Biliary Mucocele: Inspissated biliary material
(gallbladder [GB], “kiwi” fruit pattern on
ultrasound, associated with GB cystic mucosal
hyperplasia, GB hypokinesis, hyperlipidemia,
vacuolar hepatopathy, and sometimes cholecystitis
and ruptured GB; may also affect common ducts
and hepatic ducts.
Rx: Remove inspissated biliary material, GB
resection usually indicated, induce hydrocholeresis:
maintain good hydration, UDCA, and SAMe.
Culture bile/tissue: aerobic and anaerobic
bacteria, inspect cytology of bile for bacteria (may
see bacteria that fail to grow in culture due to
antibiotic treatment preceding sample acquisition).
UDCA promotes bile flow and aids elimination of
other substances excreted in bile (up-regulation
of canalicular transport and stimulated ductal
bicarbonate secretion). SAMe may augment bile
flow via enhance GSH biliary concentrations (GSH
fuels non-BA dependent bile flow). UDCA: 15 mg/
kg PO SID, SAMe: 20 mg/kg PO enteric coated
tablets on empty stomach. Appropriate antibiotics,
fat restricted diet if hyperlipidemia associated with
VH. Vitamin E if inflammatory histology.
Back to contents
A
Non-Necroinflammatory Disorders Secondary to
Systemic or Metabolic Disorders:
Vacuolar Hepatopathy (VH): In dogs, hepatocyte
distention with cytosolic glycogen secondary to
chronic stress imposed by systemic or hepatic
disease. Relates to chronic release of inflammatory
cytokines (dental disease, IBD, skin infections,
neoplasia), or Hyperadrenocorticism (iatrogenic,
spontaneous typical Hyperadrenocorticism, or
sex hormone adrenal hyperplasia).
Rx: Identify and treat underlying disease process;
e.g. sex hormone related adrenal hyperplasia
treated with lysodren rather than trilostane. IF
VH diffuse and associated with stromal collapse,
high serum or urine bile acid concentrations.
Hepatic Lipidosis (HL) cats: triglyceride
distention of hepatocytes, secondary to anorexia
and another primary disorder.
Rx: identify underlying cause of anorexia,
provide protein replete feline diet, NAC (140
mg IV over 20 min., then 70 mg/kg IV q6-12
hrs, correct hypokalemia and hypophosphatemia,
beware of electrolyte changes with re-feeding
phenomenon, supplement with taurine (250 mg
PO SID to BID), l-carnitine (250 mg PO SID
[use Carnitor®), vitamin E (10 IU/kg/day), water
soluble vitamins, determine B12 status, treat
while awaiting data (1.0 mg/cat, SC).
“Reactive” Hepatitis: diagnosed subsequent to
liver biopsy for unexplained liver enzyme activity;
a term applied to liver biopsies lacking a distinct
pattern but showing multifocal lipogranulomas
(small clusters of macrophages with Fe
[hemosiderin], minor lymphoplasmacytic portal
infiltrate, but lacking overt necrosis, fibrosis, or
architectural remodeling.
Rx: reactive hepatitis is not a disease but merely
represents the sentinel function of the liver. Beware
of recommendations to intervene with anti-
inflammatory / immunomodulatory treatments if
2006 World Congress WSAVA/FECAVA/CSAVA
morphologic description seems vague. Call and
talk with your pathologist before committing to
the chronic use of potentially toxic drugs.
Specific Considerations Interventional Strategies:
Nutrition: Balanced nutritional support is
critical including vitamin supplements (avoid
Cu supplement if high tissue Cu). Only restrict
protein in patients showing signs of HE (may
be vague, may be indicated by ammonium
biurate crystalluria, cannot depend on blood
ammonia determinations). Most animals with
acquired hepatobiliary disease DO NOT require
protein restriction, especially cats. Cats with
HL may succumb subsequent to dietary protein
restriction.
45
A
Antioxidants: Approximately 65% of dogs and
cats with necroinflammatory liver disorders have
low liver GSH concentrations.. Since oxidant
injury is better inhibited than reversed, early
preemptive therapy in necroinflammatory and
cholestatic liver disease may be most effective.
Antioxidant therapy should be combined with
disease appropriate immunomodulatory / anti-
inflammatory / antifibrotic medications to achieve
a synergistic effect. For example, glucocorticoids
intervene in membrane release of arachidonic
acid that initiates production of inflammatory
eicosonoids that play a crucial role in membrane
oxidation. Thus, concurrent of an antioxidants
may yield a synergistic benefit.
Direct Thiol / Glutathione donors - N-
Acetylcysteine, S-Adenosylmethionine, Whey
Protein ?, Silibinin (Milk Thistle), N-Acetylcysteine
(NAC): Used IV for crisis intervention, especially
during the first few days in cats with HL, and in
animals with suspected of hepatotoxicity. Dose:
140 mg/kg IV (dilute at least 1:4 with saline or
5% dextrose, give via 0.25 μmicron nonpyrogenic
filter), administer over 20-min NOT as constant
rate infusion (CRI). Follow-up dosing: 70 mg/kg
IV given 2-4 times daily as clinically indicated.
S-Adenosylmethionine (SAMe): For
necroinflammatory / cholestatic liver disease
/ VH / HL: Broad metabolic benefits may have
important metabolic implications as a GSH
donor, for methylation reactions (including l-
carnitine and phosphatidylcholine synthesis). In
HL, low vitamin B12 may contribute to SAMe
and GSH deficiency (compromised methionine
availability for transsulfuration pathway). Dose:
20 mg/kg enteric coated tablets, given on an empty
stomach. Be particular about source, Denosyl-
SD4TM, Nutramax, Inc has proven bioavailability
and increases hepatic GSH in healthy cats, cats
with portal triad inflammation, and dogs treated
with high dose glucocorticoids.
2006 World Congress WSAVA/FECAVA/CSAVA
Whey Protein: Alternative cysteine source for
GSH synthesis; other nutritional benefits claimed
but efficacy remains unproven. Consult recent
review: Marshall K: Therapeutic applications of
whey protein. Altern Med Rev. 2004;9:136-156.
Product labeled Protectamin (Fresenius Kabi,
Bad Hamburg, Germany) may provide greater
GSH substrates.
Vitamin E ( --tocopherol): “last line of membrane
defense” as lipid peroxidation chain terminator.
In membranes exists in low molar ratio:
phospholipids (especially PUFA) that are highly
susceptible to oxidation (1,000-2,000 PUFA:1 Vit.
E). Efficient recycling of oxidized (tocopheroxyl
radical) to reduced antioxidant form dependes
on an interactive group of redox antioxidant
cycles (CoQ10, ascorbate, GSH). Large doses
46
Back to contents
without interactive antioxidants may fail to
provide expected antioxidant protection and may
become pro-oxidant (accumulated tocopheroxy
radical). Vit. E also modulates cellular responses
to oxidative stress through signal-transduction
pathways (protein kinase C) providing anti-
inflammatory and antifibrogenic effects (reduces
collagen gene transcription). Since it Is not
synthesized in vivo it must be ingested (diet or
supplementation). Dose: 10 IU/kg PO / day
( --tocopherol acetate); higher dosing for bile
duct occlusion or cats with severe sclerosing
cholangitis (fat malassimilation due to disrupted
bile acid enterohepatic circulation). Water-soluble
( --tocopheryl succinate polyethylene glycol
1000 [TPGS]) form preferred if compromised
fat uptake (TPGS forms micellar solutions at low
concentrations obviating need of bile acids for
Vit. E uptake). Toxic effects of Vit E if very large
doses: may potentiate oxidant injury and interferes
with Vit. K activity (bleeding tendencies).
Silibinin / Silymarin (Milk Thistle): studied in a
considerable repertoire of clinically relevant live
animal disease models. Proven for prevention
/ recovery from certain toxins (e.g. amanita
mushroom, CCl4, ethanol). Despite numerous
studies in humans, clinical benefit in chronic
liver disease remains controversial. Imparts
antioxidant, anti-inflammatory, and anti-fibrotic
effects, promotes protein synthesis (regeneration),
and interferes with certain p450 enzymes and
toxin uptake/ activation. Hepatoprotective,
anti-inflammatory, antifibrotic, and antioxidant
effects mechanistically overlap with several
other nutraceuticals, (specifically Vit. E, SAMe,
NAC, and polyunsaturated phosphatidylcholine).
Avoid mixed herbal formulations of milk thistle,
except combination with polyunsaturated
phosphatidylcholine. Later combination has
superior advantage in hepatic disease. Dose of
silibinin complexed with PPC: 2-5mg/kg per day
(based on experimental work in other species;
current veterinary product provides Vit. E 300
IU. Zinc gluconate 45 mg with 70 mg silibinin
complexed with phosphatidylcholine.
Ursodeoxycholic Acid (UDCA): Least
controversial mechanism involves protection
against membranocytolytic bile acids in liver,
bile, and systemic blood providing direct
cytoprotection (hepatocellular membranes,
possibly blood brain barrier) and molecular
interventions accentuating survival signals. May
suppress MHC expression (target foci, MHC II) on
hepatobiliary surfaces. Also is immunomodulatory
and produces hydrocholeresis that may aid in
biliary toxin elimination. Recommended in
chronic necroinflammatory and cholestatic liver
disease, cholestatic disorders complicated by

“sludged” or lithogenic bile, but no evidence of
benefit in acute toxic injury or HL in cats. Biliary
diversion/decompression necessary if bile duct
occlusion before UDCA therapy. May blunt
peribiliary inflammation and fibrosis in EHBDO.
Unjustified for congenital portosystemic shunts,
limited benefit (if any) in short term jaundice due
to sepsis or cats with HL.
Cu Storage Rx: Reduce Cu intake (water, food),
use chelation, and impair enteric Cu uptake (zinc)
to reduce Cu accumulation. Chelation: indicated
when tissue Cu > 1,500 ug/gm dry weight liver.
Preferred chelator: d-penicillamine (15 mg/kg PO
BID, 30-minutes before meals with supplemental
pyridoxine). If patient intolerant, Trientine may
be used (author has observed Trientine associated
acute renal failure in 2 dogs). Chelation for at least
6-months; second liver biopsy used to determine
best chronic treatment. If Cu is critically lower:
may convert to chronic zinc acetate (gluconate
or sulfate). If patient zinc intolerant, use chronic
chelation (d-Pen. dose reduced by 50%). Do not
use chelation and Zn together, direct chelation of
zinc to d-Pen. Avoid ascorbate supplementation
as this may enhance transition metal oxidative
injury. All patients with high liver Cu should
receive supplemental Vit. E as an antioxidant
antifibrotic.
Zinc Supplementation: Essential trace element,
required for many homeostatic functions with
central importance to the liver, e.g. normal
protein metabolism, function of >300 zinc
metalloenzymes, and membrane integrity. Zn
sufficiency has impact on numerous physiologic
reactions including: immune and neurosensory
functions, detoxification pathways, wound
healing, appetite, imparts antioxidant effects
reducing some but not all ROS mediated injury
(antagonizing redox-active transition metals:
Fe, Cu which it competitively displaces).
Zinc insufficiency increases susceptibility to
GSH deficiency. Liver Zn should be measured
concurrent with both Cu and Fe in liver
biopsies. Supplement Zn when concentrations
< 120 ug/mg dry liver, especially when either
Fe or Cu values are high. Low tissue Zn
concentrations are common in animals with
severe liver disease, especially with acquired/
congenital PSS. Feeding a restricted protein diet
may augment this phenomenon. Association
between low tissue Zn and GSH in severe liver
disease suggests greater risk for transition metal
injury. Zn therapeutically impedes hepatic Cu
accumulation (liver binding, enteric uptake).
When used for transition metal injury, concurrent
administration of Vitamin E and a thiol donor
(SAMe) are recommended (synergistic effects).
Dose: 1-3 mg/kg elemental zinc if low tissue
Back to contents
A
zinc; 3-10 mg/kg elemental zinc for Cu toxicity
(30-min. before feeding).
Immunomodulation:
Azathioprine: Used for CH and lobular dissecting
hepatitis when infectious cause unlikely or
eliminated; reserved for dogs. Antimetabolite:
impairs purine metabolism. Dose: 1-2 mg/kg
PO SID for 3 – 4 days then every other day
(EOD). Cats do not tolerate this drug. Toxicity:
hematopoietic (acute or chronic bone marrow
toxicity: leukopenia, thrombocytopenia) and
gastrointestinal signs (vomiting and diarrhea);
occasional side effects: pancreatitis, dermatologic
reactions, and rare hepatotoxicity (cholestasis rare
in dogs, veno-occlusive lesion in human beings).
Acute bone marrow toxicity requires suspending
treatment, awai recovery, continuing treatment
with 50% or 75% initial dose. Chronic bone
marrow toxicity, pancreatitis, hepatotoxicity:
permanent drug discontinuation, use alternative
immunomodulatory agent (e.g.myocphenolate)
Good clinical response allows 50% dose reduction.
Patient response: monitored initially at weekly (4
weeks) then quarterly (CBC, liver enzymes, total
bilirubin). Many patients requiring prednisone and
azathioprine for control of chronic liver disease
CANNOT BE COMPLETELY WEANED OFF
EITHER DRUG. Chronic therapy is combined
with antioxidants (Vit. E, SAMe), and UDCA (if
high serum BA).
Mycophenolate Mofetil: Morpholinoethyl ester
pro-drug of mycophenolic acid (MPA), a selective
potent inhibitor of inosine monophosphate
dehydrogenase (IMPDH). This enzyme is critical
for de novo synthesis of guanosine triphosphate
(GTP), a purine necessary for synthesis of
DNA, RNA, proteins, and glycoproteins. MPA
is relatively selective for lymphocytes which
are dependent on a purine synthetic pathway
inhibited by MPA permitting targeting of activated
lymphocytes (inhibits clonal expansion: B and T
2006 World Congress WSAVA/FECAVA/CSAVA
lymphocytes, antibody production, and expression
of lymphocyte cellular adhesion molecules).
MPA is eliminated after hepatic glucuronidation
(inactive MPA-glucuronide); dose in canine liver
patients used by the author. Dose: 10-20 mg/kg
PO BID (20 mg/kg q 12 hours proven successful
for myasthenia gravis in dogs). Reduce dose
for long term treatment (after remission) by
50% (5-10 mg/kg PO BID). Alternative for
dogs intolerant of azathioprine (these may have
impaired azathioprine metabolism, pancreatitis,
hepatoxicity, bone marrow toxicity). Rare bone
marrow suppression (humans, dog). Limited
information for cats.
Metronidazole: Provides bactericidal, amebicidal,
trichomonacidal, cytotoxic, immunosuppressant
47
A
(cell mediated immune responses) influences
and a dose dependent antioxidant effect. Used
adjunctively with other drugs (e.g. prednisone)
improves response compared to single agent
therapy (man). Especially recommended for
liver disease associated with inflammatory
bowel disease. Limited protein binding allows
delivery to bile, bone, effusions, CSF, and
hepatic abscesses. Relies on hepatic metabolism
(30-60%) along with renal and fecal elimination;
dose adjustment required if compromised liver
function. Dose: Empirical dose reduction in liver
disease (used in veterinary patients with good
success for > 17 years): 7.5 mg/kg PO BID. Side
Effects: anorexia (metallic taste) and neurologic
effects with excessive dosing; vestibular signs
most common and usually resolve within 1 week
of drug discontinuation or dose adjustment.
Antagonize neurologic toxicity (rapid recovery)
with diazepam unless HE.
Methotrexate: A folic acid antagonist,
that reversibly and competitively inhibits
dihydrofolate reductase; undergoes renal
elimination. Used as a “rescue” or second
line anti-inflammatory- immunomodulator
in a variety of immune mediated diseases in
humans. Active against cells in which it becomes
trapped by polyglutamination; is concentrated
in lymphocytes, perhaps in biliary epithelium
(limited evidence), and achieves concentrations in
bile. May offer “targeted” therapy in lymphocyte
mediated chronic biliary inflammation. Useful
in some humans with sclerosing cholangitis, but
response is inconsistent. Proven useful in some
cats with sclerosing cholangitis as these typically
do not respond to prednisolone as single agent
immunomodulatory, and appear predisposed to
diabetes mellitus (with prednisolone therapy).
Only use when biopsy proves diagnosis of
sclerosing CCHs, infection ruled out, and with
polymodal therapy: UDCA, SAMe, Vit. E, low
2006 World Congress WSAVA/FECAVA/CSAVA
dose prednisolone, and supplemental folate.
Author prefers methotrexate to chlorambucil
in these cats. Positive response indicated by
declining bilirubin concentrations; low level
enzyme activity usually continues. Dose: use
only with low dose pulse therapy regimen (treat
ONCE weekly) to avoid side effects; 0.4 mg
total dose divided into 3 doses given on one day
at 8 hour intervals ONCE weekly. Formulate
capsules to 0.13 mg for once weekly single day
pulse dosing. Renal disease reduces clearance
and can result in drug accumulation. Use ONLY
with folate supplementation (0.25 mg/kg folate
or folinic acid daily). May be used IM or IV but
reduce dose by 50% if administered using these
routes. Very immunosuppressive and increases
risk of infection (infections observed by author:
48
Back to contents
feeding tubes, pyelonephritis, demodex, herpes
keratitis). For polymodal CCHS treatment in
cats, methotrexate replaces azathioprine or
chlorambucil. Estimated canine dose: 0.1 mg/kg
over 24 hours (divided into 3 doses) repeated q
7 to 10 days ?
Alternative immunomodulators not discussed
here: chlorambucil, cyclosporine.
Antifibrotics: A number of agents provide
antifibrotic influences: including antioxidants
(SAMe, Vit. E), UDCA, and Silibinin. However,
primary antifibrotics are: polyunsaturated
phosphatidylcholines (PPC) and colchicine.
Polyunsaturated Phosphatidylcholines: Extract
of soybeans or salmon roe; a mixture of seven
phospholipid species rich in polyunsaturated
phosphatidylcholines, sometimes classified with
the group of B-vitamins. Active component:
dilinoleoyl-phosphatidylcholine (DLPC)
accounting for approximately 50% (w/w)
of polyunsaturated phosphatidylcholine.
Attenuates hepatic fibrosis in a number of animal
models and in humans with chronic active
hepatitis. Mechanisms: hepatoprotectant, anti-
inflammatory, immunomodulatory (glucocorticoid
sparing effect permitting dose reduction
when adjunctively used with prednisone and
azathioprine), and antioxidant effect. DLPC may
directly influence hepatocyte cell and organelle
membrane structure (membrane stabilizing
effect), directly attenuate transformation /
activation of Stellate cells into myofibrocytes
(source of liver collagen), increases Stellate
cell collagenase activity (digests collagen), and
reduces platelet derived growth factor stimulation
of Stellate cells; all these effects are proven
to contribute to hepatic fibrogenesis. Study
of DLPC and SAMe (ethanol hepatotoxicity)
demonstrated similar lipid membrane enrichment,
but DLPC minimally attenuated liver enzymes
and cholestasis compared to SAMe. With an in
vitro testing system, DLPC did not, but SAMe
did restore total cell and mitochondrial GSH and
improved organelle / cell oxygen consumption.
SAMe provisioning the transmethylation
pathway enables hepatocyte phosphatidylcholine
synthesis and thus may provide similar effects.
DLPC is derived from PPC after enteric digestion,
PPC circulation to the liver, and reservoir-like
incorporation in membranes and lipoproteins.
Dose: 50 to 100 mg/kg PO SID (no greater than
3 gm suggested in man) extrapolated for dogs and
cats by the author from human and experimental
animal studies. No side effects have emerged
from use > hundred dogs with liver disease and
fewer cats.
Colchicine: Inhibits microtubular apparatus, may
arrest hepatic fibrogenesis by interfering with

transcellular movement of procollagen fibrils,
inhibiting procollagen synthesis, and fibroblast
proliferation, and by inducing collagenase.
Imposes antiinflammatory effects by suppressing
leukocyte locomotion and degranulation, and
impaired expression of surface TNF receptors.
May facilitate hepatic Cu excretion. Inconsistent
benefits shown in humans with chronic liver
disease. Used primarily in juvenile fibrosing liver
disease in dogs where there is little inflammation.
Toxicity: hemorrhagic gastroenteritis, bone
marrow suppression, renal injury, and
peripheral neuropathies. Considered a safer
therapeutic alternative than D-Penicillamine or
glucocorticoids in man. Colchicine commonly
combined with probenecid which increases its
Back to contents
A
duration of action. The form without probenecid is
preferred in liver disease since biotransformation
and elimination of colchicine is in part dependent
on the liver. May undergo reservoir accumulation
(proven in humans). Owners must be warned of
potential teratogenic and abortifacient effects
(contact through urine and tablet, provide written
warning to pregnant women). Use concurrent
with UDCA, glucocorticoids, and antioxidants.
Not recommended as concurrent treatment with
azathioprine, methotrexate, or chlorambucil
owing to similar side effects; rather use PPC
in these. Dose: 0.025-0.03 mg/kg PO SID
(probenicid free drug); used in many dogs and
fewer cats without problems.
2006 World Congress WSAVA/FECAVA/CSAVA
49
A
A - Standards of Care (How I Treat)
GIARDIA INFECTIONS

Michael R. Lappin, DVM,

PhD, DACVIM
Professor
Department of Clinical Sciences
Colorado State University
Fort Collins
Colorado 80523
USA
mlappin@colostate.edu

The genus Giardia contains multiple species of Albendazole: Canine dose-15 mg/kg, PO,
flagellated protozoans that are indistinguishable q12hr for 2 days.
morphologically. Recent genetic analysis has Febantel: Canine dose-Label dose PO,
revealed 2 major genotypes in people; assemblage daily for 3 days.
A and assemblage B. These organisms are not Feline dose-56 mg/kg, PO,
usually found in dogs and cats in the United daily for 5 days.
States. Dogs are most commonly infected with Quinacrine: Canine dose-9 mg/kg, PO,
assemblages C and D and cats are most commonly q24hr, for 6 days.
infected with assemblage F. Feline dose-11 mg/kg, PO,
Giardia spp. have specific antimicrobial q24hr for 12 days.
sensitivity patterns like bacteria. However, Furazolidone: Feline dose-4 mg/kg, PO,
some Giardia can be difficult to cultivate and q12hr for 7-10 days.
so there is little in vitro susceptibility test
results available. In addition, while there have The protozoal toxicity of metronidazole is from
been multiple drugs used for the treatment of short lived intermediates or free radicals that
giardiasis in dogs and cats, there are few studies produce damage by interacting with DNA and
that utilized dose titrations and evaluation of possibly other molecules. Metronidazole has
drugs in experimentally infected animals. In most effect against other GI protozoans, helps correct
studies, fecal samples were only assessed for bacterial overgrowth, and may be an immune
short periods of time after treatment and immune modulating agent and thus, has many potentially
suppression was not induced to evaluate whether positive effects in animals with diarrhea and
infection was eliminated or merely suppressed to Giardia infection. However, efficacy is not 100%
below detectable limits of assays used. Infection in most studies in dogs. We recently reported
with Giardia does not appear to cause permanent clinical resolution of diarrhea and cessation of
2006 World Congress WSAVA/FECAVA/CSAVA

immunity and so reinfection can occur, a finding cyst shedding in 26 of 26 cats with giardiasis
that also hampers assessment of treatment studies. when administered metronidazole benzoate
Treatment options currently available or used at 25 mg/kg, PO, twice daily for 8 days. There
historically include the following. was no recognized neurological or benzoate
toxicity and the benzoate salt was well tolerated.
Metronidazole: Canine and feline Most cases of metronidazole neurotoxicity have
dose-15-25 mg/kg, PO, occurred in animals on high or extended doses
q12-24 hr, for 5-7 days. and so the maximal total daily dose should be
Ronidazole: Feline dose (primarily used for < 50 mg/kg total daily dose. The related drugs
T. foetus)-30 mg/kg, PO, q12hr, tinidazole, ipronidazole, and ronidazole may also
for up to 14 days. be effective for the treatment of giardiasis but
Tinidazole: Canine dose-44 mg/kg, PO, there is limited information currently available.
q24hr for 3 days. Benzimidazoles may have anti-Giardia effect by
Ipronidazole: Canine dose-126 mg/liter interacting with the colchicines site in tubulin in
of water, PO, ad libitum the microtubules, resulting in the disruption of
for 7 days. assembly and disassembly. Selective toxicity is
Fenbendazole: Canine and feline dose-50 mg/ achieved because the drug is minimally absorbed
kg, PO, daily for 3-5 days. from the host intestine. Fenbendazole is very safe
50
Back to contents

in dogs and cats and was effective (approximately
90%) for the treatment of giardiasis in at least 2
short term studies of experimentally infected dogs.
However, cysts shedding was only eliminated
in 4 of 8 cats with concurrent giardiasis and
cryptosporidiosis when administered fenbendazole
at 50 mg/kg, PO, daily for 5 days. Albendazole
has been associated with hematologic toxicity in
both dogs and cats. Since albendazole efficacy is
unlikely to be greater than fenbendazole and the
drug is apparently more toxic, it should not be
used routinely. When given at the label dose for
3 days, a combination of pyrantel, praziquantel,
and febantel was safe and effective in eliminating
fecal cysts in 5 of 5 treated dogs. The canine
product was used safely in cats but a higher dose
was needed. Because febantel is metabolized in
part to fenbendazole, use of this drug may be no
more effective than using fenbendazole alone but
it is possible pyrantel or praziquantel provide an
additive effect even though they are not effective
for giardiasis when used alone. Fenbendazole,
albendazole, and the pyrantel, praziquantel, and
febantel combination have the added benefit of
having effect against other helminths and cestodes
that may be coinfecting the animal. Resolution
of clinical signs usually occurs within 7 days of
instituting treatment.
Nitazoxanide and paromomycin are used in
people with giardiasis and may prove to be
effective treatments for giardiasis in dogs and
cats. Paromomycin is an aminoglycoside and
should not be used if there is blood in the stool
because it could potentially be adsorbed and
result in renal insufficiency.
There are a number of other things that may also
aid in the treatment of giardiasis. The addition of
fiber to the diet may help control clinical signs
of giardiasis in some animals by helping with
bacterial overgrowth or by inhibiting organism
attachment to the microvillus. Immunotherapy
with the Giardia vaccine has aided in the
elimination of cyst shedding and diarrhea in some
infected dogs. However, in a controlled study in
16 experimentally infected cats, vaccination as
immunotherapy was ineffective with one strain
of Giardia.
Because clinical signs induced by Giardia spp.
can be intermittent and since some Giardia spp.
Back to contents
A
may be zoonotic, treatment of subclinically
infected animals should be considered. However,
since natural infection does not result in
protective immunity, reinfection from the same
contaminated environment is likely. In resistant
or recurrent cases, consider other underlying
disorders such as inflammatory bowel diseases,
bacterial overgrowth, exocrine pancreatic
insufficiency, and immunodeficiency. Since cyst
shedding can be intermittent, it is difficult to use
fecal flotation results to predict a cure.
REFERENCES
1. Barr SC, Bowman DD, Frongillo MR, et al.
Efficacy of a drug combination of praziquantel,
pyrantel pamoate, and febantel against giardiasis
in dogs. Am J Vet Res. 1998; 59: 1134-1136.
2. Diaz E, etal. Epidemiology and control of
intestinal parasites with nitazoxanide in children
in Mexico. Am J Trop Med Hygiene. 2003; 68:
384-385.
3. Harris JC, et al. Antigiardal drugs. Appl
Microbiol Biotecnol 2001; 57: 614-619.
4. Olson ME, et al. The use of a Giardia vaccine
as an immunotherapeutic agent in dogs. Canadian
Vet J. 2001; 42: 865-868.
5. Payne PA,et al. Efficacy of a combination
febantel-praziquantel-pyrantel product, with or
without vaccination with a commercial Giardia
vaccine, for treatment of dogs with naturally
occurring giardiasis. J Am Vet Med Assoc 2002;
220: 330-333.
6. Scorza AV, Lappin MR. Metronidazole for
the treatment of feline giardiasis. J Fel Med and
Surg. 2004; 6: 157-160.
7. Scorza AV, et al. Efficacy of a combination
of febantel, pyrantel, and praziquantel for the
treatment of kittens experimentally infected with
Giardia species. J Feline Med Surg. 2005 Jul 9;
[Epub ahead of print] 2006 World Congress WSAVA/FECAVA/CSAVA
8. Stein JE, et al. Efficacy of Giardia vaccination
for treatment of giardiasis in cats. J Am Vet Med
Assoc. 2003; 222: 1548-1551.
9. Zajac AM, et al. Efficacy of fenbedazole in the
treatment of experimental Giardia infection in
dogs. Am J Vet Res. 1998; 59: 61-63.
51
A
A - Standards of Care (How I Treat)
FLUID THERAPY FOR CRITICALLY ILL DOGS AND CATS
Michael Schaer, D.V.M.,
DACVIM, DACVECC
Professor and Assoc. Chair
University of Florida
College of Veterinary Medicine
2015 SW 16th Ave
Gainesville, FL 32608
schaer@mail.vetmed.ufl.edu
CONDITIONS REQUIRING SPECIAL FLUID
THERAPY CONSIDERATIONS
Anemia
Intravenous fluids are sometimes used excessively
in the anemic patient when the decrease in red
blood cell mass is misinterpreted as total blood
volume depletion, when in fact the plasma
volume might even be expanded. To compensate
for decreased tissue oxygen delivery, the heart
rate increases, and if these patients are subjected
to large fluid volumes over a short period of time,
pulmonary edema can occur.
Anemic cats in particular are susceptible to
intravenous overload from crystalloid infusions.
The dehydration deficit and maintenance fluid
volumes should be gradually replaced over a 24-
hour period with an isotonic crystalloid solution,
while fresh whole blood is used to replace the red
blood cells. The volume of whole blood infused
should be considered when calculating the
volume of crystalloid for infusion.
Extracellular Fluid Volume Excess
This condition is associated with an increase in
total body salt and water and occurs in a variety
2006 World Congress WSAVA/FECAVA/CSAVA
of clinical settings including congestive heart
failure, glomerulopathies, liver fibrosis, and
protein-losing enteropathy. These conditions are
associated with a decrease in “effective arterial
volume,” which stimulates the renin-angiotensin-
aldosterone cycle and the release of antidiuretic
hormones to promote renal salt and water
retention, respectively. Because of increased
venous pressure from heart failure and cirrhosis
or because of decreased plasma oncotic pressure
associated with hypoalbuminemia, the retained
salt and water move into the interstitial and other
body spaces, causing edema, ascites, or pleural
effusion. Hypervolemia amounting to 20-30% in
water excess can cause pulmonary edema.
Patients with any of these conditions are
extremely sensitive to intravenous overload
52
Back to contents
with crystalloid solutions. Treatment should be
directed toward improving the underlying primary
pathologic process. Fresh or fresh frozen plasma
should be used to volume expand animals with
hypoalbuminemia, although in glomerulopathies
and protein-losing enteropathy (PLE), beneficial
effects are usually temporary at best because of
continued protein losses especially with PLE.
Heart failure patients receiving intravenous fluids
should be closely observed for weight gain and
respiratory distress caused by intravascular fluid
overload. A rapid respiratory rate will often be the
earliest sign of overload therefore calling for close
patient observation. Under optimal conditions,
monitoring of central venous and pulmonary
wedge pressures is helpful for avoiding this
potentially fatal complication. The reader is
referred to other sources for details regarding
these techniques.
When parenteral fluid therapy is indicated in
the cardiac patient, solutions containing little
or no sodium are given after dehydration and
hypovolemia are corrected with isotonic solutions.
Either 0.45% saline or D-5-W can be used. Efforts
should be made to avoid hypokalemia by adding
potassium chloride solution to the fluids at a dose
of 7 to 10 mEq/250 ml. Periodic monitoring of
serum electrolytes is necessary for accurate
treatment adjustments.
Hypovolemic Shock
The loss of 30-40% of intravascular volume
will cause severe hypovolemia and hypotension.
Cardiac arrest occurs when 50-60% of blood
volume is lost.
Isotonic crystalloid solutions (NS, acetated
Ringer’s or LRS) are the most commonly used
replacement fluids because they are usually
effective, readily available, easily administered,
and relatively inexpensive. Severely hypotensive
patients might require at least one whole blood
volume of replacement fluids during the first hour
of treatment. Initial rapid infusion for dogs should

be 20 to 40 ml/kg IV (one-half this amount for
cats) for 15 minutes, followed by 70 to 90 ml/
kg (dogs) or 30 to 50 ml/kg (cats) administered
over one hour. This loading volume is followed
by administration of maintenance fluids at a rate
of 10 to 12 ml/kg/hr for dogs and 5 to 6 ml/kg/hr
for cats. The patient’s heart and respiratory rates
and urine volume are monitored every 15 minutes
during vascular volume resuscitation. Any signs
of fluid overload necessitate prompt decreases
in fluid delivery and consideration of diuretic
therapy. Optimally, central venous or pulmonary
arterial wedge pressure determinations should
be used to monitor the patient’s hemodynamic
status.
This particular fluid regimen is especially useful
for treating dogs and cats with trauma-induced
peracute blood loss. It has also been proved
efficacious for treating other conditions in which
plasma volume is depleted rapidly, such as
the canine hemorrhagic gastroenteritis (HGE)
syndrome. After volume loading an HGE patient
with crystalloid solution, the plasma proteins
will decrease substantially. In most cases this
will begin to correct itself after the first 24-hour
period of treatment.
Vomiting
Vomiting is the principle sign of gastric disease,
but it can also accompany disorders of the small
or large bowel, liver, and pancreas, as well as
disorders occurring outside of the digestive
system. Vomiting can deplete the body of a
substantial volume of fluids and electrolytes.
The specific types of electrolyte deficiencies
and acid-base abnormalities depend on the
location of the primary disorder. Vomiting
caused by pyloric outflow obstructions typically
can lead to dehydration, metabolic alkalosis,
hypochloremia, hypokalemia, and hyponatremia.
NS supplemented with potassium chloride (3 to
10 mEq/kgBW every 24-hours) is the fluid of
choice.
Fluid losses through vomiting associated with
systemic illness or intestinal disease are best
replaced with lactated or acetated Ringer’s
solutions. The patient’s serum electrolyte
status should be monitored and corrected when
indicated.
Gastric Dilatation-Volvulus (GDV)
The GDV complex causes hypovolemic shock
as well as gastric sequestration of fluids and
electrolytes. Although the hypovolemia can
cause tissue hypoxia and eventually metabolic
acidosis, there are several instances in which the
gastric hydrogen and chloride ion sequestration
can offset the acidosis and perhaps even cause
Back to contents
A
a metabolic alkalosis. Although most dogs with
GDV are initially volume resuscitated with LRS,
their acid-base parameters should be monitored if
possible in order to detect any need for a change
in fluid type.
Oliguric and Anuric Renal Failure
The urine output of all critically ill patients
should be monitored, especially during periods of
intensive fluid therapy. Fortunately, many oliguric
patients will begin producing urine after they
receive one half of their estimated dehydration
deficit values during the first one to two hours of
treatment. If urine production is inadequate, the
following protocol is recommended:
1. Insert an indwelling urethral catheter and
empty the urinary bladder of any residual urine.
2. Administer the calculated dehydration deficit
fluid volume over the first two to four hours of
treatment.
3. Once rehydration has occurred, administer
furosemide (4 mg/kg IV push) and/or mannitol
(0.5 gm/kg IV) over a 10-minute period.
4. If no urine flow occurs, readminister furosemide
(8 mg/kg IV push) or administer dopamine (1 to 2
Fg/kg/min IV).
5. If oliguria or anuria persists, the amount of
fluids infused per day will consist of the sum of
the measured urine output, the insensible water
loss (13-20 ml/kg/day), and the extra losses caused
by vomiting or diarrhea. Peritoneal dialysis will be
required to rid the body of uremic toxins
Plasma volume expansion should be accomplished
with LRS or NS; the latter is preferred if
hyponatremia is present. Maintenance fluids can
initially consist of Ringer’s lactate or acetate
but can eventually be reduced in concentration
to one-half strength in the absence of any renal
sodium-losing disorder.
2006 World Congress WSAVA/FECAVA/CSAVA
Diarrhea
The fluid deficit from massive diarrhea can
be efficiently corrected with LRS because
it resembles the type of fluid lost, is readily
available, and provides uniformly good results. In
markedly hypotensive patients, the intravenous
fluids should be given as described previously
(see Hypovolemic Shock).
Hyperosmolar Conditions
The common causes of extreme hyperosmolality
in the dog and cat include hyperosmolar
nonketotic diabetes mellitus, hypernatremia
associated with water deprivation in diabetes
insipidus patients, and essential hypernatremia
(in dogs). In hyperosmolar diabetes, dehydration
53
A
is easily detectable through skin turgor evaluation;
in the latter two conditions, the interstitial water is
often retained because of a shift of fluid from the
intracellular space, thereby allowing for normal skin
turgor. Eventually, however, the subcutaneous water
will become depleted. In each of these conditions,
hypovolemia can be life-threatening.
It would seem logical that a hypotonic solution such
as D-5-W (252 mOsm/L) would be the fluid of
choice; however, this solution rapidly exits from the
intravascular space (two thirds of the infused volume
exits within the first hour), and thereby does little to
expand the intravascular fluid space. The preferred
initial fluid, therefore, is NS because of its isotonicity,
its tendency to persist within the intravascular space
for a reasonable length of time, and its hypotonicity
relative to the patient’s hyperosmolar plasma. After
adequate plasma space resuscitation, the infusion
can be changed to 0.45% saline with or without
2.5% dextrose added.
In marked hypernatremia (serum Na+ > 165 mEq/L),
the goal of treatment is reduction of the serum sodium
level by 0.5 to 1.0 mEq/L per hour, replenishing one
half of the water deficit in 12 to 24 hours and the
remainder in another 24 hours. This gradual water
replacement will prevent cerebral edema and death,
which can be caused by too rapid correction of the
serum sodium level.
Hypotonic Disorders
A hypotonic disorder is one in which the serum
osmolality and sodium levels are reduced in
2006 World Congress WSAVA/FECAVA/CSAVA
54
Back to contents
parallel. Clinically significant hyponatremia
is most often due to an inability to excrete a
maximally dilute urine.
The goal of treatment in hyponatremia is to
correct body water osmolality and restore cell
volume by raising the sodium-to-water ratio
of extracellular fluid. Acute hyponatremia
occurs when the decline in serum sodium
exceeds 0.5 mEq/L/hr. When levels fall below
120 mEq/L, with associated brain dysfunction,
the condition should be treated immediately.
Hypertonic saline (3% or 5% is administered at a
rate of at least 1 mEq/L/hr to replace sodium.
Chronic hyponatremia is more common than the
acute form and occurs when the rate of decline is
less than 0.5 mEq/L/hr. Slow correction, essential
for preventing central pontine myelinosis,
is accomplished by administering NS and
furosemide at a rate of less than 0.5 mEq/L/hr.
Hypercalcemia
Many patients with hypercalcemia are volume
depleted. Initially, NS should be infused to
normalize intravascular volume. Because the
renal excretions of sodium and calcium are linked,
a forced saline diuresis using furosemide and
isotonic saline will accelerate calciuresis. Close
monitoring of serum electrolyte levels, especially
potassium, is essential to detect and correct
possible hypokalemia. All patients receiving
rapid saline diuresis should be monitored for
signs of intravascular fluid overload.

A - Standards of Care (How I Treat)
ACUTE ADRENOCORTICAL INSUFFICIENCY
Michael Schaer, D.V.M.,
DACVIM, DACVECC
Professor and Assoc. Chair
University of Florida
College of Veterinary Medicine
2015 SW 16th Ave
Gainesville, FL 32608
schaer@mail.vetmed.ufl.edu
Etiology
Adrenocortical insufficiency can result from
the following causes: iatrogenic adrenocortical
atrophy from glucocorticoid administration,
o,p’-DDD-induced adrenocortical destruction,
hemorrhage or infarction of the adrenal
glands, mycotic or neoplastic involvement,
surgical adrenalectomy, anterior pituitary gland
insufficiency, and, primary hypoadrenocorticism.
Pathophysiology
The pathophysiologic consequences of
primary adrenocortical insufficiency are a
direct result of glucocorticoid and aldosterone
deficiencies. Glucocorticoid depletion results
from impaired function of the zona fasciculata.
The hypocortisolemia causes impaired
gluconeogenesis and glycogenolysis, decreased
sensitization of blood vessels to catecholamines,
impaired renal water excretion, and decreased
vitality as characterized by poor appetite, lethargy
and impaired cerebration.
Aldosterone is a mineralocorticoid hormone that
plays an important role in sodium and potassium
homeostasis. Hypoaldosteronism occurs from
impaired function of the zona glomerulosa and
causes renal sodium and chloride ion wasting and
potassium and hydrogen ion retention. The clinical
and pathophysiologic effects of hyponatremia
include lethargy, mental depression, nausea,
hypotension, impaired cardiac output and renal
perfusion, and hypovolemic shock. Hyperkalemia
causes muscle weakness, hyporeflexia, and
abnormal cardiac excitation and conduction. The
addisonian crisis most often occurs in the setting
of moderate to marked hyponatremia (serum
sodium <132 mM/L) and hyperkalemia (serum
potassium > 7.0 mM/L).
The hypoaldosteronism is the chief reason for
the hyperkalemia. The hyponatremia, which
occurs mostly with glucocorticoid deficiency, is
caused by elevated arginine vasopressin levels
and the resulting increased free water retention,
Back to contents
A
decreased sodium pump activity and the resulting
shift of extracellular sodium into cells, and
decreased delivery of filtrate to diluting segments
of the nephron as a result of decreased glomerular
filtration rates.
Differential Diagnosis
The differential diagnosis of hypoadrenocorticism
includes any illness that can characterize as
vomiting, depressed appetite, weight loss,
muscular weakness, or acute collapse. Some
of the more common differentials include
gastrointestinal disorders, renal failure, various
intoxicants, liver disease, and cardiac disorders.
Diagnosis
A tentative diagnosis of acute adrenocortical
insufficiency can be made on the basis of the
history and physical examination findings.
Historically, the dog might have had a chronic
period of weight loss, vomiting and/or diarrhea,
and lethargy. Polydipsia and polyuria are rarely
present in some patients. The chronicity might
vary from weeks to months duration and then
suddenly culminate in an acute hypotensive state
of collapse. On the other hand, the addisonian 2006 World Congress WSAVA/FECAVA/CSAVA
crisis can occur acutely without any prior signs
of illness.
The physical examination findings of the acutely
decompensated patient will depict a generally
ill patient that is either hypo- or normothermic.
Hydration varies from normal to varying degrees
of dehydration. The mentation is dull, and muscle
weakness is usually marked. The respiratory
rate can be normal or rapid, the latter due to
either shock and/or attempted compensation for
a metabolic acidosis. The mucous membranes
are usually pink, but the capillary refill time is
prolonged. Cardiac auscultation can detect either
normal sinus rhythm or arrhythmias, especially
bradyarrhythmias. The pulse quality is weak, and
the rate varies from normal to slow.
The electrocardiogram is a useful diagnostic tool
55
A
for the detection of the various conduction and
complex abnormalities that are associated with
hyperkalemia. The most common abnormalities
include flattened P-waves, increased positive
or negative deflected T-waves, broadened
QRS complexes, bradycardia, sinoventricular
complexes, and atrial standstill. These
electrocardiographic abnormalities do not occur
until the serum potassium exceeds 7.5 mM/L,
but they can occur at 7.0 mM/L when the serum
sodium is < 130 mM/L.
The tentative clinical diagnosis of Addison’s
disease is based on clinicopathologic test results.
The hallmark findings include hyperkalemia
and hyponatremia (Na/K < 25:1). Some atypical
addisonian patients can have hyponatremia
with normokalemia or hyperkalemia with
normonatremia. Other causes of hyponatremia
with hyperkalemia have to be differentiated
from adrenocortical insufficiency. These include
renal failure, gastroenteritis, decompensated
diabetes mellitus, ascites and chylothorax. Some
addisonians might have normal electrolytes yet
have hypocortisolemia. Additional associated
clinicopathologic abnormalities include
mild to moderate hypochloremia, azotemia,
hyperphosphatemia, metabolic acidosis, and
rarely hypothyroidism. Mild hypercalcemia is
oftentimes present, but of no clinical significance.
Hypoglycemia occurs rarely, but may be the
only presenting abnormality in an atypical
addisonian.
Although the above historical, physical,
clinicopathological and electrocardiographic
abnormalities are strongly suggestive of acute
hypoadrenocorticism and usually constitute
the basis for the clinical diagnosis and the need
for immediate therapy, the absolute diagnosis
depends on the demonstration of absent or
minimal adrenocortical response to an injection of
corticotropin (ACTH). The following procedure is
2006 World Congress WSAVA/FECAVA/CSAVA
recommended soon after the patient’s admission
in order to avoid any unnecessary delay of therapy
for the sake of performing a diagnostic test.
(1) Draw blood for hemogram, serum biochemistry
and basal cortisol determinations.
(2) Begin the intravenous fluids and give 2-5
mg/kg of dexamethasone sodium phosphate
intravenously.
(3) Immediately give 0.25 mg of alpha 1-24
cosyntropin (dogs) (Cortrosyn-Organon)
intramuscularly or intravenously. Cats should
receive 0.125 mg.
(4) Withdraw a second blood sample for plasma
cortisol determination 45-60 minutes later.
The patient will derive the benefit of undelayed
treatment while simultaneous confirmatory
56
Back to contents
diagnostic tests are performed with the above
technique. The post ACTH injection cortisol blood
level will barely increase above the basal value
in typical hypoadrenocorticism. Blood levels of
< 1.0 Fg/dl are typical, while those stimulating
to only 2-3 Fg/dl also suggest hypoadrenocortical
function.
Treatment
Treatment should begin immediately whenever
the index of suspicion is strong for diagnosis
of an addisionian crisis. The therapeutic
objectives include (1) intravascular volume
resuscitation, (2) correcting the hyponatremia and
hyperkalemia, (3) providing glucocorticoids, and
(4) recognizing and reversing any life-threatening
cardiac arrhythmias.
Sodium chloride 0.9% is the fluid of choice
and should be delivered through an indwelling
intravenous catheter. The saline should be infused
at a rate of approximately 75 ml/kg body weight
during the first 1 to 2 hours of treatment if the dog
is markedly hypotensive. Care should be taken to
avoid an iatrogenic intravascular fluid overload
because of the addisonian patient’s theoretical
intolerance to acute water loading. Central
venous pressure determinations should be done in
order to safeguard against this complication. For
the remaining 24-hour period, the isotonic saline
can be evenly infused at a maintenance rate of
approximately 60 ml/kg body weight so long as
the serum sodium concentration does not increase
by more than 8-12 mM/L (or 0.5 to 1.0 mM/L per
hour) during the first 24-hours if the initial serum
Na+ was < 125 mM/L. The intravenous fluids
are discontinued when hydration, urine output,
serum electrolytes, the BUN levels are restored
to normal (usually following 48 to 72 hours of
treatment), and the patient begins eating.
Although intravenous saline will help correct
the hyponatremia and hyperkalemia, the patient
must also receive a mineralocorticoid drug
that will enhance renal distal tubular sodium
reabsorption and potassium excretion. When
desoxycorticosterone acetate (DOCA) was
available the dose ranged from 1.0 mg for a
small dog to 5.0 mg for a large dog and was
given once daily intramuscularly. In many
patients, the subsequent daily doses of DOCA
was decreased to approximately one-half of
the initial dose due to the synergistic effects of
fluids, DOCA and glucocorticoid medications.
Currently DOCP (0.5 mg/kg IM) can be used in
its place although its rate of onset is slower than
DOCA. When DOCA or DOCP are unavailable,
fludrocortisone acetate (Florinef; Bristol-Meyers
Squibb Company) should be given orally at an
initial dosage 0.1 mg/5 kg body weight per day.

Re-assessment of the serum electrolyte levels
will serve as a helpful treatment guide for further
dosage adjustments.
The glucocorticoid deficiency is best corrected with
rapid-acting drugs such as prednisolone sodium
succinate or dexamethasone phosphate. These
glucocorticoid drugs should be given intravenously
once initially at doses of 5-10 mg/kg and 2-5 mg/kg
body weight, respectively for prednisolone sodium
succinate and dexamethasone phosphate. Subsequent
glucocorticoid requirements are fulfilled by
administering 1 mg/kg body weight of prednisolone
orally, intramuscularly, or intravenously every 12
hours through the second day and then reducing
the dose to 0.25 to 0.5 mg/kg body weight every 12
hours for the remainder of hospitalization.
Hydrocortisone sodium succinate can be given
for glucocorticoid replacement taking advantage
of the fact that this particular glucocorticoid
contains some mineralocorticoid activity. The
emergency dose for shock is 20-25 mg/kg body
weight IV every 6 hours. There has been no
proven advantage with the use of hydrocortisone
sodium succinate.
Serum potassium concentrations greater than
7.0 mM/L can cause progressive abnormalities in
myocardial excitation and conduction. The degree
of hyperkalemic myocardial toxicity ranges from
mild to severe based on the electrocardiographic
changes, and only with severe changes is special
therapy warranted. In such cases treatment
should consist of 10% calcium gluconate, sodium
bicarbonate, and/or insulin-dextrose solutions.
Ten percent calcium gluconate solution is
given at a dose of 0.5 to 1.0 ml/kg body weight
intravenously over a 5- to 10-minute period,
accompanied by continuous electrocardiographic
monitoring. It directly antagonizes the myocardial
toxic effect of hyperkalemia, but it will not lower
the serum potassium level. Calcium gluconate
takes its affect within minutes. To accomplish
this latter effect, sodium bicarbonate solution
is given at a dose of 1-2 mEq/kg body weight
intravenously over a 5- to 10-minute period.
Back to contents
A
Bicarbonate takes its affect after approximately
15 minutes. Regular crystalline insulin at an
intravenous dose of 0.25 unit/kg body weight will
also lower the serum potassium level. Two to three
grams of dextrose per unit of insulin administered
should also be given by intravenous push in order
to avoid the anticipated hypoglycemic effects of
insulin. The insulin dextrose treatment will lower
the serum K+ after approximately 30 minutes.
The above emergency measures for the treatment
of myocardial toxicity are required only once and
need not be repeated.
Complications
The majority of dogs with Addison’s disease
have an excellent prognosis for a normal quality
of life. Early complications that might alter a
favorable outcome include acute renal failure
resulting from renal ischemia associated with
protracted hypotension and cardiac dysfunction.
If the patient is oliguric or anuric following the
initial period of intravascular volume expansion,
mannitol should be given intravenously at a dose
of 0.5 gm/kg body weight in order to promote an
osmotic diuresis. Furosemide (1-2 mg/kg IV) and
dopamine (2-5 µgm/kg/minute) can also be used
to counteract oliguria. An indwelling urethral
catheter should be inserted to quantitate the urine
output until it is deemed adequate.
Central pontine myelinosis can occur as a result of too
rapid correction of the serum sodium concentration.
The parenchymal central nervous system tissue
changes associated with this condition can cause
signs of seizures, behavioral changes and paresis.
The mechanism involves an osmotic dysequilibrium
between the brain parenchyma and the plasma that
occurs when the onset of hyponatremia is over 24
hours duration and is corrected at a rate exceeding
0.5 to 1.0 mM/L per hour. When the initial
serum sodium concentration is < 125 mM/L
it should not be allowed to increase by more
than 8-12 mM/L over the first 24-hours in order
2006 World Congress WSAVA/FECAVA/CSAVA
to avoid this complication.
57
A
A - Standards of Care (How I Treat)
ACUTE PANCREATITIS
Joerg M. Steiner, Dr.med.vet.,
PhD, DACVIM,
DECVIM-CA
Gastrointestinal Laboratory
Department of Small Animal
Clinical Sciences College
of Veterinary Medicine and
Biomedical Sciences
4474 TAMU
College Station, TX 77843-
4474
USA
jsteiner@cvm.tamu.edu
Introduction
Acute pancreatitis can be mild or severe and can
be associated with systemic and/or pancreatic
complications. The therapy of patients with acute
pancreatitis is mainly dependant on the presence
of such systemic or pancreatic complications.
Supportive Care
Whenever possible the inciting cause should
be removed. Exposure to unnecessary drugs,
especially those implicated in causing pancreatitis
in dogs, cats, or other species, should be avoided.
Also, aggressive fluid therapy is the mainstay of
supportive therapy regardless of the underlying
cause of the disease process. Fluid, electrolyte,
and acid-base imbalances need to be assessed and
corrected as early as possible.
Alimentation
The traditional recommendation for any patient
with pancreatitis is to give nothing per os for three
to four days. This recommendation is justified in
patients that vomit, but there is little evidence to
justify this strategy in patients that do not.1 The
2006 World Congress WSAVA/FECAVA/CSAVA
issue is complicated further in cats by the fact
that cats with pancreatitis often develop hepatic
lipidosis.2 Preferred routes of alimentation are
a jejunostomy tube or total parenteral nutrition.
However, these strategies are impractical in many
cases and a gastrostomy tube or a nasogastric
tube are acceptable alternatives if a patient does
not vomit. However, in dogs or cats that do vomit
the patient should be held NPO for 3-4 days.
In cats alternative routes to oral alimentation must
be pursued if the cat has been anorectic before
presentation or if there is evidence to support
concurrent hepatic lipidosis. After holding
a patient NPO water is slowly reintroduced,
followed by small amounts of a carbohydrate-
rich and low-fat diet.
58
Back to contents
Analgesia
Abdominal pain is commonly recognized in dogs
but not in cats with pancreatitis.3,4 However, the
presence of abdominal pain should be assumed
and analgesic drugs are indicated in all small
animal patients with pancreatitis. Meperidine,
butorphanol tartrate, or morphine can be used
parenterally. Other alternatives are a fentanyl
patch or the intraabdominal administration of
lidocaine.
Plasma
Studies in dogs suggest that when α2-
macroglobulin, one of the scavenger proteins
for activated proteases in serum, is depleted
death ensues rapidly. Fresh frozen plasma
(FFP) and fresh whole blood not only contain
α2-macroglobulin, but also albumin, which has
many beneficial effects in patients suffering from
severe pancreatitis. In clinical trials in human
patients with acute pancreatitis there was no
benefit of plasma administration. However, the
author believes that FFP is useful in dogs with
severe forms of pancreatitis.
Antibiotic Therapy
In contrast to human beings, infectious
complications of pancreatitis are rare in dogs
and cats with pancreatitis. Therefore, the use of
antibiotic agents should be limited to those cases
when an infectious complication can be identified
or is strongly suspected.
Anti-inflammatory Agents
There is no data on the use of anti-inflammatory
agents in dogs and cats with severe pancreatitis,
but no benefit was found in human patients. In dogs
and cats with severe pancreatitis corticosteroids
should only be used in secondary cardiovascular
shock. Corticosteroids may be needed to treat
small animal patients with IBD and concurrent

pancreatitis, and do not appear to be harmful
in these patients. Also, immune-mediated
pancreatitis is recognized with increasing
frequency in humans with pancreatitis.5 While
immune-mediated pancreatitis has not been
described in small animals the author believes
that such a disease entity also exists in small
animal patients.
Other Therapeutic Strategies
Many other therapeutic strategies, such as
the administration of trypsin-inhibitors (e.g.
trasylol), platelet activating factor inhibitors
(PAFANTs), dopamine, antacids, antisecretory
agents (i.e. anticholinergics, calcitonin, glucagon,
somatostatin), or selenium, and peritoneal lavage
all have been evaluated in human patients with
pancreatitis. With the exception of PAFANTs and
selenium, none of these have shown any beneficial
effect at this point. The efficacy of selenium,
which has also been shown to decrease mortality
in dogs with pancreatitis in an uncontrolled study,
needs to be further evaluated before its use can be
recommended.
Prognosis
The prognosis for dogs and cats with acute
pancreatitis is directly related to disease severity,
Back to contents
A
extent of pancreatic necrosis, occurrence of
systemic and pancreatic complications, duration
of the condition, and the presence of concurrent
disease.
References
1. Williams DA, Steiner JM. Canine pancreatic
disease. In: Ettinger SJ, Feldman EC. eds.
Textbook of Veterinary Internal Medicine. St.
Louis: Elsevier Saunders, 2005; 1482-1488.
2. Akol KG, Washabau RJ, Saunders HM, et al.
Acute pancreatitis in cats with hepatic lipidosis.
J Vet Int Med 1993; 7: 205-209.
3. Hess RS, Saunders HM, Van Winkle TJ, et al.
Clinical, clinicopathologic, radiographic, and
ultrasonographic abnormalities in dogs with fatal
acute pancreatitis: 70 cases (1986-1995). J Am
Vet Med Assoc 1998; 213: 665-670.
4. Washabau RJ. Acute necrotizing pancreatitis.
In: August JR. ed. Consultations in feline internal
medicine. St. Louis: Elsevier Saunders, 2006;
109-119.
5. Klöppel G, Lüttges J, Löhr M, et al.
Autoimmune pancreatitis: Pathological, clinical,
and immunological features. Pancreas 2003; 27:
14-19.
2006 World Congress WSAVA/FECAVA/CSAVA
59
A
A - Standards of Care (How I Treat)
CATS WHO BITE PEOPLE WHO PET THEM
Karen L. Overall, MA,
VMD, PhD
Diplomate ACVB
ABS Certified Applied Animal
Behaviorist
Center for Neurobiology and
Behavior
Psychiatry Department - Penn
Med Translation Research
Laboratory
125 S. 30th St.
Philadelphia, PA 19104
overallk@mail.med.upenn.edu
http://psych.ucsf.edu/
K9Behavioral/Genetics/
Epidemiology of cat bites: Problem aggression
is second only to elimination disorders in
commonness of complaints about cat behavior.
Given the multifaceted role played by scent in
feline social systems, this should not be surprising.
Unfortunately, the extent to which the interaction
between feline aggression and elimination
disorders is involved in tough problems is under-
appreciated. Feline aggression is emerging as a
common and worrisome problem, especially
when viewed with regard to its potential to cause
serious illness in people.
Cat scratch disease: 22,000 cases - 1.8-10 cases
/ 100,000 people - of cat scratch disease are
reported each year in the U.S.; 2,200 people are
hospitalized, annually. The presumptive agent
in cat scratch disease (CSD) is the rickettsial
organism Bartonella (formerly Rochalimaea)
hensalae, and a contributory role has been
postulated for the bacteria Afipia felis. 38/45
patients with CSD had titers of >/= 1:64 for
2006 World Congress WSAVA/FECAVA/CSAVA
Bartonella hensalae. CSD is most commonly
seen in the late summer and fall and coincides
with seasonality in births of kittens (spring) and
the entry of these kittens into the house in the
winter. Fleas infestation may be associated with
a higher incidence of the CSD and most patients
have at least 1 kitten that has fleas. Patients with
CSD are more likely to have a kitten less than
or a year of age, or to have been scratched by
a kitten than are non-patients. While patients
in kitten-owning households are more likely to
have been scratched or bitten than patients in
non-kitten owning households, there appears to
be no association with patients’ cats and those of
controls with regard to indoor / outdoor status,
litter box use, and hunting behaviors.
Cats transmitting CSD appear healthy although
they have active B. hensalae infections that last
60
Back to contents
months. People with CSD tend to have localized
skin lesions that are followed by regional lymph
node involvement 3 weeks post exposure. Lymph
nodes remain enlarged for several months.
Systematic illness is rare, but fever, headache,
splenomegaly, and malaise are common.
These are usually self-resolving; however,
arthritis, neuroretinitis, pleurisy, pneumonia,
osteolytic lesions, granulomatous hepatitis, and
encephalitis, with coma and seizure, can be an
unusual sequela. Individuals with AIDS or those
immunosuppressed for other reasons are at risk
for more severe disease, including bacillary
angiomatosis.
In addition to being a human health hazard, CSD
is costly: the cost of treatment for ambulatory
patients averages $5.2 million per year, and the
cost of treatment for hospitalized patients exceeds
$6.9 million per year, in 1990s USD.
Cat scratch disease is an occupational hazard for
those working in veterinary medicine. When cats
are fearful or distressed, they try to escape and
withdraw. As a precursor to withdrawal, or as a
means to make withdrawal possible, cats will bit
and scratch. Understanding how to better handle
cats in veterinary settings and how to teach clients
to better accustom cats to veterinary visits should
reduce the number of injuries to humans.
Aggressive behaviors: Survey studies indicate
that, over their lifetime, 80% of cats hiss at each
other, 85% swat at each other, 70% fight with each
other occasionally, 25% hiss / growl at people and
60% of them scratch or bite people occasionally.
53.6% of the cats in this study exhibited hissing
sometimes (1 time per month) or frequently
(1+ times per week), 63.1% exhibited swatting
sometimes or frequently, and 44.5% exhibiting
fighting sometimes or frequently.
Statistical examination of data collected by

Borchelt and Voith (1987) indicate that cats are
more often aggressive to other cats than people
in situations involving defensive and territorial
aggression (p<0.05; Gadj=32.627 and 11.442,
respectively), but are more often aggressive to
people when compared with cats in circumstances
involving play aggression (p<0.05; Gadj=25.091).
Their study did not evaluate a baseline of normal
behaviors (perhaps cats are not involved in play
aggression often with cats because they are
corrected by the other cats sufficiently early in
the sequence of play to avoid frank aggression),
but suggests situations in which people might be
at risk.
The aggressive behavior of the cats may not
be manifest the same way towards all people.
There are few actual data on cat bites, and those
that have been published generally provide no
statistical examination of the data, but if authors
publish their data, others can do I as have done,
and provide the analysis. Careful examination
of data published by Borchelt and Voith (1987)
indicates that for cats that are deemed “frequently”
aggressive, there is no difference between the
frequency of growling or hissing that is directed
towards strangers compared with that directed
towards family members (ns; Gadj=0.209), but that
family members are more frequently subjected to
swatting, scratching and biting without breaking
the skin, and bites that break the skin (p<0.05;
Gadj=21.197,30.014, and 9.554, respectively).
Closer statistical investigation reveals that
family members are more frequently victimized
than are strangers by cats that break the skin,
only by cats that have inflicted 3,4, or more
than 8 bites (p<0.05; Gadj=3.874, 4.179, 22.311,
respectively).
Categories of feline aggression - associations
with human / cat aggression: It’s important
to remember that some of the circumstances
in which humans will be injured by cats may
involve “normal” aggressive behavior on the
part of the cat. Cats who protect their kittens
when there is really a threat are not showing
manifestations of a diagnosis of maternal
aggression. Likewise, cats who are afraid of a real
threat are behaving normally and appropriately,
rather than demonstrating manifestations of
fearful aggression. Seen within this context, much
of the aggression demonstrated at veterinary
practices is normal aggression associated with
fear. Accordingly, we can address this by either
learning how to anticipate the problem, and
lesson the result, and, or by preventing it.
The easiest way to prevent such aggression is to
acclimate the cat to the situation. Cats respond
most plastically to novel stimuli between 5
and 9 weeks of age, and their ability to remain
Back to contents
A
flexible in response to novel stimuli decreases
greatly by 14 weeks of age, if they have not
been previously exposed to novel situations.
Although the data have not been completely
collected, early exposure to a variety of stimuli
that are not terrifying may be necessary for the
cat to learn to learn. In other words, if the cat
is “protected” from the world, they may have
decreased plasticity in their responses to changes
in social and environmental stimuli later in life.
We can use this information to benefit the cat’s
overall “wellness” and mental health: simply, any
client with a kitten should take advantage of the
cat’s natural curiosity and energy and stimulate
the kitten to explore and interact with as many
environments as possible.
First, clients should fit their kittens with harness
and light-weight lead and encourage the cat to go
for walks outside of the house or apartment. If
the cat is slightly nervous, he or she can just sit
on the client’s lap and be an observer until the
cat decides to venture forth. Even if the clients
have a back yard, it is safer, more humane, and
more considerate for neighbors if the cat is kept
on a lead or a trolley. For these to be safe, clients
need to supervise the cat. If clients wish to give
their cat the experience of the outdoors without
supervising them, outdoor habitats can now be
built with very little effort or custom made to
encircle trees, branches, decks, and windows.
Second, clients should be encouraged to carry and
use treats for cats as they do for dogs. Most kittens
will readily work for small shrimp, dried liver or
bacon, or a dab of some of the salty, fermented
spreads (e.g., Marmite, Veg-e-mite). The key is
convincing the clients that their little balls of fluff
are intelligent, cognitive, curious beings who can
be trained to work with the client. If clients would
interact with their cats in this manner both of their
cognitive lives would be enriched.
Third, clients should be encouraged to take the
cat with them - temperature permitting - in the car
2006 World Congress WSAVA/FECAVA/CSAVA
whenever they can. Cats can be restrained in car
harnesses, in an open crate, or using pet gates.
Fourth, clients should be encouraged to take their
cat visiting to the vet’s multiple times during the
cat’s first year of life. If the cat visits the vet and all
that happens is that the cat is petted, fussed over,
played with, and given treats, the cat will learn
that this is good place to visit. Routine exams will
then become easier, if the vet continues buying
into and encouraging the concept of positive
rewards and interactions. For example, if the
cat is not worried about getting into the carrier
and going to the vets, then when he gets there he
might be far more interested in the food treat that
is smeared on the exam table than he is in fighting
the vet.
61
A
Getting vets to buy into the idea of using toys and
treats at every visit is not a trivial problem. Most
vets are concerned about their tightly booked
appointments and the time / money conundrum.
However, most of us fail to accurately account for
all the time we struggle with patients and clients,
all the times we need more hands than we have to
restrain an animal, and for the real cost to us and
the patient - in both physical and emotional terms
- of such struggles. Were we to do an accurate
accounting, we would be investing in any strategy
that lowers our frustration time and our patients’
stress levels.
An easy way to get vets to start working with cats
differently is to hold kitten classes. While many
practices hold puppy classes, few practices in the
US hold kitten classes (but many in Australia do:
see Training Your Cat by Kersti Seksel, Hyland
House, Australia, 2001). These are ideal for
kittens 8-13 weeks of age, and if conducted in 2
sessions allows the veterinary staff to cover all
relevant preventative behavioral and medical
topics, and also permits adequate time to teach
clients how to play with cats, to encourage clients
to watch normal cat behavior, and to teach the
cats to sit, stay, come, do a trick, and to walk on
lead and harness.
Tables 1 and 2 contain a summary of information
to discuss at the first appointments, or - preferably
- in kitten classes. If it is impossible to cover all
of this information during the first examination,
a series of short-examinations, arranged as a
package at one price, or a long first puppy or kitten
visit (2 hours can be a realistic estimate) arranged
as part of a package deal with all vaccinations can
be options. Videos, client handouts, and support
staff participation are invaluable. If the puppy
or kitten is going to undergoing a series of three
vaccinations, the information can be outlined at
the first visit and a schedule of topics to cover
at that and subsequent visits developed. There
2006 World Congress WSAVA/FECAVA/CSAVA
are many variants on this approach and ALL are
somewhat labor intensive; however, that labor
pays off. Clients want information and will
pay for it and treatment later if they received it
first. Also, pets that are killed because of later
behavioral problems do not generate income
and do not contribute to an attitude and bond
that encourages the generation of income. What
veterinarians should NOT do on the first visit,
is rush the pup or kitten through in 5 minutes
(because it is generally healthy) and quickly (and
scarily - to the pet) vaccinate it.
First visits may not even involve a vaccination
- that activity may be better executed the next day
(when it could be done quickly after a temperature
check if the first visit included a thorough physical
examination). The first visit should involve
62
Back to contents
acquaintance with the staff, play, fuss, treats, a
physical examination, and possibly, a vaccination
sneaked in at the end of play. Encourage clients to
return between appointments to just visit - this is
great for the puppy or kitten and them. Of course
they will ask your staff questions, but they can
also be told up front, when invited to drop in, that
if the staff is too busy for the visit they will say
so.
These activities are outlined in the checklists
in Tables 1 and 2. Clients should practice these
activities often, whether the pet “needs” them or
not. Obviously, toe nails should not be clipped or
filed unless needed, but the client can manipulate
the kitten’s toes and hold them in the way they
would when they clip them. This will make the
actual activity easier. Repeated exposure of the
new pet to these activities will help the client in
two respects: (1) they will help render then pet
more tractable and less fearful of manipulation,
and (2) they will familiarize the client with
“normal” so that they can report deviations from
this to you.
When considering whether a cat’s aggression
is contextually appropriate or ‘normal’, it is
important to bear in mind the evolutionary
derivation of domestic cats, especially since this
differs dramatically from that of dogs.
Feline social systems differ from those of dogs
in the extent to which solitary versus social
daily activities are prevalent. Cats are primarily
solitary hunters, ingesting prey that is smaller
than they are, whereas most wild canids work
in groups to obtain prey larger than themselves.
These forces will act to shape social relationships
within groups. Cats can hunt sufficiently for one
meal alone, while dogs use this only as a back-
up foraging strategy. Dogs are more aligned with
the “binge and gorge” eating style than are cats.
Because cats don’t rely on running down prey
and exhausting them before the group moves in
to attack, stealth is much more important to cats
than it is to dogs, and it may be associated with
the cat’s normal tendency to hide when stressed
or distressed. Finally, it’s really important to
remember that the history of cats and humans is
the history of disease control: cats were attracted
to rodents who are always attracted to human
garbage. Cats killed the rodents that carried
diseases or vectors of disease. Consequently, there
has been little artificial selection by humans on
how cats behave. In fact, selection for how they
look is fairly recent and only taken place intensely
in the past 200 years. Dogs were selected because
of their shared behaviors with humans to help
humans in tasks in which both species engaged.
Hence, breeds in dogs have their roots in the jobs
the dogs did - not what they looked like.

As a consequence of their evolutionary system,
matrilineal social system, and skewed sex ratios
for mating in free-ranging domestic casts, Most
normal aggression between cats appears to occur in
contexts involving territory and social rank which
are complexly interrelated. It is not surprising that
the types of inappropriate aggression witnessed
by owners differ from those that we perceive in
dogs, and that they are understandable given the
evolutionary context of feline social systems and
the developmental context of sensitive periods.
Attention has been paid to the extent to which
feline aggression is covert, rather than overt and
defensive, rather than offensive (Table 3). These
can be useful distinctions in understanding and
intervening in the interactions between cats and
other individuals involved in the aggressive
circumstances. Clients must learn to read the
signs of these behaviors to correctly interpret
the ongoing interaction and to help us to treat
the problem appropriately. Offensive aggression
generally involves components that decrease the
distance between the individuals. These behaviors
can include approach (as a threat with subsequent
flight of the other individual) and attack.
Regardless, the aggressor controls the interaction
through the use of threat or the escalation of
violence. Defensive aggression involves passive
behaviors designed to encourage avoidance and
withdrawal. This serves to remove the stimulus
for further aggression (Young, 1988). Spraying
can act as a defensively aggressive behavior
when it serves this purpose.
Client often have trouble recognizing aggression
within their feline household because they are
only aware of overt forms of aggression. It will
help them if you emphasize that cats are not
small dogs: the most common form of aggression
in cats is subtle, covert aggression that involves
posturing on the part of the aggressor and
deference on the part of the recipient of the
aggression. Assertions that cats are not social
have interfered with our ability to understand
both these types of aggressions when they occur
between cats and when they are directed by the cat
to people (assertion or status-related aggression).
Cats generally exhibit overt aggression when they
perceive each other as equal rivals and neither cat
defers to the other. This situation is more common
in crowded situations like laboratory colonies,
households with too many cats, or urban, stray
groupings. Covert aggression is more likely to
occur if cats know each other well, and if all cats
involved either agree that they do not see each
other as equals, or if some cat is not sufficiently
confident to overtly challenge another cat.
Spraying and non-spraying marking can play a
role in both of these circumstances.
Back to contents
A
Categorization of feline aggression is similar
to that of canine aggression; differences in
the manifestation of the aggressions may be
attributable to differences in mating behaviors
and differences in social hierarchies. Diagnoses of
feline aggression that involve humans include:
1. - aggression due to lack of socialization
2. - play aggression
3. - fearful aggression
4. - pain aggression
5. - redirected aggression
6. - assertion or status-related aggression
These are the behavioral, functional,
phenomenological classifications of aggression.
It should be noted that cats, like dogs, can
be aggressive because of or as a sequelae to
underlying organic disease. Medical rule-outs for
feline aggression include hepatoencephalopathy,
feline ischemic encephalopathy, lead poisoning,
hyperthyroidism, epilepsy, and rabies. To the
extent that pain aggression is sometimes associated
with illness, it should act as a flag for a possible
underlying condition; however, in the sense that
the term is used here, the aggression is the result of
the pain, not of the underlying condition.
1. Aggression due to a lack of socialization:
The effect of exposure during sensitive or
developmental periods in young animals has
been debated. In the 1950s Scott and Fuller
investigated the role of developmental periods
within the first few months of dogs’ lives on their
ability to develop appropriate social behaviors.
While these periods, called “sensitive” periods
by Bateson exist, they are best viewed in the
context of risk assessment. Animals for whom
all sensitive period requirements were met can
still have problems, and animals who missed
socialization for the relevant periods can do well;
however, the risk of having problems attendant
with the respective socialization or sensitive
period increases if exposure during the that 2006 World Congress WSAVA/FECAVA/CSAVA
period is missed.
For example, cats who have not had contact
with humans prior to 3 months of age have
missed sensitive periods important for the
development of normal approach responses
to people. Karsh and Karsh and Turner (1988)
examined the extent to which the social
environment experienced by cats affected their
ability to interact with people. Among their
findings, which are more fully discussed in the
chapter on normal cat behavior, were that cats
that were not handled until 14 weeks of age, were
fearful and aggressive to people, regardless of the
circumstances. These cats would not volitionally
approach humans, and were aggressive if they
could not escape. In contrast, cats handled for as
63
A
little as 5 minutes per day from the day they were
born until they were 7 weeks of age were quicker
to approach and solicit people for interaction and
gentle play, were quicker to approach inanimate
objects, and were quicker to play with toys. This
suggests that there are complex, far-reaching
consequences of early interaction with people.
Lack of such social interaction with other cats
may result in the same lack of normal inquisitive
response to other cats. This negative response
can be augmented by sub-optimal nutritional
conditions for the pregnant queen. Kittens
born to such queens generally have a delayed
developmental skills in addition decreased ability
to learn, and increased (and usually inappropriate)
reactivity to novel situations and stimuli, and an
inappropriate response to other cats (this is more
fully discussed in the chapter on normal feline
behavior). The chance of such cats responding
normally to most situations involving any
interaction is diminishingly small. Furthermore,
total isolation from cats can have negative
consequences for future interaction with humans.
This constellation of deprivation scenarios may
be contributory to many of the aggressions seen
in urban, feral cats. These cats will never be
normal, cuddly pets, although they may attach
to one person or a small group of people over a
period of time. If forced into a situation involving
restraint, confinement, or intimate contact, these
animals may become extremely aggressive.
2. Play aggression: Cats who were weaned early
and then hand raised by humans may never have
learned to temper their play responses. Social
play in cats peaks early and is replaced by more
predatory activities by weeks 10-12 and by social
fighting by week 14. Cats who, as kittens, never
learned to modulate their responses may play too
aggressively with owners. These cats may not
have learned to sheathe their claws or inhibit their
bite. 7/27 cats studied by Chapman and Voith
2006 World Congress WSAVA/FECAVA/CSAVA
(1990) were diagnosed with play aggression. The
frequency of this aggression is likely to be directly
related to the demographic environment of the cat
community - urban practices may have more cats
with a history consistent with the development of
play aggression.
It is not clear if there is a component of oral
response associated with an owner who bottle
fed the cat. Were the kitten to nurse too hard on
the mother or hurt her in play, the mother would
have swiftly corrected the kitten. This appears
to be less common among owners playing the
nursing role, possibly because they are concerned
about injuring the kitten. This is a valid concern;
however, if they mimic feline behaviors such as
neck bites an growls or hisses, the kitten learns
to respond and inappropriate play behavior
64
Back to contents
and play aggression may not develop. Should
these problems still ensue, they are treatable
using behavior modification that interrupts the
inappropriate behavior and replaces it with a
more appropriate one. For example, the kitten
that is playing roughly can be blasted with a water
pistol or a compressed air canister at close range
to startle it; this is most effective if the startle
occurs as the cat is commencing the inappropriate
behavior. Then, when the cat seeks out the
owner’s company, the owner can strike, massage,
and provide the cat with food treats whenever it
is acting calm. Owners must be vigilant for the
first signs of any inappropriate behavior (pupils
dilating, claws unsheathed, ears back, legs and
shoulders stiffening, tail twitching) and correct
the cat using a correction designed to startle as
early in the sequence as possible. The startle
technique, whether tapping on the nose, blowing
in the face or using a water pistol or air canister,
should be humane: this means that the lowest
level of stimulus that gets the desired effect of
aborting the behavior and moving on to another
is the one that should be used.
3. Fearful, fear, or fear-induced aggression:
Fearfully aggressive cats will hiss, spit, arch
their backs, and piloerect, if flight is not possible.
Flight, a defensive activity, is virtually always
a component of fearful aggression in cats. As
they are pursued with increasingly less escape
space, cats will draw their head in, crouch, growl,
roll on their back if approached (this is NOT a
“submissive” behavior in cats - it is an overt,
defensive behavior), and paw at the approacher.
If the approacher continues his or her pursuit,
the fearfully aggressive cat will try to strike
at him or her, and follow this with holding the
approacher, using the forepaws, while kicking
with the pack feet and biting around the neck.
Most people who have seen or experienced
rough play from cats are also familiar with this
sequence of behaviors. When fearful aggression
involves other cats, the cats that are fearfully
aggressive generally do not seek out the other cat
for aggressive interactions. Fearful aggression
usually involves a combination of offensive
and defensive postures and overt and covert
aggressive behaviors (Leyhausen, 1979).
There are genetically friendly cats and genetically
shy cats. It is unclear the extent to which shy cats
have the potential to become fearfully aggressive,
but there are cats who, despite the best socialization
possible, become aggressive whenever fearful.
These cats also may become fearful without an
apparent stimulus. Regardless, if threatened, any
cat will defend itself. Depending on the outcome
of the treat, the cat can learn to become fearfully
aggressive. This is particularly important if

small children are involved, since they may
not know how to appropriately respond to a cat
that is crouching. Any animal that is cornered
and cannot escape has the potential to attack.
It is imperative that the cat not learn that his or
her only recourse is aggression since this could
lead to them becoming aggressive in response
to any approach. Behavior modification can be
very effective early in the development of the
condition. Pharmacological intervention can be a
useful adjuvant. It is not clear if any intervention
can be successful if the condition is genetic.
4. Pain aggression: As is true for dogs, cats that
are painful, either because of an injury or as a
sequelae to an underlying medical condition, can
be painful upon manipulation. Practitioners can
often induce this type of aggression in injured or
arthritic and dysplastic cats. It can often become
fearful aggression if it is result of long-term
painful treatment. It is a defensive aggression, and
will respond to measures that alleviate the pain,
and minimize the potential to be exposed to it.
Companion animal analgesia is finally receiving
the attention it deserves. Appropriate use of such
analgesia can minimize painful aggression in any
animal.
Cats who have gotten their tails caught in doors are
often very aggressive whenever anyone attempt
to touch their tail. Some of this could be fear,
but even when restrained they appear to become
aggressive during manipulation. It is possible
that they have some long-standing damage that
is not apparent in medical and neurological
work-ups. Behavior modification designed to
teach them to relax and tolerate touching can be
useful, as can anti-anxiety medication. The same
phenomenon is infrequently reported for cats that
have undergone declaw and who now will not
use their feet. When their feet are manipulated
these cats are, apparently, painfully aggressive.
Full work-ups, including radiography, usually
reveal no detectable abnormality, leading to
discussions of “phantom” pain. Pain is a complex
issue and probably under-appreciated in such
circumstances. These cats also often respond well
to behavior modification designed to teach them
to relax and to anti-anxiety medication.
If there has been no painful medical intervention
and the cat appears to exhibit this behavior,
consider abuse. Cats, particularly strays, are
good victims for torture, and may represent the
first sign that untoward events are occurring in a
household where there are children.
The role of pain aggression in cat-cat interactions
has been under-explored, but, especially when
cats are mismatched by size, health status, or
temperament, is probably not a trivial problem.
This would be particularly true for cats that have
Back to contents
A
already been in fights and may have painful
abscesses - any physical contact by another
cat may cause them to react defensively in an
aggressive manner.
5. Redirected aggression: Redirected aggression
is seen in felines, as well as in canines; however,
it can be difficult to recognize and may only
be reported as incidental to another form of
aggression. In redirected aggression, any
interruption of an aggressive event between two
parties by a third party results in redirection of
the aggressive behavior to the third party or to
another, uninvolved individual. It is important
to realize that the interrupted aggressive event
may only be a threat, so that the person (or
animal) interrupting it may not realize what is
occurring. Cats appear to remain reactive for an
extended period of time after being thwarted in an
aggressive interaction. Clients need to realize this
and to be aware of the subtleties of their behavior
that communicate their intent. Since redirected
aggression is often precipitated by another
inappropriate behavior, it is important to treat that
behavior, as well. Treatment involves standard
behavior modification techniques. If there is a
socially mediated conflict within the household
cats, some environmental modification may be
necessary to decrease the extent to which the
involved cats are capable of interacting. Owners
should be encouraged to use inanimate objects
(battery operated water pistols, buckets of water,
foghorns, et cetera) to intervene between fighting
animals. This minimizes danger to the owners
and may have the benefit of aborting the behavior
while teaching the cat that there are consistent,
undesirable consequences to its inappropriate
behavior.
6. Assertion or status-related aggression: Assertion
or status aggression has been described as the
‘leave me alone bite’ and most frequently occurs
when being petted. The most similar situation
in canines is dominance aggression; however,
2006 World Congress WSAVA/FECAVA/CSAVA
the divergent evolutionary history of canine and
feline social systems argues that these are not
homologous situations. These cats share with
dogs with similar problems the need for control
of the situation. Nothing the owner did provoked
the cat; rather the cat demonstrates a desire or
need to control when the attention starts and
when it ceases. Some cats do this by biting
and leaving, while the occasional cat with take
the owners’s hand with its teeth, but not bite.
Fortunately, owners can be taught observe
signs of impending aggression (tail flicking,
ears flat, pupils, dilated, head hunched, claws
possibly unsheathed, stillness or tenseness,
low growl) and interrupt the behavior at the
first sign of any of these by standing up and
65
A
letting the cat fall from their lap or abandoning
the cat and refusing to interact until the cat
is exhibiting an appropriate behavior. Clients
should be discouraged from direct physical
correction of the cat, since the cat may view
that as a challenge and intensify its aggression.
If the cat does not respond to passive control
or redirects its aggression, it is safer to counter
the behavior with a fog horn or a battery
operated water pistol. Corrections must occur
within the first 30-60 seconds of the onset of
the inappropriate behavior to insure learning;
corrections within the first second are best.
Clients having such cats should be aware that
their cats are never going to be hugely cuddly,
although, if the client can refrain from petting
them, they may be willing to sit quietly on the
owner’s lap for extended periods.
References:
Adamec RE. The interaction of hunger and
preying in the domestic cat, Felis catus: an
adaptive hierarchy. Behav Biol 1976; 18: 263-
272.
Borchelt PL, Voith VL. Aggressive behavior in
cats. Comp Contin Educ Pract Vet 1987; 9: 49-56.
Chapman BL, Voith VL. Cat aggression to
people: 14 cases. J AM Vet Med Assoc 1990 ;
196: 947-950.
Jackson LA, Perkins BA, Wenger JD. Cat-scratch
disease in the United States. Am J Public Health
1993; 83: 1707-1711.
Karsh EB, Turner DC. The human-cat relationship.
In: The Domestic Cat: The Biology of Its
Behavior, eds. Turner DC, Bateson P. Cambridge
University Press: Cambridge, England, 1986:
159-177.
Leyhausen P. Cat Behavior. New York, Garland
STPM Press, 1979.
2006 World Congress WSAVA/FECAVA/CSAVA
Tompkins DC, Steigbigel RT. Rochalimea’s role
in cat scratch disease and bacillary angiomatosis.
Ann Intern Med 1993; 118: 288-290.
Zangwill KM, Hmilton DH, Perkins BA,
Regnery RL, Plikaytis BD, Hadler JL, Carter ML,
Wenger JD. Cat scratch disease in Connecticut -
epidemiology, risk-factors, and evaluation of a new
diagnostic test. N Engl J Med 1993; 329: 8-13.
Table 1. Techniques to demonstrate at the first
visits or in kitten classes:
1) nail-clipping - reticent clients can learn to use
an emery board; clients should be able to visualize
the vein using a mag light, and should be able to
outline its margin using a Sharpie
2) tooth brushing - using pediatric toothbrushes,
gauze, or washcloths,
66
Back to contents
3) grooming - for coat health and for fleas / ticks;
will require at least a flea comb and a good brush;
some cats should have mat combs and brushes
introduced
4) temperature taking - use a digital thermometer
- they don’t break and are easy to read, but you
will have to show clients how to clean them
without damaging them
5) pilling - particularly cats - practice with
food ball ‘blanks’ and encourage the clients to
give treats as part of the process or afterwards
afterwards,
6) ear cleaning - clients may want to purchase
a disposable otoscope so that they know what a
cat’s ear looks like
7) general lymph node palpation and mammary
gland palpation
8) fitting, adjustment, and use of harnesses
9) age and size appropriate toys
Table 2. Issues to be discussed at the first visits or
in kitten classes:
1) nail trimming, scratching rationale, scratching
posts, onchyectomy / tenectomy
2) urine and feces as communication signals and
roles for marking
3) sexual dimorphism and sexually dimorphic
behaviors: roles for neutering
4) sexual maturity (6-9 months) and social
maturity (24-48 months): what they are and how
they affect behavior
5) origin of cats, lack of selection for behavior (in
contrast to dogs) and matrilineal social systems
6) non-urine / fecal marking: roles for rubbing
and scratching
7) roles for overt and covert aggression and the
importance of understanding social signaling
Table 3: Heuristic model for thinking about
phenotypic patterns of feline aggression:
Potential axes:

overt v. covert aggression

active v. passive aggression

offensive v. defensive aggression
Sample scenarios:

overt, passive, offensive aggression: confident
cat staring when another enters room

overt, passive, defensive aggression: less
confident cat leaving room or backing up and
withdrawing into smaller space, tail tucked
vocalizing

covert, passive, defensive aggression:
vanquished or less confident marking with
mystacial glands in boundary areas or areas from
which cat had been displaced

covert, active, offensive aggression: vanquished
or less confident marking with urine or feces in

boundary areas or areas from which cat had been
displaced

overt, active, offensive aggression: chase
and attack using teeth and accompanied by
vocalization by resident cat toward new cat in
environment

overt, active, defensive aggression: attack or
response using hitting and or swatting while
Table 4: Survey questionnaire about general feline behaviors - to be used at all visits1:
1. Client(s):
3. Patient’s name:
5a. Age in weeks at which your cat was adopted? a. ________________weeks / months (circle)
5b. How many owners has your cat had?
5c. How long have you had this cat?
6a. Is your cat (please circle):
a. indoor, only
b. outdoor, only
c. indoor / outdoor
7a. Does your cat leave urine or feces
outside the litterbox?
7b. Does your cat spray?
Back to contents
A
leaning back or avoiding further pursuit

covert, active, defensive aggression: withdrawal
and marking of restricted area by victim cat

covert, passive, offensive aggression:
displacement or theft of “bully” or higher ranking
cat’s toys, bed, food, or hidden copulations (?),
accompanied by non-elimination pheromonal
marking
2a. Today’s date:
___ (day) / ___ (mo) / ___ (year)
2b. Cat’s date of birth:
___ (day) / ___ (mo) / ___ (year)
 estimated?  known?
4a. Breed:
4b. Weight: __________lbs / ________kg
4c: Sex:  M  MC  F  FS4
d: If your cat is castrated or spayed [neutered] at
what age was this done?
____________weeks / months (circle)
b.  0 1 2 3 4 5+ unknown
c. _______________months
6b. How many litter boxes does your cat have:
0 1 2 3 4 5+
6c. What types of litter do you use?
6d. How often do you change the litter box
completely?
_________times weekly / monthly (circle)
6e. How often do you scoop the box?
_________times daily / weekly (circle)
Yes No  don’t know; if you answered yes,
 urine - where specifically? 2006 World Congress WSAVA/FECAVA/CSAVA
 feces - where specifically?
both - where specifically?
Yes No  don’t know; if you answered yes,
 where specifically?
67
A
8. Do you have any concerns, complaints,
or problems with urination in the house now?
9. Do you have any concerns, complaints,
or problems with defecation in the house now?
10. Did your cat destroy any objects while
teething?
2006 World Congress WSAVA/FECAVA/CSAVA
11. Does your cat destroy any objects or
anything else by chewing, sucking, or eliminating what objects - specifically - does the cat destroy?
on them (eg, furniture, rugs, clothes, et cetera) now? Please list all of them and note which are
12. Does your cat mouth, bite, suck, or
anything or anyone?
68
Back to contents
Yes No; if you answered yes,
(a) where is the cat urinating that you find
undesirable (list all areas)?
(b) how many times per week is the cat urinating
in places you find undesirable?
(c ) at what time of day is the urination occurring?
(d) is the pattern different on days when you are
home and days you are not home?
(e) are you at work during the hours when the cat
urinates?
(f) how many times per day does your cat usually
urinate when he or she is not urinating in places
you find undesirable?
Yes No; if you answered yes,
(a) where is the cat defecating that you find
undesirable (list all areas)?
(b) how many times per week is the cat defecating
in places you find undesirable?
(c ) at what time of day is the defecation occurring?
(d) is the pattern different on days when you are
home and days you are not home?
(e) are you at work during the hours when the cat
defecates?
(f) how many times per day does your dog usually
urinate when he or she is not urinating in places
you find undesirable?
Yes No Unknown; if you answered yes,
what objects - specifically - did the dog destroy?
Please list all of them and note which - if any - you
had given the dog as toys or to play with by putting
a * next to them.
Yes No; if you answered yes,
destroyed when you are home or not home - please
note that of they destroy at both times - tick both
columns:
Object When home When gone
a. Yes No if you answered yes,
what or whom does the cat mouth?
b. Is this a problem for you? Yes No
 A
13. Does your cat exhibit any vocalization Yes No; if you answered yes,
about which you are concerned? what is / are the vocalization(s) and when do they
occur:
vocalization situation in which it occurs
 a. barking
 b. growling
 c. howling
 d. whining

14. Does your cat show any signs of growling, Yes No; if you answered yes,
barking, snarling or biting? what is / are the sign(s) and when do they occur:
sign situation in which it occurs
 a. barking
 b. growling
 c. snarling
 d. biting
15. Have you ever been concerned that Yes No; if you answered yes, why?
your cat is “aggressive” to people?

16. Have you ever been concerned that Yes No; if you answered yes, why?
your cat is “aggressive” to cats?

17. Have you ever been concerned that Yes No; if you answered yes, why?
your cat is “aggressive” to animals other than cats?

Does your cat hunt or prey on other animals? Yes No; if you answered yes,
which animals and where?

18. Has your dog even cat ever bitten or clawed Yes No; if you answered yes,
anyone, regardless of the circumstances? did you think the bite was:
 a. accidental? Why?
 b. deliberate? Why?
 c. the cat’s “fault”? Why?
 d. not the cat’s “fault”? Why?

19. Has your cat had any changes Yes No; if you answered yes,
in sleep habits? what are these, specifically?

2006 World Congress WSAVA/FECAVA/CSAVA

20. Has your cat had any changes Yes No; if you answered yes,
in eating habits? what are these, specifically?

21. Has your cat had any changes in locomotory Yes No; if you answered yes,
behaviors or it’s ability to get around what are these, specifically?
or jump on the bed, et cetera?

22. Has anyone ever told you that they were Yes No; if you answered yes,
afraid of your cat? what did they say?

23. Has anyone every told you that your cat Yes No; if you answered yes,
was ill-mannered? why - what did the cat do that made them say this?

69
Back to contents
A
24. Do you have any concerns about Yes No; if you answered yes,
your cat’s grooming behaviors? a. little to no grooming
b. sucking
c. chewing
d. licking
e. self-mutilation / sores
f. barbering / trimming
g. plucking out clumps of hair

25. Is the cat exhibiting any behaviors Yes No; if you answered yes,
about which you are concerned, please list these behaviors below:
worried or would like more information?

Table 5 Feline Aggression Screen1
KEY: NR = no reaction; S = stare; B = bite; H
= hiss, howl, growl, vocalize (not purr); SW =
swat / scratch; P = piloerect / arch / puff up; TS =
switch or twitch tail; NA = not applicable
This screen can be used in three ways: (1) to note
the presence or absence, at any time, of any of the
behaviors, (2) to keep as a log about the baseline
behavior, noting how many times the behavior
occurs, given the number of times it is attempted,
per unit time (i.e., per week), and (3) to keep a log
about frequencies of the occurrence behaviors,
given the number of times the circumstance has
been encountered, during treatment so that these
numbers can be compared with (2). Please note if
the reaction is consistent in style, or only directed
towards one person, or only present in one
restricted circumstance. If using this screen as a
client log, the circumstances must be evaluated
for all people to whom the cat reacts. For any
of the uses it is worth noting whether the cat is
subjectively becoming more or less intense [or
harder or easier to interrupt] in its behavior {>I,
<I, relatively}. If using this screen only for the
first use, note if the cat has been worsening in
intensity or frequency in any category.
Please note - we want to know what your cat does
when you routinely interact with it - if you don’t
know how your cat would react in the following
circumstances, please do not try to find out. You
may provoke the cat.

NR S B H SW P TS NA
1. take cat’s food dish with food
2. take cat’s empty food dish
3. take cat’s water dish
4. take food (human) that falls on floor
5. take real bone
6. take food treat
7. take toy
2006 World Congress WSAVA/FECAVA/CSAVA

8. human approaches cat while eating

9. another cat approaches cat while eating
10. human approaches cat while playing
with toys
11. another cat approaches cat while
playing with toys
12. dog approaches cat while eating
13. dog approaches cat while playing
with toys
14. human walks past cat in doorways
15. human approaches/disturbs cat
while sleeping
16. cat approaches/disturbs cat while sleeping
17. step over cat
18. push cat off bed/couch
19. reach toward cat

70
Back to contents
 A
NR S B H SW P TS NA
20. reach over head
21. put on harness or collar
22. push on shoulders or rump
23. pet cat when in lap
24. pet cat when not in lap
25. towel when wet
26. bathe cat
27. groom cat’s head
28. groom cat’s body
29. trim cat’s nails
30. put on nail caps
31. stare at
32. stranger enters room
33. cat in yard - person passes
34. cat in yard - dog passes
35. dog enters room where cat is
36 human physically carries cat
37. cat in vet’s office
38. cat in boarding kennel
39. cat in groomers
40. cat yelled at
41. cat physically punished - hit
42. squirrels, cats, small animals approach
43. cat sees another cat through window
44. cat sees squirrels, birds, dogs
through window
45. human approaches cat who is
at top of stairs
46. cat removed from hiding place
47. human body parts move under covers
on bed
48. crying infant
49. playing with 2-year-old children
50. playing with 5-7-year-old children
51. playing with 8-11-year-old children
52. playing with 12-16-year-old children

1 From: Overall KL. Manual of Clinical Behavioral Medicine for Small Animals, Elsevier, to be
published 2007.
2006 World Congress WSAVA/FECAVA/CSAVA

71
Back to contents
A
Standards of Care (How I Treat)
CANINE COMPETITIVE AGGRESION TO OWNERS
Dr. Moisés Heiblum
Veterinary Hospital
Universidad Nacional
Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
Private Practice in Small
Animal Behavior, Naucalpan,
Mexico
moisesheiblum@yahoo.com
Classification of aggression can vary according to
a combination of eliciting stimuli:
Context, function, motivation, behavioral
sequences.(1,2) It is the most frequent cause for
behavioral consultations in Mexico city because
it’s implications for public health issues.(1) The
majority of problems that arise between dog
and owners are due to social conflicts between
both species.(2) In order to prevent and control
competitive aggressive behavior to owners,
veterinarians must have a proper knowledge of
canine social organization and communication.
At the VH UNAM the first phase in the treatment
of any aggression problem is to consider all the
risk factors to decide if the case could be treated
with a minimum safe warrant to the owners.
Avoiding the situations that elicit an aggressive
response minimizes danger. Once the competitive
aggression towards the owner is diagnosed, the
goal for the treatment plan is to train the dog to
assume a gradually more submissive position
in the family. If the risk analysis is too high
euthanasia must be considered.(1,2,3)
2006 World Congress WSAVA/FECAVA/CSAVA
The treatment protocol includes different
elements:
• Behavior modification
• Medication
• Neutering in males
The first phase in the treatment of any aggression
problem is learning to avoid the situations that
elicit an aggressive response; allowing aggressive
behavior to occur reinforces the tendency for the
dog to act aggressively.(3)
When the dog growls, it is only possible for the
person to act in 2 ways: withdraw or confront the
dog, in the first case the dog realizes that growling
allows the dog to reinforce his dominance. In the
second case there is a high risk of getting bitten.
Both alternatives are unacceptable, therefore the
only possible choice is to avoid both scenarios.(3)
72
Back to contents
•Not touching the dog while eating
•Not punish the dog
•Avoid any situation in which aggression has
previously been showed
•Avoid gestures that elicit aggression
•Be consistent with the dog, it is important for the
whole family group to interact with the dog using
the same rules. Give the dog a reliable way of life
making routines that are highly predictable.
•Feed the dog after the family, don’t give food
from the family table
•Avoid rough games like wrestling or tug of war
Use an obedience training program, obedience
training does not solve behavior problems by
itself and it should not be used as a substitute
for a behavioral treatment, but as a support
element.(1,2,3)
•Teach the dog to sit and stay using positive
reinforcement while relaxing, in a variety of
circumstances; this is the foundation for teaching
the dog context-specific appropriate behavior; the
goal is not to get the dog to sit, sit is just a tool;
the goal is teach the dog to relax.(3)
•Ignore attention soliciting behaviors and reward
submissive and calm behaviors.
Teach the dog to earn a salary for desirable
behaviors; here is where obedience is of great
help, the goal is to control good things in life,
therefore the dog has to differ to the owner in
order to have access to everything he wants.(1,3)
Use desensitization and counterconditioning
techniques and /or shaping
Use behavioral accessories such as a Gentle
leader® and leash to have a better control of the
dog. If there is a high risk to teach obedience,
habituate the dog to use a basket muzzle first.
Neutering: even though its efficacy is not
completely estimated and the simple fact of
castrating a dog is not enough to control aggression,
in certain situations there is a hormonal influence

in the development of certain behaviors such as
territorial marking and dominance, therefore is
worthwhile to add favorable conditions to the
treatment. (1,2). It is contraindicated in bitches
unless the aggressive episodes are related to
estrous.
Pharmacotherapy:
No drugs are approved for the treatment of
aggression in dogs. Any psychotropic medication
can have unexpected results, including increased
arousal and disinhibition of aggression.(3) Clients
need to be informed that there are no quick
fixes for complex behavior and that aggression
problems can be controlled and not cured. The
use of medications must be considered as a
way of complement the behavior modification
program and not as the only resource.
Back to contents
A
The choice of medication or the combination
of drugs will be according to the intensity and
duration of the problem as well as if there is any
anxiety or impulsivity component associated.
The drugs of choice are:
Fluoxetine 1mg/kg/24h
Amitryptiline 2mg/kg/12h
References:
1. Heiblum, M educación continua “actualización
en el diagnóstico y tratamiento de problemas de
conducta en perros y gatos” UNAM 2001
2. Memorias de etología clínica en el perro y el
gato, diplomado de educación continua UNAM-
UAB 2002
3. University of Georgia, continuing education
courses February 1999 Problems of aggression
in dogs
2006 World Congress WSAVA/FECAVA/CSAVA
73
A
Standards of Care (How I Treat)
SEPARATION ANXIETY IN DOGS
Dr. Moisés Heiblum
Veterinary Hospital
Universidad Nacional
Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 52240
Private Practice in Small
Animal Behavior, Naucalpan,
Mexico
moisesheiblum@yahoo.com
Clinical separation anxiety occurs when dogs
exhibits inappropriate behaviors specifically
caused by their owners leaving them alone or when
the dog does not have access to them.(3) In dogs
these behaviors typically include vocalization,
destructiveness, inappropriate elimination when
the owner is away and excessive attachment
behavior when the owner is home. It is the most
prevalent canine anxiety disorder diagnosed in
Mexico city.(1)
At the VH UNAM we diagnosed, propose
a treatment plan which normally includes 4
phases:
a) Client education, explaining what is SA and
its causes
b) Environmental modification, by the means
of adjusting the place for the dog to be safe and
restrict the dog access to areas where destruction/
elimination can occur
c) Behavioral modification by the means of
different learning techniques to teach the dog
to become more independent, like downplay
departures and arrivals, extinguish pre-departure
2006 World Congress WSAVA/FECAVA/CSAVA
cues, graduated departures with a safety cue to
teach the dog to habituate to different levels of
owner’s absences.
d) Medication therapy if needed which must
always be accompanied by environmental and
behavioral modification.
Usually treatment lasts several weeks
and requires a high compliance from the
owners.(1,2,3)
Environmental modification:
•Restrict dog’s access to areas where destruction/
elimination can occur.
- Crate
- Dog day care
- Pet sitter
Vary the toys that are available to the dog.
74
Back to contents
Behavior modification:
Increase physical activities.
Obedience training does not solve behavior
problems by itself and it should not be used as
a substitute for a behavioral treatment, but as a
support element.(1,2)
•Teach the dog to sit or down and stay using
positive reinforcement while relaxing, in a variety of
circumstances; this is the foundation for teaching the
dog context-specific appropriate behavior; the goal is
not to get the dog to sit or down, sit or down are just a
tool; the goal is teach the dog to relax.(1,2,3)
•Ignore attention soliciting behaviors and reward
submissive and calm behaviors.
Downplay departures and arrivals.
•Ignore the dog while preparing to leave the
house, don’t say goodbye, having elaborate
farewells may increase the dogs anxiety about the
owner leaving.
•Ignore the dog when return, until can redirect
into a “sit”. When the owner comes home after
being gone for a while must not interact with
the dog until he is calm, by doing this the owner
makes his arrival less exiting to the dog and
therefore decrease the dog’s anticipation for that
moment (1,3)
Extinguish pre-departures cues
•Keys, briefcase, purse, working shoes, security
system etc.
- Owner picks up keys (CS)→dog anxious
(CR)
- Owner picks up keys (CS)+does not
leave(no US)→ Dog anxious (CR)
- Owner picks up keys (NS) → dog no longer
anxious (no CS). Extinction of of the dog’s
reaction to pre-departure cues is easily done.
Simply expose the dog to the cues that he
already knows predict the owner’s absence, but
do so in a way that will not allow the dog to
have a full anxiety reaction.

After the dog’s reactions to the departure cues
have been extinguished the dog is ready to begin
desensitization.
Desensitization is a process where the owner
very gradually expose the dog to the stimulus that
makes him anxious (owner’s absence), but will
do so in a way that will not allow the dog to have
a full blown anxiety response.
1. Give the dog situations in which he will succeed.
Do not progress to a next step of the schedule,
unless the dog is calm for previous steps.
2. If at any point the dog shows anxiety, back up
to an easier step.
3. Desensitization is a slow process. The owner
can only progress as fast as the dog is capable
of progressing (3). Graduated departures using a
safety cue; visual, olfactory or auditory cue not
known by the dog and given to the dog which is
associated with the owner returning shortly.
We tell the owner to choose a place in the house
where he would like his dog to be able to stay
while gone. The dog has to associate this area
with positive things, the owner has to give the
dog special treats and toys whenever the dog is
there, and also reward when the dog goes there
by himself. Then start by putting the dog in that
area and leave him alone for very short periods
and very gradually increase the time the dog is
left alone in that area. We also tell the owner not
to use that area for any kind of punishment.
The benefit of this technique is that the dog
does not need to be fully calm when the owner
leaves and the owner needs to return before the
dog exhibits full blown symptoms. The owner
must perform these exercises where he wants
the dog to be able to stay by himself later on. It
is important to only use this safety cues during
practice departures, otherwise they will lose their
meaning, and extend the time the dog is left alone
very gradually.
Pharmacological treatment:
The use of medications must be considered as a
way of complement the behavior modification
program and not as the only resource.
Back to contents
A
The choice of medication or the combination
of drugs will be according to the intensity and
duration of the problem.
There is an FDA approved medication for
separation anxiety in dogs: Clomipramine
“Clomicalm”™ a tricyclic antidepressant, but as
we don’t have access to it in México, we have to
use the presentation for humans “Anafranil”™ at
1 mg/kg q 12h for the first 2 weeks → 2 mg/kg q
12h. next 2 weeks → 3 mg/kg q 12h for the next
4 weeks and wean off the dose very gradually at
the end of treatment.
Sometimes we can combine Clomipramine
+ Alprazolam at 0.01/0.1 mg/kg q 8h. If the
symptoms are too intense and we wean off
Alprazolam by the end of the 3rd or 4th week of
treatment.
The prognosis depends on:
•The severity of the problem
- Mild symptoms has better prognosis that
severe
•The duration of the problem
- Short duration of the problem has better
prognosis than longer duration of the
problem
•Compliance of owners
- High compliance will lead to better
prognosis
References:
1. Heiblum, M memorias de etología clínica en el
perro y el gato , diplomado de educación continua
UNAM-UAB 2002
2. University of Georgia, continuing education
courses March 1999 Psychopharmacology and
treatment of phobias in dogs and cats
3. University of Georgia, continuing education
courses November 2001 Update on diagnosis and
treatment of small animal behavior problems.
4. University of Georgia, continuing 2006 World Congress WSAVA/FECAVA/CSAVA
education courses October 2005 Veterinary
Psychopharmacology: Selecting the best drug,
monitoring the patient
75
A
Standards of Care (How I treat)
INTERVERTEBRAL DISC DISEASE
Richard A. LeCouteur, BVSc,
PhD, Diplomate ACVIM
(Neurology), Diplomate ECVN
University of California
Davis CA 95616
USA
ralecouteur@ucdaviss.edu
Type I Disk Extrusion
The appropriate treatment for animals with
type I disk extrusion depends on an individual
animal’s neurological status. Medical treatment
directed at decreasing spinal cord edema by
means of corticosteroids is indicated only in
those animals with an acute onset of neurological
deficits, that are examined within eight hours of
the injury. The recommended agents and dosages
are as described for spinal cord trauma. The
use of corticosteroids in dogs with type I disk
extrusion has been associated with pancreatitis,
gastrointestinal bleeding, or colonic perforations.
Nonsurgical (medical or conservative) treatment
is recommended for animals with apparent pain
only or animals that have mild neurologic deficits
but are ambulatory and have not had previous
clinical signs associated with disk disease. These
animals should be strictly confined to a small area
such as a hospital cage or a quiet place away from
other pets for at least 2 weeks, and walked (on
a leash or harness) only to urinate and defecate.
The objective of confinement is to allow fissures
in the anulus fibrosus to heal, thus preventing
further extrusion of disk material, and allowing
2006 World Congress WSAVA/FECAVA/CSAVA
resolution of the inflammatory reaction caused by
small amounts of extruded disk material.
Use of analgesics, muscle relaxants, or non-
steroidal anti-inflammatory agents, is not
recommended in most cases as it is believed that
their use encourages animals to exercise and
risk further disk extrusion. Very cautious use of
analgesics or non-steroidal anti-inflammatory
agents occasionally may be indicated. However,
strict confinement followed by a period of
restricted exercise is imperative. Owners should
also be warned that an animal’s neurological status
may deteriorate owing to extrusion of further disk
material despite this treatment and to observe
the animal very carefully. If the neurological
status worsens, an animal’s treatment should be
reevaluated immediately. Owners should also
be warned that a recurrence of clinical signs is
76
Back to contents
common due to further disk extrusion at the same
or a different site, and subsequent episodes may
be more severe, especially in the thoracolumbar
spine.
Animals with severe cervical pain frequently do
not respond to cage rest. These dogs often have
large amounts of disk material within the spinal
canal, and dogs that do not show improvement
after 7 to 10 days of confinement should be
evaluated further by means of radiographs and
myelography, and ventral cervical decompression
should be considered.
Surgical disk fenestration has been recommended
as a prophylactic measure to prevent further
extrusion of disk material into the spinal canal.
Fenestration of the disks most likely to herniate
(C2-3 through C6-7 in the cervical spine and
T11-12 through L3-4 in the thoracolumbar spine)
is recommended in animals that have had one
or more episodes of apparent neck or back pain
and have evidence of intervertebral disk disease
on radiographs. Various surgical techniques have
been described. Fenestration of disks does not
remove disk material from the spinal canal and
therefore is not recommended as the sole surgical
procedure in dogs that have evidence of disk
material within the spinal canal and spinal cord
compression on radiographs and myelography.
The role of disk fenestration in the management
of intervertebral disk disease is controversial.
Disk fenestration in the thoracolumbar region
is not easily done, and complications such as
scoliosis, pneumothorax, and hemorrhage may
occur. Disk fenestration in the cervical region is
achieved more easily and rarely is associated with
such complications. Fenestration does not prevent
recurrence of disk extrusion in all animals. The
effectiveness of fenestration depends largely
on the amount of nucleus pulposus removed.
Completion of disk fenestration is recommended
at the time of spinal cord decompression.
Animals with neurological deficits such as
paresis or paralysis with deep pain perception

intact, animals with recurrent bouts of apparent
back or neck pain, or animals with apparent back
or neck pain (or mild neurological deficits) that
are unresponsive to strict confinement, should
be evaluated by means of spinal radiographs,
CSF analysis, and myelography. Surgical
decompression of the spinal cord and removal
of disk material from the spinal canal should be
considered. Although many dogs with moderate
or severe paresis improve neurologically if
treated with cage rest, neurologic recovery is
often more rapid and more complete in animals
following surgical decompression of the spinal
cord. In addition, the neurological status of some
dogs with type I disk extrusion, especially in the
thoracolumbar spine, suddenly worsens over a
period of hours or days despite medical treatment.
Such deterioration usually results from further
disk extrusion that may result in irreversible
spinal cord damage and permanent paralysis. This
progression of signs always is a risk with medical
treatment of animals with thoracolumbar disk
disease. Progression is impossible to predict on
the basis of history, clinical signs, or radiography.
Owners should be made aware of treatment
options and offered the opportunity of referral
to an appropriate surgical facility when animals
are initially presented. Surgical decompression
should be done as soon as possible to prevent
further spinal cord damage incurred as a result
of sustained compression or further extrusion of
disk material. In addition, if surgery is delayed 2
to 3 weeks, disk material hardens and becomes
adherent to dura mater, and becomes difficult or
impossible to remove from the spinal canal.
Prognosis for neurological recovery in animals
that retain deep pain perception postsurgically is
fair to very good. The major factors that correlate
with the degree of neurological improvement
seen postsurgically are the animal’s neurological
status prior to surgery, the rapidity of onset of
clinical signs, and the time interval between onset
of clinical signs and surgical decompression.
Animals that have severe neurological signs, a
rapid onset of clinical signs (hours), and a long
period of time before surgery generally have a
prolonged recovery period and may have varying
degrees of permanent neurological deficit.
The incidence of recurrence of clinical signs
due to disk extrusion is greater in nonsurgically
than surgically treated dogs. One author found
that one-third of dogs with type I disk herniation
that were treated nonsurgically had a recurrence
of clinical signs, and generally showed greater
severity of neurological deficits at the time of
recurrence. Another author reported a recurrence
rate of 40 per cent in nonsurgically treated dogs.
The advantages and disadvantages of various
Back to contents
A
techniques for spinal cord decompression have
been discussed. Surgical treatment is not without
risks. Anesthesia is necessary, and surgery
occasionally results in further spinal cord damage
due to surgical manipulation. Nonsurgical
treatment should be attempted in animals that
are poor anesthesia or surgical candidates or if
surgical treatment is not possible financially.
In animals with clinical signs of a complete
transverse myelopathy, without deep pain
perception for a period of more than 24 hours,
the prognosis for return of spinal cord function is
poor despite medical or surgical treatment. Some
of these animals may improve neurologically
if given sufficient time. However, it is a matter
of controversy whether surgical treatment
increases the probability of improvement or not.
In cases in which deep pain perception has been
absent for less than 24 hours, the prognosis for
return of spinal cord function is poor. However,
surgical treatment may increase the likelihood of
neurological improvement in this group.
Regardless of whether medical or surgical
treatment is instituted, animals that are paretic
or paralyzed require intensive nursing care.
Neurological improvement may take weeks or
months and this requires owner cooperation and
enthusiasm regarding care and physical therapy.
Manual expression, intermittent catheterization,
and /or indwelling catheterization of the bladder
are often required to ensure emptying of the
bladder. Weekly urinalysis, especially in animals
that do not have voluntary control of micturition,
is important in monitoring for urinary tract
infection. It is also important to keep animals
well padded, clean, and dry to prevent formation
of pressure sores, and to ensure that caloric and
water intake is adequate. Physical therapy does
not result in neurologic improvement but helps
to prevent disuse muscle atrophy associated with
paraplegia or tetraplegia. Physical therapy should
not be attempted in animals treated medically for
2006 World Congress WSAVA/FECAVA/CSAVA
at least the first 2 weeks following onset of signs,
as further extrusion of disk material may occur.
Type II Disk Protrusion
Treatment with corticosteroids may result in
neurological improvement for variable periods
of time in animals with type II disk protrusion.
However, corticosteroid therapy is not curative.
The reason for this improvement is not clear,
as intramedullary hemorrhage and edema seen
in cases of acute spinal cord injury are not a
feature of chronic spinal cord compression. In
the thoracolumbar spine, surgical removal of
protruded disk material may result in clinical
improvement. However, the neurological
status of some dogs is worsened permanently
77
A
despite careful surgical technique. The reasons
for this are not known, but increased vascular
permeability has been described in the spinal
cord associated with release of chronic spinal
cord compression and this probably plays a role
in this phenomenon. Ventral decompression in
the cervical spine allows removal of protruded
Standards of Care (How I Treat)
DISCOSPONDYLITIS
Richard A. LeCouteur, BVSc,
PhD, Diplomate ACVIM
(Neurology), Diplomate ECVN
University of California
Davis CA 95616
USA
ralecouteur@ucdaviss.edu
Etiology and Pathogenesis
Bacterial or fungal infection of the intervertebral
disks and adjacent vertebral bodies
(diskospondylitis), or of only the vertebral bodies
(spondylitis), may result in extradural spinal cord
or cauda equina compression due to granulation
tissue, bony proliferation, or pathologic fracture
or luxation. Less commonly, diskospondylitis
may lead to diffuse or focal meningitis and
myelitis.
Diskospondylitis and spondylitis result from
implantation of bacteria or fungi introduced by
migrating plant awns (grass seeds, foxtails),
hematogenous spread, extension of a paravertebral
infection, a penetrating wound, or previous disk
2006 World Congress WSAVA/FECAVA/CSAVA
or vertebral surgery.
Diskospondylitis and spondylitis occur more
commonly in dogs in areas where grass awn
infections are a problem. Several theories
exist to explain migration of grass awns to the
vertebral column. Awns may be swallowed
and migrate through the bowel wall (possibly
at the caudal duodenal flexure), through the
mesentery to the attachment to ventral epaxial
muscles, and to the vertebral column. Evidence
of scarring, however, has not been found in the
gut or abdomen of dogs with diskospondylitis.
As dogs with diskospondylitis thought to be
due to plant awn migration have lesions most
commonly in the cranial lumbar spine (L2-L4)
it has been suggested that awns may be inhaled
and migrate through the lungs to the diaphragm,
78
Back to contents
type II disk material and neurologic improvement
may occur over several months; however, some
dogs, especially those with moderate to severe
neurologic deficits prior to surgery, may manifest
temporary or permanent worsening of clinical
signs postoperatively.
and lodge at the crural insertion on the lumbar
vertebrae. Plant awns may also migrate through
skin and paravertebral or abdominal muscles
to the vertebral column. Grass seeds are able to
travel long distances owing to the direction of the
barbs. Forward progress may be aided by muscle
movements.
Hematogenous spread of bacteria or fungi
is probably the most common cause of
diskospondylitis. Sources of infection include
bacterial endocarditis, sites of dental extraction.,
and urinary tract infections. Retrograde flow in the
vertebral veins has been suggested as a possible
route of infection to the vertebral column. Many
dogs with diskospondylitis have concurrent
urinary tract infection. Diskospondylitis due to
Brucella cants infection most likely results from
bacteremic spread from a genital infection.
Affected intervertebral disks may have evidence
of degeneration (collapsed disk space, spondylosis
deformans) or trauma (traumatic disk protrusion,
vertebral luxation). Prior disease or injury to
the disk has been suggested as a factor in the
pathogenesis of diskospondylitis.
Diskospondylitis may occur with increased
frequency in immunocompromized animals.
Diskospondylitis and vertebral osteomyelitis also
have been reported associated with Mycobacterium
avium infection in basset hounds in which an
inherited immunodeficiency was suggested as a
predisposing factor German shepherd dogs may
be predisposed to fungal diskospondylitis.

Organisms most commonly isolated from
blood, affected vertebrae, and urine of dogs
with diskospondylitis are coagulase-positive
Staphylococcus spp (aureus, intermedius). Other
organisms isolated include Bacteroides capillosus,
Brucella canis, Nocardia sp , Streptococcus canis,
Corynebacterium sp, Escherichia coli, Proteus
sp, Pasteurella sp, Paecilomyces sp, Aspergillus
sp, and Mycobacterium sp. Coccidioides
immitis may cause vertebral body osteomyelitis.
Hepatozoon canis infection has been associated
with periosteal bone proliferation of the vertebrae
as well as other bones of the body. Spirocerca lupi
infection may cause productive bony changes on
the ventral aspect of thoracic vertebrae where the
aorta and the esophagus run in parallel course.
Clinical Findings
Diskospondylitis may occur in dogs or cats of any
age, however it is most commonly seen in giant
and large breeds of dog. Any level of the vertebral
column may be affected by diskospondylitis,
and multiple lesions may be seen, in either
adjacent vertebrae or nonadjacent vertebrae.
Diskospondylitis occurs more commonly in
thoracic and lumbar spine than in cervical
spine. The lumbosacral disk space frequently is
involved.
Clinical findings depend on the location of
the affected vertebra or vertebrae. The most
common clinical signs are weight loss, anorexia,
depression, fever, reluctance to run or jump, and
apparent spinal pain (which may be severe).
Hyperesthesia may be present only over the site of
the lesion or may be poorly localized, especially
with involvement of multiple sites.
Diagnosis
Diagnosis may be difficult, as clinical signs
often are nonspecific. Diskospondylitis should
always be considered in an animal with fever of
unknown origin. If the lumbosacral intervertebral
disk is involved, dogs often show a stilted, short-
strided pelvic limb gait and shifting pelvic limb
lameness. Clinical signs commonly are present
for several weeks or months before a diagnosis of
diskospondylitis is made.
Neurologic deficits associated with spinal
cord or cauda equine compression may be
present, and may reflect either a transverse or a
multifocal myelopathy. Cervical lesions most
commonly cause only apparent cervical pain,
and lumbosacral lesions may cause neurologic
deficits due to compression of nerves of the cauda
equine. Rarely, animals may demonstrate clinical
signs of diffuse suppurative meningitis associated
with extension of infection to involve the spinal
meninges. Dogs may have a history of draining
Back to contents
A
tracts in the paravertebral area associated with
grass seed migration.
Affected animals may have a normal or elevated
peripheral white blood cell count. Typical
radiographic findings are destruction of the bony
end-plates adjacent to an infected disk, collapse
of the intervertebral disk, and varying degrees of
new bone production. Early lesions may consist
only of lytic areas in affected vertebral end-
plates. More advanced lesions show a mixture of
bone lysis and extensive new bone production,
with osteophytes bridging adjacent vertebrae
containing a central destructive focus. Affected
vertebral bodies may be shortened, and bony
proliferation may result in fusion of one or more
vertebrae.
Infection may be difficult to distinguish from a
healing fracture, unstable fracture, congenital
malformation, or postoperative changes.
Diskospondylitis usually can be distinguished
from a neoplastic lesion, as neoplasms rarely
cross intervertebral disk spaces.
Diskospondylitis may be present in more than
one site in the vertebral column, therefore, it
is important to radiograph the entire spine in
animals suspected to have diskospondylitis.
Occasionally, clinical signs may occur before
characteristic radiographic changes are
evident. If diskospondylitis is suspected, and
characteristic lesions cannot be found, a dog
should be radiographed again in 2 to 4 weeks.
Advanced imaging (CT or MRI) may be useful in
identification of subtle vertebral lesions.
Collection of CSF is indicated in animals with
neurologic deficits. The CSF white blood cell
count may be normal, or may be elevated, with
an increase in PMN neutrophils in CSF from
animals with meningitis or myelitis.
Myelography is indicated in animals with
neurologic deficits indicative of spinal cord
compression and is mandatory in cases in which
2006 World Congress WSAVA/FECAVA/CSAVA
decompressive surgery is considered.
Aerobic, anaerobic, and fungal cultures of blood
and urine should be done prior to treatment in an
attempt to isolate causative organisms. Cultures of
CSF are indicated if the WBC count is elevated.
Cultures of fluid from draining sinuses may also
be done. Efforts should be made to diagnose B.
Canis infection in all dogs with diskospondylitis.
Surgical biopsy may be indicated in affected dogs
in which a causative organism is not isolated
from blood or urine, and/or animals that are
unresponsive to treatment with broad spectrum
antibiotics. Fluoroscopy-guided needle aspiration
of lesions is possible in some animals. However,
79
A
cultures of samples collected in this way are often
negative, especially if animals have been treated
with antibiotics prior to completion of a biopsy.
Treatment
Treatment consists of long-term use of an
antimicrobial that is effective against the
causative organism(s) determined by results of
blood and/or urine cultures. If an organism is not
cultured, dogs without severe neurologic deficits
may be treated empirically, assuming infection
with the most common organism isolated from
animals with diskospondylitis (coagulase-positive
Staphylococcus sp). Antibiotics that are most
effective for this purpose are cephalosporins,
or beta-lactamase resistant penicillins such
as oxacillin and cloxacillin. A trimethoprim/
sulfonamide combination or chloramphenicol is
less effective but is less expensive, and may be
effective in some cases.
Clinical signs may recur if the infection is
not completely eliminated prior to cessation
of antibiotic therapy, and repeated cultures of
blood and urine and ongoing treatment with
an appropriate antibiotic may be necessary.
Treatment is continued for at least 6 weeks, and
vertebral radiographs are done every 4-6 weeks
to monitor progression/ regression of a lesion,
and to monitor for development of new lesions.
Antibiotic administration may be necessary for
up to 6 months before radiographic evidence of
resolution of lesions is seen.
A combination of minocycline or tetracycline
2006 World Congress WSAVA/FECAVA/CSAVA
80
Back to contents
and streptomycin is recommended for treatment
of B. canis infections. Infected dogs should be
neutered to eliminate risk of transmission. B.
canis infections have public health significance,
as people may become infected.
Clinical improvement in animals with
diskospondylitis (resolution of fever, improved
appetite, reduction of apparent spinal pain) should
be seen within 2 weeks of starting antibiotic
therapy. If clinical improvement is not seen,
treatment should be reevaluated. Fungal infection
should be considered in animals non responsive
to antibiotic therapy. Use of analgesics and
restriction of exercise during the first weeks of
treatment may be helpful.
Surgical exploration of a lesion should be
considered in animals that are unresponsive
to treatment or have persistent draining tracts
suggestive of grass seed migration. Objectives
of surgery are curettage of lesions and
harvesting of material for bacterial and fungal
culture. Decompressive surgery is indicated if
evidence of spinal cord compression is found
on myelography and if animals show severe
or progressive neurologic deficits. Surgical
stabilization of the vertebrae may be necessary
following decompression.
Prognosis for animals with diskospondylitis
depends on the ability to eliminate the causative
organism(s) and on the degree of neurologic
dysfunction. Animals with severe neurologic
deficits and fungal infections have a guarded to
poor prognosis.

Standards of Care (How I Treat)
ARTHROSCOPIC TREATMENT OF CRANIAL CRUCIATE LIGAMENT
DISEASE
Brian Beale DVM, Diplomate
ACVS
Gulf Coast Veterinary Specialists
1111 West Loop South #160
Houston
Texas
77027
drbeale@gcvs.com
Introduction
Arthroscopy can be a useful tool when treating
dogs for cranial cruciate ligament rupture.
Arthroscopic-assisted debridement of the torn
ligament and treatment of meniscal tears prevents
the need for arthrotomy and incision of other
periarticular soft tissues. Meniscal release can
also be performed under arthroscopic guidance.
Lower morbidity and enhanced visualization
is achieved with arthroscopy. Second-look
arthroscopic evaluation of patients undergoing
previous stabilization for cruciate tears is indicated
for treatment of meniscal tears, meniscal release,
and evaluation of the cranial cruciate ligament,
caudal cruciate ligament, previous meniscal
procedures, osteoarthritis and synovitis. Patterns
of articular wear can be assessed in patients
having an unsatisfactory outcome following
TPLO. Second-look arthroscopy is particularly
valuable for low morbidity follow-up evaluations
of the joint in experimental studies.
Arthroscopic Changes
First look arthroscopic evaluation in patients
having cruciate ligament disease often
have substantial synovitis that may obscure
visualization. Synovitis has usually subsided
at the time of second-look arthroscopy. Villous
hypertrophy present at the time of an acute
ligament tear subsides at follow-up examination
in patients having a favorable outcome following
TPLO.
Torn fibers associated with partial tears of the
cranial cruciate ligament can be debrided at
the initial arthroscopic exam. Evaluation of the
ligament during second-look generally reveals
a healthy appearance characterized by reduced
hyperemia, no additional fiber tearing and
grossly normal tensile properties. The improved
appearance of the cranial cruciate ligament at
second-look arthroscopic examination supports
Back to contents
A
the theory that TPLO reduces strain on the cranial
cruciate ligament.
The caudal cruciate ligament appears normal in
most dogs at the time of second-look arthroscopy,
despite the probable development of caudal tibial
thrust following TPLO. The caudal cruciate
ligament frequently has mild fraying or tearing
of fibers at the time of initial arthroscopic
examination in dogs having cranial cruciate
ligament disease. These fibers can be debrided
carefully with a radiofrequency probe at the time
of TPLO and usually appear normal at the time of
second-look arthroscopy.
Meniscal changes are occasionally found at
second-look arthroscopic exam. Typically these
changes are minor and include mild fraying of the
free edge of the medial or lateral meniscus. These
tears are classified as radial tears. Small tears can
be meticulously debrided with a radiofrequency
probe, being careful to avoid the articular
cartilage. When using the radiofrequency probe
for meniscal debridement, the probe should be
applied in short bursts and lavaged continuously
with ample fluids to reduce the chance of
iatrogenic damage to adjacent cartilage. Other
meniscal changes that have been seen at
2006 World Congress WSAVA/FECAVA/CSAVA
second-look arthroscopy include bucket-handle
tears, meniscal degeneration and calcification.
Menisci typically appear healthy at second-look
arthroscopic exam if previously treated by partial
meniscectomy at the time of TPLO. Medial
meniscal release performed at the meniscotibial
ligament appears to remain functional and show
no evidence of healing at the time of second-look
arthroscopy. Midbody meniscal release performed
caudal to the medial collateral ligament also
appears to remain functional, but some healing
may occur and is grossly characterized by fibrous
tissue spanning the meniscal gap. In these cases,
the meniscus appears to be elongated with respect
to its original length before meniscal release.
Arthroscopic evaluation was recently performed
81
A
in 16 dogs (22 stifles) having a partial tear of the
CrCL and TPLO as part of an ongoing clinical
study. A meniscal release incision was performed
in 4 stifles. A second-look arthroscopic evaluation
was performed 3 to 33 months after TPLO (mean
10.4 months). Arthroscopic evaluation of the
cranial and caudal cruciate ligaments, lateral
and medial menisci, femoral and tibial cartilage,
periarticular osteophyte (PAO) formation and
degree of synovitis was performed. Pathologic
changes were identified at initial surgery and
followed over time.
Radiographic evidence of PAOs was unchanged
or minimally increased in 20 stifles and
moderately increased in 2 stifles. Progression
of PAOs was evident arthroscopically in 36%
of stifles. Cartilage wear was unchanged in 12
stifles and increased in 10 stifles. Cartilage wear
was evident arthroscopically in 7 stifles without
radiographic evidence of increased osteoarthritis.
Small radial tears of the lateral meniscus were
seen in 19 stifles at the time of initial surgery.
Six of 8 stifles treated by radiofrequency partial
meniscectomy had increased cartilage wear.
Increased cartilage wear was evident in 2 of 11
stifles with similar meniscal tears left untreated.
The severity of synovitis was unchanged in 2 and
decreased in 20 stifles. The CrCL was intact at
follow-up in 19 of 22 stifles. The caudal cruciate
2006 World Congress WSAVA/FECAVA/CSAVA
82
Back to contents
ligament (CdCL) was normal in 18 of 22 stifles at
time of TPLO. Four dogs had obvious fraying of
the CdCL at initial surgery. The CdCL was frayed
in 10 of 22 stifles at second-look arthroscopy. The
meniscal release incision was not healed in 2 of
4 stifles and was spanned with a fibrous tissue in
2 of 4 stifles.
Arthroscopy was a more sensitive indicator
of increased PAO formation following TPLO.
Synovitis was generally decreased at follow-up.
The intact portion of the CrCL had a high chance
of remaining intact following TPLO. Increased
fraying of the CdCL may be due to the increased
load following TPLO. Meniscal release incisions
did not heal or healed with fibrous tissue. Small
radial tears of the lateral meniscus may not require
treatment. TPLO does not eliminate osteoarthritis
in dogs having partial tears of the CrCL, but does
appear to avoid complete rupture.
Complications
Complications are infrequent following second-
look arthroscopy. The procedure is usually much
shorter in duration, often times completed in less
than 15 minutes. The predominant complication
is subcutaneous fluid extravasation. Infection is
rare if aseptic technique is used. Morbidity is
extremely low- patients rarely have lameness
induced by the procedure.

Standards of Care (How I Treat)
PATELLAR LUXATION
Brian Beale DVM, Diplomate
ACVS
Gulf Coast Veterinary Specialists
1111 West Loop South #160
Houston
Texas
77027
drbeale@gcvs.com
Very little is actually new in the world of patellar
luxation - but this condition certainly warrants
review and discussion due to its high prevalence
and the common occurrence of complications
following surgical repair. Patellar luxation is a
frequent presenting complaint of small dogs and
cats, and is occasionally seen in large dogs. Medial
patellar luxation predominates in both small and
large breeds, although past literature suggests
lateral luxation is much more common in large
breeds. Patellar luxation is generally graded from
1-4 based on increasing severity. Grade 1 patellar
luxations are generally not repaired, but surgical
repair is recommended for grades 2-4. Surgical
options include trochleoplasty, trochlear wedge
recession, trochlear block recession, tibial tuberosity
transposition, tibial tuberosity transposition, rectus
femoris transposition, retinacular imbrication,
derotational suture, retinacular releasing incision
and corrective osteotomy in cases of femoral or
tibial deformity. In severe cases that do not respond
to the above treatments, patellectomy and stifle
arthrodesis are a possibility; these techniques are
fortunately rarely needed (these techniques will
not be presented).
Decision-Making for Patellar Luxation Repair
Many surgical options are available when
considering repair of the luxating patella. It is
important to consider the underlying problems
associated with the particular luxation when
choosing a surgical plan. Factors to consider
include, depth of the trochlear groove, alignment
of the quadriceps mechanism (quadriceps,
patella, patellar tendon), and the presence of
excessive laxity or tension of the joint capsule
and retinacular tissues medially and laterally.
The surgical options chosen should alleviate the
underlying factor contributing to the luxation.
For example, if a dog has good alignment of the
quadriceps mechanism, but a shallow trochlear
groove- the surgical plan should include a
technique to deepen the femoral trochlea, but not
a tibial tuberosity transposition.
Back to contents
A
Methods to Deepen the Trochlea
Three methods are commonly used to deepen
a shallow trochlear groove. These methods are
described below. A head-to-head comparison as
not been performed to document superior efficacy
of one technique compared to the others. Usually
trochleoplasty is reserved for toy-breed dogs and
cats. Trochlear wedge recession and trochlear
block recession are preferred for small, medium
and large breed dogs, but also can be performed
effectively in toy-breed dos and cats with a slight
increase in technical difficulty.
Trochleoplasty: Trochleoplasty is a traditional
technique that involves removal of articular
cartilage and subchondral bone from the
trochlear sulcus, thereby deepening the sulcus.
Fibrocartilage repair is generally seen. This
technique is considered less desirable to cartilage-
sparing techniques described below, although it is
sometimes used in toy breeds very successfully.
Trochleoplasty is technically easy to perform. A
deepened groove can be quickly formed using
appropriate sized rongeurs. Attention should be
paid to ensuring adequate depth of the groove
proximally.
Trochlear Wedge Recession: Trochlear wedge
recession provides a means of adequately 2006 World Congress WSAVA/FECAVA/CSAVA
deepening the trochlear sulcus, while preserving
most of the articular cartilage. This technique
is described elsewhere, but basically involves
removal of a v-shaped wedge of bone and
cartilage from the trochlear sulcus, removal of
underlying bone, followed by replacement of
the original wedge in a recessed position. This
is an excellent technique, but technically more
demanding than trochleoplasty. The technique
is performed using a fine-tooth hand saw-blade.
Care should be taken when beginning the saw
cut, not to excoriate the adjacent cartilage due
to slippage. The cut is initiated perpendicular to
the cartilage surface adjacent to the peak of the
trochlear ridge. Once the saw blade has engaged
the subchondral bone, the blade is gradually
redirected in the proper direction, parallel to the
83
A
v-shaped trochlear groove. A cut is made from
the lateral and medial ridge, meeting deep to
the central sulcus of the groove. The wedge is
removed and carefully stored to avoid accidental
discard. The groove is further deepened by
removing a block of bone from one side of the
groove by making a parallel cut with the handsaw.
A modification of this technique is to broaden and
deepen the proximal aspect of the new, deepened
groove by performing a partial trochleoplasty
in the proximal aspect of the groove only, as
described above using rongeurs. A portion of
bone can also be removed from the underside
of the trochlear wedge to further deepen the Saw-blade cut for trochlear block recession
groove. The wedge is replaced and the adequate
depth of the groove is documented. Fixation of
the wedge is not needed due to pressure applied
from the patella lying above and the congruency
between the groove and wedge geometry.

Osteotome cut begins above intercondylar notch

Trochlear wedge or block recession is indicated

for this shallow trochlear groove

Trochlear Block Recession - Trochlear block

recession is similar to trochlear wedge recession
except that a block-shaped wedge is removed from
the trochlear sulcus rather than a v-shaped wedge.
This technique allows a deeper sulcus proximally,
2006 World Congress WSAVA/FECAVA/CSAVA

which may provide better biomechanical stability

of the patella when the stifle is in an extended Osteotome is used to elevate trochlear block
position. This is an excellent technique, but
technically more demanding than trochleoplasty.
The technique is performed using a fine-tooth
hand saw-blade, a small osteotome and mallet.
Care should be taken when beginning the saw
cut, not to excoriate the adjacent cartilage due
to slippage. The cut is initiated perpendicular to
the cartilage surface adjacent to the peak of the
trochlear ridge.

Bone is removed below the block deepening the

groove after replacing the block
84
Back to contents

Once the saw blade has engaged the subchondral
bone, the blade is gradually redirected in the
proper direction, perpendicular to the long
axis of the bone. A cut is made from the lateral
and medial ridge and each cut is carried to an
adequate depth deep to the central sulcus of
the groove. The block of cartilage and bone is
removed gently using an osteotome and mallet.
The osteotome is positioned just proximal to
the intercondylar notch beginning at the depth
of the trochlear cuts. The osteotome is directed
towards the proximal extent to the trochlear
groove. Gentle raps with the mallet will advance
the osteotome, dislodging the trochlear block.
The trochlear block is removed and carefully
stored to avoid accidental discard. The groove is
further deepened by removing a complimentary
block of bone from the deep portion of the groove
by making a parallel cut with the osteotome or
by deepening with a rongeur. A portion of bone
can also be removed from the underside of the
trochlear block to further deepen the groove.
The block is replaced and the adequate depth of
the groove is documented. Fixation of the block
is not needed due to pressure applied from the
patella lying above and the congruency between
the groove and block geometry.
Alignment of the Quadriceps Mechanism
Tibial Tuberosity Transposition: Tibial tuberosity
transposition is an excellent method of improving
alignment of the patellar mechanism in patients
having an abaxially displaced tibial tuberosity.
If the tuberosity is displaced medially, luxation
occurs medially; therefore, the tuberosity must be
transposed laterally and secured. Lateral luxations
require medial tibial tuberosity transposition. An
osteotomy is performed as previously described;
the tuberosity is transposed then secured with a
single or multiple k-wires. An attempt is made
when performing the osteotomy to leave the
distal cortical bone intact to act as a tension band
against the pull of the quadriceps mechanism. If
the tuberosity is freed completely, it is prudent
to secure the transposed bone with either a pin
and tension band or a lag screw. The tuberosity
should be transposed to a position that restores
axial alignment to the quadriceps mechanism.
Rectus Femoris Transposition:This is a technique
described by Dr. Barclay Slocum for use in bow-
legged dogs having medial patellar luxation.
This technique is done in combination with a
medial releasing incision. A trochlear deepening
Back to contents
A
technique should also be performed as needed.
The rectus femoris is transected from its pelvic
origin with a small piece of attached bone, then
laterally transposed by tunneling under the vastus
lateralis and reattaching it to the cervical tubercle
or third trochanter of the proximal femur with
wire or heavy suture. This realigns the quadriceps
mechanism, restoring a straight-line pull.
Retinacular Imbrication
Lateral imbrication is usually performed with
correction of a medial patellar luxation as a
means of creating lateral restraint. The stretching
of the lateral joint capsule and retinaculum occurs
chronically with longstanding patellar luxation.
Occasionally a traumatic luxation may result
in rupture of these tissues; imbrication is also a
good technique for repair in this case. Imbrication
is usually performed using heavy, absorbable,
monofilament suture placed in a vest-over-pants-
or horizontal mattress pattern. Care must be
taken not to tighten the retinaculum excessively
(especially if a retinacular releasing incision has
been performed on the opposite side), because
it is possible to create an iatrogenic luxation in
the opposite direction. An alternative method
of supplying lateral restraint is placement of a
lateral derotational suture from the lateral fabella
to a bone tunnel in the tibial tuberosity.
Retinacular Releasing Incision
A medial releasing incision is performed if fibrous
hyperplasia has occurred medially following
prolonged or severe medial patellar luxation. An
incision is made through the retinacular tissues
in a medial parapatellar location. The incision
should extend proximally beside the medial
edge of the quadriceps tendon. Placement of the
incision in this location will release the insertion
of the sartorius muscle, decreasing pull on the
patella. The incision occasionally has to be carried
deeper to include the joint capsule if marked joint
2006 World Congress WSAVA/FECAVA/CSAVA
capsular fibrosis has occurred creating excessive
medial restraint. The incision is left open and not
sutured.
Recently arthroscopic medial releasing incisions
have been performed by Dr. Wayne Whitney.
This technique is quick, easy to perform and has
low morbidity. Long-term follow-up is presently
unavailable. In addition, the clinical indications
with this technique are presently unknown.
85
A
Standards of Care (How I Treat)
CANINE URETHRAL SPHINCTER MECHANISM INCOMPETENCE
Professor Peter Holt
University of Bristol
Department of Clinical
Vetrerinary Science
Langford house
Langford
Bristol BS40 5DU
UK
Peter.holt@bristol.ac.uk
In dogs referred for the investigation of urinary
incontinence, urethral sphincter mechanism
incompetence (USMI) is the commonest diagnosis
made in adults and is second only to ureteral
ectopia in juveniles, particularly in females1.
It can present as a congenital or acquired condition.
Although urethral pressure profilometry can
be used to demonstrate incompetence of the
urethral sphincter mechanism2, this technique is
not readily available in general practice and is
predisposed to a number of artefacts which can
make interpretation difficult. In general practice,
therefore, the diagnosis is usually made on the
basis of the breed, history and by the elimination
of other possible diagnoses using imaging and
laboratory techniques.
This presentation will concentrate on possible
treatment options.
Approximately half of bitches with the congenital
form of USMI become continent following their
first oestrus and so should not be neutered until
they have had at least one season. Those that do
not may be candidates for medical or surgical
management (see acquired USMI below).
Oestrogens are contra-indicated in juvenile
bitches with this condition because of possible
2006 World Congress WSAVA/FECAVA/CSAVA
adverse ‘feed-back’ effects on the pituitary but
alpha-adrenergics such as phenypropanolamine
could be used, pending oestrus.
Acquired USMI usually (but not always) follows
spaying in the bitch3,4. It is a multi-factorial problem
and a variety of factors are known or suspected to
contribute to its clinical manifestation of urinary
incontinence. These factors include urethral tone,
urethral length, bladder neck position, body size
and breed, ovariohysterectomy, hormones and
obesity.
The treatment of cases of sphincter mechanism
incompetence may be difficult and most therapies
correct only one of the above factors. It is
highly unlikely, therefore, that any one form of
treatment alone will cure 100% of cases in the
long-term. The response may diminish over time5
and most therapies, medical or surgical, only cure
86
Back to contents
approximately 50% of affected animals in the
long term.
In theory, sympathomimetic or parasympatholytic
agents should improve continence control by
increasing urethral tone or reducing intravesical
pressure respectively but the results of
clinical trials are variable and possible long-
term adverse systemic effects have not been
evaluated. Currently, in the UK the most popular
medical treatment is the alpha-adrenergic
phenylpropanolamine . Affected spayed bitches
sometimes respond to oestrogen therapy but in
many animals the response ceases eventually,
despite increasing the dosage of oestrogens,
possibly due to desensitisation of oestrogen
receptors. Oestrogens sensitise the urethral
smooth muscle to alpha-adrenergic stimulation
and so a combination of oestrogen and alpha-
adrenergic (phenylpropanolamine) therapy may
be useful and reduce the dose of each individual
drug, lessening the chances of side effects
The main options for surgical treatment are to
attempt to:
•increase urethral resistance - e.g. peri-urethral
surgical slings 6, 7 or artificial sphincters 8; intra-
urethral injection of bulking agents 5, 9, 10;
•increase urethral length, using bladder neck
reconstruction techniques 11;
•re-locate the bladder neck to an intra-
abdominal position by means of colposuspension
12, 13
, urethropexy 14 or, in male dogs vas
deferentopexy 15, 16 or prostatopexy 17.
The problem with techniques intended to increase
urethral resistance is that they may increase the
morbidity by making an incontinent animal
dysuric. Similarly, increasing urethral length
carries potentially serious surgical risks and, in the
reviewer’s view, should be reserved for animals
with severe congenital urethral hypoplasia.
In the reviewer’s opinion, the technique least
likely to lead to serious complications is to re-
locate the bladder neck to an intra-abdominal
position by means of colposuspension. The

greater experiences of medical urologists treating
incontinent women suggests that colposuspension
provides firmer anchorage of the lower urogenital
tract than urethropexy and avoids urethral
trauma,. However, a review of urethropexy as
a treatment for urethral sphincter mechanism
incompetence in 100 bitches14 revealed similar
results to colposuspension although the
prevalence and severity of urethral complications
was higher. The author believes that cystopexy is
contra-indicated in these cases since it may result
in detrusor instability, a further cause of urinary
incontinence!
Colposuspension is intended to move the
intrapelvic bladder neck of bitches with urethral
sphincter mechanism incompetence to an intra-
abdominal position so that increases in intra-
abdominal pressure can act simultaneously on
the bladder and urethra. A long-term evaluation
of cases treated by the author13 indicates that a
cure-rate of 53% can be expected with most of
the remaining bitches improved. Ten percent of
bitches fail to respond at all to colposuspension
and the complication rate is low. In male dogs,
the response to medical management is poor and
the results of relocation of the intrapelvic bladder
neck to an intra-abdominal position 15-17 are not
as good as the response to bladder neck relocation
in bitches.
References and Further Reading
1. Holt PE, Urinary incontinence in dogs and
cats. Vet Rec 1990; 127: 347-350.
2. Holt PE, ‘Simultaneous’ urethral pressure
profilometry: comparisons between continent and
incontinent bitches. J small Anim Pract 1988; 29:
761-769.
3. Holt PE, Thrusfield MV, Association in
bitches between breed, size, neutering and
docking, and acquired urinary incontinence
due to incompetence of the urethral sphincter
mechanism. Vet Rec 1993; 133: 177-180.
4. Thrusfield MV, Muirhead RH, Holt PE,
Acquired urinary incontinence in bitches: its
incidence and relationship to neutering practices.
J small Anim Pract 1998; 39: 559-566.
5. Barth A, Reichler IM, Hubler M, Hassig M
& Arnold S, Evaluation of long-term effects of
endoscopic injection of collagen into the urethral
submucosa for treatment of urethral sphincter
incompetence in female dogs: 40 cases (1993-
2000). J Am vet med Ass 2005; 226: 73-76.
6. Muir P, Goldsmid, SE, Bellenger CR,
Management of urinary incontinence in five
bitches with incompetence of the urethral
sphincter mechanism by colposuspension and a
Back to contents
A
modified sling urethroplasty. Vet Rec 1994; 134:
38-41.
7. Nickel RF, Wiegand U, Van Den Brom WE,
Evaluation of a transpelvic sling procedure with
and without colposuspension for treatment of
femlae dogs with refractory urethral sphincter
mechanism incompetence. Vet Surg 1998; 27:
94-104.
8. Dean PW, Novotny MJ, O’Brien DP, Prosthetic
sphincter for urinary incontinence: results in three
cases. J Am Anim Hosp Ass 1989; 25: 447-454.
9. Arnold S, Jager, P, Dibartola SP, Lott-STolz
G, Hauser B, Hubler M, Fairburn A, Rusch P,
Treatment of urinary incontinence in dogs by
endoscopic injection of Teflon. J Am Vet Med
Ass 1989; 195: 1369-1374.
10. Arnold S, Hubler M, Lott-Stolz G, Rusch P,
Treatment of urinary incontinence in bitches by
endoscopic injection of glutaraldehyde cross-
linked collagen. J small Anim Pract 1996; 37:
163-168.
11. Holt PE, Surgical management of congenital
urethral sphincter mechanism incompetence in
eight female cats and a bitch. Vet Surg 1993; 22:
98-104.
12. Holt PE, Urinary incontinence in the bitch
due to sphincter mechanism incompetence:
surgical treatment. J small Anim Pract 1985; 26:
237-246.
13. Holt PE, Long-term evaluation of
colposuspension in the treatment of urinary
incontinence due to incompetence of the urethral
sphincter mechanism in the bitch. Vet Rec 1990;
127: 537-542.
14. White RN, Urethropexy for the management
of urethral sphincter mechanism
incompetence in the bitch. J small Anim Pract
2001; 42: 481-486.
15. Weber UT., Arnold S, Hubler, M & Kupper, 2006 World Congress WSAVA/FECAVA/CSAVA
JR, Surgical treatment of male dogs with urinary
incontinence due to urethral sphincter mechanism
incompetence. Vet Surg 1997; 26: 51-56.
16. Salomon JF, Cotard JP & Viguier E,
Management of urethral sphincter mechanism
incompetence in a male dog with laparoscopic-
guided deferentopexy. J small Anim Pract 2002;
43: 501-505.
17. Holt PE, Coe RJ & Hotston Moore A,
Prostatopexy as a treatment for urethral sphincter
mechanism incompetence in male dogs. J small
Anim Pract 2005; 46: 567-570.
87
A
Standards of Care (How I Treat)
CANINE LYMPHOMA
Gregory K. Ogilvie, DVM,
Diplomate ACVIM
(Specialties of Internal
Medicine, Oncology)
Director, CVS Angel Care
Cancer Center (www.
CVSAngelCare.com)
President, Special
Care Foundation for
Companion Animals (www.
SpecialCareFoundation.org)
100 North Rancho Santa Fe Rd #100
San Marcos CA 92024 USA
Gogilvie@aol.com
It is important that the client be given all the
options and that the best option be used first.
As a general rule, combination chemotherapy
is superior to single-agent therapy. Each time
an effective drug is added to the COP protocol,
the remission duration increases; however, so do
the cost and the potential for toxicity. It is also
important that clients realize that a second or third
remission is possible with appropriate therapy but
that these subsequent remissions are more difficult
to attain and that their duration is generally half
the duration of the previous remission.
The treatment options below are tiered according
to risk of toxicity, cost, and efficacy. First-level
protocols provide a low risk of toxicity at low
cost but have low efficacy; as the level rises, so
do efficacy, cost, and risk of toxicity.
First Level: For clients who cannot afford or
will not accept a combination chemotherapy
protocol due to the risks of toxicity, a protocol
using prednisone alone (40 mg/m2 PO daily for
7 days then every other day) or in combination
with chlorambucil (6 to 8 mg/m2 PO every other
2006 World Congress WSAVA/FECAVA/CSAVA
day) may provide palliation with few risks of side
effects. A CBC should be collected every 2 to 3
weeks to make sure that myelosuppression is not
occurring.
Second Level: The COP protocol is a relatively
inexpensive chemotherapy protocol with a low
risk of toxicity. Dogs tolerate the treatments,
and veterinarians find the protocol very
manageable. CBCs should be taken 1 week after
each dose of cyclophosphamide to ensure that
myelosuppression (if it occurs) is not severe and
88
Back to contents
that doses do not need to be adjusted.
Doxorubicin administered every 3 weeks for five
to eight treatments at a dosage of 30 mg/m2 (1
mg/kg for small dogs) is the most effective single
chemotherapeutic agent. This treatment regimen
results in a relatively high remission rate with
relatively few serious life-threatening toxicities
(<5%). With the advent of generic doxorubicin,
the cost is reasonable for most clients. Because
the drug is given every 3 weeks, this treatment
approach is less time intensive than most
chemotherapeutic protocols. A second remission
seems more likely if with doxorubicin is used as
first-line therapy and COP is used after relapse
than if COP is used first.1 Overall remission time
for the two-protocol treatment approach is similar
to that of the COPA protocol.2
Third Level: The most effective chemotherapy
protocols use a five-drug combination of L-
asparaginase, vincristine, cyclophosphamide,
doxorubicin, and prednisone. Similar remission
rates and survival times have been obtained
for the protocols that include these drugs.3-
7 Although these protocols require more
intense client–veterinarian communication
and monitoring for toxicity, the overall level of
satisfaction for owners, pets, and veterinarians is
high. Most oncologists recommend discontinuous
protocols such as VELCAP-S or the Wisconsin
protocol; however, some clients will not restart
chemotherapy when first remission is over.8,9
For dogs with T-cell lymphoma, protocols that
rely heavily on alkylating agents, such as Tufts
VELCAP-SC, should be used.10
 A
Table 47-10 WISCONSIN PROTOCOL
Vincristine is administered at 0.5 to 0.7 mg/m2 IV. L-asparaginase is given at 400 IU/kg IM. The dose
for cyclophosphamide* is 200 mg/m2 IV. Doxorubicin is administered at 30 mg/m2 IV. The dose for
prednisone is 2.0 mg/kg PO, week 1; 1.5 mg/kg PO, week 2; 1.0 mg/kg PO, week 3; and 0.5 mg/kg
PO, week 4.

Week Vincristine L-asparaginase Cyclophosphamide* Doxorubicin Prednisone

1 • • •
2 • • •
3 • •
4 • •
5
6 •
7 •
8 •
9 •
11 •
13 •
15 •
17
19 •
21 •
23 •
25 •

From week 25, repeat weeks 11 to 17, but every 3 weeks. After week 49, treatments given every 4 weeks.
Fourth Level: The addition of radiation therapy dosage levels of cyclophosphamide were used:
or, if available, autologous bone marrow support 300 mg/m2 (3 dogs), 400 mg/m2 (12 dogs), and
to allow chemotherapy dose intensification 500 mg/m2 (13 dogs). Toxicity was acceptable,
represents the best possible treatment option for a with only one dog requiring hospitalization after
dog with lymphoma. The potential for long-term transplant for complications that resolved in 24
remission and possibly cure is much higher than hours. Remission duration was not significantly
with other protocols. Dogs with T-cell lymphoma different for dogs receiving 300 mg/m2 or 400
may not benefit to the same extent as those dogs with mg/m2. For dogs receiving 500 mg/m2, the median
B-cell lymphoma. Although risks of toxicity are remission was 12.4 months, significantly longer
higher, the addition of radiation or chemotherapy than for dogs receiving 400 mg/m2, with 6 of 13
dose intensification has not negatively affected the dogs still in remission between 6 and 33 months
quality of life for treated dogs. after starting chemotherapy and 1-year survival
High-dose chemotherapy with hematopoietic of 57.1%. Using autologous bone marrow to
stem cell support or bone marrow transplantation support chemotherapy dose intensification allows
(BMT) has become an important component of dogs to receive 2.5 times the standard dose 2006 World Congress WSAVA/FECAVA/CSAVA
therapy for lymphoma and other malignancies in of cyclophosphamide without any increase in
humans. Although combination chemotherapy clinical toxicity. This dose intensification results
results in a complete remission rate of 75% in significant prolongation of remission.
or greater in dogs, relapses frequently occur
after a median of 10 to 12 months. It appears Supportive and Nutritional Treatment for Canine
that autologous BMT allows dogs to receive Lymphoma
intensified doses of myelosuppressive The induction death rate decreased markedly for
chemotherapy without increased toxicity and that the VELCAP-SC protocol compared with previous
this intensification improves remission duration protocols, despite an increase in the percentage
and overall survival. of dogs needing a dose reduction of at least one
In a reported protocol reported by AS Moore and chemotherapy drug (toxicity) and despite a higher
A Fermberger based on VELCAP-S, dogs in CR proportion of substage b dogs undergoing therapy.
at week 8 were treated with filgrastim (G-CSF) We attribute the difference in death rate to careful
followed by bone marrow collection. A high staging that required the owners’ commitment
dose of cyclophosphamide was given with mesna to therapy, as well as strict use of hospitalized
followed by prophylactic antibiotics, and bone induction for any animal that was in substage b.
marrow was administered intravenously. Three We suggest that any dog that has signs compatible
89
Back to contents
A
with substage b (particularly anorexia and other
GI signs) be admitted for intravenous fluid
therapy (maintenance x 1.5), broad-spectrum
antibiotics (cefazolin sodium or enrofloxacin),
and GI prophylaxis (metoclopramide and bland
diet). This supportive care should be continued
for at least 4 days after induction and preferably
for a week. Dogs can be discharged to the owner
as soon as they are self-supporting. Antibiotics
and prophylactic metoclopramide are continued
for the first 3 weeks of the protocol.
In addition, in one study, administration of
trimethoprim/sulfadiazine (Tribrissen®) to dogs
for 14 days, starting on the day of treatment with
doxorubicin, markedly reduced the likelihood of
GI toxicity (vomiting or diarrhea), hospitalization,
and lower quality-of-life (Karnofsky) score. The
effect was most marked in dogs with lymphoma
and may be due to reduced bacterial translocation
in damaged intestinal epithelial layers.133
Nutrition is an important part of supportive care
for any dog with cancer, particularly for dogs
with a systemic disease like lymphoma. Lactate
and insulin concentrations in untreated dogs
2006 World Congress WSAVA/FECAVA/CSAVA
90
Back to contents
with lymphoma are higher than in dogs without
lymphoma and do not improve when dogs enter
chemotherapy-induced remission.12-13
Nutrition may also play a role in prolonging
remission and survival. Polyunsaturated n-3 fatty
acids have been shown to inhibit the growth and
metastasis of tumors. In one study, 32 dogs with
lymphoma were randomized to receive a diet
supplemented with polyunsaturated n-3 fatty acids
(menhaden fish oil and arginine) or an otherwise
identical diet supplemented with soybean oil.14
Diets were fed from the start of doxorubicin
chemotherapy and continued after remission was
attained. Dogs fed the diet supplemented with n-
3 fatty acids had higher serum levels of n-3 fatty
acids (docosahexaenoic acid and eicosapentaenoic
acid) and lower plasma lactate responses to
carbohydrate testing. Increased serum levels
of docosahexaenoic acid were associated with
longer remission and survival times for dogs with
stage III lymphoma.
References: available upon request

Standards of Care (How I Treat)
CANINE OSTEOSARCOMA
Gregory K. Ogilvie, DVM,
Diplomate ACVIM
(Specialties of Internal
Medicine, Oncology)
Director, CVS Angel Care
Cancer Center (www.
CVSAngelCare.com)
President, Special
Care Foundation for
Companion Animals (www.
SpecialCareFoundation.org)
100 North Rancho Santa Fe Rd #100
San Marcos CA 92024 USA
Gogilvie@aol.com
Amputation
Surgical treatment of osteosarcoma by amputation
is palliative and increases survival by pain relief,
thereby delaying euthanasia. Amputation usually
eliminates the primary tumor and causes little to
no reduction in mobility and quality of life for
the dog. Although most clients do not initially
embrace the concept that their dog will have
three legs, the procedure is very acceptable to
caregivers after amputation. In two studies in
the United States and Europe, dogs learned to
walk well on three legs within a month, which
exceeded most clients’ expectations.1,2 It is also
our experience, after sending many hundreds of
dogs to amputation, that clients are very happy
with their decision; the veterinarian should
be confident in offering amputation to these
clients. For lesions in the forelimbs, complete
forequarter amputation, including the scapula,
provides cosmetically and functionally good
results. For distal hindlimb tumors, amputation
at the proximal third of the femur is performed.
For distal femoral tumors, a hip disarticulation is
performed; proximal femoral lesions are treated
by hemipelvectomy.
In one study, the median survival of 65 dogs
treated with amputation was 126 days; only
10.7% of dogs were alive 1 year after surgery.3 A
larger study of 162 dogs treated with amputation
corroborated these data.6 Surgery of any type
is only palliative, and dogs with appendicular
osteosarcoma should be given chemotherapy.
Limb-sparing surgery
Limb-sparing surgery is important in human
patients, for whom cosmetic appearance and
function are impaired by amputation. This
procedure may be appropriate for dogs that are
poor candidates for amputation (e.g., very large
dogs, dogs with other orthopedic or neurologic
Back to contents
A
problems) or for dogs whose owners refuse
amputation.4,5 Caution is advised because dogs
that are not good candidates for amputation may
not be good candidates for limb-sparing surgery
due to the prolonged period of postoperative
recovery. During limb-sparing surgery, a cortical
bone graft is used to replace the widely excised
tumor, and arthrodesis of the nearby joint is
usually performed. The best results are obtained
with distal radial lesions or lesions of the ulna. It
is possible to perform limb salvage for proximal
humeral or scapular lesions, but function is poor,
and the rate of postoperative complications
is high, including a high rate of incomplete
resection.6 Good functional results have been
reported for partial or complete scapulectomy in
dogs with osteosarcoma.7
Limb salvage is not an option for large lesions
that involve more than 50% of the bone, tumors
that invade adjacent soft tissue, and tumors of
the hindlimb. Complications of limb salvage
include allograft rejection and implant failure.
Complications occurred in 86 (55%) of 145 dogs 2006 World Congress WSAVA/FECAVA/CSAVA
treated with limb salvage in one study.43 Implant
failure was seen in 12 dogs (8%) and infection
in 71 (49%). Infection required allograft removal
or limb amputation in 16 dogs (11%).5 Local
recurrence of osteosarcoma is a frequent problem
with limb salvage procedures and affects up to
40% of dogs. Even at institutions that perform
limb salvage frequently and use adjunctive
chemotherapy, recurrence rates of 17% to 27%
are seen.7,8 Local recurrence is not a significant
problem when amputation is performed.
Another disadvantage of limb-sparing procedures
is the need for allografts from normal donors
(usually dogs euthanized for another disease).
These grafts must be stored, and fitting to the
patient is always approximate. Pasteurized excised
tumor has been used as an autograft for dogs with
91
A
distal radial osteosarcoma. Local recurrence and
infection rates were similar to those from the use
of an allograft.8
Some surgeons use surgical metallic ‘spacers’
attached to the surgical plate. These devices fill
the space where the tumor is excised. Benefits
include the lack of need for a bone bank and,
potentially, a lower complication rate. Another
technique adapted by surgeons at Colorado State
University has been used on a small number of
dogs with osteosarcoma that does not involve
the bone or cartilage at or near a joint. In this
procedure, the involved bone is stripped of
attachments to soft tissues. A cut is made distal
to the tumor, and the bone containing the tumor
is exteriorized surgically. The tumor in the bone
is given very high dosages of external beam
radiation therapy and then replaced in its normal
position and fixed in place with a surgical plate. .
Before limb salvage is performed, intra-arterial
cisplatin, with or without radiation therapy,
often increases tumor necrosis and reduces the
risk of local recurrence.10 In addition, a locally
implanted polymer impregnated with cisplatin
(open polylactic acid–cisplatin or OPLA–Pt)
can be used. OPLA–Pt releases cisplatin
slowly into the tumor bed, and its use reduces
local recurrence rates from 27% to 17%. The
survival time and disease-free interval for dogs
treated with OPLA–Pt are similar to those of
dogs receiving systemic cisplatin, presumably
because locally implanted cisplatin is dispersed
systemically. Because cisplatin release is slow,
systemic toxicity is reduced.
Chemotherapy
Cisplatin markedly improves survival rates to a
median survival of between 6 and 13 months and
1-year survival rates to between 30% and 62%; 2-
year survival rates are between 7% and 21%.11-16
Whether the drug is administered intravenously or
2006 World Congress WSAVA/FECAVA/CSAVA
intra-arterially does not appear to affect efficacy.
Other methods of administration have been
investigated. OPLA-Pt appears to release a
controlled amount of cisplatin over a prolonged
period as well as provide high local concentrations
in the site of limb-sparing surgery. OPLA-Pt
was implanted in the surgical wound of 39 dogs
that had an amputation. Median survival was
8 months, and 1-year survival rate was 41%,
which was similar to that achieved with systemic
chemotherapy.16 In another study, OPLA-Pt was
related to nonunion of limb salvage grafts.17
OPLA-Pt is not readily obtainable, so another
study evaluated the utility of subcutaneously
administered cisplatin and saline for slow-release
chemotherapy; renal, gastrointestinal, and bone
marrow toxicities and local tissue reaction were
92
Back to contents
seen in five of six dogs, and this treatment is
not recommended.18 Intramedullary cisplatin
administration led to resolution of osteosarcoma
in one dog with apparent survival benefit but was
not so successful in three other dogs.19 Cisplatin
is best given intravenously with saline diuresis.
Early reports of doxorubicin failed to show
efficacy.20 Larger studies have shown benefit for
the use of doxorubicin given as five biweekly
doses at a dosage of 30 mg/m2. In one study,
two or three doses were given before surgery;
subsequent doses were given the day after
surgery and 2 weeks later. Median survival was
12 months, and the efficacy approached that of
cisplatin; 50% of the dogs were alive at 1 year,
and 10% were alive at 2 years.21 Another group
of more than 300 dogs received five doses of
doxorubicin every 2 weeks, starting 2 weeks after
amputation. Median survival was 8 months, and
1-year, 2-year, and 3-year survival rates were
35%, 17%, and 9%, respectively, which is very
similar to results from cisplatin chemotherapy.
Survival times were greater in younger dogs,
lighter-weight dogs, and dogs with normal T-ALP
and B-ALP.
Carboplatin (300 mg/m2 IV) was given
adjunctively after surgery to 48 dogs.22 Median
survival was 10.5 months; 35% of the dogs were
alive 1 year after surgery. In this study, smaller
dogs had longer survival times. Slightly lower
survival rates were seen in a smaller group
of dogs, but overall results are similar to that
achieved with other drugs.
Single-agent treatment with carboplatin or
doxorubicin seems to be as effective as cisplatin
in treating canine appendicular osteosarcoma,
and the choice of which drug to offer may depend
on other factors. For example, doxorubicin may
be less expensive than either of the platinum
drugs; however, doxorubicin causes a cumulative
cardiotoxicity, the risk of which is higher in breeds
predisposed to cardiomyopathy. Many dogs with
osteosarcoma are also breeds that are at risk for
cardiomyopathy (e.g., Dobermans, great Danes),
so doxorubicin may not be a good choice for these
dogs. Even with prescreening of prospective
patients and elimination of those with early
cardiac changes or significant breed risk, more
than 7% of patients developed cardiomyopathy in
one study of more than 300 dogs treated with five
doses of doxorubicin. Similarly, the fluid diuresis
required to prevent renal toxicity of cisplatin
may make it unsuitable for a dog with clinical
or subclinical heart disease. Dogs that cannot be
admitted as day patients for fluid diuresis and
cisplatin may be better treated with carboplatin or
doxorubicin because these drugs can be given on
an outpatient basis.

Combination chemotherapy
A protocol alternating cisplatin (60 mg/m2) with
doxorubicin (30 mg/m2) every 21 days for two
cycles was delivered after amputation to 19 dogs
with appendicular osteosarcoma. The median
survival was 10 months, with 37% of dogs alive at
1 year and 26% alive at 2 years. Despite the lower
dose intensity (0.76) of the two drugs compared
with single-agent protocols, survival rates were
comparable to those for cisplatin chemotherapy
alone.23
Another study delivered doxorubicin (15–25 mg/
m2) and cisplatin (60 mg/m2) on the same day
(doxorubicin in postdiuresis fluids) to 102 dogs
with osteosarcoma. Median survival was 11.5
months, and 1-year, 2-year, and 3-year survival
rates were 47%, 28%, and 17%, respectively.24
The dose intensity of this protocol was greater
than that of either single agent (1.19–1.30). A
later evaluation of toxicity showed that a 20-
mg/m2 dose of doxorubicin was well tolerated
in these dogs.25 A small pilot study of 19 dogs
that used lower doses of doxorubicin and
cisplatin (15 mg/m2 and 50 mg/m2, respectively;
dose intensity: 1.04) showed a greater median
survival, but as more dogs were added to the
study, the median survival decreased, illustrating
the need for larger numbers to adequately assess
efficacy.
Carboplatin (300 mg/m2) and doxorubicin (30
mg/m2) were given in an alternating protocol
every 3 weeks for three cycles for a dose intensity
of 1.0. Median survival was 10.5 months, and
1-year and 2-year survival rates were 48% and
18%, respectively.26 The dogs that finished the
protocol had a median survival of 18 months.
Clients often want to know how their pet is likely
to do after completing a course of chemotherapy;
this finding serves as encouraging news for dogs
that have not developed metastatic disease during
chemotherapy.
Back to contents
A
Palliative Radiation Therapy
If caregivers refuse definitive treatment for a
pet with osteosarcoma, or if an animal is not
considered eligible for amputation or limb-
sparing surgery, consideration may be given to
palliation of tumor pain with radiation therapy.
Radiation delivered in two to four weekly
fractions of 8 to 10 Gy has been reported as a
palliative treatment for 125 dogs with pain or other
symptoms related to osteosarcoma. Improved
limb function was seen in approximately 75% of
dogs treated with either 8 Gy on days 0, 7, 14, and
21; 10 Gy on days 0, 7, and 21; or 8 Gy on days 0
and 7. Improvement lasted for a median of 2 to 3
months regardless of the protocol, and toxicities
were rare and acute.27-29 Chemotherapy appeared
to improve response rate and duration. Dogs with
large lesions extending to involve a greater length
of limb were less likely to respond for long.28,29
Many radiation therapists agree that a reasonable
clinical approach may be to deliver a single large
dose to the affected site and then to repeat a single
dose as necessary to maintain pain control.
Targeted stereotactic “radiosurgery” may offer
some advantages in delivering a single high dose
of 30 Gy to the tumor alone. Preliminary results
are encouraging.30
Other Palliative Therapy
Bisphosphonates are inhibitors of osteoclast
activity that have been used in human patients with
osteolytic disease, including metastatic neoplasia.
Pamidronate is an intravenously administered
drug that has anecdotally been associated with
decreased pain from osteosarcoma.
Pamidronate has also been used in combination
with radiation therapy; it is difficult to decide
whether the subjective improvement is due to the
combination or the individual components.
References: Available Upon Request
2006 World Congress WSAVA/FECAVA/CSAVA
93
A
Standards of Care (How I Treat)
PLEURAL DISEASE WITH CHEST TUBES
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery Texas A&M
University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu
Management of Pleural Effusion
Animals with pleural air or fluid usually exhibit
a restrictive respiratory pattern (i.e., rapid,
shallow respirations) and they may be extremely
dyspneic. Thoracentesis (see below) should be
performed prior to taking radiographs in severely
dyspneic animals with suspected pleural cavity
disease. Removal of even small amounts of
pleural effusion or air may significantly improve
ventilation, allowing safer manipulation of
the patient for radiographic procedures. Most
dyspneic animals will allow thoracentesis to
be performed with minimal restraint; general
anesthetics should be avoided. The animal should
be allowed to remain in sternal recumbency and
oxygen provided by face mask or nasal insufflation
if they will tolerate it. A negative tap does not
rule-out pleural effusion; however, if the animal
remains dyspneic after thoracentesis, underlying
lung disease (i.e., pneumonia, pulmonary edema,
pulmonary contusions, pulmonary neoplasia) or
loculated fluid should be suspected. Providing
nasal oxygen or placing the animal in an oxygen
cage may be beneficial while treatment of the
pulmonary disease is initiated.
2006 World Congress WSAVA/FECAVA/CSAVA
Needle Thoracentesis
Needle thoracentesis is performed with a small
gauge (#19 to #23) butterfly needle attached to
a 3-way stopcock and syringe, or an over-the-
needle catheter attached to an extension tubing,
3 way stopcock, and syringe. The appropriate
site for thoracentesis should be selected based
on physical examination findings or, if available,
radiographic findings. Usually, aspiration of
either side of the thorax will adequately drain the
contralateral hemithorax since the mediastinum
in dogs and cats is thin and permeable to fluid.
However, with some diseases, particularly
chylothorax and pyothorax, unilateral effusions
may occur due to thickening of the mediastinum
associated with chronic inflammation.
94
Back to contents
Perform thoracentesis at the 6th, 7th, or
8th intercostal space, near the level of the
costochondral junction. Clip the selected site
and perform a local anesthetic block, if needed
(rare!). Aseptically prepare the site and introduce
the needle into the middle of the selected
intercostal space. Use care to avoid the large
vessels associated with the posterior aspect of
the rib margins. Advance the needle into the
pleural space. Aspirate fluid while the needle is
being advanced to allow prompt recognition of
the appropriate depth of needle placement. With
the bevel of the needle facing inward, orient the
needle against the rib cage to prevent damage
to the lung surface. Gently aspirate fluid and
place 5 ml samples in an EDTA tube and clot
tube for analysis of cell counts and biochemical
parameters, respectively. Additionally, make 6 to 8
direct smears for cytologic evaluation and submit
samples for aerobic and anaerobic cultures.
Chest Tube Placement
Chest tube placement should not be attempted
in an animal with severe respiratory distress.
Generally, stabilization and improved ventilation
can first be accomplished by removing some
pleural air or fluid via needle thoracentesis. In
critically ill patients, chest tubes can occasionally
be placed without the use of general anesthesia;
local anesthesia (i.e., local anesthetic infiltration
or an intercostal nerve block) being sufficient.
However, most animals with pleural cavity
disease benefit from intermittent positive pressure
ventilation and oxygen supplementation during
tube placement. When general anesthesia is used,
control of the animal’s airway (via endotracheal
intubation and positive pressure ventilation) and
oxygen therapy should be rapidly achieved.
Treatment of pleural cavity disease varies
depending on the underlying etiology. For
traumatic pneumothorax, intermittent needle
thoracentesis may be sufficient in some animals

to prevent dyspnea while the lung heals, but
chest tubes are occasionally required. However,
chest tube placement and continuous drainage of
air in animals with spontaneous pneumothorax
that have undergone mechanical pleurodesis
is recommended to allow pleurodesis. With
some types of pleural effusion (i.e., pyothorax),
tubethoracentesis and thoracic lavage are
mandatory in the primary treatment of most
affected animals.
Incorrectly placed or improperly managed
chest tubes are extremely dangerous in animals.
However, if precautions are taken to assure that
the animal cannot remove the tube prematurely,
or that if the animal chews on the tube a
pneumothorax will not occur, chest tubes simplify
the management of some animals with pleural
effusion or pneumothorax. The choice of which
side to place the chest tube is made by evaluating
the radiographs. Occasionally, bilateral chest
tubes may be necessary; however, in most dogs
and cats the mediastinum is permeable to fluid
or air, allowing drainage of both hemithoraxes
through a single tube. The exception to this may
be in chylothorax or pyothorax.
Components of a tube thoracostomy include a
chest tube, an apparatus to connect the tube to a
syringe or to a continuous suction bottle, and a
device to collect the drained material (syringe or
collecting bottle). Commercially available tubes
are usually made of polyvinyl chloride or silicone
rubber and are less reactive than red rubber
feeding tubes. Commercial tubes come with a
metal stylet that simplifies tube placement, but
may increase the risk of perforating lung tissue
when compared to red rubber feeding tubes. The
latter are usually inserted using a large hemostat
or Carmalt clamp. Commercial chest tubes come
in various sizes ranging from 14 to 40 French. The
size of the thoracostomy tube should approximate
the diameter of the mainstem bronchus; however,
smaller tubes may be adequate for removal of air,
while larger tubes may required with more viscous
effusions. If a commercial tube is used, it can be
attached via a five-in-one connector (Christmas tree
adaptor) to either a 3-way stopcock or tubing from
a continuous suction device. The ends of red rubber
feeding tubes can be cut to accommodate a 3-way
stopcock; attaching these tubes to a continuous
suction device is generally not recommended due
to their tendency to collapse.
Guidelines For Estimating Chest Tube Size:
Cats & Dogs < 7 kg 14 – 16 Fr
Dogs 7 - 15 kg 18 – 22 Fr
Dogs 16 - 30 kg 22 – 28 Fr
Dogs > 30 kg 28 – 36 Fr
Back to contents
A
Clip and prepare the lateral thorax for aseptic
surgery. In order to allow sufficient drainage,
place additional holes in the tube by bending the
tube and removing a notch with a pair of sterile
scissor. Holes should not be greater than one-third
the circumference of the tube. If using a commercial
tube with a radiopaque line, place the last hole
through the line in order to allow identification
of its position on a thoracic radiograph. Make a
small skin incision in the dorsal one-third of the
lateral thoracic wall at the level of the 10th or 11th
intercostal space. Advance the tube subcutaneously
in a cranioventral direction for 3 to 4 intercostal
spaces and introduce the tube through the muscle
and pleura using the stylet or a large hemostat.
When using a trocar tube, firmly grasp the tube 2
to 4 cm from the body wall with one hand while
using the other hand to “pop” the tube through the
intercostal musculature and pleura. This will prevent
the tube from being inadvertently pushed further
into the thorax than anticipated and damaging the
lung or other thoracic structures. Feed the tube in
a cranioventral direction to a predetermined point
and before completely removing the trocar, clamp
the tube with a hemostat. Place a purse-string suture
in the skin around the tube (do not enter the lumen
of the tube) and leave both ends of the suture long.
Use this suture to perform a “Chinese-finger trap”
or “Roman-sandal” suture. Connect the chest tube
to a 3-way stopcock in order to increase the ease
of thoracic drainage. Use a five-in-one (Christmas
tree) adaptor or a female Luer lock (with small
tubes) between the tube and the 3-way stopcock to
ensure an air-tight seal. Use suture to secure the
tube to the connecting devices so that they will
not become inadvertently dislodged, resulting in
a pneumothorax. For added safety when the chest
cavity is not being suctioned, clamp the tube where
it exits the body wall with a hemostat or C-clamp.
Verify appropriate placement of the chest drain
radiographically, prior to covering it with a loose
bandage.
2006 World Congress WSAVA/FECAVA/CSAVA
Drainage may be either intermittent or
continuous. Generally, intermittent pleural
drainage is adequate; however, in some
situations (i.e., spontaneous pneumothorax,
pleurodesis) continuous suction is preferable.
Heimlich valves should only be used in medium
to large dogs, since small dogs and cats may
not develop sufficient expiratory pressure for
effective drainage. Additionally, these valves
are prone to malfunction if fluid is aspirated
into the apparatus. “Milking” or “stripping” of
chest tubes to prevent obstruction of the tube by
clots has been recommended in the veterinary
literature; however, these techniques generate
high intrapleural pressures and may cause
pulmonary damage.
95
A
Chest Tube Removal
With pleural effusion, remove the tube when
the drainage decreases to a volume that is
consistent with that caused by the presence
of the tube itself (i.e., 2.2 ml/kg b.w./day).
The tube can be removed in patients with
pneumothorax once negative pressure has been
achieved for 12 to 24 hours. Culture the end of
the tube following removal if the tube has been
present for several days, or if the animal shows
signs of infection. Suture the skin incision with
1 or 2 simple interrupted sutures.
Figure 1 From: Fossum, TW: Small Animal Surgery, Mosby Publishing Co., St. Louis, Mo, 1997.
Connect the chest tube to a bottle that serves
as an underwater seal (filled with 2 to 3 cm of
sterile water) which in turn is connected to a
suction bottle (also partially filled with water)
attached to a suction device. Vary the amount
of suction by raising or lowering the level of
water in the suction bottle. A rigid plastic vent
2006 World Congress WSAVA/FECAVA/CSAVA
tube opened to room air serves to allow air to be
96
Back to contents
Continuous Thoracic Suction
If fluid accumulation is so rapid that intermittent
drainage is not practical, or if adherence of
the visceral pleura to the body wall is desired,
continuous suction may be used. Two and three
bottle systems and commercial suction units are
available for veterinary use and are economical
and simple to use (Figure 1). A continuous 10 to
15 cm negative pressure on the thorax effectively
aspirates pneumothorax, increasing the likelihood
of spontaneous sealing of large pulmonary defects.
Slightly greater pressures may be necessary (up to
20 cm water) when viscous fluid is being drained.
aspirated into the bottle as the vacuum is applied.
A third bottle interposed between the chest tube
and the underwater seal bottle serves to collect
fluid and prevent the level from rising in the
underwater seal bottle as fluid is drained from
the chest. This bottle is unnecessary in animals
with pneumothorax. Alternately, a commercial
continuous suction device may be used.
 A
Standards of Care (How I Treat)
THE DYSPNEIC PATIENT WITH NASAL OXYGEN
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery
Texas A&M University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu

Oxygen Therapy can be detected. The patient must have a PCV of

Clinical signs of hypoxia include dyspnea,
cyanosis, tachycardia, tachypnea, postural
changes, anxiety, and/or central nervous system
depression. If clinical signs, arterial blood
gases, pulse oximetry, or the patient’s disease
suggest hypoxia, supplemental oxygen may
be administered via mask, tent, flow-by, nasal
catheter, or the animal may be placed in an
oxygen cage or tent.
NOTE: Remember that patients can be hypoxic
without showing signs of cyanosis because
greater than 5 g/dl of deoxygenated hemoglobin
must be present in the circulation before cyanosis
approximately 15% to have 5 g hemoglobin/dl.
Flow-by oxygen may be the easiest way to provide
supplemental oxygen in an emergency situation
(Table 1). The oxygen line is placed within 1
to 3 cm of the patient’s nose and mouth, which
creates a small area where the fraction of inspired
oxygen (FIO2) is increased. However, because it
requires a care provider to be present to hold the
oxygen line and to ensure that the patient does not
move away from it, and a high oxygen flow rate
is required, it is not always practical or the best
choice. Furthermore, it is not nearly as effective
as the other methods described below.

TABLE 1 Methods For Supplementing Oxygen

Mode of oxygen Indication Oxygen flow rate Fraction of
delivery of inspired oxygen
Face mask Short term 6-10 liters/min 35-55%
emergency (be sure face
stabilization mask fits well)
Flow-by Short term’s 6-8 liters/min 25-45%
emergency
stabilization; 2006 World Congress WSAVA/FECAVA/CSAVA
face mask
not tolerated
Tent or Nasal catheter 0.75-1 liters/min 30-40%
Elizabethan not tolerated,
collar canopy oxygen cage
not available
Nasal catheter Postoperative 1-6 liters/min; 30-50%
oxygen delivery; 50-100 ml/kg/min
prolonged delivery
Intratracheal catheter Upper airway 50 ml/kg/min 40-60%
obstruction; nasal
catheter not tolerated
Oxygen cage Prolonged delivery 40-50%
of oxygen, limited
access to patient
97
Back to contents
A
Face mask delivery of oxygen is a useful short-
term method to provide supplemental oxygen.
With an oxygen flow rate of 6 to 10 L/min and a
well-fitted mask, an FIO2 of 0.35 to 0.55 may be
achieved (see Table 1). Be aware that face masks
may not be tolerated (especially in severely
dyspneic animals) and are often difficult to fit well
to the faces of cats and brachycephalic dogs. An
alternative is to use an Elizabethan collar covered
with plastic wrap to create an oxygen-enriched
environment. The end of the oxygen tube should
be fed up through the collar and secured. To
allow elimination of CO2, make a small hole in
the plastic wrap.
Nasal catheters may be used when more prolonged
oxygen delivery is desired than can be achieved
with flow-by or face mask techniques (Table 2).
Other advantages of nasal catheter delivery of
oxygen is that it permits access to the patient
without loss of the oxygen-rich environment (vs.
an oxygen cage) and it is well tolerated in most
patients. When necessary, bilateral catheters can
be placed. The appropriate oxygen flow rate is
based upon assessment of the degree of respiratory
distress, the patient’s respiratory rate and pattern,
and the patient’s size. The recommended initial
therapeutic dose for unilateral nasal oxygen
supplementation is approximately 50 to 100 ml/
kg/min. These flow rates can achieve a tracheal
FIO2 of approximately 50%. Although high
gas flow rates can be administered through a
single nasal catheter, these high flow rates may
be associated with patient discomfort. In such
cases, administering oxygen through bilateral
nasal catheters may be justified. A recent study
showed that although FIO2 and PaO2 could be
increased with higher total oxygen flow rates,
the increase is the same whether the higher flow
is delivered through one nasal catheter, or two.
Thus, the use of bilateral nasal catheters appears
to be beneficial primarily in improving patient
comfort. When oxygen is administered via nasal
catheter for prolonged periods (i.e., greater than 6
to 12 hours), it should be humidified. Intratracheal
catheters may be used in animals that will not
tolerate an intranasal catheter (see Table 1).

TABLE 2 Nasal Oxygen Insufflation

1. Select a small, red rubber feeding tube (3.5-5 Fr for cats; 5-8 Fr for dogs) to serve as a
catheter and lubricate the tip with lidocaine gel.
2. Place one or two drops of local anesthetic (e.g., 2% lidocaine or proparacaine) in the
nostril.
3. Premeasure the catheter to the medial canthus of the eye or the caudal ramus of the
mandible.
4. Elevate the dorsal aspect of the nose and feed the lubricated catheter into the nostril the
predetermined distance.
5. Suture or glue (e.g., VetBond) the catheter to the external naris and muzzle and over the
frontal sinus or along the jaw. With cats, do not allow the tube to touch the whiskers.
6. Place an Elizabethan collar on the animal.
7. Attach the tube to an oxygen source and administer humidified oxygen to maintain oxygen
saturation at greater than 90%; typically start at 50 ml/kg/minute and adjust as needed.*
* Gastric distention may occur if the flow rate is too high.
2006 World Congress WSAVA/FECAVA/CSAVA

An oxygen cage provides a sealed environment in The major disadvantage of an oxygen cage is that
which the FIO2, ambient temperature, and humidity is isolates the patient from the clinician because
can be controlled. An ambient temperature of 70ºF each time the oxygen cage door is opened there is
and relative humidity of 40% to 50% is desired. a loss of the oxygen rich environment.

98
Back to contents

Standards of Care (How I Treat)
PSEUDOMONAS OTITIS
Craig Griffin DVM, Diplomate
ACVD
Animal Dermatology Clinic
5610 Kearny Mesa Rd
San Diego, California
USA 92111
itchypet@aol.com
The most important aspect of treating Pseudomonas
otitis is to determine the primary cause and
perpetuating factors of the otitis. Pseudomonas
ear infection is almost always a secondary cause
of otitis. After primary causes and perpetuating
factors are managed then once the Pseudomonas
is eliminated it will not recur. Often the emphasis
is placed on treating Pseudomonas otitis with a
topical antibiotic that it is sensitive to. When a
very resistant strain is encountered then many
veterinarians are asking for advice on what to
do. The answer is that treating all Pseudomonas
otitis cases should involve a multiple component
therapeutic approach.
The first part is to get the ear canal, and middle
ear if involved, as clean as possible eliminating
nidus for organisms to be protected from topical
therapies, reducing pro inflammatory toxins and
eliminating the toxins and neutrophils that may
interfere with some antibiotics by inactivating
them. This is more of a problem when polymyxin
and aminoglycosides are used as the antibiotic.
When exudation is rapidly returning and often
in ulcerative cases repetitive cleaning weekly
and occasionally even alternate day flushes at
home may be necessary. The level of cleaning is
determined by what is required to keep the ear
canal clean and free from exudate build up.
The second part is the use of disinfectants prior
to and in conjunction with a topical antibiotic,
the third component. Disinfectants have the
advantage or not inducing resistance and are
often less expensive. Multiple disinfectants are
available and effective though in general I tend
to use acetic acid containing products. Acetic
acid has been shown to be very effective in the
treatment of otitis externa in humans. It is believed
that its activity is not completely due to the pH
because other acidic products are not as effective
in killing Pseudomonas and Staphylococcus.
However it is possible to get a disinfectant effect
just by lowering the pH of the ear canal (Nuttal
and Cole 2004). Acetic acid is most effective
against Pseudomonas, with a 2% solution being
Back to contents
A
lethal within one minute of contact (Griffin 1993;
Thorp, Kruger et al. 1998). White vinegar is
generally about 5% acetic acid and it has been
recommended as an ear wash when diluted to
2.5% by mixing it in equal amounts with water
or 25% water, 25% isopropyl alcohol and 50%
white vinegar. Combinations with 2% boric
and 2% acetic acid are available commercially.
(Malacetic, Dermapet® and Otocetic™ solution,
Vedco) The disinfectant is used once daily as a
rinse prior to application of a topical antibiotic
glucocorticoid preparation. For resistant
previously non responsive strains my favorite is
the sequential use of two disinfectants followed
by the topical antibiotic. The first is acetic acid
which is then followed with a rinse with Tris-
EDTA. Tris EDTA increases the permeability
of bacterial cell membranes by binding Ca and
Mg ions. This activity is mainly apparent in gram
negative bacteria including Pseudomonas sp.
Tris-EDTA was shown to have a sparing effect
on the MIC of enrofloxacin against ciprofloxacin
resistant Pseudomonas as well as resolve clinical
cases resistant to cephalosporin or enrofloxacin
(Farca, Piromalli et al. 1997; Gbadamosis and
Gotthelf 2003). It was also shown effective in vivo
in a small number of cases when combined with 2006 World Congress WSAVA/FECAVA/CSAVA
a low level (0.15%) of chlorhexidine digluconate
(Ghibaudo, Cornegliani et al. 2004). My
preference for the tris EDTA combined with low
strength (0.15%) chlorhexidine (TrizEDTA™Plus,
Dermapet). This is not rinsed out but allowed to
be present when the antibiotic containing topical
is then applied. This combination is done twice
daily.
The third component is the use of a topical
antibiotic. In some countries Polymyxin is
available and also considered a first line antibiotic.
It is very effective even for Pseudomonas at least
in countries such as the United States where it is
not routinely used. To get good effects though it is
imperative to have a clean ear as purulent exudates
bind it and greatly diminish polymyxin activity.
Some of this may be beneficial as polymyxin E
99
A
has been shown to bind endotoxin and could result
in less inflammation and tissue damage(Senturk
2005). The most commonly used antibiotics
are gentamicin (Mometamax®, Schering-
Plough Animal Health) or fluoroquinolones
such as enrofloxacin (Baytril Otic, Bayer) or in
Europe marbofloxacin (Aurizon®, Vetroquinol).
Ototoxicity is reported with all gentamicin
topicals. However, similar to chlorhexidine, this
concern may be overstated. A study showed no
vestibulotoxic or ototoxic effects from 21 days of
otic gentamicin applied BID to ears with ruptured
tympanic membranes (Strain, Merchant et al.
1995). A topical combination of enrofloxacin
0.5% and silver sulfadiazine 1.0% (Baytril Otic,
Bayer Corp) is useful for the treatment of bacterial
and yeast otitis. It may be effective though lacks a
glucocorticoid in the formulation. Another option
is in clinic formulated drops made by combining
4ml of injectable enrofloxacin 2.27% (Baytril,
Bayer) with 4ml of injectable dexamethasone
sodium phosphate (4mg/ml) and then 8 cc of
saline or 8cc 1% miconazole lotion if Malassezia
are also present. Third line topical antibiotic
options to consider are amikacin, tobramycin and
ticarcillin. Injectable amikacin is available at 50
or 250mg per ml and is diluted so that it is used
at concentrations ranging from 25mg/ml to 5mg/
ml. The higher concentrations are used when
sensitivity testing has shown resistant organisms.
It may be mixed with other ingredients similar to
enrofloxacin though instead of saline Tris EDTA
products may give a synergistic effect for resistant
organisms.
The fourth component is the topical administration
of a potent topical glucocorticoid which is often
present in the antibiotic product. Mometasone,
dexamethasone and betamethasone are the active
agents used most commonly. They are used
to decrease the exudation and if a case is not
responsive to that alone then short term systemic
2006 World Congress WSAVA/FECAVA/CSAVA
glucocorticoids are indicated. Methylprednisolone
at 1-1.5mg/kg/day for 4 days then tapered to eod
is used until the inflammation and ulceration is
resolved.
The fifth component is systemic antibiotic
therapy. This component is only used when the
ulcerative changes are not responding to the
4 component approach or initially is there is
concurrent otitis media or marked proliferative
changes present. Antibiotic selection should be
based on a culture once cytology shows a pure,
only one type of rod present on cytology. Prior
to this empiric therapy is often used and most
100
Back to contents
commonly the initial therapy when there is
mixed rod or cocci and rod present on cytology
is high dose fluoroquinolone. Marbofloxacin
5mg/kg/ q24h or enrofloxacin 12-15mg/kg q24h
are most often used.
Since using this combination approach with
the above agents I have not had a case that
has required tobramycin or ticarcillin. Some
veterinarians have recommended Imipenim and
cilastin (Primaxin®, Merck) and Piperacillin
and tazobactam (Zosyn®, Wyeth) to be diluted
and used as ear drops for resistant Pseudomonas.
This practice should be seriously questioned as
these are some the most effective rescue drugs
for serious human infections and indiscriminate
use in the veterinary field could jeopardize their
value. I have not had a case that required these
products.
Farca, A., G. Piromalli, et al. (1997). Potentiating
effect of EDTA-Tris on the activity of antibiotics
against resistant bacteria associated with otitis,
dermatitis and cystitis. J Small Anim Pract 38(6):
243-245.
Gbadamosis, S. and L. Gotthelf (2003). Evaluation
of the in vitro effect of Tris-EDTA on the minimum
inhibitory concentration of enrofloxacin against
ciprofloxacin resistant Pseudomonas aeruginosa.
Vet Dermatol 14(4): 222.
Ghibaudo, G., L. Cornegliani, et al. (2004).
Evaluation of the in vivo effects of Tris-EDTA
and chlorhexidine digluconate 0.15% solution
in chronic bacterial otitis externa: 11 cases. Vet
Dermatol 15(1): 65.
Griffin, C. (1993). Otitis Externa and Media.
Current Veterinary Dermatology, The Science
and Art of Therapeutics. J. M. MacDonald. St
Louis, Mosby Year Book.
Nuttall, T. and L. K. Cole (2004). Ear cleaning:
the UK and US perspective. Vet Dermatol 15(2):
127-36.
Senturk, S. (2005). Evaluation of the anti-
endotoxic effects of polymyxin-E (colistin) in
dogs with naturally occurred endotoxic shock. J
Vet Pharmacol Ther 28(1): 57-63.
Strain, G., S. Merchant, et al. (1995). Ototoxicity
assessment of a gentamicin sulfate otic preparation
in dogs. Am J Vet Res 56(4).
Thorp, M., J. Kruger, et al. (1998). The
antibacterial activity of acetic acid and Burow’s
solution as topical otological preparations. J
Laryngol Otol 112(10): 925-928.

Standards of Care (How I Treat)
FELINE EOSINOPHILIC ULCERS
Craig Griffin DVM, Diplomate
ACVD
Animal Dermatology Clinic
5610 Kearny Mesa Rd
San Diego, California
USA 92111
itchypet@aol.com
Feline eosinophilic ulcers have also been referred
to as rodent ulcer or indolent ulcer and should
be considered a reaction pattern in the cat. Even
the histopathology is variable, eosinophilic,
neutrophilic or granulomatous, supporting a
multifactorial etiology. There is not any one
etiology and this lesion has been associated with
genetics, flea allergy dermatitis, atopic dermatitis,
food adverse reaction, insect reaction, excessive
grooming and infectious agents (Power and Ihrke
1995; Colombini, Hodgin et al. 2001). Over
grooming or licking for any reason may increase
the contact between the abrasive cat tongue and lip
resulting in trauma and an erosion that becomes
secondarily infected. The initiating cause or lesion
may be resolved while the subsequent infection
creates the persistent and more severe lesion.
Classic feline indolent ulcers initially occur on the
upper lip near the median raphe usually adjacent
to the canine teeth. Initially there will be erosion
and only with chronicity will a proliferative
response develop. This is an important distinction
as some cases will have a swollen lip first that later
ulcerates. In these cases eosinophilic granulomas
and reactions to insects are more likely. Owners
are not always aware of the possible insect
exposure. Historical information that should be
obtained in these cases is whether the cat likes to
play with or “hunt” insects. Even totally indoor
cats will sometimes spend a lot of time finding
spiders, flies, and various bugs in houses.
Back to contents
A
Initial examination should include cytology from
both the surface and any material that may be
expressed from the eroded or ulcerated surface of
the lesion. Whenever bacteria are seen especially
intracellular then an initial course of antibiotics
without glucocorticoids is warranted. If cocci
are seen then clavulanic acid and amoxicillin or
clindamycin are the initial antibiotics of choice.
If rods are seen then marbofloxacin is preferred
initially. Depending on how complete the response
is the clinician may obtain some clues as to the
underlying etiology. Residual ulcers especially if
some licking is still present suggest underlying
allergy. If a hypoallergenic diet trial is not
helpful then allergy testing and immunotherapy
or cyclosporin may be indicated. Cyclosporin
has been reported effective in multiple cases
(Vercelli, Raviri et al. 2006).
Colombini, S., E. C. Hodgin, et al. (2001).
Induction of feline flea allergy dermatitis and the
incidence and histopathological characteristics
of concurrent indolent lip ulcers. Veterinary
Dermatology 12(3): 155-161.
Power, H. and P. Ihrke (1995). Selected feline
eosinophilic skin diseases. Vet Clin North Am
Small Anim Pract 24(4): 833-845. 2006 World Congress WSAVA/FECAVA/CSAVA
Vercelli, A., G. Raviri, et al. (2006). The use of oral
cyclosporin to treat feline dermatoses: a retrospective
anaylysis of 23 cases. Vet Derm 17(3): 201-206.
101
A
Standards of Care (How I Treat)
IMMMUNE-MEDIATED HEMOLYTIC ANEMIA
Urs Giger, Prof. Dr. med. vet.
MS FVH
Dipl. ACVIM and ECVIM
(Internal Medicine) and ECVCP
(Clinical Pathology) Charlotte
Newton Sheppard
School of Veterinary Medicine
University of Pennsylvania
3850 Spruce Street
Philadelphia
PA 19104-6010 USA
giger@vet.upenn.edu
http://www.vet.upenn.edu/penngen
Immune-mediated hemolytic anemia (IMHA)
arises when an immune response targets directly
or indirectly erythrocytes and hemolytic anemia
ensues. In primary IMHA no inciting cause can
be identified, hence the term idiopathic IMHA
or autoimmune hemolytic anemia (AIHA).
In contrast, secondary IMHA is associated
with an underlying condition or triggered by
an identifiable agent. The various breed and
family predilections (about ⅓ of all cases of
IMHA are seen in American Cocker Spaniels)
suggest strongly the involvement of genetic
factors leading to a predisposition to IMHA.
There is ample evidence for infectious agents
to be associated with IMHA, including parasitic
(babesiosis, leishmaniasis, ehrlichiosis, and
dirofilariasis), fungal, and bacterial (leptospirosis,
chronic abscesses, discospondylitis, pyometra,
colitis, and pyelonephritis). The relationship
between infection and autoimmunity may be
explained by molecular mimicry. Furthermore,
several drugs and toxins (e.g. sulfonamides, bee
sting) and neoplastic disease processes have been
associated with IMHA.
2006 World Congress WSAVA/FECAVA/CSAVA
In dogs idiopathic IMHA (AIHA) has been
considered the most common cause of hemolytic
anemias for decades, and many anemic dogs are
presumptively managed for AIHA. Nevertheless,
an extensive search for an underlying disorder or
trigger is always warranted. This presentation will
discuss some of the challenges and controversies
in the management of IMHA in dogs. Because
of a paucity of evidence on treatment of canine
IMHA, some food-for-thought rather than a
definitive treatment regime for IMHA will be
provided.
A diagnosis of IMHA must demonstrate
accelerated immune destruction of erythrocytes.
Evidence of a hemolytic anemia is suggested
clinically by icterus and a regenerative anemia
with hyperbilirubinuria, and hemoglobinemia
102
Back to contents
and hemoglobinuria refers to an intravascular
process. However, the erythroid response in the
bone marrow may be blunted by the immune
process or the underlying disease thereby leading
to non-regenerative anemias. Beside documenting
a hemolytic anemia, one or more of the following
three hallmarks must be present to support
a diagnosis of immune-mediated hemolysis:
persistent agglutination, marked spherocytosis
and a positive direct Coombs test result.
Because the severity of IMHA ranges from
indolent to life-threatening disease, therapy has
to be tailored for each patient and depends in part
on whether the IMHA is primary or secondary
in nature. Removal of the triggering agent or
treatment of the underlying condition can bring
the IMHA rapidly under control.
Restoration and maintenance of tissue perfusion
with crystalloid fluids is important even when
it results in further lowering of the hematocrit.
When severe anemia and a dropping hematocrit
result in signs of tissue hypoxia, packed cell
transfusions appear beneficial. The increased
oxygen-carrying capacity provided by the
transfused red blood cells may be sufficient to
maintain the animal’s hematocrit for a few days
while other treatment modalities have time to
become effective. The notion that transfusions
pose an increased hazard to animals with IMHA
has been overemphasized and is not supported by
recent retrospective clinical studies. However,
the common occurrence of autoagglutination
may make blood typing and crossmatching of
the patient impossible. In these cases DEA 1.1
negative blood should be transfused.
If compatible blood is not available, the bovine
hemoglobin solution Oxyglobin may be
administered and provides increased oxygen-
carrying capacity and plasma expansion. In
contrast to blood and Oxyglobin, oxygen
inhalation therapy is of little benefit, unless the

animal is suffering form pulmonary disease
such as pulmonary thromboemboli. Thanks to
adequate transfusion support, animals with IMHA
rarely die because of anemia, but because of
secondary complications such as thromboemboli
and infections.
The insufficient understanding of the pathogenesis,
the generally guarded prognosis, the lack of good
therapeutic trials, the serious drug side effects,
and the high costs of intensive care greatly
hamper the successful management of dogs with
IMHA. The main goal of immunosuppressive
therapy is to reduce phagocytosis, complement
activation, and anti-erythrocytic antibody
production. Glucocorticosteroids are the initial
treatment of choice for canine and human
IMHA. They interfere with both the expression
and function of macrophage Fc receptors and
thereby immediately impair the clearance of
antibody-coated erythrocytes by the macrophage
system. In addition glucocorticoids may reduce
the degree of antibody binding and complement
activation on erythrocytes, and only after weeks,
diminish the production of autoantibodies. Thus,
oral prednisone at a dose of 1-2 mg/kg twice daily
is the mainstay treatment. Alternatively, oral or
parenteral dexamethasone at an equipotent dose
of 0.2-0.4 mg/kg twice daily can be used, but is
likely not more beneficial.
Additional immunosuppressive therapy is
warranted when prednisone fails, only controls
the disease at persistently high doses, or when
corticosteroids cause intolerable side effects. They
are generally used together with prednisone, but
may eventually be used independently. Historically,
cytotoxic drugs such as cyclophosphamide were
added, however a small randomized study and
several retrospective surveys failed to show any
beneficial effects, but may be associated with
greater morbidity and mortality in the acute
management of IMHA. Retrospective studies and
anecdotal reports with azathioprine, cyclosporine,
danazol, mycophenylate, leflunomide and human
intravenous immunoglobulin indicate some
efficacy and may be associated with fewer side
effects, but controlled prospective clinical trials
that document their efficacy and safety are
lacking.
Response to therapy may be indicated by a
hematocrit that rises or stabilizes, an appropriate
reticulocytosis, diminished autoagglutination,
and fewer spherocytes; this response can be
Back to contents
A
expected to be seen within days. The subsiding of
autoagglutination would allow the performance
of a Coombs’ test and thereby permit the direct
documentation of anti-erythrocytic antibodies.
As glucocorticosteroid therapy is associated with
well-known side effects, the initial dose will be
tapered by reducing the amount by one-third every
7-14 days. In secondary IMHA with appropriate
control of the underlying disease, the tapering
can be accomplished more rapidly. Because of
the potential of gastrointestinal ulceration by
steroids, gastrointestinal protectants such as
sucralfate may be considered. Because dogs with
IMHA suffer from an immune deregulation which
may have been triggered by an infections and are
treated with immunosuppressive agents, these
patients are prone to experience infections; it is,
therefore, prudent to administer preventative as
well as therapeutic antibiotics to these dogs with
IMHA on immunosuppressive therapy.
Thromboemboli and DIC are unique serious
complications that greatly contribute to the
morbidity and mortality of dogs with IMHA.
Although the pathogenesis remains unknown,
venopuncture, catheters, and glucocorticosteroids
as well as other immunosuppressive agents
may be contributing factors. Thus far, no study
has documented any successful prevention
and/or management protocol for these life-
threatening hemostatic problems in canine
IMHA. Predisposing factors should, whenever
possible, be limited, and adequate perfusion
and tissue oxygenation should be provided with
fluids and transfusions or Oxyglobin. Generally,
anticoagulation therapy is instituted after there is
some evidence or suspicion of thromboemboli.
Heparin is the most commonly used drug and is
used at a dose of 50-250U/kg sc every 6 hours
or by continuous infusion. The replacement of
coagulation factors and antithrombin III has not
been proven to be beneficial. Other antithrombotic
agents such as aspirin, low molecular weight
2006 World Congress WSAVA/FECAVA/CSAVA
heparin and novel antithrombotic agents have
been used occasionally, but their efficacy and
safety remain unproven.
Giger, U: Regenerative Anemias Caused by Blood
Loss or Hemolysis. In Textbook of Veterinary
Internal Medicine, SJ Ettinger and EC Feldman
(eds) 6th edition. WB Saunders, Philadelphia, PA,
pp 1886-1807, 2005.
103
A
Standards of Care (How I Treat)
THROMBOCYTOPENIA
Urs Giger, Prof. Dr. med. vet.
MS FVH
Dipl. ACVIM and ECVIM
(Internal Medicine) and ECVCP
(Clinical Pathology) Charlotte
Newton Sheppard
School of Veterinary Medicine
University of Pennsylvania
3850 Spruce Street
Philadelphia
PA 19104-6010 USA
giger@vet.upenn.edu
http://www.vet.upenn.edu/penngen
Thrombocytopenia, a common cause of surface
hemorrhage in dogs, can result from impaired
thrombopoiesis, increased platelet destruction
and consumption, and sequestration of platelets
(splenomegaly). Reduced platelet production may
be isolated or associated with an overall decreased
hematopoiesis due to many drug reactions
(estrogens, chemotherapeutics, azathioprine),
infections (Ehrlichia spp.), and myelophthisis
(leukemia, myeloma, myelofibrosis) but remains
often idiopathic (immune-mediated?).Accelerated
platelet destruction is commonly associated with
immune-mediated thrombocytopenia (IMT),
but enhanced platelet consumption may also
be observed with neoplasia, vasculitis and
disseminated intravascular coagulation (DIC).
IMT can be divided into primary, also known as
idiopathic thrombocytopenia purpura (ITP), and
secondary forms triggered by infections (Ehrlichia,
Rickettsia, and Babesia spp., vaccines), drugs,
and cancer. Anticoagulant rodenticide poisoning
can also be associated with mild to moderate
thrombocytopenia. However, acute and chronic
blood loss is not resulting in any significant
2006 World Congress WSAVA/FECAVA/CSAVA
consumptive thrombocytopenia unless there is
concomitantly a vasculopathy or DIC present.
Because thrombocytopenia occurs rarely in cats
and is generally associated with drug exposure
(griseofulvin, methimazole, prpylthiouracil),
viral infections, or malignant diseases, it will not
be further discussed here.
A diagnosis of thrombocytopenia is made by a
platelet estimated on a blood smear or complete
blood cell count, but any thrombocytopenia must
be verified by a review of a blood smear. Spurious
thrombocytopenia may due to instrument
limitations; e.g. megaplatelets in Cavalier King
Charles and platelet aggregates with many illnesses
and collection techniques; also Greyhounds have
generally a mild thrombocytopenia. Classic
signs of thrombocytopenia include petechiation,
ecchymosis, epistaxis, and gastrointestinal
104
Back to contents
blood loss. The most severe thrombocytopenias,
seen with IMT/ITP, often cause only mild
hemorrhage. Following a careful history, a search
for an underlying cause is warranted to identify
an infection (blood smear, serology, PCR) or
cancer (also involving lymphnodes and spleen).
Bone marrow examination is safe, but may rarely
reveal a specific cause on initial presentation.
A diagnosis of ITP is mostly based upon
excluding other causes of thrombocytopenia,
but platelet-associated antibodies can also be
determined to support an immune mechanism for
thrombocytopenia.
Therapy of thrombocytopenia is mostly
dependent on the underlying cause and severity
of clinical signs of bleeding rather than the actual
platelet count. It is well appreciated that despite
the severe thrombocytopenia due to ITP these
animals may be at lesser bleeding risk than the
ones with myelosuppressive disorders. Hence
therapy of thrombocytopenia involves treatment
of the underlying disease, withdrawal of any
potential triggering agents, supportive care, and
emergency control of bleeding and correction of
severe anemia.
Platelet transfusions are very rarely indicated
and restricted to serious uncontrolled bleeding
into the brain or other critical sites. Platelet can
only be transfused from freshly collected blood
kept for <12 hours at room temperature, albeit
there are efforts made to provide frozen or even
artificial platelets. In ITP transfused platelets are
thought to have an extremely short survival of
minutes to hours rather than normal 7-10 days.
Nevertheless, in patients with life-threatening
bleeding into nervous or cardiopulmonary
system, platelet rich plasma or concentrate
transfusions may be considered. In clinical
practice thrombocytopenic seriously bleeding
patients may be the ones that could benefit more
from a fresh whole blood transfusion to provide
platelet and red blood cell support. At 1 hour

post transfusion the anticipated platelet rise
per transfusion is only modest (20,000/ul per
10ml fresh whole blood/kg transfusion. In most
cases packed red cells and stored blood may
be sufficient to correct the anemia. Prior to any
transfusion the patient should be blood typed
and DEA 1.1 compatible blood and if previously
transfused cross-match compatible blood should
be transfused. In case the thrombocytopenia is
combined with a coagulopathy, supplementation
of coagulation factors in the form of fresh frozen
plasma may be considered.
As any drug may potentially trigger
thrombocytopenia all drugs should be withdrawn
except the ones absolutely required treating a
life-threatening condition (e.g. phenobarbital for
active seizures); a change in class of drugs may
also be helpful. Since infections are common
causes of thrombocytopenia and screens for
infectious diseases may not be back for days
(except SNAP tests), thrombocytopenic dogs are
often empirically treated with antimicrobials.
Most commonly doxycyclin at 10mg/kg BID
for 2 weeks is being used, however in certain
geographic areas other antimicrobials may also
be indicated; for instance babesiosis may cause
severe thrombocytopenia before the hemolytic
disease is recognized, and sepsis associated
thrombocytopenia requires intense parenteral
antibiotic administration. Furthermore, cancer
associated thrombocytopenia is best corrected by
treating the cancer.
In cases of ITP immunosuppressive therapy
is used to inhibit platelet phagocytosis by
macrophages and platelet-antibody production.
Glucocorticosteroids are still the first and main
immunosuppressive agents; they impair platelet
destruction by blocking macrophages, interfere
with platelet-antibody interactions, hamper
any inflammatory response, and finally inhibit
anti-platelet antibody production. While most
clinicians start off with prednisone at a dose
of 2mg/kg PO BID, dexamethasone at 0.2mg/
kg can be administered IV daily in cases with
gastrointestinal signs. Any steroids may induce
serious side effects including gastrointestinal
ulcers, thromboembolism iatrogenic
Back to contents
A
hyperadrenocorticism, and bacterial infections.
There is no evidence that dexamethasone is
superior to prednisone if used at the equivalent
dose (dexamethasone is 6-8 times more potent
than prednisone); however, some clinicians are
hesitant to use the high prednisone dose. In fact a
high initial steroid pulse dose has been suggested
to be effected but may also be associated with
more serious side effects. Interestingly there is
one additional immunosuppressive agent that is
considered highly effective and relatively safe
in the initial management of severe acute ITP.
Vincristine at a dose of 0.02mg/kg (0.5mg m2
body surface) strictly IV once (may be repeated
after a week) has been shown to accelerate the
platelet count rise, when used in combination
with prednisone. Potential mechanisms
of action of vincristine include binding of
tubulin and inhibition of macrophages. Other
immunosuppressive agents may be considered if
prednisone + vincristine fail or intolerable side
effects occur. These may include cyclosporine,
danazol, azathioprine, and intravenous human
immunoglobulin; none of these drugs have been
approved or shown to be efficacious and safe
in any clinical studies in dogs. In addition new
immunosuppressive agents are being introduced
such as mycophenolate and leflunomide. Finally,
splenectomy may be considered in refractory or
relapsing cases of ITP, but no data is available
in dogs.
The prognosis depends on the underlying cause
and type of hemorrhage on presentation. In ITP
the bleeding is often less pronounced despite
most severe thrombocytopenia. In uncomplicated
cases of ITP a response is generally expected
within days with platelet counts rising above the
critical level of 40,000/μl, where bleeding would
not be expected. Hence as soon as the platelet
count rises >40,000/μl, the immunosuppressive
therapy can be slowly tapered. In secondary forms
of IMT the thrombocytopenia often resolves
2006 World Congress WSAVA/FECAVA/CSAVA
within 2 weeks if the trigger can be removed. In
conclusion, thrombocytopenias in dogs can be
associated with many different diseases and are
highly rewarding to treat.
105
A
Standards of Care (How I Treat)
ANESTHESIA FOR CESAREAN SECTION
D . E. Mason, DVM, PhD,
Diplomate ACVA
Kansas State University, College
of Veterinary Medicine
mason@vet.k-state.edu
Anesthesia for cesarean section can be a
straightforward process, administered to a healthy
animal with full-term neonates. Sometimes
anesthesia for cesarean section may involve a dam
that is metabolically compromised, to salvage the
viability of neonates from a uterus that contains a
dead and decomposing fetus. Or a cesarean section
may be required in an animal in which no live
offspring are expected. Each of these scenarios
presents a different challenge to the anesthetist
and may require a different approach in drug
choices and intra-operative management. Prior to
choosing the anesthetic approach it is worthwhile
to understand the reason for the cesarean section.
The most important factors to consider when
choosing anesthesia for cesarean section are (1)
the health status of the mother; (2) the viability
of the offspring; (3) is the surgery an emergency?
(4) how to provide pain control for the mother
and (5) the ability to perform the surgery with the
anesthetic technique that is chosen.
The incidence of maternal complications of
cesarean section can be low if one provides
adequate patient support, including oxygenation
and fluid therapy and anesthetic monitoring.
2006 World Congress WSAVA/FECAVA/CSAVA
There are two categories of anesthesia for
cesarean section - regional anesthesia and general
anesthesia.
Regional Anesthesia
Regional techniques include line blocks and
epidural anesthesia. Epidural anesthesia involves
placing local anesthetic into the epidural space
and results in anesthesia of the caudal half of the
body so that the surgery can be completed with
no muscle tone at the operative site and virtually
no pain for the mother. However, in contrast to
human labor and delivery, epidural anesthesia
in small animals does not include the advantage
of avoiding systemic drugs that may affect her
offspring. Without some form of significant
sedation the mother is awake and may not remain
cooperative in dorsal recumbency throughout the
106
Back to contents
surgical procedure. Both dogs and cats generally
require sedation in addition to their epidural
block to achieve adequate restraint for surgery
and many of the commonly used sedatives and
tranquilizers in small animal practice have the
potential to significantly depress the fetus at the
time of delivery (see below). Epidural anesthesia
requires greater skill compared to a line block,
however the degree of block is often more
complete. A benefit of using an epidural is that
the epidural can provide pain relief AFTER the
operation for a period of hours. The addition of
an opioid such as morphine (0.05 mg/kg) to the
epidural can provide many hours of analgesia in
the mother at a dose much lower than that used
for systemic administration of the drug.
Epidural technique: An epidural can be performed
with the patient in either sternal or lateral
recumbency, but the technique is easier with
the animal in sternal recumbency. One should
palpate the space lying just caudal to the palpable
dorsal spinous process of the seventh lumbar
vertebra and in front of the sacrum. A 22 gauge
spinal needle is advanced through the skin into
the lumbosacral space. Staying at the midline will
decrease the likelihood of puncturing the venous
plexus and seeing blood upon removal of the
stylet from the spinal needle. As one advances the
spinal needle a distinct “pop” may be felt as the
needle passes through the interarcuate ligament
into the epidural space. The best test to confirm
proper placement of the needle into the epidural
space is a “loss of resistance” test. After removal
of the stylet, making sure that no CSF or blood is
present in the needle, a test injection can be made
using a syringe with several milliliters of saline
and a large air bubble. If one is in the epidural
space, there should be little resistance to injection
of saline and the air bubble in the syringe should
not be deformed while making the injection. If
there is resistance to injection, the air bubble
will deform and this indicates that you need to
try again to place the needle within the epidural

space. Administration of 1 ml/6 kg body weight
of 2% lidocaine (approximately 3 mg/kg)is
sufficient for performing cesarean section
Infiltration technique (line block): Simpler to
perform, but requiring a greater volume of local
anesthetic, the line block is only effective at the site
of the surgical incision and does not immobilize
the rear limbs of the mother, so adequate sedation
is necessary to insure cooperation of the patient
throughout the procedure. This block is performed
by multiple intradermal and subcutaneous
injections of local anesthetic while advancing
the needle along the line of the proposed surgical
incision. The amount of local anesthetic needed is
a function of the length of the incision, however
one should not exceed 8 mg/kg total dose of
lidocaine in the dog or 5 mg/kg total dose of
lidocaine in the cat. If the volume of drug at that
dose range is not sufficient to extend the length of
the incision, one can dilute the agent with 0.9%
saline. Bupivicaine (2 mg/kg maximum dose) or
ropivicaine (3 mg/kg maxiumum dose) can also
be used for infiltration anesthesia.
Other recommendations when choosing to
use regional anesthesia include the use of an
endotracheal tube, if the mother is sedated
adequately. If intubation is not possible when
using a regional anesthetic technique, deliver
oxygen by mask. Any period of hypoxemia in the
mother is also a period of hypoxemia in the fetus
and this can markedly decrease fetal viability at
birth.
General Anesthesia
General anesthesia has some advantages over
regional anesthesia for cesarean section. General
anesthesia can be induced quickly. Oxygenation
and ventilation are more easily controlled and
the airway is protected with endotracheal tube
placement. Patient restraint is optimal with
general anesthesia. However, fetal depression can
be substantial due to the systemic administration
of potent anesthetics. Hypotension is more
likely with inhalant anesthetics, which could
significantly compromise a metabolically unstable
mother and impair uterine blood flow decreasing
the viability of the fetus.
There are some general recommendations
regarding procedure when using general
anesthesia in cesarean sections. Prior to starting
anesthesia, prepare as many things as possible;
assemble equipment (anesthetic and surgical)
clip the site for surgery, and apply an initial
surgical scrub to the surgical site. It is important
to minimize anesthesia time up to the point of
delivery of the offspring. Always plan to use an
endotracheal tube in the mother to decrease the
possibility of regurgitation and aspiration, which
Back to contents
A
can occur more easily during pregnancy as a
result of increased intra-abdominal pressure and
dorsal recumbency.
Virtually all sedatives, tranquilizers, analgesics
and anesthetics used commonly in veterinary
anesthesia exert their effect after crossing the
blood-brain-barrier. If a drug crosses the blood-
brain-barrier, it crosses the placenta as well, so there
are few choices that will not have some effect on
the fetus during cesarean section. Phenothiazines,
like acepromazine are not associated with
significant fetal respiratory depression, but they
may cause hypotension in the mother and impair
uterine blood flow. Acepromazine should only be
considered in a healthy mother prior to elective
C-section with a maximum dose of 0.02 mg/kg
IV. Alpha-2 agonists can cause significant fetal
depression, often proportional to the level of
depression obtained in the mother. They are
not recommended for cesarean section. Opioids
cross the placenta and may concentrate in the
fetal blood due to lower pH. However they can
be useful due to the analgesia they provide, their
safe cardiovascular profile, and their contribution
towards sedation. The fetal depression can be
reversed by administration of naloxone to the
neonate at the time of delivery. Diazepam tends
to concentrate in the fetal blood in a 2:1 ratio
compared to the maternal circulation. Significant
fetal depression is associated with the use of
diazepam.
There have not been extensive studies of outcome
regarding various general anesthetic agents or
techniques for cesarean section, however there
is some evidence in the literature that would
suggest that puppy vigor at the time of delivery
is most impaired by techniques that include
ketamine. Ketamine may increase uterine tone
and as a result diminish uterine blood flow
nearing the time of delivery. Puppy vigor appears
to be superior when rapid intravenous induction
is achieved with propofol compared to either
2006 World Congress WSAVA/FECAVA/CSAVA
ketamine or thiopental. Inhalation agents produce
a rapid fetal effect which is proportional to the
depth and duration of maternal anesthesia. The
use of isoflurane or sevoflurane, with their low
solubility and rapid elimination can provide rapid
recovery of vigor in the neonate, provided the
puppy or kitten will breathe.
Based on this information my current approach
to cesarean section in any mother for whom
viability of the puppies or kittens is expected, is
to induce anesthesia with intravenous propofol
(3-8 mg/kg) to effect for intubation. Then the
mother is maintained under anesthesia with
sevoflurane, although isoflurane is acceptable as
well. Once the puppies or kittens are delivered,
the mother is administered an analgesic agent
107
A
to improve quality of recovery and to provide
some post-operative pain relief. Typical choices
for opioid in our practice are morphine 0.3 mg/
kg, hydromorphone 0.1 mg/kg (dogs only), or
buprenorphine (0.01 mg/kg).
Neonatal survival is also influenced by adequate
support of the puppy or kitten upon delivery. The
airway should be immediately cleared by wiping
away the fluid and membrane around the muzzle
using a clean, dry towel while holding the animal
in a head downward position. Some will advocate
suctioning the airway with a bulb syringe, although
the fluid present in the mouth and nasal passages
will generally run out with gravity and the fluid in
the lungs will be absorbed once the animal begins
expanding its lungs with respiratory efforts. The
umbilical cord should be clamped and tied within
2 to 5 cm of the abdominal wall. Vigorous but
gentle physical stimulation will promote neonatal
activity and help to initiate respiratory effort.
Continue to rub the puppy or kitten with a clean,
dry towel, occasionally stopping to observe
for respiratory effort and to palpate a cardiac
impulse through the chest wall. If an opioid was
administered to the mother prior to delivery of the
puppy, one can place a drop of naloxone under
to tongue of the neonate to reverse the opioid’s
effects on the puppy. Don’t be too hasty to give
up on the puppy or kitten. Stimulation should
continue for at least 10 minutes in any puppy
or kitten that has a palpable cardiac beat. One
to two drops of doxapram can be placed on the
tongue if the neonate is reluctant to breath, but
the efficacy of this technique is not established.
A small endotracheal tube can be made from an
18 gauge or 20 gauge over-the-needle catheter by
2006 World Congress WSAVA/FECAVA/CSAVA
108
Back to contents
removal of the stylet. This can be used to intubate
the neonate and deliver initial positive pressure
breaths in order to promote elimination of any
residual inhalation agent causing prolonged
respiratory depression. Once the neonate begins
to breathe, vocalize and move about it should
be kept in a warm environment until such time
that the mother is recovered from anesthesia and
one can introduce the puppies or kittens to their
mother.
References
Luna SP, Cassu RN, Castro GB, Teixeira
Neto FJ, Silva JR, Lopes MD: Effects of four
anaesthetic protocols on the neurological and
cardiorespiratory variables of puppies born by
caesarean section. Vet Rec 2004; 154: 387-9.
Moon-Massat PF, Erb HN: Perioperative factors
associated with puppy vigor after delivery by
cesarean section. J Am Anim Hosp Assoc 2002;
38: 90-6.
Moon PF, Erb HN, Ludders JW, Gleed RD,
Pascoe PJ: Perioperative risk factors for puppies
delivered by cesarean section in the United States
and Canada. J Am Anim Hosp Assoc 2000; 36:
359-68.
Moon PF, Erb HN, Ludders JW, Gleed RD, Pascoe
PJ: Perioperative management and mortality
rates of dogs undergoing cesarean section in the
United States and Canada. J Am Vet Med Assoc
1998; 213: 365-9.
Funkquist PM, Nyman GC, Lofgren AJ, Fahlbrink
EM: Use of propofol-isoflurane as an anesthetic
regimen for cesarean section in dogs. J Am Vet
Med Assoc 1997; 211: 313-7.

Standards of Care (How I Treat)
BACTERIAL ENTERITIS
Dr. Alex German
Department of Veterinary Clinical
Science
University of Liverpool
Small Animal Hospitál
Crown Street
Liverpool
L7 7EX
United Kingdom
ajgerman@liv.ac.uk
Introduction
The main etiological agents involved in
bacterial enteritis are reported to be Clostridium
perfringens, Clostridium difficile, Campylobacter
spp., Salmonella spp and enteropathoegnic
Escherichia coli (EPEC). However, given that
these organisms can be part of the indigenous
intestinal microflora, their role in causing clinical
disease is controversial.
Clostridium perfringens
Clostridium perfringens is an anaerobic, spore-
forming, gram-positive bacillus, which has
been typed into five toxigenic phenotypes, A-E.
Each elaborates a major toxin and other toxins,
including C. perfringens enterotoxin (CPE), a
well-characterized virulence factor. Several recent
studies have shown an association between the
presence of CPE in feces and diarrhea. Signs of
large-bowel diarrhea predominate characterized
by increased frequency of defecation, tenesmus,
fecal mucus and hematochezia. C. perfringens
has also been implicated in the acute hemorrhagic
gastroenteritis syndrome (AHG) in dogs; clinical
signs include severe vomiting and diarrhea, often
associated with blood. Onset of signs is peracute
and animals can be markedly volume-depleted.
A number of methods to diagnose C. perfringens-
associated diarrhea have been reported including
routine bacterial culture, identification of
increased spore counts on fecal smears, and
detection of CPE in feces. Although the presence
of endospores could help support a diagnosis,
detection of CPE is most reliable. An ELISA kit is
available for detection of CPE in fecal specimens
(Techlab Inc., Blacksburg, VA), but the assay has
not yet been fully validated in dogs or cats.
For most cases of C. perfringens-associated
diarrhea, animals respond to antimicrobial
therapy. Recommended antimicrobials include
macrolides (particularly tylosin), ampicillin,
and metronidazole. Supportive measures such
as dietary modification, is also recommended.
Back to contents
A
Aggressive treatment is required for AHG,
including intravenous fluid therapy (usually
colloids), and a combination of intravenous
bacteriocidal antibacterials (e.g. amoxicillin-
clavulanate and enrofloxacin). Cases are initially
maintained nil per os, but subsequently dietary
management can be instigated.
Clostridium difficile
Clostridium difficile is a gram-positive, anaerobic
spore-forming bacillus, which has been associated
with diarrhea in dogs. Two toxins, toxin A and
toxin B, are thought to be primarily responsible
for manifestation of clinical signs, although other
toxins may also play a role. C. difficile-associated
diarrhea can be diagnosed by routine bacterial
culture, identification spores on fecal smears and
detection of toxin A or toxin B in fecal specimens
with ELISA. Again the latter is reported to be
most reliable. Similar to C. perfringens, a strong
association has been found between the detection
of C. difficile toxin A and the presence of AHDS.
Clostridium difficile seems to be less prevalent
in cats compared to dogs. The antimicrobial
of choice for therapy of C. difficile-associated
diarrhea is metronidazole. 2006 World Congress WSAVA/FECAVA/CSAVA
Campylobacter spp.
Campylobacter is a small, curved, motile,
microaerophilic, gram-negative rod, which is often
isolated from healthy dogs and cats. Transmission
occurs by the feco-oral route. Campylobacter
species can be isolated in feces from animals with
clinical signs and from up to 50% of normal dogs.
Clinically significant disease is more common
in young, immunocompromized individuals, or
in colony dogs. Dogs with concurrent enteric
infections e.g. endoparasitism and viral diarrhea
are more severely affected. Although the
organism is a potential zoonosis, most cases of
human campylobacteriosis develop secondary to
food poisoning with poultry, poultry products and
unpasteurized milk. The organism most reported
109
A
to cause clinical signs in companion animals is
C. jejuni. However, other Campylobacter spp.
are frequently isolated (e.g. C. upsaliensis),
and their pathogenic significance is less clear.
Clinical signs range from mild transient diarrhea
to mucous laden bloody stools with associated
signs of colitis.
The organism can be detected on a direct fecal smear,
as a ‘seagull-shaped’ bacterium. However, infection
should be confirmed by culture of the bacterium
from feces and, given the potential for intermittent
excretion, multiple samples may be required. Given
that the organism is fragile, false-negative results
can occur if culture techniques are not optimal.
In light of the fact that, in many cases, isolation
of Campylobacter is incidental and that some
cases spontaneously resolve, If antibacterials are
thought necessary, the drugs of choice are the
macrolides (erythromycin, azithromycin) and
fluroquinolones (enrofloxacin, marbofloxacin).
Salmonella spp.
Salmonella species are Gram-negative motile rods,
which can cause significant clinical infections in
dogs and cats. However, Salmonella spp. are not
always associated with clinical disease, since
organisms can be isolated from healthy dogs
and cats. Clinical problems are most common
in young, kenneled or immunocompromised
animals, and concurrent viral infection (e.g.
parvovirus) may increase disease severity.
Transmission is via the feco-oral route, and some
species have a zoonotic potential.
Clinical signs include acute diarrhea of variable
severity, often but not invariably containing
blood. If bacterial translocation from the intestine
occurs, life-threatening septicemia may result.
Diagnosis is made by isolation of the organism
2006 World Congress WSAVA/FECAVA/CSAVA
110
Back to contents
from feces, or blood if septicemic. Given
problems with intermittent excretion, three fecal
cultures are required to confirm a negative result.
If a salmonella species is isolated from healthy
animals, or animals with acute diarrhea that are
not systemically ill, no treatment is needed, since
antibacterial use could promote resistance and a
carrier state. Treatment is only necessary when
there is evidence of sepsis, severe hemorrhagic
diarrhea, PLE or neutropenia. The choice of
antibacterial should be governed by culture and
sensitivity testing, but fluoroquinolones (e.g.
enrofloxacin, marbofloxacin) are usually suitable,
and the feces should be re-cultured to verify
eradication. Given the zoonotic risk, owners
should be advised to take appropriate precautions
to avoid self-infection.
Enteropathogenic E. coli
It is controversial whether enteropathogenic
(EPEC) and enterotoxigenic E. coli (ETEC)
are pathogenic in dogs and cats. Attachment of
ETECs and subsequent release of heat-labile,
heat-stable and Shiga-like toxins may cause
acute diarrhea. Further, EPECs may attach to
the mucosa causing effacement of microvilli,
and leading to profound malabsorption without
morphological abnormalities on histopathological
examination. Identification of pathogenic strains
requires specialized assays, such as bioassays
for toxins and genome probes for identification
of pathogenicity markers. However, because
these organisms can be seen in healthy animals,
a positive result does not necessarily prove a role
in clinical disease.
References
References available on request.
Back to contents
2006 World Congress WSAVA/FECAVA/CSAVA

111
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Al
Al in Alternative
Controversies
ontrove
Medicine

Back to contents
 Al
INVITED LECTURES - FULL PAPERS

Al - Controversies in Alternative Medicine

A CRITICAL ANALYSIS OF ACUPUNCTURE IN VETERINARY
MEDICINE
Johannes T. Lumeij, DVM,
PhD, Diplomate ECAMS
Associate Professor of Avian and
Exotic Animal Medicine
Division of Avian and Exotic
Animal Medicine
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Universiteit Utrecht
Yalelaan 108
3584 CM Utrecht
The Netherlands
j.t.lumeij@vet.uu.nl

Acupuncture has a wide following in veterinary References:

medicine, but there is no evidence for clinical
effectiveness. In this lecture the false historical
claims on which this treatment modality is based
will be exposed and the lack of evidence for this
treatment modality will be documented. Key
references for further study are included below.
Habacher G, Pittler MH, Ernst E. Effectiveness of
Acupuncture in Veterinary Medicine: Systematic
Review. J Vet Intern Med 2006; 20: 480–488.
Imrie RH, Ramey DW, Buell PD, Ernst E,
Basser SP. Veterinary acupuncture and historical
scholarship: Claims for the antiquity of
acupuncture. The Scientific Review of Alternative
Medicine, vol 5, no 3, 2001, pp 133-139

2006 World Congress WSAVA/FECAVA/CSAVA

113
Back to contents
Al
Al - Controversies in Alternative Medicine
THE END OF HOMEOPATHY
Ad Rijnberk Prof.em.Dr.DDr.
h.c
Department of Clinical Sciences
of Companion Animals,
Faculty of Veterinary Medicine
Utrecht University,
P.O. Box 80.154
3508 TD Utrecht
The Netherlands
A.Rijnberk@vet.uu.nl
Samuel Hahnemann
Christian Friedrich Samuel Hahnemann was
born in 1775 in Meissen, a town near Leipzig
in Germany renowned for its porcelain. His
father, a porcelain painter, was influenced by the
Enlightenment and strived for the best education
for his children. He wanted his children to become
“Selbstdenker”, self-thinker. Samuel Hahnemann
became an inquisitive student, who provided for
himself as a translator. From these translations
he acquired a vast knowledge, particularly of
chemistry.1
Hahnemann studied medicine at Leipzig and
Vienna, taking the degree of M.D. at Erlangen
in 1779. In 1782 he married the daughter of a
pharmacist, Henriëtte Küchler, and in 1783 the
first of his 11 children was born. From 1784
– 1789 the Hahnemann family lived in Dresden,
where Samuel probably had a meeting with the
visiting Lavoisier.2 This famous French chemist
might have stimulated Hahnemann to pursue his
way in chemistry. He earned a good reputation
for himself by introducing a method to unmask
sweetening of wine with lead and by publishing a
report on arsenic poisoning.
2006 World Congress WSAVA/FECAVA/CSAVA
In 1789 Hahnemann left the practice of medicine
and concentrated on research and publishing. In
the period between 1790 and 1805 he published
a total of 5500 pages in books, articles and
translations.1 From 1811 to 1821 Hahnemann
lectured at the university of Leipzig on
homeopathy. In 1821 the hostility of apothecaries
forced him to leave Leipzig, and at the invitation
of the duke of Anhalt-Köthen he went to live at
Köthen. Fourteen year later he moved to Paris,
where he practiced medicine with great popularity
until his death in 1843.
The similia theory
Hahnemann developed an aversion for the
practice of medicine of the late 18th century,
employing bloodletting, leeching, purging and
other procedures that did more harm than good.
114
Back to contents
In his search for other approaches the Newtonian
empiricism did not play an important role. The
role model was rather the Renaissance astrologist
Paracelsus, who pioneered the use of chemicals
and minerals in medicine. Hahnemann always
emphasised the empiric character of his method,
but he had a strong passion for speculation and
ontologic system building.1 While translating
William Cullen’s Lectures on the Materia medica
into German Hahnemann was not convinced by
the author’s explanation of the beneficial effect
of quinine in malaria patients. Cullen felt that
quinine reinforced the stomach. Hahnemann
took quinine himself and experienced symptoms
similar to those of malaria, that is similar to the
symptoms of the disordered state that quinine was
used to cure. This observation led him to assert
the theory that “likes are cured by likes”, similia
similibus curentur. Diseases are cured (or should
be treated) by those drugs that produce in healthy
persons symptoms similar to the diseases.3 His
chief work, Organon der rationellen Heilkunst
(1810; Organon of rational medicine) contains
an exposition of his system, which he called
Homöopathie.4 The term is derived from the
Greek words homoios (similar) and pathos
(suffering or disease).
Potentiation
After stipulation of his basic rule, Similia
similibus curentur, Hahnemann increasingly
tended to believe in dynamic rather than
corpuscular interpretation of the action of drugs.
He described the action of highly diluted solutions
as “dynamic”. He compared the action of drugs
with warmth, magnetism and electricity. Over
the years he tended to go for higher dilutions. In
1816 he recommended in Reine Arzneimittellehre
dilutions up to C30 for most purposes, i.e. a
dilution by a factor of 10030 = 1060
Hahnemann realized that there is little or no
chance that anything of the original substance
would remain after these extreme dilutions. But he

believed that the vigorous shaking or pulverizing
with each step of dilution promotes the release
of intrinsic curing forces. In Hahnemann’s view
these forces, thus freed from material bonds, can
affect the organism effectively.5
200 years later
Because homeopathic remedies were actually
less dangerous than those of 19th-century
medical orthodoxy, many medical practitioners
began using them. For example at the turn of
the 20th century, homeopathy had about 14,000
practitioners and schools in the United States.
But as medical science and medical education
advanced, homeopathy declined sharply. Schools
either closed or converted to modern methods.
The last pure homeopathic school in the United
States closed during the 1920s.6 Nevertheless
after 200 years, homeopathy is still practised by
physicians and veterinarians. In recent decades
it may even have gained popularity. This is
largely based upon the positive effects that have
been observed in clinical practice, i.e., clinical
experience.
Clinical experience
Several treatments are based upon no more than
clinical experience, which is the uncontrolled
conviction of the clinician that the treatment
works. Some of the treatments fall into disuse
after some period of time. Others persists for
decades or centuries. An intriguing question is,
how can ineffective treatments persist so long. At
least four explanations are possible:7,8
1. Insufficient knowledge of the natural course of
the disease - In using a generally accepted treatment
the clinician may loose sight of the spontaneous
course of the disease. For example, in the past
it was customary to treat idiopathic trigeminal
neuropathy (canine dropped jaw syndrome) with
corticosteroids. This was followed by a complete
recovery in 2 to 3 weeks. Now it is known that
the condition has an excellent prognosis without
any treatment and that corticosteroids do not alter
its course.
2. Random variation - The clinician’s experience
is often based on a limited number of cases. As a
result there is a risk of being misled by chance.
If, for example, four out of five cases are cured
by a treatment, it cannot be expected that 80%
of future patients will be cured. Consultation of
statistic tables for confidence intervals will reveal
that with 95% certainty the cure-rate will be
somewhere between 28 and 99%.
3. The placebo effect – Human patients seek medical
advice expecting to be helped. This expectation
together with the “healing environment” of the
doctor’s office often bring about a therapeutic
Back to contents
Al
effect – a positive placebo effect – no matter
which treatment is given. For a wide range of
afflictions, 30 to 40% of patients experience relief
after taking a pharmacologically inactive tablet,
a placebo.9 For veterinary medicine the situation
is quite different. From the stress associated with
the visit of an animal hospital,10,11,12 no beneficial
effect for the animal can be expected. On the
contrary (companion) animals are much better
off at home.
4. The bias of the clinician – The clinician always
hopes that the treatment will be effective and
thereby becomes a prejudiced or biased observer.
Like everyone, clinicians seek to bolster their
egos. They are like supporters of a football
club who say: “we won”, when the team wins
and: “they lost”, when it loses. Clinicians have
a tendency to ascribed success to the prescribed
treatment, irrespective of whether the patient’s
improvement could have been spontaneous.
Science and homeopathy
When considering a possible scientific basis for
homeopathy, two questions have to be answered:
(1) Is there any evidence of a likely mechanism?,
and (2) Have clinical trials demonstrated effects
better than a placebo?
1. Mechanism – The dilution far beyond
Avogadro’s number (6 x 1023) makes it very
unlikely that one molecule of the original
substance would be present in a C30 solution. Thus
a pharmacological action based upon molecular
interaction cannot be expected. What remains
is the belief of homeopaths that these dilutions
retain some “essential property” (curing force) of
the substance once present. The most sensational
attempt to prove the latter has been the study
of Benveniste and co-workers on the effects of
extremely diluted antibody solutions. They found
that aqueous solutions of anti-immunoglobulin
E (anti-IgE) still retain an ability to cause 2006 World Congress WSAVA/FECAVA/CSAVA
degranulation of human basophilic granulocytes,
even when diluted to the point where there are
no anti-IgE molecules left in the solution. The
report was accepted for publication in Nature,13
under the condition that identical results had to
be obtained when the experiment was repeated in
Benveniste’s laboratory under the observation of a
delegation composed by the editor-in-chief. When
the experiment was repeated, the activation of
basophils in tubes treated with the “homeopathic
diluted antigen” did not differ from that of the
control tubes, which were only treated with the
solvent. Also in other laboratories Benveniste’s
claim of transmission of biological information
to the molecular organization of water could not
be confirmed.14
2. Trials - In human medicine many randomised
115
Al
trials have been performed, comparing
homeopathic treatment with a placebo. Several
of the trials had major flaws in their design. In
recent years the reports have been summarized
in meta-analyses. In these critical reviews of the
publications on the effectiveness of homeopathy
there is special attention for the methodological
aspects. The early meta-analyses were somewhat
inconclusive. The authors felt that it could not
be excluded that individualized homeopathy has
an effect over placebo.15,16 Although they added
that the results of their analyses might have been
coloured positively by publication bias, that is,
a report with a positive result is more likely to
be published than a report with negative result.
Evidence of bias made some authors confess
that this weakened the original meta-analysis,
i.e., caused overestimation of the effects of
homeopathic treatments.17
In 2002 Edzard Ernst of the Department of
Complementary Medicine of the University
of Exeter in England published an analysis of
systematic reviews/meta-analyses.18 He could not
provide strong evidence in favour of homeopathy.
In particular, there was no condition responding
convincingly better to homeopathic treatment
than to placebo or other control interventions.
Similarly, there was no homeopathic remedy
that was demonstrated to yield clinical effects
of that are convincingly different from placebo.
Ernst concluded that the best clinical evidence
for homeopathy available does not warrant
positive recommendations for its use in clinical
practice. In 2005 investigators from Switzerland
and the United Kingdom reported a comparative
study of 110 homeopathic trials and 110 matched
conventional-medicine trials. Biases were present
in placebo-controlled trials of both homeopathy
and conventional medicine. When account was
taken for these biases in the analysis, there was a
weak evidence for a specific effect of homeopathic
2006 World Congress WSAVA/FECAVA/CSAVA
remedies, but strong evidence for specific effects
of conventional interventions. The authors
conclude that this finding is compatible with the
notion that the clinical effects of homeopathy are
placebo effects.19
The few well-designed trials in veterinary
medicine also failed to demonstrate efficacy of
homeopathy.20,21
The end
Homeopathy has not withstood scientific testing.22
It is felt that for too long a politically correct laissez-
faire attitude has existed towards homeopathy,
but there is some light.23 For example in the
United Kingdom a Parliamentary Committee
has issued a report about complementary and
alternative medicine, stating that “any therapy
116
Back to contents
that makes specific claims for being able to treat
specific conditions should have evidence of being
able to do this above and beyond the placebo
effect”.23 The Swiss Government has withdrawn
insurance coverage for homeopathy and four
other complementary treatments.
There is no justification for further investment
in research to perpetuate the homeopathy versus
allopathy debate. In an editorial comment in The
Lancet it was put as follows: “Now doctors need
to be bold and honest with their patients about
homeopathy’s lack of benefit, . . “.23
In November 2005 the Federation of Veterinarians
in Europe (FVE) has issued a strategy document,
including the statement that the veterinary
profession is rooted in science and evidence-
based veterinary medicine.24 In the explanatory
discussion of this strategy document it was
explicitly said that the FVE rejects non-evidence
based medicines such as homeopathy.25
Earlier in 2005 the European Board of Veterinary
Specialisation (EBVS) made a clear statement
with regard to alternative modes of treatment:
The EBVS only recognises scientific, evidence-
based veterinary medicine complying with
animal welfare legislation. Specialists or colleges
practising or supporting implausible treatments
with no proof of effectiveness run the risk of
withdrawal of their specialist status. No credit
points can be granted for education or training in
these so-called supplementary, complementary
and alternative modes of treatment.26
Notes and references
1. De Goeij CM. Samuel Hahnemann: een
verontwaardigd systeembouwer. Ned Tijdschr
Geneeskd 1994; 138:310-314.
2. Haehl R. Samuel Hahnemann, sein Leben und
Schaffen. Leipzig, W. Schwabe, 1922.
3. Hahnemann S. Versuch über ein neues Prinzip
zur Auffindung der Heilkräfte der
Arzneisubstanzen, nebst einigen Blicken auf die
bisherigen. Journal der practischen Arzneykunde
und Wundarzneykunst. Jena, 1796; 2.3:391-439
& 2.4:465-561.
4. Hahnemann S. Organon der Geneeskunst.
Translation of the 6th edition of 1921 in Dutch.
Alkmaar: VSB Geneesmiddelen, 1983: § 279.
5. In 1825 Hahnemann wrote: “Dürch Reibungen
(Schütteln) kommt die innere Arneikraft
wundersam zum Leben und befreit sich
gleichsam von den Banden der Materie, um desto
eindringlicher und freier auf den Menschlichen
Organismus würken zu können. Hahnemann S.
Belehrung für den Wahrheitssucher. Allgemeine
Anzeiger der Deutschen 1825; 194: 2387-2392.
Cited in ref. 1.

6. Barret S. Homeopathy: The Ultimate Fake.
http://www.quackwatch.org/
01QuackeryRelatedTopics/homeo.html.
7. Wulff HR. Rational diagnosis and treatment.
An introduction to clinical decision-making. 2nd
edn. Blackwell Scientific Publications. Oxford,
1981.
8 Rijnberk A. Modes of treatment. Austral Vet J
1997; 75:260-261.
9. Brown WA. The placebo effect. Scient Amer
1998(Jan):90-95.
10. Van Vonderen IK, Kooistra HS, Rijnberk
A. Influence of veterinary care on the urinary
corticoid;creatinine ratio in dogs. J Vet Intern
Med 1998; 12:431-435.
11. Zimmer C Reusch CE. Untersuchungen zum
Kortisol-Kreatinin-Verhältnis im Urin (UCC) bei
gesunden Katzen. Schweiz Arch Tierheilk 2003;
145:323-328.
12. Cauvin AL, Witt AL, Groves E, Neiger R,
Martinez T, Church DB. The urinary corticoid-
creatinine ratio (UCCR) in healthy cats
undergoing hospitalisation. J Feline Med Surg
2003: 5:329-333.
13. Davenas E, Beauvais F, Amara J, Oberbaum
M, Robinzon B, Miadonna A, Tedeschi A,
Pomeranz B, Fortner P, Belon P, Sainte-Laudy
J, Poitevin B, Benveniste J. Human basophil
degranulation triggered by very dilute antiserum
against IgE. Nature 1988; 333:816-818
14. Metzger H, Dreskin SC. Only the smile is left.
Nature 1988; 334:375.
15. Kleijnen J, Knipschild P, ter Riet G. Clinical
trials of homeopathy. Brit Med J 1991; 302:316-
323.
16. Linde K, Clausius N, Ramirez G, Melchart
D, Eitel F, Hedges LV, Jonas WB. Are the clinical
effects of homeopathy placebo effects? A meta-
analysis of placebo-controlled clinical trials.
Lancet 1997; 350:834-843.
Back to contents
Al
17. Linde K, Scholz M, Ramirez G, Clausius N,
Melchart D,Jonas WB. Impact of study quality
on outcome in placebo-controlled trials in
homeopathy. J Clin Epidemiol 1999; 52:631-636.
18. Ernst E. A systematic review of systematic
reviews of homeopathy. Brit J Clin Pharmacol
2002; 54:577-582.
19. Shang A, Kuwiler-Müntener K, Nartey L,
Jüni P, Dörig S, Sterne JAC, Pewsner D. Egger
M. Are the clinical effects of homoeopathy
placebo effects? Comparative study of placebo-
controlled trials of homoeopathy and allopathy.
Lancet 2005; 366:726-732.
20. De Verdier K, Ohagen P, Alenius S. No effect
of a homeopathic preparation on neonatal calf
diarrhoea in a randomised double-blind, placebo-
controlled clinical trial. Acta Vet Scand 2003;
44:97-101.
21. Holmes MA, Cockcroft PD, Booth CE, Heath
MF. Controlled clinical trial of the effect of a
homoeopathic nosode on the somatic cell counts
in the milk of clinically normal dairy cows. Vet
Rec 2005; 156:565-567.
22. Van Sluijs FJ. Kan de homeopathie de toets
der wetenschap doorstaan? Tijdschr Diergeneeskd
2004; 127:295-298. English translation in
Veterinary Science Tomorrow: Can homeopathy
withstand scientific testing? http://www.vetscite.
org/publish/articles/000051/article.html
23. Editorial. The end of homeopathy. Lancet
2005; 366:690.
24. FVE’s Strategy 2006-2010. Improving
the health and welfare of animals and people.
Brussels, FVE, 2005. www.fve.org
25. Minutes of the General Assembly Meeting of
the FVE, Brussels, November 2005.
26. www.ebvs.org - policies and procedures, page 9.
2006 World Congress WSAVA/FECAVA/CSAVA
117
Al
Al - Controversies in Alternative Medicine
HOLISTIC APPROACH TO VETERINARY MEDICINE
Christina Chambreau, DVM,
CVH
908 Cold Bottom Road
Sparks, MD 21152, USA
HealthyAnimals@aol.com
Most veterinary conferences, like this one, are
now including talks and workshops on one or
more of the complementary modalities and many
United States colleges of veterinary medicine
are offering course work. In 1996, Dr. Allen
Schoen said that there has been a great increase in
interest in complementary, alternative or holistic
veterinary medicine for people and animals. In
the last 2 years that interest has skyrocketed.
Have you ever been asked by clients – “Isn’t there
an alternative to surgery…or drugs…or radiation
therapy?” Have you had animals who presented
for otitis, then gum abscesses, then asthma, then
liver disease and finally cancer? Did you wonder if
some other approaches might have been helpful?
How many dogs with Flea Allergy Dermatitis do
not respond to hypo-sensitization? Once you do
surgery on megacolon cats – there are no more
options. Increase client satisfaction, improve
your rates of healing animals, deepen your
personal satisfaction with veterinary medicine
and add an additional income stream to your
practice by shifting to the holistic paradigm. You
will love having the option of choosing between
conventional therapy, homeopathy, acupuncture,
western botanicals, chiropractic and many more
2006 World Congress WSAVA/FECAVA/CSAVA
modalities to provide each individual animal
and their family with the care that is appropriate
to them. I will now cover the philosophies and
principles as well as specific treatments you can
add now to your practice.
Most health professionals have been trained in a
Cartesian and Newtonian model of the universe.
Then Louis Pasteur further solidified the idea
that “something” needed to be eliminated to cure
disease (on his death bed he says that germs did
not create disease – the soil or terrain did). Some
will argue that every treatment must be proved in
the above scientific ways, yet every day we use
drugs for something that was never proved nor
the mechanism of action never worked out. Now,
I ask you to look at a new model, I ask you to look
for what makes common sense to you; I ask you
118
Back to contents
to use what is useful and not argue at what does
not make sense.
Some owners are often content when the
symptoms are removed by whatever means, even
when they recur or they become more ill (blamed
on “aging”). Animals, especially certain breeds
are living shorter lives, with increased incidence
of serious disease such as Cushings, Diabetes
Mellitus, cancer, hyperthyroidism, inflammatory
bowel disease and many more. Some animals live
long lives with minimal treatment. However, when
the current mechanistic paradigm fails to help an
animal, the veterinarian has little to recommend
than euthanasia. Many animal guardians are now
looking for options. You will be more satisfied
and joyous when you can offer more options.
Holistic paradigm
All the ancient forms of healing shared the
premise of self-healing and an energetic basis
for the lack of health. Modern holistic healing
systems (or modern versions of ancient forms)
offer a coherent paradigm (system of thought)
with clear principles to follow that give us, as
practitioners, infinite possibilities for healing. As
long as the animal is still alive, there is a modality
or variation of a modality that can be tried. You
never run out of possibilities.
The underlying philosophy of holistic medicine is
that symptoms reflect the underlying health status
of the energy field and are the attempt of the body
to heal. They indicate:
1. Overall health status;
2. The most appropriate treatment modality;
3. How the animal is responding to the current
modalities.
The holistic approach may also address merely
the symptoms with herbs or specific acupuncture
points, combination homeopathic remedies
or even single homeopathic remedies. These
strategies could successfully eliminate the current
symptoms, but do not make the animal healthier
overall. Often the symptoms will recur or more

serious ones will develop when such ameliorating
treatments are used.
Curative approach
The goal is to have the symptoms go away, and
the animal become healthier in many other ways.
Baby, a big black cat, came to me at 9 years of age.
She had been receiving Depo Medrol injections for
8 years at an ever-increasing frequency, now every
6 weeks, to keep her from licking her abdomen
raw and bloody (diagnosed as Feline Endrocine
Alopecia). I treated her homeopathically for 9
months before her abdomen was free of lesions.
She never had skin lesions again. Within weeks
of her death she licked her hair short, but not to
bare skin. One year later, she recovered quickly
from an upper respiratory infection for which
2 other cats in the house had to be treated for
2 weeks. A year after that she again recovered
quickly with no treatment from the same fever
of unknown origin that the fourth and fifth cat in
the house suffered with for a week or so. None
of the 5 cats needed treatment again and they all
died around 17 within months of each other after
the owner sharply decreased the protein in their
diet. That is cure. This result often, though not
always happens when good holistic treatment is
given. Total health is always my goal and I teach
the animal guardians to have it be their goal also.
Holistic approach in the conventional setting
To summarize, the holistic paradigm is powerful
regardless of choice of therapy. The AHVMA
(American Holistic Veterinary Medical
Association) lists the following different
alternative modalities in their referral directory:
Acupuncture (IVAS certification), Acuscope,
applied Kinesiology, Bach Flower Remedies
(and there are many other flower essences as
well), Biotron II, Chinese Herbs, Chiropractic
(AVCA certification), Clinical Nutrition, Color
Therapy, EAV (Electroacupuncture according to
Voll), Glandular Therapy, Classical Homeopathy,
AVH Certified, British Institute Certified, Other
Homeopathy, Interro, NAET (Nambrudripad’s
Allergy Elimination Technique), Nutrition,
Magnetic Therapy, Massage Therapy, Pulsating
Magnetic Therapy, Reiki, Veterinary Orthopedic
Manipulation and Western Herbs. Additional
holistic modalities include Network Chiropractic,
Neutraceuticals, Rolphing, Ayurvedic Medicine,
Animal Communication, Intuitive Healing
Techniques (Barbara Brennan is one school),
Tellington Touch, Anthroposophical Medicine,
Prayer and more. These are defined on my blog,
www.healthypetsblog.com and web, www.
ChristinaChambreau.com. While observable
symptoms can be treated conventionally or
Back to contents
Al
holistically, the entire patient work-up and
selection of treatments will benefit from the
holistic approach. While taking a longer time, this
type of case intake is much more satisfying to the
animal, guardian and veterinarian. You observe
and ask about the current complaint. You try to
understand the underlying cause which could be
purely physiological but will likely include social
interactions, environment (toxins to vaccines),
diet, moves, etc. You will then ask about the
entire life of the animal and note prior problems
and their possible etiologies. You will observe the
animal using any and all training received so far.
The following are a few examples of differences
in intakes.
Conventional from Veterinary school: PE and the
minimal lab work needed.
Acupuncture: Tongue and pulse.
Chiropractic: Notice the details of the
musculoskeletal and nervous system by: Checking
the animal’s gait; Noting symmetry and balance of
the body; Feeling for heat, cold, pain, sensitivity;
Looking and feeling the muscular tone and bony
structure of the head, jaw, face, vertebrae, pelvis,
hips, shoulder and limbs.
Ayurveda: pulse, visual exam of urine, tongue,
skin, nails looking for color, moistness and
temperature.
Homeopathic: etiology, what makes the symptoms
better or worse, peculiar and idiosyncratic
symptoms, reactions to stimuli in the visit, odor,
texture.
After collecting the information, step back and see
the animal as a part of its environment, its family
of people and animals, its history and ancestors.
Formulate a treatment plan based on the severity
of symptoms, the desires of the owners, your
training and knowledge of potential referrals for
holistic specialties. This may include surgery to
repair the fracture, then chiropractic to keep the
body balanced during the healing process and 2006 World Congress WSAVA/FECAVA/CSAVA
homeopathy to speed the healing, alleviate the
pain and prevent the clumsiness that caused the
fracture in the first place. Every individual may
need a different treatment at different times in their
life and each practitioner knows and likes certain
techniques. There is no right and wrong. Make the
initial evaluation, prescribe a treatment, and then
evaluate the result by looking at the entire animal
as describe for the intake. Most importantly, do
not settle for less than full health.
The five main foci to helping animals be healthy
are:
1. Feed the best diet.
2. Vaccinate the least.
3. Provide the best environment for the needs of
that animal.
119
Al
4. Build up the health of the animal & support the
natural healing process.
5. Know how animals respond to treatment –
cure, temporary amelioration, suppression or no
response at all.
Many people seeking holistic medicine from
you will already be using different modalities
on their own animals and you will need to help
evaluate their efficacy and can also learn these
new techniques from your clients.
Early Warning Signs of Illness
As animals recover from their “disease”, we find
that certain “normal” things go away, too. Do not
be satisfied until most of the following symptoms
are gone. In young, apparently healthy animals,
these apparently “normal” problems may be
the only indications to start treatment. More
symptoms need to be added, if you will email.
Skin: doggy smell; attracts fleas a lot; dry,
oily, lack-luster coat; excessive shedding; not
grooming, ear problems - waxy, oily, itchy,
recurrent mites; eye discharge, tearing, or matter
in corner of eyes; raised third eyelid; spots
appearing on iris; “freckles” appearing on face;
whiskers falling out; fragile, thickened, distorted
claws that are painful or sensitive to trim.
Behavior: Fears (of loud noises, thunder, wind,
people, animals, life); too timid; too rough or
aggressive (even at play); too hard to train; barks
too much and too long; suspicious nature; biting
when petted too long; hysteria when restrained;
clumsy; indolent; licking or sucking things
or people too much; not using litter box or not
covering stool.
Digestive: Bad breath; tarter accumulation; loss of
teeth; poor appetite; craving weird things (rubber
bands, plastic, dirt, cat litter, paper, dogs eating
dog or cat stools, rocks, sticks...); sensitivity
to milk; thirst - a super healthy cat on non dry
2006 World Congress WSAVA/FECAVA/CSAVA
food will drink at most once a week; red gum
line; vomiting often, even hairballs more than a
few times a year; mucous on stools; tendency to
diarrhea with least change of diet; obesity; anal
gland problems; recurrent worms.
120
Back to contents
Stiffness when getting up, early hip dysplasia;
tires easily in hot or cold weather; can no longer
jump up on counters, or go up or down steps.
Temperature: Low grade fevers - Normal for
healthy cats and dogs is 100-101.5.
Age & Reproduction: Should live a long life
(Shepherds 17 years, Danes 12, cats 24). should
be able conceive easily, deliver normally, and not
pass on “genetic breed” problems.
Keeping a journal
One way to know the “dis” ease of an animal
and track the success of the treatments is for the
guardians to keep a journal to track the current and
past symptoms as well as energy level, emotional
state and overall quality of life. Crucial is to
also record in bright colors the good things that
happen to the pets, as this way they are focusing
on the positive, while still tracking the negative
symptoms.
Next Steps
Join your country’s holistic associations. Visit
holistic healing centers in your town or area.
Joint the internationals organizations. Ask this
conference and any others you attend to invite the
veterinarians trained in all the above modalities
to speak on them. Go to the many chat rooms and
it serves for veterinarians of each modality and
for lay people as well. Learn from your clients
and find out from them where to be trained. Go to
my website, www.ChristinaChambreau.com, or
my blogs, http://planetchambreau.typepad.com/
healthy_pets/
http://planetchambreau.typepad.com/healthy_
people/
http://planetchambreau.typepad.com/healthy_
planet/
Please email me if you would like further
coaching or information as I am committed to
deeply healing animals and having veterinarians
love their practice every day and prosper.

Al - Controversies in Alternative Medicine
PRACTICAL USE OF HOMEOPATHY IN YOUR PRACTICE
Christina Chambreau, DVM,
CVH
908 Cold Bottom Road
Sparks, MD 21152, USA
HealthyAnimals@aol.com
While no modality can resolve all problems,
homeopathy is the perfect training to evaluate
every form of therapy. In my experience,
the potential of homeopathy is to cure at the
deepest level, with all symptoms resolving
and the animal living a long and healthy life.
Only a deep understanding of the principles of
homeopathy and years of practice can enable
you to reliably cure this way. However, from
day one homeopathy can improve the overall
well being and health of the animal in spite of
the continuing presence of the original, uncured
pathology such as renal disease, Cushing’s,
cancer, diabetes and more. Homeopathy can
treat many acute conditions in your practice
saving you time and speeding healing of the
animal. This paper covers the guiding principles
of homeopathy, shows the potential healing that
can occur and gives you immediate practical
applications such as how to evaluate the
response of animals to any type of treatment.
Expanded versions are on my web site, www.
ChristinaChambreau.com.
WHAT CAN BE CURED?
The following brief summaries are of cases.
They are intended to give you an idea of the
breadth of conditions that can be successfully
treated with good homeopathy.
Perry was a 5-year-old Himalayan cat with
a firm, swollen, fistulous right mandible.
After achieving only temporary responses to
antibiotics, a biopsy was performed with results
showing undifferentiated carcinoma, probably
squamous cell carcinoma. Within one month of
being treated homeopathically, the fistula cleared
up and he resumed his normal happy behaviors.
He remains clear of cancer 10 years later.
Maggie presented with an infected, deeply
ulcerated histiocytic sarcoma on her face. With
homeopathic treatment, the tumor disappeared in
3 weeks, and has been completely gone for over
Back to contents
Al
5 years now. Her overall health has improved
tremendously.
Felix, a 5-month-old puppy, had a prolapsed
rectum. Within two hours of receiving the
remedy, the rectum was normal, and the next
day he was as playful and friendly as ever. Over
the next 3 years of follow -up, the rectum did not
prolapse again.
Gus, a 4-month-old pug, had one testicle that
had been retracted for 3 weeks. 2 weeks after the
homeopathic remedy, the testicle descended.
Isis had chronic coughing since 6 weeks then,
six hours after annual boosters at age 5, she was
admitted to the hospital for oxygen with a severe
asthma attack. With conventional treatment,
she continued having asthmatic respiration
with occasional hospitalizations for the next
2 years. Homeopathic remedies given while
she was being tapered off the drugs resolved
the asthma problem; and she has since had no
conventional drugs, no asthmatic breathing,
and less coughing. She survived the loss of her
owner and relocation with no further episodes
until her death at age 17.
Heidi was a 14 year old spayed female that
had a bleeding, swollen, angry looking growth 2006 World Congress WSAVA/FECAVA/CSAVA
attached to the third eyelid, covering the eye.
There were also 2 firm growths on the right paw
and in the middle of the chest. Remedies were
prescribed over a 9-month period with total
disappearance of the eyelid mass. She began
behaving like a young dog, and could hear again.
She did 4 mile walks with running, leading and
being adventuresome until a traumatic death a
year later.
The power of homeopathy lies in the potential
to cure to this level. The “illness” resolves and
most importantly, the animal feels better overall
emotionally and physically. Most animals have
an amelioration of symptoms and increased
energy, and some animals have the deep level
of curative response as illustrated above. Some
animals never respond to homeopathy or any
121
Al
other modality including conventional; some
respond to one modality and not others.
HOMEOPATHIC HISTORY
Although formally conceived by Samuel
Hahnemann, MD, a brilliant German physician
in 1800, the roots of homeopathy go back to
Hippocrates, Paracelsus, the Mayans, Chinese,
Greeks, Indians (Asian & American), and
Egyptians. All used the philosophy of like cures
like. Hippocrates and other Greek physicians
observed that if a person chronically ill with
one disease became infected with a more severe
disease that had similar symptoms - the chronic
disease would disappear upon recovery from the
acute, stronger disease. Dr. Hahnemann wrote
“Essay on a New Principle for Ascertaining
the Curative Powers of Drugs, and Some
Examination of the Previous Principles” in 1796.
His understanding and guidelines have been
followed since that time. Hahnemann’s basic
textbooks, The Organon of the Medical Art (first
edition 1810 to 6th in 1842, the latter not being
published until the early 1900s), The Chronic
Diseases, and Materia Medica Pura are still the
core textbooks used today.
PRINCIPLES
1. Dilutions of herbs, minerals and body substances
are tested on healthy people (provings) and the
details of symptoms produced are recorded in
Materia Medicas.
2. The animal’s guardian is questioned in detail.
Symptoms and individual characteristics are key
to identifying the imbalance in the vital force
to be counteracted in order for the animal to be
healed. “The more striking, exceptional, unusual,
and odd (characteristic) signs and symptoms of
the disease case are to be especially and almost
solely kept in view.” (O 153)
2006 World Congress WSAVA/FECAVA/CSAVA
3. The symptom picture of the ill animal is
matched to the medicine that causes that same
pattern of symptoms in the provers - like cures
like – using repertories and Materia Medicas.
4. The correct strength and repetition of the
chosen remedy is correctly given.
5. We then wait for the body to react and evaluate
if the right remedy was chosen.
6. The remedy itself does not heal - it stimulates
the body to heal itself.
Successful treatment depends on:
1. Knowledge of disease: The sum total of all
the symptoms, past and present, represents the
underlying imbalance that needs to be corrected.
2. Knowledge of medicines: In Materia Medicas.
3. Ability to match the remedy to the individual
122
Back to contents
in the right strength (potency), amount and
frequency.
4. Knowledge of the possible outcomes of
treatment
5. Knowledge of obstacles to recovery: For each
individual, learning what practices are detrimental
to continued health. Nutrition, vaccination,
environment, other drugs, supplements, etc.
Tools used in homeopathic practice are:
1. Materia Medicas - books reporting the symptoms
from the provings and from clinical experience.
2. Repertories - indexes of the Materia Medicas.
They list symptoms with the remedies known to
impact on those symptoms.
3. Remedies - purchased from reliable pharmacies.
4. Clinical judgment - from veterinary training &
practice evaluating the response.
5. Study: courses, reading, and learning, practice,
learning.
KNOWLEDGE OF DISEASE
Disease begins as an energetic imbalance, then
functional changes occur, then inflammation
and finally tissue changes (pathology). Healing
goes the reverse direction. There is one on-going
“disease”, not just separate, acute episodes.
To really heal, the totality of symptoms must
be addressed, not just the current problem(s).
Different homeopathic medicines are often
needed at different times because we only see
part of the underlying imbalance. Each remedy
choice is based both on the current symptoms and
any past ones.
The key shift that must be made is to treat the
individual animal, not merely the disease.
Sometimes treating the pathology or disease
(Dexasone injection or homeopathic Apis or a
combination homeopathic remedy for a bee sting
reaction) will make the symptoms disappear and
not further weaken the energy field. This does
not help the animal become healthier overall.
When we can find the remedy whose energy
pattern (as seen from the provings and described
in the Materia Medicas) is very similar to the
energy pattern of the individual, we are treating
the susceptibility to become ill (as seen by the
symptoms of the disease and the idiosyncrasies
and history of the patient) as well as the current
problem. They can stay alert, agile, interactive
and relatively symptom free until they have a
final illness and die, at an old age. This is a goal
worth striving for.
KNOWLEDGE OF THE MEDICINES
There are 3 dilution forms made by pharmacies
that can be purchased – centesimal or c, decimal or
x, and LM (Q). The centesimal potencies are made

as follows. One drop of the tincture is diluted in
99 drops of diluent (water or alcohol) and shaken
(succussed). This makes the 1c potency. One drop
of this is diluted in 99 drops of diluent and shaken
to make a 2c, etc. The further the potentization
process is carried out, the stronger or more potent
the remedy. A 1M potency of a remedy has a very
strong energetic effect on the body compared to
the milder potency of 6c, therefore a weak animal
may need the 6c.
The decimal dilutions are produced by diluting
one drop of the tincture with 9 drops of diluent,
(instead of 99. The LM (Q) potencies are made by
diluting a 3c with 50,000 parts diluent.
The potency of the remedy must match the
energetic level of the ill animal to be most effective
and least likely to cause stressful aggravations.
Remedies can be purchased many places. They
need only be crushed and put in the front of the
mouth, or diluted I water.
Many homeopathic books give quantity,
frequency and potency for the condition, the
disease, the symptom, size of the animal or the
remedy. This is incorrect. As stated before, the
amount does not matter and the frequency is
dictated by your evaluation. Because people
expect to be told a quantity, it is fine to tell them
a specific amount to give, but also educate them
that it is not important.
Remedies to learn at first: Arnica, Apis, Ledum,
Hypericum, Nux vomica, Caulophyllum, Rhus
tox, Phosphorus, Sulphur and Pulsatilla.
My favorite 3 books – Homeopathic Medicine
for Dogs and Cats – Hamilton; Homeopathic
Treatment of Small Animals – Day; Your Dog
and Homeopathy – Westerhuis; and The Organon,
edition VI – Hahnemann translated by O’Reilly.
Read the philosophy parts of the first 3.
BRIEF THERAPEUTIC MATERIA MEDICA
Aconite (Monkshood): Fearful, Sudden, Seizures
Apis (Bee): Swelling, allergic reaction, Better
cold applications, no thirst. Insect stings.
Arsenicum album (white arsenic): toxic effects,
especially on GIT; Parvo; Always restless, chilly,
thirsty.
Belladonna (Deadly Nightshade): Sudden, Red,
Throbbing. Painful. Angry. Compulsive. Fevers.
Seizures.
Bryonia (Wild Hops): Movement makes pains
worse, A grouchy bear. Arthritis.
Cantharis (Spanish Fly): Burns, Burning pains,
Cystitis
Back to contents
Al
Carbo vegetabilis (Charcoal): Cold, Blue,
Collapse, neonate resuscitation
Causticum (Lime/Potassium mix): Involuntary
urination, weak muscles, warts,
Trembling, Old age problems. Paralysis.
Ferrum phos (Phos of Iron): Early inflammation,
fever, <right, night, cold, dry.
Gelsemium (Yellow Jasmine): dull, Droopy,
Drowsy, Chilled. Diarrhea from anticipation.
Cats pull hair from back.
Hepar sulph (Calc. sulphide): Pain, Hyper
sensitive, Chilly, Grouchy, Smelly. Interdigital
cysts, infected ears, abscesses
Ignatia (St. Ignatius bean): Grief and ailments
from grief, paradoxical symptoms.
Ipecacuanha (Ipecac root): Nausea, Vomiting,
Bleeding, with a Clean tongue.
Ledum (Marsh tea): Punctures, Insect bites, >cold
applications, yet injury feels cold to touch. Lyme
disease.
Magnesia phosphorica: Colic, Cramps, >light
pressure and bend double.
Mercurius vivus (sol): Drooling, Offensive,
Mouth and rectum, <by cold AND <by heat, thick
and coated tongue.
Natrum muriaticum (Salt): Ailments from grief,
Wants salt, Thirsty, Loners, Worse at the seashore,
suppressed grief. Bite owners when petted.
Phosphorus: friendly, affectionate. Thirst for
cold water. Bleeding. Vomiting.
Pulsatilla nigricans (Windflower): Clinging.
Bland discharges,
>consolation, >open air, >cold. Thirstless.
Female problems. Prostatitis.
Rhus toxicodendron (Poison ivy): Creaky gate,
Skin, Restless, Joints better from walking or
motion.
Rumex (Yellow Dock): Coughs from going
from warm to cold air, Tickling, teasing cough
<pressure, <cold, prevents Sleep.
Ruta graveolens (Rue-bitterwort): Sprains,
strains, bruised bones and eyes.
2006 World Congress WSAVA/FECAVA/CSAVA
Sarsaparilla: Urinary tract problems. Has to stand
up to urinate. Horses losing hair from manes.
Silica (sand): Abscesses. Foreign bodies. Chilly
or can desire cold. Feline acne. Timid.
Thuja (Arbor vitae tree): Hair oily, grows slowly,
ringworm. Fearful - hides, cringes, freaks out in
cages, and does not want to be held, though is
affectionate.
123
Al
Al - Controversies in Alternative Medicine
HOMEOPATHIC TREATMENT OF FELINE HYPERTHYROIDISM
Peter Dobias, DVM, HMC
Healing Place
Veterinary Clinic
233 Seymour River Place
North Vancouver
BC, V7H 2N8
healingplace@telus.net
Hyperthyroidism is one of the most commonly
diagnosed problems in cats. The most frequently
used conventional treatments involve the use of
methimazole or Iodine 131. The following study
is a retrospective analysis of 13 cats diagnosed
with hyperthyroidism that were treated by using
one homeopathic remedy. The diagnosis of
hyperthyroidism was established based on the
serum thyroxine values and clinical symptoms
of increased appetite, tachycardia, weight
loss and change in behaviour. A single dose of
homeopathic remedy, Natrum Muriaticum 200
C, was administered upon the diagnosis and the
thyroxine values were rechecked in 4 or more
weeks.
The selection of the homeopathic treatment was
based on the principles of classical homeopathy.
Only one single remedy was used at the time of
treatment and no other methods were used. A dose
of the remedy was repeated only when laboratory
values confirmed increased thyroxin values or if
clinical signs of hyperthyroidism recurred.
The homeopathic preparation of Natrum
Muriaticum1 was administered in the form of
pellets in 200c potency. There was one cat (see
Table 1) that received a higher, 1M, potency later
2006 World Congress WSAVA/FECAVA/CSAVA
on during the treatment.
The goal of this study is to demonstrate the use,
efficacy and long term effect of homeopathic
treatment in cases of feline hyperthyroidism.
The second goal is to compare the patients whose
values had gone back to normal with the patients
that did not respond to homeopathic treatment.
Results
• A total of 13 cats were treated.
• The age at the commencement of treatment
ranged from 5 to 17 years
•Thyroxine values in the treated cats ranged from
39nmol/l to 175nmol/l (normal reference range is
18-40nmol/l).
• Symptoms of hyperthyroidism seen in the
treated cats included tachycardia, weight loss,
124
Back to contents
restlessness and increased appetite.
• The thyroxine values of 8 cats from this group
returned to normal and the clinical signs of
hyperthyroidism also disappeared. The average
age of these cats was 7.4 years (5 – 12 years).
Their initial thyroxine values did not exceed
60 nmol/l and ranged from 39 – 59 nmol/l
• There were 5 cats that did not respond to
treatment and were prescribed conventional
therapy of methimazole. The average age of
this group of cats was 13.8. The thyroxin values
ranged from 55 – 175 nmol/l with the average of
97 nmol/l.
• One cat, the oldest in the test group, LaRue (age
17), was originally diagnosed as sick euthyroid
due to an advanced stage of chronic renal
insufficiency. This cat’s thyroxin value initially
increased to 55 nmol/l and later returned back to
normal. Unlike the other patients that responded
to therapy, this cat continued to be unwell and
later had to be euthanised. We have put this
patient in the non-responsive group.
• All cats that responded well to therapy
maintained normal thyroxin values for at least
1 year and up to 5 years. The average number
of years each patient was followed was 2 years
with the average frequency of administration of
1.875 doses/year.
• 1M potency was used in 1 cat where fluctuation
between a normal and a hyperthyroid state was
noted. This cat’s thyroxin values returned to
normal and the clinical signs also resolved.
1
Natrum Muriaticum 200 C – is a homeopathic
preparation of sodium chloride in a 200 C
potency obtained in homeopathic pharmacy
Helios, England
 Al
Study Data

Table 1:
Succesfully treated patients

Patient Age at the start Remedy Years in Thyroxin levels (nmol/l)

of testing doses since the study
beginning
of Tx

Hobbs 7 4 2.0 39 39 29 22 30 32 32
Calli 7 4 2.5 45 32 31 33 34
Q 12 2 1.5 50 38 22
Mina 9 6 5.0 41 36 42 36 30 30 30 44 32 48** 32
Sita 5 4 2.0 41 39 37 28
Harley 6 2 2.0 41 33 28 25
Emily 7 5 2.0 41 24 21 17
Beau 6 3 1.0 59 31

** 1 M potency was administered

Table 2:
Unsuccessfully treated patients

Patient Age at Sex Thyroxin Comments

the start levels (nmol/l)
of testing

Blackie 15 F 175 145*** Started on Methimazole

prior to first visit

Pumpkin 8 M 81 79*** Owner declined further

homeopathic treatment

Nefer 15 M 63*** Owner requested

tapazole immediately

LaRue 17 M 16 55*** 17 33 Sikc euthyroid,

renal insuficiency, 2006 World Congress WSAVA/FECAVA/CSAVA
euthanized later

Tia Maria 14 F 112 100 13 45*** 56 71 Sick euthyroid,

poor compliance,
methimazole

*** Methimazole started

125
Back to contents
Al
Conclusions
This retrospective clinical study demonstrates
that Natrum Muriaticum (homeopathic
preparation of sodium chloride) can be
successfully used in the treatment of feline
hyperthyroidism without the high cost and
undesirable side effects of conventional use
of Methimazole or radioactive Iodine 131. It
appears that early diagnosis and the age of cats
are important factors in successful treatment.
Comments
Despite the fact that Natrum Muriaticum has
proven to be effective, other homeopathic
2006 World Congress WSAVA/FECAVA/CSAVA
126
Back to contents
remedies may be needed in individual patients
to achieve curative results. It is important
to remember that proper use of homeopathic
remedies is absolutely essential and treatment
should only be performed by a veterinarian
who has deep knowledge of the principles
of classical homeopathy. I would like to
emphasize that there is a tremendous need for
open minded, objective and unbiased research
and cooperation in the field of veterinary
medicine, homeopathy, acupuncture,
physiotherapy and other modalities for the
sake of the health and wellbeing of the
patients - our animal friends.
 Al
Al - Controversies in Alternative Medicine
SUPPLEMENTARY, COMPLEMENTARY AND ALTERNATIVE
MEDICINE. A SCAM IN FLAGRANT VIOLATION OF VETERINARY
ETHICS AND SCIENCE
Johannes (Sjeng) T. Lumeij,
DVM, PhD, Diplomate
ECAMS
Associate Professor of Avian and
Exotic Animal Medicine
Division of Avian and Exotic Ani-
mal Medicine
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Universiteit Utrecht
Yalelaan 108
3584 CM Utrecht
The Netherlands
j.t.lumeij@vet.uu.nl

Treatment modalities for which there is scientific References

evidence, or at least plausibility, belong to veterinary
science. Supplementary, complementary and
alternative medicine could be better abbreviated
with the acronym SCAM, because of the absence
of plausibility or scientific evidence. Application
of SCAM in veterinary practice violates the code
of conduct for the veterinarian and the guidelines
from the Federation of Veterinarians in Europe.
Although some argue that any treatment performed
on animals should be performed by veterinarians
and veterinarians who apply alternative methods
should be trained in these methods, standards
of care have no meaning if the most important
prerequisite, evidence for effectiveness, is lacking.
These standards would lend unjustified support to
unproven claims and raise false expectations. When
the beacons for the veterinary profession such as
professional organizations, veterinary faculties,
and veterinary journals are failing with regard to
showing the correct way, veterinary practitioners
will be lured into the maelstrom of quackery.
Editorial. The end of homeopathy. Lancet 2005;
366: 690.
FVE’s Strategy 2006-2010. Improving the health
and welfare of animals and people. Brussels,
FVE, 2005. www.fve.org
Habacher G, Pittler MH, Ernst E. Effectiveness of
Acupuncture in Veterinary Medicine: Systematic
Review. J Vet Intern Med 2006; 20: 480–488.
Minutes of the General Assembly Meeting of the
FVE, Brussels, November 2005.
Ramey DW, Rollin BE. Complementary and
alternative veterinary medicine considered, Iowa
State Press, 2004
Shang A, Kuwiler-Müntener K, Nartey L, Jüni
P, Dörig S, Sterne JAC, Pewsner D. Egger M.
Are the clinical effects of homoeopathy placebo
effects? Comparative study of placebo-controlled
trials of homoeopathy and allopathy. Lancet
2006 World Congress WSAVA/FECAVA/CSAVA
2005; 366: 726-732.

127
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

BB
Behaviour
havi

Back to contents
 B
INVITED LECTURES - FULL PAPERS

B - Behaviour
STORMPHOBIA
Dr. Moisés Heiblum
Veterinary Hospital Universidad
Nacional Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
Private Practice in Small Animal
Behavior, Naucalpan, Mexico,
Mexico
moisesheiblum@yahoo.com

Key words: fear, storm, phobia, adaptive, stimuli
Fear could be part of a normal behavior and
can be adaptive. We have to determine if fear is
abnormal, inappropriate or maladaptive by the
context in which it occurs.
Phobia: is the term used to refer to fear responses
that are persistent over time, consistent in terms
of what causes the fear. Phobias are learned,
irrational and not adaptive.
Normal dogs may exhibit alerting responses and
may show mild anxiety if there is a severe storm
immediately around the house.
You can call a dog thunder phobic when
symptoms are disproportionately intense relative
to the stimuli and or when symptoms occur in
response to innocuous stimuli.
Severe storms are a real challenge because there
are multiple stimuli involved.
During a storm, animals show fear to various
stimuli: wind, rain, lightening, thunder, clouds,
luminosity variations, barometric pressure, etc.
which may result in serious injury to the dog and
significant damage to property. It also generates ill
feelings on the part of the owners, thus damaging
the human-animal relationship.
An important factor to consider is that an animal
with storm phobias is subjected to a high degree
of suffering, but most dogs if treated will get
better, even though they can relapse during severe
storms.
The purpose of this paper is to present an easy
description of the common clinical signs showed
by storm phobic dogs and the treatment methods
used at the behavior service of the VH UNAM

2006 World Congress WSAVA/FECAVA/CSAVA

129
Back to contents
B
B - Behaviour
ELIMINATION BEHAVIOUR PROBLEMS IN CATS: THE INTERPLAY
BETWEEN BEHAVIOURAL AND PHYSICAL CAUSES
Jaume Fatjó,DVM,
DipECVBM-CA
Unitat de Fisiologia Animal
Facultat de Veterinària
Universitat Autònoma de
Barcelona
08193 Bellaterra
Spain
jaume.fatjo@uab.es
Dr. Xavier Manteca DVM,
MSc, PhD, DipECVBM-CA
Unitat de Fisiologia Animal
Facultat de Veterinària
Universitat Autònoma de
Barcelona
08193 Bellaterra
Spain
Feline elimination problems can be ascribed
to three main diagnostic categories: medical
conditions, aversions to the litterbox and marking
behaviour (Beaver, 2003).
For many years, the relationship between
medical and non medical causes of housesoiling
in cats has been considered mutually exclusive.
According to that, in front of a consultation
involving inappropriate elimination the
veterinarian should initially perform a thorough
medical examination including at least a physical
examination, a laboratory workup, a urinalysis
and a faecal examination (Beaver, 2003). Only
after physical conditions have been ruled out, the
other two causes, litterbox related problems and
marking must be considered. Questions like the
location and volume of urine spots, the animal’s
2006 World Congress WSAVA/FECAVA/CSAVA
body posture while eliminating and the social
and physical environment of the cat can help to
differentiate between marking behaviour and
problems related to the use of the litterbox.
However, as it has occurred with other clinical
problems in the field of veterinary behavioural
medicine, like canine aggression, medical
conditions and behavioural conditions responsible
for a problem of inappropriate elimination may to
some extent overlap.
For instance, a medical problem causing tenesmus
could create a litterbox aversion, since the cat
links the painful defecation with that particular
place. Once established, the reluctance to use
the litterbox could remain long after the medical
condition has been addressed.
An even more interesting example of the interplay
130
Back to contents
Dr. Marta Amat
Unitat de Fisiologia Animal
Facultat de Veterinària
Universitat Autònoma de Barcelona
08193 Bellaterra
Spain
between medical and non-medical causes of
inappropriate elimination can be found in some
cases of Non-obstructive Feline Lower Urinary
Tract Disease (FLUTD). The term FLUTD
refers to a very variable combination of physical
symptoms, like hematuria and pollakiuria.
However, in many cases none of these signs can
be detected by regular diagnostic techniques and
the condition is considered idiopathic (Gunn-
Moore & Cameron, 2004). Thus, the only clinical
sign that is consistently observed in these cases
is periuria (urination outside the litterbox). In
fact, in more than two thirds of cases involving
periuria no physical abnormalities can be detected
(Westropp et al, 2005).
Interestingly, around 50% of feline elimination
cases referred to small animal veterinary
behaviourists have antecedents of FLUTD
(Overall, 1997; Horwitz, 2002; Beaver, 2003).
Today, Feline Idiopathic Cystitis is understood as a
mixed medical and behavioural condition, resulting
of the interplay between many different causes,
from breed predisposition to diet composition and
the effect of social and physical environmental
stress (Westropp et al, 2005). Consequently, the
treatment protocol for this problem includes
strategies as diverse as increasing the cat’s daily
water intake, administering antianxiety/analgesic
medication, performing some environmental
enrichment and using feline facial synthetic
pheromones (Westropp et al, 2005; Gunn-Moore
& Cameron, 2004).
The main purpose of this presentation will be
to discuss the diagnostic and treatment protocol

of cases of feline housesoiling, with a special
emphasis in problems of inappropriate urination.
References
Beaver B (2003) Feline Eliminative Behavior. In:
Feline Behavior: A Guide for Veterinarians (2nd
Ed). WB Saunders, St. Louis, pp 247-273.
Gunn-Moore DA, Cameron ME (2004) A pilot
study using synthetic feline facial pheromone
for the management of feline idiopathic cystitis.
Journal of Feline Medicine & Surgery, Vol 6 (3),
pp 133-138.
Back to contents
B
Horwitz D (2002) House soiling by cats. In:
BSAVA Manual of Canine and Feline Behavioural
Medicine. Horwitz D, Mills D, Heath S (eds).
Gloucester: BSAVA, 97-108.
Westropp JL, Buffington T, Chew D (2005)
Feline Lower Urinary Tract Diseases. In: Ettinger
& Feldman (Ed) Textbook of Veterinary Internal
Medicine (6th Ed).
WB Saunders, Philadelphia, pp 1828-1850.
Overall K (1997) Feline elimination disorders. In:
Clinical Behavioral Medicine for Small Animals.
St. Louis: Mosby-Year Book, 160-194.
2006 World Congress WSAVA/FECAVA/CSAVA
131
B
B - Behaviour
UNDERSTANDING HOW DOGS LEARN: IMPORTANCE IN
TRAINING AND BEHAVIOR MODIFICATION
Karen L. Overall, MA,VMD,
PhD
Diplomate ACVB
ABS Certified Applied Animal
Behaviorist
Center for Neurobiology and
Behavior
Psychiatry Department - Penn
Med Translation Research
Laboratory, 125 S. 30th St.
Philadelphia, PA 19104
overallk@mail.med.upenn.edu
http://psych.ucsf.edu/
K9Behavioral/Genetics/
Introduction
Behavior modification is nothing more than the
process of altering an animal’s behavior. This
discussion addresses how learning affects the
overall phenotype, how the effects of the gross
environment interact with the phenotypes, and
how environmental effects at all mechanistic
levels contribute to secondary changes in the
phenotype.
The classic client and veterinarian response to
having “behavior mod” recommended as part of
a treatment plan is to exclaim that they “don’t
have time for that”. What is not understood here
is that we engage in behavior modification either
actively or passively every hour of the day and in
everything we do. The basic tenets of behavior
modification treatment are not complex, and are
put into action whether or not we consciously
acknowledge or recognize that this is so.
Accordingly, clients are often unconsciously and
accidentally employing principles associated with
2006 World Congress WSAVA/FECAVA/CSAVA
learning and behavior mod, and inadvertently
doing an excellent job of reinforcing the behaviors
about which they are most distressed!! Our focus
should be to help clients understand that learning
occurs all the time and that we can shape the
direction, rate, and complexity of the learning
process with conscious effort. This does not
mean that the clients ‘must’ engage in complex
active behavior mod. It does mean that they can
use small, relatively passive techniques to effect
huge changes.
The problem with changing any behavior is
2 fold: (1) inertia is a powerful force, and (2)
breaking behaviors down into elements that
require change and understanding how to change
them can be difficult to do. This difficulty lies in
understanding exactly what is called for in the
behavior modification technique of choice and
132
Back to contents
in the timing of the client’s response to the dog’s
behavior and communicatory gestures. Before
any client can change any animal’s behavior - or
their own - they MUST recognize (1) what normal
signaling is, (2) what signals are associated with
the problem they wish to change, and (3) what
signals precede #2. Two examples will help make
this clear.
Human example
Eating is a normal mammalian behavior.
Propensity to gain weight is an adaptive strategy
dating to human prehistory; weight gain acted as a
safe-guard to get humans through times of severe
resource restriction. In fact, although the hormone
leptin regulates fat, it actually acts to maintain
some level of function in fat cells. Overeating -
when out-of-context to the resource environment
- leads to obesity. If people want to lose weight
they have to change their behavior. Accordingly,
by recognizing when their behaviors have stepped
over the line from normal, contextual eating
in response to hunger and future expectations
of resource environments to out-of-context
overeating, people have satisfied conditions 1
and 2 above. If they wish to intervene to stop the
cycle they need to recognize the behaviors that
precede condition 2. If the condition that precedes
a trip to the refrigerator is a TV commercial about
food, the obvious answer is - in the context of
risk assessment where full information is not
available - to back away from the television set as
soon as any commercial begins. If it’s the act of
watching TV and anticipating the commercial and
food breaks that is associated with over-eating,
removing the TV from the equation can help.
Canine example
Barking is a normal canine behavior, but not

all barking is the same. Alerting barks have an
increasing tone and occasionally elements of a
howl. Barks signaling distress are often sharp,
high-pitched, repetitive, and relatively atonal. If
a dog is affected with separation anxiety and the
non-specific sign associated with the condition is
barking, the client must recognize how their dog’s
bark deviates from ‘normal’. In this example we
have satisfied conditions 1 and 2, above. If the
client wishes to intervene to change the behavior
that results in the barking, it is best to intervene
before the bark. This means that they have to
recognize behaviors that signal the target non-
specific sign is likely to occur......this is a form
of risk assessment and if clients understand
behavior mod in these terms they will find it very
easy to intervene at the appropriate time. In this
example, the dog starts to pace and pant while
the client is still at home, and the barking only
occurs once they have left. Accordingly, the best
time to intervene to alter the barking, is when
the dog begins to pace and pant, satisfying the
3rd condition, above. If the client is serious about
ablating all anxiety, they have to intervene in the
behaviors that precede the panting and pacing.
If these behaviors are also preceded by other
anxious behaviors, the client must intervene in the
behaviors that precede those anxious behaviors,
and so on. This is the behavior modification
version of ‘it’s turtles all the way down’.
These are the patterns clients have to recognize
to appropriately intervene in order to accomplish
‘behavior mod’.
In the examples and discussion above the
clients are to ‘intervene’, but intervention is
deliberately left undefined. In any situation there
are three environments available for intervention
which can be potentially modified: the physical
environment, the behavioral environment,
and the pharmacological environment. These
environments are not independent. The key to
understanding how dogs learn is to appreciate
the complexity of interaction between these
environments, and the importance of factors
affecting temporal and intensity changes and
interactions within these environments.
Basic concepts pertaining to environmental
effects at the gross or systems level
The physical environment includes perceived and
actual space considerations, any visual, olfactory,
or auditory stimuli, other animals, relevant objects
such as litter boxes, and any devices that might
change an animal’s perception, such as gauze
curtains, fences, or the presence of background
music.
While other animate objects may be part of the
physical environment, they may potentially also
Back to contents
B
interact within the behavioral environment. This
is not requisite and certainly the mere presence
of a dog that can be seen through a window
may be sufficient stimulus for an inappropriate
behavior although that dog may never be an
active participant in any behavioral interaction.
Conversely, because of the neurochemical
changes that may be induced, the olfactory cues
in the physical environment may directly or
indirectly alter the behavioral environment.
Because perception is so critical in the evaluation
of the physical environment it must be remembered
that this includes the time environment or the
schedules of the clients. Some problems, like
separation anxiety in dogs, may develop when the
only environmental change is one of time: day
length shortens or the clients schedules change.
Part of any treatment plan must address this
environmental change. The physical environment
may be modified because it is a direct part of
the problem, for example, insufficient space
for exercise, or because changing the physical
environment can help solve the problem, for
example by providing dog houses to give each
dog personal space in an unshared rain shelter.
The behavioral environment focuses on behavior
modification, rather than on the alteration of the
perceptual or tangible environmental component.
The behavioral environment includes the
individual and the social environment of anyone
(human or animal) with whom the individual
might interact. If there is another social group with
whom the individual doesn’t interact, but whose
social interaction affects the individual (i.e.: a
group of cats whose play affects the resident dog,
but who don’t interact with him directly), this is
also a component of the behavioral environment.
In the example just used, if the dog barks every
time the cats roughhouse, part of the treatment
may be to teach the cats to play elsewhere or to
not play in so rough a manner.
The third environment that can be modified may,
2006 World Congress WSAVA/FECAVA/CSAVA
in fact, be the most subtle one: the pharmacologic
environment. The pharmacologic environment
has two components: the endogenous environment
and the exogenous environment. We used to think
that these could be nicely separated. Given what
we now know about how drugs work to affect
memory at the cellular and molecular level, and
given the role of anti-anxiety medication on
indirectly affecting corticosteroids.......caution is
urged in blind faith acceptance of any simplistic
paradigm.
The endogenous or internal pharmacological
environment is influenced by sex hormones and
other physiological parameters. Effects can be the
result of neutering, in the case of sex hormones,
and disease, in the case of most physiological
133
B
parameters (including those associated with
gonads). It’s important that we acknowledge the
role of either primary or secondary physical illness
because there is a tendency to forget that an animal’s
behavior can change with physiological changes
attendant with aging or illness. Endogenous
changes in pharmacological environments affect
the manner in which the animal interacts in the
behavioral and physical environments. Because
the exogenous pharmacological environment
includes pharmacological intervention (drug
therapy), we have further effects on learning,
metabolism of brain chemistry, and re-regulation
of physiological pathways involved in stress and
distress.
When we castrate a dog we remove most of the
circulating testosterone (castration results in an
androgen drop within 6 hours; the bulk of the
hormonal decrease is complete in 72 hours);
however, this, alone, is unlike to wholly ‘fix’ any
true behavior problems. Testosterone, like most
androgens, acts as a behavioral modulator that
may facilitate the attainment and escalation of the
aggressive state. If a dog is already aggressive,
the difference between it in the neutered and
un-neutered form will be one of degree. The
intact dog will react more easily, escalate more
quickly and plateau at a higher level of aggressive
intensity, will become less reactive more slowly,
and may even remain poised for the next bout
more easily since they main return to a higher
state of vigilance post-aggressive event than at
which they started prior to the aggressive event.
Other dimorphic behaviors associated with the
presence of testosterone include urine marking
with lifted leg, roaming, and some types of
mounting. Castration results in a 90% decrease
in roaming in male dogs that roamed prior
to castration, a 75% reduction in male-male
aggression, a minimal 60% in urine marking,
and an 80% reduction in mounting (Hart 1974;
2006 World Congress WSAVA/FECAVA/CSAVA
Hopkins et al., 1976). Marking, mounting, and,
to a lesser extent because of the modulator effect
discussed above, fighting, are complex behaviors
not wholly controlled by only hormones. There
is a huge learning component to these behaviors
that people neglect to acknowledge. If marking
has been ongoing for some time, castration, alone,
will not ablate it, but may decrease it. The part of
the behavior that is a learned response remains in
the absence of deliberation modification to alter
it. The same logic holds for mounting.
Less attention has been paid to the role of female
sex hormones and aggressive behavior. There
may be a role for female hormones, but it appears
to be less direct than for male hormone. Female
puppies that were already showing aggressive
tendencies at the time of spaying may be rendered
134
Back to contents
worse by the procedure (O’Farrell and Peachey,
1990). This may be either a direct effect of in
utero androgenization or an indirect effect of
decreased feminization effects due to a lack of
female hormones (Overall, 1995). Female dogs
affected by impulse control aggression appear
phenotypically and neurochemically different
from males, and tend to have an age on onset that
is statistically significantly younger than do male
dogs diagnoses with the same condition (Overall,
et al., unpublished).
As a final cautionary word about over-emphasis
of the endogenous pharmacological environment
in the etiology and causality of behavioral
problems it is important to note that most
aggression is a social, not a hormonal, condition.
Certainly hormones can act as modulators.
Accordingly, work continues on the effects of
thyroid hormones, and those associated with
the hypothalamic-pituitary-adrenal axis. Expect
elegant complexity.
Still, it’s important to remember that none of
the three environments mentioned above is
independent: they all interact. A perturbation in
one environment can cause a shift in another.
Furthermore, all of these environments have
system and cellular / molecular effects which,
in turn, interact. This is difficult to understand
because it’s complex, and because of that
complexity we actually know very little about
how any part of the system really works.
Principles of Behavior Modification
Behavior modification utilizes six main learning
tactics or paradigms: habituation, extinction,
desensitization, counter-conditioning, flooding,
and avoidance/aversive conditioning. Within
this structure, 3 other concepts are important:
learning, overlearning, and reinforcement.
Before discussing the 6 main tactics, we need to
understand what is meant by learning. Learning is
generally defined as the acquisition of information
or behavior through exposure and repetition. At
the cellular and molecular level learning is defined
as cellular and receptor changes that are result of
stimulation of neurons and the manufacture of
new proteins. It is these new proteins / receptors,
that then change the way the cell responds when
next stimulated. It’s important to remember that
no cell / neuron acts on its own: region of the
brain, neurochemical tract, and interactions with
other cells are critical for determining response.
Overlearning is a technique often used by
performers and athletes when the specific
behavior desired is obtained through such
consistent practice (read, repeated stimulation
of the same cells in the same pathways) that the
response becomes almost automatic or a ‘gestalt’,

requiring little conscious thought (read, encoded
genetically through new protein receptors). We
need to remember that we can overlearn good
behaviors, but that undesirable behaviors can
also be perfectly elicited via overlearning (eg,
the dog jumps up on you whenever he sees you
because you pet him - the entire sequence of
alerting, moving, and elevating is now a flawless,
unconscious response).
Reinforcement is also key if we are to
successfully employ the basic tactics of behavior
modification. Reinforcement can either be
positive, encouraging repetition of the behavior,
or negative, discouraging the repetition of the
behavior. Negative reinforcement discourages
the behavior because the animal is rewarded
with a more favorable experience not just when
they cease the undesirable behavior, but as a
result of ceasing it. It’s important to realize that
negative reinforcement is completely different
from punishment where no reward structure is in
place.
These distinctions and definition are particularly
important when we consider learning at the
cellular and molecular level because LTP can
take place in different regions. Fear primarily
involves the amygdala, whereas various ‘reward’
systems involve parts of the cortex, the substantia
nigra, and miscellaneous parts of the ‘limbic
system’. In addition to regional activity, postitive
reinforcement, negative reinforcement, and
punishment primarily use different neurochemical
tracts or way-stations. Positive reinforcement uses
opiate and dopaminergic systems, punishment
involves the flight, freeze, or fight pathways of
the norepinephrinergic sympathetic systems,
and negative reinforcement likely involves some
complex association of both of these, plus the
serotonergic system. It’s important to acknowledge
that these neuroanatomical and neurochemical
associations are understood poorly, at best, and
that generalizations about them are painted in the
broadest possible strokes.
Definitions of behavior modification tactics
1. Habituation is the normal attenuation of a
response to something novel in the environment
that is attendant with an increase in intensity
or frequency of exposure to the stimulus in
circumstances where nothing horrendous happens.
For example, a doorbell may startle a new puppy,
but as she hears it more frequently in a benign
context she may habituate to it (if inappropriately
reinforced, she may not habituate to it....instead
she may develop a learned response that gets her
attention). People who move from the city to the
country habituate to bird songs and insect calls.
2. Extinction is the process by which normal or
Back to contents
B
conditioned responses are decreased or attenuated
by exposure to a stimulus that elicits the response
in the absence of the reward. The new puppy that
barks at the doorbell may get inappropriately
reinforced by well-meaning clients who pick her
up and reassure her. They are actually, and usually
unintentionally, rewarding her for barking, so she
continues to bark when the doorbell rings. This is
now a conditioned response. If they consistently
ignore her they will extinguish the response (if
the sound of her own bark has not become self-
reinforcing). Caution is urged since resistance to
extinction is a very common phenomenon and
occurs with very little reinforcement. The classic
introductory psychology course story about this
usually involves an elevator that is broken more
often than not. Still, because it operates 1/10 or
1/20 times, most people walk into the lobby and
push the button on the off chance that the elevator
is working. The higher the destination floor,
the more likely people are to push the button
because the ‘reward’ is greater, albeit rare. The
people in this example are exhibiting resistance
to extinction due to an intermittent reinforcement
schedule.
3. Desensitization is a decrement in response that
is produced by gradual exposure to a stimulus
that elicits the response. If the puppy used
above has become fearful of or stimulated by
the doorbell, her bark, or the events occurring
around the ringing of the doorbell, using a tape
recording or the doorbell could help her stop the
undesired response. If the tape is played very
softly at first so that she doesn’t react and then
only gradually increased in volume at increments
designed to elicit no response, she may be become
desensitized to the doorbell.
4. In counter-conditioning, negative or undesirable
behavior is extinguished or controlled by teaching
the animal to do another behavior (preferably
favorable and fun) that competitively interferes
with the execution of the undesirable behavior.
2006 World Congress WSAVA/FECAVA/CSAVA
This is best coupled with desensitization. Again,
using the puppy above, she will learn faster if
she is first taught to sit and stay and relax (the
key here) in exchange for a treat. She must be
absolutely quiet and calm, and convey by the
look in her eyes, her body posture, and her facial
expressions that she would do anything for her
client. Calm and lack of anxiety and calmness
are helpful because we know that hormones
associated with stress and anxiety - corticosteroids
- impede the ability to learn complex associations
(Yau et al., 2002). This is key to understanding
newer approaches (Overall, 1997) to behavior
modifcation.
Once the puppy can do relax and attend to her
person for exercises lasting a half hour or so,
135
B
true desensitization begins: the tape recording is
gradually increased in volume, always at a level
below that which provokes anything but a transient
response in the dog. Performing the adoration
act for a food salary (counter-conditioning) is
incompatible with or competitively exclusive of
barking. If at any point the puppy starts to act
anxious or to not attend to her client, the tape
recording should be lowered in volume until
she can relax again. This is the key here - the
sitting and staying is merely a facilitator for the
relaxation response. There is no sense to having
the dog sit and stay if it is panting, salivating, its
pupils are dilated, its ears are back, and it is clearly
distressed. What on earth is the dog learning? It’s
simple - the dog is learning to be more distressed
and also teaching his- or herself to become
refractory to complex learning because of arousal
of the HPA-axis (hypothalamic-pituitary-adrenal
axis). This is why simple ‘sit-stay’ programs
(Voith, 1982) so often fail: the dog sits, but is still
distressed.
The gestalt of relaxation is the first step to
changing the behavior. Counter-conditioning
coupled with desensitization is an extremely
time consuming technique. It means that one
must constantly go back and repeat the exercises
where there was a lesser response until there is
none, and it means that one must attend to all the
patient’s communicatory signals. It is hard work,
but it does work. Clients who are least successful
with this technique want both quicker fixes and
less work. Disabuse them of the possibility of
either at the outset. Clients also want their dogs
to be “quick”, “fast learners”, “A+ students”,
“achievers”. These are all words that I have heard
clients use as they whip through the counter-
conditioning and desensitization exercises so
quickly as to provoke anxiety in the dog. Such
client behavior and needinees sabotages the
program.
2006 World Congress WSAVA/FECAVA/CSAVA
Problem dogs have special needs. These needs
do not reflect on the intelligence of the dog, nor
on the abilities of the clients. These dogs can
eventually be A+ students, but they will have to
take a longer, harder path, and although the client
did not cause the dog’s behavioral problems, they
are constrained to accompany the dog on that path
if the dog is to get better. That said, the clients
should be able to give themselves permission to
break any behavior mod program into 5 minute
blocks, that they can practice when they can find
the time. If clients feel they can succeed, they will
at least try. If the instructions are ones that the
client cannot integrate with their lifestyle, they
will not try, or they will fail. Most of us can find
5 minutes multiple times a day, but we’d have
trouble finding an uncommitted ½ hour.
136
Back to contents
5. Flooding involves prolonged exposure at a
level that provokes the response so that the animal
eventually gives up. This exactly the opposite of
the approach taken in desensitization. It is far
more stressful than any of the other therapy
strategies and, used inappropriately - which
it usually is - could damage the animal. If
nothing else works for the puppy, flooding would
involve enclosing her in a small space (a crate
or small room) and constantly playing a tape of
a doorbell louder than it is until she ceases to
bark. She cannot be disturbed until this happens
and that could take a while. Caution is urged: if
the dog’s anxiety level continues to worsen you
are at risk of creating a tremulous, fearful,
or likely panicked dog. In most cases - except
those involving minor fears where physiological
and behavioral responses can be easily monitored
- flooding is a last resort and should always be
executed as humanely as possible. Furthermore,
no client should try this without discussing the
technique and it’s applicability to the situation
with someone who understands learning.
6. Avoidance or aversive conditioning [eg,
punishment] involves the presentation of an
aversive stimulus in response to an inappropriate
or undesirable behavior; the stimulus is intended to
abort the behavior and to decrease the probability
of it occurring in the future. This is the correct
definition of punishment. To be most successful
the stimulus designed to abort the behavior must
occur as early as possible but certainly within the
first 30-60 seconds of the onset of the behavioral
sequence (within tenths of a second of the
exhibition of the actual undesirable behavior) and
must be consistent and appropriate.
The critical factors in punishment include:
1. timing;
2. consistency,
3. appropriate intensity, and
4. the presence of a conditioned response.
Point 4, the presence of a conditioned response,
means that when the undesirable behavior ceases
there has to be some favorable stimulus or reward
that the dog gets even it is just praise or a pat.
This is the single most frequently ignored part
of treatment for pets with behavioral problems:
when these pet are not causing trouble almost no
one tells them how good they are. Instead, when
they are quiet, the clients ignore them, possibly
because they welcome this fragment of serenity
so greatly. Unfortunately, this is also where the
most ground is lost. If the pup is sleeping, you
don’t have to jump up and down and arouse him
to reward him. Rewards can be calm, quiet, and
passive. Instead when the puppy is sleeping,
gently and s-l-o-w-l-y say, in a low, calm,

soothing tone, ‘what a g-o-o-d boy’. If the client
MUST touch the dog, they must do so by pressing
with long, slow, firm, strokes. No one should pet
or agitate the dog when the dog is quiet, if ‘quiet’
is the response they hope to reinforce.
To reiterate, it is important to emphasize to
clients that - if it is to work - punishment must
be as closely coupled with the inappropriate
event as possible, must startle - without terrifying
- the animal to the point where they just abort
the behavior, must be appropriate in duration
and intensity (it is never appropriate to beat a
dog senseless, yet people tend to continue all
forms of punishment way after the abortion of
the event has occurred), and that all of this must
occur in a consistent manner that incorporated
aborting the inappropriate behavior every time
the undesirable behavior occurs. The latter is
the reason why dogs often appear ‘resistant’ to
learning to stay off the furniture: no one yells at
them when they sleep if they are home alone. The
sofa dog is experiencing an intermittent reward
schedule. The best way to maintain a behavior is
to use an intermittent reward schedule. This dog
has learned that she can sometimes sleep on the
sofa - all we are negotiating is the definition of
‘sometimes’.
Aversive conditioning may be best used early
in the development of the undesirable behavior.
Early warning signs of most aggressions
are recognizable if the client learns for what
to look. As emphasized above, in order for
punishment to succeed it has to occur preferably
in one second, but generally within the first 30-
60 seconds, of the onset of the inappropriate
behavioral sequence.............hidden in this phrase
is the truism that if the client learns to recognize
precursor behaviors, they will have far more
success in intervening at the appropriate time
and ‘correcting’ the undesirable behavior. The
punishment should preferably startle the animal
sufficiently only to interrupt the behavior and
abort any attempt at immediate resumption.
The pup can then be taught a more appropriate
behavior, such as sitting and staying. Sitting
here serves as a ‘time out’ for both handler
and pup, while employing a behavior that both
species recognize as a deferential one (sitting).
Done correctly, the pup learns that the human is
reliable and trustworthy and that he or she can
take all cues as to the appropriateness of his or
her behavior from the client. This is a key point,
because at the crux of behavioral problems is the
fact that these dogs are abnormal; therefore, they
are incapable of making appropriate, in-context
distinctions. These dogs exhibit inappropriate,
out-of-context behavior. Early intervention must
be aimed at getting the dog to trust the client
Back to contents
B
(excellent voice ‘control’) and teaching him or
her to make better context distinctions by taking
cues about the appropriateness of the behavior
from the client.
Finally, the best success with any aversive
paradigm is obtained if, as soon as the animal
stops the undersirable beahvior they are given
a clear cue about what is expected and what the
reward will be. If people cannot or will not do
the entire sequence appropriately, they have
absolutely no business using any form of
punishment. Really, what they are doing in the
absence of full follow- through is abuse.
People usually resort to physical punishment
as the correction method of choice when what
they have tried fails, or because this is how they,
themselves, were raised and no one taught them
differently. If clients cannot or do not believe
that they can learn to change, there is no hope for
the dog’s behaviors to change. Conversely, by
learning to treat a dog more humanely thank you,
yourself, were treated, you can become a better
person.
Notice that no where is it written that
punishment must be physical. Furthermore,
doing punishment well is just as hard work as is
appropriately executed counter-conditioning and
desensitization. Punishment is never an easy out
and has a high probability of backfiring unless the
client understands that its focus is to decrease the
probability of future inappropriate events.
Reward Structures
It’s important to understand reward structures and
what these mean at the cellular and molecular
level for behavior modification. Behaviors are
reinforced or learned best if every time they occur
they are rewarded. At the cellular level, repeated
reinforcement insures better, more numerous,
and more efficient connections between neurons
(Carter et al., 2002; Wittenberg and Tsien, 2002).
Stimulation is induced when a neurochemical
2006 World Congress WSAVA/FECAVA/CSAVA
in a synapse triggers a receptor to engage it.
This stimulation of the receptor engages second
messenger systems in the post-synaptic cell,
usually cAMP. The result is cellular memory or
long-term potentiation (LTP). By itself, this initial
process represents E-LTP or ‘early phase LTP’ and
STM (short-term memory). The process is short-
lasting, RNA and protein-systhesis-independent,
and the result does not persist or become self-
potentiating unless the stimulus is consolidated
into L-LTP ‘late phase LTP’, which is a more
permanent form (Schafe et al., 2001). E-LTP can
be induced by a single train of stimuli in either
the hippocampus or the lateral amygdala.
In contrast, L-LTP and LTM (long-term memory)
requires repeated stimulation of cAMP, induction
137
B
of cAMP response element binding protein
(CREB - a nuclear transcription factor), and is
long-lasting, protein synthesis dependent, and
is RNA transcription dependent ( Schafe et al.,
2001). When stimulation continues, BDNF
enhances neurotransmission and potentiates what
is called activity-dependent plasticity at synapses
(eg, learning), particularly in the region of the
brain most involved in learning, the hippocampus.
This effect can also occur in the lateral amygdala
and is one modality postulated to be involved in
learned or conditioned contextual fear (Schafe et
al., 2001).
This neurobiology is important to consider in
the context of reward systems. It explains why
continuous reward works best in acquiring a
behavior (E-LTP and STM) and why intermittent
reward acts best to maintain a learned behavior
(L-LTP and LTM). This neurobiology explains
why a really excellent reward (jackpot) can help
you learn or reinforce a behavior quickly and
why a really horrible experience can stimulate the
amygdala to encode learned panic or phobia
molecular - consider neuromolecular biology of
these (inability to escape from flooding). The
amygdala, itself, is an incredibly complex few
mm3. Almost all outgoing tracts that control
some higher forms of integration of behavior in
the cerebral cortex, hypothalamus, brain stem et
cetera have their efferents shaped by the location
of their origin in the amygdala (Davis, 1997).
Additionally, the lateral amygdala is likely the
site where memories of conditioned (learned)
fear are created through a process involving
neuronal plasticity (Schafe et al., 2001). In fact,
if one lesions or inactivates the lateral amygdala,
it is impossible to either acquire a fear or to
express a previously acquired fear (LeDoux et
al., 1990).
When one considers rewards - or aversive
stimuli - which best induce these quick learning
2006 World Congress WSAVA/FECAVA/CSAVA
experiences, it is important to consider them in
terms of their evolutionary value. Evolutionarily
tightly coupled rewards - ones that selection
has shaped to be of particularly high value - are
those directly coupled to survival: food, freedom,
elimination, mating. Evolutionarily less tightly
coupled rewards - ones on which survival should
not hinge - will be of lesser value: praise, play.
When one considers the molecular biology of
learning within the evolutionary context of very
pleasurable or very fearful stimuli, it should be
clear how behaviors can best be modified.
So what does this mean for very early learning
- before there are problems (eg, ‘socialization’)?
Pups who stay with breeders for extended periods
of time (3-4 months of age) without exposure to
138
Back to contents
novel circumstances and individuals, may never
respond appropriately to them. If these pups
are exposed to many people, dogs, and new
experiences, even if they stay with the breeder
for an extended period, the benefit of exposure
should generalize to strangers and changing
environments. This is probably some of the logic
for taking puppies crated to dog shows. The
problematic situation associated with lack of
exposure appears to be more common in kenneled
pups. When adopted these pups may exhibit fear
of all new, non-kennel environments. This fear
can be so crippling that these dogs are unable to
go in and out of the house or walk on the street.
With behavior modification and pharmacological
intervention these dogs can improve, but are
probably never normal. Pups who are kept in
kennels beyond 14 weeks of age are likely to
never be normal, and will exhibit timidity and
a lack of confidence (Pfaffenberger and Scott,
1959). Accordingly, pups who are brought home
at 8 weeks of age and kept inside with one or a
few humans, may also find it difficult to make the
transition to other environments.
It is clear from the above that the best time to
recommend that a client adopt a pup is about
8.5 weeks of age. At this time pups are ready
to be house-trained - this is the first time they
can cognitively make the connections important
for substrate preferences and stimulation for
elimination and, concurrently, volitionally inhibit
elimination - and are optimally poised to benefit
from exposure to all ‘socialization’ environments.
There are two caveats to this rule of thumb.
Later age is acceptable if the dog is going to be
exposed to lots of different people, instead of
just one person, at the breeder’s. Furthermore, if
house-training is important to the future client,
the breeder should start this process if the pup
remains with them. The preceding discussion
about LTP should make it clear why it is also so
hard to ‘unlearn’ something. Getting it right at the
beginning is most helpful. Remember that pups
learn from novel experiences at this age, so the
adoption process should not be scary, painful,
or associated with horrific circumstances such
as traumatic shipping, mutilation, tattooing, or
punishment (think - LTP in the lateral amygdala.....
and now you have ‘encoded’ fear!). Although
observance and understanding of the appropriate
periods is no guarantee that future problems will
not develop, the client will be able to minimize
the risk that future problems are due to lack of
exposure during these periods.
It is important to appreciate that some of the effects
of developmental/sensitive periods (Bateson,
1979) may be mitigated by the personality of
the individual puppy - not to mention the breed

- and by the intensity of attention that the animal
receives. The extent to which mitigation of the
effects of lack of exposure in early life is possible
is unclear. Certainly, the one situation where
people have definitely caused the aggressive
problem result not from lack of exposure, but
from inappropriate exposure: abuse. Dogs that are
abused may become fearful, fearfully aggressive,
or outright aggressive. Which path is taken may
have less to do with the form of the abuse than
with the underlying personality of the dog. Gene
x environment interactions are well understood
only for rigidly controlled, experimental
situations. This does not describes dogs.
Exogenous pharmcological environments
(drugs): Roles for neuronal stimulation, synaptic
plasticity, and receptor protein transcription and
translation
The best drugs to help treat behavioral conditions
are the tricyclic antidepressants (TCAs) and the
selective serotonin re-uptake inhibitors (SSRIs).
These 2 classes of drugs and their descendants
have made the use of broad-acting compounds
like progestins, tranquillizers, sedatives, and
anti-convulsants, at best, anachronistic. What
makes TCAs and SSRIs special and why
are they so useful for anxiety disorders? The
key to the success of these drugs is that they
utilize the same second messenger systems and
transcription pathways that are used to develop
cellular memory or to “learn” something. This
pathway involves cAMP, cytosolic response
element binding protein (CREB), brain derived
neurotrophic factor (BDNF), NMDA receptors,
protein tyrosine kinases (PTK) - particularly Src
- which regulate activity of NMDA receptors and
other ion channels and mediates the induction of
LTP (long-term potentiation = synaptic plasticity)
in the CA1 region of the hippocampus (Daniel et
al., 1998; Salter, 1998; Trotti et al., 1998).
There are two phases of TCA and SSRI
treatment
Short-term effects and long-term effects. Short-
term effects result in a synaptic increase of the
relevant monoamine associated with re-uptake
inhibition. The somatodendric autoreceptor of the
pre-synaptic neuron decreases the firing rate of
that cell as a thermostatic response. Regardless,
there is increased saturation of the post-synaptic
receptors resulting in stimulation of the -
adrenergic coupled cAMP system. cAMP leads
to an increase in PTK as the first step in the long-
term effects. PTK translocates into the nucleus of
the post-synaptic cell where it increases CREB,
which has been postulated to be the post-receptor
target for these drugs. Increases in CREB lead
Back to contents
B
to increases in BDNF and tyrosine kinases (e.g.,
trkB) which then stimulate mRNA transcription of
new receptor proteins. The altered conformation
of the post-synaptic receptors renders serotonin
stimulation and signal transduction more efficient
(Duman, 1998; Duman et al., 1997).
This should sound an awful lot like how learning
occurs at the molecular level through LTP -
because it is. Simply, TCAs and SSRIs work so
well because they stimulate the neurochemicals
involved in anxiety-related pathways, and
because the augment the rate at which learning
occurs because of the parallel effect on pathways
and mechanisms involved in learning.
Knowledge of the molecular basis for the action
of these drugs can aid in choosing treatment
protocols. For example, the pre-synaptic
somatodendritic autoreceptor is blocked by
pindolol (a -adrenoreceptor antagonist) so
augmentation of TCA and SSRI treatment with
pindolol can accelerate treatment onset. Long-
term treatment, particularly with the more specific
TCAs (e.g., clomipramine) and SSRIs, employs
the same pathway used in LTP to alter reception
function and structure through transcriptional
and translational alterations in receptor protein.
This can be thought of as a form of in vivo “gene
therapy” that works to augment neurotransmitter
levels and production thereby making the
neuron and the interactions between neurons
more coordinated and efficient. In some patients
short-term treatment appears to be sufficient to
produce continued “normal” functioning of the
neurotransmitter system. That there are some
patients who require life-long treatment suggests
that the effect of the drugs is reversible in some
patients, further illustrating the underlying
heterogeneity of the patient population considered
to have the same diagnosis.
Monitoring
Monitoring of side-effects is critical for any
2006 World Congress WSAVA/FECAVA/CSAVA
practitioner dispensing behavioural medication.
The first tier of this involves the same tests
mandated in the pre-medication physical and
laboratory evaluation. Age-related changes in
hepatic mass, function, blood flow, plasma drug
binding, et cetera cause a decrease in clearance
of some TCAs, so it is prudent to monitor hepatic
and renal enzymes annually in younger animals,
biannually in older, and always as warranted by
clinical signs. Adjustment in drug dosages may
be necessary with age.
It is preferable to withdraw most patients from one
class of drug before starting another. For changing
between SSRIs and MAOIs the recommended
drug-free time in humans and dogs is two weeks
(2 + half-lives: the general rule of thumb for
139
B
withdrawal of any drug). SSRIs can be added to
TCAs and may then exhibit a faster onset of action
than when they are given alone. This is due to the
shared molecular effects on second messenger
systems of both TCAs and SSRIs. Combination
treatment allows the clinician to use the lower
end of the dosage for both compounds which
minimizes side effects while maximizing efficacy.
Furthermore, benzodiazepines can be used to
blunt or prevent acute anxiety-related outbursts
on an as needed basis in patients for whom daily
treatment with a TCA or an SSRI is ongoing.
Together, the combination of benzodiazepines
and TCAs / SSRIs may hasten improvement and
prevent acute anxiety-provoking stimuli from
interfering with treatment of more regularly
occurring anxieties.
When stopping a drug, weaning is preferred
to stopping abruptly. Weaning minimizes
potential central withdrawal signs, and allows
determination of the lowest dosage that is still
effective (Overall, 1997, 1999a, 2000). Long-
term treatment may be the rule with many of these
medications and conditions, but maintenance
may be at a considerably lower level of drug
than was prescribed at the outset. The only way
the practitioner will discover if this is so is to
withdraw the medication slowly.
Factors Affecting the Success of Treatment
Five main factors contribute to the success of
treatment. These are: client compliance, age of
onset, predictability of outbursts, duration of
the condition, and the pattern of the behavioral
changes in response to environmental, behavioral,
and pharmacological intervention. Of these, client
compliance may be the most critical. Clients need
to truly understand - in their gut as well as in their
head - what is necessary to help their pet change
and improve his or her behavior. The remaining
factors are related. The younger the animal was
2006 World Congress WSAVA/FECAVA/CSAVA
when the problem started, the less predictable
the outbursts, the longer the condition has been
present, and the more frequent and intense the
rate and extent of the outbursts, the worse the
prognosis. Part of the reason for this is because
the degree to which the inappropriate behavior
has been learned increases with the changes
stated for these parameters. The ability of the
client to recognize the potential for a problematic
event and to abort it before it happens cannot be
over-emphasized. Clients sincerely committed to
treatment learn to do this wonderfully.
Words for future thought
The paradigmatic approach described above
is incomplete and may be largely wrong. The
study of behavior was left until last because
140
Back to contents
the brain is complex, and we don’t know much.
We know that the acquisition of a preferred
behavior or a fear is dependent on the genetic
and developmental template or response surface
of the individual animal. With dogs, the story
is even more complex. The story of dogs is the
story of work, and in their shared co-evolutionary
history with humans, dog breeds developed along
the lines of particular job descriptions. Hence, the
response surfaces for one breed may not be those
for another, and the way dogs learn, may not be
the same for all dogs.
So what is behavior modification, specifically?:
Behavior modification is nothing more than the
process of altering an animal’s behavior. The
classic client and veterinarian response to having
“behavior mod” recommended as part of a
treatment plan is to exclaim that they “don’t have
time for that”. What is not understood here is that
we engage in behavior modification either actively
or passively every hour of the day and in everything
we do. The basic tenets of behavior modification
treatment are not complex, and are put into action
whether or not we consciously acknowledge or
recognize that this is so. Accordingly, clients are
often unconsciously and accidentally employing
principles associated with learning and behavior
mod, and inadvertently doing an excellent job of
reinforcing the behaviors about which they are
most distressed!! Our focus should be to help
clients understand that learning occurs all the
time and that we can shape the direction, rate, and
complexity of the learning process with conscious
effort. This does not mean that the clients ‘must’
engage in complex active behavior mod. It does
mean that they can use small, relatively passive
techniques to effect huge changes.
Client fears: People are also afraid of the terms
used in behavior mod: desensitization, counter-
conditioning, conditioned stimulus, et cetera.
These are jargon - anyone who is competent
can teach clients to change their pets’ behaviors
without having to resort to these terms, and
while implementing the concepts. The key to
clear communication is to lose the jargon and
concentrate on content.
Potential problems: The problem with changing
any behavior is 2 fold: (1) inertia is a powerful
force, and (2) breaking behaviors down into
elements that require change and understanding
how to change them can be difficult to do.
This difficulty lies in understanding exactly
what is called for in the behavior modification
technique of choice and in the timing of the
client’s response to the dog’s behavior and
communicatory gestures. Before any client can
change any animal’s behavior - or their own -
they MUST recognize (1) what normal signaling

is (Overall, 1997), (2) what signals are associated
with the problem they wish to change, and (3)
what signals precede # 2.
Although we ask clients to ‘intervene’ and -
minimally - interrupt the behavior in step (3),
intervention is deliberately left undefined. In any
situation there are three environments available
for intervention which can be potentially
modified: the physical environment, the
behavioral environment, and the pharmacological
environment. These environments are not
independent. The key to understanding how
dogs learn is to appreciate the complexity of
interaction between these environments, and
the importance of factors affecting temporal and
intensity changes and interactions within these
environments.
Keys to success
Keys to successful implementation of behavior
modification include the following (Overall,
2003):
(1) The clients must cease their own exhibition
of any behaviors or behavioral sequences that
promote, trigger, cause, encourage, or correlate
with any of the behaviors in the dog or cat that
they wish to change.
(2) The clients must commit to clear signaling
and a humane and possible set of rules by which
they can interact with the cat or dog.
(3) The signals in (2) must have a canine or
feline equivalent so that the dog or cat both
can understand and have the mental space to
understand what the client wants. For example,
sitting in dogs and cats is a ‘stop’ behavior, and in
dogs this is a deferential behavior that functionally
passes the job of giving the next signal back to
the individual who engendered the ‘sit’.
(4) The behavior mod - which is a true rule
structure - should be sufficient either signal to the
dog or cat what they can expect to happen next
or to teach them that they can look to the client
for all cues about the appropriateness of their
behavior if they are concerned.
(5) The reward structure - which is another
rule structure - should be clearly defined and
appropriately reinforced at all times. Clients
need to understand at their gut level that we teach
best by rewarding every instance of appropriate
behavior and that we retain what we have learned
best by rewarding intermittently. Clients also
need to understand that intermittent is NOT
synonymous with ‘seldom”.
(6) Unless the client’s intent is to teach the dog or
cat to fear them, to teach the pet what will only
engender dissatisfaction, or to confuse the pet,
Back to contents
B
clients MUST stop all punishment, shrieking,
yelling, throwing things, et cetera, no matter how
good it feels to them.
Important points about behavior mod that should
go without saying, but don’t: The following
important points regarding behavior modification
exercises are those which are most frequently
misunderstood by clients and vets, alike.
1. Behavior modification exercises are NOT,
repeat NOT, obedience exercises. At the very
outset clients should be disabused of the notion
that this is fancy obedience.
First, while sitting is part of obedience training,
the goal of these programs is not just to have
the dog sit, but to relax and be receptive to
changing his or her behavior while doing so. It
is critical that clients understand and appreciate
this difference. Dogs that are stressed or anxious
cannot successfully learn a more appropriate
behavior and they certainly cannot associate that
behavior with having fun or with good things
happening.
Second, if the client perceives that all we are
doing is trying to teach the dog what he or she has
already learned in training class they will not see
the need to comply. If we offer nothing different,
what is the point of behavior modification? It
is the practitioner’s job to teach the client that
behavior modification is about changing the way
the dog thinks about interactions by rewarding
the physical cues associated with the underlying
physiological state. Obedience training, while
sharing many similarities with behavior
modification, differs in the premise, interactive
reward structure, goal, and outcome. Most of the
dogs that undergo behavior modification have
been through some form of training and most
know how to sit. For a dog to do this successfully
in a class (or even a show) situation, the dog does
not have to be relaxed. For behavior mod to work
as well as it can the dog MUST be relaxed. 2006 World Congress WSAVA/FECAVA/CSAVA
2. Relaxation is key here - the sitting and staying
is merely a facilitator for the relaxation response.
There is no sense to having the dog sit and stay if
it is panting, salivating, its pupils are dilated, its
ears are back, and it is clearly distressed. What on
earth is the dog learning? It’s simple - the dog is
learning to be more distressed - while sitting - and
also teaching his- or herself to become refractory
to complex learning because of arousal of the
HPA-axis (hypothalamic-pituitary-adrenal axis)
(Diamond et al., 1992; Yau et al., 2002). This is
why old-fashioned, out-moded, and simplistic
‘sit-stay’ programs so often fail: the dog sits, but
is still distressed.
3. Clients will have trouble with appropriate
timing of rewards and ‘corrections’. ‘Corrections’
141
B
should be restricted to walking away from the
dog or a quick, low vocal signal that the dog is
behaving undesirably. The point of the ‘correction’
is to interrupt the dog - not to ‘get even’. If clients
are doing any more than this, they are at risk
for potentially - albeit accidentally - exhibiting
abusive behaviors that will make the dog worse.
Dogs read non-vocal or body language far better
than do most humans (Cooper et al., 2003; Hare
and Tomasello, 1998; Hare et al., 1998, 2002;
Topal et al., 1997). It is easy for them to ‘subvert’
the exercise and shape the behavior of the client.
Problem dogs have been doing this already, and
such behaviors are NOT malicious. They ARE,
however, behaviors that logically are exhibited
by a confused, uncertain animal in an attempt
to gain information about what can be expected
- and what their response should be - within
that context. Because clients so often attribute
uncharitable ‘motivations’ to their pets someone
from the outside of the relationship needs to
be able to comment on timing problems and to
instruct the clients when to change their posture,
their tone, or their quickness of praise or reward.
Most clients are quite good at learning to do this,
but they need help. After the initial demonstration
they may even need to be able to show you what
they are doing to see if it is correct, or if you can
make recommendations. This can be done in a
quick 10-15 appointment (and support staff can
be responsible for this), or the client can send
a video, and an appointment - in person or by
telephone - can be set for a critique. If the clients
are not seeing an improvement, or are having an
actual problem either:
a) they are pushing the dog too hard, too fast
(very common in today’s hi-tech, faster-is-better
world),
b) they are giving confusing signals, or
c) their timing is wrong.
2006 World Congress WSAVA/FECAVA/CSAVA
This is hard work -- it is not magic. The practitioner
will need to help along the way.
3. The practitioner and, or the staff must work
WITH the client. In the case of a very fearful or very
aggressive dog the practitioner may not be able to
demonstrate the exercises or fit a halter during the
first visit. In such cases, after fully cautioning the
client about possible risks, the practitioner can
ask if the client feels comfortable attempting the
first round of the behavior modification protocols
while the practitioner talks them through it. For
reasons of liability it is important to explain that
this is not the desired technique; however, if the
client cannot eventually work with the dog, or
if the client is perpetually afraid of the dog, the
situation will be hopeless.
If the practitioner is able to work with the dog,
142
Back to contents
they should do so both to teach the dog the
appropriate behaviors and to demonstrate to
the clients what is desired. Again, making a
video that can be played back and critiqued
after the session can help. When the dog works
well with the practitioner, it is the client’s turn.
It is not sufficient to demonstrate the behavior
modification without then giving the client the
chance for emulation. It is of no use if the dog
is perfect for the practitioner, but a horror for
the client. -- the practitioner does not have to go
home and live with the dog. The clients must be
able to accomplish the suggested modification,
hence it is inappropriate to just send them home
with sheets of paper.
If the client’s dog cannot or will not work with
the practitioner, the practitioner should have
another dog available that can be used. This dog
should be able to work with the client so that the
client understands what an appropriate response
is. Everyone who is serious about veterinary
behavioral medicine should have a demo dog
who will teach the clients and staff to hone their
observational and functional skills. Alternatively,
these tasks can be farmed out to someone
more likely to have a good demo dog and who
is uniquely equipped to teach the practical
implementation of behavior modification: in the
USA, an Association of Pet Dog Trainers (APDT)
Certified Pet Dog Trainer (CPDT) (www.apdt.
com).
4. Finally, if there is the potential for a dangerous
behavior that will need to be altered or avoided,
it would be optimal if the client doesn’t discover
this when there is no one to help them. A run-
through of the program will minimize, but not
ablate, this chance.
A few words about rewards: Most commonly
used behavior modification programs employ
praise and food treats or other rewards. The
higher the quality of the treat the better the dog’s
response. A dog who might work for American
cheese while on the property, might need dried
liver when out in traffic. No one goes to hell for
using food treats, but to hear people’s reactions,
you’d be certain this was the case.
The approach to behavior modification discussed
here does not use hand signals or clickers. Clickers
are unforgiving with respect to timing, and to ask
a client to read a problem pet’s signals, monitor
them constantly, teach them to sit and relax,
and incorporate the clicker system of secondary
reinforcement into behavior mod, is not kind to
the clients, and can further confuse the dog.
Hand signals are commonly used in obedience and
can be useful for dogs and clients, but behavioral
patients need every bit of help that they can get.
Hand signals, here, will be a needless distraction.

Once the dogs master the programs, they will
have no problems coupling the learned vocal cues
to visual ones. Until then, these dogs should work
in calm, quiet circumstances, without distraction,
for vocal cues, and a consistent reward structure.
Dogs can learn all the words for the ‘commands’,
signals, or requests that they will need for these
programs.
Most importantly, hand signals at this stage will
only ask the dog to distract their attention from
the behavior modification process, and, for very
aggressive dogs, such signals will put the person
using them at risk. Without exception, dangling
body parts in front of an aggressive dog is not
recommended, and will make the animal more
anxious. In a worst-case scenario, hand signals
can be seen by the dog as threats.
Tips for incorporating behavior mod into everyday
life for ALL of your clients:
(1) Don’t single out only your problem patients
for behavior mod. Wouldn’t ALL of them benefit
from learning to be calm as a way of seeking
information from you or the client?
(2) Cats should learn behavior mod, too.
(3) At every single visit, teach the pet something
behavioral. This is simple: ask them to sit, cock
their head, and look at you for a food treat. Voila!
Magic!
(4) Practice 3.
(5) Have the clients practice 3 with all of their
dogs and cats: if any pet wants love, food,
affection, water, grooming, to play fetch, to
get into the car, et cetera - encourage them to
sit and look at you or the clients first. In turn
you - and the client - must be quiet and look at
the pet. Acknowledge the signaling relationship
and be clear (this works for spouses and kids,
too). Then give the pet access to that which they
requested.
(6) Every member of your staff should already be
practicing 3. If they are not doing so, why not?
(7) Fit all pets with head collars and harnesses.
Stock and sell these AND the know-how that goes
with using them. Throw out: chain leashes, choke
chains, prong collars, slip collars, et cetera.
(8) Teach clients how to pet their dogs and cats.
It’s so simple it will just plumb elude them. Ask
them what they want: a jazzed, reactive pet, or a
calm one.......logic will carry them from here.
(9) Reward spontaneously wonderful behaviors
and teach your clients to do so by example.
[Thanks for paying attention to these notes!]
(10) Encourage gentle walking on a leash by
engaging the pet in conversation....encourage
your clients to avoid learning that which must
be unlearned later (for them and the pet). This
translates to the over-used concept of preventing
- not treating - problems. While a bit overused,
Back to contents
B
the concept is valid: all management related
problems can be prevented by telling the animal
what you want in advance and encouraging those
favored behaviors.
(11) Be reliable, signal clearly, be compassionate
and humane, and let your patients make you a
better person. Then pass it on to the clients.
Dogs and cats are highly cognitive animals
(9,10). If you realize this and incorporate
behavior modification designed to take advantage
of their cognitive skills at each and every routine
appointment, you may have no real behavior
cases in your practice.
References
Bateson P. How do sensitive periods arise and
what are they for? Anim Behav 1979, 17:470-
486.
Carter AP, Chen C, Scwartz PM, Segal RA. Brain-
derived neurotrophic factor modulates cerebellar
plasticity and synaptic ultra-structure. J Neurosci
2002; 22: 1316-1327.
Cooper JJ, Ashton C, Bishop S, et al. Clever
hounds: social cognition in the domestic dog
(Canis familiaris). Appl Anim Behav Sci 2003;
81: 229-244.
Daniel H, Levenes C, Crépel F. Cellular
mechanisms of cerebellar LTD. TRENDS
Neurosci 1998; 21: 401-407.
Davis M. Neurobiology of fear responses: the
role of the amygdala. J Neuropsychiatry Clin
1997; 9: 382-402.
Diamond DM, Bennett MC, Fleshner M, Rose
GM. Inverted-U relationship between the level
of peripheral corticosterone and the magnitude
of hippocampal primed burst potentiation.
Hippocampus 1992; 2: 421-430
Duman RS. Novel therapeutic approaches beyond
the serotonin receptor. Biol Psychiatry 1998; 44:
324-335.
2006 World Congress WSAVA/FECAVA/CSAVA
Duman RS, Heninger GR, Nestler EJ. A
molecular and cellular theory of depression. Arch
Gen Psychiatry 1997; 54: 597-606.
Hare B, Tomasello M. Domestic dogs (Canis
familiaris) use human and conspecific social
cures to locate hidden food. J Comp Psychol
1999; 113: 173-177.
Hare B, Brown M, Williamson C, Tomasello
M.The domestication of social cognition in dogs.
Science 2002; 298: 1634-1636.
Hare B, Call J, Tomasello M. Communication
of food location between human and dog (Canis
familiaris). Evol Commun 1998; 2: 137-159.
Hart BL. Environmental and hormonal influences
143
B
on urine marking behavior in the adult male dog.
Behav Biol 1974, 11: 167-176.
Hopkins S, Schubert T, Hart B. Castration of
adult male dogs: effects on roaming, aggression,
urine marking, and mounting. JAVMA 1976, 168:
1108-1110.
LeDoux JE et al. The lateral amygdaloid nucleus:
sensory interface of the amygdala in fear
conditioning. J Neurosci 1990; 10: 1062-1069.
O’Farrell V, Peachey E. Behavioral effects of
ovariohysterectomy on bitches. J Sm Anim Pract
1990; 31: 595-598.
Overall KL. Sex and aggression. Canine Practice.
1995; 20(3): 16-18.
Overall KL. Clinical behavioral medicine for
small animals. Mosby, St. Louis, 1997.
Overall KL. Allow behavioral drugs ample time
to take effect. Vet Med 1999; 94: 858-859.
Overall KL. Behavior modifying drugs:
Neurochemistry and molecular biology.
Proceedings of the 18th ACVIM Forum 2000;
18: 68-71.
Overall KL. Pharmacological treatment in
behavioral medicine: The importance of
neurochemistry, molecular biology, and
mechanistic hypotheses. The Veterinary Journal
2001; 62: 9-23.
Overall KL. “How dogs learn”, PABA meeting
notes, April 2003, Guelph, Ontario.
Pfaffenberger CJ, Scott JP. The relationship
between delayed socialization and trainability in
guide dogs. J Genet Psychol 1959, 95: 145-155.
2006 World Congress WSAVA/FECAVA/CSAVA
144
Back to contents
Salter MW. Src, N-methyl-D-aspartate (NMDA)
receptors, and synaptic plasticity. Biochem
Pharm1998; 56: 789-798.
Schafe GE, Nader K, Blair HT, LeDOux
JE. Memory consolidation of Pavlovian fear
conditioning: a cellular and molecular perspective.
TRENDS Neurosci 2001; 24: 540-546.
Scott JP, Fuller JL. 1965. Genetics and the Social
Behavior of the Dog. University of Chicago
Press. Chicago, IL.
Scott JP, Marston MV. Critical periods affecting
the development of normal and maladaptive
social behavior in puppies. J Genet Psychol 1950,
77: 25-60.
Topal J, Miklosi A, Csanyi V. Dog-human
relationship affects problem solving behavior in
dogs. Anthrozoos 1997; 10: 14-224.
Trotti D, Danboldt NC, Volterra A. Glutamate
transporters are oxidant-vulnerable: a molecular
link between oxidative and excitotoxic
neurodegeneration. Trends Pharm Sci 1998; 19:
328-334.
Voith VL. Teaching sit-stay. Mod Vet Pract April
1982: 317-320.
Wittenberg GM, Tsien JZ. An emerging molecular
and cellular framework for memory processing
by the hippocampus. TRENDS Neurosci 2002;
25: 501-505.
Yau JLW, Noble J, Hibbert C, Rowe WB, Meaney
MJ, Morris RGM, Seckl JR. Chronic treatment
with the antidepressant amitriptyline prevents
impairments in water maze learning in aging rats.
J Neurosci 2002; 22: 1436-1442.

B - Behaviour
TANATHOLOGY IN SMALL ANIMALS
Dr. Moisés Heiblum
Veterinary Hospital Universidad
Nacional Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
Private Practice in Small Animal
Behavior, Naucalpan, Mexico,
Mexico
moisesheiblum@yahoo.com
What is Tanathology?
Death is a natural process and a characteristic
that we share with all the living creatures, and
it is necessary so that life, not the organisms in
particular, could continue and evolve (3,5). Even
tough death is a natural process, it will always
be difficult and painful, since it means a loss of
continuity in the existence of the individuals,
rupture of bonds, interruption of activities,
relations and projects. Before the need to
understand and to assimilate in a more suitable
way this process, in the recent years, tanathology
became an important field in medicine, which
tries to help the terminal patients so that they
could assume their own death; and at the same
time, it helps and prepares the people closest to
the patient, during the terminal stages and during
the grief.(2,3)
The biological process of death
From the physiological point of view, death has
been defined as the irreversible cessation of the
vital functions, in the vertebrates, it happens
when the nervous central system, the respiratory
and the cardiovascular systems stop functioning.
The cells and structures that integrate it are
disorganized, autolisis begins and the individual
loses the ability to interact with his environment
in a definitive form, this is known as somatic
death(1,8).
The veterinary practitioner facing pain and death
The veterinary practitioner has assumed the
“privilege” of being able to decide on the life
and death of the animals(3), therefore he needs a
suitable formation making him fully aware of the
huge responsibility that this implies, as well as
knowing his own limits.
The veterinarian has the task of educating
and sensitizing the owners about companion
animals, having acquired an animal, they acquire
a commitment with the animal, commitment to
Back to contents
B
take care until the moment of his death. Also it is
the veterinarian’s responsibility to actively take
part in the decisions of critical situations, since he
has the mission to promote the animal’s welfare,
he can influence in an important and positive way
the fate of the animals.
Euthanasia
Euthanasia (from the greek eu = good and
thanatos death) means “Good death” (2,3).
In the context of veterinary medicine, this word
has been used to designate the act of inducing
death in a calm and easy form, without stress or
pain. Medically euthanasia is considered to be
the interruption of life, by means of a painless
method, which produces a rapid unconsciousness
followed by death. It could also be defined as:
“the medical administration of a lethal agent
with the intention of relieving the patient from an
unbereable and untreatable suffering”
In Hebrew there is a term that describes euthanasia
as: “mitat jasadim”,(5) this means death with
compassion and is a form to refer to the act of
interrupting the life of an animal with the minimum
of suffering. Also the word “compassion means 2006 World Congress WSAVA/FECAVA/CSAVA
“feeling as the other”, either human or animal;
understanding kindness, tenderness, mercy, love
and the most important thing, companionship.
Compassion is to feel together with … therefore
to give an animal a compassionate death, goes
beyond the simple fact of taking the animal’s
life; it involves the responsibility of deciding the
moment and means of his death(2,4), but more
importantly not leaving him alone during this
process, so that having his human friends next to
him when his life ends, diminishes not only his
physical pain, but also his anxiety and suffering.
It must remain clear that euthanasia is not the
solution to all the problems, its purpose is to end
with an unbereable suffering(5), when there is no
other medical alternative.
Before thinking about euthanasia, an ethically
145
B
correct attitude is to provide the animal support,
attention, avoiding invasive procedures; trying at
all times, to make him as comfortable as possible,
having no thirst and no pain.
Deciding euthanasia
It is one of the most controversial topics. It is
known that the owners go so far as to form very
narrow bonds with their pets. On having died the
pet is as if they were losing one member of the
family, therefore, the intention of tackling this
topic is to offer a point of view and not to try to
convince anybody.
Medical approach
We have to continue a series of steps that should
lead us to knowing which is the problem, it’s
cause, which is the possible treatment (if there is)
and much importantly what is going to happen in
short, medium and long term with the patient.
The medical approach consists of the following
points:
Making a clinical history, physical examination,
laboratory tests, diagnosis, prognosis, treatment
Approaching the subject:
It can be much more difficult taking a decision
related to euthanasia in the middle of a medical
crisis. The veterinarians frequently have difficulty
knowing in what moment they must talk to the
owners about euthanasia in their animals and at the
same time a great discomfort exists in the owner
to tackle the topic (3,5). Both the veterinarian
and the owner will have to take sufficient time
to take the decision without being under a strong
emotional tension. There is too much pain in
these moments to add a sense of guilt. When will
be known that the moment has come?
If there are medical specific signs (seizures, pain)
that the owners could observe, the veterinarian
2006 World Congress WSAVA/FECAVA/CSAVA
will have to mention them. It is advisable to write
a list of clinical signs so that the owners could
remember easily what they must observe and look
for. The bottom line is to be able to measure the
level of deterioration and quality of life. These
are different for every owner. It is very important
to distinguish between pain and suffering. Pain
can be controlled by medication, but the suffering
can be more difficult to remedy. When it seems
that it has more bad days than good ones or more
bad moments than good ones, it will be known
that in a way there is some kind of suffering.
Euthanasia: how to face the inevitable?
To say good-bye to a pet is always difficult and
even more when this farewell is a result of a
decision as euthanasia.
146
Back to contents
The farewell:
As soon as the decision of euthanasia was taken,
it is important to allow a moment of privacy
between the owner and his partner, preferably in
a private place and alone.
We must give them the space so they could
cry, embrace and vent all the feelings inside,
sometimes the owners suppress these feelings
to avoid the embarrassing moments of people
watching. This moment of privacy will allow
that the owner could express oneself freely. This
moment is perhaps one of the most important and
as well as it is important it is unique. (2,3,5)
Supporting the patient:
The process of euthanasia for itself already
implies an apprehensive state for the pet, for what
we must reduce to the maximum any situation
that increases this tension.
It is an owner’s decision if he wants to be present
during the procedure. If the owner does not
support the idea of watching his pet die and cries
in an exaggerated form, it is preferable that he is
not present at that time not to increase the anxiety
of the patient.
Where to perform the euthanasia?
If the patient is hospitalized, in a critical situation
where risk exists to transport it, then the ideal
place is the same clinic. If it is in the house or the
conditions to be transported are good, the ideal
situation is taking it to the place where the patient
feels calmer.
How to perform euthanasia?
We must perform a procedure that allows the
patient to have a “good death”. Independently of
weather, the patient is canalized previously or not,
it is recommended to apply a tranquilizer, which
allows the patient to be sedated and diminishes
the anxiety. Once the family has said goodbye, the
vet proceeds to apply an overdose of anesthetic
until a cardio-respiratory arrest takes place.
It is important that the owner knows that when the
death comes: the eyes of the patient may remain
opened, the heart can keep on beating after the
respiration has stopped, there can be sound
emissions, there is sphincters relaxation, therefore
the bladder and intestine can be evacuated.
At the moment of the euthanasia: you have to
create a space for this moment, to avoid any
interruption and not to program it in schedule of
consultation.
Who should be present?
Undoubtedly this decision depends on every
family. The ideal thing is, that can be present all
those that are a part of the familiar group and who

obviously want and could be, if it is possible, do
not leave the patient completely alone.(2)
Disposition of the body
When the euthanasia is over, the owner may ask
what to do with the corpse, his sorrow is so big
that they usually do not speak about this. That’s
why it is the veterinarian’s responsibility to tell
the owners the options about it.
Autopsy: if the cause of the illness is still not
determined (later cremation)
To bury it: it is recommended to bury it to a depth
of 1.5 meters and the use of lime on the corpse,
to eliminate bad smells and in case of having
other animals in the house, preventing these from
digging the corpse up. Another option is to take it
to a pet cemetery.
Cremation: sometimes for lack of space or
because this way the owners prefer it.
Grief and sorrow:
To assimilate the death of a pet is a difficult and
painful process. Companion animals are usually
part of the family. The sorrow is normal and it
must be expressed. (2,3)
There are those who decide to keep mourning in
a time and not to acquire another pet soon. Others
prefer acquiring another pet immediately because
they have a lot of love to give. Keep their mind
occupied and prevent them to get depressed for
the pet that died. Finally there are those who
decide to never again have a pet, since the sorrow
of losing was so big that they do not feel capable
of supporting the same pain again.
What is the correct decision? Every person has
the freedom of feeling and of believing what they
should consider to be better.
What about the animals that stayed in the house?
Sometimes the pain that provokes the death of a
pet, makes us forget that the other animals that are
Back to contents
B
in the house need us. It is necessary to remember
that the animals can form very strong bonds, not
only with humans but also with other animals.
The animals that stay in the house can suffer
from depression on having felt the absence of his
partner. (2,3,5)
How can we help these animals to overcome the
loss?
It is important not to change the daily routine, not
to reinforce the changes of behavior, try not to
change the food, even if they stop eating for a
few days.
Support a regular physical activity
Do not overprotect him and do not give all the
attention and affection
Look for professional help if the change of behavior
is very intense or can put his life at risk.
References
1. Cotran RS, Kumar V, Robbins SL. Patología
Estructural y Funcional. 5a ed. Madrid:
Interamericana. McGrawHill; 1995; 1553
2. Graus A. Eutanasia: reflexión obligada. Revista
Investigación Clinica; 1995;47: 217-229
3. Vanda B. Revista Imagen Veterinaria 2003;3
4-14
4. Knight, B. Medicina forense de Simpson. 2ª.
Ed. México, D.F.; El manual moderno, 1999
5. Rebolledo- Mota F. Aprender a morir.
Fundamentos de Tanatología Médica. 3ª. Ed.
México, D.F.: 1999; 315
6. Rollin BE. Veterinary Medical Ethics. Ames:
Iowa State University Press, 1999; 417
7. Vanda B. Alteraciones celulares y tisulares. En
Trigo FJ,
8. Valero G. Editores. Patología General Veterinaria.
3ª. Ed. México: FMVZ-UNAM; 2002; 417
2006 World Congress WSAVA/FECAVA/CSAVA
147
B
B - Behaviour
UNDERSTANDING DOGS THAT FIGHT
Karen L. Overall, MA,VMD,
PhD
Diplomate ACVB
ABS Certified Applied Animal
Behaviorist
Center for Neurobiology and
Behavior
Psychiatry Department - Penn
Med Translation Research
Laboratory125 S. 30th St.
Philadelphia, PA 19104
overallk@mail.med.upenn.edu
http://psych.ucsf.edu/
K9Behavioral/Genetics/
To understand and help dogs that fight it is
necessary to both understand their signaling in
a larger context of overall pathological behavior,
and how to utilize these signals to distinguish
when animals are communicating and interacting
normally from abnormally. Accordingly, we must
give practitioners some guidance that can tell them
where their patients might be on the continuum
of normal, but scary to pathological, and possibly
fatal. This is nowhere more important than for
aggression between dogs because there is an
almost uniform belief that some aggression can
be ‘normal’ in dog-dog interactions. The inherent
problem is whether the aggression label is
misapplied to normal, tussling social behaviors.
An approach that educates practitioners about
behavioral patterns and sequelae can help here.
Unfortunately, these goals are impossible
to accomplish is we cleave to an outdated,
unfortunate, and unsubstantiated terminology:
that of the ‘alpha’ or ‘dominant’ dog. The modern
and evolving understanding of complex social
behaviors is going to require that we relinquish
2006 World Congress WSAVA/FECAVA/CSAVA
simplistic and damaging labels: the concept of a
‘dominant’ dog is not useful in these situations,
and asking clients and practitioners to identify
and support the ‘dominant’ dog can cause not just
further morbidity, but mortality. An unpublished
study of dozens of cases involving interdog
aggression between household dogs (as contrasted
with dogs with whom the participant(s) do not
live) (1) found that most clients had been advised
to support or reinforce the ‘dominant’ dog, and
that when they did so, the aggression worsened.
One could accordingly argue that the clients are
any not correctly identifying the ‘dominant’ dog,
but if a label is causing such difficulties, it may
be time to just let it go. The issues of ‘dominance’
and social rank on group interactions comprise
one of the oldest, most confusing, and hotly
debated areas in the behavioral literature. It’s
148
Back to contents
important that we understand why this concept
has caused problems in the practice of veterinary
behavioral medicine.
The existence of a hierarchy has been postulated
to be a stress-reducing device (2); however,
situations where hierarchies are most rigidly
maintained are also ones where measures of
stress are high (3). The traditional concepts
are represented in the article under discussion:
the animal who ‘submits’ - which is generally
undefined - or gives way to another as a result of
prior interactions is considered the ‘subordinate’
while the individual inducing such behavior is
usually considered the ‘dominant’ animal in the
pairing. ‘Dominance’ has been traditionally
defined as individual’s ability, generally under
controlled situations, to maintain or regulate
access to some resource (4-7). Given that the
definition of ‘dominance’ can be further refined as
a description of winning or losing staged contests
over resources (8), and that a winning outcome
needn’t confer priority of access to those resources
(8), we must accept that variable distributions of
resources (e.g., access to attention, beds, resting
sites, toys, food dishes, et cetera) will lead to
variable hierarchal classifications.
Concerns about such terminology primarily focus
on 2 related issues: (1) the extent to which the
labeling of an event, interaction, or pattern of
interactions may interfere with our ability to truly
understand behaviors and signals, in-context,
and (2) the extent to which, if we subscribe to
a hierarchical system, we are then tempted
or constrained to force all interpretations of
behaviors into that system. Such practices have
encouraged humans to treat dogs inhumanely
under the guise of being ‘dominant’ to them,
and have likely resulted in the injury or death
of many dogs because we have reinforced a
truly pathological animal as ‘dominant’. These
concerns are not new: the potential to mislead was

Rowell’s primary concern when she published
her ground-breaking study on the intricacies of
baboon social interactions (9). In fact, when free-
ranging baboon interactions were classified by
behavioral types (e.g., friendly, approach-retreat),
and then analyzed according to specific behaviors
of the participants, no ‘dominance’ system was
noted. A much more complex, elegant system of
interactions that reflected relatedness, age, sex,
social history, et cetera became apparent.
Most social behaviors, when fully examined, are
not characterized by agonistic encounters, but
by fluid, context-specific deferential behaviors
(10). Deference is not analogous to submission or
subordination. Deference is about relative status
that is freely given, not imposed. The animal to
which most others defer is the animal that behaves
most appropriately given the context, not the
animal which must always be at the door first, or
must eat first. In fact, a need to control regardless
of context can be neither adaptive, nor normal.
The role for deferential behaviors is suggested
by authors who have looked extensively at social
interactions when they discuss the variability in
the behavior of high ranking animals.
Accordingly, it may be easier to ask clients and
practitioners to do 1 basic thing: correctly identify
the animal in the interaction who is behaving
most appropriately and protect and reinforce this
animal. If clients and practitioners can watch
videos of the dogs interacting in low-to-no risk
circumstances, even without knowing what to
call the behaviors, they will see differences. This
is the first step in learning to better read feline
and canine signaling. If they review enough
interactions while emotionally removed from
the situation (hence the use of video - real-time
observations are notoriously unreliable), they will
be able to recognize the animal whose behavior
is most contextually appropriate. They will also
able to identify the specific behaviors and signals
of concern.
Interactions are not an event - they are a process.
A fight is a snap-shot viewed without the
reference frame of the long movie that is the
animals’ lives together. In the absence of repeated
snapshots, videos, or some other evaluation of
social interaction over time, we can learn about
variability in response and when it changes
to abnormal by viewing a series of videos
of dogs interacting with different outcomes.
Clinicians can learn to read behaviors and assign
probabilistic outcome to interactions using this
type of approach.
Clients need to know that their dogs will learn
from their interactions with each other, and both
‘combatants’ may hone their aggressive skills.
Attackers may become faster, and signal their
Back to contents
B
intent less intensely with time, and victims may
learn that they can minimize damage to themselves
if they exhibit a pre-emptive attack. In such
circumstances, it is easy to err in identifying the
aggressor v the victim. The key is to able to identify
when the behaviors are about learning normal
social roles in changing social environments,
and when they are about truly pathological
behavior. Because learning works by altering
neurochemistry (11), clients should understand
that both early intervention designed to avert
anxiety associated with underlying aggression
and pharmacological intervention can help,
but neither approach will be used appropriately
until the clients can understand the signaling and
interactions from the dogs’ viewpoints (12). That
said, some general guidelines that allow clients
to deal with a range of potentially problematic
interdog interactions from the relatively normal
to the potentially fatal can be developed. The
following example is from Step 3 of the Protocol
for Interdog Aggression (13):
3. Choose an order in which to reinforce the dogs
based on identifying which dog is behaving the
most appropriately. Remember - reinforcement
is not about rewarding the pushiest, most
‘dominant’ dog. It’s about rewarding the dog
who is most appropriate so that all the dogs get
the message that obnoxious behaviors are not
rewarded, but calm, non-threatening ones are.
This type of reward-based reinforcement works
because it mimics canine social systems and
uses deferential behaviors to get attention and
other ‘currencies’. When you reinforce the most
appropriate dog you feed that dog first, give him
or her attention first, give them access to the yard
first, et cetera. You can get hints about what will
be most successful from the dogs’ behaviors, as
follows.
a) For example, you have two dogs and the
younger one has begun to passively challenge the 2006 World Congress WSAVA/FECAVA/CSAVA
older, the older is snarling, and most of the time
the younger backs off. The older one is larger and
stronger than the younger, just as healthy, and not
that different in age. Reinforce the older over the
younger. The younger dog here is likely normal,
but just too pushy, and can learn how to have a
better relationship with his companion once the
threats subside.
b) The older dog perceives a threat from the
younger, but the younger isn’t really doing
anything active. The older is weaker than the
younger, and while the younger is sweet, she is
huge. Reinforce the younger dog and make sure
that the older receives needed attention, including
tasks he or she can still accomplish, so that the
shift in relative social relationships is more fluid.
The younger dog is actually behaving most
149
B
appropriately, and if you work with both dogs
the older dog can learn that she is not a threat.
You cannot reward the older dog because then
you would be telling him that his out-of-context
aggression - and his perception that he has to
exhibit such aggression - are acceptable when
they are not. Please remember the role of exercise
in reactivity: if the younger dog is not getting
enough aerobic exercise she will be a brat, and
pester the older dog. One solution here would be
to find a play group of young, rambunctious dogs
for the younger dog so that she is tired when she
comes home to her older companion.
c) The younger dog is actively pushing around
or challenging the older and is getting very
aggressive. The older is fighting back and the
younger is meeting the challenge. The old is
arthritic, and weaker, but the dogs are fairly
evenly matched in size. It will break your heart,
but reinforce the younger dog and see what
happens. If the younger dog then recalibrates
his or her response to the older dog, you’ll
be fine. If the younger dog is normal and just
provoking the social system around her as part
of the social learning that occurs as dogs (and
humans) enter social maturity, the younger dog
will become less aggressive. However, if there
is no return aggressive response to her threat
and she still continues to threaten, you have a
problem. This behavior is abnormal and out-of-
context, and the time to deal with it in the manner
discussed in this handout for true aggression is
NOW. Again, remember to meet the older dog’s
mental, physical, and behavioral needs, even if it
means changes in your behavioral interactions.
d) One of the dogs - regardless of age - perceives
a challenge and exhibits behaviors consistent
with deferential or disengaged behaviors (eg,
turning the head or neck away, ceasing motion or
other activity, turning the body away, displaying
the ventral neck or the groin, tucking the tail, et
2006 World Congress WSAVA/FECAVA/CSAVA
cetera), but the aggressor / challenger doesn’t
seem to care. The last time the challenged dog
rolled over on her back the other dog moved
in for the ‘kill’, and attacked the more passive
dog’s belly and neck. CAUTION. This is the
true problem scenario, and it is almost always
misunderstood and mishandled!!. Reinforce the
challenged (deferential) dog. This may be very
difficult to execute successfully, but if you are not
able to give this dog some status (regardless of
his or her age) so that the aggressive dog realizes
that this dog has a right to exist, he or she will be
a terrific victim. Remember, it is abnormal to
respond to a deferential behavior with a threat.
By definition, aggression that occurs when the
recipient is signaling that they are not a threat
is inappropriate and out-of-context. DO NOT
150
Back to contents
ASSUME THAT THE DOGS WILL NOT INJURE
EACH OTHER. They can seriously disable or kill
each other in such circumstances. If the dog that
is deferring cannot hold the status in a way that
encourages the aggressive dog to back down you
will either have to keep the dogs continuously
separated or find one of the dogs another home.
If you decide to place the challenger, that dog
can ONLY go to a home where he or she will be
the single dog. You do not know if this dog will
behave in the same manner to another dog in a
new home, but in the interest of the welfare of all
of the dogs you should assume that this could be
the case and minimize the cost of error.
Reinforcing the chosen dog has active and passive
components. First, separate them as discussed
above. Second, enforce the concept that the dog
being threatened has the right to exist by feeding
him dog first, letting him out before the other
dog(s), giving him a treat or toy first, walking
first, playing with first, grooming first, et cetera.
Make sure you understand what is really being
said here......this is NOT about ‘dominance’.
Because misunderstandings are so injurious to
dogs a short discussion about what ‘status’ means
is warranted.
You are not imposing a ‘rank’ order on these
dogs: instead, you are encouraging the normal
types of social deference that would be exhibited
by dogs under normal conditions. Unfortunately,
myths about dog-dog relations are so ingrained
that we have come to believe that dogs seize
control and force others to wait for them.
Nothing could be more wrong. By reinforcing
an appropriately behaved dog you encourage the
normal fluidity of the social system and can then
reward the aggressive dog for not reacting.
You can also more passively encourage the
aggressor to understand that the victim has some
status by allowing the victim sleep in a crate in
your room, on a bed there, or on your bed (if
you like this and the dog never growls at you
while you are sleeping), while the other dog is
banished to a room or crate outside your room.
This has nothing to do with beds and ‘spoiling’
and everything to do with the fact that access to
preferred spots or to attention is a currency for
dogs.
Regardless of how you decide to work with the
dogs, each dog needs daily individual attention.
The dog that is being reinforced should always
get the attention first, in the presence of the other
dog if this can be done quietly and without threats
or overt aggression. If necessary, restrain the
inappropriate dog using a harness.
Finally, if you are walking the dogs as a group,
make sure that if there is a dog that is “out in
front”, that dog is the one whose right to exist

in an unmolested manner you are trying to
reinforce. Under normal circumstances dogs
should not need to care about who is in front of
whom. If you are having these types of struggles
on walks your canine household has issues that
need to be addressed. If you are unsuccessful in
gently requesting that the pushier dog steps back,
consider some trial separations of the dogs to see
if one dog blossoms when not harassed. If this
happens, you need to work with the situation
immediately. Remember that in anxiety-related
conditions, like interdog aggression, many of
the provocative behaviors are exhibited to gain
information, and that part of the pathology
may be that the dog is incapable of interpreting
the response in all but the worse light for the
victim. Also, abnormal dogs may misinterpret
the behavior of a dog who pulls out in front of
the others: to the normal dog, such behavior may
just indicate that the dog is following a scent; to
an abnormal dog the dog who pulled out in front
may be seen as a deliberate threat.
In this world view, treatment is about both
understanding the neurochemical changes that
occur with learning and repeated exposure, and
about becoming humane. To do this, we must begin
to see the world from the dog’s point of view, which
minimally requires that we let go of labels which
may say more about us and our need, than they
do about the behavior. The situation with interdog
aggression demonstrate why we need to be more
mindful of terminology, issues, and approaches
which can inadvertently do more harm than good.
Back to contents
B
References:
1. Overall KL, Dunham AE. Unpublished 2004.
2. Collias NE. Social behaviour in animals.
Ecology 1953; 34: 810-811.
3. Rowell TE. Hierarchy in the organization of a
captive baboon group. Animal Behaviour 1966;
14: 430-443
4. Hinde RA. The nature of aggression. New
Society 1967; 9: 302-304.
5. Hinde RA. Animal behaviour. 2nd edition.
New, York, McGraw-Hill, 1970.
6. Landau HG. On dominance relations and
the structure of animal societies. I. effects of
inherent characteristics. Bulletin of Mathematical
Biophysics 1951; 13: 1-19.
7. Rowell TE. The concept of social dominance.
Behavioral Biology 1974; 11: 131-154.
8. Archer J. The behavioural biology of
aggression. Cambridge, Cambridge University
Press, 1988..
9. Rowell TE. A quantitative comparison of the
behaviour of a wild and a caged baboon group.
Animal Behaviour 1967; 15: 499-509.
10. Overall KL. Clinical Behavioral Medicine for
Small Animals. St. Louis, Mosby, 1997.
11. Overall KL. Pharmacological treatment in
behavioral medicine: The importance of
neurochemistry, molecular biology, and
mechanistic hypotheses. The Veterinary Journal
2001; 62: 9-23.
12. Rooney NJ, Bradshaw JWS, Robinson IH. Do
dogs respond to play signals given by humans?
Animal Behaviour 2001; 61: 715-722.
13. Overall KL Manual of Clinical Small Animal
Behavioral Medicine. St. Louis, Elsevier, 2005.
2006 World Congress WSAVA/FECAVA/CSAVA
151
B
B - Behaviour
CANINE AGGRESSION TOWARDS FAMILY MEMBERS
Jaume Fatjó,DVM,
DipECVBM-CA
Unitat de Fisiologia Animal
Facultat de Veterinària
Universitat Autònoma de Barcelona
08193 Bellaterra
Spain
jaume.fatjo@uab.es
Dr. Xavier Manteca, DVM,
MSc, PhD, DipECVBM-CA
Unitat de Fisiologia Animal
Facultat de Veterinària
Universitat Autònoma de
Barcelona
08193 Bellaterra, Spain
Canine aggression problems may impair the
welfare of dogs and can be very dangerous for
people (Guy et al, 2001). Aggression towards
family members is the most common form of
aggression seen by veterinary behaviourists,
ranging from 20 to 60% of the total of aggression
cases (Beaver, 1999).
For many years, most cases of aggression towards
family members have been linked to an underlying
hierarchical conflict between the dog and one or
more members of the human family (O’Farrell,
1992; Borchelt and Voith, 1996; Beaver, 1999). Other
reasons for a dog being aggressive towards family
members are commonly related to a fear reaction,
for instance in situations that cause pain, like severe
physical punishment (Askew, 1996; Houpt, 1998).
After a possible medical condition has been ruled
out, the diagnosis of aggression towards family
members is usually based on two main diagnostic
2006 World Congress WSAVA/FECAVA/CSAVA
criteria: the context in which aggression occurs
and the dog’s body language (Overall, 1997;
Lindsay, 2001; Mertens, 2002).
According to most clinical descriptions a
dominant aggressive dog is supposed to behave
in a very assertive way each time the owner
challenges the dog’s status or a competitive
situation arises (O’Farrell, 1992; Askew, 1996).
Besides the occurrence of aggression in some
specific contexts, the hallmark for diagnosis
of this form of aggression is the observation of
an offensive posture. Thus, the differentiation
between a dominant or a fear related attitude is
usually possible on the basis of body posture and
facial expression (Houpt, 1998).
The aforementioned paradigm for dominance-
aggression has been challenged during the past
152
Back to contents
Marta Amat, DVM
Unitat de Fisiologia Animal
Facultat de Veterinària
Universitat Autònoma de Barcelona
08193 Bellaterra
Spain
few years by an increasing number of authors.
The main reason for that is that a significant
proportion of dogs suspected to be dominant
show ambivalent signals during aggressive
episodes as well as other more general signs of
anxiety (Overall, 1997).
Also, in wild canids and particularly in wolves,
low rank individuals often display aggression
towards high rank pack members in certain
situations, like food protection Harrington & Asa,
2003; Mech, 1970).
In cases of dog aggression, baring the teeth could
be linked to behavioural traits like fearfulness
of lack of tolerance to frustration, rather than
to an underlying dominant attitude. Aggression
shown by some dogs toward their owners would
not be the outcome of a dog challenging the
social hierarchy, but the inability to withhold
an aggressive response (Reisner, 2002). As
already suggested by other authors, dominance
and dominance-related aggression are not
synonymous terms (Overall, 1997).
From a practical perspective, understanding the
true underlying motivation in a case of aggression
towards family members is crucial to develop
a correct treatment protocol. For instance, in
different species castration has proved to be
effective to control certain forms of offensive
but not defensive aggression. Also, behaviour
modification protocols and drug therapy could
be markedly influenced by the initial diagnosis
offered by the veterinarian.
The purpose of this presentation is to discuss
diagnosis as well as the treatment protocols for
cases of canine aggression directed towards
family members.

References
Askew, H.R., 1996. Treatment of behaviour
problems in dogs and cats. Blackwell Science,
Berlin, pp 109-124.
Beaver B (1999) Canine Behaviour: a guide for
veterinarians. W.B. Saunders, Philadelphia, pp
137-199.
Borchelt PL, Voith VL (1996) Dominance
aggression in dogs. In: Voith VL and Borchelt
PL (Eds), Readings in Companion Animal
Behaviour. Veterinary Learning System, Trenton,
pp 230-239.
Guy NC, Luescher UA, Dohoo SE, Spangler E,
Miller JB, Dohoo IR, Bate LA (2001) A case
series of biting dogs: characteristics of the dogs,
their behaviour, and their victims. Applied Animal
Behaviour Science. 74: 43-57.
Houpt KA (1998) Domestic animal behavior for
veterinarians and animal scientists, Iowa State
University Press, Ames.
Back to contents
B
Lindsay S (2001) Applied Dog Behaviour and
Training Vol 2: Etiology and Assessment of
Behaviour Problems. Iowa State University
Press, Ames, pp 229-272.
Mech LD (1970) The Wolf: The Ecology and
Behavior of an Endangered Species. The Natural
History Press, New York.
Mertens P (2002) Canine aggression. In: Horwitz,
D., Mills, D., Heath, S., (eds), BSAVA Manual
of Canine and Feline Behavioural Medicine.
BSAVA, Gloucestershire, pp 195-215.
O’Farrell V (1992) Manual of Canine Behaviour.
British Small Animal Veterinary Association,
Glouchestershire.
Overall KL (1997) Clinical behavioral medicine
for small animals, Mosby, St. Louis. pp 88-137.
Reisner I (2002) An overview of aggression. In:
Horwitz, D., Mills, D., Heath, S., (eds), BSAVA
Manual of Canine and Feline Behavioural
Medicine. Gloucestershire, BSAVA, pp 181-194.
2006 World Congress WSAVA/FECAVA/CSAVA
153
B
B - Behaviour
DIDY” PRESENTATION OF A CLINICAL CASE OF CDS
Moisés Heiblum DVM
Veterinary Hospital Universidad
Nacional Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
Private Practice in Small Animal
Behavior, Naucalpan, Mexico,
Mexico
moisesheiblum@yahoo.com
Gilberto Chaves DVM
Veterinary Hospital Universidad
Nacional Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
Introduction:
The term Cognitive dysfunction syndrome
(CDS) has been used to refer to the changes of
behavior related to aging with cognitive skills
deterioration, that do not stem completely from
medical conditions and that are a consequence of
a degenerative process of the SNC.(8)
Clinical signs/behavioral changes
The term cognition, refers to mental processes
that take place inside the animals and cannot be
observed directly, it includes: memory, learning,
conscience and perception. (5)
The changes of behavior related to aging can
gather in 5 categories:
1. Loss of proper elimination behavior
2006 World Congress WSAVA/FECAVA/CSAVA
2. Disorientation
3. Alteration or decrease of the interactions with
the owners.
4. Alteration of the sleep-wake cycle.
5. Decrease of general activity
The behavior problems mentioned above can
have several etiologies, therefore it is necessary
to rule out the medical causes before diagnosing
CDS. The CDS is important because it constitutes
a more frequent consultation to the veterinarian,
due to medical knowledge and technology there
is an increase number of dogs that come to an
advanced age.(5,8)
Another relevant aspect takes root in that the CDS
could be an equivalent to Alzheimer’s disease in
humans and it’s study will help to understand the
responsible mechanisms for this illness; the dog
154
Back to contents
Rocio Labastida DVM
Veterinary Hospital Universidad Nacional
Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
Alberto Tejeda DVM MSC
Veterinary Hospital Universidad Nacional
Autonoma de Mexico
Tabachines 15
Jardines de San Mateo
Naucalpan
Mexico 53240
might be considered as a geriatric patient who
presents signs related to the CDS as a model to
study the Alzheimer type dementia (ATD) and to
achieve a major advance in the investigation of
the above mentioned illness. (5,8)
Prevalence of the CDS
It is difficult to know at what age CDS can
start showing signs of, but his prevalence is
higher with the overcome of the years. The life
expectancy after the diagnosis is about 1.5 - 2
years. (1,3,5,8)
Etiology and pathogenesis
In the dogs, senility is accompanied by some
neuropathological lesions and changes in the
neurotransmitters.
It is known that the CDS in dogs is caused by the
physical and chemical changes that take place in
the brain due to aging. (2,3)
Histopathology
The neuropathology of the CDS in dogs is
located especially in the cerebral cortex and
in the hypocampus. The more significant
histopathological remarks are the accumulations
of ß-amiloyd protein and the formation of
plaques.
Phisiopathology
Abnormalities exist in the neurotransmitters:
decrease or unbalance of acetilcholine, serotonin,
norepinefrine and dopamine. The loss of dopamine
and norepinefrine can contribute to the cognitive
deficits in the brains of old animals. (8)

The enzyme MAO-B catalizes the decrease of the
dopamine, producing free radicals. Some of the
physical changes we can observe are: ventricles
dilation, decrease of the size and cerebral mass,
decrease in the blood flow, decrease in the
number of neuron cells, fibrosis in meninges,
degeneration of white brain and cerebelar mass
and deposition of protein ß-amiloyd plaques.
The decrease in the capacity of learning
as a consequence of aging seems to be
related to alterations in the function of the
hypocampus.(2,4)
The diagnosis is completely confirmed by means
of histopathologic tests of the brain tissue, since
at first, diagnosis is by means of exclusion, ruling
out possible competing pathologies and the most
subjective observation of clinical unspecific signs
that could be related to CDS.
Treatment of CDS
The CDS cannot be cured, but there are some
therapeutic possibilities that are palliative and
that can slow down the progress of the illness.
Treatment
1. Make a diagnosis to determine underlying
pathology and be able to treat it accordingly.
2. Determine stimuli that causes or reinforce the
problem.
3. Make environmental modifications that
facilitate movement and social interaction in the
patient.
4. Use behavior modification techniques to
reinforce proper behaviors.
5. Pharmacological intervention:
a) Selegiline a MAOI to enhance dopamine
b) Nicergoline an alpha adrenergic blocker
to enhance blood flow to the brain
6. Geriatric diet or the use of antioxidants to
protect cells membranes and get rid of free
radicals that are neurotoxic. (5)
“Didy”, presentation of a clinical case of CDS
Signalment: “Didy“ intact female domestic mixed
dog, 14-years-old.
Chief complaint: aggression towards another dog
in their household.
Findings in the case history: aggressiveness
against her companion dog, barks at objects,
looks at the wall for long periods, spatial
disorientation within the house (roaming without
a definite course), changes in the appetite, night
insomnia, sleeps much during daytime, moans
and vocalizes, urine and feces inside house.
Day 1, January 15th. 2005
Consultation at the HVE UNAM
Back to contents
B
Anamnesis: The owners mention that “Didy“
began to fight with her partner since November,
attacks him for no reason, then, later returns to
him and licks him as if nothing had happened.
Two weeks ago, after fighting, she remained
completely rigid and started barking, the owners
were talking to her but she was not paying any
attention, sometimes although there was no
fighting, she began to bark to the window or to
the wall. “Didy“ does not want to go out and
they have to drag her out to eliminate, the owner
told the medical staff that she has diminished her
general interaction with the human group and
they notice a notable lack of interest to be with
the human beings and to her canine partner.
She also shows some pain when getting up or
while walking, there is a remarkable halitosis and
bilateral opaqueness of crystalline.
Laboratory tests were made to know the general
Physical status of “Didy”, the results showed:
hiperbilirrubinemia and hiperphosphoremia,
(hemolisis, lipemia). Hiperproteinemia,
hiperglobulinemia and high values of
triglicerides.
She was sent home medicated with Condroitin
sulfate 1 tab PO SID and vitamin E 400 UI PO
SID until the next consultation.
Evaluation was suggested in the sections of
orthopedics, soft tissue, ophthalmology; an EKG
and dental cleanliness.
Integral profile is programmed. We arranged to
meet in 13 days for more lab tests and in one
month for a behavior consultation.
Day 31st. February 16th. 2005
Didy arrives for her behavior consultation at
the HVE for her aggression problem and other
undesirable behaviors.
Clinical History: The owners report “didy” as
showing aggressiveness against another dog, 2006 World Congress WSAVA/FECAVA/CSAVA
barking at objects, looking at the wall, getting
lost, (does not find the door), walks around the
house, collides with objects, remains a lot of time
jammed behind an armchair and has stopped
eating. The owners said also that “Didy” sleeps
very much during daytime, and does not allow
the owners to sleep at night because she strolls
and wails constantly, urinates and defecates inside
house. “Didy” does not want to go out anymore
and they have to drag her out to eliminate. She
has diminished the social interaction with the
owners and with her canine partner.
Presumptive Diagnosis: Cognitive dysfunction
syndrome associated with a loss of general
sensorial function.
We send her home with this treatment:
155
B
• Create an ideal environment for “Didy“ where
she feels comfortable and safe
• Clear off furniture and objects out of her way
• Create a much more predictable and reliable
routines in her daily activity
• Educate owners Not to punish her for vocalizing
or eliminating inside
• To supervise her in a more close by way, lead
her to eliminate more frequently out and when
this is not possible keep her in an area of easy
cleanliness
• Give her privileged attention time without the
other dog’s presence
• Supervise the interaction between both dogs,
separate them if supervision is not possible, and
favor the leadership of “Duke” over “Didy“
• Increase walks and increase stimuli with
“interactive toys”
• Relaxation massages in pleasure body spots
• Gradual change in the diet to geriatric dog food
• A daily capsule of 400 UI of Vitamine E
• Selegiline 10 mg every 24 h AM
Day 36 February 21st. 2005
“Didy´s” owners arrive at the hospital mentioning
that the problem has been increasing. The owners
told us that they can´t give “Didy” the attention
required and that the signs that “Didy” presents
are already intolerable for a good quality of life
so they ask to euthanize “Didy”.
To discard some other problems, a general physical
exam is realized, also a neurological, orthopedic,
ophtalmológic examination and laboratory tests,
since there were other differential diagnosis to
be made due to the behavior showed by “Didy“,
it was possible to think as the first differential
diagnosis a brain tumor such as meningioma or
astrocitoma.
As the second presumptive diagnosis we have the
CDS.
The euthanasia was performed.
2006 World Congress WSAVA/FECAVA/CSAVA
Findings at the necropsy
In the brain cranial cavity: the leptomeninges
presented white areas and road surfaces
compatible with calcification.
Microscopic description: presents gliosis,
satelitosis and diffuse neurofagia, some neurons
were appreciated as hyperchromatic. Likewise,
red congo material (+) is observed in the average
layer of some blood vessels compatible with
amiloidosis.
Morphologic diagnosis
Brain: Gliosis, satelitosis and diffuse moderate
neurofagia with neuronal multifocal necrosis and
deposits of congo red material (+) compatible
with amiloidosis.
156
Back to contents
Comment: The histomorphologic alterations
described earlier suggest that this animal coursed
with the illness known as “Cognitive dysfunctional
syndrome” (CDS) described in old dogs.
Discussion
The CDS is little known both by the Veterinarians
and by the owners of affected pets. The CDS
leads to behavioral changes in the patient and
these changes lead as well to a deterioration in
the human-animal bond with a dissolution of the
affective tie between owner and dog. What is then
translated in the decision of the owner to euthanize
the patient; the whole situation could be avoided
by knowing more thoroughly this pathology and
considering it to be a differential diagnosis when
a geriatric patient should arrive at the clinic.
In order to do that, it is necessary to realize a
complete clinical history and suitable physical
exam to rule out systemic illnesses by means
of laboratory tests. It is also very important to
educate owners as to have real expectations with
the treatment options, having only the option to
slow down the process of cognitive malfunction
and to increase the quality of life of the patient
during the course of the illness.
Conclusion
It is important to stress out that, on having
improved the quality of life of the small species,
there has given the opportunity to live longer,
this has increased the number of geriatric patient
attended by veterinarians that work with dogs and
cats; for which they must know the illnesses that
affect them, being one of the most common but
less recognized the CDS
References
1. Dodman N, Shuster L, Psicofarmacología de
los trastornos del comportamiento animal. Buenos
Aires República de Argentina: Intermédica 2000
2. Manteca X, Etología clínica veterinaria del
perro y del gato. 2ª ed. Barcelona España: Gráfica
In Multimédicas S.A. 2003
3. Juarbe-Diaz, Behavior problems in older dogs.
Knoxville: University of Tennesse, College of
Veterinary Medicine.
4. Manteca X, Etología clínica veterinaria del
perro y del gato. 3ª ed. Barcelona España: Gráfica
In Multimedias S.A 1997
5. Heiblum M Trastornos geriátricos. Memorias
de Etología clínica en perro y gatos; 2003
marzo 5-8; México (DF): Facultad de Medicina
Veterinaria y Zootecnia UNAM, 2003:69-75
6. Landsberg G, Hunthausen W, Ackerman .
Manual de problemas de conducta en el perro y el
gato. Zaragoza España: Acriba S.A. 1998
 B
7. Aminoff M, Greenber D. Neurología clínica. 3ª courses November 2001 Update on diagnosis and
ed. México: Manual moderno, 1998 treatment of small animal behavior problems.
8. University of Georgia, continuing education

2006 World Congress WSAVA/FECAVA/CSAVA

157
Back to contents
B
B - Behaviour
QUICK SUMMARY OF HOW AND WHY THREE KEY DRUGS WORK
Karen L. Overall, MA,VMD,
PhD
Diplomate ACVB
ABS Certified Applied Animal
Behaviorist
Center for Neurobiology and
Behavior
Psychiatry Department - Penn
Med Translation Research
Laboratory 125 S. 30th St.
Philadelphia, PA 19104
overallk@mail.med.upenn.edu
http://psych.ucsf.edu/
K9Behavioral/Genetics
Rationale: The addition of psychotherapeutic agents
to routine behavioral treatments, such as behavioral
and environmental modification, has lead to better
and faster treatment outcomes. In addition to
facilitating better treatment of domestic animals
and humans, psychopharmacological developments
have permitted hypotheses about underlying
mechanistic pathology to be tested. Mere treatment
of non-specific behavioral complaints and signs
is outdated (eg., treat barking by cutting the vocal
cords) and has been replaced with an approach
that includes ensuring that you meet the criteria
for diagnosis, prior to treatment, followed by
treatment that addresses the specific mechanism
underlying the neurochemical contribution to
the pathology (1).
The use of medication should occur and is
most effective as part of an integrated treatment
program. There is no substitute for the hard work
involved in behavior modification; however, some
medications may be able to make it easier to
implement the modification (2-4). Those seeking
2006 World Congress WSAVA/FECAVA/CSAVA
‘quick fix’ solutions will doubtless be disappointed:
inappropriate drug use will not alter the processes
or environments that produced the behavior. While
medication, alone, may render an animal globally
less anxious, if the animal is still being provoked my
social or physical environmental stimuli the benefit
of treatment with medication will be minimized. It is
partly this facile and inappropriate use of medication
that has led many practitioners to falsely believe
that medication does not work. Nothing could be
further from the truth: the newer serotonin-affecting
medications, protective neutraceutical, and enhanced
dietary regimes have a huge potential improve life
for troubled pets and their distressed people. In
fact, rational drug use should now minimally be
considered part of basic humane treatment of our
patients. The 3 most commonly used - and most
useful drugs - in veterinary behavioral medicine
158
Back to contents
come from 3 classes: benzodiazepines (alprazolam);
tricyclic antidepressants (TCAs: amitriptyline,
clomipramine); and selective serotonin re-uptakes
inhibitors (SSRIs: fluoxetine).
Adverse effects: The neurotransmitters affected by
behavioral medications are acetylcholine, serotonin,
norepinephrine (noradrenaline), dopamine, gamma
amino butyric acid (GABA), and excitatory amino
acids. Common adverse effects of psychotherapeutic
drugs are usually caused by a blockage of the
muscarinic acetylcholine receptors, which have
diffuse connections throughout the brain. These
‘common’ side effects are actually quite rare and
generally manifest themselves as transient changes
in GI function or heart rate. If these side effect ARE
NOT transient, clients need to understand that their
pet may be experiencing a serious problem. For
this reason, it is important to encourage clients to
help monitor both their anima;’s response to the
medication, and any side effects that they may
have. Clients can easily learn to take pulse rates.
Slight increases in pulse rate when treated with any
medications affecting norepinephrine - as most the
anti-anxiety agents do - are not worrisome. Huge,
sustained increases are problematic. If clients
know that their dog’s resting heart rate is 65 bpm
and with medication this changes to 150 bpm, they
can immediately bring this change to their vet’s
attention. Likewise, if the increase is minor (65 to 75
bpm) they can relax and not worry. Educated clients
will monitor their pets better, will be more willing
to use medications and behavior mod appropriately,
and will also be less likely to take the veterinarian’s
time needlessly. While many benzodiazepines (BZ)
can be sedative, newer BZ have decreased sedative
effects. Still, because dogs and cats, like humans,
can experience a huge range of effects when given
a BZ, clients should be encouraged to give any BZ
when they can monitor the patient. This practice
is extremely helpful in ensuring that we recognize

animals with atypical or serious sedative responses
so that we can find more appropriate medications
with which to treat them.
Most behavioral drugs are metabolized through
renal and hepatic pathways so knowledge of baseline
values is essential. That said, these medications can
be used in compromised animals if adjustments are
made and the animal is monitored behaviorally and
biochemically.
All psychotropic medications can interact with other
medications. For example, use of most anti-anxiety
agents will cause thyroidal values - whether or not
supplementation is involved - for read falsely low.
Many of serotnergic agents are thought to lower
seizure thresholds and so are recommended with
caution in patients treated with seizures. That said,
there is now evidence in both the human and canine
literature that anxiety may lower seizure thresholds
and so treatment of the anxiety may allow the
patient to successfully decrease the amount of
seizure medication needed.
Efficacy and mechanism of action: It’s important
for clients to understand that newer, more specific,
more efficacious drugs have a relatively long lag
time between initiation of treatment and apparent
changes in the patient’s behavior. This delay is
due to the mechanism of action of the tricyclic
antidepressants (TCAs) and the selective serotonin
re-uptake inhibitors (SSRIs) which employ second
messenger systems to alter transcription of receptor
proteins.
Serotonin (5-HT) receptors are all G-protein-
coupled receptors. There are 14 identified classes
of serotonin receptors. The 5-HT1 receptors are
linked to the inhibition of adenylate cyclase and
affect mood and behavior. Presynaptic 5-HT1A-
receptors predominate in dorsal and median
raphé nuclei; post-synaptic 5-HT1A-receptors
predominant in limbic regions (hippocampus and
septum) and some cortical layers. Activation of pre-
synaptic receptors by agonists results in decreased
firing of serotonergic neurons leading to transient
suppression of 5-HT synthesis and decreased 5-
HT release; activation of post-synaptic receptors
decreases firing of post-synaptic cells. These are
‘thermostatic’ effects, not integrated outcomes of
receptor activation. The overall effect depends on
regulation of second messengers (cAMP, Ca2+,
cGMP, IP3) and their effects on protein kinases
which then alter neuronal metabolism and receptor
protein transcription (5). The subclasses of 5-HT
receptors vary in their affects. 5-HT1A receptors
affect mood and behavior. 5-HT1D receptors affect
cerebral blood vessels and appear to be involved in
the development of migraine. These last two classes
of receptor subtypes are the primary focus of many
behavioral drugs. Urinary excretion of 5-HIAA (5-
hydroxy indoleacetic acid) is a measure of 5-HT
Back to contents
B
turnover and has been used to assess neurochemical
abnormalities in human psychiatric patients, and
has potential in this regard for veterinary behavioral
medicine.
Neutraceuticals designed to augment 5-HT or 5-HT
supplements may not engender the same response
as to pharmacologic agents because 5-HT does not
pass easily through the blood brain barrier (BBB),
and instead requires the help of a transport protein.
This transport protein is also used to move other
amino acids across the BBB, and so - even if 5HT
containing substances are absorbed unchanged
from the GI tract, they may be excreted depending
on the pharmacodynamics of the other amino acids
present (6).
Noradrenaline / norepinephrine (NE): The most
prominent collection of noradrenergic neurons is
found in the locus coeruleus of the grey matter of
the pons and in the lateral tegmental nuclei. There is
also a cluster in the medulla. NE has been postulated
to affect (1) mood [NE decreases in depression and
increases in mania], (2) functional reward systems,
and (3) arousal.
Dopamine: The distribution of dopamine in the
brain is non-uniform, but is more restrictive
than that of NE. Dopaminergic nuclei are found
primarily in: (1) the substantia nigra pars compacta
which projects to the striatum and is largely
concerned with coordinated movement; (2) the
ventral tegmental area which projects to the frontal
and cingulate cortex, nucleus acumbens, and other
limbic structures; and (3) the arcuate nucleus of
the hypothalamus which projects to the pituitary. A
large proportion of the brain’s dopamine is found in
the corpus striatum, the part of the extrapyramidal
system concerned with coordinated movement.
Dopamine is metabolized by monamine oxidase
(MAO) and catechol-O-methyl transferase (COMT)
into dihydroxyphenyl acetic acid (DOPAC) and
homovanillic acid (HVA). HVA is used as a
peripheral index of central dopamine turnover in
humans, but this use has been little explored in
2006 World Congress WSAVA/FECAVA/CSAVA
veterinary medicine. All dopaminergic receptors are
G-protein-coupled transmembrane receptors. The
D1 receptors exhibit their post-synaptic inhibition in
the limbic system and are affected in mood disorders
and stereotypies. The D2, D3, and D4 receptors are all
affected in mood disorders and stereotypies. Excess
dopamine, as produced by dopamine releasing
agents (amphetamines and dopamine agonists, like
apomorphine) is associated with the development
of stereotypies. Because of this - and because
acepromazine is a neuroleptic agent that scrambles
memory but does not prevent or treat anxiety -
ACEPROMAZINE SHOULD NEVER BE USED
AS A BEHAVIORAL MEDICATION OR AS A
TREATMENT FOR STORM PHOBIAS.
Gamma amino butyric acid (GABA): GABA,
159
B
the inhibitory neurotransmitter found in short
interneurons, is produced in large amounts only in
the brain and serves as a neurotransmitter in ~30%
of the synapses in the human CNS. The only long
GABA-ergic tracts run to the cerebellum and
striatum. GABA is formed from the excitatory
amino acid (EEA) glutamate via glutamic acid
decarboxylase (GAD), catalyzed by GABA-
transaminase (GABA-T) and destroyed by
transamination. There are two main groupings
of GABA receptors - GABAA and GABAB.
GABAA receptors, ligand-gated ion channels,
mediate post-synaptic inhibition by increasing
Cl- influx. Barbiturates and benzodiazepines
are a potentiators of GABAA; however they do
so by increasing the amount of time channels
remain open - a relatively non-specific change.
It is for this reason why these are NOT suitable
behavioral medications, and why one is more
likley to get a sedated, rather than a less anxious
dog, when the dog is treated with phenobarbital
for behavioral reasons. GABAB receptors are
involved in the fine-tuning of inhibitory synaptic
transmission: presynaptic GABAB receptors
inhibit neurotransmitter release via high voltage
activated Ca++ channels; postsynaptic GABAB
receptors decrease neuronal excitability by
activating inwardly rectifying K+ conductance
underlying the late inhibitory post synaptic
potential.
GABA also has a variety of tropic effects
on developing brain cells. During ontogeny
GABAergic axons move through areas where other
neurotransmitter phenotypes are being produced,
and so may be related to later monoaminergic
imbalances. The extent such ontogenic effects
are relevant for behavioral conditions is currently
unknown but bears investigating.
EAAs (glutamate, aspartate, and, possibly,
homocysteate): EEAs have a role as central
neurotransmitters and are produced in abnormal
2006 World Congress WSAVA/FECAVA/CSAVA
levels in aggressive, impulse, and schizophrenic
disorders. The main fast excitatory transmitters
in the CNS are EEAs. Glutamate, widely and
uniformly distributed in the CNS, is involved
in carbohydrate and nitrogen metabolism. It
is stored in synaptic vesicles and released by
Ca2+ dependent exocytosis, so calcium channel
blockers may affect conditions associated with
increased glutamate. Both barbiturates and
progesterone suppress excitatory responses to
glutamate. Pre-synaptic barbiturates inhibit
calcium uptake and decrease synaptosomal
release of neurotransmitters, including GABA
and glutamate.
Roles for neuronal stimulation, synaptic
plasticity, and receptor protein transcription and
translation: What makes TCAs and SSRIs special
160
Back to contents
and why are they so useful for anxiety disorders?
The key to the success of these drugs is that they
utilize the same second messenger systems and
transcription pathways that are used to develop
cellular memory or to “learn” something. This
pathway involves cAMP, cytosolic response
element binding protein (CREB), brain derived
neurotrophic factor (BDNF), NMDA receptors,
protein tyrosine kinases (PTK) - particularly Src
- which regulate activity of NMDA receptors and
other ion channels and mediates the induction of
LTP (long-term potentiation = synaptic plasticity)
in the CA1 region of the hippocampus.
There are two phases of TCA and SSRI treatment:
short-term effects and long-term effects. Short-
term effects result in a synaptic increase of the
relevant monoamine associated with re-uptake
inhibition. The somatodendric autoreceptor of the
pre-synaptic neuron decreases the firing rate of
that cell as a thermostatic response. Regardless,
there is increased saturation of the post-synaptic
receptors resulting in stimulation of the -
adrenergic coupled cAMP system. cAMP leads
to an increase in PTK as the first step in the long-
term effects. PTK translocates into the nucleus of
the post-synaptic cell where it increases CREB,
which has been postulated to be the post-receptor
target for these drugs. Increases in CREB lead
to increases in BDNF and tyrosine kinases (e.g.,
trkB) which then stimulate mRNA transcription of
new receptor proteins. The altered conformation
of the post-synaptic receptors renders serotonin
stimulation and signal transduction more
efficient.
Knowledge of the molecular basis for the action
of these drugs can aid in choosing treatment
protocols. For example, the pre-synaptic
somatodendritic autoreceptor is blocked by
pindolol (a -adrenoreceptor antagonist) so
augmentation of TCA and SSRI treatment with
pindolol can accelerate treatment onset. Long-
term treatment, particularly with the more specific
TCAs (e.g., clomipramine) and SSRIs, employs
the same pathway used in LTP to alter reception
function and structure through transcriptional
and translational alterations in receptor protein.
This can be thought of as a form of in vivo “gene
therapy” that works to augment neurotransmitter
levels and production thereby making the
neuron and the interactions between neurons
more coordinated and efficient. In some patients
short-term treatment appears to be sufficient to
produce continued “normal” functioning of the
neurotransmitter system. That there are some
patients who require life-long treatment suggests
that the effect of the drugs is reversible in some
patients, further illustrating the underlying

heterogeneity of the patient population considered
to have the same diagnosis.
Monitoring: Monitoring of side-effects is critical
for any practitioner dispensing behavioral
medication. The first tier of this involves the same
tests mandated in the pre-medication physical
and laboratory evaluation. Age-related changes in
hepatic mass, function, blood flow, plasma drug
binding, et cetera cause a decrease in clearance
of some TCAs, so it is prudent to monitor hepatic
and renal enzymes annually in younger animals,
biannually in older, and always as warranted by
clinical signs. Adjustment in drug dosages may
be necessary with age.
It is generally preferable - but not necessarily
required - to withdraw most patients from
one class of drug before starting another. For
most medications this is done so that one can
be sure which medication is associated with
any noted change in behavior. When changing
between SSRIs and MAOIs a washout period is
mandatory because of the potential for serotonin
syndrom.......the recommended drug-free time in
humans and dogs is two weeks (2 + half-lives:
the general rule of thumb for withdrawal of any
drug).
Polypharmacy: Oddly, because of the cytochrome
systems that metabolize medication, it may
be safer for the animal and more efficacious in
terms improvement of the condition to combine
medications. When medications are combined a
knowledge of side effects and specific mechanisms
of action is essential. That said, medications
within related classes can usually be combined
and such combination can allow a lower dose of
each of the medications to be given. Medications
of different classes can often be combined, if
the potential side effects are compatible, and
if the practitioner has a clear understanding of
what conditions will or should respond to each
medication.
For example, tricyclic antidepressants (TCAs) and
selective serotonin reuptake inhibitors (SSRIs)
can be combined with each other, and, if needed,
with other medication within the class. For this
to be done rationally, however, understanding
potentiation of effect and side effects is essential.
TCAs generally exert their largest effects on
serotonin (5-HT) receptors, norepinephrine (NE)
receptors, and some histaminic receptors (H).
Additionally, they can have effects on some of
the adrenergic receptors. The latter is important
primarily when premedication for anesthesia is
involved. SSRIs primarily affect 5-HT receptors,
and most have an affinity for the 5-HT1a subtype
receptor. Additionally, there are some weak effects
on NE receptors. TCAs that are less specific (eg,
amitiptyline) and SSRIs that are more specific
Back to contents
B
(eg, fluoxetine) will be the easiest to combine
since the overlap effects on the receptor will be
less, while the generalized sensitization of the
receptors in the class will be augmented.
Combination treatment allows the clinician to use
the lower end of the dosage for both compounds
which minimizes side effects while maximizing
efficacy. Furthermore, benzodiazepines can be
used to blunt or prevent acute anxiety-related
outbursts on an as needed basis in patients
for whom daily treatment with a TCA or an
SSRI is ongoing. Together, the combination
of benzodiazepines and TCAs / SSRIs may
hasten improvement and prevent acute anxiety-
provoking stimuli from interfering with treatment
of more regularly occurring anxieties.
When stopping a drug, weaning is preferred to
stopping abruptly (7). A model for how to do
this is found below (7). Weaning minimizes
potential central withdrawal signs, including
those associated with serotonin dyscontinuation
syndrome (8,9) and allows determination of the
lowest dosage that is still effective. If patients
are withdrawn fully, rather than weaned from
medication, they may not have the same response
to the medication that they had originally. Patients
with dyscontinuation or cessation syndrome
become moody and lethargic, but these effects
usually pass within a week. If they do not, re-
assessment of the wisdom of stopping medication
is warranted. Medications that have the longest
t1/2 of intermediate metabolites (eg, fluoxetine)
are less likely to cause problems when withdrawn
quickly than are those with short half-lives or
no functional intermediate metabolites (eg,
paroxetine). However, SSRIs that have the greatest
in vivo reuptake capabilities (eg, paroxetine) may
be more at risk for involvement in serotonin
syndrome. Long-term treatment may be the rule
with many of these medications and conditions,
but maintenance may be at a considerably lower
level of drug than was prescribed at the outset.
2006 World Congress WSAVA/FECAVA/CSAVA
The only way the practitioner will discover if this
is so is to withdraw the medication slowly.
Because of these patterns, it is best NOT to
withdraw animals from medication prior to
anesthesia, but instead to adjust the pre-medication
sedation so that fewer interactions - particularly
of the adrenegic variety - can be expected.
Finally, many animals appear to stop responding
to medication. Staying the course may be the
best decision in some of these cases because the
CPY system is an inducible one, and multiple
medication changes may just make the animal
more - not less - refractory (10). Additionally,
there is a huge range of genetic polymorphisms
that determine how this system acts (11). These
are all poorly understood in dogs because they
161
B
have been so little investigated. However, given
their importance in human psychiatry we’d be
remiss if we didn’t start to believe that such
patterns may no be independent of disease state.
Polypharmacy can be safe, rational, and cheap,
and can save animals’ lives. But this is an area
that really requires an understanding of how these
medications act. Fortunately, the functioning of
these medications is easy to understand.

Sample combinations (12) :

amitriptyline (TCA) + fluoxetine (SSRI)

amitriptyline (TCA) + fluoxetine (SSRI) + alprazolam (BZ)
amitriptyline (TCA) [anxiety] + alprazolam (BZ) [panic]
fluoxetine (SSRI) [anxiety] + alprazolam (BZ) [panic]
clomipramine (TCA - relatively specific) [anxiety] + alprazolam (BZ) [panic]
clomipramine (TCA - relatively specific) [anxiety] + diazepam (BZ) [panic / phobias]
- could be pretty sedating
amitriptyline (TCA) [anxiety] + diazepam (BZ) [panic / phobias] - could be pretty sedating
selegiline (MAO-I) (cognitive dysfunction) + diazepam (BZ) [panic / phobias]
selegiline (MAO-I) (cognitive dysfunction) + alprazolam (BZ) [panic]
paroxetine (SSRI) (social anxiety) + alprazolam (BZ) [panic / appetite stimulation in cats]

“Gestalt” of TCA and SSRI use based on t1/2 of parent compounds and active intermediate metabolites,
relative effects on NE and 5-HT, and extrapolations from multi-center human studies (7)

Diagnosis / Type of condition First drug of choice

Narcolepsy imipramine
Milder, relatively non-specific anxieties amitriptyline
Milder, relatively non-specific anxieties with avoidance nortriptyline
of sedation
Social phobias / anxieties concerning social interaction paroxetine
Panic / generalized anxiety sertraline
Outburst aggression / related anxieties fluoxetine
Ritualistic behavior associated with anxiety, including OCD clomipramine

Algorithm for treatment length and weaning schedule (7)

(1) Treat for as long as it takes to begin to assess effects:

2006 World Congress WSAVA/FECAVA/CSAVA

7-10 days for relatively non-specific TCAs

3-5 weeks minimum for SSRIs and more specific TCAs
PLUS
(2) Treat until “well” and either have no signs associated with diagnosis or some low, consistent level:
minimum of another 1-2 months
PLUS
(3) Treat for the amount of time it took you to attain the level discussed in (2) so that reliability of assessment
is reasonably assured:
minimum of another 1-2 months
PLUS
(4) Wean over the amount of time it took to get to (1) or more slowly. Remember, if receptor conformation
reverts it may take 1+ months to notice the signs of this. While there are no acute side effects associated with
sudden cessation of medication, a recidivistic event is a profound “side effect”. Full-blown recidivistic events
may not be responsive to re-initiated treatment with the same drug and, or the same dose:
7-10 days for relatively non-specific TCAs
3-5 weeks minimum for SSRIs and more specific TCAs
TOTAL: Treat for a minimum of 4-6 months

162
Back to contents

References
1. Overall KL . Veterinary behavioural medicine: a
roadmap for the 21st century. The Veterinary Journal
2005; 169: 130-143.
2. King J, Simpson B, Overall KL et al. Treatment
of separation anxiety in dogs with clomipramine.
Results from a prospective, randomized, double-
blinded, placebo-controlled clinical trial. J Appl
Anim Behav Sci 2000; 67: 255-275.
3. Mills D, Ledger R. The effects of oral selegiline
hydrochloride on learning and training in the dog:
a psychobiological interpretation. Prog Neuro
Psychopharmacol & Biol Psychiatr 2001; 25: 1597-
1613.
4. Overall KL, Dunham AE: Clinical features and
outcome in dogs and cats with obsessive-compulsive
disorder: 126 cases (1989-2000). J Am Vet Med
Assoc 2002; 221: 1445-1452.
5. Duman R.S. (1998) Novel therapeutic approaches
beyond the serotonin receptor. Biololgical
Psychiatry 1998; 44, 324-335.
Back to contents
B
6. Grimmett A, Sillence MN. Calmatives for the
excitable horse: a review of L-tryptophan. The
Veterinary Journal 2005; 170: 24-32.
7.Overall KL. Pharmacological treatment
in behavioral medicine: The importance of
neurochemistry, molecular biology, and mechanistic
hypotheses. The Veterinary Journal 2001; 62: 9-23.
8. Rosenbaum JF, Fava M, Hoog et al. Selective serotonin
reuptake discontinuation syndrome: a randomized
clinical trial. Biol Psychiatry 1998; 44: 77-87.
9. Zajeka J, Fawcett J, Amsterdam J, et al. Safety of abrupt
discontinuation of fluoxetine:a randomized, placebo-
controlled study. J Clin Psychiatry 1998; 18: 193-197.
10. American PsychiatricAssociation. TheAPATextbook
of Psychopharmacology, Washington DC, 2004.
11. Tribut O, Lessar Y, Reymann J-M, et al.
Pharmacogenomics Med Sci Monit 2003; 8: RA152-163.
12. Overall KL. Manual of clinical behavioral
medicine for small animals. Elsevier, St. Louis,
2006.
2006 World Congress WSAVA/FECAVA/CSAVA
163
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

CC
Cardiology
rdiol & Pulmonology

Back to contents

INVITED LECTURES - FULL PAPERS
C - Cardiology & Pulmonology
PROMISING CARDIOVASCULAR DRUGS – PIMOBENDAN
Christophe W. Lombard, Prof.
DACVIM (Cardiology),
DECVIM-CA
Dept. of clinical veterinary
medicine
Vetsuisse Faculty, University of
Berne
Länggass-Strasse 124, PO Box
CH-1201 Bern/Switzerland
christophe.lombard@kkh.unibe.ch
Pimobendan is a novel new cardiac pharmaceutical
termed an inodilator as it possesses both positive
inotropic and balanced peripheral vasodilatation
properties. Unlike historical positive inotropes
(e.g., digoxin, milrinone) that function by
increasing intracellular calcium concentrations
with increased energy/oxygen requirements
being a direct consequence, pimobendan acts as
a positive inotrope via enhancing the affinity of
myocardial troponin C to existing intracellular
calcium (Gwathmey et al 1987, Morgan 1991)
The result is improved contractility without
attendant increased myocardial oxygen or
energy requirements (Bohm 1991). Peripherally,
pimobendan is a phosphodiesterase III inhibitor
resulting in balanced peripheral vasodilation
through increased efflux of intracellular
calcium from vascular smooth muscle (Meel
and Dierden 1989, Verdouw et al, 1986). With
balanced vasodilatation reducing cardiac work
via reductions in preload and afterload, coupled
with the economical increase in contractility,
the dual action of pimobendan has a favourable
hemodynamic effect without an adverse effect on
myocardial energy consumption and thus does
not further compromise the failing heart.
The result has been a reduction in the activity of the
neurohormonal compensatory mechanisms (i.e.,
renin-angiotensin-aldosterone system [RAAS],
sympathetic nervous system [SNS]) active in
heart failure, evidenced by reductions in atrial
natiuretic peptide (ANP), brain natriuretic peptide
(BNP), norepinephrine, renin, and angiotensin II as
demonstrated via studies done in people (Sasaki et al,
1999, Erlemeyer et al, 1991). Additional properties
include improved reversal of desensitization of
baroreceptors (Baumann et al 1989), lusitropy
(Asanoi 1994), reduced platelet aggregation
(Batisda 1986), and an antiinflammatory effect
through cytokine reduction (Iwasaki 1999).
Back to contents
C
Canine studies with cardiomyopathy. Based
on pimobendan’s pharmacodynamic profile, it
appears to be a pharmaceutical agent well suited
suited for the treatment of heart failure due to
cardiomyopathy as well as chronic valvular
disease/mitral regurgitation. Studies in dogs with
dilated cardiomyopathy have clearly demonstrated
the improvements in quality and quantity of life
when pimobendan was added to traditional (i.e,
diuretic, ACEI, + digoxin) therapy (Luis Fuentes
et al, 2002, O’Grady et al 2003) and supported
by similar studies in people (the EPOCH study
group 2002).
A summary of the soon to be published PiTCH
study reads as follows: A multicenter randomized,
posotive-controlled double-blind trial compared
pimobendan 0.4 – 0.6 mg/kg/day orally with
benazapril 0.25 – 0.5 mg/kg/day or a combination
of both drugs, with additional furosemide allowed
as needed, in dogs with modified NYHA class
III or IV heart failure over 28 days. In a follow-
up voluntary longterm study phase, dogs were
allowed to continue on pimobendan or placebo 2006 World Congress WSAVA/FECAVA/CSAVA
until study withdrawal, death or censoring. A
total of 81 dogs with dilated cardiomyopathy
were included. Eight different clinical parameters
such as appetite, demeanour, exercise tolerance
etc. as well as ECG’s, radiographs and
echocardiograms were evaluated. Pimobendan
was well-tolerated, had a better overall efficacy
(p<0.05) and fewer treatment failures than
benazepril (8% versus 33 %, p<0.05) in the first
28 days (Lombard 2001). In the long-term study
period, median survival was 249 days in the
pimobendan group versus 34 days in the placebo
group (p<0.05). Pimobendan therefore improved
clinical signs with advanced heart failure, and
improved long-term survival compared with
placebo when added to standard treatment. So
far, the mechanism of clinical improvements
165
C
could not be elucidated and supported/buttressed
by beneficial echocardiographic changes of the
ventricular volumes or shortening fractions.
Admittedly however, these echocardio-graphic
measurements are fairly crude assessments of
ventricular function, and more advanced methods
such as Doppler-derived indicators of systolic
and diastolic function or TDI-assessment of
ventricular function are needed to document
or illustrate the cardiac improvements by such
graphical measurements.
Canine studies with chronic valvular disease/mitral
regurgitation. The recently published VetSCOPE
study (Lombard et al, 2006)documented
similar beneficial of Pimobendan effects
2006 World Congress WSAVA/FECAVA/CSAVA
166
Back to contents
in dogs with congestive heart failure due
to valvular regurgitation. Besides superior
clinical improvements over Benazepril and
smaller drop-out rates during the mandatory
56-day study period, Pimobendan caused a
significant reduction of heart size assessed
by the VHS-method (Buchanan and Bucheler
1995) and therefore showed beneficial effects
of reverse remodelling, one of the important
goals of modern therapy for congestive heart
failure. In the optional longterm arm of the
VetSCOPE study, Pimobendan again proved
superior to Benazepril and caused significantly
longer median survival times (415 vs. 128
days.

C - Cardiology & Pulmonology
DRUGS USED IN THE MANAGEMENT OF RESPIRATORY DISEASES
Professor David Church
Department of Veterinary Clinical
Science
The Royal Veterinary
Hawkshead Lane
North Myjme
Hatfield
Hertfordshire, AL9 7TA.
dchurch@rvc.ac.uk
Respiratory diseases in dogs and cats can be clas-
sified into respiratory problems brought about as
a result of a specific abnormality of the respirato-
ry system; so called primary respiratory disease,
and bronchopulmonary problems which occur as
a consequence of heart failure; so called second-
ary respiratory disease. This section will concen-
trate predominantly on considerations regarding
the treatment of non-infectious aspects of prima-
ry respiratory diseases. This includes agents used
to facilitate bronchodilation, to reduce coughing
and various expectorants and mucolytics.
In order to understand the indications for, and
action of, various drugs used in the treatment of
respiratory disease an understanding of normal
respiratory physiology is important and these
considerations will be dealt with in the relevant
sections.
BRONCHODILATORS
Relevent pathophysiology
Physiological bronchial tone is mediated by three
neuroendocrine systems:
(i) the parasympathetic system, the dominant
efferent pathway in animals, which provides the
baseline tone of mild bronchoconstriction that
characterizes the normal respiratory tract
(ii) the sympathetic system which mediates these
inherent bronchoconstrictive effects through
β2-adrenergic-mediated bronchodilation and α1-
mediated bronchoconstriction as well as possibly
α2-mediated reduction of parasympathetic
bronchoconstriction
(iii) the non-adreneric, non-cholinergic (NANC)
system which apparently further mediates
bronchodilation through various neurotransmitters
such as vasoactive intestinal peptide.
The mechanisms involved in cholinergic
bronchoconstriction are complex and incompletely
understood. Intracellular effects depend in
part on modifications of intracellular levels of
cyclic adenosine monophosphate (cAMP) and
Back to contents
C
cyclic guanosine monophosphate (cGMP). The
effects of these two secondary messengers are
reciprocal; hence increased concentrations of
one are associated with decreased concentrations
of the other. Cyclic AMP is increased by β2-
receptor stimulation and decreased by activation
of α1-adrenergic receptors. In contrast a variety
of different inflammatory mediators, activation
of H1 receptors, increased intracellular Ca
concentrations and muscarinic effects of
acetylcholine increase cGMP levels.
Acetylcholine’s actions are mediated via a number
of mechanisms which are not all cAMP or gAMP-
dependent. These include increasing intracellular
concentrations of inositol 1,4,5-triphosphate (ITP)
and diacylglycerol (DAG) as well as promoting
Ca influx through L-type Ca channels. The ITP
effects are thought to be responsible for the initial
phase of bronchial smooth muscle contraction,
mediated via a transient increase in intracellular
calcium concentration through release from the
sarcoplasmic reticulum. Despite this apparent
cAMP-independence, it has been postulated that it
may be a cholinergic mediated decrease in cAMP
which is the cause of the increased intracellular
ITP concentration.
Although this first phase may be AMP- 2006 World Congress WSAVA/FECAVA/CSAVA
independent, both ITP and DAG levels appear to
be involved in the maintenance of contraction via
modification of cAMP levels through unknown
mechanisms.
As mentioned above adrenergic stimulation
can result in both α1-adrenoreceptor mediated
bronchial constriction, α2-adrenoreceptor
mediated bronchodilation probably through
inhibition of cholinergic bronchoconstriction
or bronchodilation through activation of β2
adrenoreceptors. The bronchodilatory effects
of β2 adrenoreceptors are mediated not only
through increasing cAMP concentrations but
also perhaps more importantly through a cAMP-
independent pathway that involves activation of
a large-conductance calcium-activated potassium
167
C
channel. Activating this channel allows an
extracellular potassium efflux, increase in trans-
membrane potential and hence a reduction in Ca
influx through the voltage-dependent L-type Ca
channels, thereby resulting in bronchodilation.
Consequently bronchodilation may be achieved
via anticholinergic agents (including α2agonists),
β2 adrenergic receptor agonists and agents
such as the methylxanthines which produce
bronchodilation at least in part due to increased
intracellular cAMP levels in bronchial smooth
muscle.
Clinical Indications
The use of bronchodilators in various disease
states is based on the assumption that clinically
significant bronchoconstriction exists. Although
this has been shown in a small proportion of dogs
with inflammatory bronchopulmonary disease, it
is in cats where bronchoconstriction is a frequent
feature of inflammatory bronchial disease. As
the signs of bronchconstriction can dominate the
clinical syndrome, feline inflammatory airway
disease is frequently referred to as “feline asthma”
as it is thought to resemble the human syndrome
of the same name.
It is worth noting that in the cat, as in man,
“asthma” can no longer be thought of simply
as reversible airway obstruction or “irritable
airways”. Current information suggests “asthma”
should be viewed as an inflammatory disease that
has bronchial hyperreactivity and bronchospasm
as one of its consequences. Although some
affected individuals will have an allergic basis to
this inflammatory process others will not.
Asthmatic inflammation is initiated by the
release of an enormous variety of inflammatory
mediators, each having more than one effect on
airway inflammation. The resultant vasodilation,
and increased vasopermeability produces an influx
into the bronchial tissues of inflammatory cells
2006 World Congress WSAVA/FECAVA/CSAVA
which then release their own mediators with their
own inflammatory effects. The chronic results
are airway edema, smooth muscle hypertrophy,
epithelial shedding and bronchial hyperreactivity
to non-specific stimulii.
The complexity of this inflammatory process,
driven by multiple mediators of inflammation
with each mediator having numerous effects,
would suggest that a drug affecting one
mediator is unlikely to have substantial benefit,
simply because there are so many mediators
participating in the process. In addition, it seems
likely that drugs which broadly address asthmatic
inflammation are likely to be of more therapeutic
benefit than agents that are basically modifiers of
bronchoconstriction.
In man, recent clinical trials comparing the
168
Back to contents
benefits of anti-inflammatory treatment with
those of bronchodilator therapy in asthmatics
have shown the usefulness of addressing the
inflammatory process as the underlying problem,
rather than attempting to correct some of the
more dramatic clinical consequences of asthmatic
inflammation.
Nevertheless symptomatic bronchdilator therapy
remains a therapeutic option and certainly may
have substantial benefit in some cases.
The following sections will concentrate on
specific bronchodilators as well as the use of
leukotriene-receptor antagonists, a group of
drugs that can potentially modify a number of the
mediators of asthmatic inflammation.
Adrenergic agonists
All adrenergic agonists have variable α and β
receptor affinity. In view of the distribution of a
and b receptors, non-selective β receptor agonists
such as isoprenaline or mixed α and β receptor
agonists such as adrenaline are more likely to
produce cardiovascular side effects than similarly
administered selective β agonists. Consequently,
drugs with preferential affinity for β2 receptors are
likely to provide more effective bronchodilation
with fewer side effects.
A possible exception may be with the treatment
of acute allergic bronchospasm. In this situation,
the α2receptor-mediated inhibition of cholinergic
bronchospasm may be helpful. For this reason,
the use of an adrenergic agent with both β2
and α2 agonist activity may be beneficial in the
peracute management of allergic bronchospasm.
However, in view of the risks associated with
administering systemic non-selective adrenergic
agonists to a potentially hypoxic and already
tachycardic patient, it is clearly preferable for
them to be administered by inhalation rather than
systemically.
Even when selective β2 agonists are used, the
preferential activation of pulmonary β2 receptors
may be enhanced by inhalation of small doses
of the drug in aerosol form. This approach
typically leads to rapid and effective pulmonary
β2 receptor activation with low systemic drug
concentrations.
Aerosol administration relies upon the delivery of
drug distal airways which in turn depends on the
size of the aerosol particles and various respiratory
parameters such as tidal volume and inspiratory
flow rate. Even in such a cooperative patient
as man only approximately 10% of the inhaled
dose enters the lungs. Effective aerosol therapy
is possible for dogs and cats especially for short
periods or in emergency situations. However the
general inconvenience of long-term bronchodilator
therapy raises significant compliance issues.

Although there are a large number of selective β2
receptor agonists commercially available for use
in man, most are presented in various inhalant
preparations which generally are unsuitable for
regular use in small animals. The two principal ß2
agonists currently marketed in preparations that
can be readily and regularly used in small animals
are terbutaline sulphate and albuterol sulphate.
Terbutaline sulphate: Terbutaline is a selective
β2 receptor agonist which produces relaxation of
smooth muscle found principally in bronchial,
vascular and uterine tissues. Terbutaline is
available as tablets, elixir and an injectable
preparation suitable for subcutaneous use. The
dose rate has been reported from as low as 0.1-
0.2mg/kg/8h for the dog and cat given either
orally or subcutaneously to as high as 1mg/kg/8h
for an oral dose in the dog.
Albuterol sulphate: Albuterol is a selective β2
receptor agonist with pharmacological properties
similar to terbutaline. Albuterol is available as
tablets and syrup as well as various inhalants.
The dose rate in the dog is 0.02mg/kg/12h. This
dose should be maintained for 5 days and if there
has been no improvement nor any adverse effects
the dose may be increased to 0.5mg/kg/8-12h. In
animals that respond at this higher dose the dose
should be reduced until the lowest effective dose
has been determined for each patient.
Recent studies have confirmed albuterol and
prednisolone act synergistically in producing
bronchodilation in response to a standard
bronchoconstricting stimulus. Consequently
concurrent glucocorticoid therapy may be worth
considering in patients proving refractory to
albuterol’s bronchodilatory effects. This may be
given either as oral preparations or topically (see
below).
Topical bronchodilator therapy can be achieved
effectively in cats using a standard pediatric
spacer equipped with a cat face mask on the
‘patient’ end. Most clinicians recommend using
both a B-blocker (such as albuterol) and topical
glucocorticoids such as fluticasone. The dose
of aluterol is two ‘puffs’ from a generic inhaler
and is combined with a standard dose of inhaled
fluticasone of 220ugm. Both are vaporised in the
spacer, the face mask placed over the cat’s face
and it is allowed to breath through the mask for
7-10 seconds.
The inhalation procedure is usually given
every 12 hours and is started in addition to oral
prednisolone if the cat is symptomatic at the time.
Usually the prednisolone can be stopped after 5-
10 days and the inhalation continued for at least
a further month. Assuming adequate control,
the dose of fluticasone can then be reduced to
110mgm every 12 hours for another month and
Back to contents
C
then stop. Whether or not the albuterol is required
throughout this period is debatable. Some
clinicians do not use albuterol except at times
when cats are symptomatic.
Methylxanthines
The methylxanthines share several
pharmacological actions of therapeutic interest.
They relax smooth muscle, particularly bronchial
smooth muscle, stimulate the central nervous
system, are weakly positive chronotropes and
inotropes as well as being mild diuretics. However
it is as bronchodilators that they have been most
widely used in small animal veterinary practice.
Theophylline and Aminophylline: Caffeine,
theophylline and theobromine are three naturally
occurring methylated xanthines. All three are
relatively insoluble and this solubility can be
enhanced by the formation of complexes with
a wide variety of compounds. The best known
of these complexes is amminophylline which
is the ethylenediamine complex of theophylline
with differing quantities of water of hydration.
100mg of hydrous and anhydrous aminophylline
respectively contains 79 and 86 mg of
anhydrous theophylline. Conversely, 100mg of
anhydrous theophylline is equivalent to 116mg
of anyhdrous aminophylline and 127mg of
hydrous aminophylline. When dissolved in water,
amminophylline readily dissociates to its parent
compounds.
The pharmacokinetics of theophylline has been
extensively studied in a number of species.
After oral administration rate of absorption is
limited principally by dissolution of the dosage
form in the gut. Bioavailability in both cats and
dogs is generally 100% when non-sustained
release preparations are used. However sustained
release preparations may have a more variable
bioavailability. One study in dogs suggested
four different sustained release preparations has
bioavailabilities varying from 30-76% however
2006 World Congress WSAVA/FECAVA/CSAVA
other investigators found bioavailability to be
greater than 95% in studies using two of these
four products.
Theophylline is only weakly protein bound (7-
14%) with a relatively low volume of distribution
(0.82 L/kg, dogs; 0.46 L/kg, cats). Because of this
low volume of distribution and theophylline’s
poor lipid solubility, it is recommended that obese
animals be dosed on a lean body mass basis.
Because of theophylline’s relatively low
therapeutic index and pharmacokinetic
characteristics, dose rates should be determined
on lean body mass. Dose conversions between
aminophylline and theophylline can be
determined from the information present in the
chemical structure section.
169
C
The dose rate of theophylline varies depending
on the preparation used. In standard preparations
the recommended dose rate in dogs is 10mg/
kg/6-8h and cats 4mg/kg/8-12h. When using the
sustained release preparations a dose of 20mg/kg/
12h for dogs and 25mg/kg/24h for cats should be
considered. Although there have been reports of
varied bioavailability with different proprietary
forms of sustained release preparations, Theo-
Durr and Diffumal have both been shown to
reliably have bioavailability greater than 95% in
dogs.
The dose rate of aminophylline is 11mg/kg/8h in
dogs and 5-6mg/kg/12h in cats.
ANTITUSSIVES
Relevent pathophysiology
The cough reflex is complex, involving the
central and peripheral nervous system as well as
the smooth muscle of the bronchial tree. It has
been suggested that irritation of the bronchial
mucosa causes bronchoconstriction, which in
turn stimulates cough receptors located within
the tracheo-bronchial tree. Afferent conduction
from these receptors is via the vagus too possibly
multiple centres within the medulla that are
distinct from the actual respiratory centre. The
drugs that can affect this complex mechanism
are quite diverse. For example when coughing as
a result of bronchoconstriction may be relieved
by bronchodilators acting simply to dilate
airways while other antitussuve agents might act
primarily on the peripheral or central nervous
system components of the cough reflex. Generally
however the most effective antitussives have
been shown to elevate the threshold for coughing
by poorly understood centrally mediated
mechanisms.
Clinical Indications
2006 World Congress WSAVA/FECAVA/CSAVA
Almost all respiratory tract disorders involving
the large and small airways result in coughing.
Frequently this can be viewed as a protective
physiological process resulting in clearing of
viscoid secretions produced by chronic airway
inflammation. As prolonged contact between
inflammatory mediators in the mucus and
epithelial cells perpetuates inflammation any
form of cough suppression needs to be instituted
cautiously. However once clinical signs suggest
the coughing is resolving, cough suppression
may be desirable as chronic coughing tends
to increase airway inflammation, increasing
the risk of a vicious cycle of cough leading
to mucosal irritation which creates further
coughing. Additionally, chronic coughing for
any reason will increase the risk of irreversible
170
Back to contents
emphysema. Consequently cough-suppression
may be particularly helpful in certain situations.
Perhaps the most common condition where cough
suppression plays an integral part in successful
management is dynamic airway disease.
Typically drugs used to suppress coughing are
categorized as opiod or non-opiod antitussive
agents. Unfortunately, although most of the non-
opiod antitussives are effective against coughing
induced by various experimental techniques, the
ability of these tests to predict clinical efficacy
is limited. Consequently in different patients,
therapeutic trials with various antitussives may
be required in order to achieve effective cough
suppression.
Non-opioid antitussives
Dextromethorphan hydrobromide: Dextrometh-
orphan hydrobromide is a synthetic cough
suppressant which acts centrally to elevate the cough
threshold. It does not have addicitve, analgesic or
sedative action and in usual doses does not produce
respiratory depression nor inhibit ciliary activity.
Dextromethorphan binds to central binding sites
that appear to be distinct from standard opiod
receptors. The non-opiod nature of these sites is
reinforced by the inability of naloxone to reverse
dextromethorphan’s effects.
Dextromethorphan is generally marketed in
“over the counter” formulations usually syrups or
lozenges) combined with various antihistamines,
bronchodilators and mucolytics. A dose of
approximately 2 mg/kg has been suggested
although, as with most of the antitussive agents,
higher doses are often required. Antitussive
effects may persist for upto 5 hours. In the
author’s experience, dextromethorphan’s efficacy
is significantly less than the various opiod
antitussives. Its main advantage in most situations
is its ease of availability and convenience.
Diphenhydramine: Among other drugs which
have been used as antitussives, the antihistamine
diphenhydramine is perhaps the most ubiquitous.
Its antitussive mechanism of action is unclear and
controlled studies on its efficacy in dogs and cats
are not available. As diphenhydramine may produce
drowsiness in recommended doses its value as
an antitussive in dogs and cats remains at best
debatable.
Opioid antitussives
Codeine phosphate. Due to reduced first-pass
hepatic metabolism codeine has a high oral-
parenteral potency for an opiod with oral
administration of codeine providing around 60%
of its parenteral efficacy. Once absorbed, codeine
is metabolized by the liver with the largely
inactive metabolites excreted predominantly

in the urine. In man approximately 10% of
administered codeine is demethylated to form
morphine and both fee and conjugated forms of
morphine can be found in the urine of patients
receiving therapeutic doses of codeine. In man,
codeine’s plasma half-life is around 2 to 4 hours.
Codeine phosphate is contained in numerous
“over the counter” analgesic preparations as well
as in 30 and 60mg tablets which have restricted
scheduling. The starting antitussive dose has
been as low as 0.1-0.3mg/kg/8-12h and as high
as 1-2mg/kg/6-12h. Whatever the starting point,
the dose may need to be increased to achieve a
satisfactory effect.
Hydrocodone tartrate: Hydrocodone exhibits
the properties of other opiate agonists however
has reportedly increased antitussive properties
compared to codeine. The mechanism of this
effect seems to be direct suppression of the cough
centre within the medulla. It has been suggested
that hydrocodone may also reduce respiratory
mucosal secretions through undetermined
mechanisms.
In dogs the antitussive effect generally lasts
between 6-12hours.
The dose rate in dogs is 0.25mg/kg/6-12h.
Hydrocodone is only marketed in combination
with homatropine as both an elixir and tablet
formulations. The addition of homatropine is
designed to enhance any reduction in respiratory
secretions, which may come about as a result of
the administration of hydrocodone.
Dihydrocodeine tartrate: Hydrocodeine also
acts centrally to raise the cough threshold. Its
other CNS activities seem to be markedly less
than codeine. Dihydrocodeine is marketed as
an elixir, which is relatively palatable and well
absorbed. A starting dose rate of 2mg/kg/8-12h
is recommended although higher doses may be
required for satisfactory therapeutic effect.
Butorphanol: Butorphanol is an effective
antitussive as well as analgesic. In dogs it has
been shown to elevate CNS respiratory centre
threshold to pCO2 but unlike other opiod agonists
it does not suppress respiratory centre sensitivity.
Butorphanol is well absorbed orally however
a significant first-pass effect results in less than
20% appearing in the systemic circulation. It is
well distributed and in man approximately 80%
protein bound.
The antitussive dose of butorphanol in dogs is
0.55 - 1.1mg/kg/6-12h orally or 0.055 – 0.11mg/
kg/6-12h subcutaneously.
Diphenoxylate: General pharmacokinetics and
pharmacodynamics: Diphenoxylate is an opiod
agonist traditionally thought of exclusively as an
antidiarrheal agent. However it also has effective
antitussive acitivty, presumably through direct
Back to contents
C
suppression of the cough center. In most countries
it is only available in combination with atropine
as an anti-diarrheal agent. In dogs, diphenoxylate
can be used in this combination as an effective
antitussive with minimal side effects. The dose
rate is approximately 0.25mg/kg8-12h orally.
MUCOLYTICS
Relevant pathophysiology
The viscosity of pulmonary mucus secretions
depends on the concentrations of mucoproteins
and deoxyribonucleic acid (DNA). While
mucoprotein is the main determinant of viscosity
in normal mucus, in purulent inflammation the
mucoid concentration of DNA increases (due
to increased cellular debris) and so does its
contribution to mucoid viscosity.
Clinical indications
In a proportion of patients with respiratory tract
disease, significant bronchial inflammation will
be associated with the presence of large amounts
of relatively viscous, inflammatory exudate and
mucus which is firmly attached to the lining
of bronchioles and bronchii. By effectively
increasing bronchial wall thickness, this thick
adherent mucus can exacerbate the “lumen-
narrowing” effects of bronchial constriction,
enhance the overall inflammatory process as well
potentiating persistent coughing. In this situation
mucolytic therapy may have some value in
facilitating resolution of the inflammatory airway
disease.
The two most frequently prescribed mucolytics
in veterinary practice are described below. In
man, guaifensin has been proposed as an oral
expectorant or mucolytic. However, evidence for
its efficacy in this role is lacking in animals and
currently its use in veterinary practice is confined
2006 World Congress WSAVA/FECAVA/CSAVA
to its significant muscle relaxant activity. It is
also worth remembering that normal saline,
directly administered to the airways by effective
nebulisation therapy, is an extremely effective
mucolytic and expectorant.
Bromhexine hydrochloride
Bromhexine increases mucus viscosity by
increasing lysosomal activity. This increased
lysosomal activity enhances hydrolysis of
acid mucopolysaccharide polymers, which
significantly contribute to normal mucus viscosity.
It should be remembered that in purulent bronchial
inflammation, bronchial mucus viscosity is more
dependent upon the large amount of DNA fibres
present. As bromhexine does not effect these
171
C
DNA fibres, its mucolytic action is limited in
these situations.
It has also been suggested that bromhexine
increases the permeability of the alveolar/
capillary barrier resulting in increased
concentrations of certain antibiotics in luminal
secretions. Furthermore over time (2-3days)
bromhexine results in a significant increase in γ-
globulin concentrations and a decline in albumin
and γ-globulin concentrations in respiratory
secretions. The increased g-globulins are IgA and
IgG while IgM levels remain unchanged. It has
been hypothesized that because of these effects
concurrent administration of bromhexine and an
antimicrobial agent will facilitate treatment of
infectious tracheobronchitis.
The mucolytic dose of bromhexine hydrochloride
in dogs and cats is 2mg/kg/12h orally for 7 to 10
days then 1mg/kg/12h for a further 7-10 days.
2006 World Congress WSAVA/FECAVA/CSAVA
172
Back to contents
Acetylcysteine
When administered directly into airways,
acetylcysteine reduces viscosity of both purulent
and nonpurulent secretions. This effect is thought
to be a result of the free sulphydryl group on
acetylcysteine reducing the disulphide linkages
in mucoproteins which are thought to be at least
partly responsible for the particularly viscoid
nature of respiratory mucus. The mucolytic
activity of acetylcysteine is unaltered by the
presence of DNA and increase with increasing
pH.
For effective mucolytic activity, an acetylcysteine
solution should be nebulised and administered
directly to the respiratory mucosa as an aerosol.
The dose rate in dogs and cats is 50ml/kg for 30
minutes every 12 hours.
Acetylcysteine is available as 10% and 20%
solutions of the sodium salt in various sized vials.
This solution can be readily used in a nebuliser
undiluted although dilution with sterile saline
will reduce the risk of reactive bronchospasm.

C - Cardiology & Pulmonology
CLINICAL APPROACH TO THE CARDIOPULMONARY PATIENT
Philip R. Fox, DVM, MSc
Vincent Astor Chair in
Comparative Medicine
Dipl. ACVIM/ECVIM (Cardiology),
ACVECC
Caspary Institute
The Animal Medical Center
510 East 62nd Street
New York
NY 10021, U.S.A.
philip.fox@amcny.org
The history and physical examination form
the cornerstone for diagnosis and management
of cardiopulmonary disease. This information
represents the “glue” which binds together subjective
aspects of patient evaluation with technical details
from diagnostic tests. An insightful history coupled
with a thorough and detailed examination is a
prerequisite for accurate diagnosis, assessment of
treatment efficacy, and optimal outcome.
WHAT THE HISTORY ACCOMPLISHES
A good history uncovers the body system or disease
process associated with clinical signs and client
complaint. The history solicits information intended
to: 1) distinguish between cardiac and pulmonary
disease, 2) establish a diagnosis, 3) determine the
frequency and extent of clinical impairment,
4) assess response (or lack of response) to
therapy, 5) detect other medical conditions, and
6) establish a doctor-client relationship.
Taking The History
The history comprises a complete and
comprehensive set of well planned questions.
The owner is asked to relate their observations
and concerns. This offers a glimpse of the
clients’ emotional state, health care experience,
intelligence, and provides information about the
clinical condition. It also gives the client the
satisfaction of being heard. The pet owner will
not often volunteer all relevant information due to
incomplete observation of clinical signs, incorrect
description of signs through misinterpretation,
emotional status, and a sometimes, a sense of
denial that serious illness is present. The clinician
then directs the client using well planned questions
to evaluate relevant clinical observations: 1) onset
of signs, their related chronology, and severity; 2)
precipitating factors; and 3) response (or lack of
response) to therapy.
Congenital heart disorders may be implied if
siblings, dam or sire have been effected with
known cardiovascular disease. Results from
diagnostic procedures (radiographs, ECG’s,
echocardiograms, clinical pathology) performed
Back to contents
C
at other veterinary practices are important
to evaluate. When drugs have already been
prescribed, knowledge of doses, compliance and
therapeutic response can offer valuable insights.
Signalment (age, breed and gender). Many
congenital and some acquired diseases have certain
predilections regarding age, breed and gender.
Cardiopulmonary History Dyspnea, exercise
intolerance, syncope, coughing, and cyanosis are
common to both cardiac and respiratory disease.
Dyspnea. Acute dyspnea suggests pulmonary
edema, pneumonia, airway obstruction,
pneumothorax, or pulmonary thromboembolism.
Chronic, progressive dyspnea may occur with
right-sided heart failure, pericardial orbronchial
disease, pleural effusions, progressive anemia,
or pulmonary neoplasia. Inspiratory dyspnea
suggests upper airway obstruction; expiratory
dyspnea suggests lower airway obstruction,
parenchymal lung disease, heart failure, chronic
obstructive lung disease, and other conditions.
Paroxysmal dyspnea can accompany brady- or
tachyarrhythmias, especially if accompanied
by episodic weakness or syncope. A history
indicating that dyspnea diminished or resolved
following cardiac drugs suggests heart failure.
Cough. Most coughs sound alike and more than
one etiology may coexist. Cardiogenic pulmonary 2006 World Congress WSAVA/FECAVA/CSAVA
edema in dogs results from left-heart volume
overload (mitral regurgitation, endocardiosis) or
dilated cardiomyopathy. Coughing from acute
pulmonary edema is usually less than a few days
duration and progresses rapidly in severity. The
cough is generally soft, mild, and accompanies
exertional dyspnea. Chronic pulmonary
congestion may cause mild intermittent coughing
and nocturnal dyspnea or cough. Fulminant
edema yields small quantities of frothy, pink-
tinged foam from the mouth or nares. In dogs
impingement of the left main stem bronchus by a
left atrium enlarged by chronic mitral regurgitation
contributes to chronic coughing. Cats appear not
to cough, even when severe pulmonary edema is
present.
Large airway disease causes chronic paroxysmal
173
C
coughing characterized as harsh, resonant, dry, and
“goose honking” in nature. Coughing may persist
for years, is paroxysmal, and elicited by excitement.
Dogs with collapsed trachea usually have normal
exercise capacity between coughing episodes.
Weakness and exercise intolerance. When caused
by decompensated heart failure, lack of exercise
ability, lethargy, or fatigue results. Additional causes
include obstruction to ventricular outflow, cardiac
tamponade, arrhythmias, anemia, systemic and
metabolic diseases, hypotension, and respiratory
disease.
Syncope. This results from transient loss of
consciousness from inadequate cerebral blood flow.
It occurs most commonly in coughing, excited, small
breed dogs with chronic, severe mitral regurgitation,
who’s paroxysmal coughing is immediately followed
by transient collapse (cough syncope). Syncope may
occur with severe subaortic stenosis, pulmonary valve
stenosis, hypertrophic obstructive cardiomyopathy,
pulmonary hypertension, right-to-left cardiac shunts
(tetralogy of Fallot, PDA), tachy- or bradyarrhythmias
(e.g., completeAV block) and conduction abnormalities
such as sick sinus syndrome.
THE PHYSICAL EXAMINATION
Examination of the cardiopulmonary system
involves 1) extern al patient inspection at rest and
during activity to assess respiratory effort and
rate; 2) assessment of the nares, oropharynx, and
larynx for obstruction, 3) palpation of the neck for
tracheal conformity and masses; 4) observation of
the external jugular veins for abnormal distension
or pulsations; 5) palpation of the femoral arterial
pulses for strength, regularity and contour
(normal, hypokinetic, hyperkinetic, etc.); 6)
palpation of the precordium for cardiac apex beat
(location, strength of pulsation, point of maximal
impulse) and thrills (vibratory sensations which
are palpable manifestations of loud, harsh, low
frequency murmurs); 7 thoracic percussion, and
8) heart and lung auscultation.
2006 World Congress WSAVA/FECAVA/CSAVA
Auscultation
The Stethoscope. The most effective instruments
are made of plastic tubing 10 to 12 inches (25-
30 cm) long with an internal diameter of 1/8
inch (3mm). They should be connected to large,
comfortable ear pieces that fit tightly. The bell
is applied with light pressure and collects low
frequency sounds (e.g., 3rd and 4th heart sounds,
diastolic murmurs of mitral and tricuspid origin).
The diaphragm is applied with firm pressure and
collects high frequency sounds best (e.g., 1st and
2nd heart sounds, systolic clicks, high pitched
murmurs). Electronic stethoscopes are also
available.
General Principles of Auscultation. Auscultate in a
quiet room. The animal should be relaxed, standing
or comfortably positioned, not panting, barking or
purring. Palpate the left and right precordium to detect
174
Back to contents
the presence of thrills (vibrations) and determine the
cardiac apex beat. Assess heart rate. Simultaneously
palpate the femoral arterial pulse (a peripheral pulse
occurs just after the 1st heart sound). Pulse deficits
suggest an arrhythmia. Vagal maneuvers may slow
the heart rate during tachycardia.
Develop a systematic approach beginning at the
left apex where the 1st heart sound is normally
loudest, then inching forward, then dorsally. Take
note of various factors that effect loudness of
heart sounds and murmurs. Increased loudness:
a thin chest, sympathetic stimulation, thyrotoxicosis,
and anemia. Decreased loudness: include obesity,
pericardial/pleural effusions, intrathoracic masses,
pneumothorax, abdominal herniation into the chest
or pericardium, and myocardial failure.
Principal areas of cardiac auscultation include:
1) Pulmonic area- left 2nd to 4th ICS just above
the sternum (cat-2nd to 3rd ICS about 1/3 distance
from the sternum to the vertebrae), 2) Aortic
area- left 4th ICS at the CCJ (cat- left 2-3ICS, just
dorsal to the pulmonic area); apex: 3) Mitral area-
left 5th ICS at the CC (may be left 5th to 6th ICS
and more sternal in cats), 4) Tricuspid area- right
3rd to 5th ICS at the CC (cat- right 4th or 5th ICS
toward the sternum). Auscultation should not be
limited to these sites only.
Utilize selective listening. Focus on one part of
the cardiac cycle at a time. Listen separately to the
1st heart sound (S1), then the 2nd heart sound (S2),
the systolic interval, then the diastolic interval.
Determine the intensity, quality, and splitting of
each sound. The systolic and diastolic intervals
should then be listened to for additional heart
sounds or murmurs.
Heart Sounds. The cardiac cycle consists of two
periods: A) contraction (systole) when the heart
ejects blood, and B) relaxation (diastole) when
the heart chambers fill. Ventricular systole follows
closure of mitral and tricuspid valves (related to
the 1st heart sound, S1). When ventricular pressure
increases and exceeds aortic and pulmonic
pressure, aortic and pulmonic valves open,
causing rapid ejection of blood. Later in systole,
ventricular pressure falls, ejection is reduced and
ultimately ceases. Ventricular diastole follows
closure of aortic and pulmonic valves (related to
the second heart sound, S2). Following the early
diastolic filling phase, atrial contraction occurs,
contributing up to 20-25% of ventricular filling.
The initial heart sounds occur at the beginning
of ventricular systole (S1, the 1st heart sound).
The 2nd heart sound, S2, occurs at the end of
ventricular systole. The period between S1 and
S2 is represents ventricular systole; the interval
following S2 and up until the following S1
represents ventricular diastole.
Heart sounds and murmurs. These are
characterized according to: 1) Location- i.e., the
valve area where murmur is heard best (point
of maximal intensity). 2) Intensity or loudness-

Loudness of murmurs can be graded on a 1 to
6 scale as follows: I/VI- heard after only intense
concentration; II/VI- heard immediately, but
faint; III/VI- moderately loud; IV/VI- quite loud
but without a palpable thrill; V/VI- loud with a
precordial thrill, VI/VI- loudest murmur with a
thrill; audible without a stethoscope. 3) Timing-
occurring during systole, diastole, or both. 4)
Frequency- The number of sound waves cycles/
second generated by a vibrating body determines
the pitch, a subjective sensation indicating whether
a tone is high, low or medium on a musical scale.
High frequency sounds indicate a greater number
of wave cycles/second and are best heard with
the diaphragm applied firmly. A low frequency
indicates fewer wave cycles/second and are best
heard with the bell placed lightly on the skin. 5)
Quality- e.g., blowing, harsh, rough, musical.
Murmurs often have identifiable shape to their
sound: crescendo/decrescendo (diamond-shaped),
decrescendo, crescendo, plateau. Murmurs can
be described as ejection (i.e., diamond-shaped),
regurgitant (i.e., plateau) or continuous based on
phonocardiographic description. 6) Duration-
length of time the sound is heard. 7) Radiation-
other locations murmur is heard.
First (S1) and second (S2) heart sounds - S1
heralds the onset of ventricular systole. S1 is
caused by closure of the mitral (M1) and tricuspid
(T1) valves. It is a high frequency sound heard
best with the diaphragm at the apex where it is
slightly louder, longer and lower pitched than
S2. Pathologic splitting of S1 is rare. Occasional
causes include right bundle branch block and
PVC’s. S2 indicates the termination of systole
and is classically related to closure of the aortic
(A2) and pulmonic (P2) valves; Aortic valve
closure normally precedes the pulmonic valve
because systemic pressure exceeds pulmonary
pressure and this forces the aortic valve to close
earlier than the pulmonic valve. S2 is normally
louder at the left cardiac base, shorter and more
highly pitched than S1. Normal or physiological
splitting of S2 occur If both components of S2
are separately distinguishable. This is normally
heard on inspiration where a decrease in
intrathoracic pressure increases right heart venus
return, prolonging right ventricular systole and
delaying P2 closure. High heart rates in dogs
and cats make detection of physiological spitting
difficult. Causes of abnormal S2 splitting include
1) “fixed” (persistent) splitting due to delay in
pulmonary closure from right heart lesions or
diseases. The split widens during inspiration and
may narrow with expiration. Causes of delayed
pulmonic closure include pulmonic stenosis,
heartworm disease, RBBB, LV ectopic beats.
Causes of early aortic closure include shortened
LV mechanical systole due to severe MR or
VSD [L to R], normotensive ASD; 2) reversed
(“paradoxic”) splitting where the split increases
Back to contents
C
during expiration and decreases with inspiration.
Causes of delayed aortic closure include LBBB,
RV ectopic beats, prolonged LV mechanical
systole (LBBB, AS, systemic hypertension,
severe AI, PDA.
Third (S3) and fourth (S4) heart sounds - These
are referred to as gallop sounds. S3 is associated
with early (proto) diastolic rapid ventricular
filling. Low frequency, it is heard best with the
bell. Causes include 1) high cardiac output states
(anemia, hyperthyroidism, large left-to-right
shunts [e.g., PDA, VSD), 2) rapid ventricular
filling (MR, TR, AI), and 3) myocardial failure. S4
is associated with active ventricular filling during
late diastole and follows atrial contraction just
before S1. Like S3 it is a low frequency sound in
relation to decreased ventricular compliance and
is called an atrial or presystolic gallop. Causes of
right-sided S4 include pulmonary hypertension,
cardiomyopathy and PS; causes of left-sided S4
include systemic hypertension, AS, and HCM.
Isolated S4 may be related to 2 o or 3o degree
AV block.
Ejection sounds and cliks - systolic high-pitched
sounds heard best with the diaphragm. Early
systolic clicks usually coincide with full opening
of semilunar valves while mid systolic clicks can
be associated with mitral valve prolapse.
Heart Murmurs Differential diagnosis of cardiac
disease is often based upon the timing and
location of murmurs. Systolic murmurs heard
loudest at the left base include SAS, PS, and
ASD; Tetralogy of Fallot may be heard at the left
base and right sternal border. Mitral regurgitation
is loudest at the left apex. Systolic murmurs heard
loudest over the right chest (2nd-4th ICS) can
include SAS. Tricuspid regurgitation and VSDs
are heard loudest at the 3rd-5th ICS. Diastolic
murmurs associated with aortic/pulmonary
insufficiency are heard over the related valve
regions. Continuous (“machinery”) murmur
associated with PDA may be focal and heard over
the left cranioventral chest.
2006 World Congress WSAVA/FECAVA/CSAVA
References:
Atkins CE. Evaluation of cough in dogs with mitral
valve insufficiency. The Compendium.1994; 16:
1547-1552
Sisson D, Ettinger SJ. The Physical Examination.
In Fox PR, Sisson DD, Moise NS (eds): Textbook
of Canine and Feline Cardiology Principles and
Fox PR. The History. In Fox PR, Sisson DD,
Moise NS (eds): Textbook of Canine and Feline
Cardiology Principles and Clinical Practice. 2nd
Ed, WB Saunders, Philadelphia, 1999, p 41
Piirilä P, Sovijärvi ARA. Crackles: recording,
analysis, and clinical significance. Eur Respir J
1995; 8: 2139-2148
175
C
C - Cardiology & Pulmonology
CRITICAL CARE CARDIOLOGY
Philip R. Fox, DVM, MSc
Vincent Astor Chair in
Comparative Medicine
Dipl.ACVIM/ECVIM (Cardiology),
ACVECC
Caspary Institute
The Animal Medical Center
510 East 62nd Street
New York,NY 10021
U.S.A.
philip.fox@amcny.org
Cardiogenic pulmonary edema, cardiogenic
shock, ventricular underfilling, hemodynamically
unstable arrhythmias, and arterial
thromboembolism are common life threatening
conditions.
Acute pulmonary edema (Congestive Heart Failure)
Acute pulmonary edema commonly results from
chronic degenerative valvular disease (severe mitral
regurgitation) or dilated cardiomyopathy in dogs, or
diastolic heart failure associated with hypertrophic
or restrictive cardiomyopathy in cats. Treatment
requires aggressive resolution of the congestive
state and restoration of pulmonary function. Key
in this strategy is furosemide given as IV boluses
(2-4mg/kg q 30-60min) or by constant rate infusion.
Vasoactive drugs are added to promote venodilation
and/or arterial dilation. Typically, this may include
nitroglycerin ointment for mild to moderate
edema. In states of life threatening edema in the
dog, the potent vasodilator sodium nitroprusside is
administered by CRI (2-20ug/kg/min) but requires
constant arterial blood pressure monitoring.
Alternatively, hydralazine, a potent arteriolar
dilator, can be given (2mg/kg PO bid) with mitral
2006 World Congress WSAVA/FECAVA/CSAVA
regurgitation.
Inotropic support using dobutamine (constant rate
infusion) is indicated when severe myocardial
failure or cardiogenic shock is present (e.g.,
dilated cardiomyopathy). Digoxin is often added
(dog- 0.005-0.01mg/kg lean body weight q 12 hrs;
cat- ¼ of 0.125mg tablet q 24-48 hrs), especially
when right-sided heart failure or atrial fibrillation
is present. Antiarrhythmic therapy is administered
when needed to suppress or abolish ventricular
tachyarrhythmias, or to control ventricular rates
with supraventricular tachyarrhythmias such as
atrial fibrillation. Mechanical removal of effusions
and supplemental oxygen are standard supportive
measures. ACE inhibitors and pimobendan are often
considered in chronic management strategies.
Reversible causes of heart failure should be
176
Back to contents
considered and treated if present. Myocardial
failure has been associated with taurine and
carnitine deficiency. Heartworm disease is a
treatable cause of right-sided CHF. Volume
overload secondary to patent ductus arteriosus
is correctable by surgical or coil occlusion
techniques. Other systemic and metabolic disorders
may cause or contribute to heart failure including
endocarditis, myocarditis, pheochromocytoma,
diabetes, and hyperthyroidism.
With recurrent heart failure, upward drug
titration may be necessary. Serum digoxin
concentrations should be monitored. Diuretic
resistance may occur as heart failure progresses,
and some animals are likely to benefit from
intravenous furosemide therapy which has higher
bioavailability. A second and third diuretic (e.g.,
thiazide, 5 to 20 mg daily, or spironolactone- 12.5
to 25 mg once to twice daily) may be added. It
is prudent to assess BUN, creatinine, electrolytes
and blood pressure.
Cardiogenic shock
Myocardial failure is most commonly associated
with dilated cardiomyopathy. Less frequently,
chronic volume overload (eg, mitral regurgitation,
left-to right shunts) or sepsis may be causative.
The principal hemodynamic feature of
cardiogenic shock is systemic hypotension caused
by reduced ventricular pumping (ie, myocardial
failure/systolic dysfunction). Pulmlonary edema,
systemic congestion, hypotension, and tissue
hypoxia result. Acute management requires
inotropes (dobutamine CRI), diuretics to reduce
congestion, and vasodilators such as sodium
nitroprusside. ACEI, digoxin, pimobendan and
sometimes neutriceuticals are added for chronic
management
Ventricular underfilling
Conditions which interfere with return of
blood to the heart may result in decreased

cardiac preload, compensatory neuroendocrine
activation, and a clinical condition known as
cardiac tamponade. This is generally associated
with pericardial disease (typically neoplasia in
dogs; or FIP or idiopathic effusions in cats). Less
common causes include space occupying atrial
or ventricular masses including blood clots or
tumors. Initial management requires therapeutic
pericardiocentes. Avoid using drugs that decrease
preload or cause vasodilation.
Hemodynamicaly unstable arrhythmias
Tachyarrhythmias may depress cardiac output,
cause hemodynamic impairment or hypotension,
and result in organ ischemia. Shortened diastolic
filling decreases coronary blood flow, reduces
myocardial oxygen supply, causes ischemia and
results in more serious arrhythmias. Certain
tachyarrhythmias may deteriorate by becoming
electrically unstable. Hemodynamic impact of
tachyarrhythmias are influenced by factors related
to underlying cardiac disease and the particular
type of arrhythmia (i.e., (a) loss of synchronized
atrial systole, (b) altered ventricular activation
sequence, (c) rapidity of ventricular rate, (d)
timing of ectopic beats relative to preceding P-
QRS-T complexes, (e) background vasomotor
tone, (f) cardiac effects of antiarrhythmic
drugs, and (g) underlying cardiac dysfunction
or health). Because cardiac output = heart rate
x stroke volume, sustained tachycardia may
reduce cardiac output and artial blood pressure.
In atrial fibrillation with rapid ventricular
response, ventricular filling shortens due to loss
of atrial contraction, variation in cycle length
and high ventricular rate. This is worsened by
concurrent myocardial dysfunction (eg, dilated
cardiomyopathy) or exercise. Impulses originating
in the ventricle (eg, ventricular tachycardia)
alter patterns of electrical activation and reduce
stroke volume. Rapid, sustained ventricular
tachycardia decreases cardiac output, results in
hypotension and organ ischemia. Ventricular
flutter causes precipitous deterioration and all
circulation ceases with ventricular fibrillation.
Short paroxysms of atrial tach with normal
ventricular activation may not cause clinical
consequences; multifocal atrial or ventricular
tachycardia are more likely to compromise
hemodynamics, especially if ventricular function
is abnormal. Electrical instability is increased by
rapid ventricular rates and multifocal impulse
origination. Additional factors include timing of
the ectopic impulse (ie, the earlier the premature
complex relative to the preceding T wave, the
greater electrical liability). Depolarizations
occurring within the preceding T wave are
extremely dangerous). The underlying state of
Back to contents
C
ventricular function, systemic and metabolic
alterations, and concurrent drug or anesthetic
agents influence electrical stability. Electrical
instability is increased by rapid ventricular rates
and multifocal impulse origination. Additional
factors include timing of the ectopic impulse (i.e.,
the earlier the premature complex relative to the
preceding T wave, the greater electrical liability).
Depolarizations occurring within the preceding T
wave are dangerous. The underlying ventricular
function, systemic and metabolic alterations, and
concurrent drug or anesthetic agents influence
electrical stability. Tachycardia = ventricular
rate >240bpm in cats; > 180bpm in small breed
dogs; > 160bpm in large breeds, and >220bpm
in puppies. With supraventricular tachycardias,
vagal maneuvers may occasionally convert the
arrhythmia. Supraventricular arrhythmias may be
treated with digitalis glycosides, calcium channel
blockers, beta blockers, and other agents. Acute
management of ventricular tachycardia includes
treatment of the underlying cause and lidocaine.
Pacemaker implantation may be required to treat
high grade AV block.
Evaluating the critical patient
Assessment of the unstable patient is aided by a
careful history, complete general examination,
and complete data base.
Noninvasive Monitoring of Hypoxemia (Pulse
Oximetry): The saturation of hemoglobin with
oxygen in arterial blood (SaO2) is a useful indicator
of hypoxemia. Pulse oxymetry is a noninvasive
technique to allow continuous monitoring of
arterial oxyhemoglobin saturation. Blood contains
4 species of hemoglobin (Hb): 1) oxyhemoglobin
(HbO2), 2) reduced Hb, 3) methemoglobin
(MetHb), and 4) carboxyhemoglobin (COHb).
In healthy individuals, the latter 2 are in small
concentration. Pulse oximetry measures functional
hemoglobin saturation [SaO2= HbO2 divided by
HbO2+Hb x 100], and thereby assesses arterial
2006 World Congress WSAVA/FECAVA/CSAVA
oxygenation. It does not assess ventilation (CO2
elimination). Hypoxemia may be a late onset sign
of deteriation in some cases of respiratory failure,
especially when compensatory tachypnea has
maintained normal oxygen levels. Accurate pulse
oximeter readings are not always possible in every
animal owing to probe placement issues, thick or
pigmented skin, movement artifact, and other
factors. Thus, hemoglobin saturation determined
by pulse oximetry should always be evaluated I
light of the patients clinical condition. Arterial
blood gas analysis should be considered whenever
pulse oximetry estimation is in question.
Noninvasive Blood Pressure Monitoring:
Hypertension may predispose certain “target”
organs to injury, particularly the eyes, kidneys,
177
C
and cardiovascular and neurovascular systems.
Hypotension is a common consequence of shock,
dehydration, and certain drug toxicities. Systolic
blood pressure >160 suggests hypertension;
SBP>200 mmHg recorded on 2 occasions at least
24 hours apart indicate hypertension, unless the
animal was excited. End-organ injury provides
supportive evidence of hypertension. SBP <90
indicates hypotension.
Central Venous Pressure (CVP): CVP directly
measures pressure in the great thoracic veins
as blood returns to the right heart. Serial or
continuous CVP measurement helps assess
right heart filling and status of intravascular
volume. Evaluation of the direction of change in
CVP measurements over time is more relevant
than basing diagnostic/therapeutic changes on
isolated measurements. CVP generally decreases
as venous return decreases. Low CVP suggests
hypovolemia. Elevated CVP measurements
suggest either right ventricular failure or
intravascular volume overload.
Electrocardiography: Assessment of heart rate
and rhythm provideS information about cardiac
chamber enlargement, implies the presence
of severe pericardial or pleural effusion, and
2006 World Congress WSAVA/FECAVA/CSAVA
178
Back to contents
can help assess certain suspected systemic and
metabolic disorders (e.g., marked disturbances
of potassium or calcium, ischemia, infarction).
Continuous ECG monitoring, event recorders,
or Holter recordings are useful to detect transient
arrhythmias.
Radiography: The radiograph 1)confirms
disease suspected from the history and physical
examination, 2) assesses disease severity,
3) distinguishES between cardiac and respiratory
disease, 4) confirms tube/catheter placement,
5) screens for unsuspected conditions, 6) discovers
complications, and 7) and helps monitor (from
repeated studies) response to therapy.
Echocardiography: Diagnostic ultrasound assists
cardiac examination when the heart is obscured
by pleural effusion; diagnoses pericardial
effusion; provides quantitative assessment of
cardiac structure (valves; chamber dimensions,
wall thickness); assesses systolic (contractile)
and diastolic function; quantifies gradients via
Doppler echocardiography; detects disturbances
of blood flow; detects intracavitary masses (clots,
tumors); and helps characterize congenital and
acquired heart diseases.

C - Cardiology & Pulmonology
SYNCOPE, WEAKNESS, ARRHYTHMIAS AND SUDDEN DEATH
Dr. N. Sydney Moise, DVM,
MS
Diplomate ACVIM
(Cardiology and Internal Medicine)
Professor of Medicine
Cornell University
Ithaca
New York
USA
nsm2@cornell.edu
What is the differential for weakness as it pertains
to cardiac disease? The most common diseases
for which dogs are presented with this complaint
when the underlying cause is cardiogenic include
dilated cardiomyopathy, pericardial effusion,
advanced AV valve regurgitation, or cardiac
arrhythmias. Other causes that are less common
include congenital heart disease that affects
cardiac output or oxygenation.
What are the diagnostics that are done in
the evaluation of weakness and collapse?
Radiography will reveal evidence of pulmonary
pathology and usually give an appreciation
of cardiac size. Electrocardiography will
provide the evidence for the diagnosis of the
rhythm disorder. Echocardiography will give
the structure and functional characteristics to
determine the specific disease. Finally, blood
pressure and laboratory tests will clear the animal
of other diseases and provide the foundation to
know that drug therapy is not contraindicated if
underlying organ dysfunction is severe. When
these tests do not provide the answer then 24-hour
ambulatory (Holter) monitoring, event recorders,
or implantable recording devices can reveal the
abnormal rhythm.
What are the rhythm abnormalities that can result
in weakness or collapse? When the heart rate is
too slow or too fast, weakness can occur. The
degree of these extremes dictate the severity of
the clinical signs. The parameters include both
the rate and the duration of the extreme in rate.
Critical to this factor is the generation of the
systemic blood pressure. For example a heart rate
of greater than 260 bpm is more devastating than
a rate of 200 bpm, but if the faster rate persist
for only a few seconds and the latter for hours
the bad consequences are greater. This same
thought follows through with the length and rate
of bradycardias. When the extreme rates cause a
loss of cerebral blood flow (inadequate pressure)
for more than 8 seconds, then collapse or syncope
will result. The most common tachycardias that
Back to contents
C
can cause weakness include atrial fibrillation,
atrial tachycardia, and ventricular tachycardia.
The most common bradycardias include third
degree heart block, advanced second degree heart
block, and sick sinus syndrome.
Often dogs with dilated cardiomyopathy are
seen with heart failure and atrial fibrillation.
This combination can be a challenge to manage
medically. The control of excessive heart rate in
atrial fibrillation is critical.
What are the problems when striving for rate
control? Remember, you can get the heart to slow
down if you use enough drug. But there lies the
problem. There is a ‘ceiling’ effect with digoxin.
That is, the therapeutic/toxic dose of digoxin
prevents titrating up to get the desired slowing
in some dogs. The amount of digoxin required to
slow the heart enough is beyond the therapeutic
level. With calcium channel blockers or beta-
blockers there is more room for titration; however,
at the doses needed to reach the heart rate goal the
negative inotropic effect or drop in systemic blood
pressure can bring disappointment to reaching the
target heart rate. The latter is not as much of a
problem in dogs that have lone atrial fibrillation
with maintained myocardial function. In these
dogs the dose of either diltiazem or atenolol can be 2006 World Congress WSAVA/FECAVA/CSAVA
titrated to achieve the desired heart rate. We have
most commonly found a good rate control with a
combination of diltiazem (extended-release) and
digoxin. Most dogs even with myocardial failure
tolerate this drug combination. It may be that the
negative inotropic effect is offset by the dramatic
improvement in myocardial perfusion that occurs
with adequate rate control.
In a dog with acute heart failure due to dilated
cardiomyopathy and marked tachycardia due to
atrial fibrillation the goals must be prioritized. Most
of the time severe dyspnea is present in addition
to the tachycardia of the atrial fibrillation. The
dog must breath before all else. Aggressive, short
term treatment with diuretics is given with acute
treatment with nitroglycerin, and some may use
179
C
nitroprusside in those handful of places that have
continuous monitoring. The dilemma is whether
to treat the dog with dobutamine or diltiazem. The
dobutamine for the inotropic support or diltiazem
to slow the heart rate (some of these dogs have
rates greater than 240 bpm). A second dilemma
concerns the route of drug administration. In the
dog that is in complete distress the intravenous
route is obvious, but not all dogs are in this
most dire position. Some could be treated orally.
Response to oral diltiazem can be rapid; however,
if there is a negative response the effects can be
more protracted if the long acting preparations
are used such as Dilacor®. The effects of regular
diltiazem do not last long in the dog and require
frequent administration; however, this can be
an advantage in a dog where the IV route is
not selected, but the long acting medication is
2006 World Congress WSAVA/FECAVA/CSAVA
180
Back to contents
not desirable as yet. The unfortunate problem
is that with calcium channel blockers and beta-
adrenergic blockers the heart rate control comes
with the price of hypotension in many dogs with
myocardial failure. This is why a combination
of treatment with digoxin can be advantageous,
but the dog must live long enough to have all
the medications achieve adequate blood levels.
The role of other drugs such as pimobendan or
levosimendan in these acute situations needs to
be explored too. It has been our experience that
if a dog is not in severe myocardial failure, the
dose of diltiazem is higher than expected to
achieve heart rate control. We commonly use 3 to
4 mg/kg twice daily of extended release diltiazem
for long-term treatment. Some dogs may require
even higher doses. We monitor patients with
24-hour electrocardiographic monitoring.

C - Cardiology & Pulmonology
APPROACH AND TREATMENT OF THROMBOVASCULAR DISEASE
Dr. N. Sydney Moise, DVM,
MS
Diplomate ACVIM
(Cardiology and Internal Medicine)
Professor of Medicine
Cornell University
Ithaca
New York
USA
nsm2@cornell.edu
Key words: cardiomyopathy, thromboembolism,
cats, hyperkalemia, reperfusion
Thromboembolism occurs most commonly as the
result of cardiac disease in the cat with a clot lodged
in the distal aorta and iliac arteries. The arterial
occlusion alone is not the cause of the reduced
circulation, but the effects of the thrombus cause
a cascade of vasoconstriction events that reduce
collateral circulation. In order to reproduce the
clinical disease experimentally, arterial ligation
with the injection of bovine thrombin is required.
Thus, it is not primary channel blockade that causes
the ischemic neuromyopathy. The cat has many
collateral vessels to call upon from the vertebral
arterial system, but when this fails to happen the
clinical syndrome ensues. Additionally, it is the
reopening of these collateral vessels in the 12 to 24
hours after the thromboembolic event that result in
the reperfusion injury that kills many cats.
A thrombus develops when blood stasis,
endothelial damage and increased coagulation
develop. Endothelial damage is present in cats
with cardiomyopathy. Furthermore, a fundamental
question to answer concerns the vulnerability of cats
to thromboembolism.
When the clot dislodges from its site of formation,
travels in the arterial system, and decreases blood
flow, the clinical consequences of thromboembolism
occur. These manifestations are the result of nerve
and muscle damage. Ischemic neuromyopathy
is characterized by both functional and structural
alterations. Although Doppler and perfusion studies
can aid in the assessment of the perfusion deficit,
only time permits a clear view of the permanent
nerve and muscle damage.
The skeletal muscle is more susceptible to ischemic-
reperfusion damage than the nerve. Ischemic
myopathy affects the cranial tibial muscle to the
greatest extent although the gastrocnemius muscle
can be severely damaged.
In contrast to the heart and brain, the peripheral nerve
is relatively resistant to structural ischemic changes
because of the low energy needs, high energy
Back to contents
C
stores, ability to adapt to anaerobic metabolism, and
extensive anastomoses.
It is the type and extent of neuropathology that
determines the level of recovery of nerve function.
Wallerian-type degeneration and paranodal
demyelination (affected successive nodes not
random as in demyelinating neuropathies) occur.
The physical examination of cats with aortic
thromboembolism might include (1) the absence
of femoral pulses, (2) firm to hard cranial tibial
and gastrocnemius muscles, (3) pale to black cold
foot pads, (4) absence of deep pain response, (5)
absence of limb motion below the upper thigh, (6)
hypothermia, (7) lack of anal tone and distended
bladder, (8) abdominal pain if the mesenteric
artery also has been embolized, (9) tachypnea and
tachycardia (seen with cardiovascular compromise,
stress and pain), (10) bradycardia or irregular cardiac
rhythm, (11) heart murmur or gallop sound, or (12)
varying degrees of depression.
It is in the first few hours that control of pain and
anxiety are considered somewhat important. Pain
and anxiety increase the sympathetic tone and this
is very detrimental to cats with cardiomyopathy.
Consequently, treatment with medication that would
relieve these symptoms is ideal so long as the price
is not excessive sedation and hypotension. In the 2006 World Congress WSAVA/FECAVA/CSAVA
past, acepromazine has been recommended for such
treatment; however, this drug is not recommended.
Today butorphanol at 0.2 to 0.4 mg/kg subcutaneously
every 4 hours or hydromorphone at 0.05 to 0.1
mg/kg subcutaneously are most frequently used.
Butorphanol will not give as much analgesia as
the hydromorphone, but the latter is more likely to
cause dysphoria. Over-sedation can compromise the
ability to judge the status of cardiovascular shock
and mentation. Other medications such as fentanyl
patches are not recommended because they take too
long be effective. This is an important consideration
because pain in cats with thromboembolism last a
relatively short time of less than 6 to 10 hours.
The diagnostic evaluation of the cat with
thromboembolism includes blood pressure,
echocardiography, thoracic radiography, serum
181
C
chemistry, and electrocardiography. Although the
blood pressure determination in the hindlimbs
will not be accurate, an assessment from the
forelimbs is important to gauge the overall status
of the cat. Echocardiography will reveal the type of
cardiomyopathy, the severity of the hypertrophy and/
or fibrosis, systolic and diastolic dysfunction, size of
the atria, presence of pleural effusion, and presence
intra-atrial blood stasis or clots. Thoracic radiography
permits the determination of pulmonary edema or
pleural effusion. Pulmonary edema can exist even
if not suspected from the auscultation of the lungs.
Moreover, tachypnea is seen in the majority of these
cats. The cause can be either pulmonary edema,
pain, or both. The radiograph helps to determine if
treatment for fluid retention is required.
Serum chemistry abnormalities are common and
extensive. Azotemia, hyperglycemia, elevation in
muscle enzymes (creatine phosphokinase, aspartate
aminotransferase and alanine aminotransferase),
hyperkalemia, acidosis, hyperphosphatemia, and
hypocalcemia can be documented. Azotemia
is usually due to poor perfusion to the kidneys
and it is this same mechanism that explains the
hyperphosphotemia. Hyperglycemia is hypothesized
to be due to two factors: stress and increased lactate.
Stress causes an increase in adrenergic hormones
that inhibits insulin secretion and this in turn causes
the increase in blood glucose. Also contributing to
the stress response are high glucagon and cortisol
levels. Concomitant with this is that lactate levels
are high due to muscle anaerobic glycolysis.
Lactate is a major gluconeogenic precursor to cause
hyperglycemia. It is believed that insulin resistance is
likely not responsible for the hyperglycemia in cats.
Elevation in muscle enzymes particularly that of
creatine phosphokinase, can be dramatic in cats with
thromboembolism due to the muscle necrosis. Poor
renal perfusion accounts for the hyperphosphatemia,
but again the death of muscle serves as a source for
massive quantities of phosphorus. The excessive
phosphorus binds to calcium and this accounts for
the hypocalcemia. Metabolic acidosis develops
2006 World Congress WSAVA/FECAVA/CSAVA
in response to the lactic acidosis reaching levels
that demand specific treatment. All of these
biochemical alterations change over time after the
thromboembolic event. The ideal situation is for
them to return to normal; however, it is important to
particularly watch the potassium concentration as it
can increase as reperfusion develops.
Electrocardiography is vital on admission not only
for the evaluation of the rhythm, but to ascertain
the electrocardiographic evidence of the potassium
concentration. Frequently, the ECG on admission
is normal, but once reperfusion begins (as early
as 6 hours after thromboembolism) the potassium
concentrations can elevate quickly. Monitoring of
the ECG provides a means to monitor the serum
potassium level. Attention should be paid to the
P wave, S wave and T wave. Most frequently cats
182
Back to contents
will develop S waves, the P wave flattens and the
T wave flips to positive as an indicator that the
potassium is increasing. (Figure 5) It is vital that
the serum potassium be rechecked so that treatment
can be started early enough to be of benefit. Severe
abnormalities in conduction and rhythm progress as
the potassium levels increase.
For years the use of heparin in acute thromboembosis
has been purported in the acute situation. We need to
all consider the evidence for this treatment and its
value. We actually do not have any evidence of its
effectiveness in improving the state of these cats.
Cats will suffer from reperfusion injury to varying
degrees depending on the vascular hyperpermeability,
hyperkalemia, edema and acidosis present. The
aggressiveness in the treatment of hyperkalemia
depends on its severity. Treatment can include
modest fluid therapy with NaCl (careful to watch for
pulmonary edema), intravenous glucose (but if the
cat is already hyperglycemic this is not effective),
sodium bicarbonate (effective for the acidosis
too), very low doses of insulin (give with glucose
and monitor), to intravenous calcium (directly
counteracts the cellular effects of hyperkalemia).
It is clear that these cats need treatment to prevent
reembolization which occurs at the rate of about
25% as reported in the most recent reports, but what
is uncertain is how this is accomplished. For many
decades some have suggested the use of aspirin,
while others say it does no good. Studies in th early
1970’s showed that experimentally cats treated with
aspirin, if thromboembolism did occur, had less
severe clinical signs and recovered quicker. But still,
thromboembolism occurs. In humans aspirin alone is
frequently inadequate to control thromboembolism,
whereas, anticoagulation treatment decreases the
recurrence. However, treatment with anticoagulants
such as coumadin requires rigorous monitoring that
is rarely possible in cats. The LMWH could be an
alternative, although when these have been used
thromboembolism still developed and the target levels
were never obtained at the dose used and the half-life
appears short. The latter is problematic because the
drug must be administered parenterally and it appears
that twice daily administration is inadequate. This
type of treatment is likely not practical. Recently,
an alternative treatment has been suggested which
is antiplatelet rather than anticoagulation.. This
drug is clopidogrel (Plavex) and recent studies have
shown this to be a safe drug in cats. Clinical trials to
determine its effectiveness are required.
In summary, the treatment of thromboembolism in
the cat entails multitasking and attention to detail..
An understanding of the pathophysiology will
guide us in designing studies to answer the clinical
questions. We have made progress in the treatment
of this disease, but there is still a long way to go.
The fortunate situation is that there are cats that can
survive despite our limited knowledge.

C - Cardiology & Pulmonology
ADVANCES IN DIAGNSOTIC IMAGING
Philip R. Fox, DVM, MSc
Vincent Astor Chair in
Comparative Medicine
Dipl. ACVIM/ECVIM
(Cardiology), ACVECC
Caspary Institute
The Animal Medical Center
510 East 62nd Street
New York
NY 10021, U.S.A.
philip.fox@amcny.org
Recent years have witnessed a substantial
increase in the use of imaging and therapeutic
radiology procedures. Contributing to this trend
has included dramatic technologic advances,
expanding applications in clinical medicine,
improving economy, and increasing reliance on
high technology.
Traditionally, imaging has been separated into
two distinct areas: (1) functional, and (2)structural
imaging. Applications of functional imaging
includes nuclear medicine such as SPECT (single
photon emission computed tomography) and
PET (positron emission tomography), and MRS
(magnetic resonance spectroscopy). Applications
in structural (i.e., anatomical) imaging includes
planar radiography, CT (x-ray computed
tomography), and MRI (magnetic resonance
imaging). Distinctions between these modalities
and applications have begun to converge with
the development of multi-modality (SPECT/CT,
PET/CT) scanners.
Particularly in relation to veterinary medicine,
advances in CT, MRI, and echocardiography
are increasingly relevant. For example, CT is
significantly more sensitive for detecting soft-
tissue masses than thoracic radiographs. MRI can
detect and reveal the presence and distribution
of myocardial fat and thus help diagnosis and
follow specific forms of heart muscle diseases.
Improvements in basic echocardiographic
Back to contents
C
instruments including off line data assessments
have markedly expanded the utility of this
modality. Furthermore, enhancements in three-
dimensional echocardiographic imaging has now
made this technique useful for evaluating certain
acquired and congenital diseases. Moreover,
quantitative tissue Doppler examinations
including strain rate imaging can contribute to
assessment of myocardial performance.
REFERENCES
Chrysanthopoulou A, Kalogeropoulos A, Terzis
G, et al. Trends and future needs in clinical
radiology: Insights from an academic medical
center. 2006 Apr 17; [Epub ahead of print]
Bailey DL. Imaging the airways in 2006. J
Aerosol Med. 2006 19: 1-7
Nemanic S, London CA, Wisner ER. Comparison
of thoracic radiographs and single breath-hold-
helical CT for detection of pulmonary nodules
in dogs with metastatic neoplasia. J Vet Int Med
2006; 20: 508-515
Vitarelli A, Montesano T, Gaudio C, et al. Strain
rate dobutamine echocardiography for prediction
of recovery after revascularization in patients 2006 World Congress WSAVA/FECAVA/CSAVA
with ischemic left ventricular dysfunction. J Card
Fail. 2006 May; 12(4): 268-75
183
C
C - Cardiology & Pulmonology
ADVANCES AND CLINICAL UTILITY OF AMBULATORY ECG
MONITORING
Dr. N. Sydney Moise, DVM,
MS
Diplomate ACVIM
(Cardiology and Internal Medicine)
Professor of Medicine
Cornell University
Ithaca
New York
USA
nsm2@cornell.edu
Frequently the routine ECG is inadequate to
determine the need for and the response to
antiarrhythmic therapy. The 24-hour ambulatory
ECG or Holter monitor is better suited for these
determinations. The technology for Holter
monitoring has made advances relative to the
digitalization of the recordings, yet the accuracy
of the analysis is still lacking for many of the
arrhythmias that dogs and cats display. Despite the
latter difficulty, it is still evident that to make the
best judgments with regards to the management
of arrhythmias, there is no replacement for this
diagnostic ability.
During this brief communication the use of the
Holter monitor will be demonstrated. An actual
analysis will be demonstrated. Also, the results
from patients will be used to illustrate the utility
of this important diagnostic tool.
Reduction of heart rate as a indicator of oxygen
consumption.
In both reported major studies above, as well as
in previously published canine studies and in
humans, heart failure therapy with Pimobendan
is not associated with an increase in heart rate.
2006 World Congress WSAVA/FECAVA/CSAVA
In contrary, heart rate usually drops a bit with
the general improvement of the patient and the
reduction of signs of heart failure.
Arrhythmogenesis
Sensitized to proarrhytmic effects of the PDE
III-inhibitor Milrinone found in the Promise trial
(Packer et al 1991), Pimobendan therapy was
carefully observed for proarrhythmia in several
studies (the Pico trial 1996, Remme et al 1994,
the Epoch study 2002). Convincing evidence
about increased ventricular tachyarrhythmias
with clinical significance could not be found.
A veterinary study (Rosenthal 2006) revealed
increased VPC’s in 6/8 dogs with DCM
investigated with Holter-ECG’s approx. 3 weeks
after initiation of Pimobendan-therapy.
In the major multicenter trials cited above
184
Back to contents
(PiTCH, VetScope)however, no proarrhythmic
effect was found.
Comparison to another calcium sensitizer drug
Levosimendan
Levosimendan is a very similar compound that
has similar cardiovascular effects, but more
calcium sensitising and less vasodilating effects
through PDE III-inhibition than Pimobendan.
Levosimendan is used by intravenous infusions,
and prolonged lasting effects up to several weeks
after discontinuation of the drip are attributed to
one of its metabolites OR-1896 in man (Kivikko
et al 2003). This drug is being studied and
prepared for licensing for the veterinary market
as well, but results haven’t been published yet.
Apparently, dogs metabolize the drug differently
without the presence of this effective metabolite.
References
Asanoi H, Ishizaka S, Kameyama T, et al.
Disparate inotropic and lusitropic response to
pimobendan in conscious dogs with tachycardia-
induced heart failure. J Cardiovasc Pharmacol
1994; 23: 268-274.
Bastida E, Escolar G, Rodriguez-Gomez J, et
al. UD-CG 115, a benzimidazole-pyridazinone
compound with cardiovascular activity
inhibits platelet thrombus formation. Abstract.
Thrombosis Res 1986; 42(Suppl 6): 145.
Baumann G, Ningel K, Permanetter B.
Cardiovascular profile of UD-CG 115BS -
pimobendane and reversibility of catecholamine
subsensitivity in sever congestive heart failure
secondary to idopathic dilated cardiomyopathy. J
Cardiovasc Pharmacol 1989; 13: 730-738.
Bohm M, Morano I, Pieske B, et al. Contribution
of cAMP phosphodiesterase inhibition and
sensitization of the contractile proteins for
calcium to the inotropic effect of pimobendan in
the failing human myocardium. Circ Res 1991;
68: 689-701.

Buchanan JW, Bucheler J. Vertebral scale system
for cardiac mensuration. J Amer Vet Med Assoc
1995; 206: 194.
The EPOCH Study Group. Effects of pimobendan
on adverse cardiac events and physical activities
in patients with mild-to-moderate heart failure
- The effects of pimobendan on chronic heart
failure study. Circ J 2002; 66; 149-157.
Erlemeier HH, Kupper W, Bleifield W.
Comparison of hormonal and hemodynamic
changes after long-term therapy with pimobendan
or enalapril - a double-blind randomised study.
Euro Heart J 1991; 12: 889-899.
Gwathmey JK, Copelas L, MacKinnon R, et
al. Abnormal intracellular calcium handling in
myocardium from patients with end-stage heart
failure. Circ Res 1987; 61; 70-76.
Iwasaki A, Matsumori A, Yamada T, et
al. Pimobendan inhibits the production of
proinflammatory cytokines and gene expression
of inducible nitric oxide synthase in a murine
model of viral myocarditis. J Amer Coll Cardio
1999; 33: 1400-1407.
Kivikko M, Lehtonen L, Colucci WS.Sustained
hemodynamic effects of intravenous
Levosimendan. Circulation 2003; 107: 81-86
Lombard CW: Pimobendan in congestive heart
failure. Proc 21th ACVIM Forum: 104, 2003
Lombard CW, Jöns O, Bussadori CM: Clinical
efficacy of Pimobendan versus Benazepril for the
treatment of acquired atrioventricular valvular
disease in dogs. J Am Anim Hosp Assoc 2006;
42: 249-261
Luis Fuentes VL, Corcoran B, French A,
Schober KE, Kleeman R, Justus C. A double-
blind, randomized, placebo-controlled study of
pimobendan in dogs with dilated cardiomyopathy.
J Vet Int Med 2002; 16: 255-261.
Back to contents
C
Meel JC, Dierden W. Hemodynamic profile of
the cardiotonic agent pimobendan. J Cardiovasc
Pharmacol 1989; 14(Suppl 2) :S1-S6.
Morgan JP. Abnormal intracellular modulation of
calcium as a major cause of cardiac contractile
dysfunction. N Engl J Med 1991; 325: 625-632.
O’Grady MR, Minors SL, O’Sullivan LM, Horne
R. Evaluation of the efficacy of pimobendan to
reduce mortality and morbidity in Doberman
pinchers with congestive heart failure due
to dilated cardiomyopathy. Abstract 248.
Proceedings 21st ACVIM Forum 2003; 1011
Packer M, Carver JR, Rodeheffer RJ, et al. for the
PROMISE study research group. Effect of oral
milrinone on mortality in severe chronic heart
failure. N Engl J Med 1991; 325: 1468-1475.
The PICO-trial: Effect of Pimobendan on exercise
capacity in patients with heart failure: main results
from the Pimobendan in Congestive Heart Failure
(PICO) trial. Heart 1996; 76: 223-31
Remme WJ, Krayenbühl HP, Baumann G et al.
Longterm efficacy and safety of Pimobendan in
moderate heart failure
Europ Heart J 1994, 15: 947-56
Rosenthal SL, Ferguson MJ, Lefbom BK et al.
Association of Pimobendan with ventricular
arrhythmias in dogs with congestive heart failure.
Proceedings 24th ACVIM Forum 2006; 756.
Sasaki T, Kubo T, Komamura K, Nishikimi T.
Effect of long-term treatment with pimobendan
on neurohumoral factors in patients with non-
ischemic chronic moderate heart failure. J Cardio
1999; 33: 317-325.
Verdouw PD, Hartog JM, Duncker DJ, et
al. Cardiovascular profile of pimobendan, a
benzimidazole-pyridazinone derivative with
vasodilating and inotropic properties. Eur J
Pharmacol 1986; 126: 21-20.
2006 World Congress WSAVA/FECAVA/CSAVA
185
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Cr
Crl CCare
Critical
ritica
& Anaesthesiology

Back to contents

INVITED LECTURES - FULL PAPERS
Cr - Critical Care & Anaesthesiology
A PICTURE IS WORTH 1000 WORDS
Michael Schaer, D.V.M.,
DACVIM, DACVECC
Professor and Assoc. Chair
University of Florida
College of Veterinary Medicine
2015 SW 16th Ave
Gainesville, FL 32608
schaer@mail.vetmed.ufl.edu
The key to making a correct diagnosis depends on
obtaining an accurate patient history and doing
a complete physical examination. Obtaining a
history is as much an art form as it is a scientific
inquiry. It must be done as objectively as possible
in order to obtain a truly accurate description of the
patient’s problems. The findings from the physical
examination begins with the cognitive skills of
the observer and then the correct interpretation
of these findings. The mental images that are
preserved from such clinical experiences are
oftentimes the key for making future diagnoses
of the same type of disorder. Therefore, it is no
wonder that we can often say that “a picture is
worth a thousand words”. Because this seminar is
strictly an image presentation, the written version
will emphasize the clinical signs of several
common clinical disorders.
Platelet Disorders
Petechia are foci of pinpoint hemorrhages that can
involve any of the soft tissues of the body. They
usually signal the presence of a platelet disorder
although they can also occur with vasculitis.
Platelet disorders can arise from inadequate
numbers (quantitative) or from impaired function
(qualitative). Quantitative problems result from
either peripheral destruction, impaired production
or increased consumption. Platelet disorders
commonly present clinically as small skin or
mucous membrane pinpoint or ecchymotic
hemorrhages or as melena associated with upper
gastrointestinal bleeding. Rarely, the bleeding
can be more dramatic as with frank hematuria.
The most important diagnostic tests include the
platelet count and the bleeding time. Think before
doing a bleeding time test in a thrombocytopenic
patient because the procedure can be complicated
by uncontrolled hemorrhage
Back to contents
Cr
Factor Deficiencies
Coagulation factor deficiencies characterize
as frank hemorrhaging into the body tissues;
hematomas are of rather common occurrence.
Ecchymoses and overt hemorrhagic diathesis
require a rapid evaluation of the coagulation
system with tests such as the prothrombin (PT)
and partial thromboplastin times (PTT) and the
activating clotting time (ACT). Factor deficiencies
do not cause petechia unless a disorder involving
platelets coexists (DIC). The history (including a
drug history) should help to differentiate between
congenital and acquired disorders.
Hemolysis
In vivo hemolysis is the destruction of red blood
cells within the vascular and extravascular
spaces. Its causes are many ranging from toxins,
infections, and drugs to autoimmunity. The classic
picture of intravascular hemolysis includes:
weakness, nausea, anemia, hemoglobinemia,
icterus, and hemoglobin- and bilirubinuria. Note 2006 World Congress WSAVA/FECAVA/CSAVA
that “HEMOLYZERS” HEMOLYZE while
“BLEEDERS” BLEED. Coagulogram profiles are
generally normal with hemolytic disease unless a
co-existing disorder such as DIC is present.
Hemoglobinuria vs. Hematuria vs Myoglobinuria
vs Bilirubinuria
Hemoglobinuria is a product of hemolytic disease
characterized as a dark port-wine-like colored
urine that contains few intact RBC’s. Hematuria is
a typical red color and reflects bleeding anywhere
along the urinary tract. Patients with a bleeding
tendency can also bleed into their normal urinary
tract. It is possible for some upper urinary tract
lesions, such as a bleeding renal tumor, to have
both hemoglobinuria (as a result of the blood
becoming hemolyzed in the urinary bladder
187
Cr
during storage) and hematuria. It is also possible
for a fresh renal bleed to form clots in the urinary
bladder and cause urinary outflow obstruction.
Myoglobinuria accompanies rhabdomyolysis.
It will cause reddish brown pigmenturia and
a positive test for blood on dipstick, but the
sediment is devoid of RBC’s.
Vomiting vs. Regurgitation vs. Retching
Vomiting is the actual forceful oral expulsion
of gastrointestinal contents accompanying
many different digestive tract disorders as well
as those involving other organ systems as well.
Regurgitation is the more passive bringing up
of esophageal contents that most commonly
accompanies esophageal disorders. Retching is a
forceful but unproductive attempt to vomit that
can occur with constrictive esophageal pathology.
It can also occur following a coughing episode.
Localizing Significance of the Various Types of
Vomitus
Clear mucoid-esophageal, gastric. Red blood-
esophagus, stomach. Dark red (“coffee grounds”)-
gastric, pylorus, very proximal duodenum. Bile
stained-small bowel; bile in vomitus attests to
pyloric patency. Brown, malodorous (feculent)-
distal small bowel, large bowel.
Blood in Stool
In general, bright red blood can originate anywhere
distal to the mid-jejunum while dark brown-to-
black stool (melena) comes from the stomach
and proximal small bowel. However, a major
bleed in the proximal bowel and its subsequent
rapid passage can show as hematochezia. Oral or
nasal bleeding can cause melena from swallowed
blood.
Stranguria vs. Obstipation
The most important situation where this
2006 World Congress WSAVA/FECAVA/CSAVA
differentiation becomes significant is that
involving the cat or dog with urinary obstruction.
Stranguria in male dogs and cats almost always
signifies urinary outlet obstruction and is therefore
always considered as a medical emergency.
The male cat with urethral obstruction will
make repeated trips to the litter box, sometimes
accompanied by vocalization reflecting the
animal’s discomfort. Over a matter of hours the
cat will become anorectic, begin to vomit, and
become mentally depressed. The obstipated
patient shows a better systemic tolerance for its
GI dilemma. It should be pointed out that females
can also experience urinary outflow obstruction
and trying to decide on patency by way of
telephone might compromise the patient’s well
being.
188
Back to contents
Polyuria vs. Incontinence
The polyuric patient typically produces and
voluntarily passes copious volumes of dilute
urine often accompanied by polydipsia.
Urinary incontinence is an unconscious
passage of urine that occurs while the patient
is lying down or sleeping; these animals
urinate normally.
Blindness vs. Dementia
At first glance these two conditions might
resemble each other to the uncritical observer.
The blind patient will certainly bump into objects,
especially in unfamiliar surroundings, and it will
fail to respond to a menace gesture, but its other
neurological functions are normal. The demented
patient might not menace mainly because the
brain is malfunctioning and consequently cannot
register the threatening gesture while its visual
pathways might very well be normal. This
patient will have accompanying neurological
abnormalities.
Neurologic vs. Metabolic Weakness
The signs accompanying neurological weakness
will depend on the nature of the primary
disorder. Most are usually continuous, sometimes
progressive. They are commonly segmental or
lateralizing in their distribution when caused by
a focal lesion. Other neurological signs such as
pain might be present if there is meningeal or
dorsal nerve root pathology.
Metabolic weakness can also be continuous and
progressive, but it can also be episodic as well.
Patients with metabolic weakness tend not to
segmentalize or lateralize their neurological
abnormalities. The oculocephalic and pupillary
light reflexes are usually retained with metabolic
encephalopathy.
Lameness vs. Weakness
Lameness is the favoring of a limb because of
discomfort. Depending on the distribution of
the lesion, one or more limbs may be involved.
In general the more distal the lesion, the less
weight bearing that occurs. Pain and gross
morphologic abnormalities can usually be
detected. Weakness can be accompanied by
pain, but it more commonly presents in the
absence of pain and any favoring of a particular
limb. Weakness can be regional or diffuse in its
distribution.
Pain
Pain is any localized discomfort associated with
a bodily disorder. It can originate from any organ
system and be a source of major incapacitation
to the patient. Animals will manifest its presence

with either outward signs of discomfort
(vocalization, biting, various motor movements),
or they will show opposite signs characterized
by a withdrawn behavior along with anorexia
and mental depression (as commonly seen in
cats). Identifying the source can sometimes be a
challenge to the most experienced diagnostician.
Seizure vs. Syncope
Seizures are usually complex motor movements
associated with abnormal cerebral function;
alterations in the state of consciousness
to varying degrees are commonly present.
Typically, seizures have preictal, ictal and
postictal components. Syncope is a loss of
Back to contents
Cr
consciousness that lacks the three components of
a seizure. Although most syncopal disorders are
due to cardiac dysfunction it is possible where
a cardiac cause of syncope can be accompanied
by enough hypoxia to establish a seizure focus
in the same patient. It is most commonly caused
by abnormal cardiac excitation or conduction
although it can more rarely occur with certain
metabolic disorders as well. It is important
(but not always easy) to be able to differentiate
narcolepsy and cataplexy from seizures and
syncope.
PRIMUM NON NOCERE
2006 World Congress WSAVA/FECAVA/CSAVA
189
Cr
Cr - Critical Care & Anaesthesiology
CLINICAL MANAGEMENT IN THORACIC TRAUMA
Luis H. Tello. DVM, MS
Clinica Veterinaria Las Condes
Geronimo De Alderete 1567 -
Vitacura
Santiago De Chile
ltello@uchile.cl
INITIAL APPROACH
Team work is the essence and the name of the
game dealing with Thorax trauma and every
member of the emergency team needs to know
and understand his assignment.
Main sources for thorax trauma in DOGS:
• Hit by car
• Dog fights / bites
• High rise syndrome
• Mistreatment, kicks, punches and other type of
blows
• Penetrating wounds (bullets, knives, etc.)
Main sources for trauma in CATS:
• Fights / bites
• Mistreatment, kicks, punches and other type of
blows
• Penetrating wounds (bullets, knives, etc.)
• High rise syndrome
• Hit by car
Blunt trauma can be related to car accidents, fall
from a height or high rise syndrome, kicks or
“human beings” interaction, penetrating trauma,
bites or fight, specially small – large animal
2006 World Congress WSAVA/FECAVA/CSAVA
interactions, projectiles, stabbing.
In a patient with severe or multiple trauma initial
assessment is made at the same time as other
things are initiated to stabilize the patient. Fluid
therapy and shock treatment are started at the
same time the patient is being evaluated. Survey
asking a detailed history of the trauma incident
may provide vital clues.
Time lapse since the trauma occurred is an
important information that has to be asked to
the owners. Many times because of anxiety, the
time lapse cannot be thoroughly determined, but
whenever possible is a very useful data and can
help with some actions to be taken.
Detailed inspection of the animal would reveal
external or even internal injuries. Clipping the
hair may facilitate visualization of bruises.
Hypoxia and hemorrhage are two of the main
190
Back to contents
causes of death among traumatized patients.
Every traumatized patient whom present in shock
with no evidence of external bleeding, third space
accumulation of blood must be assessed and ruled
out.
The physical evaluation must be done in an
orderly fashion, always keeping in mind the
ABC concepts, no matter this subject has suffer
modifications in the latest times: Respiratory,
cardiovascular, nervous, digestive, and muscle /
skeletal systems
Inspection: initial overall observation of the
patient
Palpation: superficial and deep.
Percussion: free fluid? gas? pain?
Thorax Auscultation: Decreased vesicular
murmur, muffled or absent respiratory - heart
sounds?
Other: draw blood for preliminary lab data: blood
work and chemical panel, bladder catheterization:
urine sample, rectal palpation: pain, fractures
Preliminary assessment: Rectal temperature,
Heart rate and respiratory rate, Color of mucous
membranes, Capillary refill time and hydration
status, Pulse quality and rhythm, External
bleeding assessment, skin integrity and lesions,
Level of consciousness (Mentation)
Respiratory system: Adequate ventilation,
Imbalance between ventilation and perfusion,
Upper airway disturbances, Need tracheotomy?
Pneumothorax? Think about thoracocentesis,
Diagnosis or therapeutic, Trauma or lung
injuries? Ruptured diaphragm? Hemo, hydro or
chylothorax?, Does any lesion require immediate
surgery?
Cardiovascular system: Any external visible
hemorrhage?, Any hypovolemic or shock signs,
Arterial blood pressure, Pulse oxymetry, Rhythm
and pulse characteristics, Cardiac auscultation,
Venous distention?, IV catheter placement and
open IV pathway, Replace any volume deficiency,
Colloids requirements, Does any lesion require
immediate surgery?

Nervous system: Level of consciousness? Alert,
ambulates, reflexes, Unconscious?, Gait?,
Depressed, paretic, paraplegic?
Has the patient received any medication that may
alter the examination?
Some pathological changes in the central or
peripheral nervous system?
Does any lesion require immediate surgery?
Digestive system: Abdominal trauma can be a
challenge to diagnose. 50% of serious lesions are
miss diagnosed in human being patients !!!!
It is highly important to keep in mind a suspicion
for abdominal trauma every time we deal
with traumatized patients. Any signs of acute
hemorrhage? Ruptured spleen? Other hemorrhage
sources like kidneys, liver, mesenteric vessels?:
abdominocentesis / diagnostic peritoneal lavage
(DPL) GI tract assessment. Abdominal viscera
exploration (i.e. urinary bladder, ureters, gall
bladder, pancreas): Ultrasound scan, radiograph
Possible peritonitis? Need for immediate
exploratory laparotomy?
Muscle skeleton system: Gait abnormalities or
lameness, Any visible signs of open fracture or
luxation? Joint exploration, Tendon laceration or
avulsion?
Ancillary diagnostics
X-rays must be taken if possible before any
centesis or DPL is performed since these
procedures may introduce air / fluid into the
abdominal cavity.
Plain or contrast studies? Ultrasound?
CT scan or MRI? Do we always need such
expensive studies?
Thorax: Asses and palpate for thoracic movement
and respiratory pattern
Rib fractures. Do we need to pain treatment? Flail
chest? Support bandages?
Penetrating wounds. Locate heartbeat
Abdomen: Look for pain, Evidence for free fluid
or abdominal distention.
Diagnostic peritoneal lavage more accurate
(20ml/kg of warm saline or lactated Ringers),
Identify every palpable organ whenever possible,
retroperitoneal space evaluation.
Spine and appendages: Temperature of
extremities, Evaluate for fractures or luxations,
Check for wounds or any evident deformity,
Retroperitoneal space can be involved in spinal
and / or pelvic fractures.
Nervous system: Evaluate aptitude to stand up and
walk, Position of the extremities and presence of
paresis / paralysis, Flaccidity or rigidity, Cranial
and peripheral reflexes
Head and neck: Blood loss coming from the
natural openings?, Look after injuries in the
head, eyes, ears, nose and nostrils, Check for
Back to contents
Cr
pain and range of motion of the head, Open
the mouth and explore it for tongue or dental
lesions. Remember palate fractures in high rise
syndrome. Airway obstruction due to saliva and
blood clots?
SPECIFIC THORAX APPROACH
Maybe, the major decision in the approach
of small animal patient with thoracic trauma,
is to recognize the real need for surgical
intervention, while most of thoracic injuries can
be appropriately managed by simple measures
aimed to correct hypoperfusion and hypoxemia.
Emergency thoracotomy should be considered
in every unstable patient who has the source of
instability potentially corrected by surgery.
Tap it before Rad it: This is “almost always” rule.
Most of the lesions should be diagnosed by needle
thoracocentesis, instead of chest radiograph.
A simple technique, a butterfly catheter, 10 cc
syringe and 3 way-lock. Cats with respiratory
effort because thorax trauma, needs a very gentle
management, and normally they refuse adopt
positions according radiology examination.
Attempts to force them can cause the death of the
cat.
Open pneumothorax: There is a free
communication trough a chest wall between
the pleural space and atmosphere. Can be life
threatening according of the size of the wound.
Patients came into clinic showing respiratory
efforts and a rapid shallow restrictive respiratory
pattern. Auscultation shows muffled thorax
sounds: heart and respiratory. Diagnosis should
made base on thoracocentesis and suction of
variable amount of free air. Treatment involves
the repair of the chest defect and place a drainage
tube to keep the pleural space with negative
pressure.
Close pneumotorax (tension pneumotorax): This
lesion arise when a one way valve phenomenon
on the lungs, allowing the air leak the lung space
2006 World Congress WSAVA/FECAVA/CSAVA
and increase the pressure and gas accumulation.
Normally is a self limiting condition and just
require supportive care like oxygen and fluid
administration.
Diagnosis and initial treatment should be done
by thoracocentesis and fine needle gas aspiration.
Further treatment need chest tube placement and
permanent gas suction system.
Hemothorax: Massive lesions are rare in dogs
and cats compare with human beings. If the
thoracocentesis reveals the presence of blood
in a considerable volume, the patient should be
treated as hypovolemic and fluid infusion using
crystalloids, colloids or blood products.
191
Cr
Cr - Critical Care & Anaesthesiology
ACUTE PAIN MANAGEMENT IN EMERGENCY
Prof. Pablo Otero DVM
Facultad de Ciencias Veterinarias
Universidad de Buenos Aires
Av. Chorroarín 280
C1427CWO
Ciudad de Buenos Aires - Repú-
blica Argentina
potero@fvet.uba.ar

Introduction Therapeutics options

Pain is frequently underestimated as a promoter
of hemodynamic imbalance during emergency
that results in increased morbidity and mortality
indices. Acute pain can occur as result of trauma,
bone fractures, ligament distention and a wide
range of medical conditions, mainly those
associated with inflammatory processes. These
inflammatory processes can be related not only
with damage in somatic tissues but also with
injuries in internal organs, as a consequence
of surgical procedures. On these patients, pain
should be quickly treated to promote welfare
(comfort) and to avoid futures hemodynamic
compromises.
Many therapeutics alternatives are available
to treat acute pain such as opioids, alpha-2
adrenoceptor agonists, NMDA antagonists, non-
steroidal antiinflammatory drugs, corticosteroids
and local anesthetics, but the election should be
made carefully. For the election of the analgesic,
several factors has to be considered, especially
those associated with pharmacological aspects
of the chosen drug. Other factors are determined
by the severity of pain, the duration of treatment,
2006 World Congress WSAVA/FECAVA/CSAVA
Opioids
Opioids are mostly the first option to treat acute
pain. The main characteristics of these drugs can
be enumerated as following:
• Titrate analgesia (not ceiling effect for mu-receptor
agonist).
• Rapid onset for fentanyl and analogous (the peak
effect being evident 2 min after i.v. injection).
• Intravenous infusion can be set for long duration
treatment (morphine, fentanyl, alfentanil,
sufentanil, remifentanil, etc.).
• Bradycardia, resulting in increase of venous
returns and cardiac contractility.
• Respiratory depression, slower rate and deeper
amplitude (contributing to increase increasing of
venous returns and cardiac contractility).
• Reduce the amount of anesthetic agent required
for about 80% in critical patients.
• Epidural administration is also possible under
critical conditions (morphine persists in the
cerebrospinal fluid much longer than in plasma).
• Side effects at suggested doses: unusual.
• Morphine frequently induces vomiting when
given in conscious dogs by i.m. and i.v. route;

the effective dosages and the preexisting medical however, this side-effect is seldom observed in
conditions, as well as the available nursing care animals suffering from acute pain.
and monitors. • In head injured patients, they should be avoided
until diagnosis. When increased intracranial
Key Points: pressure is present, opioids should be combined
• Knowledge of the basic physiology of pain with mechanical ventilation to reduce the PaCO2.
mechanisms and the basic pharmacology of
analgesic drugs is essential for effective pain
prevention or alleviation.
• Multiple classes of analgesic drugs administered
simultaneously are more effective than a single
class of analgesic.
• Pain therapy should not just revolve around
drugs; therapies such as surgery and physical
therapy also have an important role in providing
effective pain relief.
• The best time to start analgesic therapy is as soon as
possible in the case of trauma or acute pain
192
Back to contents
 Cr
Table 1: Opioids in canine. Doses and intervals

Drug Dose Route Duration(hours)

Morphine 0.1-0.5 mg/kg SC; IM; PO; (IV) 4-6
CRI: 0.05 mg/kg/h
Pethidine 3.5-10 mg/kg IM 2.5-3.5
Codeine 1–2 mg/kg PO 6-8
Methadone 0.1-0.25 mg/kg IM; SC; IV 4-6
Oximorphone 0.05-0.2 mg/kg IM; SC; IV 2-4
Fentanyl 2 - 10 µg/kg IV 0.3-0.5
CIR: 5-10 µg/kg/h
Sufentanil 0.75 - 2 µg/kg IV 0.1-0.25
CRI: 1-2 µg/kg/h
Alfentanil 15–30 µg/kg IV 0.25
CRI: 30-80 µg/kg/h
Remifentanil CRI: 0.025–0.1 µg/kg/min IV CRI
Buprenorphine 5-20 µg/kg IM; SC; IV 6-12
Butorphanol 0.2–0.6 mg/kg IM; SC; IV; PO 2-4
Nalbufine 05-1 mg/kg IM; SC; IV 4-6
Pentazocin 1–4 mg/kg IM; IV 2-4
Tramadol 1–2 mg/kg IM; IV; PO 6-8
Dextropropoxiphen 2-5 mg/kg IV; IM; PO 4-6

CRI: Constant rate infusion

Table 2: Opioids in feline. Doses and intervals

Drug Dose Route Duration
Morphine 0.1-0.2 mg/kg SC; IM 6-8 hour
CRI: 0.03 mg/kg/h
Pethidin 3.5-10 mg/kg IM 2-3 hour
Codeine 1-2 mg/kg PO 6-8 hour
Methadone 0.1-0.2 mg/kg SC; IV 2-3 hour
2006 World Congress WSAVA/FECAVA/CSAVA
Oximorphone 0.01-0.1 mg/kg IM; SC; IV 2-4 hour
Fentanyl 1-5 µg/kg IV 20-30 min
CRI: 5 µg/kg/h
Sufentanil 0.1-0.5 µg/kg IV 10-15 min
CRI: 0.5-1 µg/kg/h
Buprenorphine 5-20 µg/kg IM; SC; IV; PO 3-8 hour
Butorphanol 0.2-0.8 mg/kg IM; SC; IV 2-4 hour
Nalbufine 0.5-3 mg/kg IM; SC; IV 2-4 hour
Pentazocin 1-4 mg/kg IM; IV 4-6 hou
r
Tramadol 1-2 mg/kg IM; IV; PO 6-8 hour
Dextropropoxiphen 2 mg/kg IV; IM; PO 4-6 hour

CRI: Constant rate infusion

193
Back to contents
Cr
Non-steroidal antiinflammatory drugs (NSAIDs)
NSAIDs are a group of drugs with antiinflammatory,
analgesic and antipyretic properties. These agents
act by inhibiting the ciclooxygenases (COX 1, 2
and 3). NSAIDs are widely used to treat acute
pain. The analgesic effects can be increased by
the combination with opioids, which is a common
practice during trauma.
Benefits are listed line-down.
• Good analgesic effects to treat visceral pain
(ketoprofen, flunixin meglumine, metamizol).
• Efficacious plasma levels of NSAIDs are
reached after approximately 1 hour after oral
administration.
• For pain caused by acute inflammatory diseases
NSAIDs seem to be more effective than opioids.
• Newer NSAIDs (carprofen, meloxicam, etodolac)
has high safety margins in dogs.
• Intravenous fluids should be administered before
NSAIDs use and the blood pressure should be
monitored because of renal concerns.
• NSAIDs should not be administered to patients
with renal or hepatic diseases, dehydration,
hypotension, coagulopathies and concurrent use
of other NSAIDs or corticosteroids.

Table 3: NSAIDs in canine. Doses and intervals

Drug Dose Canine Via Interval

Paracetamol (Acetominophen) 15 mg/kg PO 6-8 hour
Acetylsalicylic acid 10-25 mg/kg PO 8-12 hour
Tolfenamic acid up to 4 mg/kg SC, PO 24 hour
Carprofen 2-4 mg/kg PO 12-24 hour
Deracoxib 2-4 mg/kg PO 24 hour
Dipyrone (Metamizol) 20-30 mg/kg IV, SC, IM 8 hour
CRI: 10 mg/kg/h
Etodolac 10-15 mg/kg PO 24 hour
Phenylbutazone 10-25 mg/kg PO 8-12 hour
Flunixin 0.5-1 mg/kg IV, SC, IM 24 hour
Ibuprofen 5-10 mg/kg PO 24-48 hour
Ketoprofen 1-2j mg/kg IV, SC, IM, PO 24 hour
Ketorolac 0.3-0.5 mg/kg IV, IM 8-12 hour
Meloxicam 0.1- 0.2 mg/kg IV, SC, PO 24 hour
Naproxen 1-2 mg/kg PO 24 hour
Piroxicam 0.3 mg/kg PO 24 hour
Tepoxalin 10 mg/kg PO 24 hour
Vedaprofen 0.5 mg/kg PO 24 hour
2006 World Congress WSAVA/FECAVA/CSAVA

Table 3: NSAIDs in feline. Doses and intervals

Drug Dose Feline Via Interval

Paracetamol (Acetominophen) Contraindicated ------------- -------------
Acetylsalicylic acid 10-15 mg/kg PO 48 hour
Tolfenamic acid 4 mg/kg SC, PO 24 hour
Carprofen 4 mg/kg PO 24 hour
Metamizol 20-30 mg/kg IV, SC, IM 8 hour
Phenylbutazone 10-25 mg/kg PO 8 a 12 hour
Flunixin 0.5-1 mg/kg IV, SC, IM Only one dose
Ketoprofen 1-2 mg/kg IV, SC, IM, PO 24 hour
Ketorolac 0.25 mg/kg IM 12 hour
Meloxicam 0.1-0.2 mg/kg IV, SC, PO 24 hour
Piroxicam 1 mg/cat PO 24 hour

194
Back to contents

Alpha-2 adrenoceptor agonists
Alpha-2 agonists xylazine, medetomidine
and dexmedetomidine are commonly used in
small animals and possess analgesic, sedative
and muscle-relaxant properties. Despite the
fact that these drugs are usually reserved for
healthy animals because of the cardiopulmonary
depression that accompanies their use, its use
during acute pain could be beneficial.
• Produce profound sedation (alpha-2 agonists
are some of the most potent sedatives available).
• Potent analgesics (can be as effective as opioids
in many situations).
• Adverse affects depending on dose, rate and the
concurrent use of other CNS depressants.
Cr
• Their short duration (20-40 min depending on
the agent) can be increased with constant rate
infusion in small doses.
• Good bioavailability by the oral route.
• The combination of low doses of alfa-2 agonists,
opioids and benzodiazepines results in a
synergistic response.
• Good immobilization when combined with
ketamina.
• The hemodynamic effects can be lessened by
administering in small doses.
• Alfa-2 agonists may be used as an infusion after
a loading dose.
• This group of drugs has specific antagonists for
their reversal.

Table 4: Alfa-2 agonists and antagonists in small animals

Drug Canine Feline Via

Xilazine 0.4-1 mg/kg 0.2-0.5 mg/kg IM; (IV)
CIR:0.1 mg/kg/h CIR:0.1 mg/kg/h
Medetomidine 10-40 µg/kg 40-80 µg/kg IM; (IV)
CIR:1-3 µg/kg/h CIR:1-3 µg/kg/h
Dexmedetomidine 5-20 µg/kg 20-40 µg/kg IM; (IV)
CIR:0.5-1 µg/kg/h CIR:0.5-1 µg/kg/h
Romefidine 40-80 µg/kg 80-160 µg/kg IM; (IV)
Yohimbine 0.1-0.15 mg/kg 0.1 mg/kg IV; (IM)
Atipamizol 0.2 mg/kg 0.2 mg/kg IV; (IM)

NMDA Antagonist (Ketamine) References

The NMDA receptor plays an important role in
central sensitization, and there is much interest
in developing drugs that can inhibit this receptor.
Ketamine is widely use in clinical practice to
provide anesthesia and restraint. It is, however, a
potent analgesic in its own right. Low doses (1.0-
2.0 mg/kg, canine and feline) are used to provide
both preemptive analgesia and acute pain control.
In low doses, ketamine acts in a synergic manner
with opioids enhancing its analgesic effects.
Recently, the opioids-sparing effects of ketamine in
dogs after major surgery have been demonstrated.
1. Frecknell, P.; Waterman-Pearson, A. Pain
management in animals. WB Saunders Co.
London, UK 2000.
2. Matthews, K.A. Management of Pain. Vet Clin
North Am Small Anim Pract 2000; 30: 703-967.
2006 World Congress WSAVA/FECAVA/CSAVA
3. Otero E. Pablo. Dolor. Evaluación y tratamiento
en pequeños animales. Editorial Inter-médica.
Argentina, 2004.

195
Back to contents
Cr
Cr - Critical Care & Anaesthesiology
FELINE AS IN HOSPITAL PATIENT: TRAUMA MODEL
Luis H. Tello. DVM, MS
Clinica Veterinaria Las Condes
Geronimo De Alderete 1567
- Vitacura
Santiago De Chile
ltello@uchile.cl
Many people think that domestic feline cat, are
really a home “introduced” especie. Cats have
independent, mysterious and unpredictable
personalities, but this is not the only way that cats
are unique. Their response to disease and medical
therapy represents a challenge in the veterinary
medicine practice, making clear the famous
sentence: “cat is not a dog in emegency or critical
care”
Despite the fact that dogs and cats have the same
clinical entities in emergency, they frequently do
not show the same symptoms and clinical signs.
Cats are very sensitive to hypotension and they
are very difficult to resuscitate from hypotensive
shock. The response to hypotension in cats is very
different because they have vagal fibers close to
sympathetic fibers and hypotension can stimulate
both, showing a normal or slow heart rate, instead
of the tachycardia showed by other species like
dogs. In a research with hypotensive cats (blood
pressure less than 80 mmHg systolic), 100% of
cats were found to have normal or slow heart rates.
As cardiac output is the result of contractility and
rate, the fact of have normal or slow cardiac rate,
diminish the cat patient compensatory response
to shock, aimed at the goal of maintaining oxygen
2006 World Congress WSAVA/FECAVA/CSAVA
delivery to the tissues and hemodinamic stability
like blood pressure and capillary blood flow.
The hyperdynamic signs of shock, commonly
seen in dogs are rarely seen in the cat. Shock
in the cat is most commonly decompensatory,
evidence by normal or slow heart rate, severe
hypothermia, weak or non palpable peripheral
pulses and profound mental depression. The
mucous membranes are gray or white and
capillary refill is not evident. The bradycardia
and low cardiac output leads to hypothermia, and
hypothermia accentuates the bradycardia. There
are many aspects of critical care that are unique
for the cat.
Organic response
The very unique physiology of the domestic cat
196
Back to contents
patient, facing a trauma episode deserve special
consideration. Is well knowed that the magnitude
of the inflammatory response to trauma is directly
proportional to the exchange of energy and the
extent of injury. Cat suffering severe multiple
trauma is at much higher risk for the development
of a significant systemic inflammatory response,
any trauma will incite the same series of
events, including the release of many different
inflammatory mediators.
In the dog, in cases of massive bleeding,
sympathetic response leads to splenic contraction,
releasing of up to 30% of their volume but in cats
the spleen does not react in the same way.
Shock due to trauma results when organic
response is no longer able to compensate, leading
to maldistribution of blood and impairment of
oxygen delivery. The response to a traumatic
insult also involves the production of acute phase
proteins by the liver like Protein C and many
others cytokines who are involved in control
the inflammatory response, inhibiting enzymes
and modulating coagulation. Feline endothelium
cells has a very important role in modifying and
regulating the body’s response to injury and is
particularly susceptible to hypoxic injury.
The increased nutritional demands plus a a
generalized catabolic state can quickly lead to
negative balance of nitrogen, leading the patient
to malnutrition, that is very important in cats,
as they are at a higher risk for hepatic lipidosis
and more likely to refuse to eat in a hospital
environment.
Tissue hypoxia causes an increase in intracellular
calcium that is cytotoxic, impairs inmmune
celular function, and begins the production and
release of oxygen-free radicals. In severe case of
trauma with a massive inflammatory response,
endothelial disruption activates the coagulation
cascade resulting in a procoagulant status in the
feline trauma patient. However, Disseminated
Intravascular Coagulation is a very rare syndrome
in cats compare with traumatized dogs.

Approach to the feline trauma patient
The goal of treatment in feline trauma patients
is the same as any critically ill patient: Optimize
perfusion and oxygen delivery to the tissues.
The initial approach should be focused on
major body systems examination, with specail
atention to respiratory and cardiovascular
systems. Stabilization should be begin with the
classic ABC: Airway, Breathing, Circulation (or
Cardiovascular). Extra attention should be paid
to the neurologic and renal systems as damage
are common in cats and both can result in life
threatening injuries.
Treatment goal in the feline trauma patient
is to maximize oxygen delivery. The oxygen
content in the blood is a significant determinant
of oxygen delivery. Many sequels of trauma in
the cat can lead to pulmonary complications that
result in decreased hemoglobin saturation as well
as decreased PaO2.
The initial assessment of the respiratory system
should begins with observation of the cat
avoiding any stress during handling. Evaluation
of the rate, effort and pattern of breathing prior
to any additional stress is important. Panting cat
means the possibility of severe respiratory tract
condition. Always supplemental oxygen should
be provided in a traumatized cat.
Airway is commonly affected by traumatic
injuries in cats. Jaw fractures, skull fractures
are commonly seen in vehicle accidents, while
tracheal avulsion, or direct injury to the laryngeal/
pharyngeal area are common in dogs-cats or cat-
cat fights. If the airway is not patent, tracheostomy
should be considered.
Phisical exam and auscultation may reveal
clinical evidence of pulmonary contusions,
pneumothorax or hemothorax. If pleural space
conditions needs to be rule out, do no lead the
patient for radiographs, thoracocentesis should be
performed. In the author experience complications
are rare when is done correctly.
Assessment of pulmonary function by arterial
blood gas analysis is not common in practice,
but another methods like pulse oximetry is
more doable. However, this test can lead to
numerous mistakes and care must be taken in the
interpretation of the results. Hypothermia, very
common in the post trauma cats, poor capillary
perfusion, anemia, movement and pigmented
mucosa can lead to inaccurate results.
Thoracic radiographs should be dely until cat
is stable. Pulmonary contusions, rib fractures,
diaphragmatic hernia, as well as pleural space
disease can be diagnosed by X ray examination,
but also stress of restraint can be life threatening
in an unstable cat. Many thoracic injuries are
commonly seen in the trauma cat: penetrating chest
Back to contents
Cr
wounds, hemothorax, pneumothorax, pulmonary
contusions and tension pneumothorax.
Cat lungs are very sensitive to hypoxemia due
to poor perfusion, leading to increased capillary
leak and inflammatory lung disease secondary
to severe trauma, so much attention should be
paid to the respiratory status of any cat after any
significant trauma, even in cases where there was
no direct thoracic trauma.
Cardiac output is another important determinant
of oxygen delivery, and is commonly diminished
in the trauma patient. Hemorrhage, arrhythmias,
direct cardiac injury and myocardial dysfunction
can all lead to impairment of adequate cardiac
output. Initial evaluation includes assessment of
heart rate and rhythm, mucous membrane color,
capillary refill time, pulse rate and pulse quality.
Assessment of blood pressure can be difficult
in cats. Direct blood pressure is not common
in practice: excesive handling, pain, need to
anesthesia or sedation, and side efects are the main
reason. Indirect determination of arterial blood
pressure can be done by doppler measurement,
but studies done in healthy cats have shown that
these measurements underestimate the systolic
blood pressure. However there are no studies
about the accuracy of doppler measurements in
sick cats.
The cardiovascular response to poor tissue
perfusion and impaired oxygen delivery in the
dog is tachycardia, but this is not the case in cats
patients, where low heart rates are common in
critical care cats.
This response seems to be unique to the feline
species, and still there is no explanation about the
mechanism. Theories goes to cytokine-associated
myocardial depression who may play a role.
Hypothermia who is very common in critically
ill cats has been suggested as responsible for the
bradycardia, but no research has demonstrate a
correlation.
Cardiac arrhythmias should be investigate in
2006 World Congress WSAVA/FECAVA/CSAVA
any trauma injured cat with evidence of poor
tissue perfusion (tachycardia or bradycardia, pale
mucous membranes, prolonged capillary refill
time, weak pulses) by regular ECG assesment.
Treatment begins with fluid administration,
always starting with isotonic crystalloids. In
cats, bolus of 30-50 ml/kg of crystalloids plus
5-10 ml/kg of colloids. Care should be taken
when administering fluids to injures cats as
fluid overload is common: pulmonary edema
and pleural effusion are common in this patient
population. Cats on inflammatory conditions
has increased vascular permeability, myocardial
dysfunction and decreased colloid oncotic
pressure due to hypoalbuminemia.
It is recommended start with small boluses of
197
Cr
10 – 20 ml/kg and monitor the effect of this
volume like blood pressure normalization No
matter is the cat patient is hypothermic, always
warm fluids before the administration. Therefore
external warming should be used with air heating,
circulating water blankets, or incubator. Always
monitore temperature
Consider that may be possible that cats have a
previous anemia (FeLv - FIV infections) leading
to low hemoglobin, decrease oxygen delivery and
add the consideration of decreased ability of the
feline spleen to contract, if so, blood transfusion
should be administered. But remember that cats
can have naturally occurring antibodies, leading
to transfusion reactions, even in those cats that
never previously received a blood transfusion.
Neurologic Neurologic damage in the trauma
patient can occur through direct trauma to the
brain tissue or secondary to hypoxic tissue
damage from poor perfusion to the CNS. A
complete neurologic evaluation should be
done after initial resuscitation to determine any
necessary therapeutics and establish a baseline for
further monitoring. Additional details on therapy
for patients with head trauma will be discussed
below.
In general, maintenance of adequate perfusion
to the CNS is imperative in both treating and
preventing neurologic damage. Renal Signs of
damage to the renal system are often not evident
on initial presentation of the trauma patient.
These manifestations may not be detected for
several hours and require close monitoring after
the traumatic incident. Abnormalities such as an
uroabdomen, uroretroperitoneum, direct renal
trauma or urethral damage can be life threatening.
Close monitoring of the urine output, BUN,
creatinine and potassium should be done in any
2006 World Congress WSAVA/FECAVA/CSAVA
198
Back to contents
cat in which renal system damage is suspected.
Additional diagnostics such as abdominal
radiographs, abdominal ultrasound or intravenous
contrast studies may be necessary in some cats.
Neurologic trauma considerations
Head trauma is commonly seen in cats vehicle
accident or cats falling due to high rise syndrome.
The primary goal in the treatment of head trauma
is optimizing tissue perfusion and maintaining
cerebral perfusion pressure (CPP). Supplemental
oxygen, elevation of the head 30º, avoidance of
any neck twist position or occlusion of the jugular
veins should be instaured.
The goal of maintain CPP is made by strict control
on mean arterial blood pressure and intracranial
pressure. Keep an eye on mean arterial pressure is
imperative in these cats, and aggressive treatment
for any intracranial hypertension is necessary. A
well discussed issue in hypotensive head trauma
cats is using hypertonic saline at a dose of 3 – 5
ml/kg. Still there is no clear information about it,
but some evidence show that hypertonic fluids
improves intravascular volume and helps decrease
intracranial pressure. If there is clinical evidence
suggesting cerebral edema and increased ICP,
Mannitol at 0.5 – 1 g/kg iv should be given over
30 – 60 minutes.
Nursery
After first aid and stabilization and assessment of
the major body systems, additional considerations
include clipping, flushing and cleaning of any
wounds as well as stabilization of any fractures
prior to definitive surgery. Evaluation of the oral
cavity for any fractures, dislocations or pain is
important in the cat, as any trauma that may lead
to anorexia must be addressed.

Cr - Critical Care & Anaesthesiology
EPIDURAL ANESTHESIA AND ANALGESIA
Prof. Pablo Otero DVM
Facultad de Ciencias Veterinarias
Universidad de Buenos Aires
Av. Chorroarín 280
C1427CWO
Ciudad de Buenos Aires -
República Argentina
potero@fvet.uba.ar
Introduction
The use of epidural anesthesia provides excellent
analgesia as well as good muscle relaxation due
to its ability to produce a sensory and motor
blockade, respectively.
The local anesthetics used for epidural anesthesia
are shown in table 1 and table 2. Lidocaine,
bupivacaine and ropivacaine are similar in terms
of their anesthetic profile when used for epidural
blockade. Lidocaine may possess a slightly shorter
onset time, while bupivacaine and ropivacaine
produce a longer duration of anesthesia. Both
bupivacaine and ropivacaine are widely used
for surgical procedures. They are of particular
value for continuous epidural blockade during
acute pain like trauma. When used as a 0.1% or
0.25% solution they provide satisfactory sensory
analgesia with minimal motor blockade. Thus,
the animal can be rendered pain free and still
be able to move itself or maintain spontaneous
ventilation even when the cephalic spread is
high. Bupivacaine and ropivaciane usually
provide 2-4 h of adequate analgesia, although this
depends greatly on the dosage.
The quality of epidural blockade will be
influenced primarily by the local anesthetic
employed. Others factors that may influence the
adequacy of epidural blockade include:
1. Dose, volume and concentration of the local
anesthetic agent.
2. Addition of a vasoconstrictor to the local
anesthetic solution.
3 . P atient position.
4. Patient age, epidural space volume and
clinical status.
The volume of the anesthetic solution administered
into the epidural space may influence the cephalic
spread of anesthesia. However, the relationship
between spread and volume of anesthetic is
neither lineal nor predictable. The essential
qualities of epidural anesthesia are related to the
mass of drug rather than to the variation in volume
or concentration of solution (see table 1).
Back to contents
Cr
Epinephrine is frequently added to local
anesthetics solution (lidocaine and bupivacaine)
used for epidural anesthesia. The adition of
epinephrine is related primarily to its effect on
the local vasculature, which causes a decrease in
absorption of the local anesthetic. Bupivacaine
and ropivacaine administered epidurally do not
appear to benefit as much as lidocaine from the
addition of a vasoconstrictor.
Although the use of epidural anesthesia alone
is in theory possible, it is not advisable. In
fact, the addition of light general anesthesia
facilitates patient manipulation and contributes
to a “stress free anesthesia”. A contraindication
to supplementary anesthesia would occur in only
few cases where there is marked depression, such
as in a cesarean with coexisting fetal depression
or in patients with hemodynamic compromises.
In most cases, the contribution of epidural
anesthesia to the anesthetic protocol allows the
practitioner to significantly decrease the total
dose of central depressants, thus decreasing the
risks and the negative impact of these drugs in
patients with underlying diseases.
Opioids such as morphine have been used
intrathecally or epidurally for the treatment of both
acute pain and various chronic pain conditions. 2006 World Congress WSAVA/FECAVA/CSAVA
Although opioids administered by any route bind
to spinal cord opioids receptors, it was speculated
that epidural or intrathecal administration would
provide preferential delivery and binding of
opioids to spinal cord receptors, thereby allowing
a lower total dose to be used. Opioids for epidural
injection are diluted with an appropriate volume
of sterile saline (see table 3), and use of the basic
technique.
In most cases, the entry into the epidural space
is accomplished via puncture at the lumbar-sacral
level (L7-S1). The epidural space is situated
between the internal and external dural sheaths.
These two sheaths get separated at the level of
the foramen magnum and extend caudally. The
external leaf forms the periosteum of the spinal
199
Cr
channel, while the internal one comprises the true
spinal dura mater.
Spinal (intrathecal) administration of analgesics
is rarely used to provide clinical pain relief in
animals. There are very few drugs which are
marketed for epidural or spinal use. Many of the
drugs used for epidural analgesia are available
in preparations designed for systemic use and
contain neurotoxic preservatives. Therefore, to
avoid complications, special care should be taken
in choosing a correct formulation.

Table 1. Local anesthetics used for epidural anesthesia in dogs

Drugs Dose Spre ad Onset(min) Duration(hours)

Lidocaine 2% 0.22 ml/kg L1 5-15 1-1.5

1.5-2 w/e
Lidocaine 2% 0.31 ml/kg T12 5-15 1-1.5
1.5-2 w/e
Lidocaine 2% 1.0 ml/4.5 kg L1 5-15 1-1.5
1.5-2 w/e
Lidocaine 2% 1.0 ml/3.5 kg T9 5-15 1-1.5
1.5-2 w/e
Lidocaine 2% 0.5-0.8 ml/10 cm* L1 5-15 1-1.5
1.5-2 w/e
Lidocaine 2% 1.0 ml/10 cm* T9 5-15 1-1.5
1.5-2 w/e
Lidocaine 2% 3.0-5.0 mg/kg L1 5-15 1-1.5
1.5-2 w/e
Bupivacaine 0.5% 1.0-2.5 mg/kg L1 10-20 4-6
Bupivacaine 0.5% 0.22 ml/kg L1 10-20 4-6
Bupivacaine 0.5% 0.31 ml/kg T12 10-20 4-6
Bupivacaine 0.5% 1.0 ml/4.5 kg L1 10-20 4-6
Bupivacaine 0.5% 1.0 ml/3.5 kg T9 10-20 4-6
Bupivacaine 0.25% 1.0 ml/10 cm* T10-9 10-20 4-5
Bupivacaine 0.25% 1.5 ml/10 cm* T5-2 10-20 4-5
Bupivacaine 0.1% 1.5 ml/10 cm* T5-2 10-15 2-4
Ropivacaine 0.5% 0.8 ml/10 cm* L1 10-20 2-4
Ropivacaine 0.5% 1.2 ml/10 cm* T9-5 10-20 2-4
2006 World Congress WSAVA/FECAVA/CSAVA

Ropivacaine 0.2% 1.0 ml/10 cm* T10-9 10-20 1-1.5

Ropivacaine 0.2% 1.5 ml/10 cm* T5-2 10-20 1-1.5
Ropivacaine 0.1% 1.5 ml/10 cm* T5-2 10-15 2-4
Ropivacaine 0.05% 1.5 ml/10 cm* T5-2 10-15 1-2
Mepivacaine 2% 3.0-4.5 mg/kg L1 5-10 1.5-2
Levobupivacaine 0.5% 0.8 ml/10 cm* L1 10-20 4-6
Levobupivacaine 0.5% 1.2 ml/10 cm* T9-5 10-20 4-6
Levobupivacaine 0.25% 1.0 ml/10 cm* T10-9 10-20 4-5
Levobupivacaine 0.25% 1.5 ml/10 cm* T5-2 10-20 4-5
Levobupivacaine 0.1% 1.5 ml/10 cm* T5-2 10-15 2-4
Bupivacaine 0.25% 0.2 mg/kg/hr CIR --- ---
Ropivacaine 0.2% 0.2 mg/kg/hr CIR --- ---

• *The dose was calculated according to the spine length, measured from the occipital bone to the first
coccygeal vertebra.
• CIR: constant infusion rate; L: lumbar vertebra; T: Thoracic vertebra; w/e: with epinephrine
200
Back to contents
 Cr
Table 2. Local anesthetics used for epidural anesthesia in cats

Drugs Dose Spread Onset(min) Duration (hours)

Lidocaine 2% (con epinefrina) 1.0-1.5 ml L1-T9 5-15 1.5-2
Lidocaine 2% (con epinefrina) 1.0 ml/5 kg L1 5-15 1.5-2
Lidocaine 2% (con epinefrina) 1.0 ml/3.5 kg T4 5-15 1.5-2
Bupivacaine 0.5% (con epinefrina) 1.0-1.5 ml L1-T9 10-20 4-6
Bupivacaine 0.5% (con epinefrina)) 1.0 ml/5 kg L1 10-20 4-6
Bupivacaine 0.5% (con epinefrina) 1.0 ml/3.5 kg T4 10-20 4-6
Ropivacaine 0.5% 1.0-1.5 ml L1-T9 10-20 2-4
Mepivacaine 2% 1.0-1.5 ml L1-T9 5-10 1.5-2
Levobupivacaine 0.5% 1.0-1.5 ml L1-T9 10-20 4-6

Table 3. Epidural opioids - Dose and intervals

Drug Dose(mg/kg) Volume*(ml/kg) Onset(min) Duration(hours)

Morphine 0.1 mg/kg 0.13-0.26 30-60 10-24
Meperidine 0.5-1.5 mg/kg 0.2-0.26 10-30 5-20
Oxymorphone 0.05-0.1 mg/kg 0.26 20-40 7-10
Hidromorphone 0.05-0.1 mg/kg 0.26 --- ---
Methadona 0.7-1.0 mg/kg 0.26 5-10 4-9
Fentanyl 1.0-5.0 µg/kg 0.26 15-20 3-5
Sufentanil 0.7-1.0 µg/kg 0.26 10-15 1-4
Butorphanol 0.25 mg/kg 0.26 10-20 3-4
Buprenorphina 5.0-15.0 µg/kg 0.26 60 16-24
Xylazine 0.02-0.25 mg/kg 0.26 20-30 2-5
Medetomidine 10.0-15.0 µg/kg 0.26 20-30 1-8
Dexmedetomidine 1.0-2.0 µg/kg 0.26 20-30 1-8
Morphine +Xilacina 0.1 mg/kg 0.26 30-60 10-20
0.02 mg/kg 20-30
Morphine + 0.1 mg/kg 0.26 30-60 10-20
Medetomidine 1-5 µg/kg 20-30
Morphine + 0.1 mg/kg Diluted in local 10-15 16-24
Bupivacaine 0.5% 1.0 mg/kg anesthetic
2006 World Congress WSAVA/FECAVA/CSAVA
Morphine CIR 0.3 mg/kg/24 h 3.0 ml/h --- ---
Morphine CIR + 0.3 mg/kg/24 h Diluted in local --- ---
Bupivacaine 0.5% 0.75 mg/kg/24 h anesthetic
Ketamine 2.0 1 ml/4.5 kg 5-10 ---
(ClNa)
*Drugs for epidural injection are diluted with an appropriate volume of sterile saline

References 3. Otero E. Pablo. Dolor. Evaluación y tratamiento

1. Frecknell, P.; Waterman-Pearson, A. Pain en pequeños animales. Editorial Inter-médica.
management in animals. WB Saunders Co. Argentina, 2004.
London, UK 2000.
2. Matthews, K.A. Management of Pain. Vet Clin
North Am Small Anim Pract 2000; 30: 703-967.

201
Back to contents
Cr
Cr - Critical Care & Anaesthesiology
TREATMENT OF THE KETOACIDOTIC DIABETIC
Michael Schaer, D.V.M.,
ACVIM, DACVECC
Professor and Assoc. Chair
University of Florida
College of Veterinary Medicine
2015 SW 16th Ave
Gainesville, FL 32608
schaer@mail.vetmed.ufl.edu
Fluid and Electrolytes
Disturbances in hydration and electrolyte balance
are of great importance in diabetic ketoacidosis
(DKA) and require expedient correction when
present. The calculated fluid requirements include
the patient’s dehydration deficits, the 24 hour
maintenance needs, and extra losses that result
from vomiting or diarrhea. The dehydration
status is approximated on a scale ranging from a
mild (5%) to extreme (12%). The needed isotonic
replacement volume is calculated by either of the
following two methods:
(1) dehydration volume deficit (ml) =
= % dehydration x kg body wt x 1000
(2) dehydration volume deficit (ml) =
= % dehydration x lb body weight x 500
The 24 hour maintenance volume is roughly
estimated (assuming adequate urine output) at
60 ml/kg (30 ml/lb). Therefore, the initial first
24 hour total fluid volume is the sum of the
dehydration and the maintenance volumes plus
any on-going losses.
If the animal is 8-12% dehydrated, 2 of the
estimated dehydration deficit should be
2006 World Congress WSAVA/FECAVA/CSAVA
administered intravenously over the first 2-4
hour period of hospitalization with the remaining
replacement and maintenance volumes given
over the following 20-22 hour period. When
hypovolemic shock is present, the initial first
hour’s fluid dose is 70-90 ml/kg for a dog or 35-
40 ml/kg for a cat. Close patient monitoring is
essential during rapid intravenous infusions.
It is important to remember that hydration alone
can decrease the levels of the blood glucose
and certain counterregulatory hormones. Most
investigators believe that the mechanism of
lowering the blood glucose by hydration is caused
by increased osmotic diuresis and glucosuria.
It is suggested that prior hydration will make
the response to insulin more predictable. I prefer
to correct hypovolemia with isotonic solutions
such as lactated Ringer’s or 0.9% saline.
202
Back to contents
Acetated solutions, on the other hand, are not
recommended since they may theoretically
result in increased ketone body production.
Recommended maintenance solutions include
0.4 5% saline or 2-strength lactated Ringer’s
solution. These half-strength solutions are also
used for the hyperosmolar patient. Dextrose
solutions (22-5%) are reserved for use when the
patient’s blood glucose declines to 250 mg/dl
(13.7 mm/L) or less in the setting of continued
insulin administration.
Hyponatremia is corrected with intravenous
0.9% saline solution in order to avoid any plasma
hypoosmolality that might occur when the
hyperglycemia is reduced with insulin treatment.
Plasma hypoosmolality can cause a reversal of
osmotic gradients and an overexpansion of the
intracellular compartment, particularly in the
central nervous system where cerebral edema can
occur.
Hypokalemia is the most common and probably
most important serum electrolyte disorder in
DKA. The reasons for potassium loss include cell
catabolism, osmotic diuresis and vomiting. This
loss is furthered by additional losses from: (1)
serum dilution from rehydration; (2) continued
urinary losses brought about by sodium ion
delivery to the distal renal tubule; (3) correction
of acidosis and the accompanying cellular influx
of potassium ions; and (4) increased cellular
uptake of potassium due to insulin. One way of
avoiding hypokalemia initially is to allow for the
infusion of potassium supplemented fluids for the
first 2-4 hours before any insulin is administered.
Potassium supplementation is best provided
with potassium chloride (KCl) solution, which
is added to the parenteral fluids. If concurrent
hypophosphatemia is present, potassium
phosphate solution can be added and cautiously
administered as well. Potassium supplementation
is best begun after the first 2 hour period of fluid
replacement when hydration, blood pressure, and
urine output are improved. If the patient is initially

hypokalemic, KCl can be added to the hydrating
solution, but the infusion is slowed down to
where one-half of the dehydration replacement
volume is delivered over an additional 1- to 3-hr
period. The recommended amount of potassium
supplementation to be administered over a 24-
hour period is as follows:
1. Mild hypokalemia (serum K+ = 3.0-3.5 mmol/L):
give 2-3 mEq KCl/kg.
2. Moderate hypokalemia (serum K+ = 2.5-3.0
mmol/L): give 3-5 mEq KCl/kg.
3. Severe hypokalemia (serum K+ = < 2.5 mmol/L):
give 5-10 mEq KCl/kg.
The daily potassium dose for the average diabetic
is 3-5 mEq/kg. Potassium chloride can also be
added to the parenteral fluids in amounts ranging
from 20-60 mEq/L depending on the severity of
the hypokalemia.
Daily serum electrolyte determinations and the
necessary treatment adjustments are made until
normal values are obtained. The intravenous fluids
are discontinued when serum biochemistries are
normal, euhydration is present, and the patient is
able to eat.
Hypophosphatemia is known to occur in some
patients with DKA. Although plasma phosphate
may fall to levels that are experimentally shown
to be associated with altered consciousness,
rhabdomyolysis, muscle weakness, impaired
cardiac function, hemolysis, and respiratory
failure; phosphate depletion in DKA is usually
clinically silent and shows up only in clinical
measurements. Nevertheless, if the clinician is
concerned about severe hypophosphatemia that
is present before treatment (usually < 1 mg/dl or
0.32 mmol/L), phosphate supplementation can
be provided in the form of potassium phosphate
solution at the recommended dose of 0.01 to
0.03 mmol of phosphate/kg/hr followed by
repeat serum phosphorus determinations every 6
hours. Caution should be exercised to avoid any
consequences resulting from hyperphosphatemia
which can include soft tissue mineralization and
hypocalcemia.
Sodium bicarbonate treatment is another matter
of controversy in treating DKA. The advocates
of treatment express their concern that severe
acidosis can adversely effect cardiac function,
as seen experimentally, while opponents of
bicarbonate therapy base their concerns on its
cause and effect relationship with paradoxical
central nervous system acidosis. The use of
sodium bicarbonate is often restricted to those
patients with a blood pH < 7.1. During most
treatment courses, the metabolic acidosis will
reverse due to: (1) the cessation of ketogenesis;
(2) metabolic conversion of ketones to bicarbonate
following commencement of insulin treatments;
Back to contents
Cr
(3) improved renal function, and (4) conversion
of the lactate in lactated Ringer’s solution to
bicarbonate. In severe metabolic acidosis, where
the anion gap > 30 mEq/L and the arterial pH
< 7.1, sodium bicarbonate can be given at the
following dose schedule:
• amount NaHCO3 = base deficit x 0.3 x body
weight kg
• needed (mmol)
The base deficit equals the difference between the
desired serum bicarbonate level and the measured
level. Subsequent alkali treatment will depend on
the results of repeated plasma pH measurements;
it should be discontinued when the blood pH is
restored to a level of 7.2 or greater.
Insulin
Regular crystalline insulin is used when the DKA
patient has signs of depression, dehydration,
anorexia, and vomiting. The advantages of
regular insulin include: (1) various routes of
administration (IV, IM and SQ); (2) rapid onset
of action; and (3) short duration of action.
These properties allow adequate insulin titration
throughout the day according to the animal’s
needs. The clinician must acknowledge that blood
glucose levels decline much earlier than ketone
levels and therefore anticipate the persistence of
some ketonemia and ketonuria for the first 48-72
hr. In other words: “Don’t chase ketones.”
Bolus intravenous doses of insulin offer the
advantage of an immediate onset of action for the
critically hypotensive patient. The recommended
amount for a medium-sized to large dog is 1-2
units/kg. In the small dog and cat, the dose is
reduced to 0.5 units/kg. Subsequent doses are
given at the same or varying amounts every 2-3 hr
until the blood glucose levels decrease to less than
250 mg/dl, at which time subcutaneous insulin
injections can be given approximately every 6 hr.
The disadvantages of this technique include the 2006 World Congress WSAVA/FECAVA/CSAVA
need for intensive care monitoring with frequent
(every 1-2 hr) blood glucose determinations, the
likelihood of hypoglycemia and hypokalemia,
and the possibility of cerebral edema resulting
from a too-rapid fall in blood glucose levels.
Mannitol is the preferred treatment should this
complication occur. The maximum route of blood
glucose decline should not exceed 75-100 mg/dl/
hr or 4.1-5.5 mmol/L/hr.
When laboratory facilities are unavailable, blood
glucose reagent strips can be used to determine
approximate blood glucose levels. Several
reflectance colorimeters are now commercially
available to enhance the accuracy of these reagent
strips.
To help avoid the occurrence of the
aforementioned side effects associated with
203
Cr
intravenous bolusing, a continuous low-dose
insulin infusion can be used. One successfully
applied technique in the dog involves adding 5
units of regular insulin to a 500 ml bottle of lactated
Ringer’s solution after the first 2 hr of rehydration
and adjusting the pediatric infusion set or pump
whereby 0.5-1.0 unit/hr is delivered to the patient.
Care must be taken to avoid intravascular fluid
overload in the small animal which might result
from the technique. This can be accomplished by
infusing the insulin containing solution through
a separate intravenous catheter. Blood glucose
determinations should be made every 1-2 hr.
Low-doses of regular insulin can also be given
intramuscularly. Initially 2 units are given into
the thigh muscles of cats and dogs weighing less
than 10 kg. For dogs weighing more than 10 kg,
the initial dose is 0.25 unit/kg. Subsequent hourly
injections of 1 unit for cats and small dogs and
2006 World Congress WSAVA/FECAVA/CSAVA
204
Back to contents
0.1 unit/kg for larger dogs are given until the
blood glucose level is less than 250 mg/dl, at
which time the subcutaneous route can be used
on an every 6 hr or as needed basis. The low
doses used in this technique can be accurately
measured with low-dose insulin syringes.
Subcutaneous regular insulin treatment is a
suitable alternative to the intravenous and
intramuscular methods when intensive care
monitoring is unavailable. The initial dose is
0.5 unit/kg followed by subsequent doses every
6-10 hr depending on need.
The patient is regarded as stable and able to receive
intermediate action (NPH) bid or ultralong-acting
(PZI or Glargine) insulin when normal hydration
is restored, blood glucose levels range between
150-250 mg/dl (75-12.5 mmol/L), serum or urine
ketones are minimal to absent, and oral feedings
are accepted.
 Cr
Cr - Critical Care & Anaesthesiology
PRACTICAL APPROACH TO RECOGNITION OF DIC
Michael Schaer, D.V.M.,
DACVIM, DACVECC
Professor and Assoc. Chair
University of Florida
College of Veterinary Medicine
2015 SW 16th Ave
Gainesville, FL 32608
schaer@mail.vetmed.ufl.edu

Disseminated intravascular coagulation (DIC)
is a pathologic process that is caused by a
coexisting serious medical or surgical disorder. It
results from the activation of both the coagulation
and fibrinolytic systems and is triggered by the
activation of tissue factor. The most common
causes and mechanisms of DIC in the dog and cat
are shown below. Most begin with the production
of excess tissue factor which feeds into and
activates the coagulation process.

Clinical Setting Mechanism

Infection: bacterial Especially common in Gram negative sepsis where
viral, fungal endotoxin stimulates monocytes and endothelial cells to express
tissue factor.
Neoplasia Malignant cells cause endothelial damage and allow the expression of
tissue factor as well as other procoagulant materials.
Trauma Burns, hypo- and hyperthermia, rhabdomyolysis, and hypoxia damage
endothelial cells and allow for the exposure of tissue factor.
Liver disease Both acute and chronic. In acute form, tissue factor is expressed,
but in the chronic form, the liver cannot clear the system of fibrin
split products which have their own fibrinolytic effect.
Also in chronic disease the liver can cease producing
coagulation factors.
Vascular disease Commonly seen in hemangiosarcomas because of damaged
endothelial cells, release of tissue factor.
2006 World Congress WSAVA/FECAVA/CSAVA
Envenomation Varies with species and toxin. Endothelial cells can beDamaged
and tissue factor released.
Transfusion reaction and Release of tissue factor. DIC can be severe.
acute hemolytic reaction

Clinical Findings wherever pathologic thromboses occur, and this

The complications are related to the primary
disease process in addition to the bleeding
and/or thrombosis that predominates. The skin
and mucous membranes can have petechia and
ecchymotic hemorrhages, and bleeding can occur
just about anywhere in the body including the GI,
urinary and central nervous system. Bleeding can
also occur from any orifice, venipuncture sites
and surgical wounds.
Signs resulting from organ ischemia can occur
Back to contents
might become evident as intestinal infarction,
stroke, and myocardial dysfunction. Other signs
reflecting other sites of involvement will also
occur.
Diagnosis
The clinical suspicion occurs whenever sudden
thrombosis or hemorrhage occurs in any patient
that has a condition known to predispose to this
disorder. The typical laboratory findings include a
205
Cr
prolonged prothrombin and partial thromboplastin
times, low platelet and serum fibrinogen levels,
increased fibrin split products, and increased D-
dimer blood levels. Other findings include the
presence of fragmented red cells and low specific
clotting factor assays for Factors II, V, VII, VIII,
and IX.
Treatment
The treatment priorities should be toward
treating the primary disease process concomitant
to providing hemodynamic stabilization with
intravenous fluids. Coagulation factor replacement
is necessary if overt bleeding is present. The
factor needs can be met with fresh frozen plasma
2006 World Congress WSAVA/FECAVA/CSAVA
206
Back to contents
(FFP) while fibrinogen needs are replenished
with cryoprecipitate. If severe thrombocytopenia
is present (platelet count <10,000), platelet
transfusions are indicated. Vitamin K, should also
be administered subcutaneously.
If thrombosis is apparent, heparin can be given
at a dosage ranging 50-200 units/kg. Iatrogenic
hemorrhage due to heparin is lessened if it is
given slowly by constant rate infusion (cri) after
the initial bolus injection. It can also be given
SQ every 6 hours. It is common in veterinary
medicine to administer the FFP and the heparin
simultaneously. Heparin might not be beneficial
where chronic liver disease decreases the
production of antithrombin 3 globulin.

Cr - Critical Care & Anaesthesiology
LOCAL ANESTHETIC AND ANALGESIC TECHNIQUES
Prof. Pablo Otero DVM
Facultad de Ciencias Veterinarias
Universidad de Buenos Aires
Av. Chorroarín 280
C1427CWO
Ciudad de Buenos Aires - Repú-
blica Argentina
potero@fvet.uba.ar
Introduction
Recently local and regional anesthetic techniques
have gained widespread acceptance in small
animal practice. The mechanism of action of
local anaesthetics (lidocaine, mepivacaine,
ropivacaine and bupivacaine) is to interrupt
nervous conduction by occupying a specific
receptor site located in axonal Na+ channels,
thus restricting passage of this ion through
the channel. Usually, the effect is restricted to
the site of application and the action of these
agents is quickly reversed due to its short half-
Table 1: Local anesthetics properties
Agent pKa Onset time
Procaine 8,9 Long
Lidocaine 7,9 Rapid
Bupivacaine 8,1 Intermediate
Ropivacaine 8,1 Intermediate
Mepivacaine 7,6 Rapid
Etidocaine 7,7 Rapid
Prilocaine 7,7 Rapid
Differential sensory/motor blockade
An important clinical consideration is the ability
of local anesthetic agents to cause a differential
blockade of sensory and motor fibers. Small
nerve fibers tend to be more susceptible to the
action of local anesthetics than large nerves
fibers. Some local anesthetics (bupivacaine,
ropivacaine) selectively block sensory rather
than motor function. The required time for
tissue desensitization (onset-time) is higher
in ropivacaine than lidocaine, but similar to
bupivacaine. Ropivacaine in an equal analgesic
dose produces a shorter duration of the motor
blockade than bupivacaine. This may be an
advantage when the proposed blockade involves
Back to contents
Cr
life and subsequent decrease in concentration.
Local anesthetics are organic bases of the amide
group, with a pKa ranged between 7.6 and 8.1
with a high affinity for tissue proteins. These
characteristics, as well its low systemic toxicity
make the use of local anesthetics a valuable
option in regional anesthetic techniques. These
agents are often used with opioids, alfa2-receptor
agonists, dissociatives and anti-inflammatory
drugs as part of multimodal strategy to manage
pain in small animals.
Protein binding Duration(min)
5% 30–60
60 % 60-120
95 % 240-360
91 % 180-300
75 % 90-180
90 % 180-300
55 % 100-200 2006 World Congress WSAVA/FECAVA/CSAVA
muscle structures taking part in respiratory
movements or translation. However there are
reports indicating that the difference between both
drugs is not significant for lower concentrations
(0.125%) mostly used in pain treatment.
Techniques
Local and regional anesthetic techniques are
easier to perform in small animals that have been
sedated or anesthetized. Some indications are
obvious, but the local anesthetic techniques have
a broader application than just surgical procedure.
To perform it, practitioners should review
the sensory innervation to the zone to block.
Percutaneous desensitization, after induction
207
Cr
of anesthesia, is also suggested; however the
veterinarian must be familiar with landmarks.
Nerves frequently blocked
A. Dental nerve blocks: There are a number of
conditions for which we can use dental nerve
blocks. The obvious indication is for preemptive
and postoperative analgesia for dental extractions;
however dental nerve blocks provide excellent
analgesia for many procedures in the oral cavity
and head.
1. Infraorbital Nerve block
2. Mandibular Alveolar Nerve block
3. Maxillary or Caudal Infraorbital Nerve block
4. Mental Nerve block.
Most nerves can be blocked with 0.5 to 1.0 mL
of 2% lidocaine, 0.25-0.5% bupivacaine or 0.2-
0.5% ropivacaine.
B. Cervical and thoracic nerves blocks: The
regional blockade of cervical and thoracic nerves
provides analgesia for surgical procedures and
pain relieves involving forelimb and thorax.
During forelimb amputation, desensitization of the
brachial plexus may be carried out intraoperatively
by infiltration of 0.25% bupivacaine 15 minutes
prior to transection.
1. Brachial plexus
a) Axillary approach: useful for pain
treatment located in structures distal elbow.
Dose: 0.8 mL/kg 1.5% lidocaine with
epinephrine, 0.25% bupivacaine or 0.2%
ropivacaine.
b) Paravertebral approach: Nerves of
brachial plexus (C6; C7; C8 and T1) are
blocked as they exit intervertebral foramina.
Dose: 0.5 to 1.0 mL of 2% lidocaine, 0.25-
0.5% bupivacaine or 0.2-0.5% ropivacaine.
Useful to improve analgesia and muscular
relaxation of the shoulder and elbow.
2. Intercostals nerves. Intercostal nerve block
2006 World Congress WSAVA/FECAVA/CSAVA
during thoracotomy is performed by infiltration
of 0.25% bupivacaine on the posterior aspect of
the rib close to the spinal column while avoiding
the intercostal artery and spanning at least 2
intercostal spaces each side of the incision.
C. Thoracic and pelvic limbs nerves: Selective block
of radial, ulnar, median and musculocutaneous
nerves in forelimb or lumbar and sacral nerves
208
Back to contents
in hindlimb and perineum, may provide analgesia
as well as facilitate anesthetic management
during surgical procedures. Most nerves can
be blocked with 1.2 to 2.0 mL of 2% lidocaine,
0.25-0.5% bupivacaine or 0.2-0.5% ropivacaine.
During hindlimb amputation, desensitization
of femoral and sciatic nerves may be carried
out intraoperatively by infiltration of 0.25%
bupivacaine 15 minutes prior to transection. Sciatic
nerve is a very big branch and, as well as with the
brachial plexus, is mandatory the infusion of large
amount of the local anesthetic to produce a solid
block (0.8 mL/kg 1.5% lidocaine with epinephrine,
0.25% bupivacaine or 0.2% ropivacaine).
In cats, prior to onychectomy of the fore paw,
injection of 0.2 mL of 1% lidocaine or 0.25%
bupivacaine subcutaneously at each site of the
dorsomedial aspect of the carpus, just proximal
to the joint (block of the superficial branches of
the radial nerve), and medial and lateral to the
carpal pad (block of median nerve and palmar
and dorsal cutaneous branches of the ulnar
nerve) will confer analgesia for approximately 30
minutes to four hours depending on the solution
used. For the hind paw, subcutaneous injection on
the dorsomedial aspect of the tarsus just distal to
the joint (selective block of distal branches of the
common peroneal and tibial nerves) and on the
ventromedial aspect of the tarsus just distal to the
joint (superficial branches of the tibial nerve are
blocked) will give approximately 30 minutes to
four hours of analgesia.
References
7. Lemke KA, Dawson SD. Local and regional
anesthesia. Vet Clin N Amer:Sm Anim Pract.
2000; 30(4): 839-857.
8. Otero E. Pablo. Dolor. Evaluación y tratamiento
en pequeños animales. Editorial Inter-médica.
Argentina; 2004.
9. Skarda RT. Local and regional anesthetic and
analgesic techniques: In: Thurmon JC. Tranquilli
WJ, Benson GJ, eds. “Lumb and Jones”
veterinary Anesthesia, Baltimore, MD, Williams
and Wilkins, 1996, pp 426-447.
10. Tranquilli WJ.; Grimm KG.; Lamomt LA.
Pain management for small animal practitioner.
Jackson, Wy: Teton New Media; 2000.
Back to contents
2006 World Congress WSAVA/FECAVA/CSAVA
Cr

209
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

DD
Dermatology
rmat

Back to contents

INVITED LECTURES - FULL PAPERS
D - Dermatology
CANINE MICROBIAL OVERGROWTH
Didier-Noël CARLOTTI, Dip
ECVD
Aquivet clinique vétérinaire
F-33320 Bordeaux-Eysines
France (EU)
dncvetderm@aol.com
Microbial overgrowth may be defined as a
clinical disease due to the colonisation of the
skin by microbes. In the dog, this includes
Malassezia overgrowth (MOG) due to Malassezia
pachydermatis and bacterial overgrowth (BOG)
due to Staphylococcus intermedius.
MALASSEZIA DERMATITIS (OR MOG) IN
THE DOG
The lipophilic but not lipodependent yeast
Malassezia pachydermatis is a component of the
normal cutaneous flora of the dog. Around 50 %
of healthy dogs are carriers (external ear canal,
skin - anal area, lips and extremities - , haircoat).
The response of the host to the yeast includes
non-specific defense mechanisms (phagocytosis
by neutrophils) as well as cell-mediated
specific defense mechanisms. Local delayed
hypersensitivity responses and/or innate immune
mechanisms (transferrin limiting microbial access
to iron) play an important role.
Aetiology and pathogenesis
Alterations of the cutaneous microclimate or
host defense mechanisms allow Malassezia
pachydermatis to multiply and to become
pathogenic. These changes may be due to
underlying causes (ectoparasitic, allergic,
endocrine and keratinization disorders, treatment
with glucocorticoids or antibiotics). It has also
been suggested that innate immunity is abnormal
in case of MOG. Particularly, a defect in the
production of antimicrobial peptides (AMP) and
Toll-like receptors may be implicated since they
may be important in innate skin immunity against
fungi. Also, specific immunological dysfunction
(cell-mediated immunity, IgA secretion) could
promote the growth of the Malassezia population
on the skin and its pathogenicity.
Malassezia produce many enzymes (including
Back to contents
D
lipases and proteases) which can contribute to
cutaneous inflammation through proteolysis,
lipolysis (which alters the lipid cutaneous film),
changes of cutaneous pH, eicosanoid release and
complement activation. In addition, it has been
shown that Malassezia pachydermatis could play
an allergenic role in regard to a type 1 (immediate)
hypersensitivity. Skin-testing with a Malassezia
extract may show immediate hypersensitivity
reactions. Recently, the functionality of anti-
Malassezia IgE has been demonstrated through
passive transfer using the Prausnitz-Küstner
technique. Some major allergens of Malassezia
pachydermatis have been identified: proteins
with 45, 52, 56 and 63 kDa molecular weight.
The delayed hypersensitivity response is less
well known. Patch-testing (epicutaneous tests)
has been evaluated recently and may be a good
tool to explore delayed hypersensitivity caused
by the yeast.
Epidemiology
There is no age or sex predilection. Some breeds
are predisposed to Malassezia dermatitis (e.g. 2006 World Congress WSAVA/FECAVA/CSAVA
West Highland white terrier and Basset hound).
Malassezia dermatitis is often seasonal (summer).
There is no indication that Malassezia dermatitis
is contagious.
Clinical signs
Pruritus is always present and severe. Animals
are presented with a strong odour of rancid fat.
At the beginning of the disease there is localized
or diffuse erythema, erythematous papules and
macules, and a keratoseborrhoeic disorder with
scaling, crusting, alopecia and a greasy aspect
of the skin and hair. This is followed rapidly by
secondary lesions such as lichenification and
hyperpigmentation. Malassezia dermatitis may
be localized, e.g. on the ventral side of the body
211
D
(neck, axillae, ventrum and inguinal area), face
(ear pinnae, lips, muzzle), peri-anal area and
legs (forearms, caudal thighs and feet). It may
also be generalized. Concurrent otitis externa is
common.
Diagnosis
Diagnosis of Malassezia dermatitis is based
upon history, physical examination, appropriate
complementary diagnostic aids to show the
presence of Malassezia on the skin, response
to specific therapy and exclusion of other
dermatoses.
Cytological examination may show yeasts and
allow for a semi-quantification. The result is
immediate using the immersion power objective
after staining with a rapid method. Several
cytological techniques can be used: impression
smear, « scotch test » using pieces of tape (clear
cellophane) strip, scrape smear, swab smear.
Impression and above all tape strip smears
appeared to be the most reliable methods. Swab
smears should be reserved for the external ear
canal. Cytological examination will show oval or
elongated cells of 3 to 5 µm in diameter, with a
typical single polar budding. The minimal number
of yeasts which indicates the possibility of a true
Malassezia dermatitis is not precisely known.
In addition there are variations between breeds
and body sites. Lastly there are cases in which a
small number of yeasts trigger a hypersensitivity
reaction.
Fungal cultures may show the presence of
Malassezia on the skin and hair of dogs
(Sabouraud’s dextrose agar with chloramphenicol
and cycloheximidine and modified Dixon’s agar
which grow all species). As the yeast is a normal
component of the cutaneous flora of the dog, by
itself a positive culture has little or no value.
Cutaneous histopathology may sometimes show
the yeasts on the surface of the epidermis and
2006 World Congress WSAVA/FECAVA/CSAVA
in the infundibula, particularly in PAS stained
sections (although they are occasionally visible
on HE stained sections). However if they are not
discovered this does not exclude their presence
(biopsy in a non-infected area, removal of
the stratum corneum during processing, etc).
Cutaneous histopathology is a less sensitive
technique than cytology. There are common
findings in biopsies from dogs with Malassezia
dermatitis, including supepidermal linear
alignment of mast cells (SLAM). Signs of
concurrent bacterial folliculitis or BOG are not
uncommon.
The therapeutic challenge is in fact the ultimate
tool to confirm that in a particular case the
commensal Malassezia has become a pathogen.
Differential diagnoses include many pruritic
212
Back to contents
dermatoses with erythema, hyperpigmentation
and seborrhoea including parasitic and allergic
skin diseases, bacterial folliculitis and all causes
of seborrhoea with cutaneous inflammation.
Treatment
Systemic therapy is necessary in many cases,
particularly when clinical signs are severe and
when the lesions are extensive. Ketoconazole is
the most commonly used drug. The dose is 10 mg
kg-1/day (up to 200 mg/day). It is recommended
to give the drug with some food. Tolerance is
usually good but periodic biochemistry panels are
necessary if the drug is give n over an extended
period of time. Itraconazole may also be used (5
to 20 mg kg-1every day or other day).
Topical therapy is an alternative to systemic
treatment, particularly for localized lesions
(creams, gels, lotions or sprays). A soothing
astringent topical spray (Dermacool®, Virbac),
has been proved effective in Malassezia
pododermatitis (Carlotti and Rème, 2004).
For extensive lesions antifungal shampoos or
lotions are preferable. They can be used with
systemic therapy, which speeds up recovery.
This form of topical therapy should not be
used alone as a diagnostic challenge, but it
can maintain a remission, thus confirming the
diagnosis. Shampoos containing miconazole
(2%), chlorhexidine (at least 3%), a combination
of both (2% each) and ketoconazole (2%) are
the best whereas the most appropriate leave-
on rinses (lotions) are lime sulfur and above all
enilconazole (10 % diluted 50 times i e 0.2 %).
Topical treatments should be administered 2 to 3
times a week for 2 weeks then once a week.
Therapeutic follow-up is very important. Pruritus
usually decreases within one week, whereas
lesions will clearly decrease after 2 weeks. The
duration of treatment should be at least one
month. Usually therapy is continued for 7 to 10
days beyond clinical cure. Otitis externa should be
treated vigourously to limit the fungal reservoir.
It is important to diagnose and treat appropriately
an underlying cause.
BACTERIAL OVERGROWTH
Bacterial overgrowth has been recently
recognized (Pin D, Carlotti DN et al, 2006),
although indications in the veterinary literature
have suggested its existence for more than 10
years.
Aetiology and pathogenesis
The disease is due to a staphylococcal
(Staphylococcus intermedius) overgrowth at
the surface of the skin of affected dogs. The
pathogenesis of the disease is in fact unknown.

Low levels of anti-staphylococcal IgE exclude a
hypersensitivity process but high levels of IgG
suggest that the affected animals have experienced
a staphylococcal infection. Bacterial toxins can
have an allergic role and can act as superantigens
triggering non-specific inflammatory reactions.
An important phenomenon to be considered
in BOG is quorum sensing: when a certain
density level of staphylococci is exceeded, they
express particular characteristics and switch
their metabolism from cell proliferation to toxin
production.
It is likely that a number of cases are secondary
to an underlying allergic skin disease and perhaps
also to glucocorticoid therapy, which could
be a perpetuating cause. In fact, it has been
demonstrated that bacterial adhesion is higher
in atopic dogs than in normal dogs (Simou,
Thoday et al, 2005). In addition, atopics are
lacking antimicrobial peptides (cathelicidins,
beta-defensins) and this contributes to microbial
colonization. There is evidence from an
experimental model of canine cutaneous type
I hypersensitivity that injection of a mast cell
degranulator or histamine intradermally renders
the overlying epidermis more permeable to
bacterial antigens (Mason and Lloyd, 1990). Last
but not least microbial colonization triggers an
auto-sensitization by molecular mimicry, which
may be a component of the pathogenesis of atopic
dermatitis in humans.
Epidemiology
No data is available but it is likely that breed
predispositions to atopic dermatitis will more or
less apply to BOG. The affected dogs are adult (3
to 10 years) and have suffered chronic dermatitis
for years.
Clinical signs
The chief complaints are pruritus and an
offensive odour. The lesions include erythema,
lichenification and hyperpigmentation,
seborrhoea oleosa, excoriations and self-induced
alopecia. They may be localized (cranial aspect
of the neck, axillae, ventrum) or generalized.
Associated otitis externa is common. Usually,
there is no lesion of pyoderma associated with
BOG (no papules, pustules, epidermal collarettes
or crusts).
Diagnosis
Diagnosis of BOG is based on history,
physical examination, cytology, bacteriology,
dermatopathology and response to therapy.
Cytology is the most useful technique to
demonstrate BOG. The tape strip technique is
the most appropriate. A rapid staining is done
Back to contents
D
and microscopic examination shows numerous
colonies of cocci. These can also be found in sites
without lesions, indicating that the BOG is more
widespread than the lesions might suggest, being
in fact a more or less generalized condition.
Bacteriological cultures can be done using a swab
that is rolled onto the skin, but this is usually done
only in severe cases, when cytology shows rods
(rare) and/or in case of poor response to therapy.
Dermatopathology shows a non-specific mild to
moderate superficial, perivascular, sometimes
interstitial, irregular hyperplastic and spongiotic
dermatitis, in both affected and non-affected areas.
Cocci may be observed in the stratum corneum
but their absence should not rule out the disease
(perhaps because of a non-linear distribution
of the organisms and/or by the removal of the
stratum corneum during the processing). SLAM
and pigmentary incontinence can be seen. No
lesions of pyoderma are observed. In fact,
dermatopathology is less useful than cytology to
establish the diagnosis of BOG.
Response to therapy is the ultimate diagnostic
criterion.
Differential diagnosis includes all dermatitis with
pruritus and seborrhoea, including ectoparasitic
and allergic skin diseases, as well as Malassezia
dermatitis. In fact BOG and MOG can be
clinically and cytologically associated, and
both can be secondary to allergic skin diseases,
particularly atopic dermatitis.
Treatment
Systemic therapy is indicated as for pyoderma.
Appropriate antibiotics should be selected based
on appropriate kinetics and good cutaneous
penetration, activity against staphylococci,
bactericidal activity rather than bacteriostatic
activity particularly in severe cases, easy
administration (oral, q12h or q24h), absence
of secondary effects, and reasonable cost. The
choice is most often empirical: cephalexin,
2006 World Congress WSAVA/FECAVA/CSAVA
clavamox, trimethroprim-sulfa, fluoroquinolones,
or clindamycin. The use of cephalexin at a dose
of 30 mg kg-1 divided bid during 28 days,
without associated topical therapy, was effective
in a group of 8 dogs, significantly decreasing
both the cutaneous and mucosal staphylococci
populations and also the cutaneous signs. An
interesting finding was that the staphylococci
populations were not completely eliminated, but
rather reduced, closer to that of the normal flora
of healthy dogs (Pin, Carlotti et al, 2006).
Topical therapy is beneficial in canine BOG.
Clipping may be useful, at least in the most
severely affected areas. The main useful
topical products are chlorhexidine (lotion and/
or shampoo), povidone-iodine (lotion and/or
213
D
shampoo), benzoyl peroxide (shampoo and
eventually gel), and ethyl lactate (shampoo).
They should be used frequently, e.g. once a day,
at the beginning of therapy. Later, frequency of
application may decrease. It is justified to treat
BOG with compounds that decrease microbial
adherence and increase the production of
antimicrobial peptides, along with specific
antimicrobial therapy.
Topical or systemic glucocorticoids should never
be used in BOG, even in case of severe pruritus,
because they can perpetuate the disease and cause
severe relapses (« rebound effect »).
The patients should be treated for one month
at least and an appropriate follow-up is very
important. This allows performing both a clinical
and a cytological evaluation of the response
to therapy. If a certain level of pruritus is still
present an underlying pruritic dermatosis should
be suspected (parasitic or allergic in origin)
2006 World Congress WSAVA/FECAVA/CSAVA
214
Back to contents
whereas if the animal remains seborrhoeic without
pruritus, an underlying cause of seborrhoea
should be envisaged, such as an endocrine
disorder. Therapy of an underlying skin disease is
obviously mandatory and prevents relapses.
CONCLUSION
MOG (Malassezia dermatitis) and perhaps BOG
are relatively common skin diseases in dogs
and can mimic and be secondary to a number of
other dermatoses. They may be associated with
one another. Cytological examination and an
appropriate systemic treatment should be used to
confirm the diagnosis. In all cases, an underlying
cause should be considered. However, there is no
doubt idiopathic (« primary ») MOG and BOG
exists.
REFERENCES
Can be provided upon request.

D - Dermatology
UPDATE ON THERAPY OF CANINE PYODERMA
Professor David Lloyd
Department of Clinical Veterinary
Science
Royal Veterinary College
Hawkshead Campus
North Mymms
Hertfordshire AL9 7TA
UK
david-lloyd@ntlworld.com
Introduction
Canine pyoderma is a complex of diseases
involving bacterial infection at different levels
of the skin (Table 1) and requiring different
approaches to therapy. These diseases are nearly
always secondary and so it is important to
identify underlying factors. Commonly these are
allergies but endocrinopathy, immunodeficiency,
ectoparasitic infestation, follicular dysplasia
and breed predisposition may be involved.
Diagnosis of underlying conditions may not be
easy. Treatment during the diagnostic phase
should be designed to advance diagnosis and
avoid camouflaging diagnostic clinical signs.
Antibiotic therapy is a good diagnostic strategy
as it eliminates pyoderma and helps expose
underlying conditions.
This presentation assumes that a diagnosis has
been made and deals with current approaches to
the treatment of the different forms of infection.
Treatment of underlying causes is not covered.
Table 1. Classification of Canine Pyoderma
Surface pyoderma
• Acute moist dermatitis
• Skin fold pyoderma
• Microbial overgrowth*
Superficial pyoderma
• Impetigo (“puppy pyoderma”)
• Mucocutaneous pyoderma
• Superficial spreading pyoderma
• Superficial folliculitis
Deep pyoderma
• Muzzle folliculitis & furunculosis
• Localised deep pyodermas (nasal, pedal
& pressure point pyodermas, pyotraumatic
folliculitis & furunculosis)
• Generalised deep pyoderma
• Bacterial granulomas
*Not strictly pyoderma. Commonly both
pathogenic staphylococci and Malassezia are
present.
Back to contents
D
Surface Pyoderma
Acute Moist Dermatitis. Prevention of further
trauma is essential and will sometimes allow
healing without further therapy. Ensure that
there is no underlying folliculitis or furunculosis.
Because the epidermal damage is a consequence
of trauma, healing is rapid. However, lesions are
often painful and topical therapy, requiring direct
contact with skin, can be hazardous. Topical
antibiotic and steroid gels or creams are effective
but spraying with a soothing, antimicrobial,
astringent preparation has been shown to be
as effective1 and is likely to be less hazardous.
Lesions should be substantially healed in 7-10
days. Where there is marked pruritus, systemic
glucocorticoids may be required.
Skin Fold Pyoderma. Ideally, folds are removed
surgically. If surgery is not feasible, measures
to render the microenvironment within the fold
inhospitable to bacteria and yeasts are required.
Cleansing every 2-3 days with an antimicrobial
shampoo is effective. Benzoyl peroxide,
chlorhexidine, and chlorhexidine and miconazole
are effective. Chlorhexidine is quite unstable
and so it is advisable to select well-formulated
preparations with published efficacy against both
bacteria and Malassezia.2 (Lloyd 1999) Benzoyl
2006 World Congress WSAVA/FECAVA/CSAVA
peroxide must used with care as animals may
develop sensitivity and it can be irritant. Ethyl
lactate may be effective in milder cases and has
low irritancy. Intervals between shampooing may
be extended by the use of antimicrobial creams
and gels. Spraying with a soothing, antimicrobial,
astringent preparation may also be effective.
Superficial Pyoderma
Impetigo normally responds to antimicrobial
shampoos. Use on two or three occasions over
a period of 7-10 days should be effective in
uncomplicated cases. Spontaneous resolution
commonly occurs.
Mucocutaneous Pyoderma may respond
to treatment with antibacterial shampoos,
215
D
as described above, followed by the use of
antibacterial ointment, such as mupirocin. Daily
treatment for two weeks and then once or twice a
week may be effective. Following resolution, the
disease may remain in abeyance but commonly
repeated treatment is required. With deeper or
more extensive infection, or if topical treatment
is difficult, systemic antibiotic is required.
Treatment for 4 weeks or more may be necessary.
If not successful, further diagnostic procedures,
including biopsy, are required.
Superficial Folliculitis and Superficial Spreading
Pyoderma. Normally systemic antibiotic therapy
is used. Bacteriostatic antibiotics are effective
but bactericides are preferable. Treatment
for at least one week beyond clinical cure is
advisable. Recovery may be promoted by use of
antibacterial shampoos containing chlorhexidine
or benzoyl peroxide, or in milder cases ethyl
lactate, which aid removal of crusts and reduce
surface bacterial populations.2,3 Mild superficial
pyoderma can be treated with such shampoos
without systemic antibiotic but this is labour-
intensive; shampooing every 2-3 days is required.
Once lesion resolution occurs, shampooing can
be reduced to once or twice a week; in winter
weekly to monthly shampooing may be sufficient
to maintain remission.
Where there is recurrent infection and underlying
causes cannot be identified or controlled, long-
term treatment options need to be considered.
Regular shampooing with antibacterial shampoo
may give control. Otherwise, the main options are
pulse therapy with antibiotics and staphylococcal
vaccination. Vaccination is a better choice. Well-
prepared autogenous vaccines (bacterins) are
effective in about 50% of cases; responding dogs
do not need other therapy.4 An American bacterial
lysate prepared from S. aureus, has also been
shown to reduce the frequency of folliculitis and
decrease the need for repeated antibiotic therapy.5
2006 World Congress WSAVA/FECAVA/CSAVA
Pulse or continual low dose therapy6 should be
a last resort as it may promote development of
antibiotic resistance, although recent evidence
indicates that this risk may be low.
In view of the fact that the causative pathogen
may be harboured on the mucosae, particularly
of the upper respiratory tract and anus, some
clinicians have used topical antibiotic to treat the
nasal and or anal mucosae. Experimental studies
have shown that S. intermedius populations can
be eliminated by this method using fusidic acid.7
Anecdotally, this has helped in some cases of
recurrent pyoderma.
216
Back to contents
Deep Pyoderma
When deep infection occurs, there are local
factors causing skin damage and more serious
deficiencies in the immune system of the affected
animal. If these can be resolved, recovery should
be complete. Determined efforts to identify the
underlying factors should be made. Demodecosis
is a common cause.
With discharging lesions, antimicrobial washes
and soaks are useful to remove pus and debris,
and may accelerate recovery. Clipping is helpful,
enables the extent of lesions to be demonstrated
and can be useful in persuading clients to comply
with treatment. Prolonged systemic antibiotic
treatment with bactericidal antibiotic is necessary
and must continue for at least two weeks beyond
clinical cure. Where lesions are in areas with poor
blood supply or large granulomatous lesions,
fluoroquinolones, which penetrate well, are
particularly useful. On rare occasions it may be
necessary to use unusual antibiotics to achieve
penetration, such as rifampicin.
In some cases, unusual organisms such as
actinomycetes or mycobacteria are involved,
and there may be concurrent infection with
fungi. Careful diagnostic procedures, including
discussion with the laboratory concerned, may
be required as routine methods may not be
effective.
Choice of Antibiotics and Dosage
Although antibiotics can be selected empirically,
where recurrent infection occurs or there is a
lack of response, microbiological culture and
sensitivity should be carried out.8,9 Ensure
that you use a reliable laboratory and question
unusual results e.g. very broad resistance in an
organism identified as S. intermedius; this could
turn out to be a methicillin-resistant S. aureus or
S. schleiferi.10,11 Remember that several different
strains of pathogenic staphylococci may be present
on a single animal. Thus a single sensitivity test
may not give the full picture. Failure of a particular
antibiotic may mean you have only eliminated
part of the causative bacterial population. If in
doubt always retest. Ensure your sample contains
material from deep within the lesions; biopsy
may be necessary for this.
Generally, manufacturer’s recommended dose
rates will be effective. Occasionally you will
need to use higher doses to achieve effective
levels of antibiotic within lesions or to overcome
low level resistance. The range of antibiotics
commonly used in veterinary dermatology and
their properties and use are reviewed in a special
issue of Veterinary Dermatology published
in 1999, which is still relevant and provides
excellent summaries.12

References
1. ASCHER F, MADIN F, GUAGUERE E et al.
Intérêt d’une solution topique non antibiocorticoide
dans le traitement de la dermatite pyotraumatique
du chien. Pratique Médicale et Chirurgicale de
L’Animal de Compagnie. 1995; 30:345-354.
2. LLOYD DH, LAMPORT AI. Activity
of chlorhexidine shampoos in vitro against
Staphylococcus intermedius, Pseudomonas
aeruginosa and Malassezia pachydermatis.
Veterinary Record 1999; 144: 536-537.
3. DE JAHAM C. Effects of an ethyl lactate
shampoo in conjunction with a systemic
antibiotic in the treatment of canine superficial
bacterial pyoderma in an open-label, non placebo-
controlled study. Veterinary Therapeutics 2003;
4: 94-100.
4. CURTIS CF, LAMPORT AI, LLOYD DH.
Blinded, controlled study to investigate the
efficacy of a staphylococcal autogenous bacterin
for the control of canine idiopathic recurrent
pyoderma. Proceedings of the 16th Annual
Congress of the ESVD-ECVD, Helsinki, Finland,
August 1999. p. 148.
5. DEBOER DJ, MORIELLO KA, THOMAS CB,
et al. Evaluation of a commercial staphylococcal
bacterin for management of idiopathic recurrent
pyoderma in dogs. American Journal of Veterinary
Research 1990; 51: 636-639.
6. CARLOTTI DN, JASMIN P, L. GARDEY L,
SANQUER A. (2004): Evaluation of cephalexin
intermittent therapy (weekend therapy) in the
Back to contents
D
control of recurrent idiopathic pyoderma in
dogs: a randomized, double-blinded, placebo-
controlled study. Veterinary Dermatology 2004;
15 ( s1): 7-8.
7. SAIJONMAA-KOULUMIES L., PARSONS
E., LLOYD, DH. Elimination of Staphylococcus
intermedius in healthy dogs by topical treatment
with fusidic acid. Journal of Small Animal
Practice 1998; 39: 341-7.
8. HOLM BR, PETERSSON U, MORNER A, et
al. Antimicrobial resistance in staphylococci from
canine pyoderma: a prospective study of first-
time and recurrent cases in Sweden. Veterinary
Record 2002; 151: 600-5.
9. KRUSE H, HOFSHAGEN M, THORESEN
SI, et al. The antimicrobial susceptibility of
Staphylococcus species isolated from canine
dermatitis. Veterinary Research Communication
1996; 20: 205-14.
10. LOEFFLER A, BOAG AK, SUNG J,
et al. Prevalence of methicillin-resistant
Staphylococcus aureus among staff and pets in a
small animal referral hospital in the UK. Journal
of Antimicrobial Chemotherapy 2005; 56: 692-7.
11. FRANK, LA, KANIA, SA, HNILICA, KA,
et al. Isolation of Staphylococcus schleiferi from
dogs with pyoderma. Journal of the American
Veterinary Medical Association 2003; 222 (4);
451-4.
12. Special Issue on Antibiotics in Veterinary
Dermatology. Veterinary Dermatology 1999; 10:
161-262.
2006 World Congress WSAVA/FECAVA/CSAVA
217
D
D - Dermatology
NEW APPROACHES TO COMMON CANINE ECTOPARASITES
Peter J. Ihrke, VMD, Diplomate
ACVD
Professor of Dermatology, Chief
- Dermatology Service, VMTH
Department of Medicine &
Epidemiology
School of Veterinary Medicine
University of Kalifornia
One Shields Avenue
Davis, California 95616-8737,
U.S.A.
Fleas and Flea Allergy Dermatitis
A. Introduction
1. Flea allergy dermatitis is not only the most
common skin disease seen in small animal
practice in most countries in the world; it is
the most common disease of any organ system
seen in small animal practice worldwide. Fleas
parasitize animals in virtually every area on
earth with the exception of locations above 1500
meters elevation and regions such as deserts with
very low humidity.
2. The cat flea, Ctenocephalides felis is the primary
flea species associated with flea infestation and
flea allergy dermatitis in both the dog and the cat
in most studies. The average car flea life cycle
involving development through egg, larvae, pupa
and cocoon, and the adult and takes between 3 and
4 weeks. However the life cycle can be as short
as 12 days or as long as 140 days. Adult cat fleas
are obligate permanent ectoparasites, attracted to
the host by warmth, movement, changes in light
intensity, and respiratory carbon dioxide.
3. New advances in the understanding of the
biology of the flea and new methodologies
2006 World Congress WSAVA/FECAVA/CSAVA
available to combat multiple life stages of the flea
both on and off the animal have revolutionized
our ability to deal with this disease. It is crucial
to remember that the adult cat flea is an obligate
parasite. However, since the bulk of the flea
lifecycle (eggs, larvae, and pupa) occurs in the
environment, environmental issues must always
be addressed. Historically, flea control has required
treating both the animal and the environment with
a combination of insecticides and, more recently,
insect growth regulators. Today, either topical
or systemic anti-flea therapy may be the only
management required. The new agents that have
created this paradigm shift include imidacloprid,
fipronil, selamectin, nitenpyram, lufenuron,
methoprene, and pyriproxifen.
4. Skin disease associated with fleas is a
218
Back to contents
complex group of hypersensitivity phenomenon
involving at least four immunologic processes;
immediate hypersensitivity, late-onset immediate
hypersensitivity, delayed hypersensitivity, and
cutaneous basophil hypersensitivity. Blood
consumption by female averages 13.6 microliters/
day (75 female cat fleas can consume 1 ml/day).
The majority of blood is passed out as partially
digested feces to feed flea larvae.
5. The management of flea allergy dermatitis
requires the prevention of flea bites plus the
disruption of the life cycle of the flea. New
products that have become available over the past
15 years have exponentially increased our ability
to initiate flea control and manage flea allergy
dermatitis.
B. Modern Flea Control
1. New, considerably less toxic prescription
products that also are much easier to use are
available that kill adult fleas and disrupt the flea
life-cycle. Most insecticides can effectively kill
fleas; preventing reinfestation is the problem.
Insuring long-term pet owner compliance
is required for on-going flea control. The
comparatively recent development of both
insecticides and insect growth regulators with
novel and convenient dosage forms (such as
spot-ons, collars, and oral products) coupled
with prolonged residual activity has dramatically
improved pet owner compliance and hence
prevented reinfestations. Although insecticidal
resistance most often is suspected when flea
control measures have failed, lack of control
more often results from lack of understanding of
flea biology, poor application technique, and too
infrequent reapplication of the products.
2. The goals of flea control should be elimination
of existing fleas on affected animals, continued
elimination of fleas acquired from infested
premises, and the prevention of reinfestation. In
order to accomplish these goals, an integrated

flea control plan must be instituted. Effective
residual adulticides must be used to kill fleas
plus provide residual killing activity and insect
growth regulators must be use to used to disrupt
flea reproduction. In addition, mechanical control
procedures such as cleaning pet’s blankets, beds,
pet carriers, and throw rugs and vacuuming or
removing furniture that can house pre-adult fleas
must be instituted. Preventions of pests that can
carry fleas (rats, opossums, squirrels, raccoons,
skunks, feral cats) from entering crawl spaces,
foundation vents, porches and garages also is
important.
C. Modern Flea Control Products
1. New spot-on prescription products are
excellent products with superior efficacy, safety,
and residual activity. These products need to be
applied directly to the skin, not to the haircoat.
Our very strong clinical impression at UC
Davis is that dogs and cats with severe flea
hypersensitivity experience much better efficacy
with these products applied every 3 weeks instead
of monthly. Our clinical impression remains that
either bathing or swimming degrades the efficacy
of all of these products. Over-the-counter (OTC)
competing products commonly are advertised
as ‘just as good as what you can get from your
veterinarian’ plus ‘less expensive’. In general,
these products contain concentrated permethrin
or other synthetic pyrethroids. All indications are
that these OTC products do not have either the
efficacy, residual activity, or the safety profile of
the spot-on prescription products
2. Imidacloprid (Advantage®, Bayer)
a. Advantages – larvicidal on the animal and
kills/debilitates adult fleas on contact, ease
of application
b. Disadvantages – does not have repellent
action, diminished efficacy after bathing or
swimming, does not have activity against
ticks, occasional application site reactions
c. Bottom-line – Good narrow-spectrum
product for fleas
(Canada – Imidacloprid & Moxidectin -
Advantage Multi®, Bayer)
(Europe – Imidacloprid & Moxidectin -
Advocate®, Bayer)
3. Fipronil & S-Methoprene (Frontline® Plus,
Merial), Fipronil (Frontline® Spray, Merial)
a. Advantages – kills adult fleas, disrupts
flea life cycle, ease of application, kills ticks,
spray – rapid dispersion and coverage,
b. Disadvantages – does not have repellent
action, some diminished efficacy after
bathing or swimming, occasional application
site reactions, spray is labor-intensive
Back to contents
D
c. Bottom-line – Good broader spectrum
product
4. Imidacloprid & 44% permethrin (Advantix®,
Bayer)
a. Advantages – larvicidal on the animal
and kills/debilitates adult fleas on contact,
interrupts flea life cycle, repellant ‘flushing’
activity of permethrin, ease of application,
also kills ticks and mosquitoes
b. Disadvantages – dog only product, do not
use on cats, diminished efficacy after bathing
or swimming, occasional application site
reactions?
c. Bottom-line – Good broader spectrum
product, dog only product
5. Selamectin (Revolution® [USA]; Stronghold®
[Europe], Pfizer)
a. Advantages – broad spectrum against
many internal and external parasites, kills
adult fleas plus larvae and eggs, kills ticks,
kills some ectoparasitic mites (Sarcoptes,
Notoedres, Cheyletiella, Otodectes), ease of
application,
b. Disadvantages – does not have repellent
action, diminished efficacy after bathing or
swimming, slower efficacy?, application site
reactions?
c. Bottom-line – Good broader spectrum
product
6. Nitenpyram (Capstar™, Novartis)
a. Advantages – very rapid response with
visual results, kills 100% of adult fleas
within 6 hours, short-acting, ease of oral
administration, give every 24-72 hours
(half-life in dogs is 2.8 hours, half-life in
cats is 7.7 hours) very safe product, adverse
reactions not seen yet
b. Disadvantages – does not have repellent
action, does not disrupt flea life cycle, short-
acting, does not have activity against ticks
c. Bottom-line – Good narrow spectrum
product, use with spot-ons initially for
2006 World Congress WSAVA/FECAVA/CSAVA
rapid response, not for use as sole therapy,
use in dogs requiring frequent shampooing,
compliance problems?
7. Lufenuron (Program®, Novartis; Sentinel®
[lufeneron + milbemycin oxime])
a. Advantages – oral product, very safe
product without known mammalian toxicity,
adverse reactions not seen yet,
b. Disadvantages – does not kill adult fleas
or pupa, time lag – 60-90 days required to
disrupt flea life cycle, does not have repellent
action, adult flea must feed on animal to
ingest, does not have activity against ticks,
must give with food
c. Bottom-line – use with spot-ons for long-
term control, not for use as sole therapy
219
D
unless very closed environment, treat all
animals, use in dogs requiring frequent
shampooing, compliance problems?
8. Pyriproxifen (Nylar®) containing collars –
Pyriproxifen & amitraz collars (Preventic PLUS®,
Virbac), dogs only!, no longer available in the
USA
Pyriproxifen & 2% permethrin (KnockOut®
Collar for Dogs, Virbac), no longer available in
the USA
Pyriproxifen (KnockOut® Cat & Kitten Collar for
Dogs, Virbac), no longer available in the USA
a. Advantages – ovicidal and larvicidal for
fleas, UV stable juvenile hormone analogue,
translocates to bedding, IGR efficacy
for 3 months, Preventic Plus® adds tick
protection
b. Disadvantages – long-term residual status
may affect beneficial insects
c. Bottom-line – very useful adjunct to
spot-ons or spray products, useful in dogs
requiring frequent shampooing
9. Synthetic pyrethroid containing pump sprays
(variety of manufacturers
a. Advantages – daily use in dogs requiring
frequent shampooing
b. Disadvantages – frequency of application,
compliance, poor residual activity
c. Bottom-line – rarely used as sole therapy
unless very closed environment, use in dogs
requiring frequent shampooing, compliance
problems?
D. Personal Recommendations
1. Flea control must be regionalized and often
personalized based on severity of possible
infestation in your locale, number of dogs and
cats in the environment, indoor/outdoor/run
free status, infested pests and strays in the
2006 World Congress WSAVA/FECAVA/CSAVA
environment, finances of the owner, and severity
of disease vs. magnitude of the infestation
2. ‘The average dog or cat’ will respond to fipronil
and S-methoprene, imidacloprid with or without
lufenuron, or selamectin as sole therapy.
3. Severely flea allergic dogs will require
fipronil and S-methoprene or imidacloprid plus
permethrin, plus either nitenpyram, with or
without lufenuron.
4. (Severely flea allergic cats will require spot-
on preparations plus nitenpyram with or without
lufenuron. Pump-sprays also may be beneficial.)
5. Animals with tick exposure benefit from fipronil
and S-methoprene, imidacloprid plus permethrin
(dogs only!), and pyriproxifen & amitraz collars
(dogs only!)
220
Back to contents
Ticks
A. Introduction
1. Tick infestation and tick bite hypersensitivity
are highly variable regional skin diseases. In
some parts of North America, ticks are a major
problem, while they are comparatively rare in
many other areas. Ticks cause morbidity either
by direct irritation from their bites, initiate
hypersensitivity, or act as vectors for multiple
bacterial, viral, rickettsial, or protozoal diseases.
B. Modern Tick Control Products
1. Fipronil & S-Methoprene (Frontline® Plus,
Merial), Fipronil (Frontline® Spray, Merial)
a. Advantages – kills ticks, ease of
application, residual activity, also kills fleas
b. Disadvantages – does not have repellent
action, some diminished efficacy after
bathing or swimming, occasional application
site reactions
c. Bottom-line – Good product for tick
control
2. Imidacloprid & 44% permethrin (Advantix®,
Bayer)
a. Advantages – kills ticks, ease of
application, also kills fleas and mosquitoes
b. Disadvantages – dog only product, do not
use on cats, diminished efficacy after bathing
or swimming, occasional application site
reactions?
c. Bottom-line – Good broad spectrum
product, dog only product!
3. Selamectin (Revolution® [USA]; Stronghold®
[Europe], Pfizer)
a. Advantages – kills ticks, also broad
spectrum against many internal and
external parasites, kills adult fleas, kills
some ectoparasitic mites (Sarcoptes,
Notoedres, Cheyletiella, Otodectes), ease of
application,
b. Disadvantages – diminished efficacy
after bathing or swimming, application site
reactions?
c. Bottom-line – Good product for tick
control
4. Amitraz containing collars – (Preventic®,
Virbac), dog only product
a. Advantages – detaches and kills ticks,
residual activity for 3 months
b. Disadvantages – dog only product
c. Bottom-line – good product for tick
control
C. Personal Recommendations
1. Tick control must be regionalized and often
personalized based on severity of possible
infestation in your locale, number of dogs,
indoor/outdoor/run free status, infested pests

and strays in the environment, finances of the
owner, and severity of disease vs. magnitude of
the infestation
2. ‘The average dog’ will respond to fipronil and
S-methoprene, imidacloprid and permethrin,
selamectin, or an amitraz collar as sole therapy.
3. Severely affected dogs benefit from the
combination of a spot-on product (fipronil and
S-methoprene, imidacloprid and permethrin, or
selamectin) plus an amitraz collar.
Acariasis – Sarcoptic Acariasis, Notoedric
Acariasis, Cheyletiellosis
A. Introduction
1. Canine sarcoptic acariasis “Scabies” is an
intensely pruritic, highly contagious, transmissible
canine dermatoses caused by the epidermal mite
Sarcoptes scabei var. canis. Transmission is
usually by direct contact with an infested dog.
There is evidence that clinical disease is a multi-
factorial hypersensitivity reaction. Sarcoptic
acariasis may be increasing in prevalence with
the advent and increased popularity of newer
insect-specific flea control products. Formerly,
we may have stopped scabies infestation when
we were simply attempting to kill fleas.
2. Notoedric acariasis or feline scabies is a
rare contagious mite infestation caused by the
sarcoptid mite Notoedres cati characterized by
crusting with extreme pruritus. The disease is
rare in most parts of the United States, but may
be found in localized endemic areas. Similar
to sarcoptic acariasis, notoedric acariasis may
be increasing in prevalence with the advent of
some newer insect-specific flea control products.
Notoedres is highly contagious in cats and
occasionally, may affect dogs or humans.
3. Cheyletiellosis or Cheyletiella dermatitis is
a contagious mite infestation seen in domestic
animals, wildlife and humans characterized
primarily by scaling and crusting caused by
different, but very similar, species of Cheyletiella
mites. It may be seen more commonly in areas
of the world where concerted flea therapy is not
necessary or not consistent. Cheyletiella dermatitis
may be increasing in prevalence on a wider basis
with the advent of some newer insect-specific flea
control products. Infestations have been reported
in dogs, cats, rabbits, squirrels, poultry, foxes and
humans. This disease may not be as uncommon
as previously thought since many veterinarians
have a very low index of suspicion and do not
look for it. It is reported that the mites may live
in an animal’s environment for extended periods
of time.
B. Modern Acariasis Control Products
1. It is beneficial for the management of all 3
Back to contents
D
diseases to isolate the affected animal(s) and clean
the premises, disposing of the animal’s bedding
or thoroughly cleansing it. For the management
of canine sarcoptic acariasis, all dogs on the
premises and any other dogs with significant
contact with the affected dog should be treated.
For the management of feline notoedric acariasis,
all cats on the premises and any other cats with
significant contact with the affected cat should
be treated. The treatment of in-contact cats in
households with canine sarcoptic acariasis and the
treatment of in-contact dogs in households with
feline notoedric acariasis are more controversial.
If skin disease is present or if initial species-
restricted therapy is ineffectual, treatment of
the other species should be considered. All dogs
and cats on the premises and any other dogs or
cats with significant contact with the affected
animal should be treated when Cheyletiellosis is
diagnosed.
2. The traditional approach of using weekly
keratolytic shampoos followed by parasiticidal
dips has been superseded by newer less labor-
intensive methods of therapy. Lime sulfur
(LymDip®, DVM Pharmaceuticals) is still used in
circumstances where safety is an issue especially
in very young animals.
3. Systemic corticosteroids may be used
adjunctively to control pruritus during the first
week of therapy. Paradoxically, pruritus may
actually increase initially because of increased
antigenic load.
4. Selamectin (Revolution® [USA]; Stronghold®
[Europe], Pfizer)
a. Selamectin is used for mite infestations
most commonly at label dosages every 2
weeks for a minimum of 3 applications.
b. Advantages – kills all 3 ectoparasitic
mites, approved for use on dogs and cats,
label claims, ease of application, also kills
adult fleas and ticks, also broad spectrum
against many internal and external parasites
2006 World Congress WSAVA/FECAVA/CSAVA
c. Disadvantages – none
d. Bottom-line – Good product to treat small
animal acariasis
5. Ivermectin (Ivomec®, Merial; DVMectin®,
DVM Pharmaceuticals)
a. Ivermectin 230 micrograms/kg or 1/10
cc/10 lbs body weight per os, for a minimum
of four weekly dosages. Certain dog breeds
are potentially more sensitive to this drug
owing to the MDR1 mutation which
diminishes the functionality of the blood-
brain barrier. At the dosages used for scabies,
this problem is of most concern for Collie
Dogs and Shetland Sheep Dogs. Serious
adverse neurologic reactions to ivermectin
have been seen in Collie Dogs, Shetland
221
D
Sheep Dogs, Border Collies, Australian
Shepherds, and, less commonly, a variety of
other breeds.
b. Advantages – inexpensive, efficacious
b. Disadvantages – toxicity in dogs with
MDR1 mutation, Ivomec® is a product
licensed for use in cows
c. Bottom-line – efficacious product to treat
small animal acariasis
5. Milbemycin oxime (Interceptor®, Novartis
Animal Health)
a. Another avermectin, is also efficacious
to treat acariasis. Recommended dosages
vary from 1X to 2X the monthly heartworm
dose given once weekly for four weeks.
Milbemycin may be a ‘safer’ avermectin
that ivermectin, but caution should still be
exercised in at-risk breeds.
b. Advantages – efficacious, licensed for use
in dogs, more safe than ivermectin?
b. Disadvantages – toxicity in dogs with
MDR1 mutation
c. Bottom-line – efficacious product to treat
small animal acariasis
6. Amitraz (Mitaban®, Pharmacia & UpJohn)
a. Amitraz is an MAO inhibitor and should
not be used on dogs or applied by anyone
taking other MAO inhibiting drugs. Amitraz
should not be used on cats. Amitraz rinsing
should be performed either outdoors or in an
open garage. Rubber gloves should be worn
by the applier.
b. Advantages – efficacious, licensed for use
in dogs
c. Disadvantages – greater potential for
toxicity
d. Bottom-line – other products with equal
or greater efficacy have less potential for
toxicity.
2006 World Congress WSAVA/FECAVA/CSAVA
222
Back to contents
C. Personal Recommendations
1. It is important to maintain an index of
suspicion for all 3 mite infestations as a cause
of pruritus in dogs and cats. Cheyletiellosis may
present as exfoliation with minimal pruritus. All
3 contagious mite infestations may be increasing
in frequency of occurrence.
2. Most dogs and cats with mite infestations
will respond to selamectin, ivermectin, or
milbemycin.
3. Based on approval for use on dogs and cats for
mite infestations, selamectin is the drug of choice
for all 3 mite infestations. If financial constraints
preclude usage, ivermectin can be used as an
alternative.
Recommended Reading
Carlotti DN, Jacobs DE. Therapy, control and
prevention of flea allergy dermatitis in dogs and
cats. Vet Dermatol. 2000; 83-98.
Dryden MW. Flea biology and epidemiology:
clinically relevant issues. 16th Annual George H.
Muller Veterinary Dermatology Seminar 2000;
4-10.
Dryden MW. Flea control for the twenty-first
century. 16th Annual George H. Muller Veterinary
Dermatology Seminar 2000; 4-10.
Rust MK. Advances in the control of
Ctenocephalides felis (cat flea) on cats and dogs.
Trends Parasitol. 2005; 21: 232-236.
Rust MK, Dryden M. The biology, ecology, and
management of the cat flea. Ann Rev Entomol.
1997; 42: 451-473.
Scott DW, Miller WH & Griffin CE. (2001)
Muller & Kirk’s Small Animal Dermatology, 6th
edn. pp. 476-484, WB Saunders Co, Philadelphia:
WB Saunders Co, 2001; 476-484.

D - Dermatology
OPTIMISING TOPICAL THERAPY IN THE DOG
Didier-Noël CARLOTTI, Dip
ECVD
Aquivet clinique vétérinaire
F-33320 Bordeaux-Eysines
France (EU)
dncvetderm@aol.com
Topical (locally acting) therapy is important
in the management of many dermatological
conditions because the skin is readily accessible
to medications. Several formulations are
available for the prescribing veterinary surgeon
and may include many active ingredients. The
active ingredients penetrate the skin through
the intercellular spaces (lipophilic molecules),
through the epidermal cells (ion compounds) and
above all through the hair follicles in animals,
particularly for ionized molecules. Canine skin
is often more sensitive than is human skin due
to anatomical and physiological differences,
including differences in the thickness of the
stratum corneum, skin pH and hair follicle density
which can facilitate cutaneous penetration of
active ingredients. The use of shampoos will
be emphasized in this paper; antiparasitic and
auricular topical products are beyond its scope.
OINTMENTS, CREAMS AND GELS
Creams and ointments are a mixture (emulsion)
of oil and water. They are usually used on dry
skin, and not on oozing (exudative) areas. Creams
(made of oil dispersed in water) are more aqueous
than ointments (made of water dispersed in oil).
Gels are composed of a thixotropic (gel at rest,
but fluid when agitated) base (usually containing
propylene glycol), pass through the haircoat to
the skin and are less messy and occlusive than
creams and ointments. These bases are used as
vehicles for many agents:
• Topical glucocorticoids are useful in veterinary
dermatology and perhaps have been neglected.
They have anti-inflammatory and antipruritic
properties as well as antiproliferative and
immunosuppressive effects. These formulations
are useful for localised lesions (e. g. cheilitis,
blepharitis, pododermatitis, nasal lesions,
excoriations and pyotraumatic dermatitis). Many
molecules are available in human dermatology,
classified from class I (the least potent) to
class IV (the most potent). Some potent human
Back to contents
D
formulations can be used in the dog (e.g. clobetasol
propionate); most of the veterinary formulations
contain less potent agents. Tachyphylaxis,
atrophy and microbial infections can occur in
cases of overuse.
• Immunomodulators: tacrolimus, a calcineurin
inhibitor has been shown to be effective in the
treatment of localized lesions of canine atopic
dermatitis; imiquimod, an inhibitor of gamma-
interferon synthesis, may be helpful in treating
some preneoplastic and neoplastic diseases
(papillomas, Bowen’s disease, actinic keratosis,
basal and squamous cell carcinomas).
• Antibiotics: formulations containing fucidic
acid and mupirocin are useful for treating
localized lesions of pyoderma.
• Antifungals: human products containing azole
derivatives, nystatin or amphotericin B can be
used on localized lesions of dermatophytosis,
Malassezia dermatitis or candidiasis.
• Combined formulations: some veterinary
products contain a weak glucocorticoid and an
antibiotic (e.g. neomycin and hydrocortisone)
or more active ingredients also including an
antifungal agent (e.g. neomycin, thiostrepton,
triamcinolone and nystatine). These are useful in
non infectious lesions, for their anti-inflammatory 2006 World Congress WSAVA/FECAVA/CSAVA
and preventive anti-microbial properties but
should not be used to treat pyoderma or fungal
diseases.
LOTIONS, RINSES AND SPRAYS
Lotions are liquids in which active agents are
dissolved or suspended. Rinses are concentrated
and must be diluted before use. Pump-sprays
containing lotions are commonly used in canine
dermatology (after or in between shampoos).
They contain different agents:
• Antibacterials: chlorhexidine can be used
in lotions, as an antibacterial agent. Piroctone
olamine is used in sprays for its antimicrobial
properties.
• Antifungals: a lotion containing enilconazole
223
D
is effective against both dermatophytosis and
Malassezia dermatitis.
• Glucocorticoids: small containers allow
the treating of localized lesions, as creams
and ointments do. Several glucocorticoids are
available, usually not the most potent. Large
containers (e.g. triamcinolone) can be very useful
to treat generalized conditions.
• Nonsteroidal antipruritic formulations,
e.g. containing pramoxine, colloidal oatmeal or
aloe vera can be very useful. A spray containing
Hamamelis extract and menthol as become
popular to treat localized lesions and has been
shown to kill Malassezia. A lotion has been
developed to complement a shampoo specifically
designed for canine atopic dermatitis (see below).
It contains, in a fluid emulsion excipient, mono
and oligosaccharides (free and in Spherulites®),
vitamin E and linoleic acid.
• Moisturisers: skin hydratation is less in dogs
with scaling than in normal dogs. Moisturisers
lubricate, rehydrate, soften the skin and restore
an artificial superficial skin film. Diluted in water,
they can be massaged into the skin or applied as
a lotion/rinse. Undiluted, they may be sprayed
on after a shampoo. They should not be rinsed
off. Lipid emollients borrowed from human
dermatology and used as an emulsion in tepid
water, improve coat condition, but have a greasing
effect. Non-lipid emollients have rehydrating
and softening properties. They reduce odour and
improve coat appearance without the greasing
effect. The high molecular weight of their active
ingredients and their hygroscopic nature make
them effective surface-protecting therapeutic
agents. Examples include lactic acid, glycerine,
propylene glycol, urea and chitosanide.
• Recently a micro-emulsion spray and a spot-on
formulation containing phytosphingosine have
been launched. Phytosphingosine is a proceramid
and a natural component of the epidermis,
2006 World Congress WSAVA/FECAVA/CSAVA
with restructuring, antiseborrhoeic and also
antimicrobial effects.
SHAMPOOS
Traditional shampoo formulations are composed
of surfactants (cleansing agents, foaming agents
and conditioners) as well as thickeners, softeners,
sequestering agents, preservatives, fragrance and
sometimes opacifiers and colouring additives.
Surfactants are amphiphilic molecules, i.e.
molecules with a dual affinity, both for water and
oil. Surfactants are composed of a hydrophilic
part (hydrophilic “head”) and a lipophilic part
(“lipophilic tail”). They are called surfactants
(surface active ingredients) due to their propensity
for absorption on various interfaces (oil/water,
air/water...), modifying the properties of the
224
Back to contents
interface (decreasing the interface tension and
stabilisation of the interface). In water, surfactants
form micelle structures allowing surfactant to
emulsify, render soluble and disperse oils, dirt
and debris. Surfactants can be classified into 4
groups, according to their ionic nature: anionic,
cationic, non-ionic, and amphoteric surfactants.
Pet shampoos are formulated combinations
of surfactants combining superior cleansing
properties, a perfect local tolerance (assessed in
vitro and in vivo), a physiological pH adapted to
the canine skin and easiness of rinsing. Shampoos
are ideal vehicles to treat the haired and sensitive
skin of dogs.
How to use veterinary shampoos
Ideally, a shampoo possessing both cleansing and
therapeutic properties should be applied twice at
each use. The mechanical effect (elimination of
scales and crusts) is beneficial in all cases. Water
rehydrates the stratum corneum although this
effect is temporary in the absence of moisturisers.
A shampoo can be used in a limited area (e.g.
chin, feet, dorsolumbar, ventral areas), or more
commonly all over the body surface. At the
second application, the shampoo must be left on
for 5 to 15 minutes, to allow the active ingredients
to be properly absorbed. The skin should then be
rinsed thoroughly. The shampoo may be applied
several times a week for 2 weeks. The frequency
is then reduced to give the longest interval over
which treatment is still effective, usually about 1
to 2 weeks.
Efficacy of shampoos
Clinical improvement is the main criterion in
evaluating the efficacy of a shampoo. The efficacy
of shampoos on skin hydration, the surface lipid
film and stratum corneum, which is of great
importance in keratoseborrhoeic disorders,
can be evaluated objectively using a variety of
techniques, including transepidermal water loss
(TEWL) measurement and many others, but
they have been deemed to be not reproducible
and thus useless. Prolonging the action of active
ingredients has been made possible: liposomes
prolong the moisturizing effect and Spherulites®
increase bioavailability of therapeutic agents and
promote immediate and residual moisturising
properties (reinforced by chitosanide). Also,
microemulsions enhance bio-availability of active
ingredients, which readily diffuse, and they also
have an effective cleansing effect.
Shampoo therapy in keratoseborrhoeic disorders
1 - Keratomodulating agents work in two different
ways:
• Restoration of normal keratinocyte multiplication
and keratinisation. Some of them probably exert a

cytostatic effect on basal cells, thereby reducing
their rate of division. Agents working in this way
are called keratoplastic (keratoregulating);
• Elimination of excess corneal layers, by
increasing desquamation (ballooning of
corneocytes rendering the stratum corneum
softer and a reduction of intercellular cohesion
that increases their shedding). Agents that work
in this way are called keratolytic.
Salicylic acid is a keratolytic agent. Its
efficacy varies with concentration. Coal
tar is a keratoplastic (cytostatic) agent. It is
also antiseptic and antipruritic and has many
different sources and varieties. Side-effects are
possible. Sulphur is mildly keratolytic. It is also
keratoplastic and antiseptic. Salicylic acid and
sulphur act synergistically in particular when both
substances are incorporated into the shampoo in
equal concentrations. Selenium disulphide is
keratolytic and keratoplastic but has detergent,
irritant and drying effects. Ammonium lactate
has keratoplastic and keratolytic activity. It has
important moisturising properties and is very
well-tolerated, even when used over prolonged
periods. Phytosphingosine helps restructuring
the stratum corneum.
2 - Antiseborrhoeic agents inhibit or reduce
sebum production by the sebaceous glands, and
help clear the ducts. Sulphur (see above) is a
classic antiseborrhoeic agent, and may trigger
a rebound effect. Selenium disulphide (see
above) is antiseborrhoeic and may also cause a
rebound effect. Benzoyl peroxide, in addition
to being antibacterial, is antiseborrhoeic, and
exerts a follicular flushing action which is very
useful when treating comedone disorders and/or
follicular hyperkeratosis. Side-effects (drying
effect, irritations, erythematous rash) have been
reported especially in concentrations above 5%.
Zinc gluconate has antiseborrhoeic properties by
downregulating sebum production. Vitamin B6
(pyridoxine) also plays a role in sebum secretion
and there is a synergistic effect, of unknown
mechanism, with zinc. Phytosphingosine helps
controlling seborrhoea.
3 - Essential fatty acids and moisturisers: various
veterinary shampoos have incorporated essential
fatty acids for their softening and moisturising
properties. Some shampoos contain moisturisers
such as glycerine, lactic acid and fatty acid
polyesters.
4 - How to use shampoos in keratoseborrhoeic
disorders: long-haired dogs with severe
seborrhoeic disorders may be clipped. The
therapeutic agent often needs to be changed
following the development of side effects,
rebound effects or changes in clinical presentation
(e.g. transition from greasy seborrhoea to dry
Back to contents
D
seborrhoea). The more severe the dermatitis is,
the more active and potent the shampoo must be
and the more frequent will be the applications.
For mild and/or pityriasiform keratoseborrhoeic
disorders, keratolytic agents should be selected
whereas for severe and/or psoriasiform disorders,
keratoregulating (keratoplastic) agents will also
be used. In all cases but particularly in greasy
seborrhoea, antiseborrhoeic agents may be
useful.
Shampoo therapy in canine pyoderma
Antibacterial shampoos reduce the cutaneous
bacterial population and also remove tissue
debris and exudate, allowing direct contact of
the active ingredient with the organism. Mild
cases of superficial pyoderma can be treated with
shampoos alone. However in most cases systemic
antibiotics will be administered, the shampoo
playing a supporting role. In dogs that are prone
to recurrent folliculitis antibacterial shampoos
may have a prophylactic effect if used regularly.
In cases of deep pyoderma, clipping is preferable
to prevent the formation of a sealing crust and
allow the product to contact the lesions (furuncles,
ulcers). Chlorhexidine (0.5 to 4%, diacetate or
digluconate) is very effective against most bacteria
(Gram + and -), excepting some Pseudomonas
and Serratia strains. It has a prophylactic effect
as some remains on the skin despite rinsing
and is well tolerated. Povidone-iodine releases
iodine to tissues (0.2 to 0.4 per cent). It has also
a prophylactic effect but is relatively drying, can
be irritating and staining. Benzoyl peroxide (2
to 3 %,) has a strong microbiocidal activity, an
excellent prophylactic effect but irritation can
occur at higher concentrations (erythema, pruritus
and pain). Ethyl lactate is used at a concentration
of 10 %, which rarely causes undesirable side
effects (irritation, erythema, pruritus). When
used twice weekly it can reduce the length of the
course of systemic antibiotics required in canine
2006 World Congress WSAVA/FECAVA/CSAVA
superficial pyoderma. Piroctone olamine is
an antifungal agent (see below) which also has
antibacterial properties.
Shampoo therapy in fungal diseases
Antimycotic shampoos (ketoconazole,
miconazole, 1:1 combination of miconazole and
chlohexidine) reduce the infectivity in cases of
dermatophytosis but are not effective in treating it
as sole therapy. Keratomodulating shampoos can
be used before antifungal topical therapy. Topical
therapy is an alternative to systemic treatment
in Malassezia dermatitis. For extensive lesions
antifungal shampoos or lotions are preferable.
Topical therapy alone should not be used to
confirm the diagnosis, but it can maintain the
225
D
patient in remission with systemic therapy, thus
confirming the diagnosis. Shampoos containing
miconazole (2%), chlorhexidine (2 to 4%), a
combination of both (2% each), ketoconazole
(2%), a combination of chlorhexidine (2%) and
ketoconazole (1%) or piroctone olamine are the
most appropriate.
Shampoo therapy in allergic diseases
All shampoos are likely to remove allergens from
the skin, which is believed to be helpful in canine
atopic dermatitis. They also help to rehydrate
dry skin. Shampoos with an antipruritic effect
(1% hydrocortisone, 0.01% fluocinolone, 2%
diphenhydramine, colloidal oatmeal) can be good
adjunctive treatments. A shampoo specifically
designed for canine atopic dermatitis contains
linoleic acid and gamma linolenic acid, mono
and oligosaccharides, vitamin E, and piroctone
olamine and has been shown to be useful.
2006 World Congress WSAVA/FECAVA/CSAVA
226
Back to contents
CONCLUSION: OPTIMISING TOPICAL
THERAPY
Topical therapy is symptomatic and
complimentary, and thus often used along
with specific treatments, mainly systemic. An
appropriate formulation, judiciously selected
active ingredients and the appropriate frequency
of application make it essential. The prescription
varies according to each case and must take into
account the nature and extent of the lesions,
the concurrent specific treatment, the animal’s
temperament and willingness of the owner to
devote the necessary time, and the concentration
and potential side effects of the active ingredients.
Choices should be made on both a short and long
term basis. Communication is important and
should underline the great value of medicated
shampoos for the treatment of skin diseases of an
animal with a haired skin.
REFERENCES
Can be provided upon request.

D - Dermatology
ISCHEMIC SKIN DISEASE IN THE DOG
Peter J. Ihrke, VMD, Diplomate
ACVD
Professor of Dermatology, Chief
- Dermatology Service, VMTH
Department of Medicine &
Epidemiology
School of Veterinary Medicine
University of Kalifornia
One Shields Avenue
Davis, California 95616-8737,
U.S.A.
A. Introduction, General Information, and
Definitions
1. Vasculitis is defined as a process by which
inflammation is directed against vessel walls.
Microhemorrhage into surrounding tissue is a
frequent sequela.
2. ‘Cell poor’ vasculitis or ‘vasculopathy’ is a
subgroup of vasculitis characterized by vascular
damage, vascular depletion, and only sparse
inflammation. Loss of endothelial cells and
thickening of the vessel wall are noted.
3. Ischemic dermatopathy is a term used to
group multiple vasculopathic syndromes
unified by similar clinical and histopathologic
characteristics.
4. Diascopy is a useful and simple clinical tool
used in the diagnosis of skin diseases with a
vascular component. A clear microscope slide
is pressed onto skin to determine if erythema
is due to dilated blood vessels or hemorrhage
into the skin. Blanching of the skin indicates
that erythema is due to dilated blood vessels
and inflammation. If erythematous skin does
not blanch, diascopy confirms hemorrhage and
suggests either vasculitis or vasculopathy.
B. Classification of Ischemic Dermatopathies
1. Canine familial dermatomyositis (DM) – A
juvenile onset heritable inflammatory disease of
uncertain etiology affecting skin and muscle, seen
predominantly in the Collie, Shetland Sheepdog,
and their related cross-breeds.
2. Dermatomyositis-like disease (DM-Like)
– A juvenile-onset ischemic dermatopathy that
is clinically and histopathologically identical to
canine dermatomyositis, but in a breed without
proven breed predilection, and therefore without
known familial predisposition.
3. Localized post-rabies vaccination panniculitis
(Post-Rabies) - A localized ischemic skin disease
associated with a rabies vaccination site and
temporal link with the vaccination.
Back to contents
D
4. Generalized vaccine-induced ischemic
dermatopathy (GVIID) – A generalized ischemic
skin disease with a temporal linkage with rabies
vaccination, but with more severe generalized
post-rabies vaccination-associated disease.
5. Generalized idiopathic ischemic dermatopathy
(GIID) – An adult-onset generalized ischemic
dermatopathy without a correlative history
indicating the likelihood of induction by a rabies
vaccine reaction.
6. These 5 syndromes are united by very similar
clinical and histopathologic similarities. Groups
1 and 2 above develop as juvenile onset disease
and are clinically indistinguishable from each
other. Group 3 develops as focal skin disease at
the site of vaccination. Group 4 and 5 develop
as generalized, more severe, and usually adult-
onset skin disease. Skin disease seen with group
4 and 5 may be generalized beyond the expected
distribution pattern of most cases of DM (group
1) and DM-like disease (group 2).
7. The term, “canine familial dermatomyositis”
currently should be reserved for dogs with clinical
and histopathologic evidence of a juvenile onset
heritable inflammatory disease affecting skin and
muscle in a breed known to be at increased risk. 2006 World Congress WSAVA/FECAVA/CSAVA
C. Etiology and Pathogenesis
1. The etiology of ischemic dermatopathies is not
known. Multifocal immunologic damage to blood
vessels probably results in ischemic damage to
the skin and other susceptible organs. Cutaneous
hypoxia probably leads to follicular atrophy and
other associated chronic hypoxic skin changes.
2. Post-rabies vaccination associated disease
is presumed to be due to an idiosyncratic
immunologic reaction to rabies antigen that
partially targets vessels. Rabies viral antigen
can be documented in the walls of dermal blood
vessels and in the epithelium of hair follicles via
immunofluorescent testing. Since this syndrome
is seen predominantly in very small dogs, it is
227
D
tempting to speculate that the disease may be
partially linked to increased antigenic load in
comparison to the body size of the dog, since
the same volume of rabies vaccine is given to all
dogs subcutaneously.
3. Hereditary or individual predispositions,
coupled with a secondary environmental trigger
have long been hypothesized for dermatomyositis
in humans. Similar factors probably initiate
and drive canine ischemic dermatopathy.
Autoimmune and viral etiologies coupled with
hereditary predilection have been postulated for
dermatomyositis in humans.
4. All ischemic dermatopathies share both clinical
and histopathologic features that could result from
cell-poor vasculitis leading to a long-term lack
of cutaneous vascular sustenance. Skin hypoxia
could lead to follicular atrophy and associated
chronic skin changes. Lesions that occur over
bony prominences can be explained by enhanced
susceptibility to trauma and lesions on distal
extremities can be explained by poor collateral
circulation that does not allow appropriate
vascular sustenance.
5. Complement-mediated microangiopathy
leading to ischemia is considered to be the
pathophysiological basis of skin lesions in human
dermatomyositis. Complement C5b-9 membrane
attack complex has been demonstrated in small
blood vessels within muscle from a dog with
vaccine-induced ischemic dermatopathy and cell
poor vasculitis.
D. Comparison of Clinical Features
1. Clinical features shared by all 5 subgroups of
canine ischemic dermatopathy given above include
alopecia with crusting and post-inflammatory,
mottled pigmentary change. Hyperpigmentation
is seen in breeds predisposed to enhanced
pigmentation secondary to inflammation; in other
breeds, hypopigmentation can occur. Erosion and
2006 World Congress WSAVA/FECAVA/CSAVA
ulceration occurs in more severe cases, especially
if trauma, secondary infection, or coexistent
pruritic disease are present.
2. Dogs with Canine familial dermatomyositis
(DM) and Dermatomyositis-like disease (DM-
Like) (Group 1 & 2) share identical clinical
features and hence will be grouped in the
discussion below.
3. Dogs with Generalized vaccine-induced
ischemic dermatopathy (GVIID) & Generalized
idiopathic ischemic dermatopathy (GIID) share
similar clinical features and will be grouped in
the discussion below. However, dogs with GVIID
usually have a demonstrable focal lesion at the
subcutaneous vaccine site compatible with the
lesions seen with localized post rabies vaccination
panniculitis. Even dogs without a correlative
228
Back to contents
history of recent rabies vaccination should have
likely vaccination sites checked for compatible
lesions, as the focal lesions may be subtle and
easily missed.
E. Histopathologic Features (adapted from T.L.
Gross)
1. The histopathologic features of all ischemic
dermatopathies are similar. Diagnosis of cell-poor
vasculitis relies on recognition of subtle ischemic
changes in the skin. Altered staining of collagen
and ‘fading’ atrophy of hair follicles are the
most characteristic features. The epidermal and
dermal changes overlying post-rabies vaccination
panniculitis are identical to those seen with other
ischemic dermatopathies.
2. Scattered degeneration of individual basal cells
and prominent degeneration of follicular basal
cells are noted.
3. Secondary dermal-epidermal vesiculation
occurs in more severely affected animals.
Vesicles contain red blood cells and occur above
the basement membrane. Artifactual dermal-
epidermal separation “usable artifact of Stannard”)
may occur at biopsy specimen margins.
4. Dermal inflammation consists of diffuse, mild
lymphocytic and histiocytic inflammation that
encircles hair follicles.
5. Diffuse pallor of dermal connective tissue with
pale-staining, smudged, collagen probably results
from tissue ischemia.
6. Vascular lesions are subtle. Loss of endothelial
cells, mummification of small vessels, or hyaline
mural alteration may be seen. Leukocytoclasia
may be present.
7. Severely atrophic or faded, atrophic hair
follicles may be a direct consequences of ischemia
and basal cell degeneration.
8. Myositis with mixed inflammation, regeneration,
fibrosis, and atrophy may be present. Random
biopsy may not show muscle lesions.
9. Localized post-rabies vaccination panniculitis
also shows a nodular localization of lymphocytes
and other mononuclear cells in the lower dermis
and panniculus. Amorphous basophilic deposits
resembling vaccine product may be present.
F. Canine Familial Dermatomyositis (DM) &
Dermatomyositis-like disease (DM-Like) (Group
1 & 2)
1. Signalment predilections
a. Breeds - DM - Shetland Sheepdogs,
Collies, and related crossbreeds.
b. Breeds - DM-like - Chow Chow,
Beauceron Shepherds, Welsh Corgi,
Lakeland Terrier, German Shepherd Dog, and
Kuvasz (published). Additionally, Miniature
Schnauzers, Miniature Dachshunds, Fox

Terriers, and other breeds have been
confirmed by Ihrke or Gross.
c. Age - Both are juvenile-onset diseases;
lesions usually occur by 6 months of age. d.
Sex - Sex predilection has not been noted.
2. Initial lesions - Rare transient papules, pustules,
and vesicles eventuating in crusted erosions,
ulcers, and alopecia.
3. Chronic lesions - Scarring is seen with
chronicity. Pigmentary aberrations give rise to
poikilodermatous change with either hyper or
hypopigmentation.
4. Sites - Initial lesions occur over bony
prominences (sites of mild trauma), especially on
the muzzle; in periorbital and perioral locations;
and on the dorsal paws. Similar lesions occur on
distal extremities with poor collateral circulation,
and on pressure points susceptible to shearing
injury and trauma. The pinnal tips, pinnal folds,
nail folds, tip of the tail, other bony prominences
can be affected. Nail dystrophy and sloughing
may be seen.
5. Pain and pruritus occur if ulceration or
secondary pyoderma are present.
6. Relapse - Photo-aggravation, trauma or estrus
can trigger relapse.
7. Muscle involvement - Subtle, may be
limited to the temporal and masseter muscles.
Difficulties with mastication and swallowing can
occur. Concurrent clinical, electromyographic,
or histologic evidence of muscle disease aids in
diagnosis.
8. Severely affected dogs - Growth retardation,
megaesophagus, lameness, and widespread
muscle atrophy. The tongue may fasciculate
causing difficulty in prehension. Infertility can
occur in severe dermatomyositis.
9. Diagnosis - Compatible skin lesions,
confirmatory skin biopsy, muscle disease.
10. Prognosis - Mildly affected dogs may achieve
clinical remission. Severely affected dogs with
generalized disease exhibit cyclical lifelong
disease.
G. Localized Post-Rabies Vaccination Panniculitis
(Post-Rabies)
1. Signalment predilections
a. Breeds - Marked breed predilection for
Toy & Miniature Poodles, and Bichon
Frises. Shih Tzu, Lhasa Apso, Maltese,
Silky Terrier, Yorkshire Terrier, Chihuahua,
Toy Manchester Terrier, American Eskimo,
Poodle crossbreeds, and Miniature
Dachshunds also have been confirmed by
Ihrke or Gross.
b. Age & sex predilections have not been
noted.
Back to contents
D
2. Initial lesions - An alopecic macule or plaque
develops at the site of prior subcutaneous rabies
vaccine deposition. The time between vaccination
and noting of the lesion usually is between one
and three months. Average lesion size is 2 to 10
cm in diameter. Smaller satellite lesions may
be present. A few hairs may remain within the
boundaries of the lesion. Visible inflammation
commonly is minimal.
3. Chronic lesions - Hyperpigmentation may be an
occasional sequela, especially in black Miniature
Poodles and other breeds that tend to respond to
inflammation by hyperpigmentation.
4. Sites - Neck and shoulder region near the scapula
where most subcutaneous rabies vaccinations are
given. Gravitational drift may result in lesions
ventral to vaccination site.
5. Systemic signs - A small subgroup of dogs
display lethargy, depression, and fever. Elevated
liver enzymes have been noted. Systemic
signs may precede the skin lesion or occur
concomitantly.
6. Diagnosis – History of vaccination, compatible
skin lesions, confirmatory skin biopsy.
7. Prognosis – Most lesions remain small and are
asymptomatic. Exacerbation has been observed
after revaccination.
H. Generalized vaccine-induced ischemic
dermatopathy (GVIID) & Generalized idiopathic
ischemic dermatopathy (GIID)
1. Signalment predilections
a. Breeds – Miniature and Toy Poodle,
Shih Tzu, Shetland Sheepdog, Lhasa Apso,
Pomeranian, and Yorkshire Terrier may be at
increased risk for both types of adult-onset
generalized ischemic dermatopathy. Long-
haired toy or miniature breeds seem to be at
greater risk.
b. Age & sex predilections have not been
noted. 2006 World Congress WSAVA/FECAVA/CSAVA
2. Clinical skin lesions – Individual lesions are
those of DM and DM-like disease but may be
more severe and more generalized. More severe
lesions are located over bony prominences and on
distal extremities. Similar, but usually less severe
lesions are seen over much of the skin surface.
3. Muscle atrophy – Variable, but may be
marked.
4. Systemic signs – Some dogs with GVIID display
lethargy, depression, and fever. Elevated liver
enzymes have been noted. Systemic signs may
precede the skin lesion or occur concomitantly.
5. Prognosis - Generalized vaccine-induced
ischemic dermatopathy may gradually diminish
in severity over time. Dogs with GIID usually
exhibit lifelong disease with some cyclical
229
D
recrudescence. Revaccination can exacerbate
disease.
I. Other reported Ischemic Dermatopathies
1. Other syndromes have been reported that
share features with cell-poor vasculopathies and
ischemic dermatopathies.
2. Reported diseases include familial cutaneous
vasculopathy of German Shepherd Dogs, and
cutaneous vasculitis in Jack Russell Terriers.
J. Familial Cutaneous Vasculopathy of German
Shepherd Dogs
1. Familial cutaneous vasculopathy of German
Shepherd Dogs is a rare vascular disease affecting
predominantly the pawpads of German Shepherd
Dog puppies. Pedigree analysis indicated
probable autosomal recessive inheritance. Most
published cases (26 dogs) were seen in Canada,
with another from the United States, and another
from Italy.
2. Immunologic attack on collagen has been
hypothesized as a mechanism.
3. A temporal association with puppy vaccination
and recrudescence with repeat vaccination
was seen in some of the dogs, similar to some
ischemic dermatopathies.
4. Clinical features - The prime clinical feature
is depigmented, swollen pawpads. Erosions,
ulceration, and hairloss with adherent crusting
occur
5. Sites - Pawpads are affected preferentially.
Similar lesions may be present on the pinnae, tail
tip, and nasal planum.
6. Other clinical signs - Lymphadenopathy may
occur. Systemic signs include pain, lethargy,
pyrexia, and pain on ambulation.
7. Histopathologically identical lesions were seen
in the pawpads of a Fox Terrier and Miniature
2006 World Congress WSAVA/FECAVA/CSAVA
Schnauzer with presumed ischemic lesions
affecting the muzzle and ears (T.L. Gross).
‘Pawpad vasculopathy’ may be one manifestation
of ischemic dermatopathy in some breeds.
Coexistent mild skin lesions may be overlooked.
K. Cutaneous Vasculitis in Jack Russell Terriers
1. A syndrome characterized by cutaneous
vasculitis has been reported in 5 Jack Russell
Terriers. The most prominent histologic feature
was a cell poor vasculitis.
2. The range of reported age of onset and clinical
features both were wide.
3. Familial predisposition is suggested by all
affected dogs being of the same breed.
4. Most likely, these cases also reflect canine
ischemic dermatopathy.
230
Back to contents
L. Diagnosis & Differential Diagnosis –
Overview
1. All of the ischemic dermatopathies are
diagnosed by clinical features and skin biopsy.
Electromyographic examination is recommended
if DM or DM-like disease are suspected.
2. Clinical differential diagnoses for canine DM
and DM-like disease include juvenile-onset
demodicosis, dermatophytosis, facial pyoderma,
and discoid lupus erythematosus.
3. The diagnosis of post-rabies vaccination
panniculitis is simplified by localization to a site
of prior vaccination, breed predilections, plus a
temporal link to vaccination.
4. More severe cases of GVIID and GIID must be
differentiated from other inflammatory diseases
where extensive alopecia and pigmentary
changes are seen. Differential diagnoses include
other vasculitides, severe erythema multiforme
and epitheliotropic lymphoma. Generalized
demodicosis and generalized dermatophytosis
also may resemble ischemic dermatopathy. Most
cases of GVIID have a focal lesion at a prior
vaccine site. Skin scrapings should be performed
to rule out demodicosis and fungal culture should
be performed to rule out dermatophytosis. Skin
biopsy is required for definitive diagnosis.
M. Management of Ischemic Dermatopathies -
Overview
1. Management of ischemic dermatopathies
is challenging. Response to therapeutic
manipulations can be slow and perception of
response is highly subjective.
2. Minimally affected dogs require little
management; the disease may be largely
cosmetic.
3. Severely affected dogs are difficult to manage.
Dogs with substantial concomitant muscle
disease (DM & DM-like) may have difficulties
in prehension and swallowing. Megaesophagus
leading to aspiration pneumonia occurs in
severely affected dogs.
4. Medications aimed at diminishing or preventing
inflammation may be beneficial.
a. Omega-3 and Omega-6 fatty acid
supplementation may offer some benefit.
b. Vitamin E (200 – 800 IU/day) may be
beneficial.
5. Pentoxifylline (Trental®, Hoechst-Roussel),
available as a 400mg coated tablet (200 – 400
mg/day / 10-30 mg/kg/day). The drug is a
methylxanthine derivative with rheologic and
immunomodulatory effects. Pentoxifylline
increases red blood cell deformability, alters tissue
response to multiple cytokines, and diminishes
production of TNF-alpha.

6. The use of corticosteroids for the treatment
of ischemic dermatopathies is controversial.
Anti-inflammatory effects may be beneficial,
but overuse is detrimental. Potent topical
corticosteroids may diminish epidermal thickness
leading to increased skin fragility. Systemic
corticosteroid overuse can lead to iatrogenic
hyperglucocorticoidism and highly deleterious
side effects such as ‘corticosteroid-induced-
owner-loss-of-hope!
N. Factors Complicating Management –
Adjunctive Recommendations
1. Restrict potential for cutaneous trauma - Rough
play with other dogs, especially puppies can lead
to profound exacerbation of skin lesions.
2. Prevent self-trauma in response to concomitant
skin diseases – Any coexistent skin disease
characterized by pruritus must be relentlessly
managed long-term to prevent the cycle of self-
trauma followed by further ischemic damage.
The most commonly present troublesome
coexistent pruritic skin diseases include flea
allergy dermatitis, canine atopic dermatitis, and
food allergy.
3. Secondary infection or bacterial or yeast
overgrowth - Either Staphylococcus or Malassezia
can markedly exacerbate inflammation and
pruritus and contribute to additional pruritus and
self-trauma complicating management.
4. Long-term surveillance to prevent recurrence
of pruritic skin diseases or secondary pyoderma
and Malassezia dermatitis - Surface cytologic
examination looking for organism overgrowth
should be performed whenever inflammation
seems to be exacerbating in an ischemic
dermatopathy.
5. Minimize solar exposure – Sun exposure can
exacerbate ischemic dermatopathies.
6. Localized demodicosis restricted to the site of
the skin lesions of dermatomyositis has been noted
in multiple Shetland Sheepdogs. The significance
of these findings is not known, but may indicate
focal aberrations in immune surveillance.
O. Suggested Readings
Crowson, A.N. & Magro, C.M. (1996) The role
of microvascular injury in the pathogenesis of
cutaneous lesions of dermatomyositis. Hum
Pathol, 27, 15-9.
Back to contents
D
Fondati, A., Fondevila, M.D., Minghelli, A. et
al. (1998) Familial cutaneous vasculopathy and
demodicosis in a German shepherd dog. J Small
Anim Pract, 39, 137-9.
Gross, T.L., Ihrke, P.J., Walder, E.J. & Affolter,
V.K. Skin Diseases of the Dog and Cat: Clinical
and Histopathologic Diagnosis. Blackwell
Scientific, 49-52, 247-250, 503-505, 538-541,
2005.
Ihrke, P.J. & Gross, T.L. (1993) New Thoughts on
the Pathophysiology, Diagnosis, and Treatment of
Alopecia in the Dog. Proceedings of the William
Dick Bicentenary 1793-1993, University of
Edinburgh, 89-94.
Kovacs, S.O. & Kovacs, S.C. (1998)
Dermatomyositis. J Amer Acad Dermatol, 39,
899-920.
Magro, C.M., Crowson, A.N. & Regauer, S.
(1996) Granuloma annulare and necrobiosis
lipoidica tissue reactions as a manifestation of
systemic disease. Human Path, 27, 1, 50-6.
Parker, W.M. & Foster, R.A. (1996) Cutaneous
vasculitis in five Jack Russell Terriers. Vet
Dermatol, 7, 109-15.
Scott, D.W., Miller, W.H. & Griffin, C.E. (2001)
Muller & Kirk’s Small Animal Dermatology, 6th
edn. pp. 940-6. WB Saunders Co, Philadelphia.
Sontheimer, R.D. (1999) Dermatomyositis.
In: Dermatology in General Medicine (I.W.
Freedberg, A.Z. Eisen, K. Wolff, K.F. Austen,
Goldsmith L.A., & T.B. Fitzpatrick), pp. 2009-
2022. McGraw-Hill, New York.
Vitale, C.B., Gross, T.L., & Magro C.M. (1999)
Vaccine-induced ischemic dermatopathy in the
dog. Vet Dermatol, 18, 131-42.
Weir, J.A., Yager, J.A., Caswell, J.L. et al. (1994)
Familial cutaneous vasculopathy of German
shepherds: Clinical, genetic and preliminary
pathological and immunological studies. Can Vet 2006 World Congress WSAVA/FECAVA/CSAVA
J., 35, 763-9.
Wilcock, B.P. & Yager, J.A. (1986) Focal
cutaneous vasculitis and alopecia at sites of
rabies vaccination in dogs. J Am Vet Med Assoc,
188, 1174-7.
231
D
D - Dermatology
DIAGNOSIS & MANAGEMENT OF ADVERSE FOOD REACTIONS IN
THE DOG
Professor David Lloyd
Department of Clinical Veterinary
Science
Royal Veterinary College
Hawkshead Campus
North Mymms
Hertfordshire AL9 7TA
UK
david-lloyd@ntlworld.com

Introduction and non-immunological (food intolerances or

Adverse reactions to food (AFR) cover a spectrum
of conditions including dietary indiscretion
and food aversion as well as food allergy and
intolerance (Figure 1). This review will be
restricted to AFR recognised as differential
diagnoses for non-seasonal pruritic diseases
of the skin in dogs and which may also cause
gastrointestinal, respiratory, urinary tract (cystitis)
and neurological problems.1,2 These reactions are
thought to include immunological (food allergies)
2006 World Congress WSAVA/FECAVA/CSAVA
non-allergic food hypersensitivities) causes,
although differentiation between these causes is
rarely made in veterinary clinical practice.
The prevalence of canine AFR remains
controversial.5,6,7 Within referral populations,
studies have estimated AFR to be responsible for
5% of canine dermatoses8 and 10-15% of canine
allergic dermatoses.9,10 More recently, AFR has
been described as the sole cause of skin disease in
20-35% of dogs with non-seasonal pruritus.6,7,11

Clinical Signs in AFR Cutaneous signs normally include pruritus

Signs are nearly always non-seasonal but can and erythema, which may affect any part of
be related to seasonal factors e.g. concurrent the skin. There is often otitis externa and, in
atopy or flea allergy, ectoparasites, or seasonal severe cases, otitis media. Secondary pyoderma,
variation in diet. Signs may be related to skin pyotraumatic dermatitis, microbial overgrowth
and/or to the gastrointestinal tract. In addition, and signs related to chronic pruritus (hair loss,
cystitis, respiratory or neurological signs have hyperpigmentation, lichenification, excoriation
been reported.1,2 and ulceration) commonly occur.11 Often there is
232
Back to contents

scaling and poor coat. Lesions can be restricted
to parts of the skin and, rarely, may be unilateral.
Cutaneous signs may mimic those of other pruritic
dermatoses including ectoparasitic infestations,
such as scabies and cheyletiellosis, and atopy
and flea allergy, diseases which may also occur
concurrently. However, perineal pruritus may be
a pointer towards AFR.
Gastrointestinal signs occur with increased
frequency in pruritic dogs with AFR.11 Signs
may include increased defecation frequency,
soft faeces, intermittent diarrhoea and flatulence.
However, in some dogs with AFR resulting in
cutaneous disease, gastrointestinal signs are
absent.
Diagnosis of Adverse Reactions to Food
Clinical signs of pruritic disease consistent with
allergy should always raise suspicion of AFR,
particularly with concurrent gastrointestinal signs
and/or perineal pruritus. However, diagnosis
cannot be made on the basis of the clinical
presentation as AFR can mimic other pruritic
diseases.
Several procedures have been described for
the diagnosis of AFR. These include serology,
cutaneous tests (intradermal, patch), gastroscopic
provocation and intestinal permeability tests.
However, these procedures have not been
validated12-19 and dietary elimination trials
followed by dietary provocation remain the
procedure of choice.
Diets for diagnostic trials can either be home-
prepared foods or commercial products. Home-
prepared diets are traditionally recommended
as the “gold standard” for diagnosis of canine
AFR as they can be tailored to each dog’s dietary
history individually avoiding foods to which the
animal has already been exposed.20,21 However,
such diets are labour-intensive for owners
and ingredients novel to the dog may not be
readily available. They are also not adequate for
maintenance after diagnosis or for diagnosis in
young, growing dogs.22,23
Commercial diets using limited and less
commonly fed ingredients have been shown
to be inferior to home-cooked diets in most
comparative studies in diagnosis of AFR.11,24,25,26
Furthermore, individual dogs have been
described that tolerate home-prepared ingredients
but not their commercially prepared versions,
raising concerns over processing additives.1,25,27,28
However, allergenic food additives have not been
characterised in dog foods.28
More recently, hydrolysed veterinary diets have
been introduced for diagnosis of canine AFR.
During hydrolysis, protein sources (chicken,
poultry liver, casein, soy) are broken down
Back to contents
D
to polypeptides, changing and reducing their
allergenic properties. Two clinical investigations
into possible AFR in pruritic dogs, one using a
chicken hydrolysate diet,10 the other a soy-based
hydrolysate,7 reported similar frequencies of
AFR as in a study with home-prepared diets.6 A
subsequent retrospective study examining home-
cooked diets and the chicken hydrolysate diet in a
referral centre suggested that were equally useful
in the diagnosis of canine AFR.29
The clinical approach to diagnosis of AFR in
pruritic dogs should involve:
1. Selection of dogs with non-seasonal pruritus or
a history suggestive of AFR.
2. Careful recording of clinical signs and owners’
observations relating to pruritus, lesions and
gastrointestinal signs.
3. Tests for ectoparasitic infestation. These may
include serology for sarcoptic mange and
examination of skin scrapings, coat brushings of
hair pluck samples.
4. Flea control, on the dog and in the environment,
and trial therapy to eliminate ectoparasitic
infestation and remove flea challenge.
5. Treatment of pyoderma or microbial overgrowth
with systemic antibiotics and/or topical therapy
until all lesions are eliminated.
6. Maintenance of a rigorous food-restriction trial
for 6 to 8 weeks. In addition to the chosen diet,
only water may be given to drink. Home-cooked
or limited ingredient commercial diets are selected
based on the dietary history of the dog; a protein
and a carbohydrate source seldom or never fed
previously are selected. With hydrolysed diets,
palatability may be important. If dry, moistening
the diet may improve palatability; generally dogs
adapt to the diet after a few days.
7. Maintenance of contact with the owner to
monitor the results and ensure that all treatments
and the diet are properly instituted.
8. Dietary challenge, after the trial, with the 2006 World Congress WSAVA/FECAVA/CSAVA
foods, drinks and treats formerly given.
Some owners may refuse to challenge the dog
once a good response has been obtained and
wish to continue with the restriction diet. With
home-cooked diet it will be necessary to provide
supplements to make it balanced, or persuade
the owner to use an equivalent commercial
diet. Remember that you have not yet proved
that this problem is AFR; beware of seasonal or
other factors which may have led to the animal’s
improvement.
9. Evaluation and recording of changes in clinical
signs and owners’ observations in response
to treatment, the restriction diet and dietary
challenge.
10. If there is complete response to diet and signs
recur on challenge, AFR can be diagnosed’
233
D
11. Where there has been partial response and
signs recur on challenge, AFR concurrent with
other pruritic disease can be diagnosed. Because
of the rule-outs, this disease is likely to be atopy.
Management of Dogs with Adverse Reactions to
Food
Diagnosis of AFR should be presented to the
owner as a “good news” story. Now the disease can
be controlled only by dietary management. Often
the animal will show improvements associated
with improved gastrointestinal function which
will please the owner, such as elimination of
flatulence, improved appetite, reduced scaling, a
glossier coat, more energy. It is useful to draw
such changes to the attention of the owner.
It is important to make the owner feel responsible
and part of the “team” dealing with the problem
as dietary control will need to be maintained
for the rest of the dog’s life. Keeping in regular
contact is essential as occasionally the diet will
be broken and pruritus, pyoderma and other signs
of the disease will recur and need to be treated.
The owner may also begin to experiment with
forbidden treats and may not appreciate that signs
of reactivity can take several days to appear. In
addition, other pruritic diseases or allergies may
develop and the dog may become sensitive to
additional dietary components and may need to
be worked up and tested again.
References
1. ROSSER EJ. Diagnosis of food allergy in dogs.
Journal of the American Veterinary Medical
Association 1993 203 259-262.
2. GUILFORD, W.G. (1996) Adverse reactions
to food. In: Guilford WG. et al. eds. Strombeck’s
Small Animal Gastroenterology. 3rd edn.
Philadelphia: W.B.Saunders 1996 436-450.
5. WALTON GS. Skin responses in the dog and
2006 World Congress WSAVA/FECAVA/CSAVA
cat to ingested allergens. Observations on 100
confirmed cases. Veterinary Record 1967 81 709-
713.
6. CHESNEY CJ. Food sensitivity in the dog:
a quantitative study. Journal of Small Animal
Practice 2002 43 203-207.
7. BIOURGE VC, FONTAINE J, VROOM MW.
Diagnosis of adverse reactions to food in dogs:
efficacy of a soy-isolate hydrolysate-based diet.
Journal of Nutrition 2004 134 2062S-2064S.
8. WILLEMSE, T. Adverse reactions to diet: an
update on clinical manifestations. Royal Canin
Symposium on Adverse Reaction to Food, 5th
World Congress of Veterinary Dermatology,
Vienna, August 25th 2004, pp. 8-9.
9. ACKERMAN L. Food hypersensitivity: a rare,
234
Back to contents
but manageable disorder. Veterinary Medicine
1988 83 1142-1148.
10. CARLOTTI DN, REMY I, PROST C. Food
allergy in dogs and cats. A review and report of
43 cases. Veterinary Dermatology 1990 1 55-62.
11. LOEFFLER A, LLOYD DH, BOND R. et
al. Dietary trials with a commercial chicken
hydrolysate diet in 63 pruritic dogs. Veterinary
Record 2004 154 519-522.
12. JEFFERS JG, SHANLEY KJ, MEYER
EK. Diagnostic testing of dogs for food
hypersensitivity. Journal of the American
Veterinary Medical Association 1991 198 245-
250.
13. KUNKLE G, HORNER S. Validity of skin
testing for diagnosis of food allergy in dogs.
Journal of the American Veterinary Medical
Association 1992 200 677-680.
14. ELWOOD CM, RUTGERS HC, BATT RM.
Gastroscopic food sensitivity testing in 17 dogs.
Journal of Small Animal Practice 1994 35, 199-
203.
15. MUELLER R, TSOHALIS J. Evaluation
of serum allergen-specific IgE for the diagnosis
of food adverse reactions in the dog. Veterinary
Dermatology 1998 9 167-171.
16. FOSTER AP, KNOWLES TG, HOTSTON
MOORE A et al. Serum IgE and IgG responses
to food antigens in normal and atopic dogs, and
dogs with gastrointestinal disease. Veterinary
Immunology and Immunopathology 2003 92 113-
124.
17. JACKSON HA, JACKSON MW, COBLENTZ
L, HAMMERBERG B. Evaluation of the clinical
and allergen specific serum immunoglobulin
E responses to oral challenge with cornstarch,
corn, soy and a soy hydrolysate diet in dogs with
spontaneous food allergy. Veterinary Dermatology
2003 14 181-187.
18. HALLIWELL REW, GORDON C, HORVATH
C et al. IgE and IgG antibodies to food antigens in
sera from normal dogs, atopic dogs and dogs with
adverse food reactions. Veterinary Dermatology
2004 15 (Suppl.1) 2.
19. ISHIDA R, MASUDA K, KURATA K et al.
Lymphocyte blastogenic responses to inciting
food allergens in dogs with food hypersensitivity.
Journal of Internal Veterinary Medicine 2004 18
25-30.
20. REEDY, LM., MILLER, WH. & WILLEMSE,
T. (1997) Food hypersensitivity. In: Reedy LM.
Et al. eds. Allergic skin diseases of dogs and cats.
2nd edn. London: W.B.Sauders 1997 173-188.
21. SCOTT DW, MILLER WH, GRIFFIN CE.
Skin immune system and allergic skin diseases.

In: Scott DW, Miller WH, Griffin CE. eds. Muller
& Kirk’s Small Animal Dermatology 6th edn.
Philadelphia: W.B. Saunders 2001 543-666.
22. ROUDEBUSH P, COWELL CS. Results
of a hypoallergenic diet survey of veterinarians
in North America with a nutritional evaluation
of homemade diet prescriptions. Veterinary
Dermatology 1992 3 23-28.
23. STREIFF EL, ZWISCHENBERGER B,
BUTTERWICK RF et al. A comparison of the
nutritional adequacy of home-prepared and
commercial diets for dogs. Journal of Nutrition
2002 132 1698S-1700S.
24. TAPP T, GRIFFIN C, ROSENKRANTZ W. et
al. Comparison of a commercial limited-antigen
diet versus home-prepared diets in the diagnosis
of canine adverse food reaction. Veterinary
Therapeutics 2002 3 244-251.
25. ROUDEBUSH P, SCHICK RO. Evaluation
of a commercial canned lamb and rice diet for the
management of adverse reactions to food in dogs.
Back to contents
D
Veterinary Dermatology 1994 5 63-67.
26. LEISTRA MHG, MARKWELL PJ,
WILLEMSE T. Evaluation of selected-protein-
source diets for management of dogs with adverse
reactions to foods. Journal of the American
Veterinary Medical Association 2001 219 1411-
1414.
27. RUTGERS HC, BATT RM, HALL J. et al.
Intestinal permeability testing in dogs with diet-
responsive intestinal disease. Journal of Small
Animal Practice 1995 36 295-301.
28. HANNUKSELA M, HAAHTELA T.
Hypersensitivity reactions to food additives.
Allergy 1987 42 561-575.
29. LOEFFLER, A. SOARES-MAGALHAES,
R., BOND, R. et al. A retrospective analysis
of case series of home-prepared and chicken
hydrolysate diets in the diagnosis of adverse
food reactions in 181 pruritic dogs. Veterinary
Dermatology 2006. In press.
2006 World Congress WSAVA/FECAVA/CSAVA
235
D
D - Dermatology
NEW APPROACHES TO THE TREATMENT OF CANINE ATOPY
Craig Griffin DVM, Diplomate
ACVD
Animal Dermatology Clinic
5610 Kearny Mesa Rd
San Diego, California
USA 92111
itchypet@aol.com
Canine atopic dermatitis is a chronic often
frustrating disease to treat. In the last few years
there have been several new therapies that have
been shown to be helpful or possible valuable in
managing atopic dermatitis.
Cyclosporine (Atopica®) was initially shown to
be effective for treating atopic dermatitis in 2002.
(Olivry, Rivierre et al. 2002; Olivry, Steffan et
al. 2002) Those along with many other studies
have extensively evaluated the drug. It is the
first alternative therapy to glucocorticoids that
has shown similar efficacy to prednisolone and
methylprednisolone. Cyclosporin has multiple
effects on the skin immune and inflammatory
response. Originally the mode of action was felt
to be relatively specific for effects on T helper
lymphocytes. Cyclosporin complexes bind
calcineurin and inhibit the signal transduction
to the nucleus resulting in blocked or impaired
synthesis of multiple cytokines, most notably
interleukin-2 (IL-2) and inhibits T-cell
proliferation and the formation of cytotoxic
lymphocytes. Cyclosporine is also thought to
inhibit, via suppression of calcium-mediated
signal transduction, mast cells and IgE-mediated
2006 World Congress WSAVA/FECAVA/CSAVA
immediate and LPR reactions. A recent study in
dogs showed that suppression of mRNA for IL-
2, IL-4 and gamma interferon but not TNF alpha
as described in humans.(Kobayashi, Momoi
et al. 2006) In additions dogs do not have an
up regulation of TGF beta as in man. These
results suggest species differences may occur.
Multiple studies have demonstrated influences
on mast cells, Langerhans cells, keratinocytes,
eosinophils and lymphocytes. Cyclosporine has
immunosuppressive and antiproliferative affects
rather than cytotoxic or myelotoxic effects. It
is likely that the numerous disease and types of
disease that may respond to cyclosporine attest to
the multitude of effects the drug may have.
The dose is 5mg/kg q24h. Once a response is
seen then the dose may be tapered. In some cases
it is better to continue the induction dose until
236
Back to contents
clinical improvement is complete or reached
a steady state of response. Tapering is done by
maintaining the dose at 5mg/kg but changing
to q48h and with continued response is further
tapered to q72 or every q 4-7d dosing. In some
cases long term remissions may be seen once the
drug is discontinued, though the frequency of this
needs to be determined in more controlled study.
It make take several months for signs to return
and this effect is another way to manage some
cases, by going on and off the drug long term.
This is another way to keep the costs of therapy
within a clients comfort level. Some dogs may
end up on relatively low levels of drug long
term by doing the tapering or going on an off the
drug. This makes the overall cost low enough
to have even large dogs that initially may seem
to expensive to treat actually respond well at an
affordable cost.
Adverse reactions have been reported in a study
of up to 268 atopic dogs(Steffan, Parks et al.
2005). The most commonly encountered side
effects are vomiting and diarrhea. Vomiting is
often short term or administration with food may
alleviate it. In other cases temporary concurrent
use of metoclopromide 0.2 to 1mg/kg q24h may
allow continued use. For diarrhea temporarily
stopping the drug then treating again with the
addition of metronidazole or fiber to the diet may
alleviate the diarrhea. However this has been the
most common medical reason the drug has to be
discontinued. Hirsutism and gingival hyperplasia
have also been seen at the doses used for
atopic disease. Hirsutism is often a generalized
thickened more dense hair coat often associated
with increased shedding. In other cases there are
patterns where the hair growth is exceptionally
long. This seems to most often affect the paws and
head or face region. Papillomatous hyperplasia
may also be seen and infrequently is viral and
more often bacterial. Bacterial infections may
appear as atypical lesions. Nephrotoxicity and
hepatic toxicity has not been observed in dogs, as

a significant problem. This is more of a concern
when ketoconazole is used for concurrently either
for Malassezia or as dose sparing agent. Elevated
blood pressure is concern in humans and though
rare in dogs should be monitored for. In humans
there is an increased risk for malignancy especially
skin neoplasia with cyclosporine use.
Topical Immunomodulators (TIMs) are a new
class of drugs that have been approved in humans
for the treatment of atopic dermatitis. The initial
approved formulation, Tacrolimus, has also been
shown effective in dogs with atopic dermatitis,
especially localized disease.(Marsella, Nicklin
et al. 2004; Bensignor and Olivry 2005)
Tacrolimus is a 23-member macrolide produced
by Streptomyces tsukabaensis and the topical
formulation is called Protopic® an ointment
available as a 0.1% or 0.03%. The other approved
drug in this category is Pimecrolimus (Elidel®)
which is an ascomycin macrolactam derivative
that acts similar to Tacrolimus. It is used similar
to Protopic though studies documenting it efficacy
have not been done. No comparisons have been
done in dogs but anecdotal reports suggest that in
some dogs it is less irritating and the cream base
is preferred by some clients.
The TIMs have topical anti inflammatory effects
without the atrophogenic effects and metabolic
effects of topical glucocorticoids. The mechanism
of action is similar to cyclosporine by inhibition
of calcineurin, but 10 to 100 times more potent.
Large multicenter human studies indicate it is a
very safe drug with minimal systemic absorption.
However animal studies have shown an increase
risk for skin cancers and there is a concern
that humans with long term use may also be
predisposed to skin cancers including melanoma
and possible lymphoma. This led the Food and
Drug Administration to include this warning on
the label and now recommend these drugs in more
limited settings when other forms of therapy have
been ineffective.
These drugs are used for localized atopic dermatitis
that is not effective to topical glucocorticoids.
Initial treatment is a light application of the
ointment or cream until it is completely rubbed
in twice daily for two weeks. If a response is seen
the frequency may be lowered to once daily or
less. To date problems other than irritancy have
not been noted in dogs.
Interferons (INF) are a group of glycoprotein
cytokines produced by a variety of inflammatory
cells and fibroblasts that have numerous
immunologic effects. There are several
recognized interferons and they do vary in their
immunologic effects. The initial commercial
form of interferon is the recombinant human
INF alpha-2b (Roferon-A®) and more recently
Back to contents
D
a veterinary product became available. Carlotti
used recombinant feline INF-omega (Virbagen®,
Omega) has been shown helpful in an open trial
of atopic dogs. A small open pilot trial with canine
interferon gamma also suggests efficacy at high
doses.(Iwasaki, Park et al. 2005) Interferon alpha
(Roferon®) comes as a 3 million IU/ml solution
and is diluted in 999ml lactated ringers and then
divided into 30 ml ampoules that anecdotally
will remain stable if frozen. Once thawed it is
kept refrigerated for thirty days. The refrigerated
ampoule is then used at 0.33 ml, 1,000IU given
orally daily. The oral administration is done by
injecting the solution in the buccal cavity as it
is believed the absorption is from the upper oral
mucosa. Anecdotally they are cases convinced
that this low dose regimen if effective and also
have used it concurrently with allergen specific
immunotherapy. Controlled studies are needed to
see if it improves the efficacy of ASIT.
Nutraceuticals and herbal remedies are also being
evaluated in management of chronic pruritus and
atopic disease. Controlled studies and studies on
mechanism are needed. It has been suggested that
some ingredients may be helpful but since many
new diets have higher levels of omega 3 fatty
acids this may also improve these patients.
References
Bensignor, E. and T. Olivry (2005). “Treatment
of localized lesions of canine atopic dermatitis
with tacrolimus ointment: a blinded randomized
controlled trial.” Vet Dermatol 16(1): 52-60.
Iwasaki, T., S. Park, et al. (2005). Effect of
treatment with recombinant canine IFN-g on
the clinical signs, histopathology and Th1/Th2-
cytokine mRNA profiles in Shih Tzu dogs and a
Basset hound with atopic dermatitis. Advances
in Veterinary Dermatology. A. Hillier, A. Foster
and K. Kwochka. Oxford, Blackwell Publishing.
5: 82-88. 2006 World Congress WSAVA/FECAVA/CSAVA
Kobayashi, T., Y. Momoi, et al. (2006).
Cyclosporine inhibits IL-2, IL-4 and IFN-gamma
mRNA expression, but not TNF-alpha in canine
peripheral blood mononuclear cells. Nt Am Vet
Derm Forum, Palm Springs.
Marsella, R., C. F. Nicklin, et al. (2004).
“Investigation on the clinical efficacy and safety
of 0.1% tacrolimus ointment (Protopic) in canine
atopic dermatitis: a randomized, double-blinded,
placebo-controlled, cross-over study.” Vet
Dermatol 15(5): 294-303.
Olivry, T., C. Rivierre, et al. (2002). “Cyclosporine
decreases skin lesions and pruritus in dogs
with atopic dermatitis: a blinded randomized
prednisolone-controlled trial.” Veterinary
Dermatology 13(2): 77-87.
237
D
Olivry, T., J. Steffan, et al. (2002). “Randomized
controlled trial of the efficacy of cyclosporine in
the treatment of atopic dermatitis in dogs.” J Am
Vet Med Assoc 221(No 3): 370-377.
D - Dermatology
DEALING WITH MRSA IN SMALL ANIMAL PRACTICE
Professor David Lloyd
Department of Clinical
Veterinary Science
Royal Veterinary College
Hawkshead Campus
North Mymms
Hertfordshire AL9 7TA
UK
david-lloyd@ntlworld.com
Introduction
Methicillin-resistant Staphylococcus aureus
(MRSA) infection is now recognised as a
worldwide problem in human medicine.
Epidemic hospital strains (EMRSA) are a
common in human medical institutions and
strains that are distributed amongst people in
the community (community-acquired MRSA)
are being recognised increasingly. The very
broad antimicrobial resistance profile of MRSA
makes it a major hazard in human hospitals and
to vulnerable individuals in the community; it is
significant cause of human mortality.1
In 1988 colonisation of a cat with MRSA was first
recognised when in-contact patients in a geriatric
ward developed recurrent MRSA infection2 and
this case demonstrated that transfer from animals
to man could occur. There are now many reports
2006 World Congress WSAVA/FECAVA/CSAVA
documenting transfer of MRSA, most commonly
hospital EMRSA, from humans to animals,3 and
colonisation and infection of dogs and cats with
MRSA is increasingly recognised in veterinary
practice4, particularly in the USA and UK.
The consequence of the occurrence of MRSA in
domestic pets is that practitioners are now obliged
to consider more carefully 1) the possibility that
animals they are treating may be carriers or
infected with MRSA, 2) the consequences this
may have for treatment of affected animals and
3) the risks of transfer to other animals and to
veterinary staff.
Recognising MRSA Infection and Colonisation
in Dogs and Cats
Staphylococcal infection is well-recognised in
238
Back to contents
Steffan, J., C. Parks, et al. (2005). “Clinical trial
evaluating the efficacy and safety of cyclosporine
in dogs with atopic dermatitis.” J Am Vet Med
Assoc 226(11): 1855-1863.
small animal veterinary practice. Normally S.
intermedius is the cause and isolates seldom have
very broad antimicrobial resistance. The risks to
associated humans are very low. S. aureus causes
similar clinical presentations but infection in
pets is much less common. In the past, S. aureus
strains associated with pet animal infections have
often shown a broader range of antimicrobial
resistance than S. intermedius but with the advent
of highly resistant MRSA, S. aureus presents a
much greater challenge.4
In the British Isles, two reports in 2004, provided
warning that MRSA infection was becoming
a problem in small animal practice. Rich and
Roberts5 reported in 2004 isolation of 95 MRSA
from specimens submitted to a veterinary
diagnostic laboratory during 2003. In March
2004, Boag et al.6 reported an increase in cases
of MRSA infection seen at a small animal referral
hospital; 12 cases had been confirmed in dogs
and cats over the previous 5-months.
There is now increasing evidence that veterinary
staff can become colonised by MRSA at relatively
high frequencies and that transfer amongst staff
and animals in veterinary practice can readily
occur.3 Furthermore, owners of MRSA-infected
animals may be the original source of infection,
particularly if they have had contact with human
healthcare facilities, or may become colonised
by MRSA from their infected or colonised pets.
Thus animals that are susceptible to bacterial
infection, especially those being treated with
antimicrobials, are at risk of acquiring MRSA
from owners or veterinary staff and from other
MRSA-infected or colonised animals, and may

then be much more difficult or impossible to treat
effectively.
Recognition of MRSA infection in pet animals
should occur when diagnostic microbiology is
carried out on appropriate samples but this is not
always the case. Laboratories that are expecting to
isolate S. intermedius may misidentify S. aureus
particularly those strains which have very low
levels of golden pigmentation. Suspicion should
be raised if an isolate reported as S. intermedius
has a very broad resistance profile, especially if
it is resistant to cefalexin. Any case of bacterial
infection that does not respond to properly
administered antimicrobial drugs or suffers from
recurrent infections should also be suspected. If
there is doubt, the laboratory should be asked to
recheck the identity of isolates or new specimens
should be submitted with a request that checks be
made for the presence of S. aureus.
Treatment of MRSA Infection in Pets
MRSA can be very highly resistant. In some cases
there may be no antimicrobials that are effective
against them. Fortunately, isolates from animals
have generally proved to be susceptible to
potentiated sulphonamides and oxytetracycline,
and also topical products including fusidic acid
and mupirocin.3 Clindamycin sensitivity is quite
common but inducible resistance to this antibiotic
has been reported in 71% of 285 MRSA animal
isolates and screening for such inducible
resistance is recommended if clindamycin is to
be used.7
There is evidence indicating that when small
animals become infected with MRSA, the nasal
mucosae commonly become colonised. This
colonisation may persist for a substantial time.
Thus when animals are found to be infected or
colonised with MRSA, the need for decolonisation
must be considered. Otherwise the animals may
continue to pose a risk to themselves, to other
animals and to people who are in contact. No
well-established methods for decolonisation
have been described but combination of systemic
therapy with treatment of mucosal sites with
topical antimicrobials to which the MRSA is
sensitive may be effective. Fusidic acid has been
shown to be effective, at least in the short-term,
with S. intermedius.8 Treatment for about three
weeks with topical mucosal application twice or
three times daily may be effective.
Controlling Transfer of MRSA Infection in
Practice
Preliminary data indicate that owners and
veterinary staff in contact with MRSA-infected
dogs and cats may often be colonised by MRSA.
Although in healthy individuals the risk posed
Back to contents
D
by MRSA appears to be no greater than that of
methicillin-sensitive strains, the risk of transfer to
susceptible animals or people must be considered.
There is now abundant evidence that this occurs
and infection of animals under veterinary
treatment, particularly those with wounds or
subjected to surgery, has been documented. In
addition, transfer of MRSA to the environment can
readily occur and survival of such organisms in the
environment for many months is possible.9
Thus veterinary surgeons need to monitor
possible MRSA colonisation amongst their staff,
and MRSA infection and colonisation amongst
the animals they treat. Hospital hygiene methods
need to be rigorously maintained at a high level of
efficiency and when MRSA infection is recognised
or suspected, comprehensive disinfection must be
carried out. Members of staff need to be given
appropriate training so as to understand the
risks posed by MRSA and enable them to adopt
appropriate disinfection and aseptic techniques.
Isolation facilities should be reserved for infected
animals or if these cannot be supplied, strict
barrier nursing must be maintained.
In the UK, the British Small Animal Veterinary
Association has published very useful guidelines
for dealing with MRSA in small animal practice
at its website (http://www.bsava.com/resources/
mrsa/mrsaguidelines/).
References
1. APPELBAUM PC. MRSA - the tip of the
iceberg. Clinical Microbiology and Infection
2006; 12 Suppl 2: 3-10.
2. SCOTT GM, THOMSON R, MALONEY-
LEE J, RIDGWAY GL. Cross-infection between
animals and man: possible feline transmission
of Staphylococcus aureus infection in humans?
Journal of Hospital Infection 1988; 12: 29-34.
3. LOEFFLER A, BOAG AK, SUNG J,
et al. Prevalence of methicillin-resistant 2006 World Congress WSAVA/FECAVA/CSAVA
Staphylococcus aureus among staff and pets in a
small animal referral hospital in the UK. Journal
of Antimicrobial Chemotherapy 2005; 56: 692-7.
4. DUQUETTE RA, NUTTALL TJ. Methicillin-
resistant Staphylococcus aureus in dogs and cats:
an emerging problem? Journal of Small Animal
Practice 2004; 45: 591-7.
5. RICH M, ROBERTS L. Methicillin-resistant
Staphylococcus aureus isolates from companion
animals. Veterinary Record 2004; 154: 310.
6. BOAG AK, LOEFFLER A, LLOYD DH.
Methicillin-resistant Staphylococcus aureus in
small animal practice. Veterinary Record 2004;
154: 411.
7. RICH M, DEIGHTON L, ROBERTS L.
239
D
Clindamycin-resistance in methicillin-resistant
Staphylococcus aureus isolated from animals.
Veterinary Microbiology 2005; 111(3-4): 237-40.
8. SAIJONMAA-KOULUMIES L., PARSONS E.,
LLOYD, DH. Elimination of Staphylococcus
intermedius in healthy dogs by topical
2006 World Congress WSAVA/FECAVA/CSAVA
240
Back to contents
treatment with fusidic acid. Journal of
Small Animal Practice 1998; 39: 341-7.
9. WAGENVOORT JH, SLUIJSMANS W,
PENDERS RJ. Better environmental survival of
outbreak vs. sporadic MRSA isolates. Journal of
Hospital Infection 2000; 45: 231-4.

D - Dermatology
NEWLY DESCRIBED FELINE SKIN DISEASES
Peter J. Ihrke, VMD, Diplomate
ACVD
Professor of Dermatology, Chief
- Dermatology Service, VMTH
Department of Medicine &
Epidemiology
School of Veterinary Medicine
University of Kalifornia
One Shields Avenue
Davis, California 95616-8737,
U.S.A.
A. Introduction
1. Skin disease in general is less common in cats
than in dogs or humans.
2. Diagnosis of feline skin diseases may be more
challenging since feline skin seems to have a
limited number of ways to react. Both clinically
and histologically, there seem to be less classical
reaction patterns than in other species.
3. Many practitioners seem to fear feline
dermatology as ‘so many feline skin diseases look
the same’. In the past, the development of feline
dermatology was hampered by the rapid response
of many feline skin diseases to corticosteroids or
progestational compounds and the seeming safety
of these medications in cats.
4. Increased frequency of skin biopsy has allowed
the diagnosis of an increasing number of feline
skin diseases.
B. Miscellaneous Newly described feline skin
diseases
1. Feline degenerative mucinotic mural folliculitis
2. Feline paraneoplastic alopecia
3. Feline thymoma-associated exfoliative dermatitis
4. Proliferative necrotizing otitis of kittens
5. Erythema ab igne
6. Feline superficial demodicosis
C. Feline Degenerative Mucinotic Mural
Folliculitis
1. A rare, unique, presumptively immunological
skin disease of cats characterized by striking
clinical features.
2. Clinical features - diffuse, generalized alopecia
of variable severity, facial skin (especially
the muzzle) becomes alopecic, thickened,
and swollen, bilaterally symmetric, highly
characteristic thickening of the lid margins and
narrowing of the space between the eyelids. The
affected skin of the muzzle becomes shiny and
waxy, and has a rubbery feel. Scaling and crusting
may be present. Alopecia commonly begins on
Back to contents
D
the muzzle and neck, and after generalization,
becomes most pronounced on the head, neck, and
shoulders.
3. Pruritus is a feature in some cats.
4. Systemic signs - Lethargy, weight loss, general
health screening tests do not show consistent
abnormalities.
5. Histopathology – Degenerative inflammatory
mucinotic mural folliculitis.
6. Therapy – The management of this disease
has not been successful. Corticosteroid therapy
may be slightly helpful in improving mood and
diminishing lethargy
D. Feline Paraneoplastic Alopecia
1. A rare and highly characteristic skin disease
that is a marker for underlying visceral neoplasia,
usually pancreatic adenocarcinoma. This
syndrome conforms to criteria established for a
‘paraneoplastic syndrome’.
2. Clinical features - Precipitous hair loss is
the prime presenting clinical feature. Alopecia
usually commences on the ventral abdomen,
thorax, and legs before generalization. The pinnae
and periorbital regions also may be affected 2006 World Congress WSAVA/FECAVA/CSAVA
preferentially. Excessive grooming contributes
to the alopecia. Remaining hair epilates easily.
Regions of alopecia have a peculiar and highly
distinctive smooth, shiny, and glistening
appearance, even in areas that have not been
groomed. There may be adherent crusts or scale
in cats that have not groomed. The pawpads are
dry, scaly, and shiny with multiple, concentric,
circular rings of scale that give a striking targetoid
appearance. Pawpad pain may be seen. Secondary
Malassezia dermatitis may occur.
3. Cats commonly excessively self-groom inferring
pruritus.
4. Systemic signs - Signs of underlying visceral
neoplasia include lethargy, inappetence, and
weight loss. Constitutional signs may develop
in concert with skin disease or may precede it.
241
D
Lesions generally evolve rapidly over 1 to 3
months. Metastasis of the tumor to the liver or
lungs generally has occurred by the time of
diagnosis of skin disease. Most cats die or are
euthanized within a month of diagnosis.
5. Feline paraneoplastic alopecia occurs in older
cats.
6. Histopathology - Moderate to severe
acanthosis, stratum corneum absent (but when
present usually parakeratotic), cornified layer
lifts from the underlying epidermis, hair follicles
are diffusely miniaturized in telogen, dermal
inflammation commonly absent unless ulceration
is present.
7. Therapy – As mentioned above, metastasis
usually precedes diagnosis of the skin disease.
E. Feline Thymoma-Associated Exfoliative
Dermatitis
1. This is a rare feline paraneoplastic syndrome.
Exfoliative skin disease usually precedes systemic
signs associated with the underlying tumor.
Many paraneoplastic syndromes of putative
immunological basis are seen in conjunction
with thymomas in humans. The paraneoplastic
nature of feline thymoma-associated exfoliative
dermatitis has been proven by the regression
of clinical signs after surgical removal of the
neoplasm. In humans, thymomas have been
shown to generate new aberrant populations
of autoantigen-responsive, CD4+ T cells. This
disease probably is a reaction pattern indicative
of T cell-driven immunity.
2. Clinical features - Erythema and exfoliation
develop with increasing severity. Secondary
alopecia is noted. The head, neck, and pinnae
commonly are affected first, before the syndrome
generalizes. Large visually striking sheets of
exfoliated stratum corneum develop, and become
entrapped in the remaining haircoat.
3. Pruritus usually is absent, unless secondary
2006 World Congress WSAVA/FECAVA/CSAVA
yeast or bacterial infection is present.
4. Systemic signs - Coughing and dyspnea may
occur, less diagnostic systemic signs of anorexia
and lethargy may be present in advanced cases.
5. Feline thymoma-associated exfoliative dermatitis
primarily affects middle-aged to older cats.
6. Histopathology - Epidermal and follicular
apoptosis and hyperkeratosis, interface dermatitis
is invariably present, and extends to superficial
hair follicles to the level of the isthmus,
striking follicular interface inflammation with
scattered basal cell apoptosis, lymphocytes and
macrophages predominate,
7. Diagnosis is centered on identification of a
thymic mass.
8. Therapy – Skin disease regresses in early cases
after surgical removal of the thymic mass.
242
Back to contents
F. Proliferative Necrotizing Otitis of Kittens
1. Proliferative necrotizing otitis of kittens is a
rare, highly characteristic syndrome of uncertain
etiology. The syndrome is seen only in cats less
than one year of age. An immunologic basis is
suspected based on similarities to hyperkeratotic
erythema multiforme. No evidence currently
exists to link this syndrome to infectious viral
diseases. PCR testing for feline herpesvirus 1 was
negative in five cats.
2. Clinical features – The primary lesion is a well-
demarcated erythematous plaques with adherent,
thick keratinous debris. Lesions occur on the
medial aspect of the pinnae, the entrance to the
auditory canal, and the preauricular region of
the face. Lesions eventuate rapidly and coalesce.
Adherent crusts often are trapped in the hair
coat. Erosion and ulceration occur as the lesions
progress. Most lesions are asymptomatic. The
syndrome is seen in kittens between 2 months
and 6 months of age and regress, apparently
spontaneously, by 12 to 24 months. Most cases
have occurred in Domestic Shorthaired Cats.
3. Diagnosis – The syndrome is visually
distinctive. Skin biopsy is confirmative.
4. Histopathology – Striking parakeratosis
intermingled with neutrophilic crusts is present
on the surface. Scattered apoptotic keratinocytes
are present within the hyperplastic epidermis and
superficial follicular epithelium.
5. Therapy – The syndrome seems to regress
spontaneously by 1 or 2 years of age.
G. Erythema Ab Igne (Synonyms: Chronic
moderate heat dermatitis; chronic radiant heat
dermatitis)
1. ‘Erythema ab igne’ is a term borrowed from
human medicine used to describe skin disease
caused by repetitive, prolonged exposure to
chronic radiant or conductive heat. Clinically,
this syndrome is characterized by erythema and
mottled pigmentary changes. In humans, the most
commonly reported heat sources include stoves,
heating pads, steam radiators, and hot water
bottles. Predisposing factors include venous
stasis and aging. Pre-cancerous thermal keratoses
and thermal carcinomas have been reported
in humans. Reported heat sources in animals
include heating pads, heated kennel mats, electric
blankets, plant warmers, metal heat register
covers, infrared lamps, sun-heated driveways,
and cable television boxes.
2. Clinical features - Alopecia is the most
common clinical sign. Erythematous scaly or
crusted macules and plaques give rise to mottled
hyperpigmentation. Linear and intersecting
lattice-like hyperpigmentation with alopecia is
a highly characteristic feature. Lesions are seen

most commonly on the ventral or lateral chest,
abdomen, and flank and neck.
3. Diagnosis – Lesions are not particularly visually
distinctive. Clinical suspicion and exposure
history are helpful. Biopsy may be confirmatory.
4. Histopathology – A cell poor interface reaction
that features mild apoptosis of basal cells is seen.
Deeply staining basal cell nuclei (karyomegaly)
may be seen. Eosinophilic, wavy elastic fibrils
may be seen in the superficial dermis (‘Red
spaghetti of Walder’).
5. Therapy – Access to the source of chronic
radiant heat must be eliminated.
H. Feline Superficial Demodicosis
1. Feline demodicosis in general is a rare or
regional skin disease caused by at least three
different species of demodectic mites. Feline
superficial demodicosis is a contagious,
transmissible frequently pruritic generalized
skin disease caused by the surface dwelling mite,
Demodex gatoi. In comparison, feline follicular
demodicosis caused by the feline follicular mite,
Demodex cati resembles Demodex canis infection
in dogs.
2. Feline superficial demodicosis does not have a
canine counterpart. It is believed to be rare in most
of North America, but is found more commonly
in localized enzootic regions of the southern
and southeastern U.S.A. The disease may be
increasing in frequency where modern insect-
specific parasiticides that do not kill acarids are
used for flea control.
3. Clinical features - Clinical features vary from
asymptomatic alopecia to alopecia with variable
pruritus and self-trauma. If pruritus is absent, cats
can present with diffuse, bilaterally symmetric
alopecia, plus or minus scaling, affecting the
ventral and lateral trunk and caudal legs. Pruritus,
if present, usually is intense leading to erythema,
crusting and excoriation. Skin scrapings may not
yield mites or eggs in pruritic cats since excessive
grooming can remove surface-living mites. Skin
scrapings of non-pruritic cats may yield large
numbers of mites.
4. Diagnosis – Superficial skin scrapings, fecal
examination and skin biopsy all can yield
definitive diagnosis.
5. There is good evidence-based information to
recommend lime sulfur rinses (LymDyp) (2%)
weekly for the treatment of feline demodicosis.
There is fair evidence to support the use of
amitraz rinses (0.0125%) weekly.
I. General References
Scott, D.W., Miller, W.H. & Griffin, C.E. (2001)
Muller & Kirk’s Small Animal Dermatology, 6th
edn, WB Saunders Co, Philadelphia.
Back to contents
D
Gross TL, Ihrke PJ, Walder EJ & Affolter VK.
Skin Diseases of the Dog and Cat. Clinical and
Histopathologic Diagnosis. Blackwell Scientific,
2006.
Degenerative mucinotic mural folliculitis in cats
Gross, T.L., Olivry, T., Vitale, C.B. et al. (2001)
Degenerative mucinotic mural folliculitis in cats.
Vet Dermatol, 12, 279-83.
Feline paraneoplastic alopecia
Brooks, D.G., Campbell, K.L., Dennis, J.S. et al.
(1994) Pancreatic paraneoplastic alopecia in three
cats. J Amer Anim Hosp Assoc, 30, 557-63.
Heripret D. (2000) Dermatological manifestations
of systemic disease. In: A Practical Guide to
Feline Dermatology (E Guaguère, P. Prélaud),
pp. 14.1-14.10. Blackwell Science, Oxford.
McLean, D.I. & Haynes, H.A. (2003) Cutaneous
manifestations of internal malignant disease:
Cutaneous paraneoplastic syndromes. In:
Fitzpatrick’s Dermatology in General Medicine,
6th edn. (I.M. Freedberg, A.Z. Eisen, K. Wolff,
K.F. Austen, L.A. Goldsmith, & S. I. Katz), pp.
1783-1796. McGraw-Hill, New York.
Pascal, A., Olivry, T., Gross, T.L. et al. (1997)
Paraneoplastic alopecia associated with internal
malignancies in the cat. Vet Dermatol, 8, 47-52.
Tasker, S., Griffon, D.J., Nuttall, T.J. et al. (1999)
Resolution of paraneoplastic alopecia following
surgical removal of a pancreatic carcinoma in a
cat. J Sm Anim Pract, 40, 16-9.
Feline Thymoma-Associated Exfoliative
Dermatitis
Forster-Van Hijfte, M.A., Curtis, C.F. & White,
R.N. (1997) Resolution of exfoliative dermatitis
and Malassezia pachydermatis overgrowth in
a cat after surgical thymoma resection. J Small
Anim Pract, 38, 451-454.
Heripret, D. (2000) Dermatological manifestations
of systemic disease. In: A Practical Guide to 2006 World Congress WSAVA/FECAVA/CSAVA
Feline Dermatology (E Guaguère, P. Prélaud),
pp. 14.1-14.10. Blackwell Science, Oxford.
Feline Thymoma-Associated Exfoliative
Dermatitis
Forster-Van Hijfte, M.A., Curtis, C.F. & White,
R.N. (1997) Resolution of exfoliative dermatitis
and Malassezia pachydermatis overgrowth in
a cat after surgical thymoma resection. J Small
Anim Pract, 38, 451-454.
Heripret, D. (2000) Dermatological manifestations
of systemic disease. In: A Practical Guide to
Feline Dermatology (E Guaguère, P. Prélaud), pp.
14.1-14.10. Blackwell Science, Oxford.
Scott, D.W., Yager, J.A. & Johnston, K.M.
(1995) Exfoliative dermatitis in association with
thymoma in three cats. Fel Pract, 23, 4, 8-13.
243
D
Walder, E.J. & Kornet, M.E. (1999) Necrolytic
dermatitis in a cat with sclerosing thymoma. Vet
Pathol, 36, 5, 507.
Scott, D.W., Yager, J.A. & Johnston, K.M.
(1995) Exfoliative dermatitis in association with
thymoma in three cats. Fel Pract, 23, 4, 8-13.
Walder, E.J. & Kornet, M.E. (1999) Necrolytic
dermatitis in a cat with sclerosing thymoma. Vet
Pathol, 36, 5, 507.
Proliferative necrotizing otitis of kittens
Gross TL, Ihrke PJ, Walder EJ & Affolter VK.
Skin Diseases of the Dog and Cat. Clinical and
Histopathologic Diagnosis. Blackwell Scientific,
2006.
Erythema Ab Igne
Schwartz R.A. & Stoll H.L. (1999) Epithelial
precancerous lesions. In: Dermatology in General
Medicine (I.W. Freedberg, A.Z. Eisen, K. Wolff,
K.F. Austen, Goldsmith L.A., & T.B. Fitzpatrick),
pp. 823-39. McGraw-Hill, New York.
Walder, E.J. (1994) Chronic radiant heat dermatitis
in a dog. 10th Proceedings of the AAVD/ACVD
Meeting, Charleston, South Carolina, p 70
(abstract).
Declercq, J. & Vanstapel, M.-J. (1998) Chronic
radiant heat dermatitis (erythema ab igne) in two
dogs. Vet Dermatol, 9, 269-75.
2006 World Congress WSAVA/FECAVA/CSAVA
244
Back to contents
Walder, E.J. & Hargis, A.M. (2002) Chronic
moderate heat dermatitis (erythema ab igne) in
five dogs, three cats and one silvered langur. Vet
Dermatol, 13, 283-92.
Schwartz, RA (1996) Premalignant keratinocytic
neoplasms. J Am Acad Dermatol, 35, 223-42.
Feline Superficial Demodicosis
Beale, K.M. Contagion and occult demodicosis in
a family of 2 cats. 14th Proceedings of the AAVD/
ACVD Meeting, San Antonio, Texas, 1998, p 99
(abstract).
Morris DO, Beale KM. Feline demodicosis. In
Bonagura JD (ed): Kirk’s Current Veterinary
Therapy XIII, Philadelphia, WB Saunders
Company, 2000, p 580.
Mueller RS. Treatment protocols for demodicosis:
An evidence-based review. Vet Derm 2004 15:75-
89.
Gross TL, Ihrke PJ, Walder EJ, Affolter VK:
Skin Diseases of the Dog and Cat: Clinical and
Histopathologic Diagnosis. Blackwell, Oxford,
pp 222-225, 2005.
Back to contents
D

2006 World Congress WSAVA/FECAVA/CSAVA

245
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

De
D
ntistre
Dentistry
y

Back to contents

INVITED LECTURES - FULL PAPERS
De - Dentistry
BIOFILM: MICROBIAL COMMUNITIES AND PERIODONTAL
DISEASE
Prof. Dr. Zlatko Pavlica DVM
University of Ljubljana
Veterinary Faculty
Ljubljana
Slovenia
Zlatko.Pavlica@vf.uni-lj.si
Introduction
Throughout life, all the interface surfaces of the
body are exposed to colonization by a wide range
of microorganisms. In general, the establishing
microbial population size is restricted by the
microenvironmental conditions and the organisms
live in harmony with the host. In the oral cavity,
however, teeth provide a permanent, moist, non-
shedding surface on which extensive bacterial
deposits can develop. The accumulation and
metabolic activity of these deposits, i.e. bacterial
plaque, is considered the primary cause of dental
caries, gingivitis, periodontitis and stomatitis.
Understanding the nature of plaque, how it forms
and matures assists in the treatment and control
of these diseases. Knowing that dental plaque is
a biofilm adds to understanding its nature. Over
the past few years, biofilm has been extensively
studied due to its importance in both general
environmental management and in medicine, both
of which have major implications for human and
animal health. Elucidation of biofilm dynamics is
pertinent to both veterinary and human dentistry,
improving our understanding of the nature of
plaque 1,2.
It has been estimated that more than 99% of all
the planet’s bacteria live as adherent biofilm under
conditions very different from those provided in
laboratory environments. This is not surprising
as living in a biofilm is highly advantageous to
the organisms present. They are protected from
extreme conditions by the external “slime”
matrix they secrete and they can cooperate to
make maximal use of available resources. This
protection and cooperation confers increased
resistance to the effects of antimicrobial
agents, hence the poor response to antibiotics
of infections involving biofilms. It is therefore
encouraging that researchers are now cultivating
dental plaque organism in biofilms in constant
Back to contents
De
depth film fermenters as this method should more
accurately predict clinical response of plaque to
antimicrobial drugs3.
Formation of biofilms
The first bacteria to attach to a smooth surface attach
either via their glycoclyx mucopolysaccharides or
by electrostatic forces. Once bacteria stick, they
also begin producing hemoserine lactone, which
acts as a communication signal stimulating other
free-roving bacteria to produce sigma factors
that activate genes that stimulate them to join the
community4. Next, new arrivals of varied genus
and species of bacteria, many of which produce
fibrillar polysaccharide exopolymers, form a thick
slime layer. New sigma factors also cause the
expression of genes needed for communal living,
and the suppression of other genes, which were
needed during their prior planktonic existence.
They are now phenotypically distinct from their
planctonic counterparts5.
The biofilm bacteria act very much like tissue cells
of multicellular organisms, in which the wider
needs of the community take precedence over
2006 World Congress WSAVA/FECAVA/CSAVA
those of the individual. Its neighbours as nutrients
use toxic wastes produced by one species. Non-
useful wastes are transported away by circulating
fluids. The cells’ biochemical resources are pooled,
allowing the community to use varied enzyme
systems to break down potential food supplies
that are otherwise unavailable to the individual
organisms. Communication, cell specialization,
and a basic circulatory system are all present in
biofilms. Biofilms even have their own predators,
internal and external parasites in the form of
bacteriophagic amoeba and nematodes. Many
bacteria can only be grown in culture when others
are included to provide required nutrition’s. This
characteristic is similar to an organ that cannot
survive outside its supporting organism. Biofilm
247
De
communities are units of existence, activity,
ecology, proliferation, survival and evolution6.
Within a biofilm, the surrounding slime matrix
effectively protects its resident bacteria from
antimicrobial drugs. The exact nature of this
protection remains unclear. The matrix is difficult
to dissolve, and resident bacteria can develop
resistance to antimicrobial drugs by producing
more polysaccharides to form a thicker layer.
The matrix itself may mechanically protect
bacteria against desiccation, bacteriophages,
amoeboid predators, protozoa, and immune
system clearance. The mechanism of hindrance
of antimicrobial drugs remains unclear, but may
involve a neutralizing ability rather than or in
addition to inhibition of diffusion. The bacteria
themselves, although genetically identical to
their planctonic counterparts, make use of a
very different biochemistry due to their newly
expressed set of genes. As many as 30-40% of
bacterial cell wall proteins differ, sometimes
eliminating antimicrobial target sites. Their
lower metabolic activity and slower absorption
of environmental factors increase the chances
they can acquire enhanced resistance to chemical
antimicrobial compounds. Biocide rinses,
including powerful chlorine-based disinfectants
and bleach solutions, are largely ineffective
and could even select for resistant organisms.
A disinfectant may need to be 1000 to 500,000
times more concentrated to kill the bacteria in
biofilms than in a monoculture, and bacteria in
biofilms can be up to 1500 times more resistant
to antimicrobial drugs than the same bacteria in
a single colony. However, simple mechanically
disruption of the biofilm, as occurs if their
substrate is wiped with a brush or other abrasive
material, can easily disperse the organisms and
make them susceptible7.
Significance of biofilm behaviour in plaque
2006 World Congress WSAVA/FECAVA/CSAVA
control
Dental pellicle, a thin clear layer of glycoprotein
deposited from saliva and gingival crevicular
fluid, adheres to mineralised tooth surfaces
within minutes after cleaning. This facilitates the
attachment by the pioneering species of bacteria
that start the biofilm (plaque) formation. These first
bacteria are typically gram-positive organisms,
often Actinomyces spp. and streptococci. As the
biofilms thickens and matures, the community
attracts new residents and provides an environment
that is conducive to the growth of anaerobes and
gram-negative organisms. As with other biofilms,
mechanical disruption remains the best method of
removing plaque. Although once or twice daily
tooth brushing of pets’ teeth by their owners
may be ideal, this may sometimes be difficult or
248
Back to contents
impractical. A method that enhances the abrasive
dental self-cleaning that occurs when an animal
chews fibrous foods can be very helpful. Various
dietary factors can influence the accumulation of
plaque and the calcified residue of dead plaque,
i.e. calculus. Food particle size, shape density,
moisture level, fibre content and source can
all have an influence. Abrasive diets are more
successful in some individuals and certain teeth
than others due to variability in occlusion, tooth
crowding, and eating habits8.
The realization that plaque is a biofilm helps us
understand its formation, development, removal,
and control. Since plaque bacteria are protected
physically and metabolically from disinfectants
and antibiotics, mechanical removal represents
the best method of control.
Microbial destructive processes of periodontium
Periodontal disease is initiated and sustained by
factors produced by the subgingival microbiota.
Microbial biofilm accumulation on the surface
of teeth adjacent to the gingival tissues brings
the oral sulcular and junctional epithelial cells
into contact with the waste products, enzymes,
antigens, toxins and surface components of
colonizing bacteria. Some of these substances
can directly injure host cells and tissues. Other
microbial constituents may activate inflammatory
or cellular and humoral immune systems, which
secondarily damage the periodontium. It is
the latter pathway, which accounts for most
periodontal injury5,6.
Plaque microorganisms may damage cellular and
structural components of the periodontium via
release of their proteolytic and noxious waste
products. As well as the formation of noxious
substances by the microbiota of the gingival
pocket, microbial invasion of soft tissues should
be considered. Invasion of the dentogingival
epithelium by spirochetes has been conclusively
documented in acute necrotizing ulcerative
gingivitis3.
Microorganisms produce a large variety of
soluble enzymes in order to digest extracellularly
host proteins and other molecules and thereby
obtain nutrients for growth. They also release
numerous metabolic products, such as ammonia,
indole, hydrogene sulfide and butyric acid.
Among the enzymes released by bacteria are
proteases capable of digesting collagen, elastin,
fibronectin, fibrin and various other components
of the intercellular matrix of epithelial and
connective tissues.
The effect of many structural, enzymatic and
waste products is to stimulate, probably noxiously,
host cell cytokine production. The cytokines thus
produced are predominantly pro-inflammatory

and possess multiple effects, which serve to
enhance the inflammatory response. They also
enhance matrix metalloproteinase activity as well
as recruiting leucocytes to the area4,5.
Microbes are capable of producing a variety of
substances, which either directly or indirectly
harm the host. The main detrimental effect,
however, may be the host’s own immune response
to the foreign microbial antigens1.
References:
1. Lang NP, Mombelli A, Attstrom R. Dental
plaque and calculus. In: Clinical periodontology
and implant dentistry. Lindhe J, Karring T, Lang
NP eds. 3rd ed, Munksgaard, 2002, pp. 102-34.
2. Jensen I, Logan E et al. Reduction in
accumulation of plaque, stain, and calculus in
dogs by dietary means. J Vet Dent 1995; 12: 161-3.
3. Williams JF, Molinari JA, Andrews N.
Microbial contamination of dental unit waterlines:
Back to contents
De
Origins and characteristics. Compend Cont Educ
Dent 1996;17:538.
4. Shearer BJ. Biofilm and the dental office. J Am
Dent Assoc 1996;127: 181-9.
5. Costerton JW, Lewandowski Z, Caldwell DE
et al. Microbial biofilms. Ann Rev Microbiol
1995;49: 711-45.
6. Gorrel C, Rawlings JM. The role of tooth
brushing and diet in the maintenance of
periodontal health in dogs. J Vet Dent 1996;13:
139- 43.
7. Greenfield JI, Sampath L et al. Decreased
bacterial adherence and biofilm formation
on chlorhexidine and silver sulfadiazine-
impregnated central venous catheters implanted
in swine. Crit Care Med 1995;23: 894-900.
8. Rateitschak KH. Color atlas of dental medicine.
Periodonology.New York, Thieme, 1989.
2006 World Congress WSAVA/FECAVA/CSAVA
249
De
De - Dentistry
PERIODONTAL MEDICINE
Prof. Dr. Zlatko Pavlica DVM
University of Ljubljana
Veterinary Faculty
Ljubljana
Slovenia
Zlatko.Pavlica@vf.uni-lj.si
The presence of systemic disease
The presence of systemic disease in dogs with
chronic periodontal disease has been suggested
as an co-factor in various other diseases,
particularly respiratory disease, cardiac disease,
atherosclerosis, hepatic disease, renal disease and
low birth weight1,2,3. In most cases there is as yet
no conclusive proof of a direct link, but there are
multiple plausible explanations for such links4.
Frequent bouts of bacteraemia and endotoxaemia
occur due to minor trauma at sites of periodontal
inflammation.Those bacteria that survive within
the circulation may cause infection or stimulate
inflammation and disease at distant sites.Any
individuals with defective defence mechanisms
are likely to be predisposed to distant and
systemic effects of periodontal disease due to
increased invasion by micro-organisms and
both more severe bacteraemia and greater local
production of cytokines5.
Respiratory disease
Bacteria from the oral cavity may cause
respiratory infection on many different ways6.The
most common is aspiration of saliva containing
pathogenic bacteria from oral cavity to the
lungs. Periodontal pathogens release enzymes
2006 World Congress WSAVA/FECAVA/CSAVA
and other factors that promote tissue adhesion
and invasion both in the oral cavity and at other
sites such as respiratory epithelia. Cytokines that
are released in inflammation process in the oral
cavity enter the systemic circulation and affect
distant sites, including the respiratory epithelium
which is altered to become more susceptible to
establishment of infection and its progression.
Periodontal pathogenic bacteria cause the release
of cytokines IL-1,IL-6,IL-8 and TNF-α from
the tissues of the respiratory tract, particularly
endothelial and connective tissue cells7.These
proinflammatory cytokines attract inflammatory
cells and activate neutrophils,which tend to
degranulate causing further tissue damage.
Respiratory diseases and chronic obstructive
pulmonary disease are quite common in dogs. The
250
Back to contents
numbers of organisms involved in periodontal
disease is phenomenal so the likelihood of
occasional aspiration of sufficient pathogens to
permit development of infection is high. Even
if common respiratory diseases are not caused
by aspiration of, or bacteraemia with, oral
pathogens, their effects are likely to influence the
development and progression of such diseases.
Cardiovascular disease
It has been recognised that periodontal disease is a
significant risk factor for development of cardiac
disease, thromboembolism and stroke, which
are still the leading causes of death in people.
Anaerobic bacteria, such as Porphyromonas
gingivalis, that enter the circulation activate
thrombocytes resulting in their aggregation
and obstruction of small blood vessels, which
for example can result in insufficient flow
through coronary arteries.Such bacteraemias
may also cause degenerative changes on heart
valves, coronary and other vessels, endocarditis,
myocarditis or endocardiosis as well9,10.
Inflammatory periodontal disease is believed
to be one of the factors in development of
atherosclerosis8. P. gingivalis has been isolated
from atheromas of carotid and coronary artery,
and has been cultivated in vitro or identified by
PCR in the endothelium cells of endocardium
and aorta11.Patients with periodontal disease and
atherosclerosis often have a common genetically
determined phenotype of hyperinflammatory
monocytes, which in contact with endotoxins (of
periodontal and other gram negative microflora)
release increased amounts of IL-1, PGE2 and
TNF-α: cytokines which accelerate development
of atherogenesis and thrombosis.
Cardiovascular disease of various types is
frequently identified in dogs, particularly those
older than ten years of age, i.e. animals that are
likely to have had periodontal disease for many
years. Miniature and toy breeds are a risk group
for development of both cardiovascular and
periodontal disease and it is suspected that there

may be genetic factors involved as there are in
people. The most common pathology in a recent
necropsy study of small poodles was chronic
degeneration of the heart valves and swellings in
the wall of coronary vessels in all cases. It cannot
be excluded that in dogs with periodontal disease
and endocardiosis there is concurrent impairment
of microcirculation, leading to capillary
rarefication and subsequent ischemia of the
periodontium and myocardium, predisposing to
periodontal disease and endocardiosis occurring
in parallel, as seen in man8. A further pathway
that may link periodontal and cardiac disease is
the influence of systemic inflammatory mediators
on the myocardium. It has been shown that pro
– inflammatory cytokines such as TNF α and IL
– 6 may cause anabolic changes in the myocytes
through the activation of intracellular signaling,
which leads to hypertrophy of the myocardium8.
Liver disease
Extrahepatic bacterial infections that are
associated with bacteraemia can cause intrahepatic
cholestasis, and both parenchymal inflammation
and portal fibrosis have been associated with
periodontal disease in dogs2. The level of
histopathological changes in the poodle livers
in the above mentioned study was statistically
significant according to gender. In male dogs
there was typically a moderate focal or diffuse
inflammation and/or mild focal or multifocal
fibrosis. In female dogs there were milder changes,
primarily diffuse parenchymal or portal system
inflammation. It is speculated that the difference
in liver pathology between genders is connected
with the greater total dental circumference, and
consequently a larger average area of periodontal
disease burden in the male population. Combined
mild mononuclear infiltrates of portal tracts,foci
of liver cells surrounded by neutrophils and
macrophages, and mild hepatocellular vacuolar
change were common findings. These changes,
which are indicative of current or recent immune
stimulation, can occur secondarily to a wide
variety of extrahepatic disorders, such as chronic
disease anywhere in the gatsrointestinal tract
including the oral cavity12. As the oral cavity was
the only site with gross evidence of inflammation
in the studied animals, it is likely that the oral
inflammation was a significant factor even if not
the primary cause. It is considered likely that the
significant correlation found between periodontal
disease burden and liver pathology is an accurate
indicator of the tendency for one or more of
LPS from Gram negative periodontopathogenic
bacteria,intact bacteria filtered from the
circulation during bacteraemia,and inflammatory
cytokines absorbed from periodontal lesions to
Back to contents
De
activate the defensive cells of liver parenchyma
resulting in the hepatic pathology.
Kidney disease
Pyelonephritis and interstitial nephritis may also
result from bacteraemia related to oral infection
in dogs. Immune mediated kidney disease,
particularly glomerulonephritis, is also considered
to be a potential consequence of chronic low-
grade bacteremia associated with periodontal
disease2. Glomerular localization of exogenous
antigens occurs in bacteraemia associated with
periodonto-pathogenic bacteria. These bacteria
appear to have an affinity for endothelium and
serum filtration in the kidneys will increase the
likelihood of glomerular capillary walls being
affected. Bacteria, free LPS and other antigens
react with specific immunoglobulins to form
immune complexes either locally within the
kidney or in the circulation with deposition
of complexes in the glomeruli associated
with the process of serum filtration as urine is
produced13,14. Once formed, immune complexes
activate complement and stimulate production
of bioactive mediators such as cytokines,
eicosanoids, growth factors and nitric oxide. They
also stimulate mesangial cell proliferation and
the production of the intracellular microfilament
actin α SMA and extracellular matrix proteins.
The glomerular and interstitial changes seen
in necropsy studies of periodontal disease
susceptible dogs are suggestive of immune
complex- mediated damage, though this is yet to
be confirmed. However, The strong correlation
found between periodontal disease burden and
extent of renal pathology suggest that periodontal
disease contributes to the development of these
lesions, most likely through chronic, persistent or
repetitive insult to the kidney.
References:
1. Beck DJ, Slade GD, Offenbacher S. Oral
2006 World Congress WSAVA/FECAVA/CSAVA
disease, cardiovascular disease and systemic
inflammation. Periodontology 2000; 23: 110
– 120.
2. DeBowes LJ. The effects of dental disease
on systemic disease. In: Holmstrom SE, (ed).
Canine Dentistry – The Veterinary Clinics of
North America. Saunders, Philadelphia, 1998:
1057-1062.
3. Mehta JL, Saldeen TGP, Rand K. Interactive
role of infection, inflammation and traditional
risk factors in atherosclerosis and coronary artery
disease. J Am Coll Cardiol 1998; 31: 1217-1225.
4. Renvert S, Wirkstrom M, Mugrabi M, Claffey
N. Histological and Microbiological Aspects of
Ligature-induced
251
De
Periodontitis in Beagle Dogs. J Clin Periodontol
1996; 23: 310-319.
5. O’ Reilley PG, Claffey NM: A history of oral
sepsis as a cause of disease. Periodontology 23:
13 – 18, 2000.
6. Scannapieco FA: Systemic Effects of
Periodontal disease. Dent Clin N Am 49: 533
– 550, 2005.
7. Wilson M, Reddi K, Henderson B. Cytokines
– inducing components of periodontopathogenic
bacteria. J Periodontal Res 1996; 31: 393 – 407.
8. Franek E, Blach A, Witula A, Kolonko A,
Chudek J, Drugacz J and Wiecek A. Association
between Chronic periodontal Disease and Left
Ventricular Hypertrophy in Kidney Transplant
Recipients. Transplantation 80: 3-5, 2005.
9. Nieto JF. Infections and atherosclerosis: New
clues from an old hypothesis? Am J Epidemiol
1998; 148: 937 – 948.
10. Offenbacher S, Madianos PN, Champagne
2006 World Congress WSAVA/FECAVA/CSAVA
252
Back to contents
CME, Southerland JH,Paquette DW,Williams RC,
Slade G, Beck JD. Periodontitis- atherosclerosis
syndrome: an expanded model of pathogenesis. J
Periodont Res 1999; 34: 346-352.
11. Haraszthy VI, Zambon JJ, Trevisan M, Zeid
M, Genco RJ. Identification of periodontal
pathogens in atheromatous plaques. J Periodontol
2000; 71:1554-1560.
12.Taboada J, Meyer DJ. Cholestasis associated
with extrahepatic bacterial infection in five dogs.
J Vet Intern Med 1989; 3: 216 – 220.
13. Cook HT and Sullivan R. Glomerular
nitrite synthesis in in situ immune complex
glomerulonephritis in the rat. Am J Pathol 1991;
139: 1047 – 1052.
14. Ortiz A, Gomez- Chiarri M, Lerma JL,
Gonzales E, Egido J. The role of platelet- activating
factor (PAF) in experimental glomerular injury.
Lipids 1991; 26: 1310- 1315.

De - Dentistry
ORAL DIAGNOSIS – CLINICAL APPROACH
Dr. David Crossley
Animal Medical Centre
511 Wilbraham Road
Manchester M24 5AJ
UK
wsava2006@dacross.net
Many conditions affect the oral cavity and the
teeth. Many surveys have been undertaken
looking at the incidence of various oral and dental
conditions in pets, most showing high levels of
disease: 60% to 80% of middle aged and older
cats and dogs presented in small animal practices
having sufficient disease to warrant immediate
professional treatment. The most frequent disease
seen is periodontitis associated with bacterial
plaque and calculus build-up. Traumatic lesions
are also quite frequent, but other problems are
much less frequent. All conditions require a
thorough diagnostic work-up.
Oral Diagnosis
There are many anatomical and physiological
variations between species and breeds. These
features need to be known before it is possible
to decide whether what is present is normal or
not, i.e. to diagnose health or disease during
either the initial conscious examination or the
later definitive examination which needs to be
undertaken under general anaesthesia.
The oral cavity
a. Soft tissues may be completely pigmented,
partially pigmented or unpigmented.
b. Lips. Clear distinction between haired skin
and the smooth hairless keratinised stratisfied
squamous external lip epithelium. Lip epithelium
merges with oral lining epithelium.
c. Oral lining mucosa. This is the highly sensitive
covering of the insides of the lips and cheeks, is
also found on the floor of the oral cavity and under
surface of the tongue. It is a loosely attached
unkeratinised stratisfied squamous epithelium
with a smooth moist surface. There are multiple
minor salivary glands beneath its surface. The
major salivary gland duct openings pass through
it: mandibular and sublingual caruncle lateral
to frenulum, zygomatic and parotid papillae on
buccal surface opposite maxillary carnassial and
first molar. There is a distinct “muco-gingival
line” separating it from the gingiva.
Back to contents
De
d. Gingiva and palate. The gingiva is a firmly
attached and relatively insensitive keratinised
epithelium found adjacent to the teeth. Its surface
is slightly pitted like orange skin. A similar
but ridged epithelium covers the hard palate.
There is frequently inflammation at the gingival
margin where it contacts the teeth. In true health
the gingival margin is attached to the tooth by
hemidesmosomes. In practice this is unlikely to
be the case as inflammation and some swelling is
normally present leading to creation of a gingival
sulcus. Progression of disease may result in loss
of gingiva or periodontal detachment.
e. Teeth. The enamel of the tooth crowns should
be smooth and near white without surface
deposits. Adult dogs typically have 42 adult
teeth (6 incisors, 4 canines, 16 premolars and
10 molars). These should all be fully erupted by
about 9 months of age. Cats have evolved to have
a reduced number of teeth, their dentition being
adapted to a truly carnivorous diet. The 28 teeth
typically present in adult cats are made up of 6
incisors, 4 canines, 10 premolars and 4 molars.
f. Occlusion. The teeth are normally arranged
so that those in the maxilla and mandible
come together in a functional arrangement.
The conformation of many breeds disturbs this
arrangement. 2006 World Congress WSAVA/FECAVA/CSAVA
Recognition of disease
When the normal and its variations can be
recognised, disease can be diagnosed. The
animal’s history and presenting signs need to be
considered, but an oral examination is essential.
The initial examination is generally performed on
a conscious patient. The extent of this will vary
with species and temperament, but even in the
most cooperative animal of a species that can open
its mouth wide it is still not possible to complete a
full examination as this requires exploration and
probing which are potentially painful. In addition,
radiography is essential for determination of the
extent of sub-epithelial dental/jaw disease.
253
De
Disease patterns
The most frequent oral disease is periodontal
disease. This encompasses gingivitis and
periodontitis and may progress to extensive tissue
damage and destruction. Whilst the accompanying
redness and swelling is usually clearly visible
in gingivitis, periodontal involvement may be
hidden, hence the need to probe for areas of
lost tooth attachment to the adjacent bone. As
periodontal disease is on the vast majority of
cases related to bacterial plaque deposits on the
tooth surfaces, and bacterial growth conditions
are generally bilaterally symmetrical, the pattern
of disease is expected to be nearly symmetrical
though one side may be affected to a greater
degree than the other.
Diagnosing oral disease
As with other areas of medicine, oral diagnosis
involves obtaining a basic database on the patient,
obtaining the clinical and management history
from the client and determining the reason for
presentation. This may not be the reason stated
by the client as it is quite common for owners to
be concerned about something else, for example
the possibility of “cancer” or they may be
embarrassed about the problem the animal has.
Once a history is available a routine physical
examination is required. This should not
concentrate on the primary problem until a
general health assessment has been performed
unless the primary problem is life threatening.
Once the general examination is completed a
closer examination of the oral cavity is indicated.
It is very important to inform clients that it is
not possible to adequately assess this area in a
conscious animal (poor visibility, poor patient
compliance, need to explore and probe dentition
2006 World Congress WSAVA/FECAVA/CSAVA
254
Back to contents
plus need for radiography to assess tooth roots and
supporting bone etc.). The conscious examination
may be sufficient to make a diagnosis. But it will
not be a complete diagnosis and should generally
be considered as provisional and needing
confirmation.
After discussing differential diagnoses, what
further investigations are needed and the
likely treatment requirements with the owner,
arrangements should be made for more definitive
examination under general anaesthesia. With the
patient anaesthetised and the airway secured with
an endotracheal tube the detailed definitive oral
examination can be performed and the results
recorded. There are many types of dental chart
available from many sources. (Examples are
available for free download from the download
page at www.dacross.com.) Use of dental charts
(plus radiographs and photographs) makes record
keeping and explanation of findings to clients
easy. Client satisfaction can be greatly enhanced
by giving them a copy of the dental chart and
an appropriate information leaflet concerning
the condition their pet has and how to manage/
control/prevent recurrence of it.
Treatment and follow-up
Once a diagnosis has been made it is possible to
plan treatment appropriately. Unfortunately we
do not always get the diagnosis correct! Follow-
up of cases is extremely important so that we
can check that there is an appropriate response
to treatment, and in the longer term that control
measures for prevention of recurrence have
been effective. Should the patient not respond to
treatment as expected or further signs appear the
whole cycle of examination and diagnosis needs
to be repeated:

Reference sources used and suggested further
reading
Bojrab & Tholen. Small Animal Oral Medicine
and Surgery. Lea & Febiger 1990
Crossley & Penman (eds) (1996) BSAVA Manual
of Small Animal Dentistry. BSAVA, Cheltenham
Harvey & Emily. Small Animal Dentistry. Mosby
1993
Linde. Textbook of Clinical Periodontology.
Munksgaard 1983
Marx RE, Stern D. Oral and Maxillofacial
Pathology: A Rationale for Diagnosis and
Back to contents
De
Treatment. Quintessence Publishing 2002
Page, Schroeder. Periodontics in man and other
animals. Karger 1982
Ten Cate AR. Oral Histology: Development,
Structure and Function, fifth edition. Mosby, St
Louis 1998
Wiggs RB, Lobprise HB, Veterinary Dentistry:
Principles and Practice. Lippincott - Raven,
Philadelphia 1977
2006 World Congress WSAVA/FECAVA/CSAVA
255
De
De - Dentistry
ORAL DIAGNOSIS: RADIOGRAPHY AND RADIOLOGY

Dr. David Crossley

Animal Medical Centre
511 Wilbraham Road
Manchester M24 5AJ
UK
wsava2006@dacross.net

Introduction Root deformity

Radiography is indispensible to human medicine Root fracture
and dentistry. It is an established part of general Root resorption
veterinary medicine, but unlike human dentists, Supernumerary teeth
vets seem reluctant to use this essential tool c. Recognition of other oral pathology:
routinely for dental assessment. Clients expect Abscesses
a high level of service from our profession. Bone atrophy
This requires that suitable investigation such as Craniomandibular osteopathy
radiography is undertaken prior to therapy. As Foreign body
tooth roots, the largest part of most teeth, and Metabolic bone disease
their associated support structures are hidden Orthodontic assessment
within the jaws we cannot complete a dental Osteomyelitis
examination without radiography, so why is it not Pathological fracture
even offered by many practices as part of their Traumatic injury
dental service? Tumours
Concern relating to monetary cost is a possible
reason, but this is for the client to decide, not the Not knowing all the facts about a case can put
vet. Another reason for failure to perform dental the patient at risk! Advanced periodontal disease
radiography and radiology is the assumption is common and leads to loss of alveolar bone.
that it is difficult. Well possibly it is, but so The only practical way to assess this in general
are radiography and radiology of the general practice is by radiography. Failure to identify
skeleton, yet it is rare for orthopaedic surgery to cases with advanced bone loss commonly leads
be undertaken without radiographic control. to iatrogenic jaw fracture due to improper
handling during examination and treatment. The
Table 1: Indications for oral radiography timing of radiography during examinations can
a. Identification of normal features: be varied. In cases with indications of advanced
periodontal lesions the best time is immediately
2006 World Congress WSAVA/FECAVA/CSAVA

Anatomical variation
Deciduous tooth root resorption on induction of anaesthesia, the latter being done
Differentiation between with extremely gentle handling and avoidance
Presence of permanent dentition pre eruption of applying pressure to the mandibles. In cases
Tooth root development with minimal periodontal involvement it may
be appropriate to wait until after scaling and
b. Recognition of dental pathology: polishing of the teeth so that the oral cavity is
Avulsion or luxation clean and a more pleasant area to work in. In
Caries or resorptive cavities many cases further radiographs are required at
Crown fractures different times during a procedure to complete
Delayed tooth eruption a diagnosis, investigate new findings or monitor
Developmental abnormalities treatment progress.
Endodontic assessment
Monitoring treatment Oral Radiography
Periodontal abscessation Obtaining diagnostic radiographs of oral
Periodontal bone loss structures is sometimes complicated by their
Periapical pathology anatomical arrangement, but by applying the
Retention of deciduous teeth basic principles used with radiography in other
256
Back to contents

areas, the crowns, roots and supporting alveolar
bone of almost all teeth can be demonstrated
clearly in dogs and cats. It is a little more difficult
in herbivores due to their longer oral cavities,
longer teeth and limited oral opening.
At least two views are needed in order to
adequately assess three dimensional anatomical
structures. In the mandible there is limited space
for hidden abnormalities medial and lateral to the
teeth so a single view will demonstrate the majority
of lesions. Even in the maxilla, with use of intra-
oral film placement to minimise superimposition
of other structures on the image, a single view
is often all that is required to confirm anatomical
relationships and locate pathology. Additional
films are readily obtained using a differing view
for the identification and specific localisation of
suspect lesions once their presence is known. The
occlusal view (with the x-ray beam directed along
the length of tooth roots) is particularly useful for
locating retained root tips.
In order to obtain a realistic image of the subject,
it should generally be positioned close to and as
near parallel to the film as possible, with the central
x-ray beam perpendicular to the film, ie. using
“parallel technique. With long bone radiography
this is usually straightforward, but is much less so
for most teeth. In the carnivores, only the caudal
mandibular premolars and molars can be imaged
in this manner. The bisecting angle method is
an alternative for use when parallel positioning
is not practical. In this technique the x-ray beam
is directed perpendicular to a line which bisects
the angle between the long axis of the object
being imaged and the film plane. The bisecting
angle technique makes use of the geometry of the
isosceles triangle, the two halves of which have
the same dimensions giving the image the same
length as the object being imaged. The image
will show increasing magnification of those parts
further from the film so the image is not a perfect
representation of the teeth.
Whilst it is possible to use a conventional x-ray
machine for dental radiography, it is much easier
if a dental x-ray machine is used. When dental
radiography is integrated into dental procedures
(it should be considered essential not optional)
the frequent use of the machine will rapidly
pay for its purchase and maintenance allowing
it to become a profit centre for the veterinary
practice.
Obtaining good radiographs
Radiologists have individual preferences
regarding x-ray images, some prefering light
films, others dark ones. As there is a reasonable
range of image densities which provide sufficient
contrast and definition for film assessment the
Back to contents
De
actual image density is unimportant providing
the film is of diagnostic quality. Guidelines for
producing radiographs of this standard are given
in Table 2.
Table 2. Guidance on obtaining diagnostic dental
radiographs
Immobilise the patient as even a small
movements will lead to blurring of the image.
Dental radiography, as with thorough intra-oral
examination, requires general anaesthesia so the
two can be performed at the same time.
Position the patient, film and x-ray machine to
demonstrate the features of interest. As mentioned
above, a dental x-ray machine simplifies
positioning.
Use a film or film/screen combination to provide
optimum definition whilst minimising exposure.
Use the appropriate x-ray exposure for the
area under investigation. Exposures can be
varied a little to satisfy the radiologist‘s density
preferences.
Process the film correctly and ensure that
subsequent handling and storage are meticulous
to maximise final image quality and longevity
(see appendix 1).
Suitable viewing conditions are almost as
important as correct exposure and processing.
The best method of viewing radiographs is to
work with subdued room lighting. Avoid looking
at bright light sources for several minutes prior
to examining radiographs. The film is placed
on a viewing box and the area around the film
collimated to cut out unwanted light prior to
switching on the illumination. A bright area
adjacent to the film will tend to dazzle the viewer
significantly reducing ability to resolve fine detail
and subtle changes. The light intensity should be
varied according to the film density in the area of
interest, particularly dark areas on a film being
viewed with bright spot illumination, just the
same as in general radiology. Ones eyes need
2006 World Congress WSAVA/FECAVA/CSAVA
to dark adapt to the level of light transmitted
through the film so a quick glance will not suffice.
In dentistry the assessment of fine detail such as
suspected root resorption in cats requires the
additional use of magnification (Figure 6).
Dental radiographic film
Dental radiographic film is non-screen film cut to
appropriate sizes for use in the human oral cavity.
There are different “speeds” of dental film.
The slower Ultraspeed films have the highest
exposure latitude and finest grain. Ektaspeed
film requires only half the exposure (having a
thicker emulsion) but has a lower contrast range
and larger silver grain size and is less tolerant of
exposure and processing errors. Recently even
257
De
faster films have been introduced with the aim of
reducing patient exposure, but these also require
very precise exposure and processing to get the
best results. Digital dental radiography systems
have been introduced. These require a lower
exposure than film systems but most of those
in general use have a much lower resolution.
A big advantage is the ability to manipulate
image contrast, brightness and magnification for
viewing. With modern digital cameras the same
effects can be achieved by viewing photographs
of conventional films on a computer.
Three sizes of dental film are in common use
in veterinary dentistry: paediatric periapical eg.
Kodak DF54 (22 x 35 mm), standard periapical
eg. Kodak DF58 (31 x 44 mm), and occlusal eg.
Kodak DF 50 (57 x 75 mm). Human dentists use
several other sizes so have a look in catalogues
and see whether any of these may be of use to
you. The majority of dental films have a small
indentation in one corner as a positioning marker.
The raised dot is on the side facing the patient/
tooth/x-ray machine.
When processing the film it is necessary to
separate it from the packaging. Processing film
plus packaging or just a layer of backing card doe
not work ;-) Unfortunately the small size of dental
films and their thick emulsion preclude their
development in ordinary automatic processors.
Whilst special automatic processors are available,
manually processing is quick and easy using
either conventional chemicals or rapid processing
solutions (eg. Kodak Rapid Access Developer
and Fixer). There are even films supplied with
their own processing chemicals within the film
sachet. Processing is simplified in this manner,
but image contrast and keeping quality tends to
be poor. Whatever processing method is used it is
important that the films are thoroughly fixed and
washed. Re-fixing and thorough washing under
2006 World Congress WSAVA/FECAVA/CSAVA
running water is advisable after initial viewing of
hand processed films to ensure keeping quality
once dried.
258
Back to contents
In cats a full mouth dental survey, using a
combination of parallel and bisecting angle views,
can be obtained using six standard periapical film.
In dogs a larger number of films are usually needed
in a combination of sizes. When one has had a
little practice the whole series can be obtained
in a matter of minutes. It then takes a while to
examine the films properly, but it is always time
well spent. An additional benefit of routine dental
radiography is that there is something to show
clients at the end of the procedure and correctly
processed films combined with the dental chart
will become part of the permanent case record for
future reference.
Suggested Reading
Colmery B, DeForge D. Atlas of Veterinary
Dental Radiology. Iowa State University Press
2000, ,
Crossley and Penman, BSAVA Manual of
Small Animal Dentistry, 2nd edition. BSAVA,
Cheltenham 1995.
Harvey and Emily, Small Animal Dentistry,
Mosby, 1993
Verstraete FJM, Kaas PH, Terpak CH. Diagnostic
value of full-mouth radiography in dogs.
American Journal of Veterinary Research 1998,
59, 686-691
Verstraete FJM, Kaas PH, Terpak CH. Diagnostic
value of full-mouth radiography in cats. American
Journal of Veterinary Research 1998, 59, 692-
695
Wiggs, Lobprise. Veterinary Dentistry, Principles
and Practice. Lippincott - Raven, Philadelphia
1997,
Zontine EJ. Dental Radiographic technique and
Interpretation.. Vet.Clinics N. America, 1974, 4:
4, 741-750
Zontine WJ. Canine dental radiology; radiographic
technic, development, and anatomy of the teeth.
Journal of the American Veterinary Radology
Society 1975, 16: 3, 75-83

De - Dentistry
PERIODONTAL DEBRIDEMENT
Loic Legendre, DVM, FAVD,
Diplomate AVDC, EVDC
Northwest Veterinary Dental Ser-
vices Ltd
4037 Sunset Boulevard
North Vancouver
B.C. V7R 3Y7
Canada
ledentiste@aol.com
Periodontitis is by far the main oral pathology
encountered, and its universal characteristics
are attachment loss, pocket formation, and
ultimate tooth loss. Researches show that 80
% of dogs over the age of 3 suffer from some
form of periodontal disease. It is also the most
common disease worldwide, on the human side;
periodontal treatment costs totaled $51 billions in
North America in 2003, 75% of all dental costs.
The initiating factor is the presence of pellicle.
It gives rise to plaque. Plaque, in cats and dogs
is comprised of over 700 different bacteria; it
is the enemy. With time plaque mineralizes and
becomes calculus.
The disease progresses through several stages:
Stage 1. Marginal gingivitis, where the only sign
is the inflammation of the edge of the gingiva; the
red line sign.
Stage 2. Moderate gingivitis. The gingiva is
edematous and inflamed.
Stage 3. Severe gingivitis. The entire gingiva
is edematous, it bleeds easily, and periodontal
pockets start to form.
Stage 4. Moderate periodontitis. The inflammation
is severe, pockets and pus are present, there is
some bone loss and slight mobility.
Stage 5. Severe periodontitis. There is advanced
bone loss, definite tooth mobility, and tooth loss.
Stage 6. Exfoliation of the tooth. Healed alveolus.
Often see atrophy of the dental ledge. Can also
see the development of oronasal fistulas.
The first 2 stages represent gingivitis, a condition
that is reversible. Once attachment is lost it is
almost impossible to regain it. In other word,
periodontal disease is irreversible and incurable,
only controllable.
Etiology
The main pathogens in dogs are: Bacteroides sp,
Porphyromonas sp., Prevotella sp., Fusobacterium
sp., and a few aerobic organisms. In cats the main
culprits are: black pigmented Porphyromonas sp.,
Peptostreptococcus sp., Actinomyces sp.. In cats
these species are also found in healthy gingiva.
Back to contents
De
Pathogenesis
G-organisms cause rapid tissue destruction,
resulting in pocket formation. There is loss of
integrity of the sulcular epithelium. Bacteria and
their by-products migrate into the periodontal
ligament space. The periodontal ligament breaks
down and ultimately teeth are lost.
Clinical signs
Affected patients present with halitosis, ptyalism,
face rubbing, nasal discharge, and facial swelling.
As the research done by Dr. L. Debowes
determined, the signs can also be associated with
disease to the organs affected by periodontal
disease (heart, kidney, liver, skin, lungs and
brain). It has also been shown that periodontal
disease interacts with endocrine conditions
such as diabetes mellitus, hyperthyroidism and
hypothyroidism.
The oral signs of periodontitis are pocket
formation and attachment loss. There are three
types of pockets listed. Pseudopockets, as the
name implies, are not due to attachment loss but
rather to gingival hyperplasia creeping up the side
of teeth and creating deeper gingival sulci than
normal. In suprabony pockets, the bone recedes
at the same rate than the periodontal ligament
so that the bottom of the pocket is above the 2006 World Congress WSAVA/FECAVA/CSAVA
bone level. On x-rays, this is seen as horizontal
bone loss. In infrabony pockets, the periodontal
ligament recedes faster than bone and thus the
bottom of the pocket ends up within bone. On x-
rays, this is recognized as vertical bone loss.
The consequences of periodontitis are patients
with difficulty chewing, chronic periodontal
abscesses, bacteremias, weight loss, poor physical
condition and pain.
Treatment
To determine the extent of the disease one should
rely not only on visual inspection, but also on
palpation, probing and x-rays.
No matter what stage your patient is in, the
first treatment step is to perform a complete
dental cleaning. Actually, for stage 1 and 2 all
that is required is prophylaxis, irrigation and
259
De
establishment of a good home care program.
Stage 3 requires subgingival scaling in addition.
For stage 4 subgingival curettage and root
planning are needed. Root planning is the removal
of infected cementum on the surface of a root.
It is performed using a curette. Curettage is the
removal of the inflamed connective tissue on the
inside of the gingival sulcus. It is also performed
using a curette. Both procedures are often
indiscriminately referred to as curettage. The two
procedures should always be done together and
are jointly referred as subgingival scaling.
Subgingigval scaling is the simplest of the
periodontal procedure and is virtually done at
every dental cleaning. Curettes are essential; they
need to be very sharp to properly lift the calculus
away from the dentin surface. If they are dull,
which too often the case, they only burnish the
surface of the calculus but do not actually remove
it. They also have to be manipulated properly.
They are slid into the sulcus with the curvature
of the working tip following the curvature of the
root. Once at the bottom of the pocket, they are
rotated so that their distal shank is parallel to the
surface of the root, and they are pulled. They only
function in a pull motion. Because one relies on
the bends in the shank to reach the desired surface,
several curettes are necessary to adequately clean
all the root surfaces in the mouth. Subgingival
scaling is designed to address pockets 5mm deep
or less. Deeper pockets cannot be thoroughly
cleaned with scaling alone.
External bevel gingivectomy is a technique
De - Dentistry
ADVANCED PERIODONTAL THERAPY
Loic Legendre, DVM, FAVD,
Diplomate AVDC, EVDC
Northwest Veterinary Dental Ser-
2006 World Congress WSAVA/FECAVA/CSAVA
vices Ltd
4037 Sunset Boulevard
North Vancouver
B.C. V7R 3Y7
Canada
ledentiste@aol.com
DEFINITIONS
Attachment loss. It is the absolute measure of the
loss of periodontal support. It is measured from
the junctional epithelium to the C.E.J.
Curettage. Cleaning of the inside surface of the
free gingiva that forms the outer wall of the
gingival sulcus.
Root planing. Cleaning of the calculus and the
infected cementum, witihin the gingival sulcus.
260
Back to contents
designed to deal with moderate gingival
hyperplasia or pseudopockets. It is performed by
measuring the pocket with a probe, marking the
outside of the gingiva with the point of the probe,
aligning the scalpel blade at a 45% angle with the
surface of the root, and cutting. This should leave
a pocket less than 2 mm deep.
It is an easy operation, but its major disadvantage
is an important loss of gingiva.
Internal bevel gingivectomy, is a technique where
a scalpel is used instead of a curette to perform the
curettage of the pocket. It is intended for suprabony
pockets, moderate gingival hyperplasia, and to
facilitate wound healing. It is a harder procedure
than the external bevel gingivectomy, especially
in small patients. To accomplish this technique;
measure the pocket depth with a probe, mark the
gingiva, align the scalpel blade to have it stop
on the crestal bone, cut and remove the band of
granulating connective tissue with the help of a
curette.
In cases where periodontal pockets are deeper than
5mm, more advanced surgical flaps, created with
vertical releasing incisions, are also required.
Before performing any periodontal surgery, be
sure the client can carry out daily home care. If
the client is unable or unwilling to do so, most
of your procedures will fail or produce only
temporary improvements. Periodontal surgery
is performed only after a complete prophylactic
cleaning.
Finally, never forget that there is no cure for
periodontal disease, only control.
Infrabony pocket. Periodontal pocket whose
bottom is situated coronal to the crest of the
surrounding alveolar bone.
Pseudopocket. Pocket whose bottom is at
the C.E.J., and whose increased depth is due
to gingival hyperplasia rather than to loss of
periodontium.
Root planing. Cleaning of the root surface inside
the gingival sulcus.

Subgingival scaling. Combination of curettage
and root planing.
Suprabony pocket. Periodontal pocket whose
bottom is situated apical to the crest of the
surrounding alveolar bone.
Before performing any periodontal surgery be
sure the client can carry out daily home care. If
the client is unable or unwilling to do so, most
of your procedures will fail or produce only
temporary improvements. Periodontal surgery
is performed only after a complete prophylactic
cleaning. Always, always leave at least 2 mm of
attached gingiva at the end of the procedure.
BASIC TECHNIQUE
Subgingival scaling.
This procedure is composed of two parts: root
planing and curettage. Root planning is the
removal of infected cementum on the surface
of a root. It is performed using a sharp curette.
Curettage is the removal of the inflamed
connective tissue on the inside of the gingival
sulcus. It is also performed using a curette. Both
procedures are often referred to as curettage.
These are the most common procedures used
in periodontal therapy. They are most effective
when dealing with pockets less than 5mm deep.
TECHNIQUES INVOLVING TISSUE RESECTION
Gingivectomy.
(Def. elimination of gingival pockets by resection
of gingival tissue from the inside of the pockets).
The oldest method still in use.
External bevel gingivectomy
Indications: 1. Shallow suprabony periodontal
pockets. 2. Moderate gingival hyperplasia.
3. Asymmetrical gingival topography. 4. Soft
tissue impaction causing a dental inclusion.
Contraindications: 1. Infrabony pockets. 2. Pockets
extending beyond the mucogingival junction, or
in cases where there remain very little attached
gingiva. 3. Inflamed tissues. 4. When the
procedure compromises the esthetic.
Technique: Measure the pocket with a probe,
mark the outside of the gingiva with the point of
the probe, align the scalpel blade at a 45% angle
with the surface of the root, and cut. This leaves a
pocket less than 2 mm deep.
It is an easy operation, but used only in the
presence of pseudopockets (gingival hyperplasia),
in veterinary dentistry. Its major disadvantage is
an important loss of gingiva.
Internal bevel gingivectomy
It is actually an incision that can be combined
with other periodontal treatments.
Back to contents
De
Indications: 1. Suprabony pockets. 2. To facilitate
wound healing. 3. Moderate gingival hyperplasia.
4. Asymmetrical gingival topography. 5. Soft
tissue impaction causing a dental inclusion.
Contraindications: 1. Infrabony pockets. 2. Pockets
with little attached gingival left. 3. Very inflamed
tissue. 4. Need to access bone support.
5. When it compromises the esthetics.Advantages:
1. Facilitates wound closure. 2. Diminishes post-
op complications.
Disadvantages: Harder procedure than the
external bevel gingivectomy.
Technique: Measure the pocket depth with a
probe, mark the gingiva, align the scalpel blade
to have it stop on the crestal bone, cut and remove
the band of granulating connective tissue with the
help of a curette.
Apically positioned flap without osseous
reduction.
This technique requires one or two vertical
releasing cuts, past the mucogingival margin,
with Periosteal elevation of the flap.
Indications: 1. Supra and infrabony pockets.
2. Subgingival root caries. 3. Crown lengthening.
4. Need to increase epithelial tissue coverage.
Contraindications: May cause cosmetic
problems.
Advantages: 1. Decreases pocket depth. 2. Facilitate
wound healing. 3. Allows access to bony support,
to roots, to furcations, and to subgingival caries.
Disadvantage: Limits the treatment of infrabony
pockets.
Technique: Same steps as before plus vertical
releasing incisions and elevation of a flap.
Cleaning of the granulating connective tissue
with a curette. Apical repositioning of the flap
with elimination of the pocket. Suturing to
reattach the flap.
Apically positioned flap with osseous reduction
Indications: 1. Moderate infrabony pockets.
2006 World Congress WSAVA/FECAVA/CSAVA
2. Subgingival root caries. 3. Asymmetrical
gingival topography. 4. To facilitate restorative
processes.
5. To facilitate cleaning.
Contraindications: 1. Roots too short for the
size of the crown. 2. Esthetic considerations.
3. Furcation exposure. 4. Excessive mobility of
the tooth. 5. Inadequate amount of gingiva. 6. Too
important a loss of attachment.
Advantages: 1. Reduces pocket depth. 2. Preserves
gingiva. 3. Allows access to bony support, to
roots, to furcations, and to subgingival caries.
4. Facilitates dental restorations.
5. Facilitates exposed root surfaces examination.
Disadvantages: 1. Complex technique. 2. Possibility
of removing too much periodontal attachment.
261
De
Technique: Same steps as before except that
when the flap has been elevated, an osteoplasty is
performed to redefine the osseous margins.
Root resection
Indications: 1. Important bone loss around
one or several roots. 2. Class II or III furcation
exposures. 3. Adjacent tooth roots too close.
4. Fracture, perforation, caries, or resorption
of one or several roots. 5. When endodontic
treatment of a root seems impossible.
Contraindications: 1. Insufficient bony support
around the remaining roots. 2. Endodontic
treatment of the remaining roots is impossible.
3. When the remaining roots are useless. 4. When
the remaining roots cannot be restored.
Advantages: 1. Preservation of part of the tooth.
2. Easy access for cleaning. 3. Decrease in the
morbidity of the tooth.
Disadvantages: 1. Complex technique. 2. Difficult
case selection.
Technique: Finish the endodontic treatment of the
tooth before amputating the root. Make sure that
you close the gingiva after extracting the root.
Ensure that the area will be easy to keep clean.
TISSUE ATTACHMENT
Definition of the terms used in this section.
Reattachment: Union of connective tissue with
the surface of the root on which live periodontal
tissue is present.
Repair: Healing of a wound without completely
repairing architecture or function of the part
in question (i.e.: formation of long junctional
epithelium).
New attachment: Union of connective tissue with
the surface of a denuded root. This can happen
with or without the formation of new cementum.
Regeneration: Reconstitution of a damaged or
lost part.
2006 World Congress WSAVA/FECAVA/CSAVA
Curettage (Removal of pocket epithelium )
It removes infiltrated granulating connective
tissue, but causes of pronounced tissue shrinkage.
It is adequate for 3 to 5 mm deep pockets. Deeper
pockets are difficult to clean and require the
creation of flaps. The flaps heal by way of long
junctional epithelium formation. Curettage is not
indicated if the goal of the procedure is to obtain a
new attachment. Always combine this technique
with root planning.
Modified Widman flap
Indications: 1. Moderate to deep periodontal
pockets. 2. Preservation of esthetic. 3. Improved
262
Back to contents
access to root surfaces and supporting bone.
Contraindications: 1. Shallow pockets (less than
3 mm). 2. If in need of new attachment.
Advantage: Yields a comfortable, functional,
healthy dentition.
Disadvantage: Heals by repair.
Technique: First cut in an internal sharp bevel
directed toward the crestal bone. Second cut,
intrasulcular. Partially elevate the flap. Third cut,
at right angle with the root surface, at the base of
the sulcus.
As mentioned above, repair is done by the
formation of a long junctional epithelium.
Research done on animals where they use a
ligature, around the base of the tooth, to create
a periodontitis, shows no difference in the
formation of pockets whether the attachment is
long or short (normal) junctional epithelium.
REGENERATIVE METHODS
Autografts
They act via osteoproliferative, osteoconductive,
and osteoinductive mechanisms. Autografts are
the only ones to be osteoinductive. The results
are good when dealing with infrabony defects
(normally more than 50% filling of the defects),
but they are less successful with crestal bone or
furcation defects.
Freeze-dried allografts
Satisfactory for filling infrabony defects but
have minimal success with furcation exposures.
A mixture of autograft and freeze-dried allograft
yields better results with furcation exposures.
Decalcified freeze-dried allografts
Sometimes allows regeneration of periodontium
during infrabony defects treatment. The material
is inductive, conductive, resorbed, and replaced.
Implants
Tri calcium phosphate (TCP. Ceros 82, Synthograft,
and others). Resorbable, osteoproductive, good
as filler but is of no use for regeneration work.
Hydroxyapatite (HA, Alveograf, Bio-Oss,
Calcitite, Ceros 80, Interpore 200, Osprovit,
Periograf, and others). Not resorbable, otherwise
similar to TCP.
Guided tissue regeneration
(GTR) it is a whole different story!

De - Dentistry
SIMPLIFYING DENTAL EXTRACTION
Dr. David Crossley
Animal Medical Centre
511 Wilbraham Road
Manchester M24 5AJ
UK
wsava2006@dacross.net
There are many possible indications for extraction
of teeth:
• Advanced periodontal disease
• Extra (retained deciduous + supernumerary) teeth
• Malformed, malpositioned + overcrowded teeth
• Unerupted (impacted and embedded) teeth
• Destructive (caries + resorptive) lesions
• Pulp exposure, pulpitis, necrosis
• Fractured teeth and jaws
• Treatment failure
• Other disease
In all except advanced periodontal disease the
teeth are likely to remain strongly attached to the
jaws making tooth removal anything but simple.
Even when there has been extensive alveolar
bone loss and teeth are mobile extraction can still
be difficult and prone to complications such as
jaw fracture.
The main problem associated with extraction
is inadequate diagnosis and treatment planning
so that the operator embarks on the procedure
unprepared. Animals vary considerably in their
anatomy, not just between species but also
between breeds and even individuals of the same
breed. Different teeth have different purposes
and as a result different structures and they suffer
from a variety of types of pathology.
The first means of simplifying extraction
is to perform a thorough visual, tactile and
radiographic examination so that an appropriate
treatment plan can be devised to accommodate
the particular anatomy of individual teeth. Once
planning is complete the operating site can be
prepared for the surgery by cleaning (supra and
subgingival scaling, polishing and thorough oral
lavage) and disinfection (application of a 0.1 to
0.2% aqueous solution of chlorhexidine) with a
3-5 minute preoperative contact time just as for
any other surgery. During scaling and disinfection
the appropriate sterile instrumentation can be
prepared and laid out.
Once the oral cavity and surrounding skin are
disinfected the animal should be positioned to
allow easy access to and visualisation of the teeth
Back to contents
De
requiring extraction, the surgical site then being
isolated by draping.
The actual method of extraction will depend on
the structure of the tooth:
• Small single rooted tooth with conical root
structure
• Small multi-rooted tooth
• Large multi-rooted tooth
• Large single rooted tooth
and its location in the oral cavity.
Most small single rooted teeth can be extracted
using a “closed” extraction technique, working
through the gingival sulcus without creating
an access flap, although a flap often makes it
easier, particularly if several adjacent teeth are
to be removed. The most efficient method of
separating the periodontal ligament of these small
teeth is use of a thin tipped highly tapered tipped
extraction instrument (a dental luxator or modern
design elevator, but not a traditional chisel type
dental elevator). This is used to cut the accessible
portion of the periodontal ligament and stretch
the alveolus to make it wider so that the tooth
can be tipped within the socket (Figure 1) and the
luxator inserted further.
By locking the inserted luxator against the tooth
root and rotating the instrument on its long axis a 2006 World Congress WSAVA/FECAVA/CSAVA
large rotational leverage force (Figure 2) can be
applied in a very controlled manner over a short
distance. As the tooth and bone are forced apart
the un-cut periodontal ligament is stretched, and if
tension is held long enough, torn well beyond the
tip of the instrument. By working systematically
around the circumference of the root it will be
loosened to the point where it can simply be lifted
from its socket.
263
De

Figure 1. Luxation technique

If extraction forceps are used great care is required due to the long thin fragile structure of dog and cat
tooth roots. This is particularly important when dealing with deciduous teeth which are proportionally
longer and weaker than their permanent replacements.
2006 World Congress WSAVA/FECAVA/CSAVA

Figure 2. Rotational leverage:

Large radius of instrument handle compared with tip width

By sectioning the crown using a high speed
bur, after creating a shallow envelope flap, the
individual roots of small multirooted teeth can be
extracted in the same manner.
Large multi-rooted teeth are likely to require
release of some of the bone they are attached to
in order to ease extraction. These teeth should be
sectioned as for smaller teeth and the access flap
then enlarged to permit access for bone removal
using a sterile low speed bur or bone chisels
264
Back to contents
(dental elevators and luxator designs are based
on bone chisels, so they are eminently suitable
for cutting and removing thin and soft bone). If a
bur is used a sterile isotonic irrigant (eg. lactated
ringers i/v solution) should be used to wash away
bone debris and keep the bur cool. High speed
dental handpieces deliver non-sterile (usually
bacteria contaminated) air/water spray into the
site and so are NOT suitable for use for cutting or
removal of bone.

The buccal bone overlying the coronal half of
the tooth root is released by burring around
the margins or removed completely and the
tooth roots loosened using luxation technique.
In some cases instrument tips can also be
positioned horizontally between sectioned tooth
segments and rotational leverage used to tear
the periodontal attachments. This method is also
useful in determining whether sectioning between
roots is complete; there should be some relative
De
movement between the tooth sections as a force
is applied between them.
Large single rooted teeth can be extracted
similarly to individual roots of large multi-rooted
teeth by gaining access, releasing the lateral
alveolar wall for half of the root length and
luxation of the remaining attachment. Should this
not prove effective then the whole lateral wall of
the alveolus can be released (Figure 3).

2006 World Congress WSAVA/FECAVA/CSAVA

Figure 3. Illustration of the use of a combination of an access flap,
bone release and luxation technique for extraction of the maxillary
canine tooth in dogs. This method can be adapted for extraction of
maxillary third incisors and mandibular canine teeth.

Suggested further reading

BSAVA Manual of Small Animal Dentistry
(second edition). Crossley & Penman (editors).
BSAVA, Cheltenham, UK. 1995.

265
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Di
Dsiti imagine
Diagnostics
agno

Back to contents
 Di
INVITED LECTURES - FULL PAPERS

Di - Diagnostics imagine
THE RADIOLOGISTS APPROACH TO MUSCULOSKELETAL
DISEASES
Johann Lang, Dr.med.vet., Dip
ECVDI
Division of Clinical Radiology
Department of Clinical Veterinary
Medicine
Vetsuisse Faculty Bern
Länggassstrasse 128, Postfach
CH-3001 Bern
johann.lang@kkh.unibe.ch
http://kleintierklinik.unibe.ch
Introduction Radiography, Ultrasonography, Scintigraphy CT
Diagnostic work up of musculoskeletal disorders or MTRI may used, alone or in any combination
in the dog and cat usually includes a radiographic with the method finally selected depending on the
examination, and/or other diagnostic imaging history, clinical findings and the questions that
procedures. The imaging modalities are used to should be addressed by the examination (Table1).
further characterise clinically localised problems Other important criteria include the physical
and to differentiate disease processes: congenital properties considering strengths and limitations
and developmental disorders, degenerative, of a method in question, of course whether or not
traumatic, inflammatory, neoplastic, and a method is available on site, radiation hazards,
metabolic processes. In orthopaedic disorders and the costs (cost - effectiveness) involved.
of unknown origin, diagnostic imaging may be Economic aspects often decide whether an
used to localise the problem, and in hereditary animal undergoes complete diagnostic work up
disorders of the musculoskeletal system they are and treatment or not.
used as screening methods.

Fig. 1: Typical imaging protocol in

orthopaedic disorders
a) conventional x-ray with
radiographic signs that are typical
for a specific diagnosis (e.g.
flattening of humeral head for
OCD). Other imaging procedures
2006 World Congress WSAVA/FECAVA/CSAVA
are not required or indicated.
b) An examination with equivocal
findings (e.g. irregular borders
and radiolucency of supraglenoid
tubercle) for DDx “trauma” and
“neoplasia”. Additional imaging
procedures (e.g. Ultrasound) are
indicated. Often, a sequence of
2 or more diagnostic methods is
necessary to eliminate differential
diagnosis fro the initial list and to
establish the correct diagnosis.
modified from: Skelettradiologie
von Adam Greenspan

267
Back to contents
Di
Table 1. Imaging modalities used in musculoskeletal disorders
and core biopsies
Conventional radiography Bone scintigraphy
Includes standard projections, positional and Screening method, very sensitive method for
stress views. Excellent spatial resolution: Bone most inflammatory and neoplastic, traumatic and
architecture and morphology degenerative bone and joint pathologies, low
spatial resolution, not specific for bone and soft

Special procedures
Arthrography – except shoulder joint rarely used
tissue pathologies
Computed tomography (CT)
Structural abnormalities of bone, morphology
of joints, complex fractures, extent and
characterisation of bone tumours.

Sonography Magnetic resonance Imaging (MRI)

Musculature, tendons and ligaments; bone Any soft tissue (musculature, tendons, joints
surface, arthrosonographyUS-guided fine needle including joint capsule and ligaments, and
Menisci in stifle joints

Radiography: In the imaging of musculoskeletal which may include up to 6 or 7 projections,

diseases conventional radiography still is of basic
and relevant importance. The method is readily
available, cost efficient and has an excellent spatial
resolution. However, a lesion has to be localised by
a thorough physical examination before imaging
is considered, Radiography is not an adequate tool
to localize a disease process and the sensitivity of
radiography depends on the disease process and
the structure involve. Abnormal findings may
not be associated with clinical signs and may
be misleading. For example, mildly dysplastic
and osteoarthritic hip joints are clinically silent
in most dogs. Radiographic standard projections
usually include at least two projections. However
these are often not sufficient for a radiographic
diagnosis: in particular, a thorough radiographic
examination of joints often includes flexed and
extended views from different angles. An example
2006 World Congress WSAVA/FECAVA/CSAVA
depending on the disease process in question.
Positional and stress radiographs may be used
to confirm or eliminate joint instability. Invasive
radiographic methods, such as arthrography, are
mostly used in the shoulder joint; however, with
increasing availability and expertise of other
imaging techniques arthrography becomes less
important.
Thorough knowledge of the radiographic
anatomy including species and breed specific
variations, age dependent changes and the
skills in interpreting of a radiograph are of
equal importance as the radiographic technique.
Characterization of bone lesions not only includes
the description of the abnormality, but also the
distribution and localisation in the skeleton,
localisation in a specific bone, and so on (table
2). Diagnosis is based on description, the ID of

is the radiographic protocol in elbow dysplasia, patient and clinical signs

Table 2. Interpretation criteria for skeletal radiographs

Radiographic abnormality
• alteration of architecture (size, shape, border) and proportion, of opacity and structure (osteoporosis/
atrophy, osteolysis, osteosclerosis, osteopetrosis)
Intraskeletal distribution
• generalized, (oligo-) polyostotic, monostotic
Localisation
• within the skeleton: bone or bones affected
• within the bone longitudinal: proximal or distal epiphysis, physis (growth plate), metaphysis,
and/or diaphysis
• cross sectional: bone marrow, endosteum, compact bone, periosteum, soft tissues
Complications
• e. g. metastases, effects on other structures/joints
Aggressivity of a lesion
268
Back to contents

Bone-scintigraphy is often used as screening
method in lameness in horses and less
commonly in small animals in order to localize
an occult skeletal lesion, and to screen for
metastases in tumour cases. Scintigraphy reflects
metabolic activity. An injection of 99m Tc-Sc-
methylendiphosphate at a dosage of 16.3 MBq/kg
bodyweight is required for osseous radiolabeling.
99mTc produces gamma radiation with an energy
of 140 keV, which collected and visualized
Di
using a gamma-camera. The distribution can be
registered as an angiographic study immediately
after injection, a pool phase some minutes, and
the metabolic phase 2-3 or more hours after
injection (Fig. 2). In small animals a maximum of
300 k-counts per region are recorded. Comparing
the metabolic activity of a specific structure to
the controlateral body part is essential. Increased
or decreased activity reflects abnormal perfusion
and/or metabolism.

Fig. 2: Bone scan of a dog

with clinically not clearly
localized lameness of the
right hindlimb. Equal
orientation of the two
hindlimb- scans facilitates
the comparison to the
controlateral part. Note
the difference in activity
of the two stifle-joints.

Kidneys and urinary tract eliminate unattached

tracer-particles. Therefore image editing is needed to
correct the highly active urine in the urinary bladder
overlaying less active bony structures. In the present
bladder-activity is suppressed by imaging software
(black spot).
Bone scan (dorsal view) of the same dog: metabolic
activity of separate regions of the hindlimbs can be
compared directly positioning of the legs is symmetric.
The right stifle shows intensive enhancement clearly
distinct from the left stifle.
red: peak of activity; dark blue: lowest activity

2006 World Congress WSAVA/FECAVA/CSAVA

Sonography: Standard method for soft tissue
diagnostics, particularly for abdominal
examinations where it is often performed as
single examination. To some extent this is also
true in musculoskeletal disorders, e.g. for tendinal
lesions in the horse. In small animals, sonography
most often is used as an adjunct diagnostic tool.
Lesions of the bones have to be ruled out by
radiography. Clinically relevant examinations
include tendons (biceps tendon, Achilles tendon)
and tendon sheath’s after trauma or control after
surgery, joints (shoulder joint, stifle, hip joint) in
order to differentiate between fluid accumulation
and soft tissue proliferations ( e.g. suspicion of
neoplasia), US controlled assessment of joint-
stability (alternatively to stress radiographs),
sonographic examination of post traumatic
musculature (ruptures, hematoma), suspicion of
tumour or abscess, US guided FNA or biopsy.

269
Back to contents
Di

Fig. 3. Left: Sonography of a dog showing clear signs of a ruptured Achilles tendon which was verified
and repaired surgically. Only after the dog did not improve clinically, a radiographic examination was
performed. The lateral projection of the stifle joint revealed a distally dislocated sesamoid bone of the
lateral gastrocnemius muscle, a radiographic sign of an avulsion of the respective muscle.

Computed tomography (CT) and magnetic
resonance imaging (MRI): Both techniques
are becoming very popular also in veterinary
medicine. Whenever available, they are used as
additional diagnostic tools whenever radiographic
or sonographic findings are equivocal, as
an alternative for arthroscopy, or for further
characterisation (extent and nature of a lesion) of
a known lesion. In general CT is used primarily
for bone disorders; MRI, on the other hand, is the
method of choice for soft tissue imaging. CT is
useful to visualise complicated fractures ( joints,
pelvis) preoperatively - a three dimensional CT-
reconstruction can be very helpful for the surgeon
planning the surgery. Furthermore CT is used
as gold standard to explore malformations and
2006 World Congress WSAVA/FECAVA/CSAVA
Characterisation and assessment of the extent of
primary bone tumours or bone affecting tumours
preoperatively or pre-radiation-therapy are other
indications for CT.
MRI has the highest contrast resolution for soft
tissues and has become method of choice in
neurological disorders. In orthopaedic disease
MRI is useful for soft tissue pathology, e.g.
imaging of internal derangement of joints such as
the stifle-joint. Ruptured cruciate ligaments, tears
and other pathologies of the menisci, disease of
articular cartilage, and joint capsule are readily
imaged (fig. 4). By choosing the appropriate
planes and sequences, MRI is sensitive and
specific for many musculoskeletal pathologies.
Since increase in cell- or fluid content within

developmental disorders of complex joints: The bones can also be seen in MRI, bone-tumors,
sensitivity of radiographs of a fragmented medial osteomyelitis and post-traumatic bone marrow
coronoid process is below 50%, the sensitivity edema are also detectable.
and specificity of a CT is close to 100%.

270
Back to contents
 Di

Fig. 4: lateral radiograph (left) and sagital plane section of a stifle-joint with ruptured cranial cruciate
ligament. Radiological findings are unspecific. With MRI the intact caudal cruciate ligament (white
arrow) and the thickened remainder of the ruptured cranial cruciate ligament are visible (black
arrow).

Suggested reading Hoskinson, J. J. and R. L. Tucker. 2001. Diagnostic

Carrig, C. B. 1997. Diagnostic imaging of
osteoarthritis. Vet. Clin. North Am. Small Anim
Pract. 27: 777-814.
Davis GJ., Kapatkin AS., Craig LE., Heins
GS., Wortman JA: Comparison of radiography,
computed tomography, and magnetic resonance
imaging for evaluation of appendicular
osteosarcoma in dogs; J Am Vet Med Assoc. 2002
220(8): 1171-6.
Fitch RB., Wilson ER., Hathcock JT., Montgomery
RD: Radiographic, computed tomographic and
magnetic resonance imaging evaluation of a
chronic long digital extensor tendon avulsion in a
dog; Vet Radiol Ultrasound. 1997 38(3): 177-81.
Gemmill TJ.; Mellor DJ., Clements DN.,
Clarke SP., Farrell M., Bennett D., Carmichael
S: Evaluation of elbow incongruency using
reconstructed CT in dogs suffering fragmented
coronoid process; J.Small Anim Pract. 2005;
46(7): 327-33.
imaging of lameness in small animals. Vet. Clin.
North Am. Small Anim Pract. 31: 165-80, vii.
Liptak JM, Pluhar GE, Dernell WS, Withrow
SJ:Limb-Sparing Surgery in a Dog with
Osteosarcoma of the Proximal Femur, Veterinary
Surgery 2005; 34: 71-77.
Thrall DE: Textbook of Veterinary Diagnostic
Radiology 4th edition. W.B. Saunders Company,
2002.
Wallack ST., Wisner ER., Werner JA., Walsh
PJ., Kent MS., Fairley RA., Hornof WJ:
Accuracy of magnetic resonance imaging for
estimating intramedullary osteosarcoma extent
in pre-operative planning of canine limb-salvage
procedures; Vet Radiol Ultrasound 2002 43(5): 2006 World Congress WSAVA/FECAVA/CSAVA
432-41.
see also manuscript on MRI of the musculoskeletal
system

271
Back to contents
Di
Di - Diagnostics imagine
PHENOTYPE OF HEREDITARY ORTHOPEDIC DISEASE – AND THE
ROLE OF DIAGNOSTIC IMAGING
Johann Lang, Dr.med.vet., Dip
ECVDI
Division of Clinical Radiology
Department of Clinical Veterinary
Medicine
Vetsuisse Faculty Bern
Länggassstrasse 128, Postfach
CH-3001 Bern
johann.lang@kkh.unibe.ch
http://kleintierklinik.unibe.ch
Sandra Martig, Dr.med.vet.
Division of Clinical Radiology
Department of Clinical Veterinary
Medicine
Vetsuisse Faculty Bern
Länggassstrasse 128, Postfach
CH-3001 Bern
INTRODUCTION
The role of diagnostic imaging in congenital and
inherited disorders depends on many factors.
In the following article the focus is on the
goals, possibilities and limitations of diagnostic
imaging in the context of breeding programs.
The phenotype of an inherited disorder depends
mainly on the genetic trait and whether the
changes are present at birth or develop later in life.
Only in dominant genetic disorders every carrier
of a specific gene will present as a phenotypically
affected individual - independent whether the
allele is present as homo- or heterozygote.
In contrast, in recessive and even more so in
polygenetic traits the disorder may be passed
to the progeny through several generations by
phenotypically normal carriers. The pattern of
2006 World Congress WSAVA/FECAVA/CSAVA
inheritance of many orthopedic diseases, as for
example canine hip dysplasia, indicates a complex
trait controlled by the interaction of several
genes and environmental factors (nutrition, dog
keeping). In such polygenetic hereditary disorders
it is extremely difficult to conclude from the
(radiologically) phenotype to the genotype of an
individual. Therefore, knowledge of the mode of
inheritance of a disease is important for using the
information’s gained from radiographs or other
imaging modalities in an appropriate way. The
second major problem in many inherited skeletal
disorders is the fact that the abnormalities are
often not present at birth, and develop only later
in adult animals. In some diseases the primary
disease process can not readily be detected
radiographically and the diagnosis depends on
secondary sings. An example is the fragmented
272
Back to contents
Anaïs Güdel, med.vet.
Division of Clinical Radiology
Department of Clinical Veterinary Medicine
Vetsuisse Faculty Bern
Länggassstrasse 128, Postfach
CH-3001 Bern
medial coronoid process where the diagnosis
often depends on the presence of secondary
osteoarthritis. Many hereditary defects are
associated with the standard of a breed. An
example for this is the Dachshund where chondroid
degeneration of intervertebral discs is associated
with chondrodystrophy, the gene defect used to
develop the standard of the breed. Recognition of
chondrodystrophy is easy, however recognition
of intervertebral disc degeneration at a young age
is a diagnostic challenge. The method proposed
to use radiographs with intervertebral disc
mineralization as a marker has to be done at an
age of 18-36 months.
Not every congenital defect (radiological
detectable abnormality) is a genetic inherited
disorder. A fetus with sound genes may be exposed
during gestation to teratogenic impacts (e.g.
pharmaceutics, infections). Such abnormalities
are congenital but not anchored in genes and are
therefore not passed to the progeny. Examples
are sporadically observed abnormalities such as
hemimelia, syndactylia, or ectodactylia.
GOALS OF DIAGNOSTIC IMAGING
In relation with inherited disorders there are
mainly two tasks for diagnostic imaging.
1. Diagnosis and prognosis in a diseased
individual: In a given case and within the
financial scope of the owner, a combination
of any diagnostic imaging technique such as
radiography, bone scintigraphy, Ultrasonography,
CT and or MRI can be applied. In addition or as
alternative arthroscopy as minimally invasive

diagnostic technique (therapeutic option) may be
considered.
2. Phenotypical screening in the context of
breeding schemes: All breeding programs are
based on the positive identification of affected
individuals. Affected animals should be
recognized as early in life as possible, preferably
before the animal is being introduced to breeding
or before a lot of time and money are invested into
education of a working dog. Ideally, a screening
method is inexpensive, not invasive and has
a high sensitivity and specificity. In disorders
where genetic testing is not possible, screening is
based on the phenotype. In the ideal situation the
phenotype reflects exactly the genotype, and no
false negative and false positive results are seen.
An almost ideal disorder for phenotypical
screening using diagnostic imaging is polycystic
kidney disease in Persian cats. The dominant
genetic trait and the fact that the cysts develop
early in life made Ultrasound to an almost perfect
diagnostic tool with very high sensitivity even in
animals far below 1 year of age. In orthopaedic
disorders, the situation is often far more
complicated. Dominant or simple recessive traits
are rare. The avascular necrosis of the femoral
head (Legg-Calvé-Perthes disease) is a non-
inflammatory (aseptic) necrosis with subsequent
deformation of the femoral head and neck
resulting in pelvic limb lameness. In Minitiature
Poodles and West Highland White Terriers the
disease is a simple (autosomal) recessive trait,
and radiography can be used for assessing the
femoral heads. Eliminating all affected individuals
and littermates from breeding (if the genetic basis
allows such a strict program) will eradicate the
problem in a few generations.
Real challenges for radiologists, genetists, and
breeders are disorders with polygenic traits. An
excellent example is the canine hip dysplasia
(CHD). The pattern of inheritance indicates
that canine hip dysplasia is a complex trait
controlled by the interaction of several genes and
environmental factors and the phenotype often
is only recognized in the adult animal. Because
there are several genes and environmental factors
responsible for the disease, till now there is no
simple genetic test on the market. For the same
reasons, the recognition of the genetic burden
using diagnostic imaging in a single individual is
not possible as well. The problem therefore has
to be addressed combining imaging methods with
refined breeding schemes on the basis of mass-
selection and open database or other methods
such as breeding value estimation.
Canine hip dysplasia is a disturbance of growth,
which is characterized by the presence of an
enhanced passive laxity of the joint, and - in
Back to contents
Di
the course of the disorder - incongruent joints,
deformity of the azetabulum, femoral head an neck,
and osteoarthritis. Several genes with different
loci and environmental factors (up to 80%) take
part in the phenotypical development of CHD. To
make the situation even more complicated, there
may be inductive or protective loci that control
expression of hip OA that are independent from
the “CHD-genotype”. The risk of a German
Shepherd dog with a 50% joint laxity to develop
OA is higher than for a Rottweiler with the same
amount of laxity. Using the classical methods,
the radiographic diagnosis depends on primary
signs such as passive laxity and secondary joint
deformities and OA. However, because there is
no simple genetic test available, radiographic
examination of the hip joint in the scope of
breeding against CHD and other polygenetic
disorders still plays an important role. The
goal of testing is to find the best approximation
of the phenotype of an individual or group of
individuals and the genotype. Furthermore, the
test has to be reliable, safe and inexpensive. For
assessing primary signs of disease, independent
from the presence of OA, measurements of the
Norberg angle and distraction indices have been
developed. Ultrasonographic examinations,
which are used in infants as a screening method,
did not achieve acceptance in dogs (yet) because
of several reasons. This is also true for biometric
procedures as proposed by R. Beuing.
It has been shown, that the joint laxity measured by
the distraction index by Smith, and other methods
as described by Flückiger or Ohlerth have a high
prognostic value. Already in 16-18 weeks old
animals, the status of joints of adults could be
predicted using the Smith method. For example
60% of the 4 months old German Shepherds
with a DI > 0.3 developed OA and CHD at an
older age. However, the joint laxity seems to be
breed specific and these values cannot be alienate
from one breed to another. Some breeds appear
2006 World Congress WSAVA/FECAVA/CSAVA
to display different susceptibilities to CHD based
on their DI’s and some breed may tolerate more
passive hip laxity than other breeds. Labradors
with DI values of less than 0.3 have a greater
than 80% probability of not developing hip OA
whereas those with DI’s greater than 0.7 have
a high probability of developing hip OA. The
upper DI value in German Shepard’s is 0.5. An
advantage is that hip laxity has a higher heritability
(0.6) than estimates based on the standard method
(0.2 - 0.45). Therefore, measuring joint laxity
using a standardized method might improve the
radiographic assessment of hip joints; however,
because of several (non medical) reasons the
method is not yet accepted in Europe. Puerto
et al even postulate the combination of several
273
Di
methods for the finishing/terminal assessment of
the hip joints.
OTHER DISORDERS
Appendicular skeleton
Standard radiographic and evaluation
protocols exist for many inherited orthopedic
disorders. Examples are elbow dysplasia (ED),
osteochondrosis (several joints), or avascular
necrosis of the femoral head (Legg-Calvé-
Perthes disease). In radiographic diagnostic of
elbow dysplasia, often the fragmented medial
coronoid process (FCP) can not readily be
identified using radiographs and the diagnosis
depends on the identification of osteoarthritis.
Computed Tomography (CT), the method of
choice to identify affected joints can not be
used as screening method up to now, because
CT is not readily available and too expensive
as a screening tool. In contrast to the FCP the
overall accuracy of a radiographic examination
to correctly identify isolated anconeal process
(IPA) and ostechondrosis OCD) of the elbow
joint is very high. The heritability is similar
as described in CHD. Incomplete ossification
of the humeral condyle (IOHC: autosomal
recessive trait?) in some breeds such as Cocker
-, Brittany -, Springer -, Clumber -, and CKC
Spaniel, (but also Labrador Retriever, Rottweiler,
German Shepherd dog, German Wachtelhund),
medial and lateral Patellar luxation and many
other congenital and hereditary disorders of the
appendicular skeleton exist where radiography
and other imaging modalities are important to
diagnose or characterize the problem. However
it is beyond the scope of this paper to list and
describe all these diseases.
Axial skeleton
Spondylosis of Boxers show an average to high
2006 World Congress WSAVA/FECAVA/CSAVA
heritability (up to 0.6; depending on the author,
model and localization of the spondylosis), even
though the mode of inheritance has not been
reported (Langeland, others). Often, 1.5 years
old boxers already show advanced spondylosis
which are readily identified on radiographs,
making radiographic screening very promising.
Some Kennel Clubs and countries already have
established breeding schemes, while others seem
not to be interested.
Mineralized intervertebral discs are reliable
signs of intervertebral disc degeneration. The
risk for a chondrodystrophc dog suffering from
an intervertebral disc hernias, which often leads
to neurologic deficits, seems to increase with
the number of mineralized discs. Furthermore
heritabilities of over 0.4 have been estimated for
274
Back to contents
mineralized discs. Dachshunds show a considerable
predisposition of mineralized intervertebral
disc, and several countries introduced screening
methods based on the number of mineralized
intervertebral discs (Jensen). Radiographic
imaging shows mineralized intervertebral discs
easily and reliable. However, The number of
mineralized discs in an individual varies over
time. After an increase in the first 2 years of age,
mineralization without herniation may disappear
over time (mineral is reabsorbed) and the optimal
time for screening is between 18 and 36 months
of age.
Examples of non-skeletal diseases
Many other inherited disorders where imaging
techniques are used have been described.
Ultrasonography is used in cardiac diseases
with hereditary background such as in Boxers
(subaortic stenosis), Cavalier King Charles
Spaniels (av-valve dysplasia), several large
breed dogs (dilated cardiomyopathy), or Maine
Coon cats (hypertrophic cardiomyopathy).
Several breeds (Cairn Terrier, Golden Retriever,
Irish Wolfhound, Labrador Retriever, Maltese,
Miniature Schnauzer and Yorkshire Terrier) have
a higher risk to develop a portosystemic shunt and
Ultrasound and Scintigraphy are used as screening
methods. Magnetic Resonance Imaging is used
in dogs with idiopathic epilepsy, and in Cavalier
King Charles Spaniel with Syringohydromyelia
(Arnold-Chiari type I malformation).
SUGGESTED READINGS
Biller DS et al: Inheritance of Polycystic Kidney
Disease in Persian Cats. J Hered 87 (1): 1-5
(1996)
Eaton KA et al: Autosomal Dominant Polycystic
Kidney Disease in Persian and Persian-cross
Cats. Vet Pathol 34: 117-26 (1997)
Flückiger M et al: A Radiographic Stress
Technique for Evaluation of Coxofemoral Joint
Laxity in Dogs. Vet Surgery 28: 1-9 (1999)
Flückiger M et al: Correlation between Hip Joint
Laxity and subsequent Coxarthrosis in Dogs.
Zentralbl Veterinarmed A. 45 (4):199-207 (1998)
Henninger W und Köppel E: Die Bedeutung
des kraniolateralen Pfannenrandes für die HD-
Beurteilung. Tierärztl Prax 22: 278-85 (1994)
Jensen, V. F. 2001. Asymptomatic radiographic
disappearance of calcified intervertebral
disc material in the Dachshund. Vet. Radiol.
Ultrasound 42:141-148
Jensen, V. F. and K. A. Christensen. 2000.
Inheritance of disc calcification in the dachshund.

J. Vet. Med. A Physiol Pathol. Clin. Med. 47:331-
340.
Langeland M und Lingaas F: Spondylosis
Deformans in the Boxer: Estimates of Heritability.
J Small Anim Pract 36(4):166-9 (1995)
Lust G et al: Joint Laxity and its Association with
Hip Dysplasia in Labrador Retrievers. Am J Vet
Res 54: 1990-99 (1993)
Ohlerth S et al: Comparison of three Distraction
Methods and Conventional Radiography for
early Diagnosis of Canine Hip Dysplasia. J Small
Anim Pract 44 (12): 524-9 (2003)
Popovitch CA et al: Comparison of Susceptibility
for Hip Dysplasia between Rottweilers and
German Shepherd Dogs. J Am Vet Med Ass 206:
648-50 (1995)
Puerto et al: Relationship between Results of
the Ortolani Method of Hip Joint Palpation and
Back to contents
Di
Distraction Index, Norberg Angle, and Hip Score
in Dogs. J Am Vet Med Ass 214: 497-501 (1999)
Ruvinsky A and Sampson J: The Genetics of the
Dog. CABI Publishing Oxon UK and New York
(2001)
Smith, G. K., C. A. Popovitch, T. P. Gregor, and
F. S. Shofer. 1995. Evaluation of risk factors
for degenerative joint disease associated with
hip dysplasia in dogs. J. Am. Vet. Med. Assoc.
206:642-647.
Smith, G. K., D. N. Biery, and T. P. Gregor. 1990.
New concepts of coxofemoral joint stability and
the development of a clinical stress-radiographic
method for quantitating hip joint laxity in the
dog. J. Am. Vet. Med. Assoc. 196:59-70.
Young AE et al: Feline Polycystic Kidney Disease
is linked to the PKD1 region. Mammalian
Genome 16: 59-65 (2005)
2006 World Congress WSAVA/FECAVA/CSAVA
275
Di
Di - Diagnostics imagine
INTERPRETING RADIOGRAPHIC SIGNS IN THE ABDOMEN

Christopher R. Lamb MA,

VetMB, DipACVR,
DipECVDI, ILTM, MRCVS
Department of Veterinary Clinical
Science
The Royal Veterinary College,
Hawkshead Lane,
North Mymms,
Herts AL9 7TA
U.K.
clamb@rvc.ac.uk

The radiologic (Roentgen) signs are abnormal: Abnormal position

• number Potential causes of abnormal position in the
• position abdomen:
• size • Congenital (ectopia - rare)
• shape • Displacement
• opacity - Mass effect
• margination - Abnormal mobility
Memorise this list and apply it routinely when Ruptured diaphragm
considering any potential abnormality that you Hernia
have identified in any diagnostic image. Although Volvulus, e.g. stomach
this sounds very basic, these abnormalities are Torsion, e.g. spleen
the basis for all radiologic diagnoses and this list - Adhesions
of criteria applies equally well to radiography, • Surgical implantation
ultrasonography, CT and MRI. - Kidney
Abnormal number Problems with assessment of organ position in
Ability to count structures radiographically the abdomen
depends on their correct identification. This is • Radiographic descriptions of organ position
not always possible because, for example, many and borders are often limited because they are
normal anatomical structures are not visible deduced from relatively few projections, say
radiographically (e.g. adrenal glands). Conversely, lateral and ventrodorsal.
certain structures that are normally visible may Abnormal position, i.e. as a result of displacement
be obliterated as a result of physiological variants of an organ, may be the principal radiographic
(e.g. lack of body fat) or disease. sign that a mass is present, and is a particularly
Potential causes of abnormal number in the important sign if the mass itself is not visible.
2006 World Congress WSAVA/FECAVA/CSAVA

abdomen: Consider a dog with a hepatic mass: caudal

Decreased displacement of the stomach may be the only
• Congenital absence (rare) radiographic abnormality. The caudal surface of
• Small organ, e.g. kidney, bladder the liver that contacts the stomach is not normally
• Displaced organ visible radiographically; therefore the presence of
- Ruptured diaphragm a mass cannot change its appearance. On the other
- Perineal rupture hand, the position of the lumen of the stomach is
- Hernia influenced by the position of the caudal border
• Organ not recognised, e.g. because it is deformed of the liver and is normally visible because of
- Renal mass the gas it contains. Therefore, a change in the
Increased position or shape of the gastric lumen is likely to
• Enlargement of normally invisible structures be the only sign of a hepatic mass bulging from
- Lymph nodes the caudal surface of the liver.
- Uterus It is often possible to make an assessment of the
• Lesion mimicking normal organ origin of a mass by the direction of displacement
- Paraprostatic cyst mimicking bladder of adjacent organs. Mobile abdominal viscera,
- Adrenal mass mimicking kidney principally the small intestine, are displaced
276
Back to contents
 Di
away from the point of origin of the mass. For different breeds of dog and between individuals
example, a mass originating by the bladder will of the same breed that tend to limit the usefulness
be expected to displace small intestine cranially; of organ measurements. As a result there are
a mass originating in the mesenteric root will very few measurements that are useful aids to
displace the intestine peripherally. The larger diagnosis – don’t bother trying to measure the
the mass, the more marked any displacement is liver or spleen, for example.
likely to be. Even relatively fixed organs, such • Rather than a direct measurement, radiographic
as the kidneys may be displaced by a gradually measurements of organ size frequently use a bone
enlarging mass. landmark as a reference point to take account of
the effects of magnification and variations in body
Abnormal size size, e.g. the canine kidney is about 3xL2.
Potential causes of abnormal size in the abdomen:
Increased Abnormal shape
• Hypertrophy Note that the silhouette of an irregular object
- Compensatory hypertrophy of contralateral varies greatly depending on its orientation
- kidney in unilateral renal disease whereas the silhouette of a rounded, regular
• Hyperplasia object does not. Perhaps radiologists are fortunate
- Prostatic that many important pathological structures,
• Congestion/oedema including primary neoplasms and metastases, are
• Infiltration (usually diffuse) roughly spherical so may be recognised whatever
- Acute inflammation the radiographic projection.
- Neoplasia, e.g. lymphoma Only a very uniform, diffuse disease (e.g.
- Fat, e.g. affecting the liver in diabetes mellitus congestion/oedema, acute inflammation) is likely
- Glycogen, e.g. affecting the liver in to change the size of an organ without affecting
hyperadrenocorticism its shape. Whereas a change in shape is usually
• Obstruction the result of a focal or multifocal lesion(s).
- Gastric outflow Potential causes of abnormal shape in the
- Intestinal abdomen:
- Ureteral • Mass
- Urethral - Physiological enlargement, e.g. urinary
- Uterine/vaginal bladder
Decreased - Neoplasm
• Congenital (hypoplasia) - Haematoma
• Atrophy - Inflammatory lesion, e.g. abscess
• Chronic inflammation - Obstruction causing dilatation
• Hypovolaemia, e.g. small liver in - Cyst (or pseudocyst)
hypoadrenocorticism - Torsion, e.g. spleen, retained testicle
• Previous resection • Scarring
- Chronic inflammation
Problems associated with recognition of abnormal - Previous surgery
organ size in the abdomen • Impingement by adjacent structure 2006 World Congress WSAVA/FECAVA/CSAVA
• We can recognise abnormal organ size only - Displaced organ
when we know how fairly precisely big the - Mass
normal organ is in an animal of the same body
weight as the patient in question; however, there
are marked variations in conformation between

277
Back to contents
Di
Abnormal opacity
Summary of potential opacity changes in disease:
Normal opacity Change in opacity Examples
↑ ↓
Gas/air - Soft tissue Intraluminal gastric mass
Calcification Bone in GI tract
Fat - Calcification Fat necrosis
Soft tissue Gas Gas-forming infection
Hollow foreign body
Calcification Urinary calculi
Chronic haemorrhage
Bone Soft tissue Bone cyst, lytic lesion
Metallic Surgical implants

Abnormal margination organs may be particularly sharp in an animal

A difference in opacity must be present between with pneumoperitoneum. Hence in the abdomen,
adjacent structures for their edges to be visible margination of the various organs tends to reflect
radiographically. changes in their surroundings rather than organ
Imagine a typical radiograph of an animal. The disease per se.
bones are visible because they are more opaque Potential causes of abnormal margination in the
than the adjacent tissues (cartilage, muscle, abdomen:
ligament) as a result of their higher physical Decreased clarity of organ margins
density and calcium content. The edge of the • Surrounding fluid
bone (= periosteal surface) is a bone: soft tissue - Retroperitoneal
interface. Changes in the appearance of bone - Peritoneal
margins, such as irregular or indistinct margins, • Serosal lesion
which may represent a periosteal reaction, are - Adhesions (chronic peritonitis)
important signs of diseases affecting the bone. - Carcinomatosis
Similarly, the edges or margins of various - Adherent clots (blood, proteinaceous)
abdominal organs are normally visible because • Lack of surrounding fat
they are more opaque that the surrounding - Juvenile patient
fat, which appears as a darker grey around the - Chronic disease causing weight loss
liver, spleen, kidneys, etc. If no fat is present, - Enhanced margins
for example if the patient is very thin due to • Surrounding gas
chronic illness, the difference in opacity that - Retroperitoneal
produced the organ edges initially is no longer - Peritoneal
present and therefore the organs are invisible. • Calcified margins
If the fat is infiltrated by inflammatory cells or
2006 World Congress WSAVA/FECAVA/CSAVA

- Paraprostatic cyst
displaced by peritoneal fluid the margins of the • Contrast study
abdominal organs may become indistinct or
blurred. Conversely the margins of abdominal

278
Back to contents

Di - Diagnostics imagine
OLD RADIOGRAPHIC TECHNIQUES FOR THE ABDOMEN
REVISITED
David S. Biller, DVM
Diplomate, American College of
Veterinary Radiology
Professor and Head of Radiology
Kansas State University
College of Veterinary Medicine
Department of Clinical Sciences
1800 Denison Ave
Manhattan, KS 66503
USA
biller@vet.ksu.edu
Abdominal Compression Radiography
Abdominal compression radiography is the
use of a radiolucent device to compress an area
of interest, thus decreasing subject thickness
and allowing anatomic isolation of a structure.
This technique provides for evaluation of the
size, shape, location, and opacity of a specific
organ, without the degree of superimposition of
structures seen on survey radiographs. Indications
include a suspected abnormality on survey
abdominal radiographs, which is inconclusive due
to superimposition of structures. Compression
radiography of the abdomen provides additional
information in cases, which helped with diagnosis,
prognosis, and therapeutic options.
The equipment necessary is minimal and consists
of varying sizes of wooden or plastic (Lucite or
Plexiglas) stirring spoons or paddles. Any rigid
radiolucent material may be used. The size of
the compression surface should be based on the
area of interest. Ideally the compression surface
should be 1.5 times the area of the target organ.
The field size should be collimated to include
only the region of interest. This will improve
image quality and decrease personnel exposure
by decreasing scatter radiation. It is important
to recognize that compression of the animal
will decrease the subject thickness, therefore
exposure factors should be adjusted accordingly.
A decrease in kVp by approximately 10% to 15%
is usually adequate. The animal can be measured
while compressed if exposure factors are in
question. Failure to decrease technique will result
in overexposure. Tranquilization may be helpful
to aid in positioning, but is not required.
This technique should not be used when there
is a large increase in uterine size with suspected
pyometra because there is the potential of
uterine rupture. The same holds true for very
large masses which are cystic in nature, such
as hemangiosarcoma. Diaphragmatic hernia
Back to contents
Di
is a contraindication because of the potential
to further displace abdominal contents into
the thoracic cavity. Compression radiography
can also be used in combination with contrast
procedures of the gastrointestinal or upper and
lower urinary tract.
Compression radiography is helpful in delineation
of the origin of a mass, size and shape of an organ,
and abnormal opacities (gas or mineralization)
such as renal, ureteral, or cystic calculi. This
technique has also been used when assessing
for fetal death. This allows for improved detail
of fetal skeletal structures when checking for
normal alignment.
Cases for compression should be selected based
on the area of interest and the size of the animal.
The region of interest must be a compressible
area. For example, this technique could not be
used on structures underlying the rib cage. Cats
and small to medium size dogs are more readily
examined because abdominal organs are easier to
separate. This technique has been used on giant
breeds with success. Compression can be used
with any position, although lateral recumbency is
most common.
2006 World Congress WSAVA/FECAVA/CSAVA
Contraindications include enlarged organs in
which rupture of the structure may occur. Examples
would include a severely enlarged uterus or
severe splenic enlargement due to a cystic mass.
Diaphragmatic hernia is also a contraindication
because compression may displace abdominal
viscera into the thoracic cavity.
Positional Radiography
Radiography of the gastrointestinal tract is
indicated in cases of foreign body ingestion,
vomiting, regurgitation, abdominal pain,
abdominal distention, weight loss, anorexia, and
abnormal abdominal palpation. Standard survey
abdominal radiographs include a ventrodorsal
and either a left or right lateral recumbent view.
279
Di
The determination of which lateral radiograph is
obtained is often personal preference. There are
differences in the appearance of various organs,
such as the kidneys, spleen, and gastrointestinal
tract, between the right and left lateral recumbent
radiograph. This varied appearance is particularly
noticeable in the gastrointestinal tract, which
is dependent on gas to provide contrast for
visualization of the mucosal surface.
Fluid and gastric contents are extremely mobile
and tend to move to the dependent portion of the
stomach during postural changes. Gas will rise
to the non-dependent portion of the stomach.
For example, in right lateral recumbency gas
accumulates in the fundus, and in left lateral
recumbency redistribution to the pyloric region
occurs.
Gas within the gastrointestinal tract serves as a
negative contrast media. Specifically, the change
in positioning of the animal for the opposite
lateral abdominal radiographs will allow for
the redistribution of gas already present in the
stomach, small, and large intestines. The position
of gas in the stomach changes in the following
manner. If the animal is in left lateral recumbency
gas will be present in the pylorus if the stomach
is in its normal location. Conversely, if the animal
is in right lateral recumbency gas will be present
in the fundus. It is important to realize that the
amount of gas will have and effect on which
portions of the stomach will contain gas. In a
severely gas distended stomach, gas may be in all
portions of the stomach on both lateral abdominal
radiographs. Even in these situations the location
of the pylorus can be determined. The right
lateral recumbent radiograph is recommended
in determining gastric dilatation from gastric
dilatation with volvulus.
Even in cases in which ileus is detected it is often
helpful to gain additional information to help
with surgical planning and prognosis.
2006 World Congress WSAVA/FECAVA/CSAVA
The fluid filled pylorus is an area, which can be
misdiagnosed as a cranial abdominal mass when
the right lateral recumbent radiograph is taken.
When the left lateral abdominal radiograph is
obtained the pylorus will be filled with gas.
This technique may not always be useful if there
is minimal air within the gastrointestinal tract.
Air can be introduced via and orogastric tube and
is especially useful in disorders of the stomach.
Pneumogastrogram
Indications for the use of contrast in evaluation of
the stomach include:
1) Suspicion of luminal or mural gastric masses.
2) Radiolucent gastric foreign bodies.
3) Hematemeisis.
4) Recurrent or non-responsive vomiting.
280
Back to contents
5) Gastric localization, identification, size, shape,
and margination.
6) To evaluate motility.
Preparation of the patient include survey
radiographs which should always precede
contrast studies. Survey radiographs allow
evaluation for subsequent adjustment of
technical exposure settings for the contrast
study. The animal should be fasted 12-24 hours
before radiography. Cleansing enemas should
be done the night prior and 2-3 hours before the
procedure. Contrast procedures should always be
individualized. If a patient has acute abdominal
pain or there is a potential for time delay which
may make a difference the enema and fasting
should be overlooked. Many drugs affect motility
and these drugs should be discontinued for an
appropriate interval before any contrast study is
done. Contrast agents include negative (room air)
and positive (barium sulfate suspension which is
micropulvarized). If perforation is suspected an
organic iodinated solution like Iohexol should
be used. Other equipment includes mouth gag
and an orogastric tube. Gastrograms are most
often used as part of an otherwise standard
upper GI series (the small bowel evaluation
follows the introduction of a positive contrast
media). Technique includes dosage of barium of
approximately 5 mls/lb that is administered via
a gastric tube. Radiographs are routinely taken
in right lateral and ventrodorsal but for complete
and accurate evaluation of the stomach a DV and
left lateral films may be taken. Films are taken
immediately to evaluate the complete stomach,
before it starts to empty.
Partial Barium Enema / Pneumocolon
A helpful technique in differentiating distended
small intestine from large intestine is a partial
barium enema. This technique also helps localize
the colon in the abdomen. Technique includes
introduction of either barium or gas (room air) at
a dosage of 6 ml/Kg. Introduce it with a flexible
catheter as far into the colon as possible. Then
take a ventrodorsal and well as right and left
lateral abdominal radiographs.

Di - Diagnostics imagine
HOW TO PRODUCE A GREAT THORACIC RADIOGRAPH
David S. Biller, DVM
Diplomate, American College of
Veterinary Radiology
Professor and Head of Radiology
Kansas State University
College of Veterinary Medicine
Department of Clinical Sciences
1800 Denison Ave
Manhattan, KS 66503
USA
biller@vet.ksu.edu
Diagnostic radiology is an extremely valuable tool
probably the most important in the diagnosis of
thoracic disease. It usually reveals more specific
information than can be gained from taking a
history and performing a physical examination
relatively cheap and quickly and providing rapid
results. Although we know that all the information
gained is important towards developing a list of
differential diagnosis.
History and physical examination changes
associated with thoracic disease can be ambiguous.
Therefore indications for thoracic radiography
(noncardiac) can be numerous and varied.
Some Indications for Thoracic Radiographs
include:
• Cough
• Dyspnea
• Post-trauma
• Geriatric preanesthesia
• Post-operative
• Swallowing dysfunction
• Hyperthyroid work-up
• Metastasis check
Understanding the factors involved with the
production of a quality radiograph are important,
because diagnosis can be limited or made
incorrectly by poor quality.
Common Quality Errors include:
• Not including entire thorax on film
• Not centering thorax on film
• Not taking film on inspiration
• Poorly positioned patient
• Patient motion
• Appropriate technique (mAs, kVp)
• Not short enough exposure
• Film processing error
• Poor environment for evaluating radiograph
The entire thorax (not to mistaken for the entire cat)
including thoracic inlet and the entire diaphragm
should be on the radiograph. The radiograph
should also include the caudal cervical trachea.
The lateral radiograph should be centered at the
Back to contents
Di
caudal edge of the scapula when the exposure
is taken. Make sure the animal is straight. This
is best accomplished on the lateral radiograph
by having the spine and sternum parallel and
equidistant from the table in the lateral view.
Padding under the sternum will help accomplish
this. Oblique positioning artifact is common
and can make the heart appear falsely enlarged
and create confusing lung shadows. Proper
positioning should also include the extension of
forelimbs forward off the chest and parallel to
each other. Head in neutral position in lateral view
(Flexion of head and neck often causes confusing
deviation of thoracic trachea). Do not stretch the
animal as this will distort the thorax. Radiographic
signs of malpositioning on the lateral radiograph
include: lack of superimposition of costochondral
junctions, dorsal arches of ribs not at same level
on each side, and thoracic vertebral bodies not
individually and distinctly visualized. Right
lateral recumbency preferred due to a more
constant cardiac position. Left lateral recumbency
produces a less consistent cardiac position,
although it is useful in evaluation of suspected or
questionable right sided pulmonary lesions.
Radiographic signs of malpositioning of the VD
or DV views include: spine and sternum not
2006 World Congress WSAVA/FECAVA/CSAVA
superimposed, costal cartilages not symmetrical,
dorsal processes of the vertebrae do not appear
as oval central opacities superimposed over the
vertebral bodies, and contralateral ribs different
lengths. Oblique positioning although good
for evaluation of extrapleural or thoracic wall
lesions (disease) can create confusing artifactual
abnormalities such as giving a false appearance
of mediastinal shift of the heart or create the
appearance of an abnormal heart shape. The
dorsoventral (DV) radiograph shows a more
constant cardiac position. Pulmonary ventilation
is more uniform especially for the caudodorsal
lungs and it is less stressful on the respiratory
compromised patient. Small very ventral lesions
of the right middle and caudal subsegment of the
281
Di
left cranial lung lobe may not be visualized in
the DV radiograph. The cardiac position is less
constant on the ventrodorsal (VD) radiograph, and
appears longer on the VD. The VD radiograph is
useful in the evaluation of the heart when small
volumes of pleural fluid are present. Fluid falls to
dependent areas (paravertebral gutter) and avoids
silhouetting (border effacing) the heart.
The most common error associated with poor
quality thoracic radiographs is motion of the
animal during exposure. This may be due to
motion of the animal resisting restraint or from
respiration or heart beat (this blurring can cause
mis-interpretation). A short exposure time
(< 1/30th of a second - 1/60th ideal) is the best
way to avoid motion. Things that are helpful in
decreasing exposure time include: rare earth film,
faster intensifying screens, and x-ray machines
that allow short exposures (shorter mAs can
be achieved by increasing kVp by 15% and
decreasing mAs by half).
High kVp, low mAs gives a high latitude / low
contrast radiograph (long scale of contrast) which
is ideal for the thorax (makes evaluating things
like the small pulmonary vessels possible). Use of
a grid is important when patient thickness exceeds
10 cm therefore reducing scatter. Assessment of
2006 World Congress WSAVA/FECAVA/CSAVA
282
Back to contents
adequate penetration can be made on the VD or
DV radiograph by faint visualization of the spine
through the cardiac silhouette (or intervertebral
disc spaces should be faintly visible through
the cardiac shadow), and on the lateral by faint
visualization of the dorsal spinous processes of
the cranial thoracic vertebrae (or cranial thoracic
vertebrae should be moderately underexposed
and the mid-thoracic vertebrae should be easily
seen). Ribs will also be poorly visualized over
the cardiac silhouette. The peripheral lung fields
should not be over exposed (high kVp / low mAs
technique will help prevent this).
Thoracic radiographs should be taken during
peak inspiration with few exceptions (greatest
air/tissue ratio and it is the contrast provided by
this air/tissue ratio that allows us to visualize
intrathoracic structures). The key to making
the exposure at full inspiration is to take the
radiograph while the animal is breathing in. These
differences can equal or mimic those caused
by pathology. Expiratory films can sometimes
be useful in: detection of dynamic collapse of
intrathoracic trachea or bronchi, demonstrate
small degree of pneumothorax, and demonstrate
air-trapping by the lungs.

Di - Diagnostics imagine
THE NORMAL THORACIC RADIOGRAPH: WHY YOU MUST
UNDERSTAND NORMAL TO RECOGNIZE ABNORMAL
David S. Biller, DVM
Diplomate, American College of
Veterinary Radiology
Professor and Head of Radiology
Kansas State University
College of Veterinary Medicine
Department of Clinical Sciences
1800 Denison Ave
Manhattan, KS 66503
USA
biller@vet.ksu.edu
If you can accurately describe a radiographic
lesion you are well on your way to identifying
the disease process. There are 3 phases to
interpretation of a radiograph. First phase is
called the Recognition phase. In this phase we
compare all parts of the radiographic image to
normal . If any abnormalities are recognized we
must consider whether they are a normal variant,
an artifact, or due to improper patient positioning.
The second phase is Descriptive phase. In this
phase we describe how the lesion varies from
normal including: changes in opacity, size, shape,
contour (margination), location, position, and
number. We also describe the extent of the lesion
(involve entire left cranial lung or just the cranial
subsegment). Lastly we describe the distribution
of the lesion (focal, multifocal, or diffuse). The
last phase is the Analysis phase. Take all the
information regarding radiographic changes
from normal, historical information (patient
signalment) and abnormalities found on physical
examination and develop a list of differential
diagnosis. Prioritize this list by probability. At this
point additional information may be necessary and
require additional tests (radiographs, ultrasound,
computed tomography, blood work, culture and
biopsies/fine needle aspirates).
Chest wall
Evaluation of the chest wall or extrathoracic
structures should always include the cranial
abdomen and caudal cervical regions. Liver
size, abdominal distension, free abdominal gas
and presence of peritoneal fluid can usually be
diagnosed. Position of abdominal viscera may
be partially evaluated in suspected cases of
diaphragmatic hernia. In cats the appearance of
the falciform fat triangle, just ventral to the liver
can also be used for this evaluation.
Evaluation of the chest wall radiographically
includes: soft tissues, ribs, sternum, and spine.
Back to contents
Di
The chest wall should first be examined from a
distance for symmetry. The ribs should also be
examined for symmetry. Fractures, penetrating
wounds and neoplasia may cause displacement
of or destruction of ribs. The chest wall should
be evaluated for changes in opacity (focal/
diffuse opacities or lucencies). One of the
biggest problems associated with interpretation
of the thorax is associated with the normal
chest wall,is skin folds. Skin folds can be
confused with lobar borders causing erroneous
diagnosis of pneumothorax. Subcutaneous
masses and dirt (ticks) can also add confusion
when evaluating chest wall and pulmonary
parenchyma. Deformities (ie. scoliosis, lordosis,
kyphosis, pectus excavatum) are rarely of clinical
significance but can cause marked changes in
appearance of the internal thoracic structures.
Lesions of the chest wall include: trauma
(fractures, swelling, SQ emphysema), infections,
degeneration, and neoplasia. Many chest wall
lesions present as masses, and if they project into
the thorax may demonstrate an extrapleural mass
sign:
1. Well defined convex border facing the 2006 World Congress WSAVA/FECAVA/CSAVA
pulmonary surface.
2. Tapered edges which blend into the chest wall,
3. Adjacent rib lesion (destructive &/or
productive reaction). These signs may be difficult
to demonstrate unless the x-ray beam catches the
mass tangentially.
Diaphragm
The position of the diaphragm depends upon
muscle tension and the trans-diaphragmatic
pressure. The diaphragm is not actually visualized
as a separate structure; the density seen (or what
we call the diaphragm) is mainly the cranial aspect
of the liver. If the diaphragm is seen separately
as a thin band it is indicative of free gas in the
abdomen (pneumoperitoneum).
283
Di
The inability to visualize the diaphragm may
be due to border effacement or its rupture.
Border effacement may occur secondary to
alveolar pattern in the caudal lung lobes or
pleural effusion. Rupture of the diaphragm or a
diaphragmatic hernia may occur as an acquired
disease from trauma or congenital for example:
hiatal, or peritoneopericardial.
Radiographic signs of a traumatic diaphragmatic
hernia include: interruption of diaphragmatic
outline (incomplete visualization of diaphragm),
abdominal viscera displacement (presence of
abdominal structures in the thorax-abdominal
radiograph maybe helpful), pleural effusion &/or
thoracic mass lesion which may contain loculated
gas, ± rib fractures, and mediastinal shift. Pleural
effusion maybe asymmetrical. The irregular
herniated organs compress the lungs on one side.
The spaces between the lungs and the organs
fill with fluid, obscuring the organs. Additional
studies which may be useful in the diagnosis of
a diaphragmatic hernia: abdominal radiographs,
UGI, positive contrast peritoneography, and
multiple positional radiographs. Differential
diagnosis for loss of diaphragmatic outline
include: pleural fluid, pleural masses, mediastinal
densities, and pulmonary densities.
Mediastinum
Mediastinum is a body compartment or potential
space between pleural cavities lined on each side
by pleura (mediastinal pleura). This is a nebulous
anatomic area which may be difficult to evaluate
because of a lack of any contrasting tissue
densities. Radiographic diagnosis of disease may
be difficult because: 1) number of incompletely
visualized organs (lack of contrasting tissue
densities), 2) superimposition of spine on VD/
DV film, and 3) normal fat accumulation there.
It extends from dorsal to ventral and from the
thoracic inlet to the diaphragm. On the lateral
2006 World Congress WSAVA/FECAVA/CSAVA
view a fluid opaque area can be visualized
between the thoracic inlet and carina and from
the ventral edge of the spine to just ventral to
the trachea. This is the craniodorsal mediastinum
which contains a number of important structures
including: trachea, esophagus, heart, great vessels
(ie., aorta, caudal and cranial vena cava), thoracic
duct, and major nerves, lymph nodes, and thymus
(young animals). The mediastinum is poorly seen
as a distinct structure on the lateral radiograph.
On the DV radiograph the cranial and caudoventral
borders are apparent. Normal thickness of the
cranial mediastinum is 1.5 to 2 times the width
of the vertebral bodies in the cat. Should have
smooth, rather straight margins. Wide cranial
mediastinum in young animals (< 1 year) usually
due to thymic shadow (sail sign). Esophagus,
284
Back to contents
outer tracheal walls, major subdivisions of the
aorta, cranial vena cava, and azygos vein are not
normally seen; their visualization would indicate
the presence of gas within the mediastinum
(pneumomediastinum). Esophagus may be seen
without surrounding gas if it contains gas or
material (fluid, food, barium).
The right and left hemithoraces are essentially
equal in size when evaluated on the VD/DV
radiograph. Any difference in size is referred to
as a mediastinal shift. This can result from uneven
inflation of lungs (right versus left) caused by a
unilateral increase or decrease in lung volume or
a unilateral increase or decrease in intrathoracic
pressure (volume).
Mediastinum should also be evaluated for
presence of diffuse or focal widening which may
indicate a infiltrative process or mass lesion.
Diffuse mediastinal widening, indistinctness or
border effacement of contained structures, and
narrowing or displacement of the trachea can
be seen with fluid accumulation (mediastinitis,
hemorrhage-coagulopathy, trauma).
Mediastinal masses are common in cats and
appear as thoracic densities near midline and
frequently cause displacement of adjacent
structures. If a mass is in contact with a
mediastinal structure it will be border effaced.
Mediastinal masses are frequently divided
up by location: cranioventral, craniodorsal,
perihilar, caudoventral, and caudodorsal.
Radiographic changes associated with mediastinal
masses include: increased opacity or opaque
cranial thorax (mediastinum), displacement
of normal mediastinal structures( displaced
and or compressed trachea and/or esophagus-
esophagram is helpful), widened mediastinum,
and loss of distinct mediastinal borders.
Differential diagnoses as well as confusing lesion
that may mimic mediastinal disease includes:
normal thymus young animals, obese animals,
lung mass (especially of the cranial tips of L and
R cranial lungs and accessory lung), and perihilar
edema.
Pleura and Pleura Space
The pleural space is a potential space between
the visceral (pulmonary) and parietal (costal,
mediastinal, and diaphragmatic) pleura. The
lung remains inflated and occupies the pleural
space rather than demonstrating its normal elastic
retractile property because of the surface tension
of the pleural fluid and sub-atmospheric pressure
present in the thorax. The normal pleural spaces
(right and left) are not visualized radiographically,
although a small amount of fluid is present and
acts as a lubricant reducing friction between
pleural surfaces. They usually communicate

with each other through fenestration of the
mediastinum, but not with other compartments of
the body. Interlobar fissures are reflections of the
visceral pleura on the lung lobes, not normally
seen. Three criteria must be met for the pleura to
be visualized radiographically:
1) projection of pleura on end (tangential beam
striking pleural margin or border),
2) thickened pleura or increased pleural fluid
present, and
3) well aerated lung adjacent to diseased lung to
contrast the pleura. We usually do not see pleural
fissures because the x-ray beam strikes the pleural
margin obliquely. When seen they will appear as
very thin, sharp lines in typical locations. It is
more common to see interlobar fissures in the
older animal secondary to pleural thickening
(aging change).
Radiology plays an extremely important role
regarding pleural disease: detection, location,
estimation of volume, distribution, and mobility of
the air or fluid, placing needle for thoracocentesis,
and evaluation for associated disease (chest wall,
pulmonary, mediastinal, diaphragmatic). The are
2 broad categories of pleural disease:
1) increased opacity to the pleural space (pleural
effusion or mass lesion),
2) decreased opacity of the pleural space
(pneumothorax).
Back to contents
Di
Pulmonary Parenchyma
The overall opacity of the lung depends upon the
ratio between air within the alveoli and bronchi
and soft tissue of the vessels and interstitium. Any
process that alters this ratio alters the appearance
of the lungs. The components of the lung
include: airways and alveoli, vessels, interstitium
(lymphatics, supporting framework for vascular
and bronchial structures, interalveolar septa), and
bronchi. The pulmonary opacity can be increased
by conditions other than pathology including:
poor inspiration, severe obesity, under exposure,
and advanced age. The lungs are usually divided
into 3 regions for evaluation and include: central
(perihilar), middle, and peripheral.
Pulmonary lesions may be described as: solitary,
multiple, focal or disseminated (diffuse). Other
descriptive terms that can be used in describing
lesions of the lungs include: well defined, ill
defined, irregular, rounded, nodular, fluffy,
homogeneous, inhomogeneous, cavitary, and
solid. Pulmonary parenchyma lesions may also
include generalized increases and decreases in
pulmonary opacity.
2006 World Congress WSAVA/FECAVA/CSAVA
285
Di
Di - Diagnostics imagine
MRI OF THE MUSCULOSKELETAL SYSTEM
Johann Lang, Dr.med.vet., Dip
ECVDI
Division of Clinical Radiology
Department of Clinical Veterinary
Medicine
Vetsuisse Faculty Bern
Länggassstrasse 128, Postfach
CH-3001 Bern
johann.lang@kkh.unibe.ch
http://kleintierklinik.unibe.ch
In human medicine examination of musculoskeletal
abnormalities of the appendicular skeleton is the
most common non-neurologic application of
magnetic resonance imaging (MRI). The knee
(menisci, ligaments), shoulder (rotator cuff), and
hip joints (avascular necrosis) are the joints most
often examined, but other joints and soft tissues
also are assessed with MRI. In veterinary medicine
there is an increasing number of reports describing
normal MRI anatomy and pathology of the distal
limbs in clinically normal and lame horses. In
small animals reports using MRI as a diagnostic
tool in orthopedic diseases are still sparse. They
are concentrating on technical aspects including
contrast procedures, specific regions such as the
knee joint, assessment of specific diseases such
as bone tumors and research on pathophysiology
and treatment of osteoarthritis using the dog as
model (e.g. Pond Nuki model for the development
of osteoarthritis).
The following paragraphs will give a short review
on applications of MRI in orthopedic diseases in
small animals and discuss possible indications,
benefits and limitations. Radiography is still
the single most important diagnostic tool for
the detection and diagnosis of musculoskeletal
2006 World Congress WSAVA/FECAVA/CSAVA
diseases, and Ultrasonography is an excellent
method for soft tissue pathologies. Computed
tomography (CT) and MRI are used as
complementary techniques in selected cases. It is
widely accepted that computed tomography has
advantages over MRI in imaging the morphology
of normal bone and in traumatology, whereas
MRI is the method of choice in imaging soft
tissues such as the muscles, tendons, ligaments,
joint capsule and menisci, but also diseases of the
bones leading to alteration in the bone marrow
composition. The examination time of MRI
is longer than for CT especially if helical CT
scanners are used. This has consequences for the
anesthesia and increases the costs.
286
Back to contents
Martin Konar, Dr.med.vet.
Division of Clinical Radiology
Department of Clinical Veterinary Medicine
Vetsuisse Faculty Bern
Länggassstrasse 128, Postfach
CH-3001 Bern
martin.konar@kkh.unibe.ch
Properties of MRI
• very high soft tissue (contrast) resolution
• individual sequences and contrast media allow
differentiation of different types of soft tissues
and pathologies
• imaging in any desired plane facilitates three-
dimensional understanding of morphology
Sequences
• STIR or other fat saturation sequences: high
contrast, low spatial resolution – screening
for lesions in general, bone marrow, menisci,
muscles
• FE T2*: good contrast and moderate spatial
resolution - ligaments in general, menisci
• FE 3D MPR or SPGR (T1) - native/+C : high
spatial resolution – contrast sensitive, cartilage
• Completely balanced sequences (BASG; True
FISP, B-FFE3D; other) – ligaments/cartilage.
• FSE T2: high contrast moderate spatial
resolution – tendons; trouble shooting for high
SI in ligaments (cranial cruciate Ligament)
• SE T1 in combination with post contrast
studies
Review
MRI is an excellent tool for screening for bone
metastases with a compared to scintigraphy
higher sensitivity for specific soft issue tumors.
However, assessment of bone marrow pathology
requires knowledge of the MRI features of the
normal bone marrow in different age groups. The
different patterns are associated with the different
composition of the bone marrow in growing,
adult and aging bones. Fat suppression sequences
such as the STIR (Short TI Inversion Recovery)
will exhibit a bright signal in the diaphysis of
long bones in 3 to 6 month old dogs because of
the “red” bone marrow. In adult dogs, this will
be replaced by fatty marrow and will be dark in
the same sequence. However, reconversion to
hematopoietic marrow is also described in older
individuals.
In a series of 10 dogs with osteosarcoma of long
bones, radiographic examination underestimated

tumor length substantially in 1 limb and slightly
in another limb. CT and MRI were least accurate
but did not underestimate tumor length in any of
the limbs. Obviously, MRI is overestimating the
extent of osteosarcoma because it is very sensitive
for any change in the adjacent bone marrow such
as inflammatory reaction or hyperemia.
Most joints including the shoulder joints are rare
indications to perform an MRI in dogs. Unlike
as in humans where rotator cuff tear is the most
typical indication for MRI of the shoulder,
bicipital injuries are far more common in the dog.
However, the supra- and infraspinatus muscle and
tendon insertion, the bicipital tendon and tendon
sheath, and the shoulder are readily assessed
using ultrasonography and are rare indications
for MRI.
As in humans, the knee joint is also the joint
with the highest number of MRI reports in the
dog. The primary indication for MRI of the knee
is evaluation of internal derangement. MRI is
helpful when physical examination findings
and the results of other imaging modalities are
equivocal or for assessing the entire joint with
all its components. MRI primarily assesses the
menisci and ligaments, but the joint capsule, the
integrity of the osseous structures and muscles
also can be evaluated. MRI is a sensitive method
for assessing the menisci non-invasively. MRI
of meniscal injuries of the knee in the dog is not
fully understood yet and there are differences in
the appearance depending on the field strength
of the magnet. However, a meniscal tear usually
appears as increased signal that reaches the
articular surface within the normally dark menisci.
Ligamentous injuries of the knee typically present
as abnormally high signal and lack of a normal
course for the ligament in question. MRI therefore
is an excellent method for evaluation of cranial
cruciate ligament tears and associated pathologies
of the menisci and underlying bone of the tibial
plateau and femoral condyles including for the
presence of osteophytes. Bone marrow edema
like lesions (“bone bruise”) will appear dark on a
STIR sequence, is usually masked by the fat in T2
sequences und will appear dark on T1 sequences.
They may or may not take up contrast.
Due to its small thickness being in the range of
the achievable resolution of the applied MR-
sequences, cartilage imaging is still a challenge in
veterinary MRI. Whereas in human medicine very
high resolution sequences with fat suppression
pulses are of great value, the best sequence for
cartilage evaluation in veterinary MRI still has
to be determined. However, because of its high
sensitivity for bone marrow changes, a cartilage
lesion can be suspected due to changes of the
subchondral bone.
Back to contents
Di
Muscular lesions are readily identified using fat
suppression techniques (e.g. STIR). They are
preferred to normal SE or FSE T2 sequences
because hyperintense lesions may be masked
by the hyperintense surrounding fat. In a STIR
sequence, the normal muscle will appear dark,
a lesion usually will present with high SI. They
may or may not take up contrast material; if
contrast medium is used, fat – water separation
techniques will highlight contrast enhanced
lesions. Fat suppression techniques are also
helpful in distinguishing fatty degeneration of
muscles from other lesion. Fatty degeneration
(atrophy) will present with volume loss (usually)
and relatively high SI in T1 and T2 sequences.
These areas will present with low SI using fat
suppression techniques.
Suggested readings
1. Baird, D. K., J. T. Hathcock, P. F. Rumph, S.
A. Kincaid, and D. M. Visco. 1998. Low-field
magnetic resonance imaging of the canine stifle
joint: normal anatomy. Vet. Radiol. Ultrasound
39: 87-97.
2. Baird, D. K., J. T. Hathcock, S. A. Kincaid, P.
F. Rumph, J. Kammermann, W. R. Widmer, D.
Visco, and D. Sweet. 1998. Low-field magnetic
resonance imaging of early subchondral cyst-
like lesions in induced cranial cruciate ligament
deficient dogs. Vet. Radiol. Ultrasound 39: 167-
173.
3. Banfield CM, Morrison WB. Magnetic
resonance arthrography of the canine stifle joint:
technique and applications in eleven military
dogs. Vet Radiol & Ultrasound 2000; 41: 200-
213.
4. Carrig, C. B. 1997. Diagnostic imaging of
osteoarthritis. Vet. Clin. North Am. Small Anim
Pract. 27: 777-814.
5. Davis, G. J., A. S. Kapatkin, L. E. Craig, G. 2006 World Congress WSAVA/FECAVA/CSAVA
S. Heins, and J. A. Wortman. 2002. Comparison
of radiography, computed tomography, and
magnetic resonance imaging for evaluation of
appendicular osteosarcoma in dogs. J. Am. Vet.
Med. Assoc. 220: 1171-1176.
6. Gonzalo-Orden JM, Altonaga JR, Gonzalo-
Cordero JM et al. Magnetic resonance imaging
in 50 dogs with stifle lameness. Eur J Comp An
Pract 2001; 11: 115-118.
7. Hoskinson, J. J. and R. L. Tucker. 2001.
Diagnostic imaging of lameness in small animals.
Vet. Clin. North Am. Small Anim Pract. 31: 165-
80, vii.
8. Konar, M., Kneissl, S., Vidoni, B.,
Lang, J., Mayrhofer E. Niederfeld-
Magnetresonanztomographie am Kniegelenk
287
Di
des Hundes Teil 1: Untersuchungsprotokolle und
Sequenzen. Tierärztl. Prax. 2005; 33 (K); 5-14
9. Konar, M.,Vidoni B., Kneissl, S., Doherr,
M., Mayrhofer, E., Lang, J. Niederfeld-
Magnetresonanztomographie am Kniegelenk
des Hundes Teil 2: Verteilung pathologischer
Veränderungen und Korrelation mit
Operationsbefunden. Tierärztl. Prax. 2005; 33
(K); 73-82
10. Nolte Ernsting CC, Adam G, Buhne M et
al. MRI of degenerative bone marrow lesions in
experimental osteoarthritis of canine knee joints.
Skeletal Radiol 1996; 25: 413-420.
11. Ohlerth S, Lang J, Scheidegger J et al.
Magnetic resonance imaging and arthroscopy of
a discoid lateral meniscus in a dog. Veterinary and
Comparative Orthopaedics and Traumatology
2001; 14: 90-94.
12. Sanders TG, Medynski MA, Feller JF et
al. Bone contusion patterns of the knee at MR
imaging: footprint of the mechanism of injury.
Radiographics 2000; 20: 135-151.
13. Snaps, F. R., J. H. Saunders, R. D. Park, B.
Daenen, M. H. Balligand, and R. F. Dondelinger.
1998. Comparison of spin echo, gradient echo
and fat saturation magnetic resonance imaging
sequences for imaging the canine elbow. Vet.
Radiol. Ultrasound 39: 518-523.
14. Snaps, F. R., M. H. Balligand, J. H. Saunders,
R. D. Park, and R. F. Dondelinger. 1997.
Comparison of radiography, magnetic resonance
imaging, and surgical findings in dogs with elbow
dysplasia. Am. J. Vet. Res. 58: 1367-1370.
15. Snaps, F. R., R. D. Park, J. H. Saunders, M. H.
Balligand, and R. F. Dondelinger. 1999. Magnetic
resonance arthrography of the cubital joint in
dogs affected with fragmented medial coronoid
processes. Am. J. Vet. Res. 60: 190-193.
2006 World Congress WSAVA/FECAVA/CSAVA
288
Back to contents
16. van Bree, H., B. Van Ryssen, H. Degryse,
and F. Ramon. 1995. Magnetic resonance
arthrography of the scapulohumeral joint in dogs,
using gadopentetate dimeglumine. Am. J. Vet.
Res. 56: 286-288.
17. van Bree, H., H. Degryse, B. Van Ryssen,
F. Ramon, and M. Desmidt. 1993. Pathologic
correlations with magnetic resonance images of
osteochondrosis lesions in canine shoulders. J.
Am. Vet. Med. Assoc. 202: 1099-1105.
18. Wallack ST., Wisner ER., Werner JA.,
Walsh PJ., Kent MS., Fairley RA., Hornof WJ:
Accuracy of magnetic resonance imaging for
estimating intramedullary osteosarcoma extent
in pre-operative planning of canine limb-salvage
procedures; Vet Radiol Ultrasound. 2002 43(5):
432-41.
19. Widmer WR, Buckwalter KA, Braunstein
EM et al. Radiographic and magnetic resonance
imaging of the stifle joint in experimental
osteoarthritis of dogs. Vet Radiol & Ultrasound
1994; 35: 371-383.
20. Widmer, W. R., K. A. Buckwalter, E. M.
Braunstein, D. M. Visco, and B. L. O’Connor.
1991. Principles of magnetic resonance imaging
and application to the stifle joint in dogs. J. Am.
Vet. Med. Assoc. 198: 1914-1922.
21. Yabe, K., K. Yoshida, N. Yamamoto, S.
Nishida, C. Ohshima, M. Sekiguchi, K. Yamada,
and K. Furuhama. 1997. Diagnosis of quinolone-
induced arthropathy in juvenile dogs by use of
magnetic resonance (MR) imaging. J. Vet. Med.
Sci. 59: 597-599.

Di - Diagnostics imagine
CLINICAL UTILITY OF THE RIGHT INTERCOSTAL WINDOW FOR
ULTRASONOGRAPHY OF THE RIGHT CRANIAL ABDOMEN
David S. Biller, DVM
Diplomate, American College of
Veterinary Radiology
Professor and Head of Radiology
Kansas State University
College of Veterinary Medicine
Department of Clinical Sciences
1800 Denison Ave
Manhattan, KS 66503
USA
biller@vet.ksu.edu
For many sonographers, a standard abdominal
ultrasound examination is performed by
scanning the ventral abdomen from a subcostal
approach with the animal in dorsal recumbency.
Unfortunately, right cranial abdominal structures,
such as the right aspect of the liver, portal hilus
(hepatic lymph nodes, common bile duct, caudal
vena cava, and portal vein), right limb and body
of the pancreas, duodenum, right kidney, and
right adrenal gland are often not visible from
the standard subcostal approach. Evaluation of
right cranial abdominal organs via the subcostal
approach may be difficult in dogs that are deep-
chested, have microhepatia, have large amounts
of gas in the gastrointestinal tract, or have large
volume peritoneal effusion.
Normal Anatomy
Access to the liver in dogs may be difficult
because portions are located beneath the rib
cage. In large and deep-chested dogs, complete
evaluation of the liver may require a right lateral
intercostal approach from the last 3-4 intercostal
spaces
The right lateral intercostal approach is essential
in evaluation of the portal hilus and nearby
vessels. Important structures in this region that
can be seen include the aorta, caudal vena cava,
portal vein, and common bile duct.
The aorta is the most dorsal of the vessels in the
region of the portal hilus. It can be found dorsal
to the caudal vena cava and the diaphragm. The
margin of the diaphragm blends with the ventral
wall of the aorta. In some cases, the azygos vein
may be seen running parallel and to the right of
the aorta
The caudal vena cava is ventral to the aorta and
runs through the foramen venae cavae of the
diaphragm to the right of midline in the mid-
dorsal diaphragm. It is surrounded by the caudate
Back to contents
Di
and right lateral liver lobes. The caudal vena
cava can be differentiated from the aorta by the
presence of hepatic veins entering.
From the right lateral intercostal window, the
portal vein is ventral and to the left of the caudal
vena cava and dorsal to the common bile duct.
The common bile duct is ventral and to the right
of the portal vein. The common bile duct may or
may not be seen, but should be less than 3 mm
in diameter in a normal dog. This structure is
often not seen from the standard ventral approach
because of intestinal gas. With the right lateral
intercostal approach, the liver is used as an
acoustic window.
Complete evaluation of the pancreas is difficult
from the standard ventral abdominal approach.
Reasons for this difficulty include intestinal
gas and cranial abdominal pain in cases of
pancreatitis. The right lateral intercostal window
is useful in evaluation of the right lobe and body
of the pancreas. From this approach, the right
lobe of the pancreas lies ventral to the right
kidney, ventrolateral to the portal vein, and dorsal
or dorsomedial to the descending duodenum.
The body of the pancreas unites the right and 2006 World Congress WSAVA/FECAVA/CSAVA
left lobes caudal to the pylorus and lies ventral
to the portal vein and craniomedial to the right
kidney. The colon is caudoventral to the pancreas.
The pancreaticoduodenal vein, which drains into
the portal vein may be seen in the right lobe of
the pancreas, running parallel to the descending
duodenum. This vessel is not visible in the other
pancreatic lobes. To ensure thorough evaluation
of the right lobe of the pancreas, the entire
descending duodenum should be followed.
Because of its cranial location, the right kidney
is difficult to examine in many dogs from a
subcostal approach. It often lies dorsal to small
intestine, which can be a barrier if it contains gas.
Positioning the dog in left lateral recumbency and
placing the transducer dorsally in the intercostal
space can allow better access to the kidney. The
289
Di
right kidney can be found by angling or moving
the transducer caudally from the portal hilus.
Because of its cranial location, the right adrenal
gland is difficult to access from the standard
subcostal ventral approach. The level of difficulty
is increased when there is gas in the pylorus and
the duodenum and in dogs >10 kg. The right
lateral intercostal approach is useful for finding
this structure. Landmarks for locating the right
adrenal include the caudal vena cava, the origin
of the celiac and cranial mesenteric arteries, and
the craniomedial aspect of the right kidney. To
find the gland in long axis, the caudal vena cava
is located caudal to the portal hilus.
Multiple lymph nodes can be assessed from the
right lateral intercostal window. The hepatic
lymph nodes are found next to the portal vein,
1-2 cm caudal to the portal hilus. The left hepatic
nodes range from 1 to 6 cm in length and are found
in the lesser omentum dorsal to the common bile
duct. The right hepatic nodes are smaller and are
found next to the body of the pancreas.
Clinical indications
The right lateral intercostal approach is useful
for diseases involving the right lateral, right
medial, and caudate lobes of the liver. This
view is especially helpful in diseases that cause
microhepatia, such as cirrhosis or congenital
portosystemic shunts. Ultrasonographic findings
associated with cirrhosis include, microhepatia,
hyperechoic parenchyma, irregular margination,
ascites, and regenerative nodules. Mass and
nodular lesions of the liver may also be evaluated
from the right lateral intercostal approach,
especially in large and deep chested dogs. These
lesions could easily be missed in these dogs if the
examination is limited to the subcostal approach.
Diseases involving the portal vasculature are
indications for the right lateral intercostal view.
This view is indicated in any animal suspected to
2006 World Congress WSAVA/FECAVA/CSAVA
have a portosystemic shunt. A single extrahepatic
shunt is difficult, if not impossible, to identify
from the standard subcostal approach, especially
in large dogs. The right lateral intercostal view is
useful in detection of intrahepatic portosystemic
shunts as well
Portal vein thrombosis, an uncommon condition
that is rarely diagnosed in live dogs, can be
diagnosed using the right lateral intercostal scan
plane.
Diseases of the biliary system are often
incompletely evaluated via the subcostal approach.
The right lateral intercostal approach is useful in
these cases. One indication for this approach is
suspected biliary tract obstruction, especially for
assessment of the common bile duct.
The right intercostal approach is useful in cases
290
Back to contents
of pancreatitis. These animals are painful, and the
intercostal approach avoids the pain induced with
scanning from the subcostal approach. The most
consistent landmarks for the right pancreatic lobe
are the duodenum and the right kidney. The right
lobe of the pancreas is found dorsomedial to the
duodenum and ventral to the right kidney. With
inflammation and bowel gas associated with
pancreatitis, vascular landmarks are often not
visible.
Diseases of the right kidney and right adrenal
gland may be more thoroughly evaluated via
the right intercostal view than the standard
subcostal approach. This is also a good view for
comparison of the echogenicities of the liver and
renal cortex.
The hepatic and sometimes the pancreaticoduodenal
and gastric lymph nodes can be assessed via the
intercostal window. Normal lymph nodes may not
be seen because their echogenicities are similar
to surrounding fat and muscle. Inflammation and
neoplasia will cause lymph nodes to enlarge and
become hypoechoic, making them more easily
detectable.
Percutaneous ultrasound-guided fine-needle
aspirate and biopsy are two commonly performed
procedures due to their low cost and relative lack
of invasiveness. Using ultrasound guidance, rather
than blind techniques, makes it less likely to end
up with a non-representative sample. Lesions of
the right cranial abdomen might not be accessible
from a standard ventral subcostal approach. The
right intercostal approach may allow access to
these lesions.
Conclusion
In conclusion, a ventral subcostal approach is
often inadequate for a complete ultrasonographic
examination. The right lateral intercostal scan
plane allows for a complete evaluation of the
liver, portal hilus, pancreas, duodenum, right
kidney, right adrenal gland, and cranial abdominal
lymph nodes. Animals in which this approach is
most useful are large and deep-chested dogs, dogs
with gas in the gastrointestinal tract, cases of
microhepatia, peritoneal effusion, and abdominal
pain.
Back to contents
Di

2006 World Congress WSAVA/FECAVA/CSAVA

291
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

EE
Endocrinology
doc

Back to contents

INVITED LECTURES - FULL PAPERS
E – Endocrinology
UPDATE ON FELINE DIABETES MELLITUS
Claudia E. Reusch,
DiplECVIM-CA
Clinic for Small Animal Internal
Medicine
University of Zuerich
Winterthurererstrasse 260
CH-8057 Zuerich
creusch@vetclinics.unizh.ch
In cats, diabetes mellitus represents one of the
most common endocrinopathies. Currently it
is assumed that the so-called administrative
incidence is 1:100 – 1:400. Risk factors are
increasing age, male gender, neutering and high
body weight. Approximately 80% of cats seem
to have type 2 diabetes mellitus (2DM) based
on islet histology and clinical characteristics of
the disease. 2DM is characterized by disorders
of both insulin action and insulin secretion; both
are usually present at the time of diagnosis. As
in humans there is a strong link between obesity
and 2DM, about 70 - 80% of cats are obviously
obese at the time of diagnosis. The association
with obesity is of practical and scientific
importance. Obesity is the main risk factor and
it is also the most obvious target for measures
to prevent diabetes. From a scientific viewpoint,
the mechanism by which obesity is diabetogenic
remains unexplained. It has been shown that cats
which increase their body weight by 2 kg had a
50% decrease in insulin sensitivity.
Administration of insulin and dietary
management are the mainstays of treatment in
diabetic cats. Treatment of diabetes mellitus
should be initiated as soon as possible after
diagnosis. Good glycemic control reverses
the effect of high glucose on -cells (glucose
toxicity) and increases the chance of remission
of diabetes. Glucose toxicity is a phenomenon,
which should be understood when managing
diabetes mellitus. It is defined as impaired insulin
secretion from beta cells as a result of prolonged
hyperglycemia. Initially, suppression of beta cells
is reversible, later, structural changes will lead
to an irreversible status. Glucose toxicity is the
reason why measuring insulin concentration is
usually not helpful to predict if the cat will go
into diabetic remission. We recently investigated
if differences in the response to arginine exist
between transient and non-transient cats. Cats
Back to contents
E
with DM had significantly lower insulin levels
during the arginine test than healthy cats and the
glucagon response was significantly higher. 5 of
the 10 cats studied went into diabetic remission
within 6 to 14 weeks. Insulin and glucagon
response did not differ between cats with transient
and non-transient course of disease.
In Zurich treatment is usually initiated with
a porcine zinc insulin of intermediate action
(Caninsulin®) twice daily: cats weighing < 4 kg
receive 1U/cat BID, cats weighing > 4 kg usually
receive 1.5 – 2.0 U/cats BID. Dosage changes
are performed with increments of 0.5U/cat BID.
Dosage changes are done no more often than
every 5 to 7 days. Time until adequate regulation
is achieved is somewhere between 1 and 3
months. The majority of cats is well regulated
with a dosage of < 1U/kg body weight BID. In
a recently performed multicenter study 72% of
the cats treated with Caninsulin were considered
well regulated. Initial insulin dosage was 0.34 +
0.14 U/kg BID, after 4 months the dosage was
0.64 + 0.32 U/kg BID. Diabetic remission was
achieved in 17% of cats within the study period 2006 World Congress WSAVA/FECAVA/CSAVA
of 4 months.
Recently, insulin analogues have been developed
in order to improve pharmacodynamic properties,
e.g. absorption. In humans, insulin glargine, a
long acting synthetic insulin analogue, is thought
to be a peakless insulin with a long duration of
action (> 24 hours).
In cats only few data on the use of Glargine are
available so far. According to a recently published
study, once-daily Glargine may be as effective as
twice-daily Lente-type insulin. Another group of
investigators described a remission rate of 100%
when Glargine was used BID.
During the last years opinion on diets for diabetic
pets has changed. The fact, that cats are true
carnivores recently came into focus again. As
such they have a high protein requirement and
293
E
the activity of hepatic enzymes responsible
for phosphorylation of glucose for subsequent
oxidation or storage is lower than in omnivores.
Several studies show that using low-carbohydrate-
high-protein diet results in better clinical control
and increased rates of diabetic remission. In
previous years, when we did not limit the type
of food our remission rate was 15-25%. We were
able to increase the remission rate to 50-70% by
using a low carbohydrate-high-protein-diet.
Diabetes mellitus is a chronic disease that requires
continuing medical care and owner education
to prevent acute complications and to enable
adequate life quality.
Until recently long-term management of diabetic
cats relied on the owners observation of clinical
signs and on periodic evaluation by a veterinarian.
The latter includes evaluation of the owners’
observations, measurement of body weight
and determination of blood glucose and serum
fructosamine. Cats, which eat and drink normal
and do not loose weight are usually well regulated.
Blood glucose concentrations in well regulated
cats range mostly between 15 mmol/l (prior to
insulin) and 5 mmol/l (nadir), fructosamine then
is either within the normal range or moderately to
slightly elevated (up to 450 μmol/l).
Serial blood glucose curves (BGCs) are necessary
to assess insulin efficacy, glucose nadir, time of
peak insulin effect, duration of the insulin effect,
degree of fluctuations in blood glucose (BG)
concentrations and to recognise the Somogyi
phenomenon. Until recently, the vast majority
of BGCs were performed in the hospital because
most pet owners are unable to collect blood
samples by venipuncture. However, a variety of
problems are associated with the determination of
BGCs in hospitalised patients. The process is time
consuming and relatively expensive and therefore,
is not performed as frequently as required. Stress
or lack of food intake can markedly influence BG
2006 World Congress WSAVA/FECAVA/CSAVA
concentrations. Cats in particular are sensitive
to stress caused by an unfamiliar environment
or by veterinary manipulation. Consequently,
the BGC may show a continuous increase in
the blood glucose concentrations, or it may be
elevated from the start. When the latter occurs,
it is not possible to differentiate between stress-
associated hyperglycemia, insulin under-dosage
and the many causes of insulin ineffectiveness and
resistance. Hospitalized diabetic cats frequently
refuse to eat, which may result in a marked
decrease in blood glucose concentration. It is then
difficult for the veterinarian to decide whether
anorexia or overdose of insulin is the cause of
low glucose concentration. Therefore, in-hospital
BGCs can be difficult to interpret or may even
be useless. During the last years, methods have
294
Back to contents
been developed for obtaining capillary blood
(mostly from the inner ear) by means of lancing
devices manufactured for humans. Measurement
of blood glucose concentration is performed
using one of the many portable glucose meters
(PGM). Attention should be paid to the fact that
performance differs largely between the different
PBG, and validation for use in cats is essential.
We have positive experience with the PBGM
Ascensia Elite (formerly Glucometer Elite,
Bayer Diagnostics) or with the latest generation
Ascensia Contour (Bayer Diagnostics). The latter
currently is the smallest PBGM on the market,
requires only small volumes of blood (0.6 μl) and
measurement is not started when blood volume is
too low, omitting the potential error of previous
PBGM generations.
Measurement of capillary blood glucose (home
monitoring, HM) has been part of the routine
protocol for long-term management for diabetic
cats in our clinic since 1999. Cat owners are
introduced to HM about 3 weeks after starting
therapy. We recommend determine fasting blood
glucose twice weekly (to practice blood sampling,
to detect hypoglycemia) and a BGC for 12 hours at
least once a month. BGC and appropriate changes
in treatment are then discussed over the phone.
Periodic re-assessments of the entire procedure in
the hospital are mandatory. For the first months
the patient is re-assessed at least once a month,
later on frequency is reduced to a minimum of
twice a year. Over the years we performed a
variety of studies on HM regarding technical
problems, comparison between blood glucose
measured at home and in hospital and long-term
compliance. Problems frequently encountered
initially include failure to produce negative
pressure with the lancing device, producing a
blood drop, absorption of the blood drop, correct
use of the test strip and restraining the cat. By
means of repeated explanation and demonstration
most problems can be solved. About 70% of our
cat owners are willing and able to perform HM.
Also long term compliance appears to be good.
In a recent study 76% of the owners performing
HM used the technique for more than one year
for up to 4 years. HM did not appear to influence
the frequency of re-evaluations in the hospital.
Most owners did not change insulin dosages
on their own, but called for advice. All cat
owners believed that HM had raised their self-
confidence with regard to their ability to manage
the disease in their pets. When blood glucose
curves generated at home and in the hospital were
compared with regard to treatment decisions, in
about 60% of cases treatment decisions would
have been the same. In 40% decisions would have
been different, in some cases even completely

contrary. We usually base our treatment decisions
on the curves generated at home. It is difficult
to proof whether hospital or home curves reflect
the true blood glucose concentrations. In our
study the percentage of well regulated cats was
higher than in comparable studies not using HM.
Therefore we assume that curves generated at
home reflect the true metabolic situation better
than those performed in the hospital. The success
of HM greatly depends on careful preparation and
instruction of the owners. They must have ready
access to veterinary support if needed. Initially,
most owners call for advice, and several of them
need repeated explanation or demonstration
of the procedure. One of the major advantages
of HM is that it enables frequent generation of
BGC. In complicated cases, more than one curve
can therefore be performed at home before a
treatment decision is made.
References
Appleton DJ, Rand JS, Sunvold GD. Insulin
sensitivity.decreases with obesity, and lean cats
with low insulin sensitivity are at greatest risk of
glucose intolerance with weight gain. Journal of
Feline Medicine and Surgery 2001; 3: 211-228.
Casella M, Wess G, Reusch CE. Measurement
of capillary blood glucose concentrations by pet
owners: a new tool in the management of diabetes
mellitus. Journal of the American Animal Hospital
Association 2002; 38: 239-5.
Casella M, Wess G, Hässig M, Reusch CE. Home
monitoring of blood glucose concentration by
owners of diabetic dogs. Journal of Small Animal
Practice 2003; 44: 298-305.
Goossens MMC, Nelson RW, Feldman EC,
Griffey SM. Response to insulin treatment and
survival in 104 cats with diabetes mellitus (1985
– 1995). Journal of Veterinary Internal Medicine
1998; 12: 1-6.
Back to contents
E
Kley S, Casella M, Reusch CE. Evaluation of
long-term home monitoring of blood glucose
concentrations in cats with diabetes mellitus:
26 cases (1999-2002). Journal of the American
Veterinary Medical Association 2004; 25: 261-
266.
Marshall RD, Rand JS. Treatment with glargine
results in higher remission rates than lente or
protamine zinc insulins in newly diagnosed
diabetic cats. Abstract. Journal of Veterinary
Internal Medicine 2005; 19: 425.
Rand JS, Martin GJ. Management of feline
diabetes mellitus. In: Behrend EN, Kemppainen
RJ (eds). The veterinary clinics of North
America, Small Animal Practice, Endocrinology.
2001, Volume 31, Number 5. W.B. Saunders,
Philadelphia. 881-913.
Rand J. Pathogenesis of diabetes mellitus in the
cat. The European Journal of Companion Animal
Practice 2004; 14: 131–34.
Thompson MD, Taylor SM, Adams VJ, Waldner
CL, Feldman EC. Comparison of glucose
concentrations in blood samples obtained with
a marginal ear vein nick technique versus from
a peripheral vein in healthy cats and cats with
diabetes mellitus. Journal of the American
Veterinary Medical Association 2002; 221: 389-
92.
Weaver KE, Rozanski EA, Mahony OM, Chan
DL, Freeman LM. Use of glargine and lente
insulins in cats with diabetes mellitus. Journal of
Veterinary Internal Medicine 2006; 20: 234-238.
Wess G, Reusch CE. Capillary blood sampling
from the ear of dogs and cats and use of portable
meters to measure glucose concentration. Journal
of Small Animal Practice 2000; 43: 60-6.
Wess G, Reusch CE. Laboratory assessment of
five portable blood glucose meters for use in cats.
American Journal of Veterinary Research 2000;
61: 1587-92.
2006 World Congress WSAVA/FECAVA/CSAVA
295
E
E – Endocrinology
THE DIAGNOSTIC APPROACH OF HYPERCORTISOLISM IN
DOGS AND CATS
Dr. Hans S. Kooistra, Dipl
ECVIM-CA
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
Yalelaan 108
3584 CM UTRECHT
THE NETHERLANDS
H.S.Kooistra@vet.uu.ni
Introduction
Hypercortisolism can be defined as the physical
and biochemical changes resulting from
chronic glucocorticoid excess. In dogs and
cats there are two main endogenous forms:
the adrenocorticotrophic hormone (ACTH)-
dependent form, which accounts for about 85% of
the cases, and the ACTH-independent form, which
is due to autonomous glucocorticoid-secreting
adrenocortical tumour(s). A combination of the
two forms may also occur.
ACTH is synthesized from a well-characterized
precursor molecule, proopiomelanocortin
(POMC), which also gives rise to a number of
other peptides that are co-released with ACTH. In
the canine and feline pituitary, POMC- producing
cells are present in both the anterior lobe (AL)
and the pars intermedia (PI). ACTH secretion by
the AL is regulated by the hypothalamus and the
central nervous system via hypophysiotrophic
hormones such as corticotrophin-releasing
hormone (CRH) and vasopressin. Glucocorticoids
inhibit ACTH release at the level of the AL and
the hypothalamus. The POMC producing cells of
the PI are resistant to glucocorticoid suppression
2006 World Congress WSAVA/FECAVA/CSAVA
due to the absence of glucocorticoid receptors on
these cells. The dopaminergic influence of the
hypothalamus is held responsible for inhibiting
the expression of glucocorticoid receptors on PI
cells.
Pituitary-dependent hypercortisolism (PDH)
or Cushing’s disease results from chronic
overproduction of glucocorticoids due to
excessive secretion of ACTH by the pituitary
gland, resulting in hypersecretion of cortisol
and in hyperplasia of the adrenal cortices. In
dogs and cats, PDH is most often caused by a
corticotroph adenoma that may originate in the
AL or the PI. One of the functional hallmarks
of corticotroph adenomas is that they are less
sensitive to the suppressive feedback effects of
glucocorticoids.
296
Back to contents
Adrenocortical tumours (AT) causing
hypercortisolism occur in both dogs and cats.
Most are unilateral lesions. The left and right
adrenal glands are affected about equally.
Bilateral tumours occur in about 10% of cases.
Histological types range from small well-
encapsulated adenomas to large adenocarcinomas
with liver and lung metastases (Rijnberk, 1996).
In both dogs and cats, spontaneous
hypercortisolism is a disease of middle-aged and
older animals. In dogs there is no pronounced
sex predilection, whereas in cats the great
majority of the reported cases are females. In
dogs the disease is seen more often in small
breeds such as Dachshund, miniature Poodles
and Yorkshire Terriers. Clinical manifestations
of dogs chronically exposed to excess cortisol
include polydipsia, polyuria, polyphagia,
abdominal enlargement, alopecia, panting,
muscle weakness and lethargy. The course of the
disease is often slowly progressive and often the
signs and symptoms are regarded by the owner
as a consequence of aging. In cats the cutaneous
manifestations are initially less pronounced than
in the dog. Polyuria and polydipsia in cats with
hypercortisolism may in most cases be the result
of concurrent diabetes mellitus. Cats seem to be
more susceptible than dogs to the diabetogenic
effects of glucocorticoids. Only about 10%
of dogs with hypercortisolism develops overt
diabetes mellitus.
Among the routine laboratory data a consistent
finding is an elevation of the plasma concentration
of alkaline phosphatase (AP). In dogs, this is
mainly due to the induction of an isoenzyme
which has greater stability at 65 degrees Celcius
than other AP-isoenzymes and is therefore easily
measured by a routine laboratory procedure.
In the majority of dogs with hypercortisolism
decreased plasma total thyroxine levels are found.
In addition, a low plasma urea level, lymphopenia
and eosinopenia, an elevated plasma glucose
level, and elevated liver values may be found.

Diagnosis
When the physical and biochemical changes fit in
with hypercortisolism, diagnostic tests have to be
performed to prove chronic glucocorticoid excess.
Measurement of the plasma cortisol concentration
has little diagnostic value, as the pulsatile
secretion of ACTH results in fluctuating plasma
cortisol levels that may at times be within the
reference range. The diagnosis hypercortisolism
should therefore rely on:
1) Determination of elevated urinary corticoid
excretion
2) Determination of a decrease in sensitivity to
the negative feedback effects of glucocorticoids
By determination of the urinary corticoid
excretion an integrated reflection of adrenal
glucocorticoid secretion is obtained, thereby
adjusting for fluctuations in plasma levels. The
urinary corticoid (largely cortisol) concentration
is related to the urinary creatinine concentration,
thus providing the urinary corticoid/creatinine
ratio (UCCR), in order to obtain a value
independent of the degree of urine concentration.
Determination of the UCCR requires little time
from the veterinarian, is not invasive (no blood
collection), and has a high diagnostic accuracy
(Rijnberk et al., 1988). In addition, the test
procedure has the advantage of combining a test
for basal adrenocortical function and a dynamic
test for differential diagnosis (see below).
The UCCR is a very sensitive reflection of
adrenocortical cortisol secretion. Therefore,
stress during or prior to the urine collection (e.g.
urine collection in veterinary practice or during
hospitalisation) should be avoided as much
as possible, since this activates the pituitary-
adrenocortical axis and thus elevates cortisol
excretion (van Vonderen et al., 1998). In addition,
an elevated UCCR may be found in dogs
with non-adrenal illness (Gieger et al., 2003).
However, when the physical and biochemical
changes point to hypercortisolism a false-positive
result is highly unlikely.
In the second approach the sensitivity of the
hypothalamic-pituitary-adrenocortical system to
feedback suppression is tested by administering
a synthetic glucocorticoid in a dose that
discriminates between healthy dogs and dogs with
hypercortisolism. For this purpose, the potent
glucocorticoid dexamethasone is used, because
dexamethasone is not measured in the cortisol
assay. In this so-called dexamethasone screening
test or low-dose dexamethasone suppression
test (LDDST), 0.01 mg dexamethasone per
kg body weight is administered intravenously.
Blood for cortisol measurement is collected 8 h
after dexamethasone administration. In healthy
Back to contents
E
dogs the plasma cortisol concentration is still
depressed (< 40 nmol/l) at this time, whereas in
animals with hypercortisolism the plasma cortisol
concentration remains high or may have escaped
from initial suppression. In case of adrenocortical
tumours the cortisol excess may be only moderate,
which may pose diagnostic problems.
Another popular test to screen for the presence of
hypercortisolism is the ACTH stimulation test. In
principle, this test has been designed to diagnose
hypoadrenocorticism (Addison’s disease) and to
distinguish between iatrogenic and spontaneous
hypercortisolism in dogs (Feldman and Nelson,
1996; Rijnberk, 1996a). The sensitivity of the
ACTH stimulation test differs in dogs with a
functional adrenocortical tumour and those
with PDH. About 85% of dogs with PDH will
have an exaggerated cortisol response to ACTH,
while only 55% of dogs with a functional
adrenocortical tumour will have such a result.
The main advantages of the ACTH stimulation
test are its simplicity and the short duration of
the test. However, the diagnostic accuracy for
hypercortisolism of this test is less than that of the
UCCR and the LDDST. Therefore, this test is no
longer recommended in the diagnostic approach
of dogs with hypercortisolism (Feldman, 2005).
Differentiation between PDH and adrenocortical
tumour
Once the diagnosis of hypercortisolism has been
made it is necessary to distinguish between
pituitary-dependent hypercortisolism (PDH) and
hypercortisolism due to adrenocortical tumour.
Differentiation of the cause of hypercortisolism
is necessary to provide a more accurate prognosis
and instigate a suitable treatment protocol.
Despite a decreased sensitivity to suppression by
glucocorticoids, the ACTH secretion of most dogs
with PDH can be suppressed with a 10-fold higher
dose of dexamethasone (0.1 mg/kg), resulting in
decreased cortisol secretion. The autonomous
2006 World Congress WSAVA/FECAVA/CSAVA
hypersecretion by adrenocortical tumours will not
be influenced by the high dose of dexamethasone.
Two procedures are used, one employing plasma
cortisol as a reflection of adrenocortical secretion
and the other the urinary corticoid/creatinine ratio
(UCCR). In both, a greater than 50% decline from
baseline values is regarded as diagnostic for PDH
(Galac et al., 1997).
This high-dose dexamethasone suppression test
(HDDST) does not require a second test procedure
when for the diagnosis of hypercortisolism the
UCCRs are used. After collection of two
basal urine samples the owner is asked to
administer dexamethasone tablets in a dosage
of 0.1 mg dexamethasone/kg body weight at 8-
hourly intervals. When the UCCR in the third
297
E
urine sample is 50% lower than the mean of the
first two ratios, the diagnosis of PDH is justified
(Galac et al., 1997).
Also the LDDST may have value in distinguishing
dogs with PDH from those with a functional
adrenocortical tumour. When the plasma cortisol
concentration is not only measured at 8h but also
after 3 or 4 h after intravenous administration
of 0.01 mg dexamethasone/kg, those dogs with
decreases of the plasma cortisol concentrations
>50% of the basal concentration either at 3, 4
or 8 h can be regarded as pituitary-dependent
(Rijnberk, 1996b). In these cases the HDDST
does not need to be performed.
When suppression is less than 50% in the HDDST,
either performed with plasma cortisol or UCCR,
there is about equal chance the hypercortisolism
is due to either adrenocortical tumour or pituitary
ACTH excess that is extremely resistant to
dexamethasone suppression (Feldman et al.,
1996). In these cases, differentiation between
the two forms of hypercortisolism should rely
on measurements of endogenous ACTH and
ultrasonography of the adrenals. In the great
majority of dogs with functional adrenocortical
tumour the basal ACTH values are completely
suppressed. When an adrenocortical tumour is
found on ultrasonography it is still useful to have
ACTH measurements. If the plasma ACTH levels
are not low, further studies are warranted, as
there might be co-existent PDH (Van Sluijs et al.,
1995; Greco et al., 1999). These further studies
may include visualization of the pituitary.
Once the biochemical work-up indicates the
2006 World Congress WSAVA/FECAVA/CSAVA
298
Back to contents
presence of PDH, the pituitary is visualized if
possible (Van der Vlugt-Meijer et al., 2002).
This visualization is imperative in institutions
where hypophysectomy or pituitary irradiation
are options for treatment. If this is not the case
then visualization still gives insight into the
prognosis.
References
1) Feldman EC and Nelson RW. In: Canine and
Feline Endocrinology and Reproduction 2nd edn,
1996: 187-265.
2) Feldman EC et al. JAVMA 1996; 209: 772-
775.
3) Feldman EC. Proceedings ACVIM Forum
2005. 669-671.
4) Galac S et al. Vet Q 1997; 19: 17-20.
5) Gieger TL et al. JVIM 2003; 17: 154-157.
6) Greco DS et al. JAVMA 1999; 214: 1349-
1353.
7) Rijnberk A et al. Vet Rec 1988; 122: 178-180.
8) Rijnberk A. In: Clinical Endocrinology of
Dogs and Cats, 1996a: 61-93.
9) Rijnberk A. In: Clinical Endocrinology of
Dogs and Cats, 1996b: 205-212.
10) Van der Vlugt-Meijer RH et al. Mol Cell
Endocrinol 2002; 197: 81-87.
11) Van Sluijs FJ et al. Vet Q 1995; 17: 113-116.
12) Van Vonderen IK et al. JVIM 1998; 12: 431-435.

E – Endocrinology
CURRENT TREATMENT OPTIONS OF CANINE
HYPERADRENOCORTICISM
Sylvie Daminet, DVM, PhD, Dip
ACVIM, Dip ECVIM-CA
Prof. Internal Medicine
Dept. Small Animal Medicine
Ghent University
Salisburylaan 133
B-9820 Merelbeke
Belgium
Sylvie.daminet@ugent.be
The choice of therapy for hypercortisolism
depends on the localisation of the problem
(adrenal versus pituitary tumor), the availability
of more sophisticated methods (hypophysectomy
and radiation therapy), motivation and budget of
the owner and experience of the veterinarian. This
lecture will focus on current treatment options of
pituitary dependant hypercortisolism (PDH).
When available, transsphenoidal hypophysectomy
(surgical removal of the whole pituitary gland)
is the treatment of choice for many dogs with
PDH. Indeed, this surgery aims for the removal
of the cause of the disease. Currently this can
be performed at the University clinic of Utrecht,
The Netherlands. Travel and cost are the limiting
factors. The prognosis for dogs treated with
hypophysectomy is good if the diagnosis of PDH
is made early and the pituitary gland is only
mildly to moderately enlarged. For macrotumors
the prognosis is not that good. Many dogs require
vasopressin supplementation during the post
operative period, and all dogs require a life-long
therapy with cortisone and L-thyroxine.
Untill recently, chemotherapy with o,p’-DDD
(Lysodren® or Mitotane®) was used to treat most
dogs with PDH. This drug causes a destruction
of the adrenal cortex. Two protocols have been
described: selective (partial) or non-selective
(complete) destruction of the adrenal cortex.
The adrenal cortex is formed by 3 layers, the
zona fasciculata, zona reticularis (secretes
glucocorticoids and androgens), and the zona
glomerulosa (produces only mineralocorticoids).
This is a lypophilic drug and therefore always
needs to be administered with food. Furthermore,
gloves need to be worn when manipulating this
drug. o,p’-DDD should not be administered when
the patient is or becomes anorectic.
The selective protocol consists of an induction
period of approximately 7 days and is followed by
a life-long maintenance therapy with Lysodren®.
The protocol aims at a selective destruction of the
adrenal cortex sparing the zona glomerulosa and
decreasing cortisol secretion.
Back to contents
E
With the non-selective protocol (Utrecht
protocol), a high dosage of Lysodren® is
administered during a limited period. This
protocol aims at a complete destruction of the
adrenal cortex (zona fasciculata, zona reticularis
and zona glomerulosa). Hypocortisolism and
hypoaldosteronism will ensue. A life-long therapy
with glucocorticoids and mineralocorticoids is
mandatory.
Trilostane (Vetoryl®) has been used with success
to treat dogs with PDH since 1997. Initially,
the veterinary preparation was only available
in England. Recently it has become widely
available throughout Europe. Trilostane is a
synthetic steroid with no inherent hormonal
activity. It is a competitive inhibitor of the 3-β-
hydroxysteroid-dehydrogenase enzyme system.
Hence, Trilostane blocks the adrenal synthesis
of glucocorticoids, sex hormones and to a lesser
extend mineralocorticoids.
Recently, a consensus meeting (Amsterdam, April
19th, 2006) recommended a relatively low starting
dose of Trilostane of 2.5 mg/kg per os, once daily.
It is our experience that, especially in small dogs,
this dosage will limit side effects. Only capsules
of 30 and 60 mg are available, which can be 2006 World Congress WSAVA/FECAVA/CSAVA
problematic for small dogs. Reformulating the
capsule (when country legislation allows it) is
an option in small dogs to allow more optimal
dosaging.
Close monitoring of Trilostane therapy is
required. Decreased polyuria/polydipsia/
polyphagia and increased activity are already
often reported by the owners at the first control
visit (7-14 days after initiation of therapy).
Dermatological improvement will only occur
later. Dosage adjustments are based on the
clinical improvement, electrolyte measurements
and monitoring of the adrenal reserve. The
latter is performed with an ACTH stimulation
test, which is best performed 2-3 hours after
Trilostane administration. Indeed, the effects of
Trilostane last for only a few hours. Initial dosage
299
E
adjustments are required in most dogs. These
are often made in increments of 10-30 mg per
dog. Once the goal of therapy is achieved (good
clinical control with post ACTH cortisol level
between 40 and 150 nmol/L), check up is planned
every 3 months. Most dogs tolerate the treatment
with Trilostane well, especially when the therapy
is started with a conservative dosage (2.5 mg/kg).
The effective dosage of Trilostane varies largely
among dogs. Exceptionally, dosages of 15 mg/kg
or more need to be administered.
Possible side effects include vomiting, diarrhoea
and lethargy. These can be self-limiting or require
cessation of therapy. Rarely, hypoadrenocorticism
develops and needs to be treated. This is confirmed
by an ACTH stimulation test (absence of increase
in cortisol after ACTH administration).
Noteworthy are the ultrasonographic changes
of the adrenal cortices (increased thickness and
echogenicity) reported during Trilostane therapy.
These changes are due to increased ACTH levels
resulting from the diminished negative feed back
normally exerted by cortisol.
A study from Barker et al. showed that survival
times between dogs treated with Trilostane and
those treated with Mitotane® were not significantly
2006 World Congress WSAVA/FECAVA/CSAVA
Figure 1: Schematic representation of the adrenal steroid biosynthesis. Trilostane inhibits the action of
the 3β-hydroxysteroid-dehydrogenase enzyme in the adrenal cortex.
300
Back to contents
different (median of 662 and 708, respectively).
Because of their limited efficacy and/or potential
side effects, the use of ketoconazol and L-
deprenyl will not be discussed.
Approximately 20 % of dogs with PDH develop
neurological signs because of dorsal expansion of
the pituitary tumor. Therefore, in dogs with PDH,
medical imaging of the pituitary gland (CT scan or
MRI) should be recommended to the owners. If a
large pituitary tumor is detected, with or without
neurological signs, radiation therapy is indicated.
Indeed, pituitary tumors are relatively sensitive to
radiation. The aim here is to decrease the volume
of the space occupying pituitary mass. Dogs may
already show some improvement (i.e. improved
alertness in a dull dog) during radiotherapy but
improvement is often delayed. Most often the
treatment has no or little effect on the hormonal
secretion of the tumor. Therefore, medical therapy
is still warranted and most often started 1-3 weeks
after termination of the radiation therapy.
Prognosis for PDH with appropriate treatment and
monitoring is favorable in many dogs. However,
treatment of PDH requires a major commitment
by the owner and the veterinarian.

References
Barker EN, Campbell S, Tebb AJ, Neiger
R, Herrtage ME, Reid SWJ, Ramsey IK.
A comparison of the survival times of dogs
treated with mitotane or trilostane for pituitary-
dependent hyperadrenocorticism. JOURNAL OF
VETERINARY INTERNAL MEDICINE 2005;
19: 810-815.
British Small Animal Veterinary Association
Manual of Canine and Feline Endocrinology. 3rd
edition. Edited by CT Mooney and ME Peterson.
ME Herrtage. Canine hyperadrenocorticism. P.
150-172.
Hanson JM, van’t Hoofd MM, Voorhout G, Teske E,
Kooistra HS, Meij BP.Efficacy of transsphenoidal
hypophysectomy in treatment of dogs with
pituitary-dependent hyperadrenocorticism.
JOURNAL OF VETERINARY INTERNAL
MEDICINE 2005; 19: 687-694.
Back to contents
E
Neiger R, Ramsey I, O’Connor J, Hurley KJ,
Mooney CT. Trilostane treatment of 78 dogs
with pituitary-dependent hyperadrenocorticism.
VETERINARY RECORD 2002; 150: 799-804.
Ruckstuhl NS, Nett CS, Reusch CE. Results
of clinical examinations, laboratory tests, and
ultrasonography in dogs with pituitary-dependent
hyperadrenocorticism treated with trilostane.
AMERICAN JOURNAL OF VETERINARY
RESEARCH 2002; 63: 506-512.
Wenger M, Sieber-Ruckstuhl NS, Muller
C, Reusch CE. Effect of trilostane on serum
concentrations of aldosterone, cortisol, and
potassium in dogs with pituitary-dependent
hyperadrenocorticism. AMERICAN JOURNAL
OF VETERINARY RESEARCH 2004; 65:
1245-1250.
2006 World Congress WSAVA/FECAVA/CSAVA
301
E
E – Endocrinology
ADRENAL TUMOURS IN DOGS
Claudia E. Reusch, Dipl
ECVIM-CA
Clinic for Small Animal Internal
Medicine
University of Zuerich
Winterthurererstrasse 260
CH-8057 Zuerich
creusch@vetclinics.unizh.ch
Adrenal tumours may be functional or non-
functional. Functional tumours may arise from all
zones of the adrenal cortex or the adrenal medulla
and oversecrete cortisol, aldosterone, cortisol
and aldosterone precursors, sex-hormones and
catecholamines.
Glucocorticoid-secreting adrenocortical tumour
They are the most common adrenal tumours in
dogs. For many years, it was assumed that ATs
produce large amounts of hormone, more than the
hyperplastic adrenal glands of dogs with PDH.
However, it appears the opposite is true; in many
dogs with AT, the hormone excess and subsequent
clinical signs are only moderate. Thus, despite
the fact that ATs usually greatly exceed the size
of the normal adrenal gland, the tumour tissue
is only moderately active, and the neoplastic
transformation results in a decreased function per
unit of volume. It is also possible that the cortisol
synthesis pathway in dogs with AT is not intact.
In humans, adrenal carcinomas tend to produce
large amounts of precursors of cortisol, and a
partial or complete deficiency of 11β-hydroxylase
is common. In dogs, the existence of a similar
phenomenon has recently been suggested. In
2006 World Congress WSAVA/FECAVA/CSAVA
dogs with AT, the right and left adrenal glands
are affected with about equal frequency. Usually
there is a unilateral solitary adrenal mass,
although in approximately 10 per cent of cases,
bilateral tumours are found.
Adenomas and carcinomas probably occur with
equal frequency. Similar to other endocrine
tumours, it is difficult to distinguish between adrenal
adenomas and carcinomas. Even differentiation
between AT and pheochromocytoma may
require a pathologist with experience in special
immunohistochemical staining techniques.
Sometimes ATs that were initially diagnosed as
benign turn out to be malignant when metastases
are found later. Histological differentiation
between benign and malignant tumours is only
straightforward when there is capsular or vascular
invasion by the tumour.
302
Back to contents
It is not uncommon for AT to be associated
with pheochromocytoma; another interesting
phenomenon is the co-existence of pituitary
tumours and AT. Both situations may pose a
difficult diagnostic and therapeutic challenge.
In humans bilateral nodular hyperplasia with
HAC has been identified as a sequel to several
pathophysiological conditions. Long-standing
ACTH hypersecretion may result in nodular
enlargement of the adrenal gland. Over time,
these nodules may become autonomous or
semiautonomous. Another type of nodular
hyperplasia has been termed macronodular
adrenal hyperplasia. It is ACTH-independent
and characterized by bilateral nodules secreting
excessive amounts of cortisol. Recent studies
indicate that receptors for various hormones may
be abnormally expressed by the adrenal glands;
an example is ectopic expression of the gastric
inhibitory polypeptide receptor. It is likely that
adrenocortical nodular hyperplasia also exists in
dogs, up till now one case has been described.
Dogs with AT are usually > 6 years of age; breeds
most commonly involved are poodles, German
shepherd dogs, Dachshunds, Labrador retrievers
and various terrier breeds. Approximately 45 to
50% of dogs with AT weigh more than 20 kg i.e.
belong to medium-sized and large breeds.
Clinical signs and clinicopathological findings
are similar in dogs with AT and PDH. Typical
symptoms include pu/pd, polyphagia, truncal
obesity or abdominal enlargement (due to
hepatomegaly, muscle wasting and/or intra-
abdominal fat accumulation), thin haircoat, failure
to regrow shaved hair, alopecia (may or may not
be bilaterally symmetric, usually sparing head and
extremities), thin skin, pyoderma, panting, muscle
weakness, muscle atrophy and lethargy. Less
common signs are heat intolerance, seborrhoea,
comedones, hyperpigmentation, calcinosis cutis,
bruising, testicular atrophy, failure to cycle,
clitoral hypertrophy and facial paralysis. Rupture
of an AT with intraabdominal or retroperitoneal
haemorrhage is a rare complication, leading to

acute severe lethargy, weakness and pale mucous
membranes. Most frequent laboratory findings
are increase in ALP, ALT, cholesterol, iso- or
hyposthenuria, proteinuria and positive bacterial
culture of urine.
The further diagnostic work up is a two step
procedure. The first step is to confirm the diagnosis
of HAC, the second to differentiate between PDH
and AT. Routinely used screening tests include
the urine cortisol:creatinine ratio (UCC) and the
low dose dexamethasone test (LDDS test). With
regard to the LDDS test it has long been thought
that all dogs with AT show dexamethasone
resistance (elevated cortisol concentration 4 and
8 hours after dexamethasone administration).
However, it has now been described by us and
others that a substantial percentage of dogs with
AT may show suppression of cortisol 4 hours
after dexamethasone which has originally been
thought to be typical for PDH. Some dogs with
AT even have normal cortisol concentrations after
4 and 8 hours. It is therefore advisable to perform
additional tests with a higher sensitivity, such as
UCC and to use ultrasonography and cATCH
to differentiate between AT and PDH.Surgical
removal is the treatment of choice. Patients must
be assessed preoperatively for metastases or
invasion of the tumour into surrounding tissues.
Adrenalectomy is technically challenging and
should be performed by a skilled surgeon.
Approximately 50 per cent of patients develop
postoperative complications, which may be severe
and life-threatening and include pancreatitis,
pneumonia, pulmonary thromboembolism, acute
renal failure, sepsis and hypoadrenocorticism.
The reported death rate after adrenalectomy
varies between 10 and 34% and certainly depends
on factors such as state of disease, skills of the
surgeon, quality of perioperative management. It
is not known whether dogs with AT that undergo
long-term medical treatment before adrenalectomy
have fewer postoperative complications and
higher survival rates. Recurrence of HAC weeks
to months after surgery or persistence of clinical
signs occurs in dogs in which tumour removal
was incomplete.
Autonomous cortisol secretion results in atrophy
of the cells of the zona fasciculata and zona
reticularis; in a few dogs aldosterone-producing
cells of the zona glomerulosa may also be
atrophied. Thus glucocorticoid substitution
intraoperatively and postoperatively is necessary.
Mineralocorticoid treatment is instituted when
required.
For inoperable AT we currently use mitotane
according to a protocol aiming for complete
adrenal destruction. In some dogs, this treatment
regime results in complete tumour remission and
even disappearance of metastases.
Back to contents
E
Pheochromocytoma
Pheochromocytoma (Pheo) is the second
most common adrenal tumour in dogs. It is of
neuroectodermal origin arising from chromaffin
cells of the sympathoadrenal system. Clinical
signs result from excretion of excessive amounts
of catecholamines and rarely from the direct
presence and space occupying nature of the
tumour. Pheo is identified most commonly in
older dogs (> 7 years). There does not seem
to be a sex or breed predilection. Symptoms
are subtle, episodic and often complicated by
concurrent disease. The most common clinical
signs are generalized weakness and episodic
collapse. Further symptoms include intermittent
agitation, pacing, excessive panting, pu/pd.
Systemic hypertension may occur leading to
retinal detachment or retinal haemorrhage or
hemorrhage into the retroperitoneal space,
the abdominal cavity or the CNS. Vomiting,
diarrhea, inappetence, weight loss, tender
abdomen and cardiac arrhythmias may also be
seen. Signs related to a space-occupying process
are a palpable mass, enlarged abdomen, ascites
and rear limb edema. Collapse and death from
a sudden, massive and sustained release of the
catecholamines and massive haemorrhage due to
sudden increase in blood pressure or rupture of
the tumour is possible. Many of the clinical signs
caused by pheo are unspecific and vague and may
be associated with a variety of more frequent
diseases. There are no consistent abnormalities
on haematology, serum biochemistry and
urinalysis which would raise the suspicion of
pheo. Up till recently the majority of cases were
therefore only diagnosed at necropsy and were
not suspected antemortem. However, due to the
fact that abdominal ultrasonography including
adrenal imaging is increasingly used as part of
a diagnostic work-up, the situation has started
to improve. Often, pheo is only considered
after an adrenal mass is identified on abdominal
2006 World Congress WSAVA/FECAVA/CSAVA
ultrasonography. Although normal sized adrenal
glands do not rule out pheo, there seems to be a
relationship between tumour size and severity of
clinical signs. In most dogs with obvious clinical
signs the tumour is easily detectable. Different
to the situation in human medicine the majority
of pheos in dogs are malignant. Ultrasonography
can provide information regarding local invasion
to surrounding tissue and vessels, tumour thrombi
and metastasis to other abdominal organs. In more
than 50% of dogs with pheo tumour thrombi and/
or metasasis are present at the time of diagnosis.
Pheo and AT can occur simultaneously, and since
clinical signs may be similar it is important to rule
out HAC in questionable cases. Determination
of blood pressure is indicated in any dog with
303
E
suspected pheo and demonstration of hypertension
would be supportive of the disease. However,
catecholamine secretion by the tumour and thus
hypertension tends to be episodic. Hypertension
has been documented in only 40 – 50% of dogs
with pheo in which blood pressure had been
measured.
In human medicine, measurement of urinary
catecholamines, their metabolites metanephrine
and normetanephrine, and vanillylmandelic acid
in urine collected over 24 hours constitutes the
traditional approach to the biochemical diagnosis
of pheo. Alternatively to 24 hours urine sampling
ratios to creatinine (in particular metanephrine:
creatinine ratios) from spot urine samples can be
used. In veterinary medicine biochemical testing
has infrequently been performed due to limited
availability of techniques, lack of established
reference ranges and the problems of 24-hour
urine collection. We recently established reference
ranges for urine epinephrine-, norepinephrine-,
metanephrine- and normetanephrine:creatinine
ratios in dogs. From preliminary data from
dogs with confirmed pheo we assume that the
normetanephrine:creatinine ratio may be the most
sensitive parameter.
The treatment of choice is surgical removal
after a 2 – 3 weeks period of medical therapy to
reverse the effects of catecholamine excess. For
the latter phenoxybenzamine, an a-adrenergic
antagonist can be used. Initial dose is 0.25 mg/kg
BID, followed by gradual increase every few days
until the dog shows clinical improvement or signs
of hypotension. Maximum dosages is around 1.5
– 2.0 mg/kg BID. Prognosis is guarded due to the
malignant nature of the tumour. Reported survival
times range between 1 – 36 months.
Sex-hormone producing tumour
In humans with adrenocortical tumours abberant
synthesis pathways are well characterised.
2006 World Congress WSAVA/FECAVA/CSAVA
Those tumours may be deficient in the enzymes
involved in normal steroidogenic pathways, such
as 21β-hydroxylase or 11β-hydroxylase, leading
to an accumulation of steroid precursors proximal
to the blockade. These precursors may either
cause clinical signs similar to those seen with
cortisol excess or they may be shunted into other
metabolic pathways, and cause signs of androgen
excess.
In veterinary medicine knowledge on abnormal
steroidogenic pathways is scarce and matter of
controverse discussions. A small number of dogs
with sex-hormone producing tumours have been
described. They had clinical signs consistent
with HAC, and cortisol levels measured during
screening-tests were negative. Further endocrine
testing revealed that various precursors
304
Back to contents
resp. sex-hormones such as progesterone, 17-
hydroxyprogesterone, DHEAS, androstenedione,
testosterone and estrogen were elevated. A lot
more work is required to determine the frequency
of these tumours and to characterize the specific
enzyme-defects.
Aldosteronoma
Aldosterone-producing tumours are increasingly
reported in cats. In dogs, however, the disease
appears to be rare. One dog has recently been
described, which was presented with pu/pd.
Further work-up revealed hypokalaemia,
hypophosphataemia and alkalosis. Diagnosis was
made by demonstrating high aldosterone levels
and low renin activity and a nodule in one adrenal
gland by CT. The dog made a complete recovery
after adrenalectomy.
Adrenal tumours may not only oversecrete
aldosterone, but also its precursors. A high
index of suspicion and access to precursor
measurements are necessary to make the
diagnosis. A deoxycorticosterone-secreting
adrenal tumour was demonstrated recently in a
dog. Clinical signs were those of mineralocorticoid
excess, however, aldosterone levels were
undetectable. Deoxycorticosterone which has
mineralocorticoid activity and acts as the same
receptor as aldosterone was elevated. In another
dog with signs consistent with mineralocorticoid
excess oversecretion of aldosterone as well as of
deoxycorticosterone was shown.
References
Behrend EN, Weigand CM, Whitley EM, Refsal
KR, Young DW, Kemppainen RJ. Corticosterone-
and aldosterone-secreting adrenocortical tumor
in a dog. Journal of the American Veterinary
Medical Association 2005; 226(10): 1662-1666.
Greco DS, Peterson ME, Davidson AP, Feldman
EC, Komurek K. Concurrent pituitary and adrenal
tumours in dogs with hyperadrenocorticism:
17 cases (1978-1995). Journal of the American
Veterinary Medical Association 1999; 214(9):
1349-1353.
Norman EJ, Thompson H, Mooney CT.
Dynamic adrenal function testing in eight dogs
with hyperadrenocorticism associated with
adrenocortical neoplasia. Veterinary Record
1999; 144(20): 551-554.
Reine NJ, Hohenhaus AE, Peterson ME,
Patnaik AK. Deoxycorticosterone-secreting
adrenocortical carcinoma in a dog. Journal of
Veterinary Internal Medicine 1999; 13: 386-390.
Reusch CE, Feldman EC. Canine
hyperadrenocorticism due to adrenocortical

neoplasia. Journal of Veterinary Internal Medicine
1991; 5: 3-10.
Rijnberk A, Kooistra HS, van Vonderen IK,
Mol JA, Voorhout G, van Sluijs FJ, Jzer JI, van
den Ingh M, Boer P, Boer WH. Aldosteronoma
in a dog with polyuria as the leading symptom.
Domestic Animal Endocrinology 2001; 20(3):
227-240.
Syme HM, Scott-Moncrieff C, Treadwell
NG, Thompson MF, Snyder PW, White MR,
Back to contents
E
Oliver JW. Hyperadrenocorticism associated
with excessive sex hormone production by an
adrenocortical tumour in two dogs. Journal of the
American Veterinary Medical Association 2001;
219(12): 1725-1728.
Van Sluijs FJ, Sjollema BE, Voorhout G, van den
Ingh TS, Rijnberk A. Results of adrenalectomy
in 36 dogs with hyperadrenocorticism caused by
adreno-cortical tumour. The Veterinary Quarterly
1995; 17(3): 113-116.
2006 World Congress WSAVA/FECAVA/CSAVA
305
E
E – Endocrinology
PITFALLS IN THE DIAGNOSIS OF HYPOADRENOCORTICISM
IN DOGS
Dr. Hans S. Kooistra, Dipl
ECVIM-CA
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
Yalelaan 108
3584 CM UTRECHT
THE NETHERLANDS
H.S.Kooistra@vet.uu.ni
The terms hypoadrenocorticism and adrenocortical
insufficiency comprise all conditions in which the
secretion of adrenal steroid hormones falls below
the requirement of the animal. Two forms can be
distinguished:
1. Primary adrenocortical insufficiency, which
results from disease processes located in the
adrenal cortices.
2. Secondary adrenocortical insufficiency,
which is due to insufficient adrenocorticotrophic
hormone (ACTH) release by the pituitary.
Primary adrenocortical insufficiency
Pathogenesis. Primary hypoadrenocorticism
or Addison’s disease results from progressive
destruction of the adrenal cortices, which must
involve 90% or more before it causes signs and
symptoms. In dogs the often-found atrophy is
probably the end-result of an immune-mediated
destruction. In the end there is an absolute
deficiency of usually both glucocorticoids and
mineralocorticoids together with high plasma
levels of ACTH as a result of the loss of negative
feedback effect on the pituitary by the absence
2006 World Congress WSAVA/FECAVA/CSAVA
of cortisol. Rarely the destruction is confined
to the two inner zones of the adrenal cortices,
although it may occur more often and remain
unnoticed for quite some time as there is (initially
or permanently) no mineralocorticoid deficiency.
The reverse, that is selective destruction of the
zona glomerulosa with intact glucocorticoid
production, has also been described. Primary
hypoadreno-corticism may be part of a polyglandular
deficiency syndrome.
Other possible causes of primary adrenocortical
insufficiency include infections, haemorrhage and
metastatic disease, but they seem to be very rare.
Finally an iatrogenic cause of the disease should
be mentioned; chemotherapy with o,p’-DDD for
hyperadrenocorticism may deliberately or non-
deliberately destruct the adrenal cortices to such
an extent that hypoadrenocorticism ensues.
306
Back to contents
Clinical manifestations. Hypoadrenocorticism
is an uncommon disease of primarily young
to middle-aged dogs (mean 4 years) with a
predilection for the female. Familial occurrence
of hypoadrenocorticism has been described
for several breeds and heritability has been
investigated in Nova Scotia Duck Tolling
retrievers, bearded collies and standard poodles.
Although glucocorticoid deficiency may cause
some lethargy and weakness and this certainly
will contribute to the clinical manifestations,
Addison’s disease is primarily a syndrome
caused by mineralocorticoid deficiency. Many
of the signs and symptoms can be related to
hypotonic dehydration due to the sodium losses.
The hyperkalemia contributes to the problems by
affecting neuromuscular function, particularly
leading to conduction disturbances in the heart.
As the disease usually is caused by a gradual
autoimmune destruction of the adrenal cortices
one might expect an insidious onset of slowly
progressive weakness, fatigue, anorexia and
vomiting. Although this may be the case, more
often the animals are presented as an emergency in
a state of rather severe depression and hypotonic
dehydration. There may not have been a start
with mild signs or the signs may have remained
unnoticed by the owner and are only remembered
in retrospect. Apparently the animals can cope
with the hormone deficiencies for a long time
until a critical threshold in the maintenance of
fluid and electrolyte homeostasis is passed.
Thus commonly the cases are brought in as rather
young, suddenly very sick animals with a history
of anorexia, vomiting and weight loss. On physical
examination there is usually severe lethargy in
combination with signs of (10–12%) dehydration:
hypotonic veins and weak pulse. Radiographically
the hypovolemia becomes manifest by the small
sizes of the heart, pulmonary vessels and caudal
vena cava. The hyperkalemia causes bradycardia

with ECG changes such as low R wave, spiked
high T wave and wide or absent P wave.
Results of routine laboratory examination usually
include hypoplastic anemia (often masked
by hemoconcentration due to dehydration),
(prerenal) azotemia, hyponatremia and
hyperkalemia. In about 30% of cases there may
also be hypercalcemia, which in part may be due
to hemoconcentration.
Differential diagnosis. For the cardinal features
of the disease, i.e., rapidly worsening depression,
weakness, anorexia and vomiting, there is only
a limited number of syndromes that may have
a similar picture. These are ileus, (acute) renal
insufficiency, acute gastroenteritis and acute
pancreatitis. Initially the differentiation may pose
problems as the other conditions occasionally
are associated with electrolyte disturbances as
well. However, further diagnostic work-up and
especially the favourable result of treatment in
Addison’s disease usually brings the clinician
quickly in the right track.
Diagnosis. In cases with a characteristic
routine biochemical pattern (prerenal azotemia,
hyponatremia and hyperkalemia) and with a good
response to treatment, there may be little doubt
about the diagnosis. However, it is a diagnosis
with as a consequence life-long treatment and
therefore also in these cases it should be secured
by an endocrine test. Basal levels of cortisol,
either in urine or plasma, are low in cases of
complete primary hypoadrencorticism, but
they may also be low for other reasons, such
as previous administration of (long-acting)
corticosteroids. Therefore a test of adrenocortical
reserve capacity is necessary to establish the
diagnosis, i.e., the ACTH-stimulation test. In
this test plasma for cortisol measurements is
collected immediately before and 60 - 90 min
after intravenous administration of 0.25 mg
synthetic ACTH. Most commonly there are low
to low-normal baseline cortisol concentrations
that fail to increase after ACTH administration.
Plasma ACTH concentrations are high in dogs
with primary hypoadrenocorticism as a result of
the loss of negative feedback on pituitary ACTH
secretion. Determination of a low cortisol/ACTH
ratio and a low aldosterone/renine ratio may be
an alternative for the ACTH stimulation test in
the diagnosis of primary hypoadrenocorticism.
Ultrasonographic measurements may reveal
small sized adrenal glands, which may contribute
to the diagnosis.
Secondary adrenocortical insufficiency
In secondary adrenocortical insufficiency there
is hyposecretion by the two inner zones of the
adrenal cortices as a result of ACTH deficiency.
Back to contents
E
In its spontaneous and complete form the
condition is rare and most commonly caused
by large pituitary tumours, which usually give
rise to multiple pituitary-hormone deficiencies.
Isolated ACTH deficiency due to autoimmune
hypophysitis, as described in humans, has not
been documented for dogs, although isolated
ACTH deficiency has been reported to occur in
dogs.
The iatrogenic form due to long-term
corticosteroid therapy is much more common than
the spontaneous disease. Via negative feedback
this therapy causes chronic suppression of ACTH
production and as a consequence atrophy of the
zona fasciculata and reticularis. Thus like in the
spontaneous cases these animals have two deficits,
a loss of adrenocortical responsiveness to ACTH
and a failure of pituitary ACTH release. Upon
corticosteroid withdrawal these insufficiencies
may continue to exist for several months before
full recovery ensues.
Another iatrogenic form of the disease and a more
permanent one is of course ACTH deficiency due
to hypophysectomy.
Clinical manifestations. In secondary adrenocortical
insufficiency the mineralocorticoid production is
virtually unaffected as it is primarily regulated via
extra-pituitary mechanisms. Therefore there is not
that tendency to hypotension and shock that gives
primary adrenocortical insufficiency its dramatic
features. On the contrary, although glucocorticoid
deficiency may give rise to slight depression and
anorexia, the abnormality may remain unnoticed
for a long time. Nevertheless the condition has
to be regarded as potentially dangerous because
of the animals’ inability to cope with stress by
activating their pituitary-adrenocortical system.
Major (surgical) trauma might cause a crisis and/
or non-recovery from anaesthesia, when no extra
glucocorticoids are given.
Diagnosis. Suspicion of secondary adrenocortical
insufficiency may be strengthened when the 2006 World Congress WSAVA/FECAVA/CSAVA
urinary corticoid/creatinine ratios are low in the
absence of hyponatremia and hyperkalemia. In
an ACTH-stimulation test low initial cortisol
levels will be found, whereas after stimulation
there may be (1) a normal or somewhat impaired
cortisol response, or (2) no cortisol response.
The first mentioned outcome almost excludes
primary hypoadrenocorticism but not secondary
hypoadrenocorticism as the response might
be seen following recent onset. In the case of
absent cortisol response there is the possibility
of long-standing ACTH deficiency. However,
there is also the exceptional possibility that
there is still primary adrenocortical insufficiency
with selective atrophy of the two inner zones
and minimal or no involvement of the zona
glomerulosa (see above).
307
E
For differentiation between these possibilities
further studies are required, which should include
measurements of plasma concentrations of ACTH,
eventually together with a CRH-stimulation test.
In dogs with primary adrenocortical insufficiency
basal ACTH concentrations are high. In dogs with
secondary adrenocortical insufficiency ACTH
levels are low and non-responsive to stimulation
with CRH.
Once there is biochemical certainty about the
presence of secondary hypoadrenocorticism,
visualization of the pituitary should follow in order
to obtain some information on the morphology of
the lesion that is causing the ACTH deficiency.
References for further reading:
1. Javadi S, Galac S, Boer P, Robben JH, Teske E,
Kooistra HS.Aldosterone-to-renin and cortisol-
to-adrenocorticotropic hormone ratios in healthy
dogs and dogs with primary hypoadrenocorticism.
J Vet Int Med 2006; 20: 556-561.
2006 World Congress WSAVA/FECAVA/CSAVA
308
Back to contents
2. Melian C, Peterson ME. Diagnosis and treatment
of naturally occurring hypoadrenocorticism in 42
dogs. J Small Anim pract 1996; 37:268-275.
3. Peterson ME, Kintzer PP, Kass PH. Pretreatment
clinical and laboratory findings in dogs with
hypoadrenocorticism: 225 cases (1979-1993). J
Am Vet Med Ass 1996; 208:85-91.
4. Reusch CE. Hypoadrenocorticism. In: Ettinger
SJ, Feldman EC, eds. Textbook of Veterinary
Internal Medicine. Diseases of the dog and cat.
5th edition. W.B. Saunders Co, Philadelphia,
2000:1488-1499.
5. Rijnberk A. Adrenals. In: Clinical
Endocrinology of Dogs and Cats, ed A. Rijnberk.
Dordrecht/Boston: Kluwer Academic Publishers
1996a: 61-93.

E – Endocrinology
FELINE HYPERTHYROIDISM AND ITS RELATION WITH RENAL
FUNCTION
Sylvie Daminet, DVM, PhD, Dip
ACVIM, Dip ECVIM-CA
Prof. Internal Medicine
Dept. Small Animal Medicine
Ghent University
Salisburylaan 133
B-9820 Merelbeke
Belgium
Sylvie.daminet@ugent.be
Feline hyperthyroidism and chronic renal failure
(CRF) are common diseases in older cats. Further,
renal function is profoundly influenced by thyroid
status in several species. In cats, several studies
have shown a marked decline of renal function
after treatment of hyperthyroidism. This has been
documented with all treatments routinely available
for treatment of feline hyperthyroidism.
Physiological interactions between thyroid
hormones and renal function
Through their ino- and chronotropic effects,
excessive thyroid hormone concentrations can
lead to an increased cardiac output (CO). Further,
hyperthyroidism diminishes peripheral vascular
resistance by dilating arterioles of the peripheral
circulation. This leads to a stimulation of the
renin-angiotensin-aldosterone system, which
contributes to the increased CO. As a consequence
of these processes, an increased RBF is observed.
Opposite changes are described in hypothyroid
humans and rats.
The increased GFR associated with hyperthyroid
states is thought to result from the increased
CO and intrarenal vasodilatation and leads
to a decline in BUN and serum creatinine
concentrations. Opposite changes are observed in
hypothyroidism (human) and studies have shown
a normalisation of GFR, BUN and creatinine
values after successful treatment of hypo- or
hyperthyroidism in human medicine.
Considerations and clinical implications in
hyperthyroid cats
It is important to underline that CRF and
hyperthyroidism are both frequently encountered
diseases in geriatric cats. Therefore, finding
both diseases in one cat is not uncommon. Also,
clinical signs of both diseases can overlap.
Further as shown in table 1, renal function will
decline after treatment of hyperthyroidism in
cats. This can unmask renal failure in some
cats. Decreased muscle mass associated with
Back to contents
E
emaciation and therefore decreased production
of creatinine can contribute to the declined serum
creatinine concentrations observed in untreated
hyperthyroid cats. The presence of a hyperthyroid
state could contribute to the development or
progression of CRF. Systemic hypertension
can lead to intraglomerular hypertension,
hyperfiltration and contribute to the development
of glomerulosclerosis.
In the study of Adams et al. (1997), 9 out of
22 hyperthyroid cats had concurrent CRF at
presentation. Another study on a larger number of
cases (n=167) reported that 14% of hyperthyroid
cats had pre-existing renal disease (Milner et al.,
2006). Approximately 30% of hyperthyroid cats
are azotemic after therapy of hyperthyroidism.
Assessment of complete blood count, chemistry,
urinalysis and blood pressure are important in
hyperthyroid cats prior to treatment. Indeed,
careful evaluation of BUN, creatinine and urine
specific gravity (USG) are required prior to
instituting therapy for hyperthyroidism as these
results will influence the initial choice of therapy
for hyperthyroidism. Medical, surgical and 131I
therapy are available and effective in the treatment
of hyperthyroidism. Thyroidectomy and 131I are 2006 World Congress WSAVA/FECAVA/CSAVA
considered definitive and irreversible treatments.
Daily oral administration of methimazole (MMI)
is reversible.
Pre-existing renal failure in a newly diagnosed
hyperthyroid cat: First, in such a case, the diagnosis
of mild hyperthyroidism can be somewhat
complicated by a decline in thyroid hormones
(euthyroid sickness) within the reference range.
Second, given the further decline in GFR to be
expected after resolution of the hyperthyroid
state, it is wise to start an azotemic hyperthyroid
cat with a reversible anti-thyroid therapy (trial
therapy). Often, methimazole is used (orally or
transdermal), at a low starting dose (i.e., 1.25 mg
orally once a day). This allows assessing
the impact of anti-thyroid therapy on renal
function. These patients should be monitored
309
E
every 2 weeks. Dosage adjustments should be
made prudently. The presence of overt signs
of thyrotoxicosis (heart murmur, emaciation,
proteinuria) underlines the importance of treating
the hyperthyroidism. Management of CRF is
also warranted. If the patient stabilises and renal
function remains stable after reestablishment of
a euthyroid state, a more definitive treatment,
such as 131I, can still be considered. If renal
function declines significantly after methimazole
treatment is instituted, it seems wise to maintain
the cat on a reversible anti-thyroid therapy, which
can be adjusted individually as needed. In some
cats, maintenance of a mild hyperthyroid state
may be beneficial.
Development of renal failure after treatment of
hyperthyroidism: Resolution of the hyperthyroid
state can unmask renal failure. Excess thyroid
hormones increase GFR and treatment of
hyperthyroidism will decrease glomerular
filtration, leading to an increase in BUN and
creatinine values. Approximately 30% of the
patients develop overt CRF after treatment of
hyperthyroidism. This underlines the importance
of appropriate monitoring after therapy of
hyperthyroidism.
Predicting which non azotemic cats will develop
renal failure after treatment of hyperthyroidism
is currently difficult. Pre-treatment values of
serum creatinine, BUN, USG and urine protein
to creatinine ratio (UPC) did not appear to be
predictive for the development of post-treatment
renal failure in several studies. However, there
are some reports of hyperthyroid cats with
isostenuric urine prior to treatment who developed
post-treatment azotemia. It seems reasonable
(although not evidence-based) to recommend a
trial therapy in any hyperthyroid cat presented
with one or more of the following: BUN or serum
creatinine values at the high end of the reference
interval, a low USG, an increased UPC or marked
ultrasonographic kidney abnormalities. Currently
the most useful predictive parameter seems to be
GFR measurement. A low pre-treatment GFR was
predictive of the development of CRF in several
studies. However, measurement of GFR is often
impractical in a clinical setting. Usefulness of
urinary markers of early renal disease is currently
being investigated.
Keeping in mind the negative effects on
renal function, described in rats and humans
in hypothyroid states, it seems important to
avoid a hypothyroid state after treatment of
hyperthyroidism in cats.
The relationship between kidney disease and
hyperhyroidism in cats is complex. It can be
challenging to accurately diagnose and treat
cats with concurrent CRF and hyperthyroidism.
Follow-up of all cats treated for hyperthyroidism
is important as a significant amount will develop
CRF.

Table 1: Follow-up of renal function after treatment of hyperthyroidism in cats. Hyperthyroid: HT,
Methimazole: MMI, thyroidectomy: SX, Radioactive iodine: 131I. Mean values for USG, GFR and
creatinine are given prior to and after therapy of hyperthyroidism.

Author Number HT Therapy USG GFR Creatinine

et al. cats ml/kg/min mg/dl
2006 World Congress WSAVA/FECAVA/CSAVA

Evaluation
period
Graves n=13 SX 1038→1030 2.51±0.69 1.26±0.34→2.05±0.60
1994 (+ 11 c ontrols) →1.4±0.41
30 days
DiBartola n=27 131I 131
I 1046→1043 Not performed 1.3±0.4→2±0.6
1996 n=9 MMI MMI 1042→1037 1.7±0.9→2.7±2.5
n=22 SX SX 1033→1033 1.7±0.6→2.4±0.8
90 days
131
Adams n=22 I 1032→1028 2.2→2 (day 6) 1.3±0.6→1.9±0.7
1997 30 days
Becker n=12 MMI 1041→1033 3.83±1.82 1.32±0.21→1.81±0.96
2000 (+22 controls) →2.02±0.81
6 weeks

310
Back to contents

References
Adams WH, Daniel GB, Legendre AM, Gompf
RE, Grove CA. Changes in renal function in cats
following treatment of hyperthyroidism using
131I. Vet Radiol & Ultrasound 1997; 38: 231-
238.
Becker TJ, Graves TK, Kruger JM, Braselton
WE, Nachreiner RF. Effects of methimazole on
renal function in cats with hyperthyroidism. J Am
Anim Hosp Assoc 2000; 36: 215-223.
Bhatti S., Van Neste A., Waelbers T., Daminet S.,
Peremans K.: Treatment of feline hyperthyroidism
with radioactive Iodine (131I) in Belgium: a
retrospective study. Poster. EAVDI 2005.
den Hollander JG, Wulkan RW, Mantel MJ,
Berghout A. Correlation between severity of
thyroid dysfunction and renal function. Clin
Endocrinol 2005; 62: 423-427.
DiBartola SP, Broome MR, Stein BS, Nixon M.
Effect of treatment of hyperthyroidism on renal
function in cats. J Am Vet Med assoc 1996; 208:
875-878.
Graves TK, Olivier NB, Nachreiner RF,
Kruger JM, Walshaw R, Stickle RL. Changes
in renal-function associated with treatment of
Back to contents
E
hyperthyroidism in cats. Am J Vet Res 1994; 55:
1745-1749.
Langston CE, Reine NJ. Hyperthyroidism and the
kidney. Clin Tech in Small Anim Pract 2006; 21:
17-21.
Milner RJ, Channell CD, Levy JK, Schaer M.
Survival times for cats with hyperthyroidism
treated with iodine 131, methimazole, or both:
167 cases (1996-2003). J Am Vet Med assoc
2006; 228: 559-563.
Slater LA, Neiger R, Haller M, Mueller W,
Stevens KB, Church DB. Long-term changes
in glomerular filtration rate in hyperthyroid
cats following treatment with iodine-131. In:
Proceedings ECVIM-CA Congress, Uppsala,
Sweden, 2003, p. 154.
Syme HM, Elliott J. Evaluation of proteinuria in
hyperthyroid cats. J Vet Intern Med 2001; 15, p.
299.
Syme HM, Elliott J. Prevalence and significance
of proteinuria in cats with hyperthyroidism.
In: Scientific Proceedings BSAVA Congress,
Birmingham, England, 2003, p. 533.
2006 World Congress WSAVA/FECAVA/CSAVA
311
E
E – Endocrinology
DIAGNOSIS OF CANINE HYPOTHYROIDISM
Sylvie Daminet, DVM, PhD, Dip
ACVIM, Dip ECVIM-CA
Prof. Internal Medicine
Dept. Small Animal Medicine
Ghent University
Salisburylaan 133
B-9820 Merelbeke
Belgium
Sylvie.daminet@ugent.be

The image we have of canine hypothyroidism diagnosed with hypothyroidism. Indeed,

has changed during the last decade. We use to
consider it as the most common endocrinopathy
in dogs. Most endocrinologists will agree that
nowadays, other endocrine diseases such as
hypercortisolism, are more frequently observed.
In the past, many dogs have been erroneously
evaluation of thyroid function in dogs is not
always straightforward. The vague and non-
specific clinical signs of hypothyroidism and the
fact that numerous factors can influence thyroid
function test results are major contributors to the
difficulty in diagnosing this disease.

Tests available to assess the thyroid gland in dogs

Table: Advantages and disadvantages of the most commonly used tests to evaluate thyroid function
in dogs
Test Advantages Disadvantages
TT4 Easy Decreased with SNTD
Not expensive Decreased after administration of certain drugs
Readily available A decreased T4 alone does not allow a reliable
Normal values allow diagnosis of hypothyroidism (low specificity)
‘exclusion’ of hypothyroidism
TSH Easy 1/4 of hypothyroid dogs have TSH values within
Not expensive the reference range (low sensitivity)
Available Always use in combination with T4
FT4 Is less influenced by SNTD The only reliable method includes
or through drug equilibrium dialysis Not readily
administration than TT4 available in all countries
TSH Was and still is considered Bovine TSH is not easily available
2006 World Congress WSAVA/FECAVA/CSAVA

stimulation as the gold standard anymore → rhTSH

test Expensive4 to 6 hours lasting test
Anaphylactic reactions were described
with bTSH

SNTD: systemic non-thyroid disease

Total thyroxine (TT4) Endogenous thyrotropin

It is important to realise the limitations of a TT4
measurement. Indeed, numerous factors such as
systemic diseases (euthyroid sick syndrome) or
the administration of medications can influence
the TT4 serum concentrations. Therefore, when
TT4 serum concentration is below the reference
range, further testing is indicated.
312
Back to contents
With primary hypothyroidism, an increase in TSH
serum concentrations would be expected because
of the lack of negative feed back mechanism
of the thyroid hormones on the pituitary.
However, about one fourth of the dogs with
hypothyroidism show TSH serum concentrations
within the reference range. Because of the weak
sensitivity of the TSH measurement for the

diagnosis of hypothyroidism, this test cannot be
recommended solely. To reliably evaluate canine
thyroid function, a T4 measurement (FT4 or TT4)
is always combined with a TSH measurement. A
serum sample with decreased T4 and increased
TSH serum concentrations (>0,6 ng/ml) will
confirm with confidence the diagnosis of primary
hypothyroidism. When the measurements of
T4 and TSH give contradictory results, it is
recommended to repeat measurements 4-8
weeks later or to perform further testing (i.e. FT4
measurement, rhTSH stimulation, scintigraphy).
Free thyroxine (FT4)
In theory, the measurement of FT4 should reflect
more precisely thyroid function. The most
reliable technique used to measure FT4 involves
equilibrium dialysis, only available in some
laboratories and more expensive than measurement
of a TT4. Free T4 serum concentrations seem less
influenced by non-thyroidal illnesses than TT4.
Measuring FT4 seems therefore more interesting
to evaluate thyroid function, if measurement is
performed after equilibrium dialysis.
Thyrotropin stimulation test
Canine thyroid stimulation with bovine
TSH is less affected by the presence of non-
systemic thyroid diseases than is a baseline
TT4 measurement. Therefore the bovine TSH
stimulation test has long been considered as the
gold standard for thyroid evaluation in dogs.
Today, the bovine TSH stimulation test is less
used for several reasons: expense, 4-6 hour test,
bovine TSH is difficult to obtain and FT4 and
TSH measurements are available. However, in
non-infrequent cases with controversial results,
performing a TSH stimulation test would still
be very interesting. Sauvé and Paradis showed
that recombinant human TSH (rhTSH) will
stimulate the thyroid gland of euthyroid beagle
dogs. Major limiting factors for the use of rhTSH
in dogs resided in the cost of the product and
some practical aspects: one vial contains 1.1 mg
of lyophilized rhTSH, while the amount needed
to perform a TSH stimulation test in dogs varies
from 50 to 100 µg. We showed that rhTSH can
be stored in aliquots at 4°C for 4 weeks and at
–20°C for 8 weeks without loss of biological
activity. This allows clinicians to perform more
TSH response tests per vial.
A study performed at the University of Montreal
(Daminet et al., submitted), showed the ability
of the rhTSH stimulation test to differentiate
euthyroid dogs, dogs with hypothyroidism and
euthyroid dogs with nonthyroidal illnesses.
We have used the rhTSH stimulation test in our
clinic almost exclusively in dogs with ambiguous
Back to contents
E
thyroid function test results, especially in dogs
suspected of having hypothyroidism with
decreased TT4 serum concentrations and TSH
levels within the reference range, but also in
dogs with TT4 values within the reference
range accompanied with an increased TSH
concentration.
Antibodies against thyroid hormones
Anti-thyroglobulin antibodies (ATG) are
found in only 36 to 60% of hypothyroid dogs.
The presence of ATG in euthyroid dogs (false
positives) is now only observed in less than
5% of dogs. Epidemiological analysis of the
prevalence of ATG has shown considerable breed
and age variation. The presence of ATG does not
necessarily reflect thyroid ability to synthesise
thyroid hormones. The presence of antibodies in
combination with normal thyroid hormone values
can be an indication that hypothyroidism might
develop.
Rarely, anti-T3 and anti-T4 antibodies are
observed in hypothyroid dogs. Therefore their
clinical use is limited. These antibodies can
however interfere with radio immunoassay
determination of T3 or T4, and lead to falsely
increased values as a consequence.
Medical imaging
Scintigraphy is a very useful method for evaluation
of thyroid function. When available, it can be
used to differentiate dogs with the euthyroid sick
syndrome from truly hypothyroid dogs.
Ultrasonographic changes observed in
hypothyroid dogs were recently described and
include a decrease in thyroid volume and a
decreased echogenicity compared to normal dogs.
Quality of the ultrasonographic equipment and
experience of the ultrasonographer may negatively
impact accurate measurement of thyroid size and
will most likely limit the use of ultrasonography
for the diagnosis of hypothyroidism in current
2006 World Congress WSAVA/FECAVA/CSAVA
veterinary practice.
Influences on thyroid function tests
Numerous diseases and drugs can influence
thyroid function. Besides this many other
physiological factors such as, age, breed and
fluctuating serum concentrations, can influence
the results. Some dog breeds clearly have
thyroid hormone concentrations lower than
values observed in most breeds. For example,
Greyhounds have TT4 values that are markedly
lower (half) than in other breeds. Recently we
investigated thyroid hormone values in Whippet
dogs and also demonstrated that caution is also
advised in this breed as lower TT4 values were
found when compared to control dogs.
313
E
Summary of the effects of some drugs on canine thyroid function test results.

Drugs TT4 FT4 TSH TSH stimulation test

Glucocorticoids ↓ = or ↓ = Blunted at high dose and duration
(immunosuppressive
dosage)
Potassium bromide = = = =
Phenobarbital ↓ = or ↓ = or↓
Sulfonamides ↓ ↓ ↓ ↓
Propranolol = = = =
Carprofen = or ↓ = (↓) = or ↓ Not studied
Aspirin ↓ = = Not studied
Meloxicam = = = Not studied
Ketoprofen = = = Not studied
Etodolac = = = Not studied
Clomipramine ↓ ↓ = Not studied

Conclusion the administration of medications can lead to

Treatment of hypothyroidism is relatively simple,
but obtaining a reliable diagnosis can sometimes
be more difficult. Numerous factors can influence
thyroid homeostasis. Knowledge of these factors
can contribute to decreasing the misdiagnosis
of hypothyroidism. Non-thyroidal diseases and
2006 World Congress WSAVA/FECAVA/CSAVA
decreased thyroid hormone concentrations. As
always, laboratory results should be interpreted
in light of history and physical examination
findings.
References available upon request

314
Back to contents

E – Endocrinology
ULTRASONOGRAPHIC EXAMINATION OF ENDOCRINE GLANDS:
THE ENDOCRINOLOGISTS VIEW
Claudia E. Reusch, DiplECVIM-
CA
Clinic for Small Animal Internal
Medicine
University of Zuerich
Winterthurererstrasse 260
CH-8057 Zuerich
creusch@vetclinics.unizh.ch
During the last 10 to 15 years enormous
progress has been made with regard to quality
of ultrasound equipment. The improved
resolution has enabled consistent visualisation
of endocrine glands in dogs and cats and today
ultrasonography is routinely used in the work-
up of endocrine diseases. It is important to
remember, that ultrasonographic imaging gives
information on size, shape and parenchyma of
the endocrine organs, but not their endocrine
function. Therefore, ultrasonography should be
regarded as a test that is useful in addition (not as
replacement) to hormone testing. The presentation
will focus on the ultrasonographic examination of
adrenal glands, thyroid and parathyroid glands.
Adrenal glands
In almost all dogs and cats it is possible to
visualize the adrenal glands. Usually, a 7.5 MHz
transducer is adequate, in general the highest
frequency that will penetrate to the adrenal region
should be used. A systematic approach is critical
for a high detection rate. In our clinic the left
adrenal gland is evaluated in dorsal recumbency,
the right adrenal in left lateral recumbency. The
left adrenal gland is located ventrolateral to the
aorta between the origin of the left renal artery
and the cranial mesenteric artery; therefore
it is advisable to use those 3 blood vessels as
anatomical landmarks. In some animals the right
adrenal gland is more difficult to find, since it
is located deeper and more cranial than the left
adrenal and therefore ribs and bowl gas can
compromise visualisation. The caudal vena cava
serves as landmark, since the right adrenal gland is
firmly attached to its lateral side. In healthy dogs
the left adrenal gland appears as a peanut-shaped
hypoechoic structure (in the longitudinal plane).
The right adrenal is hypoechoic and comma-
shaped and it may be difficult to visualize the
entire length in a single-long axis view. Due to its
special shape the cranial pole of the right adrenal
gland may appear thickened and resemble an
Back to contents
E
adrenal tumour. Therefore, careful imaging of the
right adrenal and conservative interpretation of a
thickened cranial pole is of particular importance,
especially for beginners.
In cats adrenal glands are also hypochoic
compared to surrounding tissue, and they are
oval to bean-shaped. A distinct waist between the
cranial and caudal pole is usually not identified.
In dogs and cats the parenychma may appear
uniform or two layers may be seen.
Measurement of the dorsoventral dimension
(thickness) appears to be the most accurate
means of assessing adrenal size. Normal
thickness in dogs is between 3 and 6 (-7) mm,
in cats 2 – 5 mm. It should be noticed, however,
that size measurements depend on the imaging
position, therefore own reference ranges should
be established. Adrenal ultrasound is most often
used in dogs and cats with hyperadrenocorticism
(HAC) to differentiate between pituitary-
dependent disease (PDH) and HAC due to an
adrenocortical tumour (AT). In the typical case of
a dog with PDH the adrenal glands have a bilateral
symmetrical appearance. They may be enlarged
(increase in thickness), or normal-sized. Normal-
sized adrenal glands are relatively frequent (about 2006 World Congress WSAVA/FECAVA/CSAVA
30% of cases with PDH) and we assume that
they are mostly seen in dogs with short term or
mild disease. In dogs with PDH the shape of the
adrenals is usually preserved, a plump appearance
is sometimes seen. With regard to echogenicity
adrenal glands in dogs with PDH are most often
hypochechoic and homogenous. However, the
parenchyma may also appear irregular, show
focal areas of increased echogenicity or a nodular
appearance. These findings may indicate nodular
hyperplasia, however they are indistinguishable
from AT or other adrenal lesions. In some dogs
with PDH adrenal glands are not symmetrical
(one gland is thicker than the other) a situation
which resembles AT. In those latter cases further
endocrine tests (such as cACTH) are needed to
specify if the HAC is due to PDH or AT.
315
E
ATs, which are the most common endocrine
tumours, may have a large variation with regard
to ultrasonographic appearance. As a general rule,
ultrasonography does not allow to differentiate
between benign and malignant lesions nor
can the type of tumour be specified. They may
appear as focal increase in adrenal thickness
(= nodule) or a diffuse increase in thickness
and/or length, resulting in various degrees
of distortion of the normal shape (= adrenal
mass). The parenchyma may be homogenous
or heterogenous. The larger the tumour the
more likely it is malignant; however, also small
tumours may be malignant. Mineralization may
occur in benign and malignant tumours, however,
it may also be seen in hyperplastic adrenal glands
and is therefore not a marker for AT. Anechoic
lesions are preferably seen in large tumours,
they are often part of a heterogenous or mixed
pattern of echogenicity. They may represent foci
of adrenal necrosis or hemorrhage and may be
associated with fast tumour growth. Identification
of vascular invasion (most often into the vena
cava caudalis) is specific for a malignant tumour.
Although ultrasonography in general is a fast and
easy tool to detect vascular invasion it may not
be possible to differentiate vascular involvement
from compression or a blot clot in some cases.
A variety of other tumours (pheochromocytoma,
aldosteronoma, sex-steroid-producing tumour,
metastasis, myelolipoma, lipoma) or other
lesions (cyst, hematoma, abscess, granulomatous
disease) may occur in the adrenal glands and
can not be differentiated from AT by means of
ultrasonography. In a dog with an adrenal nodule/
mass a smaller than normal contralateral gland
strongly supports the suspicion of an AT. However,
in some dogs atrophy of the contralateral gland is
not visible on ultrasonography. In this situation
differential diagnosis are: unilateral AT without
visible atrophy of the contralateral gland, AT
2006 World Congress WSAVA/FECAVA/CSAVA
and concurrent PDH, PDH and another adrenal
tumour/lesion (as mentioned above), PDH with
(irregular) nodular hyperplasia. Most AT are
unilateral, however, bilateral tumours occur and
may be impossible to differentiate from PDH
with nodular hyperplasia. Endocrine tests may be
helpful to make the exact diagnosis.
The second most common adrenal tumours
are pheochromocytomas. Dogs with
pheochromocytomas may be presented with
various clinical signs; some of them are similar to
those of HAC. Pheochromocytomas have a very
wide range of size (mm – cm) and may reveal any
of the ultrasonographic patterns described above,
rendering differentiation from AT impossible.
Mineralization within a pheochromocytoma
seems to be a very rare finding; therefore, this
316
Back to contents
finding would make pheochromocytoma less
likely than AT.
Up till now information is scarce on the
ultrasonographic appearance of the adrenal
glands in cats with PDH or AT. So far, it appears
that all statements made for the dog are also valid
for the cat.
Ultrasonography of the adrenal glands may
also be helpful in the workup of patients with
hypoadrenocorticism. It is currently believed
that most cases result from an autoimmune
destruction of the adrenal cortices with bilateral
atrophy of all three adrenal zones. It has been
demonstrated that this atrophy is visible in the
form of a bilateral, symmetrical reduction in size.
In most dogs with hypoadrenocorticism adrenal
gland thickness is less than 3 mm. However, due
to their small size those adrenals are difficult to
find and a high level of experience is required
on the part of the operator. So far, no reports are
available on the adrenal gland size in dogs with
partial hypoadrenocorticism.
Thyroid and parathyroid glands
The superficial location of the thyroid gland
allows ultrasonographic examination with
high-frequency transducers. Recently, thyroid
ultrasonography has been evaluated as a
diagnostic tool for hypothyroidism. It can be
performed in dorsal recumbency or in a sitting
position, usually without sedation using a 10
MHz linear transducer. The head and neck are
moderately stretched and the point of the mandible
and sternum are kept in a straight line. Larynx
(cranial), trachea (media) and common carotid
artery (lateral) serve as anatomical landmarks.
The transducer is placed directly caudal to the
larynx in the jugular groove and the carotid artery
is identified in the longitudinal plane. From
this position, the transducer is tipped slightly
medially in the direction of the trachea until the
boat-shaped thyroid gland is apparent. Rotation
of the transducer by 90° allows the visualization
in transverse plane. In healthy dogs thyroid lobes
appear fusiform or elliptical in the longitudinal
plane and round to oval in the transverse plane.
Echogenicity compared with surrounding
musculature is hyper- or isoechoic in most cases.
From the few data available it appears that thyroid
size depends on body weight, therefore, reference
ranges need to be established for different breeds
resp. different weight categories. Primary
hypothyroidism is thought to be the result of
immune-mediated destruction of the thyroid gland
in the majority of cases. This correlates well with
the finding that thyroid volume is significantly
lower in hypothyroid dogs than in healthy or
sick-euthyroid dogs. Echogenicity in hypothyroid

dogs is either hypoechoic or heterogenous
compared to surrounding musculature. So far it is
unknown at which stage of the disease differences
in size and echogenicity can be diagnosed by
ultrasonography. The diagnostic value of thyroid
ultrasonography in dogs with subclinical and early
hypothyroidism is currently under investigation.
In dogs with suspected thyroid tumour
ultrasonography is helpful to evaluate size, uni-
or bilateral involvement, possible invasion into
surrounding tissue and to guide fine-needle
aspiration.
By means of a 10 MHz high resolution linear
transducer it is also possible to visualize the
parathyroid glands. There is a positive correlation
between body weight and size of the parathyroid
glands and the likelihood to detect all 4 glands
increase with an increase in body weight. The
size of the parathyroid gland is determined by
measuring the maximal length of the gland when
it is imaged in longitudinal plane. In dogs < 10
kg the longest dimension is 3.0 mm, in dogs
weighing between 10 and 19 kg 3.5 mm, in dogs
between 20 and 29 kg 4.0 mm and dogs > 30 kg
4.6 mm.
Ultrasonographic evaluation is an extremely
valuable tool in the workup of patients with
hypercalcemia. In dogs with hypercalcemia of
malignancy parathyroids are either small or not
detectable. In contrast visualisation of parathyroid
masses in dogs with primary hyperparathyroidism
is usually easy due to their increased size and
anechoic appearance. In our latest case series
size of parathyroid adenomas in dogs with
primary hyperparathyroidism ranged between 6
and 30 mm. Others have described smaller sizes,
which would then make differentiation from
normal parathyroid glands more difficult. As in
the other endocrine disorders discussed above,
ultrasonography is not a test of parathyroid
function and should only be used additionally
to endocrine tests (such as PTH, PTHrP).
Parathyroid ultrasonography may also be helpful
to differentiate between acute and chronic renal
failure. In a recently performed study in dogs with
severe azotemia (serum creatinine > 500 mmol/
l) we could demonstrate that dogs with chronic
renal failure had significantly larger parathyroid
glands than dogs with acute renal failure. The
number of abnormal parathyroids correlated
with the duration of the disease. Furthermore,
the parathyroid glands of dogs with chronic renal
failure were more prominent than those of healthy
dogs and dogs with acute renal failure and they
were consistently anechoic.
Back to contents
E
References
Besso JG, Penninck DG, Gliatto JM. Retrospective
ultrasonographic evaluation of adrenal lesions in
26 dogs. Radiology & Ultrasound 1997; 38(6):
448-455.
Brömel C, Pollard RE, Kass PH, Samii VF,
Davidson AP, Nelson RW. Ultrasonographic
evaluation of the thyroid gland in healthy,
hypothyroid, and euthyroid golden retrievers
with nonthyroidal illness. Journal of Veterinary
Internal Medicine 2005; 19: 499-506.
Brömel C, Pollard RE, Kass PH, Samii VF,
Davidson AP, Nelson RW. Comparison of
ultrasonographic characteristics of the thyroid
gland in healthy small-, medium-, and large-breed
dogs. American Journal of Veterinary Research
2006; 67(1): 70-77.
Hörauf A, Reusch C. Darstellung der Nebennieren
mittels Ultraschall: Untersuchungen bei
gesunden Hunden, Hunden mit nicht-endokrinen
Erkrankungen sowie mit Cushing-Syndrom.
Kleintierpraxis 1995; 40: 351-360.
Hörauf A, Reusch C. Ultrasonographic
characteristics of both adrenal glands in 15 dogs
with functional adrenocortical tumors. Journal of
the American Animal Hospital Association 1999;
35: 193-199.
Hörauf A, Reusch C. Ultrasonographic
evaluation of the adrenal glands in 6 dogs with
hypoadrenocorticism. Journal of the American
Animal Hospital Association 1999; 35: 214-218.
Reese S, Breyer U, Deeg C, Kraft W, Kaspers
B. Thyroid sonography as an effective tool
to discriminate between euthyroid sick and
hypothyroid dogs. Journal of Veterinary Internal
Medicine 2005; 19: 491-498.
Reusch C, Glaus T, Hoerauf A, Grundmann S,
Unterer S. Primärer Hyperparathyreoidismus
beim Hund – zur diagnostischen Bedeutung des
Parathyreoidea-Ultraschalls am Beispiel von 5
2006 World Congress WSAVA/FECAVA/CSAVA
Fällen. Kleintierpraxis 1999; 44(5): 317-328.
Reusch CE, Tomsa K, Zimmer C, Hoerauf A, Nett
C, Unterer S, Glaus TM, Schlittner E, Pospischil
A. Ultrasonography of the parathyroid glands
as an aid in differentiation of acute and chronic
renal failure in dogs. Journal of the American
Veterinary Medical Association 2000; 217: 1849-
1852.
Rosenstein DS. Diagnostic imaging in canine
pheochromocytoma. Veterinary Radiology &
Ultrasound 2000; 41(6): 499-506.
Zimmer C, HoeraufA, Reusch C. Ultrasonographic
examination of the adrenal gland and evaluation
of the hypophyseal-adrenal axis in 20 cats. Journal
of Small Animal Practice 2000; 41: 156-160.
317
E
E – Endocrinology
HYPERALDOSTERONISM IN CATS
Dr. Hans S. Kooistra, Dipl
ECVIM-CA
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
Yalelaan 108
3584 CM UTRECHT
THE NETHERLANDS
H.S.Kooistra@vet.uu.ni
Introduction
The mineralocorticoid aldosterone is synthesized
exclusively in the outer zone, the zona
glomerulosa, of the adrenal cortex and has two
important activities: (1) It is a major regulator
of sodium homeostasis and hence extracellular
fluid volume, and (2) it is a major regulator
of potassium homeostasis. In response to (a
tendency to) hypovolemia, renin is released
from the juxtaglomerular cells in the kidney. In
the bloodstream renin acts upon its only known
substrate, angiotensinogen, to form angiotensin
I. This angiotensin I, which is physiologically
inactive, is converted to angiotensin II by the
action of a converting enzyme (ACE). One of the
biological actions of angiotensin II is synthesis and
release of aldosterone. In addition to angiotenson
II, potassium and the pituitary hormone ACTH
are involved in aldosterone secretion.
Primary Hyperaldosteronism (PHA) is a disorder
of the adrenal cortex and can be divided in
two main subtypes: an unilateral aldosterone-
producing adenoma or adenocarcinoma (APA)
and bilateral adrenal hyperplasia or idiopathic
hyperaldosteronism (IHA)(Wheeler and Harris,
2006 World Congress WSAVA/FECAVA/CSAVA
2003). Both subtypes result in elevated circulating
aldosterone levels. The increased aldosterone
secretion gives rise to increased potassium
excretion in the urine and thus lowers the total body
potassium concentration. In addition, it increases
sodium absorption, which ultimately results in a
higher circulating volume. Consequently, the main
clinical symptoms of PHA are muscle weakness
due to hypokalemia and arterial hypertension.
Hypokalemia is, however, not always present in
patients with PHA. Eventually the hypertension
can cause failure of target organs like the heart,
eyes and kidneys.
Systemic arterial hypertension is a relatively
common clinical entity in especially middle-
aged to older cats. Arterial hypertension may
lead to blinding ocular complications, resulting
from hypertensive retinopathy, hypertensive
318
Back to contents
choroidopathy and hypertensive optic neuropathy.
In fact, ocular signs such as (recurrent) intraocular
haemorrhage or acute blindness resulting from
retinal detachment are often the reason for first
presentation of these hypertensive patients
to a veterinarian, and for the diagnosis to be
frequently made by a veterinary ophthalmologist.
If untreated, the hypertension-induced posterior
segment lesions quickly result in irreversible
damage to the retina and optic nerve and, thus, in
permanent blindness. It is therefore of paramount
importance that the diagnosis is instantly made
and an appropriate therapy is initiated at once.
The etiology of feline systemic arterial
hypertension may be quite diverse, and classically
includes chronic renal disease, hyperthyroidism
and hyperadrenocorticism. Only recently,
primary hyperaldosteronism has been identified
as an important cause of feline systemic arterial
hypertension (Flood et al., 1999; Javadi et al.,
2005).
Feline primary hyperaldosteronism has long
been considered a rare entity. Its incidence,
however, may be underestimated (Ash et al.,
2005; Javadi et al., 2005). Since feline primary
hyperaldosteronism has been identified as a cause
of progressive renal disease (Javadi et al., 2005),
quite a number of hyperaldosteronism cases
may in the past have been falsely attributed to
progressive renal failure.
The occurrence of primary hyperaldosteronism
may be suspected based upon a low plasma
potassium concentration, high arterial blood
pressure and/or indications for target organ
failure. A specific diagnosis can be made by
measuring plasma renin activity (PRA) and
plasma aldosterone concentration (PAC) and
determining the ratio between these two, i.e., the
aldosterone/renin ratio (ARR). Recently, in cats the
reference values of the aldosterone concentration
(PAC) and renin activity in plasma (PRA) have
been determined and published (Javadi et al.
2004). In case of primary hyperaldosteronism,

diagnostic imaging of the adrenals is required to
differentiate between an unilateral aldosterone
producing adenoma or adenocarcinoma (APA)
and bilateral adrenal hyperplasia or idiopathic
hyperaldosteronism (IHA) (Rijnberk et al. 2001;
Ash et al., 2005; Javadi et al., 2005.
Therapy. Depending on the underlying pathology
of the primary hyperaldosteronism, a number
of interventions are available. For cats with
unilateral adrenal neoplasia without demonstrable
metastases, unilateral adrenalectomy is the
treatment of choice. Cats with adrenocortical
hyperplasia as well as cats with bilateral or
metastasised adrenal neoplasia may benefit from
administration of aldosterone antagonists, such
as spironolactone (Aldactone®). However, in
addition to spironolactone drugs which lower
the arterial blood pressure (e.g. calcium blocking
agents such as amlodipine) and potassium
supplementation are often required to completely
normalize blood pressure and the plasma
potassium concentration.
References
Ash RA, Harvey AM, Tasker S. Primary
hyperaldosteronism in the cat: a series of 13
cases. Journal of feline medicine and surgery
2005; 7: 173-82.
Back to contents
E
Flood SM, Randolph JF, Gelzer ARM, Refsal K.
Primary hyperaldosteronism in two cats. Journal
of the American Animal Hospital Association
1999; 35: 411-6.
Javadi S, Slingerland LI, van de Beek MG, Boer
P, Boer WH, Mol JA, Rijnberk A, Kooistra HS.
Plasma renin activity and plasma concentrations
of aldosterone, cortisol, adrenocorticotropic
hormone, and alpha-melanocyte-stimulating
hormone in healthy cats. Journal of veterinary
internal medicine 2004; 18: 625-31.
Javadi S, Djajadiningrat-Laanen SC, Kooistra
HS, van Dongen AM, Voorhout G, van Sluijs
FJ, van den Ingh TSGAM, Boer WH, Rijnberk
A. Primary hyperaldosteronism, a mediator
of progressive renal disease in cats. Domestic
Animal Endocrinology 2005; 28: 85-104.
Rijnberk A, Voorhout G, Kooistra HS, van
der Waarden RJ, van Sluijs FJ, IJzer J, Boer P,
Boer WH. Hyperaldosteronism in a cat with
metastasised adrenocortical tumour. Veterinary
Quarterly 2001; 23: 38-43.
Wheeler MH, Harris DA. Diagnosis and
Management of Primary Aldosteronism. World J.
Surg. 2003; 27: 627-631.
2006 World Congress WSAVA/FECAVA/CSAVA
319
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Ex
E x
oticsx
Exotics

Back to contents

INVITED LECTURES - FULL PAPERS
Ex - Exotics
PHARMACOTHERAPEUTICS IN REPTILES: AN UPDATE AND
REVIEW
James W. Carpenter, MS,
DVM, Dipl. ACZM
Professor of Zoological Medicine
Department of Clinical Sciences
College of Veterinary Medicine
1800 Denison Avenue
Manhattan, KS 66502
carpentr@vet.ksu.edu
Introduction
Although a modest number of pharmacokinetic
studies have been conducted on reptiles, they are
really quite limited when one considers all the
drugs that are used to treat many of the extant
7500 species of this extremely diverse class of
animals. Drugs with available pharmacokinetic
data should be selected when possible. With the
extreme variations noted within Class Reptilia,
it is not surprising to find variations in the
effectiveness of certain drugs, or toxicities of
others, when one attempts to extrapolate from one
species to another. Although there are limitations
to metabolic scaling, it can be a useful tool for
some drugs when no pharmacokinetic data are
available. However, it should be noted that the
reptilian resting metabolic rate is 1/10 to 1/3
lower than the resting oxygen consumption rate
of mammals of an equivalent size.
Because sick reptiles may not absorb drugs well,
it is important to correct hypothermia (try to
maintain a preferred optimum temperature zone),
other suboptimal environmental conditions,
dehydration, malnourishment (hypoglycemia),
and electrolyte imbalance concurrent to
administration of therapeutic agents. This is
especially important when using nephrotoxic and
hepatotoxic drugs.
Like other lower vertebrates, reptiles have a
renal portal system as a unique component to
the circulatory system. Although reports exist of
nephrotoxicosis associated with the administration
of aminoglycosides, it appears that the toxicosis
was attributed to high doses of gentamicin rather
than the route of administration. This plus recent
research suggests that parenteral administration
of drugs into the caudal extremities may not
pose as great a risk as once thought2. It still
may be prudent, though, to avoid administering
Back to contents
Ex
potentially nephrotoxic drugs into the tail or
caudal extremities.
Antibiotics
Antimicrobial therapy is an important part of
medically managing reptiles with infectious
diseases. Selection of specific chemotherapeutics
is more difficult than in mammals because of
the broad range of behavioral, anatomic, and
physiologic peculiarities of the various species
within the Class Reptilia.
Culture results should be correlated with the
response to treatment. Therapeutics can be
selected or modified based on the isolate and
sensitivity data. Two areas of the culture results
must be evaluated: the quantitative results and
the minimum inhibitory concentrations (MIC)
patterns. Other factors to consider when selecting
an antimicrobial is the species being treated,
physical condition of the patient, frequency of
administration, cost of the therapy, and owner
compliance.
Most bacterial pathogens of reptiles, and many
2006 World Congress WSAVA/FECAVA/CSAVA
of these could be part of the host’s normal
flora, becoming pathogenic when the host is
immunosuppressed or stressed. Also, the presence
of gram-negative bacteria on culture does
not always indicate pathogenicity, and mixed
infections are common. Gram negative bacteria
that are most commonly isolated from reptiles
include: Aeromonas, Klebsiella, Morganella,
Pseudomonas, Provendencia, and Salmonella.
Also, anaerobic infections are quite common (yet
some of the most frequently used antibiotics in
reptiles, fluoroquinolones and aminoglycosides,
are not effective against anaerobes). Antibiotics
should not be used indiscriminately in reptiles
because of the risk of creating antimicrobial
resistant organisms.
321
Ex
Following are the antibiotics commonly used in
reptile medicine:
• Extended-spectrum penicillins (carbenicillin,
piperacillin): gram-negative bacteria
• Third-generation cephalosporins (cefotaxime,
ceftazidine): broad-spectrum, but primarily gram-
negative bacteria
• Macrolides (azalide: azithromycin): broad-
spectrum antibacterial, Chlamydophila,
Mycoplasma
• Tetracyclines (doxycycline): spectrum vs.
Chlamydophila, Mycoplasma, and ricketsial
organisms; broad-spectrum
• Chloramphenicol (chloramphenicol, broad-
spectrum bacteriostatic; florfenicol, broad-
spectrum bacteriocidal)
• Lincosamides (clindamycin, gram-positive
bacteria and anaerobes)
• Aminoglycosides (amikacin, gram-negative
bacteriocidal)
• Nitroimidazole (metronidazole, cidal vs. selected
protozoans and most obligate anaerobes)
• Trimethoprim-sulfa (trimethoprim-sulfadiazine
and -sulfamethoxazole, this synergism is bacteriocidal,
broad-spectrum)
• Fluoroquinolones (enrofloxacin, marbofloxacin;
bacteriocidal with activity vs. both gram-negative
and gram-positive pathogens; limited spectrum
vs. anaerobes)
Combination therapy (i.e., aminoglycoside and
an extended-spectrum penicillin) are often very
effective in the treatment of retiles. The Exotic
Animal Formulary (2005) lists the antimicrobial,
antiviral, antifungal, antiparasitic, and analgesic
agents used in reptiles.
AIPMMA Beads
Antibiotic-impregnated polymethylmethacrylate
(AIPMMA) beads are an effective means of
delivering an antibiotic in an infected area in
2006 World Congress WSAVA/FECAVA/CSAVA
which tissue integrity and vascular supply have
been compromised. The beads are placed in an
infected lesion after surgical debridement. Tissue
fluids penetrate the bead, and the antibiotic is
eluted into the lesion in high concentrations over
weeks to months.
In reptiles, AIPMMA beads are used to provide
controlled, local release of antimicrobials for the
treatment of infection (generally osteomyelitis or
abscesses). In addition, local release is associated
with a lower risk of toxicosis than parenteral
administration. Also, effective concentrations of
antimicrobials can be achieved and maintained
even if the site of infection is difficult to reach,
and AIPMMA beads can be used to help manage
infections in intractable animals in which systemic
administration may be difficult. The beads are
322
Back to contents
reasonably easy to make, and may be sterilized
with ethylene oxide gas.
The ideal antimicrobial for incorporation in an
AIPMMA bead would be bactericidal, have a
broad spectrum of activity, and be effective at low
concentrations; have low tissue toxicity; be heat
stable (up to 100°C); have high water solubility;
and results in low serum concentrations but high
concentrations in adjacent bone and soft tissue.
Ideally, the antibiotic should come as sterile
powder. Liquid antibiotics have been used, but
they may reduce the mechanical strength of the
PMMA. It is best to leave the beads in until the
site is no longer infected, and then to remove
them. Some of the antibiotics which have been
used include amikacin and ceftiofur.
Analgesics
Although there are few studies evaluating the use
of analgesics for pain in reptiles, it is strongly
recommended that an analgesic be administered
before (preemptive analgesia) any painful
procedures or whenever an animal may be in
pain. As with other animals, the consequences
of untreated pain are consistent with impaired
homeostasis and may impair the immune system
and inhibit healing.
The two major classes of analgesic drugs in reptiles
are opioids (butorphanol, buprenorphine) and,
more commonly, nonsteroidal anti-inflammatory
drugs (NSAIDs) (meloxicam, carprofen,
ketoprofen, and flunixin meglumine [if the latter
is used, administer for maximum of 3 days]). Of
these, butorphanol, carprofen, and meloxicam
are the most commonly used. In a study in green
iguanas, meloxicam at 0.2 mg/kg IV or IM lasted
approximately 36 hours (author suggests that 0.4
mg/kg PO q48h may be effective).
There are very few investigations that describe
the assessment of opioids and none that evaluate
the efficacy of NSAIDs in reptiles. The unknown
actions of opioids and NSAIDs in the central
nervous system of reptiles, therefore, may result
in unpredictable variations in the duration,
potency, and side effects of these drugs when
the doses are determined by extrapolation from
mammalian doses. Until more studies on the
effects of NSAIDs in reptiles are performed, it
is probably best to consider the possibility that
side effects (gastrointestinal irritation, renal
compromise, and platelet inhibition) similar to
those seen in mammals may also occur in reptiles
(Mosley). Therefore, hydration status, concurrent
medications (steroids), gastrointestinal disease,
and renal disease should be addressed before
administering these drugs.

Therapeutic Contraindications
Although there are far fewer reports of therapeutic
contraindications in reptiles than for other
species, they can occur.5 For example, ivermectin
toxicity can occur in chelonians where, even at
low dosages, it can result in paresis and death.
A dose considered safe in one chelonian species
may not be safe in another.
Metronidazole is used to treat anaerobic bacterial
and protozoan diseases in reptiles. Tortoises may
develop side effects (anorexia, head tilt, circling,
disequilibrium, and signs of hepatotoxicity) from
this drug and may not tolerate the relatively high
doses or duration of therapy necessary to treat
some conditions (i.e., amoebiasis).4 Metronidazole
treatment regimens in chelonians need to be
tailored to the individual with close monitoring
for clinical signs of toxicity. Metronidazole
toxicity has also resulted in the deaths of indigo
snakes and California and Arizona Mountain king
snakes when doses of more than 100 mg/kg were
used and in uracoan rattlesnakes at doses greater
than 40 mg/kg.
Back to contents
Ex
References
1. Carpenter JW (ed.). Exotic Animal Formulary.
3rd ed. St. Louis, Elsevier Publishers, 2005. Pp
53-131, 547-554.
2. Mitchell MA. Therapeutics. In: Mader DR
(ed.). Reptile Medicine and Surgery. 2nd ed. St.
Louis, Elsevier Publishers, 2006. Pp. 631-664.
3. Mosley CAE. Anesthesia and analgesia in
reptiles. Semin Avian Exotic Pet Med 14(4): 243-
262, 2005.
4. Norton TM. Chelonian emergency and critical
care. Semin Avian Pet Med 14(2): 106-130,
2005.
5. Rosenthal KL. Therapeutic contraindications
in exotic pets. Semin Avian Exotic Pet Med 13(1):
44-48, 2004.
2006 World Congress WSAVA/FECAVA/CSAVA
323
Ex
Ex - Exotics
PHARMACOTHERAPEUTICS IN COMPANION BIRDS: AN UPDATE
AND REVIEW
James W. Carpenter, MS,
DVM, Dipl. ACZM
Professor of Zoological Medicine
Department of Clinical Sciences
College of Veterinary Medicine
1800 Denison Avenue
Manhattan, KS 66502
carpentr@vet.ksu.edu
Introduction
Although there are many therapeutic agents
available for treating companion birds, most
drugs are based on empirical data, observations,
and experience. There are relatively few
pharmacodynamic studies in companion birds in
relation to the medications we use or potentially
use in practice.
Drug Administration
Most of the drugs given to companion birds
are given parenterally or orally in the form of
suspensions. There has been little research on
the efficacy of various drug suspensions in these
patients. It is essential for practitioners to have
a good working relationship with a licensed
compounding pharmacist. These pharmacists will
ensure that the drug is placed in the appropriate
media to remain viable in suspension and can warn
of potential risks associated with this media.
Antibiotics
Bacterial diseases are among the most common
medical problems reported in companion birds.
Because there is a concern by the medical
2006 World Congress WSAVA/FECAVA/CSAVA
profession of antibiotic resistance associated
with the overuse and abuse of antibiotics, it is
important to recognize the factors that determine
the use of antibiotic agents. Some of the decision
making factors include effectiveness of the agent
against the specific bacterial organism being
treated, ease of administration, stress of the
patient related to administration, ability of the
agent to reach therapeutic levels at the intended
site of treatment, cost, and availability of the
drug.
When selecting an antibiotic the clinician should
know if it is bacteriocidal or bacteriostatic, how
it is administered, how well an oral medication
is absorbed through the gastrointestinal tract and
disseminated through the body, species variation
relating to dose, and major side effects of the
324
Back to contents
drug. Although there are other considerations,
but if one does not apply this thought process into
the selection of antibiotics and other therapeutic
agents the success of treating avian patients will
be greatly reduced. It is generally recommended
to use bacteriocidal agents when possible, but
certain diseases respond better to agents that
may be bacteriostatic (e.g., drug of choice for
Chlamydiophila psittaci is doxycycline). A
detailed list of antibiotics, dosages, and special
considerations are listed in the Exotic Animal
Formulary (2005)1.
It is important to obtain a definitive diagnosis
whenever possible to avoid the problems
associated with the empirical dosages and to
improve efficacy in these species. Antibiotics
should be selected based on culture and sensitivity
results when possible. The use of more pathogen-
specific antimicrobials will decrease the potential
for resistant bacteria and often narrows the
potential side effects. Following are some of the
antibiotics commonly used in companion bird
medicine1:
• Antimicrobial agents commonly used to treat
bacteremia/septicemia cases include synergistic
aminoglycoside and cephalosporin therapy,
enrofloxacin with extended-spectrum penicillins,
and for anaerobic infections chloramphenicol,
clindamycin, and metronidazole.
• Cephalosporins, doxycycline, trimethoprim-
sulfa, and fluoroquinolones are often used to
treat anaerobic soft tissue infections while
clindamycins or metronidazoles are used to treat
anaerobic soft tissue infections.
• Respiratory tract infections are one of the
most common disease presentations involving
avian species. The drugs of choice for
respiratory infections are extended-spectrum
penicillins, cephalosporins, tetracyclines
(especially doxycycline), trimethoprim-sulfa,
chloramphenicol, fluoroquinolones, macrolides,
and, for anaerobic infections, clindamycin or

metronidazole. Antibiotics can be administered
through nebulization techniques and nasal
flushes.
• Trimethoprim-sulfa, fluoroquinolones, cephalosporins,
amoxicillin, tetracyclines, and metronidazole for
anaerobic infections are commonly used for
conditions that affect the gastrointestinal tract.
• Dermatological presentations are treated with
similar antimicrobial agents that one would use
for other small companion animals: amoxicillin-
clavulanate, cephalosporins, erythromycin,
enrofloxacin, and trimethoprim-sulfa.
• Bone and/or joint infections are difficult to treat
and as with any microbial infection a culture and
sensitivity will greatly aid in selecting the right
antibiotic agent to use. Choices of antimicrobial
agents to use for bone and/or joint infections
include cephalosporins, extended-spectrum
penicillins, fluoroquinolones, aminoglycosides,
clindamycin, and, for anaerobic infections,
extended-spectrum penicillins with clindamycin
and third generation cephalosporins with
clindamycin. Polymethyl methacrylate
(PMMA) beads containing aminoglycosides,
fluoroquinolones, or clindamycin may be a useful
adjunct to conventional antibiotic therapy.
• Extended-spectrum penicillins (piperacillin),
cephalosporins (ceftazidime, ceftiofur),
trimethoprim-sulfa, and fluoroquinolones, are all
commonly used for urinary tract infections.
• For central nervous system infections it is
important to choose an agent that crosses the
blood-brain barrier. The drugs of choice are
chloramphenicol and fluoroquinolones.
• Reproductive tract disorders are best treated
with chloramphenicol, trimethoprim-sulfa,
enrofloxacin, amoxicillin-clavulanate, and
clindamycin (against anaerobes).
Antifungal Agents
Fungal diseases (aspergillosis, candidiasis, and
avian gastric yeast [Macrorhabdus ornithogaster])
are relatively common in captive birds. Of these
diseases, aspergillosis is the most challenging to
diagnose and treat. Although several species of
Aspergillus may be involved in avian disease,
the most commonly encountered is A. fumigatus,
followed by A. flavus and A. niger. Particularly
susceptible species include African grey, Amazon,
and pionus parrots.
Agents most commonly used in treating mycotic
diseases in birds include:
• Amphotericin B: for aspergillosis, may be
used intravenously or topically via nebulization,
intratracheal, and direct application to lesions
within the air sac; administered PO for avian
gastric yeast; renal toxicity does not seem to be a
significant problem in birds.
Back to contents
Ex
• Nystatin: fungistatic; used to treat yeast
infections, primarily candidiasis; functions as a
topical treatment when administered PO (drug
requires contact with the yeast to be effective).
• Itraconazole: most common triazole antifungal
used in birds; fungistatic; alters the cellular
membranes of susceptible fungi, thereby
increasing and allowing leakage of cellular
contents and impaired uptake of purine and
pyrimidine precursors.
• Voriconazole: a triazole antifungal; oral; in
people with aspergillosis, treatment success with
voriconazole is often better than amphotericin or
itraconazole; some side effects in people have
been reported.
• Other triazoles: fluconazole (PO), ketoconazole
(PO), clotrimazole (nebulization), and miconazole
and enilconazole (topical).
• Terbinafine: fungicidal; an allylamine antifungal
that inhibits squalene epioxidase, thus inhibiting
fungal steroid and cell wall synthesis; well-
tolerated; administered orally or nebulized.
Respiratory tract infections in birds caused
by Aspergillus are especially difficult to treat.
The most commonly used drugs used to treat
this disease are a combination of itraconazole
with nebulization of amphotericin B. Topical
application of amphotericin B or clotrimazole aids
in the initial treatment success. Long periods of
oral antifungal drug therapy are usually required
to treat aspergillosis. Although itraconazole can
be effective, treatment failures in some species
(i.e., African grey parrots) are common. In those
cases, terbinafine or voriconazole may be used.
Analgesics
Because avian pain is likely analogous to
pain experienced by most mammals, painful
procedures or events should always be
accompanied by appropriate analgesia. As
in mammals, it is assumed that pre-emptive 2006 World Congress WSAVA/FECAVA/CSAVA
administration of analgesics reduces the
magnitude of the pain experienced by a bird as
a result of tissue damage. During gas anesthesia,
the CNS is depressed sufficiently to prevent
perception of pain, but this depression does not
provide analgesia. In fact, inhaled anesthetics can
produce extreme sensitivity to pain at very low
concentrations. The sometimes violent recoveries
in birds from anesthetic may be due, in part, to
hyperalgesia produced by low concentrations of
inhaled anesthetics. Opioids and nonsteroidal
anti-inflammatory drugs (NSAIDS) are probably
the most frequently used drugs for treating pain
in birds.
Opioids: Opioid actions are mediated by specific
membrane receptors (mu, delta, and kappa) that
are distributed throughout the CNS and peripheral
325
Ex
nervous system. In contrast to the population
of opioid receptors in the mammalian nervous
system, kappa receptors predominate in the pigeon
fore brain. Buprenorphine is a partial agonist that
binds readily to mu receptors and has some kappa
antagonist properties. Although reported to be
clinically effective in birds, buprenorphine at 0.1
mg/kg in African grey parrots did not show an
analgesic effect (higher doses may be effective in
some species).
Butorphanol is a mixed agonist-antagonist with
primarily kappa agonist action. Butorphanol (1-
3 mg/kg IM) is the correct recommendation for
opioid analgesia in parrots.
Non-steroidal Anti-inflammatory Drugs: NSAIDs
control pain by inhibiting cyclooxygenase
(COX) enzymes which prevents production
of prostaglandins (important local mediators
of inflammation that lower the threshold of
thermal, mechanical, and chemical nociceptors).
However, NSAIDs are also capable of producing
gastrointestinal ulceration and bleeding because
of inhibition of prostaglandin synthesis. NSAIDs
should not be used if there is an indication of
renal impairment, hepatic dysfunction, severe
hypovolemia, or if gastric ulceration is present.
NSAIDs can be use to relieve musculoskeletal and
visceral pain, acute pain (trauma or surgical), and
chronic pain such as osteoarthritis. Although the
most common NSAIDs used in avian medicine are
ketoprofen, carprofen, and meloxicam, the latter
two are preferred because of their widespread use
and low incidence of reported toxicities.
2006 World Congress WSAVA/FECAVA/CSAVA
326
Back to contents
Corticosteroids
Steroid use can cause severe alterations in the
normal physiology of birds. For example, studies
in pigeons have shown the deleterious affects
of steroids on the liver of birds and the possible
negative affect on breeding birds. Corticosteroids
in psittacine birds can also cause other
adverse effects, including immunosuppression,
delayed wound healing, hepatic disease, and
gastrointestinal ulceration. Since the use of
steroids in many situations is now controversial,
it may be appropriate to avoid these drugs unless
no other medication will be effective.
References
1. Carpenter JW (ed.). Exotic Animal Formulary.
3rd ed. St. Louis, Elsevier Publishers, 2005. pp
133-344; 547-554.
2. Flammer K. Common bacterial infections
and antibiotic use in companion birds. Suppl
Compend Contin Educ Pract Vet. 20(3A): 34-48,
1998.
3. Lumeij JT. Psittacine antimicrobial therapy.
Antimicrobial Therapy in Caged Birds and
Exotic Pets: International Symposium, Orlando,
1995. pp. 38-47
4. Machin KL. Avian analgesia. Semin Avian
Exotic Pet Med. 14(4): 236-242, 2005.
5. Rosenthal KL. Therapeutic contraindications
in exotic pets. Semin Avian Exotic Pet Med.
13(1): 44-48, 2004.

Ex - Exotics
GIS AS AN EPIDEMIOLOGICAL TOOL IN THE STUDY OF
INFECTIOUS DISEASES
Doc. MVDr. Jiří Pikula, Ph.D.
Department of Veterinary
Ecology and Environmental
Protection
University of Veterinary and
Pharmaceutical Sciences Brno
Palackeho 1-3, 612 42 Brno,
Czech Republic
pikulaj@vfu.cz
Recently, there have been a growing number of
applications of geographic information systems
(GIS) in epidemiology and public health. Data for
the GIS may be gathered using standard screening
methods throughout a distinct territory as well as
remote sensing from satellites. GIS databases offer
new analytic opportunities for disease assessment
and prevention. They have been used to identify
risk factors of zoonotic diseases over large
geographic areas such as environmental variables
associated with the disease and breeding habitats
of disease vectors. It is also possible to use GIS to
test epidemiological hypotheses about patterns of
disease occurrence. It may be stated that GIS make
it possible to incorporate space relationships into
epidemiological studies of diseases of animals
and humans. It is a technology consisting of input,
storage, analysis and presentation of geographic
data. Using GIS it is possible to combine a
whole number of data from various sources and
evaluate different aspects of the environment in
relation to the phenomenon studied. Analytical
possibilities of GIS are still developing and
range from a simple visual evaluation of maps to
exploratory analysis and modelling. For purposes
of veterinary administration and disease control
the GIS technology has been used by e.g., Fuchs
et al. (2001), McGinn et al. (1996), Michel
et al. (2002), Norstrom (2001), Sanson et al.
(1991), Schwermer et al. (2002), Solymosi and
Medveczky (2000) and Stark et al. (1998). Unlike
in domestic animals, the distribution of wild
animals in space depends to a great degree on
environmental factors and geographic conditions
(Pfeiffer and Hugh-Jones, 2002). That is why the
GIS technologies are suitable for the purpose of
study of occurrence and distribution of diseases
in wild animals (Delahay et al., 2000; Conraths et
al., 2003). In relation to the growing importance
of the so-called „new-emerging“ infections
(zoonoses) there is an increased interest in the
ecology of reservoir hosts (wild rodents and
Back to contents
Ex
game animals) as well as vectors of diseases. In
this respect it is possible to study the geographic
distribution of the host, outlining the maximum
territory of the disease distribution, the extent of
the disease distribution within the distribution
of the host, relation between the geographic
distribution of the host and the disease within
individual habitats, the importance of population
ecology of the host (overcrowding, seasonal
dynamics, migration activities, activities during
the day and night, survival and mortality).
Use of GIS in veterinary medicine is presented
here on examples of analysing spatial aspects of
distribution of tularaemia, a zoonosis of veterinary
and public health importance occurring in natural
foci throughout the Northern Hemisphere with
the milder biotype B prevailing in Eurasia. In
Southern Moravia (Czech Republic) it has been
known since autumn 1936 when 290 humans
contracted the external ulceroglandular form of the
disease due to handling tularaemic hares. During
the 1960s, severe epidemics of the professionally-
acquired pulmonary form of tularaemia in workers
in “cold divisions” of sugar factories occurred.
There was a 25-year period of low occurrence
of this disease in humans interrupted by another 2006 World Congress WSAVA/FECAVA/CSAVA
epidemic in 1978. In autumn 1994, the number of
tularaemia cases rose again and, during the season
of 1998-1999, 115 human cases of tularaemia
contracted mainly by handling tularaemic hares
were reported (Černý, 2001). These increased
numbers of human cases of tularaemia coincide
with the rise of seroprevalence of hares positive
for tularaemia from the common value of about
1% to 5.75% in 1994. In the last decade, apart
from the rise of numbers of positive hares, we
have been witnessing some spread of natural
foci of tularaemia into more northern areas of
Southern Moravia.
1) Ecological conditions of natural foci of
tularaemia in the Czech Republic (Pikula et al.,
2003): A new variable (xt), the mean number of
327
Ex
natural foci in a specific area, has been suggested
to analyse the environmental conditions of
distribution of natural foci of tularaemia and their
long-term persistence in the Czech Republic.
Comparing two 15-year periods, a close
correlation between the geographic distribution
and numbers of natural foci of tularaemia in the
Czech Republic in 1971 to 1985 and 1986 to 2000
(r=0.91, n=1814, t=92.50, P=0.01) was found.
Natural foci of tularaemia have been persistent,
but not stationary, over the period of 30 years and
the geographic area of their occurrence has not
been considerably growing or diminishing in the
Czech Republic. The highest numbers of natural
foci of tularaemia were in habitats of alluvial
forests (xt=7.20), geographic areas of up to 200 m
of elevation above sea (xt=9.18), 8.1-10.0 °C of
mean annual air temperature (xt=6.24), 450-700
mm of mean annual precipitation (xt=2.84), and
2001-2200 h of mean annual sunshine duration
(xt=8.77).
2) Spatio-temporal aspects of tularaemia in
Southern Moravia (Czech Republic) (Pikula et
al., 2004): The spatio-temporal development of
tularaemia in Southern Moravia (in a selected
study area of 130x90 km) was evaluated using
correlation analysis which resulted in finding
that the geographic distribution of natural foci
of tularaemia in any year correlated with the
distribution in any other year of the study period
of 1994-2001. The coefficients of correlation of
all possible combinations of distribution in years
1994-2001 vary from 0.38 to 0.96 (n = 3700,
p = 0.01). The closer the years, the closer and
more significant the correlation of distribution
of tularaemia. It can be stated that, in the study
area during the period of eight years, tularaemia
persisted rather in the same locations but, as the
coefficients of correlation do not equal 1.0, some
variation in the distribution could be observed.
3) Ecology of European brown hare and
2006 World Congress WSAVA/FECAVA/CSAVA
distribution of natural foci of tularaemia in
the Czech Republic (Pikula et al., 2004):
Quantitative data on the geographic distribution
of the European brown hare (a game animal most
important as a source of tularaemia for humans
in the Czech Republic) were analysed with
respect to selected environmental factors and
natural foci of tularaemia. The highest population
densities of the European brown hare were found
in geographic areas of up to 200 m of elevation
above sea (231.47 individuals/10km2), climatic
district No. 1 (227.91 individuals/10km2), annual
snow cover duration of 40-60 days (183.95
individuals/10km2), mean annual precipitation
of 450-700 mm (174.71 individuals/10km2),
annual sunshine duration of 1801-2000 hour
(169.72 individuals/10km2) and mean annual air
328
Back to contents
temperature of over 10.0 °C (245.00 individuals
/ 10km2). A correlation (r = 0.4431, n = 395, t =
9.7972, P = 0.01) between the population density
of the European brown hare and numbers of
natural foci of tularaemia in the Czech Republic
was found. In other words, tularaemia seems to
be the European brown hare population density
dependent.
4) Ecology of the common vole and distribution
of natural foci of tularaemia (Pikula et al., 2002):
The common vole (Microtus arvalis) is another
important reservoir animal of tularaemia in the
Czech Republic. Analysing the relation between
M. arvalis population abundance and geographic
distribution and numbers of natural foci of
tularaemia in the European hare, it was, however,
found that there is no correlation (r = 0.0765, n
= 396, t = 1.5228). In other words, tularaemia
seems to be independent of M. arvalis population
density.
5) Prediction of possible distribution of
tularaemia in the Czech Republic (Pikula et al.,
2004): A prediction map of tularaemia has been
constructed on the basis of the identified factors
favourable for the existence of current natural foci
of tularaemia in the Czech Republic. Geographic
distribution of a total of 6 different factors has
been evaluated with respect to their suitability
for harbouring natural foci of tularaemia. These
factors included habitats of alluvial forests,
geographic areas of up to 200 m of elevation above
sea, 8.1-10.0 °C of mean annual air temperature,
450-700 mm of mean annual precipitation, 1801-
2000 and 2001-2200 h of mean annual sunshine
duration and highest population densities of the
European brown hare (Lepus europaeus). Two
main territories of favourable conditions for
tularaemia were identified in the Czech Republic,
i.e., Southern Moravia and Central Bohemia.
Areas of 0, 1, 2, 3, 4, 5 and 6 factors favourable
for tularaemia cover 18 120.30, 27 960.75,
15 259.20, 7 933.05, 5 245.35, 3 337.95 and
780.30 km2, respectively, of the total area of
78 636.9 km2 of the Czech Republic.
Conclusion
Prediction modelling of possible occurrence of
a zoonosis seems to be an economical way for
the selection of areas of study and research. It
is also possible to use this knowledge for the
purpose of preventive and control measures
such as banning transfer of wild animals from
areas of existing natural foci to geographic areas
where the conditions suitable for the creation
of natural foci are met. GIS are suitable for the
State Veterinary Administration and they are
becoming part of decision-making as knowledge
on the geographical aspects of diseases including

the distribution of reservoir hosts is essential for
disease control.
Acknowledgement
Supported by the Ministry of Education, Youth
and Sports of the Czech Republic (Project MSMT
6215712402).
References
Černý Z. (2001): Changes of the epidemiology
and the clinical picture of tularemia in Southern
Moravia (the Czech Republic) during the period
1936-1999. Eur J Epidemiol 17: (7) 637-642.
Conraths, FJ., Staubach, C., Tackmann, K. (2003):
Statistics and sample design in epidemiological
studies of Echinococcus multilocularis in fox
populations. Acta Trop., 85, (2): 183-189.
Delahay, RJ., Langton, S., Smith, GC., Clifton-
Hadley, RS., Cheeseman, CL. (2000): The spatio-
temporal distribution of Mycobacterium bovis
(bovine tuberculosis) infection in a high-density
badger population. J. Anim. Ecol., 69, (3): 428-
441.
Fuchs, K., Wagner, P., Kofer, J. (2001): VETGIS®-
Styria - a geographic information system as a tool
for epidemiological research for the veterinary
administration. Wien. Tierarztl. Monat., 88, (9):
246-251.
McGinn, TJ., Cowen, P., Wray, DW. (1996):
Geographic information systems for animal
health management and disease control. J. Am.
Vet. Med. Assoc., 209, (11): 1917-1921.
Michel, JF., Dray, S., De la Rocque, S., Desquesnes,
M., Solano, P., De Wispelaere, G., Cuisance, D.
(2002): Modelling bovine trypanosomosis spatial
distribution by GIS in an agro-pastoral zone of
Burkina Faso. Prev. Vet. Med., 56, (1): 5-18.
Norstrom, M. (2001): Geographical information
system (GIS) as a tool in surveillance and
monitoring of animal diseases. Acta Vet. Scan.,
94: 79-85.
Pfeiffer, DU., Hugh-Jones, M. (2002):
Geographical information systems as a tool in
epidemiological assessment and wildlife disease
Back to contents
Ex
management. Rev. Sci. Tech . Off . Int. Epiz., 21,
(1): 91-102.
Pikula J, Treml F, Beklová M, Holešovská Z,
Pikulová J: Geographic information systems
in epidemiology-reservoir host ecology and
distribution. Acta Vet. Brno, 2002, 71: 379
– 387.
Pikula J, Treml F, Beklová M, Holešovská Z,
Pikulová J: Ecological conditions of natural
foci of tularaemia in the Czech Republic. Eur J
Epidemiol, 2003, 18(11): 1091-1095.
Pikula J, Beklova M, Holesovska Z, Treml F:
Spatio-temporal aspects of tularemia in Southern
Moravia (Czech Republic). Vet. Med. – Czech,
49, 2004 (1): 15-18.
Pikula J, Beklova M, Holesovska Z, Treml F:
Prediction of possible distribution of tularemia in
the Czech Republic. Vet. Med. – Czech, 49, 2004
(2): 61-64.
Pikula J, Beklova M, Holesovska Z, Treml
F: Ecology of European Brown Hare and
Distribution of Natural Foci of Tularaemia in the
Czech Republic. Acta Vet. Brno, 2004, 73: 267-
273.
Sanson, RL., Liberona, H., Morris, RS. (1991):
The use of a geographical information system
in the management of a foot-and-mouth-disease
epidemic. Prev. Vet. Med., 11, (3-4): 309-313.
Schwermer, H., Rufenacht, J., Doherr, MG.,
Heim, D. (2002): Geographic distribution of BSE
in Switzerland. Schweiz. Arch. Tierh., 144, (12):
701-708.
Solymosi, N., Medveczky, I. (2000): Using the
applications of the geographic information system
in veterinary epidemiology and in the control of
infectious diseases. Magy. Allatorvosok., 122,
(8): 504-507.
Stark, KDC., Morris, RS., Benard, HJ., Stern,
MW. (1998): EpiMAN-SF: a decision-support 2006 World Congress WSAVA/FECAVA/CSAVA
system for managing swine fever epidemics. Rev.
Sci. Tech. Off. Int. Epiz., 17, (3): 682-690.
329
Ex
Ex - Exotics
PHARMACOTHERAPEUTICS IN EXOTIC SMALL MAMMALS: AN
UPDATE AND A REVIEW
James W. Carpenter, MS, DVM,
Dipl. ACZM
Professor of Zoological Medicine
Department of Clinical Sciences
College of Veterinary Medicine
1800 Denison Avenue
Manhattan, KS 66502
carpentr@vet.ksu.edu
Introduction
Pharmacokinetic studies in exotic small
mammals are lacking and, therefore, most of
the dosages used in these species are based on
empirical data, observations, and experience.
Because drug uptake depends on factors such as
age, sex, physiology, disease state, diet, etc., it is
important for us as veterinarians to know some of
the pharmacobiologic, physiologic, and anatomic
characteristics of these species. It should also be
noted that most of the drugs used in exotic small
mammals are extralabel. This review outlines
drug administration sites, compounding, and some
of the issues involved in selecting an antibiotic,
analgesic, or nonsteroidal, anti-inflammatory
drugs for use in exotic small mammals.
Compounding
Exotic animal practitioners face daily challenges
to meet the pharmaceutical needs of their
small mammal patients. Because there are few
approved medications for use in these patients,
attempts to meet these challenges include:
extralabel use of human and domestic animal
products; compounding by the practitioner; use
2006 World Congress WSAVA/FECAVA/CSAVA
of compounding service; using medicated feeds;
and using imported pharmaceutical productions.
There may be both legal and ethical issues that
the practitioner must be aware in using any of the
aforementioned strategies.
Antibiotics
Antibiotics are probably the most commonly used
medications in small mammal medicine. Because
pharmacokinetic studies are lacking in these pet
species and are often empirical, it is helpful to
know the basic pharmacologic features and the
side effects of the drugs being used for maximum
safety and efficacy.
Because rabbits are herbivorous animals,
their intestinal microflora consists mainly of
gram positive bacteria and anaerobic bacteria.
330
Back to contents
Antibiotic choices in rabbits, however, are
limited because many antibiotics suppress the
healthy flora and allow pathogens to proliferate,
resulting in well documented enteric disorders.
Antibiotics which have been reported to cause
dysbiosis/enteritis/enterotoxemia in rabbits
include amoxicillin, amoxicillin/clavulanic
acid, ampicillin, cephalosporins, clindamycin,
erythromycin, lincomycin, and penicillin1. There
have also been some reports of antibiotic related
colitis in rabbits given penicillin/streptomycin,
trimethoprim/sulfamethoxazole, tetracycline,
tylosin, and gentamicin. It should also be noted
that, in some cases, enteritis can develop weeks
after the antibiotic has been discontinued. Oral use
of these medications generally is contraindicated
in rabbits; however, penicillin is occasionally
used parenterally on a limited basis2.
Unfortunately, there is a lack of data (based on
clinical trials) on the use of most antibiotics
in rabbits. Very few antibiotics have been
evaluated for their therapeutic effectiveness,
and, therefore, dosages in rabbits often rely
largely on empiric data. Antibiotics that
are generally considered safe in rabbits
include the fluoroquinolones, sulfonamides,
chloramphenicol, and metronidazole. Antibiotics
that do not cause problems with normal usage can
cause diarrhea when given in large doses.2 Even
when presumably “safe” agents are used, rabbits
on antibiotics should be monitored for signs of
gastrointestinal distress.
Inappropriate antibiotic treatment can also
result in enteritis and antibiotic-associated
clostridial enterotoxemia in rodents, especially
when antibiotics with a primary gram-positive
spectrum are given. Incidence is higher when
agents are given orally. Chinchillas, guinea
pigs, and hamsters are most susceptible.
Also, direct toxicity from streptomycin and
dihydrostreptomycin occurs in gerbils, guinea
pigs, hamsters, and mice. Procaine, included in

some penicillin preparations, can be toxic to mice
and guinea pigs. Guinea pigs and chinchillas
are highly susceptible to the ototoxic effects of
chloramphenicol and aminoglycosides at dosages
above those recommended clinically. Antibiotics
implicated in antibiotic associated clostridial
enterotoxemia in rodents include:1
• Chinchillas: penicillins (including ampicillin,
amoxicillin), cephalosporins, clindamycin,
erythromycin, lincomycin.
• Guinea pigs: penicillins (including ampicillin,
amoxicillin), cefazolin, clindamycin, erythromycin,
lincomycin, dihydrostreptomycin, streptomycin,
bacitracin, chlortetracycline, oxytetracycline,
tetracycline, tylosin.
• Hamsters: penicillins (including ampicillin,
amoxicillin), cephalosporins, clindamycin,
erythromycin, lincomycin, vancomycin,
dihydrostreptomycin, streptomycin, bacitracin,
oral gentamicin, tylosin.
Analgesics
Because small mammals are increasingly
considered by their owners to be part of the
family unit rather than just possessions, more
clients are expecting appropriate pain relief
postsurgically, posttrauma, etc., for their pets.
Likewise, veterinarians are much more aware and
proactive in providing pain management for their
patients. Analgesia results in smoother recoveries,
a decrease in systemic stress and resultant stress-
related diseases (i.e., gastric ulcers), and a more
rapid return to normal behavior and function.
Pre-emptive analgesia, or the administration of
analgesic drugs during premedication, is now the
standard when performing painful procedures.
The two main groups of analgesic medications are
opiates and nonsteroidal anti-inflammatory drugs
(NSAIDs). These can be combined or used alone.
Opioids produce both central and peripheral
alleviation of pain and have advantages of
being efficacious, safe, reversible, and versatile.
Of the opioid receptors, the one that has been
demonstrated to be extremely important in pain
control is the mu receptor.
Although opioids provide the most effective
analgesia for most types of pain, they can also
cause sedation and can be difficult to prescribe
for home use. Potent mu agonists (i.e., morphine,
meperidine, and oxymorphone) can cause
respiratory depression in small mammals. Mixed
opioid agonist antagonists (i.e., buprenorphine,
butorphanol) have fewer side effects and are most
commonly used. The effects of opiates on the
cardiovascular system are variable, depending
on the species. In ferrets and rats, opiates tend
to produce hypotension, whereas in rabbits and
mice, they are hypertensive. Use of opiates may
Back to contents
Ex
also result in ileus.
Butorphanol and buprenorphine, both synthetic
opiate partial agonists, are, therefore, the most
common opiates used in small mammals. They
have minimal respiratory effects and do not
cause significant CNS depression. Butorphanol
acts mostly at kappa and sigma opioid receptors,
whereas buprenorphine acts at mu receptors,
which may explain its relatively long duration of
action. Mammals have more mu receptors, hence
an advantage to buprenorphine.
Butorphanol (a synthetic opiate partial agonist
that is 4-7 times as potent an analgesic as
morphine) has a faster onset of action and
shorter duration compared to buprenorphine’s
slower onset of action and longer duration. Some
clinicians use both drugs concurrently in exotic
animals to provide rapid analgesia (butorphanol)
and longer duration (buprenorphine). However, it
is probably preferable to give butorphanol (i.e.,
as a preanesthetic) followed by buprenorphine
at least 2-3 hours later. Butorphanol can produce
profound sedation in ferrets, so often lower doses
are used in this species compared to other small
mammals.
Buprenorphine is 30 times more potent than
morphine and exhibits many of the same actions
as the opiate agonists. Although few adverse
effects of this drug have been reported, on rare
occasions patients have developed respiratory
depression.
Nonsteroidal, Anti inflammatory Drugs
Nonsteroidal, anti inflammatory drugs (NSAIDs)
are increasingly being used in small mammals
because of the analgesia they provide in
response to pain associated with inflammation
(i.e., arthritis and dental problems). However,
NSAIDs are not considered adequate for treating
severe pain and are usually contraindicated in the
patient that has received corticosteroids because
of the potential for gastrointestinal ulceration
2006 World Congress WSAVA/FECAVA/CSAVA
or bleeding. Other characteristics of NSAIDs
include their antipyrectic actions and many have a
long duration of action (i.e., at least 12-24 hours).
Although there is little information concerning
the safety and appropriate dosages of NSAIDs in
these animals (an off label species), these drugs
have been reported to cause gastric ulceration
in some species. Sucralfate has been shown to
protect gastric cells in vitro.
There are two different COX enzymes that have
been described in mammals: COX-1 and COX-
2. Historically, compounds with activity against
COX-1 enzymes were believed to affect the
synthesis of prostaglandins important to normal
gastrointestinal and renal function, while inhibition
of COX-2 enzymes were solely associated with
331
Ex
altering anti-inflammatory activity. However,
more recent work suggests that the activity of
the enzymes is not that well delineated. COX-2
inhibitors, though, are less likely to induce the
negative side effects associated with COX-1
inhibition.
Meloxicam is probably the most commonly used
NSAID used in exotic small mammals, and is
available in both oral and injectable forms. Its
primary action is the inhibition of cyclooxygenase-2,
which mediates inflammation. Carprofen is also
more selective for COX-2 activity, and is also
routinely used to provide analgesia in exotic pet
mammals.
There are, however, potential risks associated
with the use of NSAIDs. The four most commonly
reported clinical signs in domestic animals are
vomiting, anorexia, depression, and diarrhea.
Less commonly, gastric ulceration, intestinal
ulceration, renal failure, hepatic failure, and death
may result.
Corticosteroids
Glucocorticosteroids, which have both anti-
inflammatory and potential analgesic effects, are
still used too commonly in practice. For example,
the rabbit is considered to be a very corticosteroid
sensitive species. Steroids in rabbits cause two
types of adverse reactions: severe immune
suppression and liver toxicity.4 Small, one time
doses of a corticosteroid have been reported to
have an adverse effect in a rabbit and even topical
or ophthalmic doses can cause gastrointestinal
ulceration and immunosuppression in this species.
There are very few indications for steroids in
rabbits, and extreme caution should be observed
when steroids are administered.2
2006 World Congress WSAVA/FECAVA/CSAVA
332
Back to contents
Current Pharmacodynamic Studies
There are relatively few pharmacodynamic studies
in exotic companion pets that are relevant to the
medications we use or potentially use in practice.4
Recently Kansas State University conducted
studies to evaluate the pharmacokinetics of
three drugs that are (or potentially are) used in
rabbit medicine: marbofloxacin, meloxicam, and
tepoxalin. Results of these studies are currently
being evaluated.
Formulary for Small Mammals
The Exotic Animal Formulary (2005) and
Ferrets, Rabbits, and Rodents: Clinical Medicine
and Surgery (2004) list the antimicrobial and
antifungal agents, antiparasitic agents, chemical
restraint/anesthetic/analgesic agents, ophthalmic
drugs, and miscellaneous agents used in exotic
small mammals.1,3
References
1. Carpenter JW (ed.). Exotic Animal Formulary.
3rd ed. St. Louis, Elsevier Publishing, 2005. 564 pp.
2. Ivey ES, JK Morrisey. Therapeutics for rabbits.
Vet Clin N Am, 2000; 3(1): 183 220.
3. Quesenberry KE, JW Carpenter (eds). Ferrets
Rabbits, and Rodents: Clinical Medicine and
Surgery. Philadelphia, WB Saunders Co, 2004.
461 pp.
4. Rosenthal KL. Therapeutic contraindications
in exotic pets. Semin Avian Exotic Pet Med, 2004;
13(1): 44 48.
 Ex
Ex - Exotics
ADVANCES IN AVIAN CLINICAL BIOCHEMISTRY (PART 1 AND
PART 2)
Johannes T. Lumeij, DVM, PhD,
Diplomate ECAMS
Associate Professor of Avian
and Exotic Animal Medicine
Division of Avian and Exotic
Animal Medicine
Department of Clinical
Sciences of Companion
Animals
Faculty of Veterinary
Medicine
Universiteit Utrecht
Yalelaan 108
3584 CM Utrecht
The Netherlands
j.t.lumeij@vet.uu.nl

In these two lectures an overview will be presented Reference

of well known facts and new developments with Lumeij JT. Avian Clinical Biochemistry. In:
regard to clinical biochemistry in avian practice. Kaneko et al (eds). Clinical Biochemistry in
The lectures will be illustrated with examples Domestic Animals, 5th ed. Academic Press, 1997;
from clinical practice and experimental findings 857-883.
from the author’s facilities at Utrecht University.
Recommended study material includes the
reference below. A forthcoming new edition of
this book (2007) will contain the most recent
updates.

2006 World Congress WSAVA/FECAVA/CSAVA

333
Back to contents
Ex
Ex - Exotics
ADVANCES IN REPTILIAN HEMATOLOGY AND BLOOD
CHEMISTRY
Prof. Zdenek KNOTEK, DVM, PhD
Avian and Exotic Animal Clinic,
Faculty of Veterinary Medicine,
Univ. Vet. Pharm. Sci. Brno,
Palackeho 1-3,
Brno, CZ – 612 42,
Czech Republic
knotekz@vfu.cz
Zora KNOTKOVA, DVM, PhD
Avian and Exotic Animal Clinic,
Faculty of Veterinary Medicine,
Univ. Vet. Pharm. Sci. Brno,
Palackeho 1-3,
Brno, CZ – 612 42,
Czech Republic
knotkovaz@vfu.cz
Determination of morphologic characteristic
of different peripheral blood cells and plasma
chemistry profile of reptiles was the purpose
of many studies. Research is still continuing
on normal healthy tortoises, lizards, snakes
and crocodiles as well as on patients suffering
from different metabolic diseases. The results
of independent trials show a significant degree
of variation due to different animal selection
methods and technical differences in blood
sample treatment. Blood that is exposed to
heparin for several hours will usually not stain as
well as slides made immediately after collection.
Haemolytic destruction of chelonian cells by
EDTA was observed. Classification of white
blood cells in reptiles is inconsistent, because
2006 World Congress WSAVA/FECAVA/CSAVA
variable criteria have been used to categorise
these cells. For the more exact characterisation of
different types of blood cells in a group of healthy
tortoises (Agrionemys horsfieldi) the commercial
kits were used (Knotková et al.2000). Ten
different types of blood cells were determined:
erythrocytes, thrombocytes, lymphocytes,
monocytes, type-I cells (heterophils), type-II
cells (eosinophils), type-III cells (azurophils),
type-IV cells (basophils), type-Ia cells (toxic
heterophils) and type-V cells (polychromatophil
erythrocytes). Some authors pointed out technical
complications involved in distinguishing reptilian
small lymphocytes from thrombocytes or big
lymphocytes and monocytes (Bruder 1998, Harr
et al. 2001). We did not find these problems in
reptiles (Pejřilová et al. 2004). Lymphocyte of
lizards varies in size between small, uniformly
334
Back to contents
Sarka TRNKOVA, DVM
Avian and Exotic Animal Clinic, Faculty of
Veterinary Medicine,
Univ. Vet. Pharm. Sci. Brno, Palackeho 1-3,
Brno, CZ – 612 42,
Czech Republic
trnkovas@vfu.cz
round and large, more pleomorphic mononuclear
cells. They are characterized by light-blue to
grey-blue cytoplasm and nuclei in the central
position, differing – especially in the case of big
lymphocytes – considerably in shape. In small
lymphocytes, the cytoplasm forms only a tiny
rim surrounding the round nucleus. A detailed
examination may reveal azurophilic and/or
hyaline inclusions. Lymphocytes are the most
prolific leukocyte population in peripheral blood
of healthy iguanas. The presence of eosinophils
varies among species of reptiles. Eosinophils are
present in chelonians as well as in crocodilians.
Cells which are known as heterophils and
eosinophils are present in chelonians. The main
difference between them is the shape of granules.
Sometime it could be difficult to distinguish the
type of granules with the basic Pappenheim´s
smears, because the cytoplasm is filled with
them. We suggest that Granulocolor® would
be appreciated in cases of special importance.
Pappenheim method is absolutely sufficient
for routine laboratory examination of tortoise’s
hemogram. One peculiarity typical of green iguanas
is the light-blue colour of the round cytoplasmic
granules of the eosinophils. The nucleus is round
to oval and situated in an off-centre position.
The heterophils are characterized by oval or
sharpened bright red cytoplasmic granules.
The nucleus is bluish, in an off-centre position,
mostly segmented. The basophils in reptile blood
smears stand out by their exquisite blue granules
filling in the cytoplasm and concealing even the
nucleus situated in the central position. There is

a risk of diluting and washing away basophilic
granules in case when inconsiderate sample
processing is applied. Inconsistent classification
of monocytes and leukocytes with azurophilic
granules in the cytoplasm has been a traditional
issue in reptile haematology (Saint Girons 1970,
Sypek and Borysenko 1988). Even recently, Harr
et al. (2001) did not regard the azurophils in green
iguana as an independent leukocyte population.
Differentiating between the two types of
leukocytes in reptiles takes thorough preparation
of samples and much experience on the part of
the person doing the count. The azurophils are
mononuclear cells with a dominantly stained
nucleus mostly in an off-centre position and blue-
grey cytoplasm containing prominent azurophilic
granules. Their shares in peripheral blood differ
depending on the reptile genus and species
(Campbell 1996).
Most haematological trials focusing on reptiles
have had the form of one-off blood sample-taking
analysis. Therefore we realised a long-term
ontogenetic trial on blood-related lizards kept in
identical conditions. The trial involved 11 green
iguanas (Iguana iguana rhinolopha) that were
kept under special regime of light (12h/12 h),
temperature (24 - 35 °C and air humidity (60 – 80%).
No seasonal changes of the haematological indices
were observed, no significant differences in the
haematological indices between male and female
subpopulations were found (Pejřilová et al. 2004).
As to the number of erythrocytes, a statistically
significant drop was observed comparing the data
at 14 to 15 months of age with those at 34 to 36
months. We recorded a statistically significant
drop in packed cell volume comparing the
figures at 14 to 18 months with those obtained
at 34 to 35 months of age of the animals. Our
results confirmed a statistically significant rise
in haemoglobin concentration comparing the
data at 23 to 24 months with those at 35 to 36
months. A similar statistically significant rise was
confirmed for computed red cell indices (MCV,
MCH, MCHC), too.
Plasma chemistry profile in reptiles involves
analysis of well separated plasma for the
concentration of total protein, glucose, uric acid,
alkaline phosphatase, alanine aminotransferase,
aspartate aminotransferase, cholesterol,
triglycerids, calcium and phosphorus. The
hyperuricaemia may indicate renal damage in
reptiles, but uric acid levels do not increase
significantly until the extensive damage of kidney.
Hyperphosphataemia seems to be more reliable
indicator of renal insufficiency in iguanas (Knotek
et al. 2002). Indeed, the phosphorus-calcium ratio
could be a sensitive parameter for the diagnosis
of renal disease. Results of our previous studies
Back to contents
Ex
show a significant degree of variation in plasma
chemistry of green iguanas. Females with post-
ovulatory egg stasis or pre-ovulatory follicle
stasis had the highest mean plasma values for uric
acid and phosphorus compared to females with
acute hypocalcaemia and females with metabolic
bone disease. Females with acute hypocalcaemia
had the highest concentration of AST, the highest
phosphorus to calcium ratio and the lowest
plasma concentrations of total protein, glucose,
cholesterol and calcium (Knotek et al. 2003).
The peripheral blood concentrations of calcium,
cholesterol and triglycerides may correspond to
the metabolic activity requirement, which is lower
in adult males than in females during the breeding
season. Calcium levels in peripheral blood of
green iguana females peak within the period of
vitellogenesis. In ovariectomized females we
revealed downward trend for examined values
reaching the levels typical for males. During the
following reproductive season intact females
returned to the vitellogenic high concentrations
of calcium, cholesterol and triglycerides whereas
ovariectomized females did not (Knotková et
al. 2005). The mechanism of hormonal control
(oestrogen levels) for seasonal changes of
calcium, cholesterol and triglycerid levels in
blood of female green iguana is expected.
REFERENCES
Bruder M Blutreferenzwerte bei Grünen Leguanen
(Iguana iguana). Thesis, Univ München, 1998,
113.
Campbell TW Clinical pathology. In: MADER
DR (Ed).: Reptilie Medicine and Surgery. WB
Saunders, Philadelphia, 1996, 248–257
Divers SJ, Redmayne G, Aves EK Haematological
and biochemical values of 10 green iguanas
(Iguana iguana). Vet Record, 1996, 138: 203-
205.
Harr KE, Alleman AR, Dennis PM, Maxwell LK, 2006 World Congress WSAVA/FECAVA/CSAVA
Lock BA, Bennet RA, JAcobson ER Morphologic
and cytochemical characteristics of blood cells and
hematologic and plasma biochemical reference in
green iguanas. J Amer Vet Med Assoc, 2001, 218:
915–921.
Hawkey CM, Dennett TB Color atlas of
comparative veterinary hematology. Wolfe
Medical Publ, 1989, 192.
Knotek Z, Hauptman K, Knotková Z, Hájková P,
Tichý F Haemogram and Plasma Biochemistry
in Green Iguanas with Renal Disease. Acta
Veterinaria Brno, 2002, 71: 333-340
Knotek Z, Knotková Z, Doubek J, Pejřilová S,
Hauptman K Plasma Biochemistry in Female
Green Iguanas (Iguana iguana) with Calcium
335
Ex
Metabolism Disorders. Acta Veterinaria Brno,
2003, 72: 183–189.
Knotková Z, Knotek Z, Hájková P. Plasma
biochemistry of chelonians of the Geochelone
group. Proc.3rd EAZWV Sci. Meeting, 31.5.–4.6.
2000, Paris, 281-285.
Knotková Z, Pejřilová S, Trnková Š, Matoušková
O, Knotek Z. Influence of Reproductive Season
upon Plasma Biochemistry Values in Green
Iguanas. Acta Veterinaria Brno, 2005, 74: 515–
520.
Köhler G. Krankheiten der Amphibien und
Reptilien. Eugen Ulmer Vrlg, 1996, 166.
Saint Girons MC Morphology of the circulating
blood cells. In: Gans C, Parsons TS (Ed).: Biology
of the Reptilia, vol. 3 – Morphology C, Academic
Press London, 1970, 73-91.
Pejřilová S, Knotková Z, Knotek Z, Vrbas J Age-
Related Changes of the Haematological Profile in
Green Iguana (Iguana iguana rhinolopha). Acta
Vet Brno 2004, 73: 305–312.
Sypek J, Borysenko M Reptiles. In: Rowley
AF, Ratcliffe NA (Ed).: Vertebrate blood cells.
Cambridge Univ Press, Cambridge, 1988, 211-
256.
Walton RM. Establishing Reference Intervals.
Health as a relative Concept. Seminars in Avian
and Exotic Pet Medicine, 2001, 10: 66-71.

Table 1 Plasma chemistry values in iguanas with renal disease

Parameter Boyer et al. Knotek et al. 2002

Mean Mean ± SD
Total protein g/l 63.00 53.51 ± 15.96
Glucose mmol/l 9.55 10.07 ± 6.81
Uric acid μmol/l 428.26 306.70 ± 212.88
Creatinine μmol/l 52.20 61.07 ± 24.78
ALP μkat/l - 0.38 ± 0.33
ALT μkat/l 3.52 0.74 ± 0.64
AST μkat/l 3.11 5.02 ± 5.82
Cholesterol mmol/l - 5.29 ± 3.62
K mmol/l 6.10 4.18 ± 0.33
Ca mmol/l 1.95 2.06 ± 0.78
P mmol/l 7.69 5.95 ± 3.21

Table 2 Plasma chemistry values in females green iguana

2006 World Congress WSAVA/FECAVA/CSAVA

Season Cholesterol Triglycerides Calcium Phosphorus

mmol/l mmol/l mmol/l mmol/l
June 7.59 ± 3.34 3.55 ± 3.10 2.75 ± 0.20 2.11 ± 0.13
February 10.13 ± 3.46 6.44 ± 2.68 6.03 ± 2.24 2.60 ± 0.40
March 12.42 ± 4.74 2.40 ± 2.62 2.98 ± 0.60 1.75 ± 5.21
April 7.50 ± 3.15 5.32 ± 2.84 3.00 ± 0.20 2.76 ± 0.45
November 15.75 ± 1.47 15.62 ± 0.50 7.01 ± 1.67 6.91 ± 1.37
January 12.24 ± 4.63 10.03 ± 2.57 7.67 ± 1.30 3.37 ± 1.47

336
Back to contents

Ex - Exotics
ADVANCES IN EXOTIC ANIMAL ENDOSCOPY
Prof. Zdenek KNOTEK, DVM, PhD
Avian and Exotic Animal Clinic,
Faculty of Veterinary Medicine,
Univ. Vet. Pharm. Sci. Brno,
Palackeho 1-3,
Brno, CZ – 612 42,
Czech Republic
knotekz@vfu.cz
BIRDS
In birds, fine diameter endoscopes have been
used for diagnostic purposes since late 1970´s
(Taylor 1998). In 1992 the new endoscope and
sheath system for avian use was developed by
Taylor (Taylor 1993). This author described an
anatomic approach to better understand the most
applicable access point for avian endoscopy. The
universal equipment for endoscopy includes rigid
telescope, flexible fiber optic light cable and
cold light fountain source. The most commonly
recommended rigid endoscope is Standard
Hopkins telecope, with 4.0 mm outer diameter, 18
cm in length, 30 ° angle of view. Slender Hopkins
telescope – 18 cm in length, 30 ° angle of view,
with 1.9 - 2.1 mm outer diameter, is very useful
for extremelly small space documentation. The
rigid telescope is regulary used with a protection
sheat (3.5 mm outside diameter) or a 14.5Fr
working sheat that provides three ports (for water
inflation, aspiration, irrigation, insufflation, with
excellent operating channel). Cold light fountain
(100 – 125/220-240 VAC, 50/60 Hz, Xenon spare
lamp 175 Watt, 15 volt) enables perfect control of
all internal organs in large birds (owls, raptors).
The internal anatomical organisation of the avian
body is ideal for endoscopy examination. The
caudal thoracic air sacs are the key entry points
to the avian air sac system (Molnar 2003). The
cranial thoracic and abdominal air sacs can be
easily accessed from a single entry point into the
caudal thoracic sacs via the lateral thoracic wall.
The entry site is located by finding the point where
the semimembranous muscle crosses the last
rib. Isoflurane anesthesia is generally required.
Respiratory arrest occurs if trachea is irritated
by tracheal tube and/or endoscope (Molnar
2003). During mask inhalation the trachea can
be blocked by saliva, or during deep anesthesia,
by regurgitation of the crop content. The left
side approach is entering the caudal thoracic
air sac by inserting the endoscope in triangular
area created by last rib-pelvic bone and femoral
muscle. In larger birds the preferred insertion
Back to contents
Ex
Vladimír JEKL, DVM, PhD
Avian and Exotic Animal Clinic, Faculty of
Veterinary Medicine,
Univ. Vet. Pharm. Sci. Brno, Palackeho 1-3,
Brno, CZ – 612 42,
Czech Republic
jeklv@vfu.cz
site is the last intercostal area. Advantages of
the practical use of the rigid endoscope in the
avian medicine have already been demonstrated
in many cases (Chamness 1999, Harris 1999).
Using endoscopy in the case of the gunshot
falcon proved to be an optimum choice (Jekl et
al. 2006). A classical surgical approach would
have been more demanding and hazardous
concerning the risk of injuring major blood
vessels. Following a standard preparation of the
surgical field endoscopy was performed with the
access through the left caudal thoracic air sac in
a male of peregrine falcon. A blunt perforation
was made behind the last rib about 1.5 cm from
the lateral diapophysis. Despite the small size
of the wound the minimally invasive approach
enabled removal of a bullet without any damage
to adacent organs or blood vessels.
Recently, minimally invasive endoscopic surgery
of birds has been described in details (Hernandez-
Divers 2005). This author compared single-entry
with the double-entry as well as triple-entry
techniques. The single-entry endosurgery in birds
is limited to a single instrument that cannot be
manipulated independently of the telescope. It
is feasible for salpingohysterectomy. This form
of basic endosurgery prevented the need for 2006 World Congress WSAVA/FECAVA/CSAVA
more invasive coeliotomy and reduced surgical
trauma. It is very useful method, even for a very
small avian species. The main disadvantage
of single-entry techniques are restriction to
single instrument use (Hernandez-Divers 2005).
Double-entry techniques can facilitate endoscope-
assisted biopsy, enterotomy, enterectomy,
duodenostomy, cloacopexy, syringeal surgery,
proventriculotomy/ventricolutomy. Double-entry
techniques reduce trauma associated with standard
form of coeliotomy, the main disadvantage of this
technique is dependence of one instrument on the
sheath and telescope. The next step is the triple-
entry method, developed for avian medicine
by the same author (Hernandez-Divers 2005).
This technique enables the simultaneous use of
two instruments – independent of the telescope.
337
Ex
The use of this technique is restricted to large
patients.
REPTILES
Endoscopy in reptiles has developed from methods
for sexing monomorphic reptiles (Schildger
1998). It started to be very important method
for clinical diagnosis and different endoscopic
techniques were developed for reptilian patients
(Divers 1999, Schildger et al. 1999). Nowadays
it includes diagnostic endoscopy (with a form
of guided biopsy) and minimally invasive
endosurgery. Basic examinations of the mouth
cavity and cloaca can be realised in reptiles under
mild anesthesia. General anesthesia (isoflurane)
is required for advanced endoscopy – laparoscopy
and respiratory endoscopy. The tightly packed
coelomic cavity in the reptilian patient leaves
limited space for instrument manipulation (with
the risk of iatrogenic trauma). Gas insufflation
(carbon dioxide is the insufflation gas of choice)
is the preferred technique that is well tolerated by
the patient. For a good endoscopy examination
insufflation technique is necessary in lizards and
chelonians. For GIT endoscopy – air insufflation
is feasiblle method, for coelioscopy insufflation
with CO2 is standard. Reccommended coelomic
pressure is 2 – 4 mm Hg, with a CO2 flow
rate of 0.5 – 1.0 l/min. The most feasible
coelioscopic approach in chelonians is via the
small perforation of the prefemoral fossa skin.
Cloacal endoscopy is feasible method of direct
evaluation the contents of the urinary bladder and
indirect control of the gonads (follicles). Not only
visualization, but tissue biopsies are required
to investigate unclear pathological situations.
Endoscope-guided biopsies allow the surgeon
to collect biopsies from particular locations,
especially when only portions of the organ are
altered. The most common biopsies in exotic pets
are those of the liver, kidneys and air sacs. Small
2006 World Congress WSAVA/FECAVA/CSAVA
size biopsies are difficult to evaluate. If indicated
multiply biopsies can be taken from the same
site. Sampling a non-significant tissue mass can
mislead the final diagnosis.
Recently, new endoscopy method has been
described in snakes (Jekl and Knotek 2006). This
method serves as a modified endoscopic method
to access the coelom of snakes through the air
sac. Air passages (lungs, air sac, trachea) could be
examined directly by this method, other organs
like liver, stomach, pancreas and spleen are
assessed indirectly. This mini-invasive method
is very easy, with minimum risk for the reptile
patient. Short incision is made in aseptic prepared
skin on the right side of the snake´s body, 35 – 45%
along its length and parallel with horizontal
axis of the body. Small incision of 1 – 2.5 cm
338
Back to contents
in length is made between the second and the
third row of lateral skin scales. This is followed
with blunt perforation of the muscle layer and the
peritoneum. Two absorbable fixation sutures is
made in the wall of the air sac before its gentle
perforation. The endoscope with an examination
sheath is introduced through this small perforation
between the two sutures. This method is feasible
for direct control of the mucosa of the lungs as
well as for indirect image the surfaces of liver,
spleen, gall bladder and pancreas. The approach
through the air sac provides an alternative method
for examining the caudal segment of respiratory
system of large snakes like pythons and boas,
without the need for more expensive flexible
endoscopes (Jekl and Knotek 2006).
SMALL MAMMALS
The endoscopy is very feasible method for
clinical examination in small herbivorous
mammals, especially for clinical dentistry (Taylor
1999). The mouth cavity of small herbivorous
mammal is long and narrow, making its carefull
clinical examination technically more difficult
than in carnivores and insectivores. Molar and
premolar malocclusions are very frequent serious
health problem in small mammals. Diagnosis
and treatment of oropharyngeal disease in these
patients are facilitated perfectly with the rigid
endoscope. The technique was evaluated on a
group of 55 rabbits, 30 chinchillas, 36 guinea
pigs, 17 degus, and 12 prairie dogs suffering from
a lack of appetite, hypersalivation accompanied
by humid dermatitis, swelling of the lower jaw or
mild exophthalmus. A total of 265 examinations
were realized. Telescope with 30° optics enabled
a detailed examination of all the parts of the
mouth cavity and oropharynx. It provided precise
observation of external lesions on premolars and
molars as well as on mucosal layers of the gingiva,
the tongue, and the upper palate. Telescope with
70° optics provided an excellent control of
occlusal tooth surfaces, tooth crowns, and buccal
mucosa. Under endoscopic control collection
of bioptic samples, removal of foreign objects
and correction of malocclusion were carried out
without any risk of injury (Jekl et al. 2006).
FISH
Rigid endoscopy and minimally invasive
endosurgery offer in fish new possibilities in
research as well as in wildlife and exotic pet
medicine. Endoscopy in fish was first described
in details by Murray (1998). More advanced
form of reproductive endoscopy and endosurgery
in fish has been decribed recently (Hernandez_
Divers et al. 2005). The rigid endoscopy permits
the minimally-invasive examination of the

respiratory and gastro-intestinal systems. Saline
flushing-insufflation of the coelom helps in
examination of other visceral organs.
REFERENCES
Divers SJ. Lizard endoscopic techniques with
particular reference to the green iguana. Semin
Avian Exotic Pet Med. 1999, 8: 122-129.
Chamness CJ. Equipment for the avian and exotic
endoscopist. Semin Avian Exotic Pet Med. 1999,
8: 102-106.
Jekl V, Knotek Z. Endoscopic examination of
snakes by access through the air sac. Vet Record,
2006, 158: 407 – 410.
Jekl V, Hauptman K, Knotek Z. Clinical
examination of the oral cavity in small herbivorous
mammals. Veterinarni Klinika, 2006,3: 55–60.
Jekl V, Tukac V, Hauptman K, Knotkova Z,
Knotek Z. Endoscopic-assisted Removal of a
Bullet from the Hearth Region in a Peregrine
Falcon (Falco peregrinus). J. Avian Med. Surgery
2006, in press
Harris DJ. Rigid endoscopy: one practicioner´s
perspective. Semin Avian Exotic Pet Med. 1999,
8: 107-109.
Hernandez-Divers SJ. Minimally invasive
endoscopic surgery of birds. J Avian Med Surg.
2005, 19: 107-120.
Hernandez-Divers SJ, Bakal SR, Hickson B,
Back to contents
Ex
Rawlings CA, Wilson HG, Radlinsky MA,
Hernandez-Divers S, Blasier M, Dover SR.
Reproductive endoscopy and endosurgery of gulf
of mexico sturgeon and short-nosed sturgeon.
Proc. AAZV,AAWV,AZA/NAG Joint Conference
Omaha 14.-21.10.2005, 127–128.
Molnar L. Endoscopy of raptors and exotic birds.
Proc. Annual Meeting CAZW, Zidlochovice 4.-
5.10.2003, 31–34.
Murray MJ. Endoscopy in Fish. Endoscopy in
Birds, Reptiles, Amphibians and Fish. Endo-
Press, Tuttlingen, 1998, 59-75.
Schildger B. Endoscopy in Reptiles. Endoscopy
in Birds, Reptiles, Amphibians and Fish. Endo-
Press, Tuttlingen, 1998, 31–56.
Schildger B, Haefeli W, Kuchling G, Taylor M,
Tenhu H, Wicker R. Endoscopic examination of
the pleuro-peritoneal cavity in reptiles. Semin
Avian Exotic Pet Med. 1999, 8: 130-138.
Taylor M. Diagnostic application of a new
endoscopic system for birds. Proc. Eur. Conf.
Avian Med Surg, Utrecht 1993, 127–131.
Taylor M. Endoscopy in Birds. Endoscopy in
Birds, Reptiles, Amphibians and Fish. Endo-
Press, Tuttlingen, 1998, 7–28.
Taylor M. Endoscopy as an aid to the
oropharyngeal disease of samll herbivorous
mammals. Semin Avian Exotic Pet Med. 1999, 8:
139-141.
2006 World Congress WSAVA/FECAVA/CSAVA
339
Ex
Ex - Exotics
IS THERE A NEED FOR SPECIALIZATION IN EXOTIC PET
MEDICINE?
Johannes T. Lumeij, DVM, PhD,
Diplomate ECAMS
Associate Professor of Avian and
Exotic Animal Medicine
Division of Avian and Exotic
Animal Medicine
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Universiteit Utrecht
Yalelaan 108
3584 CM Utrecht
The Netherlands
j.t.lumeij@vet.uu.nl

Although it has taken nearly two decades to achieve
a framework for veterinary specialization in
Europe, the structure for veterinary specialization
in Europe as originally proposed by the Advisory
Committee on Veterinary Training (ACVT) in
1992 now appears to be well founded. Briefly
it consists of the various specialist colleges, the
European Board of Veterinary Specialization
(EBVS) formed by representatives of all the
colleges, and a supervising body, the European
Coordinating Committee for Veterinary Training
(ECCVT) that can approve procedures for the
recognition of European veterinary specialists.
The ECCVT is formed by representative of EBVS,
the Federation of Veterinarians in Europe (FVE)
and the European Association of Establishments
for Veterinary Education (EAEVE). Of the 21
colleges currently recognized, 8 deal with various
aspects of the traditional companion animal, like
dogs and cats, and one deals with medicine and
surgery of birds, i.e. the European College of
Avian Medicine and Surgery (ECAMS).
2006 World Congress WSAVA/FECAVA/CSAVA
programmes have an emphasis on canine and
feline medicine and diplomats of the various
colleges that cover companion animals (except
for ECAMS diplomats), although they might
have some specialist knowledge on some of the
exotic animal diseases, often do not even know
the basics like restraint and handling of exotic
companion animals.
Despite the lack of a well structured training
in exotic pet medicine there have been many
developments in this emerging field of veterinary
medicine and a is a vast amount of literature is
available. Furthermore there are a lot of exotic pet
owners who would be happy to get professional
veterinary care for their animals. Establishment
of a specialty in exotic pet medicine, like was
done in the avian field with ECAMS, might be an
answer to this problem.
It would create transparency for the public
and would alleviate veterinary schools and the
various colleges of the burden to incorporate
exotic species in their curricula.

The basic training in veterinary aspects of small

exotic mammals (rabbits, rodents, ferrets), Reference
reptiles, amphibians, fish and invertebrates varies Lumeij JT, Herrtage ME. Veterinary specialization
between the veterinary schools, but is generally in Europe. Journal of Veterinary Medical
marginal. The various specialist training Education 2006 33(2): 176-179.

340
Back to contents
Back to contents
2006 World Congress WSAVA/FECAVA/CSAVA
Ex

341
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Fe
FeMMedicine
Feline
line e

Back to contents
 Fe
INVITED LECTURES - FULL PAPERS

Fe - Feline Medicine
CATS AND CALICIVIRUS INFECTION – THE EVOLVING PATTERN
OF DISEASE
Dr. Alan Radford Dr Carol J. Porter
Senior Lecturer in Small University of Liverpool Veterinary Teaching
Animal Studies Hospital
University of Liverpool Leahurst
Veterinary Teaching Hospital Chester High Road
Leahurst Neston
Chester High Road S Wirral
Neston CH64 7TE
S Wirral UK
CH64 7TE
UK
alanrad@liv.ac.uk

Dr Karen P. Coyne Prof Rosalind M. Gaskell

University of Liverpool University of Liverpool Veterinary
Veterinary Teaching Hospital Teaching Hospital
Leahurst Leahurst
Chester High Road Chester High Road
Neston Neston
S Wirral S Wirral
CH64 7TE CH64 7TE
UK
UK
Dr Susan Dawson
University of Liverpool
Veterinary Teaching Hospital
Leahurst
Chester High Road
Neston
S Wirral
CH64 7TE
UK

Aetiology
Feline calicivirus (FCV) is a highly infectious 2006 World Congress WSAVA/FECAVA/CSAVA
pathogen of cats with a widespread distribution.
The virus typically causes moderate, self-limiting
acute upper respiratory tract disease. However,
some strains induce lameness and recently,
more virulent strains have evolved, particularly
in the USA. The prevalence of FCV is likely to
be broadly proportional to the number of cats
in the household [2, 3, 11, 26]. Privately owned
pet cats kept in small numbers have relatively
low prevalence (~10%). In contrast, cats living
in colonies or at shelters have a higher chance
of being infected [1, 12, 22]. Indeed, in some
colonies we have found prevalence values of 50-
90% over prolonged periods of time [4, 21].
The virus belongs to the Caliciviridae, a family of
RNA viruses which includes important pathogens
of man (noroviruses and sapoviruses; together the
343
Back to contents
Fe
commonest causes of infectious gastroenteritis in
people) and animals including the vesiviruses
(e.g. FCV, canine calicivirus) and the lagoviruses
(rabbit haemorrhagic disease virus and European
brown hare syndrome virus) [10].
Having an RNA genome, we should expect FCV
to have a high degree of genomic plasticity. This
is a reflection of the lack of proofreading and
associated low fidelity generally attributable to
viral RNA-dependent RNA polymerases [7].
This mechanism for error-prone replication
should afford FCV great adaptability and allow
it to exploit new environmental niches. Specific
current problems associated with FCV that are a
reflection of this include the difficulty of choosing
representative strains for inclusion in vaccines,
the presence of persistently infected cats, and the
emergence of hypervirulent strains of FCV.
Clinical signs
Oral and respiratory disease. Due to the large
number of different strains of FCV, a range of
clinical signs may be seen. The most consistent
signs are relatively mild and include oral
ulceration and ocular and nasal discharge.
Occasionally, inapparent infections or pneumonia
may also be seen. Rarely, and usually in young
kittens, the more severe respiratory infections can
be fatal [15, 16].
Lameness. Calicivirus strains can also cause an
acute febrile lameness syndrome, associated with
acute synovitis and an increase in quantity of
synovial fluid [6, 19]. It has been suggested that
lameness and oral / respiratory disease represent
two extremes of a clinical continuum, with some
individual strains tending to either extreme, and
the majority of strains being able to induce both
of these clinical signs [25].
Virulent systemic disease. More recently and
more worryingly, highly virulent strains of
FCV have emerged, that are associated with
2006 World Congress WSAVA/FECAVA/CSAVA
outbreaks of disease with high mortality termed
FCV–associated virulent systemic disease (VSD
– previously haemorrhagic-like fever) [13, 14,
18, 20, 23]. As well as upper respiratory tract
disease, affected cats show to varying degrees
pyrexia, cutaneous oedema, ulcerative dermatitis,
anorexia and jaundice, with up to 50% of cats
dying or being euthanased in extremis. Adult
cats are frequently affected more severely than
kittens, and worryingly, field vaccination does
not appear to be protective. Outbreaks start
quickly, generally effect less than 100 animals
and disappear rapidly.
So far, FCV-associated VSD has mainly been
reported in the USA. In the UK, one outbreak
in 2003 has been described affecting a group of
five cats in two households [5]. In addition, the
344
Back to contents
authors are aware of two outbreaks in France
(personal communication H Poulet) and it is
possible that considerably more outbreaks occur
than have been reported.
Lesions are widespread and include subcutaneous
oedema, ulceration of the mouth, and variable
levels of ulceration of the skin particularly on the
pinnae and pawpads and nares [18]. Other lesions
are more variable and include bronchointerstitial
pneumonia and necrosis in the liver, spleen and
pancreas.
VSD has been reproduced experimentally,
strongly supporting a role for FCV in this disease
[18], and suggesting that mutations within the
viral genome may be responsible for the highly
virulent phenotype. So far, the FCV strains
from each reported outbreak of VSD have been
genetically distinct from each other. Therefore,
if viral mutations are required to cause the
hyper-virulent phenotype, then they must evolve
independently in each outbreak. To date, no
consistent genetic motif has been reported within
the available capsid sequences to differentiate
FCV isolates associated with VSD from those
associated with more typical FCV-associated
disease. This makes diagnosis of VSD difficult.
Most outbreaks of VSD have been associated with
the introduction of cats from large rescue colonies
into another population [14]. It is possible that the
high levels of replication of normal FCV strains
in large groups of cats such as rescue shelters may
provide the required conditions necessary for the
independent emergence of these hypervirulent
strains. We have recently shown that virus
replication in endemically infected colonies of
cats is associated with markedly higher levels of
biodiversity than those normally seen within a
single strain of FCV [4, 21].
Diagnosing FCV-associated VSD in the cat
remains somewhat of a conundrum since there
are no unique clinical or laboratory markers for
the disease. The authors are frequently asked
about individual cats with suspicious signs, some
of which are also FCV positive. Such individual
cats must be treated carefully, but whether
these represent actual sporadic cases of VSD
is unknown. The index of suspicion for VSD
increases dramatically when two or more cats
present with the same clinical signs. However,
until a marker of virulence is identified, definitive
diagnosis will remain difficult.
Crucial to the control of suspect outbreaks is
early recognition / suspicion and prompt rigorous
biosecurity. It is very important that owners and
staff are all aware of the disease and what it
looks like. This includes veterinary surgeons at
neighbouring practices who may see other cases
from the same outbreak. Specific measures must

include contact tracing and quarantining of all
suspect cats. Actual and suspect cases are perhaps
best managed away from the veterinary hospital.
However, where cases must be hospitalised, they
must be kept in strict isolation and barrier nursed.
All staff should be made aware of the case, and
those who don’t own cats should preferably be
involved in the treatment of the affected animal.
The virus is generally considered to survive for
up to two weeks in the environment and therefore
can be transmitted by direct contact and fomites,
and possibly by aerosol. Affected cats are likely
to shed virus from their respiratory and oral
secretions, but any discharge from skin may also
be highly infectious. FCV has also been isolated
from faeces and urine. Areas where the cat has
been and any equipment require disinfection
using a product that has been shown to be
effective against FCV. Quaternary ammonium
compounds are generally not thought to be
completely effective [8, 9, 13, 17]. However, a
1:32 dilution of household bleach with some
household detergent does seem to be effective
providing contact time is sufficient [24]. With
these measures, all outbreaks seem to have been
successfully managed. Whether the end of each
outbreak is entirely attributable to disease control
measures or includes a cat behavioural and / or
virus evolutionary component, remains to be
determined.
Conclusion
FCV has been recognised as an important
pathogen of cats for over 40 years now. As an
RNA pathogen, it seems to rely on evolution to
maintain itself in the population. Where the virus
came from we do not know. Today we struggle
with newly emerged virulent strains and have
a clear need to improve the cross-protection
offered by our vaccines. What is certainly true
is that FCV is still changing. We must expect
the clinical features of this virus to change and
accordingly, our attempts to control it will need to
be continually updated. Sounds interesting.
References
[1]. Bannasch MJ, Foley JE (2005). Epidemiologic
evaluation of multiple respiratory pathogens in
cats in animal shelters. J Feline Med Surg, 7:
109-19.
[2]. Binns SH, Dawson S, Speakman AJ, Cuevas
LE, Hart CA, Gaskell CJ, Morgan KL, Gaskell
RM (2000). A study of feline URTD with reference
to prevalence and risk factors for infection with
FCV and feline herpesvirus. J Feline Med Surg,
2: 123-33.
[3]. Coutts AJ, Dawson S, Willoughby K, Gaskell
Back to contents
Fe
RM (1994). Isolation of feline respiratory viruses
from clinically healthy cats at UK cat shows. Vet
Rec, 135: 555-556.
[4]. Coyne KP, Dawson S, Radford AD, Cripps PJ,
Porter CJ, McCracken CM, Gaskell RM (2006).
Long term analysis of FCV prevalence and viral
shedding patterns in naturally infected colonies
of domestic cats. Vet Microbiol, in press.
[5]. Coyne KP, Jones BR, Kipar A, Chantrey J, et
al (2006). Lethal outbreak of disease associated
with FCV infection in cats. Vet Rec, 158: 544-50.
[6]. Dawson S, Bennett D, Carter S, Bennett M, et
al. (1994). Acute arthritis of cats associated with
FCV infection. Res Vet Sci, 56: 133-143.
[7]. Domingo E, Menendez L, Holland J (1997).
RNA virus fitness. Rev Med Virol, 7: 87-96.
[8]. Doultree JC, Druce JD, Birch CJ, Bowden
DS, Marshall JA (1999). Inactivation of FCV, a
Norwalk virus surrogate. J Hosp Infect, 41: 51-7.
[9]. Eleraky NZ, Potgieter LN, Kennedy MA (2002).
Virucidal efficacy of four new disinfectants. J Am
Anim Hosp Assoc, 38: 231-4.
[10]. Green K, Ando T, Balayan M, Berke T, Clarke
I, et al (2000). Taxonomy of the caliciviruses. J
Infect Dis, 181 Suppl 2: S322-30.
[11]. Harbour DA, Howard PE, Gaskell RM
(1991). Isolation of FCV and feline herpesvirus
from domestic cats 1980 to 1989. Vet Rec, 128:
77-80.
[12]. Helps CR, Lait P, Damhuis A, Bjornehammar
U, Bolta D, Brovida C, Chabanne L, Egberink H,
Ferrand G, Fontbonne A, Pennisi MG, Gruffydd-
Jones T, Gunn-Moore D, Hartmann K, Lutz
H, Malandain E, Mostl K, Stengel C, Harbour
DA, Graat EA (2005). Factors associated with
upper respiratory tract disease caused by feline
herpesvirus, FCV, Chlamydophila felis and
Bordetella bronchiseptica in cats: experience from
218 European catteries. Vet Rec, 156: 669-73. 2006 World Congress WSAVA/FECAVA/CSAVA
[13]. Hurley KE, Pesavento PA, Pedersen NC,
Poland AM, Wilson E, Foley JE (2004). An
outbreak of virulent systemic FCV disease. J Am
Vet Med Assoc, 224: 241-9.
[14]. Hurley KF, Sykes JE (2003). Update on
FCV: new trends. Veterinary Clinics of North
America: Small Animal Practice, 33: 759-772.
[15]. Kahn DE, Gillespie JH (1971). Feline
viruses: Pathogenesis of picornavirus infection in
the cat. Am J Vet Res, 32: 521-531.
[16]. Love DN, Baker KD (1972). Sudden death
in kittens associated with a feline picornavirus.
Aus Vet J, 48: 643.
[17]. Marks PJ, Vipond I, Carlisle D, Deakin D,
Fey RE, Caul EO (2000). Evidence for airborne
345
Fe
transmission of Norwalk-like virus in a hotel
restaurant. Epidem Infect, 124: 481-7.
[18]. Pedersen NC, Elliott JB, Glasgow A, Poland
A, Keel K (2000). An isolated epizootic of
hemorrhagic-like fever in cats caused by a novel
and highly virulent strain of FCV. Vet Microbiol,
73: 281-300.
[19]. Pedersen NC, Laliberte L, Ekman S (1983).
A transient febrile “limping” syndrome of kittens
caused by two different strains of FCV. Feline
Practice, 13: 26-35.
[20]. Pesavento PA, MacLachlan NJ, Dillard-
Telm L, Grant CK, Hurley KF (2004). Pathologic,
immunohistochemical, and electron microscopic
findings in naturally occurring virulent systemic
FCV infection in cats. Vet Pathol, 41: 257-63.
[21]. Radford AD, Dawson S, Ryvar R, Coyne
K, Johnson DR, Cox MB, Acke EF, Addie DD,
Gaskell RM (2003). High genetic diversity of the
immunodominant region of the feline calicivirus
capsid gene in endemically infected cat colonies.
Virus Genes, 27: 145-55.
2006 World Congress WSAVA/FECAVA/CSAVA
346
Back to contents
[22]. Radford AD, Sommerville LM, Dawson
S, Kerins AM, Ryvar R, Gaskell RM (2001).
Molecular analysis of isolates of feline calicivirus
from a population of cats in a rescue shelter. Vet
Rec, 149: 477-481.
[23]. Schorr-Evans EM, Poland A, Pedersen NC
(2003). An epizootic of highly virulent feline
calicivirus disease in a hospital setting in New
England. J Fel Med Surg, 5: 217-226.
[24]. Scott FW (1980). Virucidal disinfectants
and feline viruses. Am J Vet Res, 41: 410-414.
[25]. TerWee T, Lauritzen A, Sabara M, Dreier
KJ, Kokjohn K (1997). Comparison of the
primary signs induced by experimental exposure
to either a pneumotrophic or a ‘limping’ strain of
feline calicivirus. Vet Microbiol, 56: 33-45.
[26]. Wardley RC, Gaskell RM, Povey RC (1974).
Feline respiratory viruses - their prevalence in
clinically healthy cats. JSAP, 15: 579-586.

Fe - Feline Medicine
ANTIVIRAL THERAPY IN CATS – WHAT WORKS AND WHAT
DOESN’T
Dr. Alan Radford
Senior Lecturer in Small Animal
Studies
University of Liverpool
Veterinary Teaching Hospital
Leahurst
Chester High Road
Neston
S Wirral
CH64 7TE
UK
alanrad@liv.ac.uk
Background
We are very clever at developing therapies
against microorganisms... or rather hijacking
them from bacteria. Many of the major classes
of antibacterials, antifungals and anthelmintics
are derived from prokaryotes. What we have not
been so clever about is developing drugs to treat
viral infections. This is largely a reflection of the
most intimate relationship between a virus and its
host. Not only do viruses replicate intracellularly,
they also use many host cellular processes to
complete their lifecycle. As such, attempts to
interfere with viral growth can often be toxic to
the host cell such that the therapeutic margins for
antivirals are in many cases quite low. Despite
these difficulties, many antiviral drugs are now
being developed to treat human viral infections
including human immunodeficiency virus (HIV),
herpes simplex virus, and influenza virus.
The most commonly available antiviral drugs
are generally the result of one of three processes.
Interferons are natural chemicals produced by
vertebrate cells that have quite general effects on
viral replication. They represent the end result of
an evolutionary process that has taken place over
the millions of years of virus : host competition.
Many other synthetic antivirals have been
developed, often by trial and error. The properties
which cause a drug to be anti-neoplastic will often
enable the same drug to have antiviral activity,
and this has formed another potential route for
developing antiviral drugs. Increasingly, and
in the future, antivirals will be designed on the
basis of a deep understanding of the molecular
interactions between important viruses and their
infected cells, leading to the identification of
crucial pathways that are required for viruses to
complete their lifecycle. This scientific process is
time consuming and costly, such that it is unlikely
many antivirals will be specifically developed this
way for the veterinary market. Rather, we will
Back to contents
Fe
often have to make use of drugs first developed
for human therapies.
For the cat, two factors have greatly influenced the
clinical availability of antivirals, one positively
and one negatively. Firstly, the close and fortuitous
relationship between important viral pathogens
of cats and humans, has meant that those drugs
developed for human disease may also be useful
for feline disease. Feline immunodeficiency virus
(FIV) has been used as a model of HIV and has
meant that many of the drugs that have been
successfully developed to treat AIDS in people
have also been tested on cats. Another example is
feline herpesvirus (FeHV), which is very closely
related to human herpes simplex virus, another
virus for which antiviral therapy is routinely used
in people. Secondly, the tendency of cats to find
many drugs toxic has meant that although some
drugs may have been shown to be beneficial in
cell culture, they have proved too toxic in the cat
e.g.[8].
The main antiviral drugs available for cats are
interferon, nucleoside analogues, and amino
acids. Entry inhibitors, protease inhibitors, exit 2006 World Congress WSAVA/FECAVA/CSAVA
inhibitors and monoclonal antibodies are not yet
available but will be mentioned for completeness
because of their importance in treating human
viral infections.
Interferons
Interferons are part of our natural innate immune
response. They are rapidly induced in response
to viral infection, much faster than the acquired
immune response. They bind to cellular receptors
leading to the induction of a so-called “antiviral”
state. Their effects are mediated predominantly
by two proteins. Double-stranded RNA activated
protein kinase switches off protein translation
(synthesis) in infected cells. Ribonuclease L
chops DNA and RNA. There are two main types
of interferon. Type I (αβω) and II (γ). Although
347
Fe
interferons from one species may work in another
(human interferon has been used in cats) , they
work best in more closely related species (feline
interferon works in both cats and dogs). Virbagen
omega (Virbac) is feline interferon omega
produced by recombinant DNA technology in
silkworm cells. It is licensed across Europe for
the treatment of cats with feline leukaemia virus
(FeLV) infection and / or FIV infection in the
non-terminal stages of disease, and for canine
parvoviral disease.
In one study, cats with FeLV +/- FIV were
treated with 1MU/kg of Virbagen omega per day
subcutaneously, for five days on three occasions
starting on days 0, 14 and 60. Treated cats showed
reduced mortality (39% compared to 59% of
controls - relative risk of death in the interferon
group is 1.6 lower than in the control group) [1].
Generally, cats anaemic at the start of therapy that
have shown no improvement in the anaemia by
day 14 are considered unlikely to respond well
to treatment.
There is also some evidence that oral human
interferon α may have some beneficial effect
against both FeLV and FIV infection. A low dose
oral regime is preferable to parenteral routes
of administration, as cats treated with the latter
protocol seem to rapidly develop antibodies to
the “foreign” interferon molecule, and become
refractory to any beneficial effect. In a study of
clinically affected FIV cats, low dose oral human
interferon α was also shown to reduce clinical
disease and prolong survival times compared to
controls [7]. However, there was no effect on the
viral load in affected cats.
There is also some data to suggest a beneficial
effect against feline infectious peritonitis (FIP)
virus [2]. In this study which was not controlled,
12 clinically ill cats previously diagnosed
with FIP were treated with a combination of
recombinant feline interferon (1 MU/kg s.c.
2006 World Congress WSAVA/FECAVA/CSAVA
e.o.d until remission, then weekly injections) and
glucocorticoid (2mg/kg initially then reducing).
Complete (> 2 yrs) remission (resolution of
effusion) was seen in four cases, and partial
remission (2 to 5 months) in four further cases.
Feline interferon is also licensed for the treatment
of acute feline calicivirus disease in Japan &
Australasia. Cats receive 2.5 MU/kg i.v. e.o.d.
on three occasions. Treatment appears to be more
effective when given early in disease. However,
too my knowledge there are no widely available
peer reviewed publications on its use.
Other possible (non-licensed) uses for feline
interferon include outbreaks of FCV-associated
virulent systemic disease, FeHV ocular disease,
and feline parvovirus infection (based on licensed
use for canine parvovirus - [4]). However, to the
348
Back to contents
author’s knowledge, controlled trials showing
efficacy are lacking.
Nucleoside analogues
The building blocks of DNA are the four
nucleotides. Each consists of a sugar molecule
with an attached base on one side (A,G, C or T)
and phosphorylated on the other. Each nucleotide
is made in the cell from a nucleoside, which
is simply a nucleotide without the phosphate.
Nucleoside analogues either contain a false sugar
or a false base or both. They bind to the enzymes
responsible for making new genetic information
(polymerases) and inhibit their action. Clinically,
they are used to inhibit tumour cells and viral
replication. However, they can also interfere with
normal cell turnover leading to their potential for
toxicity.
Many nucleoside (and some nucleotide) analogues
are now available for the treatment of HIV. Some
are also useful in cats for the treatment of FIV and
FeHV, however many are too toxic in cats. The
nomenclature is confusing since each drug has a
generic name, a chemical name and a trade name.
e.g. (Retrovir – brand name, AZT – commonly-
used name (3’-azido-2’,3’-dideoxythymidine),
zidovudine (ZDV) – generic name).
Although there is a lot of data about the sensitivity
of FIV and FeLV to nucleoside analogues in vitro
(in cell culture), for most there is very little data
about their clinical usefulness. Zidovudine (AZT)
has been shown to be useful in FIV infected cats,
and in early FeLV infection. However, non-
regenerative anaemia is a common side effect
which needs careful monitoring.
As is the case in HIV treatment, it is probable that
these veterinary viruses will be swift to develop
resistance to single drug therapies (e.g. [10]),
and these may also be resistance to others drugs.
This is likely to limit the clinical usefulness of
monotherapies.
Numerous nucleoside analogs have been
developed against human herpesviruses, mainly
herpes simplex and varicella-zoster viruses.
However, many are too toxic at therapeutic levels
for oral administration to cats e.g. valacyclovir
[5]. The current treatment of FeHV keratitis is
therefore based on the topical use of nucleoside
analogues. Although in vitro, acyclovir is less
efficacious than vidarabin, idoxuridin and
trifluridin [6], it is often the most readily available
of the drugs (e.g. Zovirax ophthalmic, GSK) [16].
In one relatively small study of 17 cats variably
treated with vidarabin, idoxuridin or trifluridin,
no superior protocol could be identified [11].
Human interferon alpha reduces viral replication
and cell death in a corneal cell culture model [9],
and has a synergistic effect with acyclovir [15],

but evidence of its clinical utility in cats with
FeHV is lacking.
Other antivirals such as ganciclovir, on the basis
of in vitro studies, may prove useful in FeHV
[14].
Ribavirin is used to treat respiratory syncitial
virus infection in children. It has broad action
against a variety of feline viruses including FeLV,
FIV, calicivirus and coronavirus. However, it is to
toxic for use in cats [8].
L-lysine
L-lysine is a normal amino acid that has an
inhibitory effect against both human herpesvirus
and FeHV infection. Oral supplementation
(400mg of L-lysine in food once daily for 30
days) reduces the severity of experimentally-
induced FeHV conjunctivitis when administered
prior to infection [12] and the number of
shedding episodes associated with reactivation of
latent infection induced by re-housing [3]. It may
therefore be of use early in acute disease or as
a means of reducing the amount of disease and
virus shed at times of stress.
Other drugs
Anti-flu drugs with specific activity against
influenza viruses are particularly topical at the
moment. Amantadine and rimantadine prevent
the virus from uncoating, whereas zanamivir
(Relenza) and oseltamivir (Tamiflu) prevent
the release of viral particles from infected cells.
Although cats can be infected with the H5N1
strain of influenza with severe consequences, it is
uncertain whether these precious drugs would be
made available for use in cats.
Protease inhibitors. Many viruses produce there
own proteins as one large molecule that needs to
be chopped by specific viral proteases to release
the active proteins. This specific step is a key
target for protease inhibitors against HIV. To the
author’s knowledge, no protease inhibitors are
available for use in cats at the moment.
Monoclonal antibodies are specific antibody
clones made in mice that target individual
epitopes in their target antigen. Since they
are made in mice they induce an immune
response against themselves when injected
into other species. Recently, these antibodies
have been molecularly modified to make them
immunologically acceptable in their new host
and potentially useful as therapeutic agents. They
are being developed for the treatment of cancers
and infectious diseases in humans. In cats, there
is some experimental evidence they will work
against FCV and FeHV [13].
Back to contents
Fe
Summary
The general dogma that we can’t treat viral
infections is now gone, even for the cat.
Unfortunately there are not many double blinded
trials clearly demonstrating clinical efficacy but
these will come. In the future, new drugs and new
formulations of old drugs will be developed for
humans and may be appropriate for use in the
cat. Topical applications may abrogate toxic side
effects of drugs given parenterally. Combination
therapies give best clinical response in humans
and this will probably be the case in the cat.
References
[1]. de Mari K, Maynard L, Sanquer A, Lebreux
B, Eun HM (2004). Therapeutic effects of
recombinant feline interferon-omega on feline
leukemia virus (FeLV)-infected and FeLV/
feline immunodeficiency virus (FIV)-coinfected
symptomatic cats. J Vet Intern Med, 18: 477-82.
[2]. Ishida T, Shibanai A, Tanaka S, Uchida K,
Mochizuki M (2004). Use of recombinant feline
interferon and glucocorticoid in the treatment of
FIP. J Feline Med Surg, 6: 107-9.
[3]. Maggs DJ, Nasisse MP, Kass PH (2003).
Efficacy of oral supplementation with L-lysine in
cats latently infected with feline herpesvirus. Am
J Vet Res, 64: 37-42.
[4]. Martin V, Najbar W, Gueguen S, Grousson
D, et al (2002). Treatment of canine parvoviral
enteritis with interferon-omega in a placebo-
controlled challenge trial. Vet Microbiol, 89:
115-27.
[5]. Nasisse MP, Dorman DC, Jamison KC,
Weigler BJ, Hawkins EC, Stevens JB (1997).
Effects of valacyclovir in cats infected with feline
herpesvirus 1. Am J Vet Res, 58:1141-4.
[6]. Nasisse MP, Guy JS, et al (1989). In vitro
susceptibility of FeHV to vidarabine, idoxuridine,
trifluridine, acyclovir, or bromovinyldeoxyuridine. 2006 World Congress WSAVA/FECAVA/CSAVA
Am J Vet Res, 50: 158-60.
[7]. Pedretti E, Passeri B, Amadori M, Isola P,
Di Pede P, Telera A, Vescovini R, Quintavalla
F, Pistello M (2006). Low-dose interferon-alpha
treatment for feline immunodeficiency virus
infection. Vet Immunol Immunopathol, 109: 245-
54.
[8]. Povey RC (1978). Effect of orally administered
ribavirin on experimental FCV infection in cats.
Am J Vet Res, 39: 1337-41.
[9]. Sandmeyer LS, Keller CB, Bienzle D (2005).
Effects of interferon-alpha on cytopathic changes
and titers for FeHV in primary cultures of feline
corneal epithelial cells. Am J Vet Res, 66: 210-6.
[10]. Smith RA, Remington KM, Preston BD,
349
Fe
Schinazi RF, North TW (1998). A novel point
mutation at position 156 of reverse transcriptase
from FIV confers resistance to the combination
of (-)-beta-2’,3’-dideoxy-3’-thiacytidine and 3’-
azido-3’-deoxythymidine. J Virol, 72: 2335-40.
[11]. Stiles J (1995). Treatment of cats with ocular
disease attributable to herpesvirus infection: 17
cases (1983-1993). J Am Vet Med Assoc, 207:
599-603.
[12]. Stiles J, Townsend WM, Rogers QR,
Krohne SG (2002). Effect of oral administration
of L-lysine on conjunctivitis caused by feline
herpesvirus in cats. Am J Vet Res, 63: 99-103.
[13]. Umehashi M, Imamura T, Akiyama S,
Kimachi K, Tokiyoshi S, Mikami T (2002).
Post-exposure treatment of cats with mouse-cat
2006 World Congress WSAVA/FECAVA/CSAVA
350
Back to contents
chimeric antibodies against FeHV and feline
calicivirus. J Vet Med Sci, 64: 1017-21.
[14]. van der Meulen K, Garre B, Croubels S,
Nauwynck H (2006). In vitro comparison of
antiviral drugs against feline herpesvirus 1. BMC
Vet Res, 2: 13.
[15]. Weiss RC (1989). Synergistic antiviral
activities of acyclovir and recombinant human
leukocyte (alpha) interferon on feline herpesvirus
replication. Am J Vet Res, 50: 1672-7.
[16]. Williams DL, Robinson JC, Lay E, Field
H (2005). Efficacy of topical aciclovir for the
treatment of feline herpetic keratitis: results of a
prospective clinical trial and data from in vitro
investigations. Vet Rec, 157: 254-7.

Fe - Feline Medicine
CHRONIC RENAL FAILURE IN THE CAT
Dr Andrew H. Sparkes BVetMed
PhD DipECVIM MRCVS
RCVS Specialist in Feline
Medicine
Animal Health Trust
UK
Andy.sparkes@dsl.pipex.com
Chronic renal failure (CRF) is a common and
important cause of morbidity and mortality in
cats. The hallmark of CRF is a chronic decline in
the population of functional nephrons to a point
where the glomerular filtration rate (GFR) is no
longer adequate to maintain normal excretory
function. This leads to azotaemia (elevation in
plasma urea and/or creatinine concentrations) and
the retention of other plasma solutes and protein
catabolic products normally eliminated via the
kidneys. Ultimately, renal dysfunction and the
retention of these products results in a spectrum
of clinical signs associated with CRF, commonly
referred to as the ‘uraemic syndrome’.
Aetiology of feline CRF
The underlying aetiology of feline CRF is often
obscure although a variety of causes have been
documented. Histological evaluation of kidneys
from affected cats most commonly reveals the
presence of chronic interstitial nephritis (CIN)
characterised by the presence of progressive
fibrosis, loss of nephrons and the presence
of sterile inflammation, but the cause of this
uncertain. It has been speculated that chronic
pyelonephritis or glomerulonephritis may account
for at least some of these ‘end stage’ cases of
chronic renal failure, but whatever the underlying
cause, unlike many cases of human renal failure,
this is not predominantly a glomerular disease in
cats, but rather a tubulointerstitial disease (with
glomerular involvement) that results in nephron
loss.
Clinicopathological changes and diagnosis
The diagnosis of CRF is usually based on the
presence of appropriate clinical signs (although
these are often vague and non-specific) together
with the demonstration of azotaemia and
inappropriately concentrated urine. Because cats
often retain some concentrating ability during
CRF, isosthenuria is not necessarily observed and
indeed studies suggest that isosthenuria (urine SG
Back to contents
Fe
<1.015) may only be seen in around 50-60% of
cases of feline CRF, with the remaining having
various degrees of hypersthenuria. However,
the ability of the kidneys to concentrate urine
will depend to some extent on the severity of the
renal failure, and few cats with advanced or well
established CRF can concentrate urine above
1.035.
Because factors other than CRF can cause
azotaemia (in particular dehydration), the finding
of azotaemia alone is not sufficient to make a
diagnosis of CRF. In all cases, the presence of
azotaemia should be interpreted together with a
concomitant urine sample for measurement of
urine SG. Thus the presence of azotaemia with
a urine SG <1.035-1.040 is usually considered
evidence of primary renal failure as if the
azotaemia were associated with dehydration,
in the presence of normal renal function active
water conservation would lead to a much higher
urine SG. However, as some cats with early renal
failure ar still able to concentrate urine well, the
presence of azotaemia and a urine SG >1.040
does not rule out the possibility of CRF. Although
in most cases the diagnosis of CRF is relatively
straightforward, there may be some where this is
difficult, and additional investigations of renal 2006 World Congress WSAVA/FECAVA/CSAVA
function may be required (see below).
Stages of feline CRF
The IRIS (International Renal Interest Society)
group has defined four stages of renal failure
in cats and these may help to some extent in
targeting therapy for the disease. Absolute cutt-
off values of creatinine vales for the different
stages cannot be applied as these are affected
by numerous variables other than renal function
itself (hydration status, lean body mass etc.):
351
Fe
Stages of feline chronic renal failure (IRIS)
Creatinine Signs
µmol/l
Non- <140 None +++
azotaemic
Mild 140-250 Mild +++
azotaemia
Moderate 251-440 Transitional ++
azotaemia
Severe >440 Uraemic + +
azotaemia
Although renal failure cannot generally be diagnosed until cats have developed azotaemia, many cats
present with diseases where there is clearly renal
damage even though they have not progressed
to overt renal failure. Thus cats that present
with pyelonephritis, glomerulonephritis, renal
lymphoma etc., although they may not necessarily
be azotaemic at the time of the diagnosis of their
primary disease, there will be renal damage and
loss of functioning nephrons. In these cases,
the clear priority is specific therapy for the
underlying disease, and preventing further renal
damage through adequate disease diagnosis and
management.
By the time azotaemia has developed, it can be
assumed that around 75% of functioning nephrons
have been lost, but even at this stage, clinical signs
will be relatively mild or even non-existent early
on. If an underlying disease can be diagnosed
and specific treatment instituted this will again
provide significant benefits in preventing further
progression of disease, but in many (if not all)
cats, the CRF will progress, although often at a
slow rate. Attention is focussed on therapeutic
interventions that will help to slow down the rate
of progressive nephron loss.
2006 World Congress WSAVA/FECAVA/CSAVA
As cats progress though the period of moderate
azotaemia, there is an increasing likelihood of
clinical signs developing relating to the CRF
(development of uraemic signs), and thus as cats
progress through stage III disease and on into stage
IV disease there is an increasing need to provide
symptomatic and supportive therapy to address
the manifestations of the uraemic syndrome and
to some extent a lesser emphasis on therapies to
slow progression of disease as this becomes more
difficult in advanced renal failure.
Medical management of CRF
Treatment of underlying cause
Identifying and treating reversible causes or
contributory factors to CRF is important, although
in many cases these may not be present. However,
352
Back to contents
Specific Renoprotective Symptomatic
therapy therapy therapy
+ +
+++ +
+++ +++
+++
searching for conditions such as pyelonephritis,
glomerulonephritis and urinary tract obstruction,
or iatrogenic renal damage through administration
of non-steroidal anti-inflammatory drugs
or aminoglycoside antibiotics, may allow
intervention to arrest further renal damage, and
as such this part of the patient assessment should
not be overlooked. Full urinalysis including urine
sediment analysis, urine protein:creatinine ratio
and urine culture (especially if there is evidence of
inflammation on urine sediment analysis) should
be performed as part of the initial assessment
whenever possible.
Maintaining fluid balance
Inadequate water intake in CRF is associated
with dehydration, reduced renal perfusion and
further impairment of renal function. Some cats
are presented in acute decompensation of CRF
due to sudden volume depletion, whereas others,
particularly as CRF progresses, may experience
chronic or recurrent dehydration and renal
hypoperfusion. Acutely decompensated cats
require intravenous fluid therapy and reassessment
of azotaemia after correction of the dehydration
to permit accurate assessment of renal function.
Maintaining adequate fluid intake is of prime
importance in CRF, and owners should be made
aware of the obligatory polyuria that frequently
accompanies renal failure and, therefore the
consequent need for free access to water.
Additional water intake can be achieved in a
variety of ways
• Feeding moist rather than dry foods (this is a
priority in cases of CRF, and cats that have been
accustomed to dry food should be encouraged to
slowly switch to a moist (tinned/sachet) food
• Supplementing the diet with water or broths
• Providing running water (pet fountains) and
flavoured water, etc.
• Sub-cutaneous administration of fluids at home
by owners

Delaying progression, and managing complications
of CRF
Dietary protein restriction
The benefits of protein restriction in dogs and cats
with established CRF are not in doubt, and the
positive impact that this can have on the quality
of life and clinical disease is unquestioned.
Accumulated evidence suggests that it is likely
(though not certain) that protein restriction does
have a positive impact on the progression of renal
failure in these species, but it is generally accepted
that this effect is likely to be relatively small, and
the major benefit is through amelioration of signs
of the uraemic syndrome.
Dietary phosphorus restriction
Both findings in cat studies, and also extrapolation
from studies in dogs and other species, suggest
that dietary phosphorus restriction is an important
goal in the management of CRF. As much dietary
phosphorus is associated with protein, the use of
a protein restricted diet will reduce phosphate
intake, and commercial renal diets are specifically
phosphate restricted. It is now generally accepted
that the combined effects of dietary phosphate
restriction (direct reduction in circulating
phosphate levels, indirect reduction in circulating
PTH levels) is likely to have a very important
renoprotective effect and can significantly help to
slow the progression of renal failure. In addition,
as PTH has been implicated as a uraemic toxin,
control of dietary phosphate may also help to
improve quality of life and relieve other uraemic
manifestations.
Use of phosphate binders
If hyperphosphataemia persists (fasting serum
phosphorus >2 mmol/l) despite dietary restriction,
oral phosphate binders are indicated to control
this and are best administered along with meals.
Aluminium hydroxide was the traditional
product of choice, and although very effective
as a phosphate binder (30-90 mg/kg/day), this
was always associated with palatability issues.
In recent years, this product has been withdrawn
from the market due to concerns over aluminium
toxicity in humans. Two newer products have
become available on the human market, and
although relatively little is known about their use
in dogs and cats, anecdotally they appear to be
both safe and effective. Sevelamer (Renagel®)
has been used in cats at a dose of 200mg 2-3
times daily and lanthanum carbonate (Fosrenal®)
has been used at a similar dose.
Back to contents
Fe
Control of hypokalaemia
Hypokalaemia, probably mainly from
inappropriate kaliuresis, is a common finding in
feline CRF with a reported prevalence of around
15-20% of cats with CRF. Overt clinical signs are
generally not seen until the serum concentration
falls below around 3.0 mmol/l. However,
although polymyopathy is often regarded as the
major clinical manifestation of hypokalaemia,
there are other significant consequences that
are of particular importance in cats with CRF
and may occur with less severe hypokalaemia.
Hypokalaemia can directly contribute renal
damage (hypokalaemic nephropathy) and
the advancement of renal failure. The renal
compromise induced by hypokalaemia has a
number of facets but includes hypokalaemia-
induced renal vasoconstriction, reduced
responsiveness of the kidneys to vasopressin and
increased renal ammoniagenesis which directly
contributes to interstitial nephritis. There is also
evidence that the presence of hypokalaemia will
contribute to both the metabolic acidosis and
hypertension that can occur in CRF. Potassium
concentrations should be monitored regularly in
cats with CRF and if they fall below 4 mmol/
l, supplementation with potassium salts is
recommended.
Hypertension and chronic renal failure
Although primary hypertension is recognised,
many cases of feline hypertension are secondary
to other diseases, and the association with renal
failure is the most important of these. There is a
great degree of individual variation in response to
therapy, but in cats monotherapy with amlodipine
(a calcium channel blocker) is generally
regarded as the treatment of choice for systemic
hypertension.
ACE-inhibitor therapy in humans
At present there is too little data available to know
2006 World Congress WSAVA/FECAVA/CSAVA
whether ACE-inhibitor therapy slows progression
of feline CRF, although there is rationale and
some data to suggest that cats with elevated (and
especially markedly elevated) proteinuria levels
do benefit from therapy (especially cats with a
UPC ratio >1.0). If human data is applicable to
the cat, then in hypertensive renal failure, the first
priority is to control the hypertension, and ACEI
may not adequately do this in cats. However, a
second priority could be control of the degree
of proteinuria and it could be argued that these
two objectives might best be achieved by a
combination of an ACEI and a calcium channel
blocker, but evidence to support this as a first line
therapy is lacking.
353
Fe
Fe - Feline Medicine
FELINE LOWER URINARY TRACT DISEASE
Dr Andrew H. Sparkes BVetMed
PhD DipECVIM MRCVS
The Feline Unit
Centre for Small Animal Studies
Animal Health Trust
UK
Andy.sparkes@dsl.pipex.com
A spectrum of disease
Feline lower urinary tract disease (FLUTD) is a
spectrum of different diseases that present with
a common set of clinical signs irrespective of
the underlying cause – these include dysuria,
haematuria, pollakiuria and periuria and
behavioural changes such as aggression and
perineal overgrooming. Additionally male cats
may develop stranguria with urethral blockage
which, if left untreated, will result in acute renal
failure within 1-3 days.
Despite the common array of clinical signs
exhibited, there are a number of potential
underlying aetiologies for FLUTD which have to
be considered and achieving a definitive diagnosis
requires a logical and structured approach to the
investigation of cases.
In general, idiopathic cystitis accounts for
50-70% of cases of FLUTD and is universally
the most common diagnosis made. Urolithiasis
and urethral obstruction (which can be caused by
a single urolith, an accumulation of small uroliths,
a urethral plug, urethral stricture, or functional
spasm of the urethral sphincter) are also common
causes of disease, together accounting for up to
2006 World Congress WSAVA/FECAVA/CSAVA
40% of clinical cases.
Bacterial cystitis
While most surveys suggest bacterial cystitis
is rare in cats (<2-3% of cases of FLUTD) and
while it is undoubtedly vastly less common than
in dogs, the low prevalence in some studies may
reflect biases seen in referral populations. Some
studies suggest that up to 10% (or possibly more)
of first-opinion cases may have bacterial cystitis.
Routine sediment analysis of a urine sample
collected by cystocentesis is extremely valuable,
and in most cases of bacterial cystitis this will
reveal clear evidence of its presence (pyuria,
bacteriuria). Where evident, or where there is any
doubt, bacterial culture can confirm the diagnosis
and allows selection of the most appropriate
antibiotic. Intereference with innate defence
354
Back to contents
mechanisms (eg, repeat catheterisation and
perineal urethrostomies) are known to increase
the risk of bacterial cystitis and this is also much
more common in older cats due to ageing cats
tending to produce less concentrated urine and
thus having a microenvironment where bacterial
growth is more likely to occur.
Urolithiasis
Calcium oxalate and struvite uroliths occur
with approximately equal frequency in cats
and together account for around 90% of all
uroliths. While struvite stones can be dissolved
with appropriate dietary management, oxalate
cannot and require surgical removal. There is a
significant risk of recurrent urolithiasis in any
individual that has experienced one episode, so
taking measures to help prevent their recurrence
provides good preventative healthcare. Long-term
prevention of recurrence depends on modifying
the urine composition to reduce the risk of further
crystalluria and stone formation.
Some of the known risk factors for oxalate
and struvite urolithiasis are effectively at odds
with each other (such as urine pH, and urine
magnesium concentration), and thus diets
designed to address the specific requirements for
prevention of these two different types of stone
are ideal for maintenance in these cases. Wherever
possible the use of tinned/sachet foods rather than
dry foods is recommended to help produce less
concentrated urine.
Urethral plugs and crystalluria
Urethral plugs are possibly the single most
common cause of urethral obstruction in cats,
but their underlying cause remains uncertain.
Most plugs have a high matrix content (>50%)
of within which crystalline material, cells and
cellular debris becomes trapped. Together,
these components form the urethral obstruction.
Although the matrix is composed largely of
proteinaceous material, its source has not been

determined. However, it is likely that in at least a
proportion of these cases, the underlying cause is
idiopathic cystitis, with the bladder inflammation
contributing to increased secretion and/or leakage
of various proteins into the urine. In the vast
majority of cases, the crystalline component of
urethral plugs is struvite. The finding of struvite
crystalluria (and some other forms of crystalluria)
is not of itself an abnormality. Many healthy cats
(and indeed other animals!) produce crystalluria,
but its presence does suggest that the urine is
supersaturated with the crystalloid materials,
and this would be one risk factor for urolith
development. It is not necessarily appropriate to
modify the diet of healthy individuals producing
crystalluria, but in a cat that has previously
had an episode of urolithiasis, urine should be
monitored to ensure dietary modification has
been successful in understurating the urine (ie,
crystals should be absent). Also in cats that
have experienced urethral plugs, the diet should
be modified to undersaturate the urine with
magnesium, ammonium, and phosphate, and thus
at least eliminate the crystalloid component that
may contribute to repeat plug formation. In this
situation, although crystalluria is not the cause of
the disease, it does contribute to the formation of
a plug that cannot be passed through the urethra.
Thus dietary modification to eliminate struvite
crystalluria may help prevent recurrence.
Urethral spasm
Not just with urethral plugs, but in many other
forms of FLUTD, the disease may not be confined
to the bladder but may also involve inflammation
of the urethra. This may also be exacerbated by
iatrogenic damage to the urethra or irritation of the
urethra with the use of indwelling catheters. Such
inflammation may result in significant urethral
sphincter spasm, and there is good evidence
that in some cats this is severe enough to mimic
physical urethral obstruction. Where urethral
spasm is suspected a combination of smooth and
striated muscle relaxants should be used to relax
both the internal and external sphincter muscles.
Common recommendations are to use either
dantrolene (2-10 mg/cat PO tid) or diazepam
(2-5mg/cat PO bid/tid) together with either prazosin
(0.5 mg/cat sid-bid) or phenoxybenzamine
(2.5-7.5 mg/cat sid/bid).
Idiopathic cystitis
Idiopathic cystitis is a diagnosis that can only be
made by exclusion of known causes of FLUTD,
and thus following a logical diagnostic work-up
(see Table 2). The majority of cases of idiopathic
FLUTD (iFLUTD) spontaneously resolve within
a few days irrespective of therapy, making
Back to contents
Fe
response to treatment very hard to assess. Often,
what is taken to be improvement due to therapy
is in fact simply spontaneous recovery. A plethora
of drugs are used to treat iFLUTD, many of which
have not been the subject of any clinical trials,
and of the few published well-controlled studies,
regrettably no interventional medical therapy has
been shown to be of significant benefit in these
cases.
Nevertheless, a number of drugs have only
been evaluated in short-term studies (lasting 1-
2 weeks) of idiopathic cystitis, and the fact that
drugs such as prednisolone and amitriptyline are
not significantly different from placebo therapy
in this situation may simply reflect the rapidly
self-resolving nature of this disease. Of more
clinical value is the use of long-term placebo
controlled studies looking at frequency and
severity of recurrent episodes, but such studies
are less common as they are more difficult and
more expensive to conduct.
The importance of diet in idiopathic cystitis
Although the use of diets to specifically to
minimise production of urinary crystals has little
or no scientific rationale in the management of
iFLUTD, dietary manipulation is the single most
important component of long-term management
of this disease.
Dietary change is the only form of therapy that
has consistently been shown to be of real benefit
in cases of iFLUTD. Based on our current
knowledge, this forms the most important part of
long-term management. Several studies have now
confirmed the results of an earlier investigation
that showed cats fed a wet (tinned) diet had a much
lower rate of recurrent signs of idiopathic cystitis
than those fed a dry diet. The urine concentration
produced in response to feeding the wet diet
was much lower than that of the cats fed the dry
diet, and it is thought that producing more dilute
urine (and presumably thus also encouraging
2006 World Congress WSAVA/FECAVA/CSAVA
more frequent urination) are major mechanisms
of the observed benefit. Feeding a wet (tinned/
sachet) diet rather than a dry diet is thus always
recommended for iFLUTD, and the feeding of
a ‘pH neutral’ diet (a urine pH in the region of
6.3 is typically found in cats on a ‘natural’ diet of
rodents) that will avoid extremes of urinary pH is
also likely to be of benefit. The use of a relatively
low solute-load diet helps in the production
low urine concentration, and this is preferable
to trying to encourage greater urine production
through the addition of salt to the diet. The latter
could be associated with a number of potential
adverse effects such as volume expansion and
contributing to hypertension, and exacerbating
any renal compromise present. Encouraging
355
Fe
water intake without salt supplementation is thus
preferred and the use of ‘pet fountains’, flavoured
waters and other methods of enhancing water
intake (beyond just the use of wet diets) also has
a good role to play. In cases of recurrent iFLUTD,
a primary aim should be to reduce the urine SG
to 1.035 or less, and avoid abnormal acidification
or alkalinisation.
Drug therapy in idiopathic cystitis
Recent evidence from investigation of iFLUTD
cases has revealed a number of similarities
to interstitial cystitis in humans. Although
differences also exist there are certainly many
striking similarities. There is evidence from
careful studies that both conditions may be
associated with decreased urinary excretion
of glycosaminoglycans, an increased bladder
wall permeability, and increased circulating
catecholamine levels (although paradoxically
relatively low cortisol levels and blunted cortisol
responses to ACTH). On the basis of the similarity
between these two conditions, some of the
treatments that have been shown to be useful for
the management of interstitial cystitis in humans
have been tried in cats with iFLUTD.
Glycosaminoglycan (GAG) replacers (e.g.
pentosan polysulphate, glucosmaine) fall into
this category and are now commonly used in
cats with iFLUTD. Although the finding of
significantly reduced GAG concentrations in the
urine of affected cats provides a good rationale
for their use, clinical experience with these drugs
has been variable. In two long-term controlled
studies, GAG replacers did not appear to make
a significant difference overall to the recurrence
2006 World Congress WSAVA/FECAVA/CSAVA
356
Back to contents
of iFLUTD in affected cats. Nevertheless, of
interest is that both these studies identified some
individual cats that did seemed to consistently
respond to GAG-replacer use, and have recurrent
signs when therapy was stopped. Although still
uncertain, it seems that some cats may genuinely
benefit from this therapy, although possibly not
most. On this basis, trial therapy is certainly
warranted in refractory cases.
Amitriptyline has also been used to treat interstitial
cystitis in humans. Being a tricyclic antidepressant
drug, it certainly has some central nervous system
effects which may help in controlling iFLUTD,
especially as stress factors appear to be involved
in at least some cats. However, the drug has a
number of other potential beneficial effects in
terms of reducing neurogenic inflammation in the
bladder and controlling the discomfort associated
with the disease. Generally, amitriptyline has been
used at a dose of 2.5-10 mg per cat, given once
daily in the evening (as administration may cause
temporary sedation). Although short-term studies
have not been able to demonstrate a benefit, one
long-term open uncontrolled study did suggest
genuine benefit in some cats with long-standing
intractable cystitis. Again, in severe, intractable
cases this drug is worth considering.
Consideration should also be given to
environmental factors and potential stress
factors that could impact on affected cats.
Inter-cat aggression and dominance may be an
important trigger factor in some and the use of
environmental enrichment/modification together
with feline pheromone sprays/diffusers could
also be a consideration in some situations.

Fe - Feline Medicine
THE DIFFERENTIAL DIAGNOSIS OF FELINE ANAEMIA
Dr. Séverine Tasker
Department of Clinical Veterinary
Science
University of Bristol
Langford
Bristol BS40 5DU
United Kingdom
S.Tasker@bristol.ac.uk
CLASSIFICATION OF FELINE ANAEMIA
Anaemias can be broadly divided into
regenerative (blood loss or haemolytic) and
non-regenerative types. In cats the majority of
anaemias are non-regenerative in contrast to the
dog. However multiple causes of anaemia can be
present concurrently. This can lead to difficulties
in classification of the anaemia resulting in a
diagnostic challenge.
DIFFERENTIATING REGENERATIVE AND
NON-REGENERATIVE ANAEMIAS
Haematology
The mean cell volume (MCV) indicates
the average size of red blood cells (RBCs).
Regenerative anaemias are usually macrocytic
because reticulocytes have high MCVs. However,
macrocytosis is not just a feature of regenerative
anaemias since non-regenerative anaemias
associated with FeLV infection or myelodysplasia
can be associated with macrocytosis (Shimoda, et
al 2000, Weiss 2006b).
The red cell distribution width (RDW) is an
estimate of the degree of anisocytosis in a blood
sample and is available on some haematology
analysers. A high RDW can indicate the presence
of increased number of macrocytes, microcytes
or both.
The mean cell haemoglobin concentration
(MCHC) indicates the average concentration
of haemoglobin per RBC. A reduced MCHC is
termed hypochromic. Regenerative anaemias are
Absolute reticulocyte count (x 109/l) = % reticulocytes x RBC count (x 1012/l) x 10
Regenerative response
Negligible
Mild
Moderate
Substantial
Back to contents
Fe
usually hypochromic because reticulocytes have
higher MCVs and lower haemoglobin content
than mature RBCs.
Nucleated RBCs (NRBCs) can indicate active
regeneration but are also seen with splenic
dysfunction, shock, heavy metal toxicity and
bone marrow disorders.
The presence of polychromasia, anisocytosis
and NRBCs on blood smears may indicate
regeneration.
Reticulocyte Count
This quantifies the RBC regenerative response.
A vital stain such as new methylene blue
(NMB) allows the identification of reticulocytes.
Reticulocytes correspond to polychromatic cells
on a Romanowsky-stained blood smear. Cats
have two types of reticulocytes; punctate and
aggregate. Feline aggregate reticulocytes are
identical in appearance to canine reticulocytes,
with multiple basophilic granules, and these
only last in the circulation for about a day before
maturing further. Punctate reticulocytes have only
a few basophilic granules and are more mature
reticulocytes that survive in the circulation for up
to 10 days. Since only aggregate reticulocytes
accurately reflect recent bone marrow RBC
production, these should be counted when 2006 World Congress WSAVA/FECAVA/CSAVA
evaluating moderate to marked anaemia. With
mild anaemias, punctate reticulocyte counts
may be of benefit. Calculation of the absolute
reticulocyte count allows assessment of the
degree of regeneration for the anaemia present.
Absolute reticulocyte count (x109/l)
< 50
50-100
100-200
>200
357
Fe
REGENERATIVE ANAEMIAS:
HAEMORRHAGE
Causes of Haemorrhage in Cats
Haemorrhage is the most common indication for
feline blood transfusions (Weingart, et al 2004).
Acute haemorrhage is relatively common in cats,
particularly after trauma (including surgery).
Haemostatic disorders can arise with conditions
such as liver disease or inherited coagulopathies.
Systemic amyloidosis can cause spontaneous
hepatic rupture and abdominal haemorrhage in
Siamese and related cats. Chronic haemorrhage
is uncommon in cats but can occur due to
severe ectoparasitism in kittens or urogenital
tract/gastrointestinal bleeding. Gastroduodenal
ulceration/bleeding can arise due to neoplasia,
NSAID toxicity and inflammatory bowel disease,
but cats tend to present in a critical condition
due to shock and severe anaemia. Chronic
external haemorrhage may eventually lead to iron
deficiency.
Diagnostic Features of Haemorrhage
Reticulocytes appear in the circulation after
3-5 days and peak at 5-7 days, although PCV
may take up to 2-3 weeks to return to normal.
Regeneration is evidenced by anisocytosis,
polychromasia and sometimes NRBCs on blood
smear examination. Hypoproteinaemia may be
present in the first week after bleeding. Persistent
anaemia and hypoproteinemia suggest ongoing
blood loss. Iron deficiency anaemia is a non-
or poorly regenerative microcytic hypochromic
anaemia.
REGENERATIVE ANAEMIAS: HAEMOLYSIS
Haemolysis arises due to extravascular or
intravascular RBC destruction. Extravascular
haemolysis usually occurs by macrophage
phagocytosis in the spleen, liver and bone marrow.
2006 World Congress WSAVA/FECAVA/CSAVA
Intravascular haemolysis is less common and
occurs within the vascular system. Haemolysis
may be mediated by antibodies bound to the
surface of RBCs in immune-mediated haemolysis
(IMHA).
Causes of Haemolysis in Cats
• Infections – FeLV, haemoplasmosis, Babesia,
Cytauxzoonosis,
• Oxidant injury such as exposure to chemicals or
toxins (onions) and some disease states (diabetic
ketoacidosis, hyperthyroidism and lymphoma)
– oxidant injury can result in a Heinz body
haemolytic anaemia. Feline haemoglobin is
particularly sensitive to oxidation. Anaemia is
more likely to result if the Heinz bodies are large
and affect >30% RBCs.
358
Back to contents
• Secondary IMHA – can arise secondary to
infectious agents such as FeLV, haemoplasmas
and feline infectious peritonitis (FIP), drugs (such
as methimazole, trimethoprim-sulphonamides),
neoplasia (such as lymphoma)
• Primary IMHA – in some cases no underlying
causes of IMHA can be identified and such
cases are referred to as primary IMHA. This is
a common form of IMHA in the dog, and was
thought to be rare in the cat, but recent reports
(Husbands, et al 2002, Kohn, et al 2006) suggest
it is more common than previously believed
• Haemolytic blood transfusion reactions
and neonatal isoerythrolysis are mediated
by haemolysis of RBCs which arises due to
incompatibility of donor and recipient, or queen
and kitten, blood types respectively
• Hypophosphataemia (<0.35 mmol/l) – can result
in haemolysis of RBCs, due to depletion of energy
supply to the RBCs and has been associated with
diabetes mellitus, hepatic lipidosis, refeeding
syndrome and oral administration of phosphate-
binding antacids
• Microangiopathic haemolytic anaemia –
disseminated intravascular coagulation, trauma
• Inherited RBC defects – osmotic fragility of
Abyssinians and Somalis, pyruvate kinase (PK)
deficiency in Abyssinians, Somalis and DSHs
Diagnostic Features of Haemolysis
Haemolytic anaemias are usually strongly
regenerative after 3-5 days with anisocytosis,
polychromasia, reticulocytosis and sometimes
NRBCs. In IMHA, if the immune response is
directed at RBC precursors in the bone marrow,
as well as peripheral RBCs, the anaemia may be
non-regenerative. Unlike anaemia due to external
blood loss, serum protein concentrations remain
normal with haemolysis. Bilirubinaemia and
bilirubinuria indicate acute, severe haemolysis
(intra- or extravascular), while haemoglobinemia
and haemoglobinuria specifically indicate
intravascular haemolysis. The presence of
large numbers of Heinz bodies (precipitated
haemoglobin) suggests exposure to oxidant
damage. Heinz bodies are colourless with
Romanowsky stains but blue-green with NMB.
In cats Heinz bodies tend to be single and uniform
in size and can become very large. IMHA cases
may show autoagglutination on a blood smear.
Positive slide agglutination (following washing
of RBCs) or Coombs’ tests indicate the presence
of RBC-bound antibodies in IMHA cases.
Feline Haemoplasmosis
See notes on feline haemoplasma infections.

PK Deficiency
PK is an enzyme critical to energy metabolism
in RBCs. If deficient in PK, RBC haemolysis
occurs. PK deficiency is an autosomal recessive
inherited trait in Abyssinians and Somalis. A
molecular screening test is available to identify
affected and carrier cats.
NON-REGENERATIVE ANAEMIAS
Non-regenerative anaemias develop as the
diseased bone marrow fails to replace ageing
erythrocytes.
Diagnostic Features of Non-regenerative
Anaemias
There is minimal anisocytosis and polychromasia
with a low reticulocyte count. RBCs are
usually normocytic and normochromic although
FeLV infection and myelodysplasia can cause
a macrocytosis. Iron deficiency anaemia will
typically be microcytic and hypochromic with
a mild degree of regeneration. Concurrent
leukopenias and thrombocytopenias may occur.
Causes of Non-regenerative Anaemias
Systemic disorders tend to produce mild
subclinical anaemia whereas primary marrow
disorders tend to cause moderate to severe
anaemia.
• Primary Bone Marrow Disorders
Pure red cell aplasia (PRCA)
Aplastic anaemia/pancytopenia
Myelodysplastic syndromes (MDS)
Myeloproliferative diseases
Myelophthisis – filling of the marrow
space with neoplastic cells or fibrous tissue
(myelofibrosis)
• Systemic Causes of Bone Marrow Suppression
Anaemia of inflammatory disease (AID)
Chronic renal failure (CRF)
Retrovirus-associated
PRCA
Selective erythroid bone marrow depletion
causes anaemia. It can arise secondary to FeLV
subtype C infection which is invariably fatal, or
can be immune-mediated, as reported in young
FeLV negative cats (Stokol and Blue 1999) in
which some cats were Coombs’ test positive
and immunosuppressive treatment was often
effective.
Aplastic Anaemia/Pancytopenia
All cell lines in the bone marrow are affected.
FeLV, FIV, parvovirus, toxoplasmosis, ehrlichiosis
and FIP are potential causes. Agents such as
griseofulvin (particularly in FIV positive cats),
Back to contents
Fe
chloramphenicol and some chemotherapy agents
can also induce pancytopenia. Some cases are
idiopathic. More recently a report found aplastic
anaemia arose in association with CRF in cats
and it has been suggested that starvation may
contribute to the development of marrow aplasia
(Weiss 2006a).
MDS
Maturation defects of one or more of the
haematopoietic cell lines are known as
MDSs. These are usually characterized by
hypercellular marrow with concurrent cytopenias
in the peripheral blood. Dyshaematopoiesis
is evident and a macrocytosis may be present.
Myelodysplasia is often associated with
FeLV (Shimoda, et al 2000) although a recent
report found only 36% of cats with MDS were
FeLV positive (Weiss 2006b). Secondary
dysmyelopoiesis can arise due to IMHA in which
the immune system targets the bone marrow
resulting in a non-regenerative anaemia, and
differentiation of secondary dysmyelopoiesis
from primary MDS can be difficult as both can
show autoagglutination. MDS cases tend to have
higher numbers of blast cells in the bone marrow.
Some MDS cases respond to differentiating
agents (such as cytosine arabinoside), anabolic
steroids or haematopoietic growth factors. Some
go on to develop leukaemia.
Myeloproliferative Disorders
Neoplastic proliferation e.g. in a leukaemia, can
result in inhibition of haematopoiesis.
AID
AID is a very common cause of anaemia in the
cat, occurring in association with many diseases
including infections and neoplasia. The anaemia
is mild to moderate (PCV >17%), normocytic and
normochromic. Clinical signs are rare. AID can
develop quite rapidly in the cat (within 3-4 days) 2006 World Congress WSAVA/FECAVA/CSAVA
suggesting that a shortened RBC lifespan, as well
as reduced RBC production, contributes to the
development of anaemia. Iron sequestration by
the macrophage system, erythrocyte sequestration
and impaired bone marrow response to EPO are
all thought to contribute to the development of
AID.
CRF
Up to 40% of cats CRF are anaemic due to
decreased renal EPO production, bone marrow
inhibition by uraemic toxins, decreased RBC
survival, blood loss due to gastrointestinal
ulceration or thrombocytopathia, and impaired
iron utilization (a component of AID). Aplastic
anaemia has recently been reported in association
with CRF (Weiss 2006a).
359
Fe
Retrovirus Infection
Several mechanisms (e.g. PRCA, IMHA,
AID) can contribute to retrovirus anaemia but
most cases show evidence of non-regenerative
anaemia. FeLV and FIV testing can be done on
blood and bone marrow samples.
References
Husbands, B.D., Smith, S.A. & Weiss, D.J. (2002)
Idiopathic Immune-Mediated Hemolytic Anemia
(IMHA) In 25 Cats. Journal of Veterinary Internal
Medicine, 16, 350.
Kohn, B., Weingart, C., Eckmann, V., Ottenjann,
M. & Leibold, W. (2006) Primary immune-
mediated hemolytic anemia in 19 cats: diagnosis,
therapy, and outcome (1998-2004). Journal of
Veterinary Internal Medicine, 20, 159-166.
Shimoda, T., Shiranaga, N., Mashita, T. &
Hasegawa, A. (2000) A hematological study on
2006 World Congress WSAVA/FECAVA/CSAVA
360
Back to contents
thirteen cats with myelodysplastic syndrome.
Journal of Veterinary Medical Science, 62, 59-
64.
Stokol, T. & Blue, J.T. (1999) Pure red cell
aplasia in cats: 9 cases (1989-1997). Journal of
the American Veterinary Medical Association,
214, 75-79.
Weingart, C., Giger, U. & Kohn, B. (2004) Whole
blood transfusions in 91 cats: a clinical evaluation.
Journal of Feline Medicine and Surgery, 6, 139-
148.
Weiss, D.J. (2006a) Aplastic anemia in cats
- clinicopathological features and associated
disease conditions 1996-2004. Journal of Feline
Medicine and Surgery, 8, 203-206.
Weiss, D.J. (2006b) Evaluation of dysmyelopoiesis
in cats: 34 cases (1996-2005). Journal of the
American Veterinary Medical Association, 228,
893-897.

Fe - Feline Medicine
FELINE HAEMOPLASMA INFECTIONS
Dr. Séverine Tasker
Department of Clinical Veterinary
Science
University of Bristol
Langford
Bristol BS40 5DU
United Kingdom
S.Tasker@bristol.ac.uk
What are feline haemoplasmas?
The bacterium previously known as
Haemobartonella felis has now been renamed
Mycoplasma haemofelis (Mhf) due to its new
classification as a mycoplasmal organism. Mhf
and related erythrocytic mycoplasmal organisms
are collectively known as ‘haemoplasmas’.
Additional feline haemoplasma species have
been described; ‘Candidatus Mycoplasma
haemominutum’ (CMhm), first described in 1998,
and ‘Candidatus Mycoplasma turicensis’ (CMt),
first described last year in Switzerland (Willi, et
al 2006, Willi, et al 2005).
Prevalence of feline haemoplasmas
In worldwide prevalence studies CMhm is the
most abundant haemoplasma with CMt and Mhf
being less common, although some countries do
have a high prevalence of CMt. Studies have
found infection rates of 10-32.1% for CMhm,
1.4-6.4% for Mhf and 1.3-26% for CMt.
Pathogenesis of feline haemoplasmosis
Experimental CMhm infection rarely results
in significant clinical signs and anaemia is not
usually induced, although a fall in erythrocyte
parameters can occur. Anaemia may result in
retrovirus infected cats, although reports are
variable. In studies in naturally infected cats,
an association between anaemia and CMhm
infection is not usually found although one
study in Australian cats did find that CMhm
positive cats had significantly lower haematocrit
values than CMhm negative cats, although their
retrovirus status was not determined. CMhm-
associated anaemia has also been reported in a
cat undergoing chemotherapy for lymphoma. It is
possible that different CMhm isolates have varying
pathogenicity but CMhm should not be regarded
as being apathogenic. Interestingly a recent study
found a significant association between CMhm
infection and renal insufficiency (Willi, et al
2006). This association may have arisen because
older cats are both more likely to be infected with
Back to contents
Fe
CMhm and have renal insufficiency rather than it
being a causal relationship.
Mhf often results in a severe haemolytic anaemia
although the anaemia can be mild. Prevalence
studies in naturally infected cats have only
variably demonstrated associations between
anaemia and Mhf infection. This variation is
likely to be partly due to the different populations
of cats sampled in the studies and whether Mhf
infected cats were acutely or chronically infected.
It has been hypothesised that acute infection with
Mhf can result in severe haemolytic anaemia but
that chronically infected cats often lack clinical
signs and show no evidence of anaemia (Willi,
et al 2006).
CMt was first discovered in a Swiss cat with
a history of severe intravascular haemolytic
anaemia (Willi, et al 2005) and experimental
transmission of the CMt isolate to two SPF cats
resulted in anaemia in both cats. Many CMt
infected cats are also infected with CMhm (Willi,
et al 2006). A significant number of CMt infected
cats have been found to have concurrent diseases
such as neoplasia or FIV infection, suggesting
that co-factors and immunosuppression may be
important in the pathogenesis of disease with this
agent.
Haemoplasmas induce anaemia by haemolysis 2006 World Congress WSAVA/FECAVA/CSAVA
and sequestration. Positive Coombs’ tests and
autoagglutination have been reported in acute
haemoplasmosis cases indicating the presence
of erythrocyte-bound antibodies. We, and
others, have demonstrated the development of
cold reacting (IgM) antibodies in haemoplasma
infected cats during anaemic periods, and
these antibodies have disappeared following
resolution of the haemoplasma-induced anaemia
with antibiotic treatment, without the need for
glucocorticoid treatment.
Although most haemolysis is said to be
extravascular in nature (in the spleen, liver, lungs
and bone marrow), intravascular haemolysis has
also been reported. Splenic macrophages can also
remove haemoplasmas from the surface of the
erythrocytes (‘pitting’), returning unparasitised
361
Fe
cells back into the circulation. This may explain
the rapid increase in PCV, without reticulocytosis,
seen in some cats.
Carrier Cats
Cats which recover from infection may remain
chronically infected with haemoplasmas. Long-
term carrier status appears to be common following
CMhm infection, although suspected clearance of
infection has also been reported, with and without
antibiotic treatment (Willi, et al 2006). Mhf
infected cats often spontaneously clear infection
from peripheral blood after infection without
antibiotic treatment, and such clearance has also
been reported with CMt infection. Variation
exists in the long-term host-organism interaction.
In carrier cats reactivation of infection can occur
and may result in clinical disease (Foley, et al
1998), although this is probably quite rare.
Clinical Signs
The clinical signs seen with haemoplasma
infection depend upon a number of factors
such as the species involved, stage of infection,
whether the haemoplasma infection is primary
or secondary to another disease process or stress,
and the degree and speed of development of
the anaemia. Common clinical signs seen in ill
cats include anorexia, lethargy, dehydration,
weight loss and depression. Intermittent pyrexia
is often seen, particularly in the acute stages of
disease, as well as splenomegaly which may
reflect extramedullary haematopoiesis. Icterus is
uncommon.
Haematological Features
Pathogenic haemoplasma infection typically
causes a regenerative macrocytic hypochromic
anaemia. Significant reticulocytosis is not
always present. Normoblasts may be present.
2006 World Congress WSAVA/FECAVA/CSAVA
As mentioned above, positive Coombs’ tests and
autoagglutination may also occur.
Diagnosis
Diagnosis of haemoplasmosis used to rely on
demonstration of organisms on blood smears but
this method is known to have poor sensitivity and
specificity and is no longer recommended. The
polymerase chain reaction (PCR) assay is now
the diagnostic method of choice for haemoplasma
infection, being specific and sensitive if designed
and applied properly. PCR can amplify small
amounts of DNA so that previously undetectable
amounts become detectable. The sensitivity and
specificity of PCR assays should be made available
by laboratories offering them commercially,
so that their reliability can be evaluated by the
veterinarian. Laboratories undertaking PCR
362
Back to contents
should use appropriate positive and negative
controls to monitor for contamination or problems
with the PCR assay.
Conventional non-quantitative PCRs can detect
and distinguish feline haemoplasmas but real-
time quantitative PCRs can additionally quantify
haemoplasma DNA in blood samples (Tasker, et
al 2003). The Universities of Bristol, UK and
Zurich, Switzerland, have real-time PCR assays
available to detect and quantify all three feline
haemoplasmas in blood samples. Quantification
of the amount of haemoplasma DNA may help
determine the significance of the infection and
monitor response to treatment. Cats can become
negative by PCR during effective antibiotic
treatment (but it may take a number of days/
weeks for the haemoplasma levels to fall below
detection limits) but may become positive
again when antibiotic treatment is stopped
(Tasker 2002). Blood samples for haemoplasma
PCR should not be collected during antibiotic
treatment, although a strongly positive result will
indicate that the therapy is not being optimally
effective. PCR can detect chronically infected
and asymptomatic cats such that a positive PCR
result does not always correlate with the presence
of clinical haemoplasmosis.
Epidemiology
Recent studies looking at risk factors have
generally found that older male cats, with outdoor
access are more likely to be haemoplasma
infected. The increased incidence in male cats,
together with reports that cat bite abscesses and
outdoor roaming are risk factors, is suggestive
that horizontal transmission may occur via
fighting, and CMhm and CMt have both been
amplified from the saliva of infected cats (Dean,
et al 2005, Willi, et al 2006).
The influence of retroviral status is not fully
understood. A study of US feral cats found that
FeLV infection was associated with an increased
risk of co-infection with CMhm but not Mhf,
whereas FIV infection was associated with
an increased risk of co-infection with CMhm
and Mhf (Luria, et al 2004). However a Swiss
study failed to show any association between
retrovirus and haemoplasma infection. These
differing results may be due to differences in the
populations of cats sampled (for example feral
versus client owned) and it still seems prudent
to recommend FeLV and FIV testing in any cat
found to be haemoplasma infected.
The cat flea Ctenocephalides felis has been
incriminated in the transmission of haemoplasma
species in cats, and work has demonstrated
transient transmission of Mhf to a cat via the
haematophagous activity of Ct. felis (Woods, et
al 2005).

Treatment
Doxycycline (10 mg/kg/day PO) is probably
most commonly used to treat haemoplasma
infection but short courses (up to 21 days) have
not consistently eliminated infection. Longer
treatment courses (4-6 weeks) may be required for
clearance. Doxycycline appears to have activity
against all three feline haemoplasmas although
controlled studies have only been performed for
Mhf. Oesophageal strictures secondary to oral
doxycycline treatment have been reported so it
is recommended that oral doxycycline dosing be
followed by the administration of water by syringe,
or food, to encourage passage of the drug into the
stomach. Enrofloxacin treatment is also effective
against Mhf disease but clearance of infection, as
indicated by repeated negative PCR results, does
not always result. Diffuse retinal degeneration
and acute blindness have been reported following
enrofloxacin treatment in cats and doses higher
than the 5 mg/kg/day dose recommended by the
manufacturers should not be used. Imidocarb
dipropionate has been efficacious in some field
cases but a controlled study failed to show any
significant effect of imidocarb on either clinical
signs or haematological values in experimentally
infected cats. A four week course of
marbofloxacin, in recent studies at the University
of Bristol, did reduce Mhf copy numbers and treat
clinical disease, however consistent elimination
of infection was not demonstrated. Interestingly
CMhm did not show as favourable a response to
marbofloxacin treatment as Mhf. Future studies
should evaluate treatment regimes for each of the
feline haemplasma species.
The anaemia induced by haemoplasma infection
is in part immune-mediated and corticosteroids
have been recommended as adjunct therapy
(VanSteenhouse, et al 1993) although their value
in treatment is not proven. In our experience
clinically ill cats, including those that are Coombs’
positive, respond to antibiotic treatment alone
(Tasker 2002). Supportive care may be required,
including correction of dehydration with fluid
therapy and blood transfusion if the anaemia is
very severe.
References
Dean, R., Helps, C.R., Gruffydd-Jones, T.J.
& Tasker, S. (2005) Use of real-time PCR to
detect Mycoplasma haemofelis and ‘Candidatus
Mycoplasma haemomi nutum’ in the saliva and
salivary glands of haemoplasma-infected cats.
In: 48th Annual British Small Animal Veterinary
Association Congress. British Small Animal
Veterinary Association, Birmingham, UK.
Foley, J.E., Harrus, S., Poland, A., Chomel, B. &
Pedersen, N.C. (1998) Molecular, clinical, and
Back to contents
Fe
pathologic comparison of two distinct strains of
Haemobartonella felis in domestic cats. American
Journal of Veterinary Research, 59, 1581-1588.
Luria, B.J., Levy, J.K., Lappin, M.R.,
Breitschwerdt, E.B., Legendre, A.M., Hernandez,
J.A., Gorman, S.P. & Lee, I.T. (2004) Prevalence
of infectious diseases in feral cats in Northern
Florida. Journal of Feline Medicine and Surgery,
6, 287-296.
Tasker, S. (2002) Feline haemoplasmas -
detection, infection, dynamics and distribution.
In: PhD Thesis. University of Bristol, Bristol,
UK.
Tasker, S., Helps, C.R., Day, M.J., Gruffydd-
Jones, T.J. & Harbour, D.A. (2003) Use of Real-
Time PCR to detect and quantify Mycoplasma
haemofelis and ‘Candidatus Mycoplasma
haemominutum’ DNA. Journal of Clinical
Microbiology, 41, 439-441.
VanSteenhouse, J.L., Millard, J.R. & Taboada, J.
(1993) Feline haemobartonellosis. Compendium
of Continuing Education for the Practising
Veterinarian, 15, 535-545.
Willi, B., Boretti, F.S., Baumgartner, C., Tasker,
S., Wenger, B., Cattori, V., Meli, M.L., Reusch,
C.E., Lutz, H. & Hofmann-Lehmann, R. (2006)
Prevalence, risk factor analysis, and follow-up
of infections caused by three feline hemoplasma
species in cats in Switzerland. Journal of Clinical
Microbiology, 44, 961-969.
Willi, B., Boretti, F.S., Cattori, V., Tasker, S.,
Meli, M.L., Reusch, C., Lutz, H. & Hofmann-
Lehmann, R. (2005) Identification, molecular
characterisation and experimental transmission
of a new hemoplasma isolate from a cat with
hemolytic anaemia in Switzerland. Journal of
Clinical Microbiology, 43, 2581-2585.
Woods, J.E., Brewer, M.M., Hawley, J.R.,
Wisnewski, N. & Lappin, M.R. (2005) Evaluation
of experimental transmission of ‘Candidatus
2006 World Congress WSAVA/FECAVA/CSAVA
Mycoplasma haemominutum’ and Mycoplasma
haemofelis by Ctenocephalides felis to cats.
American Journal of Veterinary Research, 66,
1008-1012.
363
Fe
Fe - Feline Medicine
CLOTTING AND COAGULATION DISORDERS IN CATS
Dr. Séverine Tasker
Department of Clinical Veterinary
Science
University of Bristol
Langford
Bristol BS40 5DU
United Kingdom
S.Tasker@bristol.ac.uk

These affect the ability of the blood to coagulate.
Coagulation, the process of clot formation, is
achieved in vivo by a combination of primary and
secondary haemostasis (Stokol 2005). Although
clotting disorders usually refer to secondary
haemostatic disorders, primary haemostasis
will also be discussed briefly due to the close
integration and clinical need to differentiate
between the two.
OVERVIEW OF HAEMOSTASIS
Primary Haemostasis
This involves platelet adhesion, via Von
Willebrand factor (vWF), to the subendothelial
collagen, with ensuing activation and aggregation
of platelets, resulting in the formation of a
platelet plug. When platelets become activated,
phosphatidylserine (PS; previously platelet factor
3) becomes exposed on the platelet membrane and
acts as a scaffold for the assembly of coagulation
factors in secondary haemostasis. Thus primary
and secondary haemostasis are closely linked.
Primary haemostasis also involves an initial
reflex constriction of the blood vessel.
Secondary Haemostasis
This involves formation of fibrin by coagulation
factors to stabilise the primary haemostatic plug.
Classically secondary haemostasis has been
explained by the coagulation cascade which is
divided into intrinsic and extrinsic pathways
with a final common pathway (Figure 1). This
cascade is useful when interpreting diagnostic
haemostatic testing but does not reflect how
coagulation occurs in vivo. In vivo there is
extensive interaction between these pathways
with the extrinsic pathway (tissue factor) initiating
coagulation and the intrinsic pathway amplifying
it. Surface (or contact) activation is required for
in vitro clotting tests but is not required for in vivo
coagulation.

Figure 1: Schematic Diagram of Secondary Haemostasis for Test Interpretation

2006 World Congress WSAVA/FECAVA/CSAVA

364
Back to contents

Most coagulation factors are protease enzymes
which circulate in an inactive form. All
coagulation factors are synthesised in the liver.
The liver requires vitamin K for the synthesis of
Factors II, VII, IX and X.
Tertiary Haemostasis
Tertiary haemostasis consists of fibrinolysis to
break down the fibrin clot predominantly via the
action of plasmin cleaving fibrin.
Inhibitors
Limiting reactions ensure that clotting is localised
to the required area. Substances important
include antithrombin (AT) which, in association
with heparin, inactivates many of the coagulation
factors, and prostacyclin (PGI2), produced by
blood vessel endothelial cells, which inhibits
platelet aggregation and causes vasodilation.
APPROACH TO FELINE COAGULOPATHIES
History and Clinical Findings
Inherited disorders tend to present in younger
cats. It is important to find out the response of the
Table 1: Laboratory Investigation of Bleeding Disorders
Haemostatic Screening Test
Stage
Primary Platelet count (in-house estimation
Haemostasis from a blood smear*)
Buccal mucosal bleeding time
(BMBT)*
Secondary Activated clotting time (ACT)*
Haemostasis
Activated partial thromboplastin
time (APTT)
Prothrombin time (PT)
Thrombin time (TT)
* Tests which can be performed in-house.
Platelet Count Estimation
Automated cell counting machines can struggle
to count feline platelets, as described in the talk
on Thrombocytopenia. Any thrombocytopenia
should be confirmed by examination of a blood
smear.
BMBT
Since vessel wall disorders are quite rare, a
BMBT in a cat with a normal platelet count is
usually a test of platelet function. In cats with
coagulation defects the BMBT is usually normal,
Back to contents
Fe
cat to any previous trauma or surgery as severe
inherited disorders will usually have resulted in
bleeding complications. Information regarding
any bleeding problems in related animals should
be obtained. Recent exposure to toxins such as
rodenticides or drugs (e.g. aspirin, NSAIDs) that
can affect bleeding should be investigated.
Primary haemostatic disorders are characterised
by bleeding from mucosal surfaces (e.g.
haematuria, epistaxis), petechiae and prolonged
bleeding from cuts or venipuncture. Secondary
haemostatic disorders are characterised by more
severe bleeding into e.g. joints and body cavities,
haematomas, ecchymoses and delayed bleeding
from cuts.
Laboratory Investigation
Blood samples taken for the investigation of
bleeding disorders (Table 1) should be collected
before starting any therapy. Atraumatic
venipuncture, to avoid excessive activation of
haemostasis and local consumption of platelets,
is required together with appropriate sample
handling and submission.
Component Evaluated
Platelet number
Platelet (number and) function,
vessel abnormalities
Intrinsic & common pathways
Intrinsic & common pathways
but more sensitive than ACT
Extrinsic & common pathways 2006 World Congress WSAVA/FECAVA/CSAVA
Common pathway, quantifies
fibrinogen levels
but rebleeding may occur. A BMBT is carried
out under heavy sedation or general anaesthesia
using a spring-loaded bleeding time device which
makes a pair of standardized incisions in the
mucosa. Normal BMBT in cats is <3.3minutes.
ACT
Tubes for measurement of ACT are produced
commercially and contain diatomaceous earth to
act as the contact activator. Platelet phospholipid
is still required for coagulation so ACT is prolonged
in severe thrombocytopenia (<10x109/l). Clotting
365
Fe
factors must be <10% normal to prolong the
ACT. Blood is collected into the tube and the
tube inverted and the time taken for complete clot
formation recorded. Normal ACT in cats at room
temperature is <165 seconds. An ACT is also
available on the I-STAT analyser.
APTT and PT
These are usually carried out by commercial
laboratories using citrated blood (an accurate ratio
of 1:9 sodium citrate:blood is required). Samples
(usually cooled plasma) should be delivered to the
laboratory as soon as possible and samples from
a normal animal may be required as a control.
Clotting times >30% prolonged compared to
controls are considered abnormal. Individual
clotting factors need to be <30% before APTT
or PT are prolonged. Point of care coagulation
instruments (e.g. SCA2000) can determine the
APTT and PT on small amounts of fresh citrated
whole blood. These have been shown to be
reliable in dogs.
The APTT is more sensitive than the ACT and
not dependent on platelets. Since Factor VII (a
vitamin K-dependent factor) has the shortest half
life of all clotting factors, the PT will prolong
before the APTT in cases of vitamin K deficiency
or rodenticide toxicity.
TT
Not commonly performed but is prolonged in
cases of hypo- or dys-fibrinogenaemia, increased
fibrin degradation product levels or circulating
heparin as it assesses the formation of fibrin in
response to thrombin.
Specific Factor Assays
Deficiency of specific factors can be identified
by specialist laboratories although this can be
costly. The laboratory should be contacted for
submission requirements before the sample is
2006 World Congress WSAVA/FECAVA/CSAVA
taken.
ENCOUNTERED FELINE COAGULOPATHY
DISORDERS
Disorders of Primary Haemostasis
Thrombocytopenia, encountered reasonably
frequently in cats, is discussed in a later lecture.
Inherited thrombocytopathias are rarely described
in cats (Chediak-Higashi syndrome in Persians,
vWD), but hepatic, renal, neoplastic, infectious
(e.g. FIP) diseases, disseminated intravascular
coagulopathy (DIC) and drugs (e.g. aspirin) can
all cause acquired thrombocytopathias.
366
Back to contents
Disorders of Secondary Haemostasis
Inherited Disorders: The most common inherited
congenital coagulopathy in cats is Factor XII
(Hageman) deficiency (Brooks and DeWilde
2006). It is an autosomal recessive disorder
(affecting both males and females) that delays in
vitro activation of the APTT and ACT, causing
these to be prolonged (often markedly), but does
not result in bleeding in vivo. It has been reported
in the DSH, DLH and other breeds including
Siamese and Himalayan. Definitive diagnosis
rests on measurement of Factor XII activity. No
treatment is required.
Haemophilia A (Factor VIII deficiency) and
Haemophilia B (Factor IX deficiency) are sex-
linked autosomal recessive (affecting males
only) traits. In a recent study (Brooks and
DeWilde 2006) Haemophilia A and B were both
diagnosed in young cats (<1year) and were found
predominantly in DSH cats, although other breeds
have been affected e.g. Birman, Himalayan. All
haemophilic cats in this report had factor activities
of <5% of feline standard plasma and had shown
signs of bleeding: subcutaneous or intramuscular
haematomas, prolonged bleeding after neutering
and gingival bleeding from teeth eruption sites.
Haemophilic bleeding tendencies vary depending
on the factor activity present. Coagulation testing
reveals prolongation of the ACT and APTT,
although these (especially ACT) can be normal
if the factor deficiency is not severe. Definitive
diagnosis depends on measurement of Factor
VIII or IX activity.
Other inherited coagulopathies reported in cats
include combined Haemophilia A or B and
Hageman trait, Factor XI deficiency, and Factor I
(fibrinogen) ± XI deficiency in Maine Coons.
Treatment of factor deficiencies involves
replacement of the factors required. Fresh
whole blood transfusions are useful if anaemia
is present. Fresh (within 6 hours of collection)
frozen plasma contains active factors. Bleeding
cats should not be given intramuscular injections.
Avoidance of drugs with can impair haemostasis
is also important together with maintaining an
atraumatic life. Breeding should be avoided.
A hereditary vitamin K-responsive coagulopathy
in Devon Rex cats is associated with moderate
to marked decreases in the activity of Factors
II, VII, IX and X due to a defective vitamin K
metabolism enzyme. It affects both males and
females resulting in haematomas, haemarthrosis
and body cavity bleeding. APTT and PT are
markedly prolonged. These cases respond to oral
vitamin K1 at 5mg/kg/d.

Acquired Disorders: Liver disease is an important
cause of acquired coagulopathies in cats (Center,
et al 2000, Lisciandro, et al 1998) since the liver
synthesises clotting factors. Coagulopathies
can also arise in cholestatic liver disease in
which absorption of the fat soluble vitamin K is
impaired due to biliary stasis. Multiple abnormal
coagulation times can occur including prolonged
PT and APTT. Although abnormal coagulation
times are common with liver disease, clinical
signs of spontaneous bleeding are rare. Vitamin
K1 is helpful (0.5mg/kg SQ BID 2-3 times prior
to e.g. surgery, and every 7-21days thereafter) to
correct the PT and APTT. Hepatic lipidosis and
severe cholangiohepatitis cases can respond well
to vitamin K1 (Center, et al 2000).
Vitamin K deficiency also arises due to rodenticide
toxicity, although this is less common in cats than
dogs (Kohn, et al 2003). Cases present with
lethargy, inappetance, haematomas, dyspnoea
due to thoracic haemorrhage and/or collapse.
The PT prolongs before the APTT. Mild
thrombocytopenia may be present. Treatment
comprises vitamin K1 (2.5mg/kg SQ 1st day then
0.25-2.5mg/kg PO in divided doses) for at least
a week (up to 6weeks), with monitoring of the
PT 24 hours after stopping treatment to dictate
whether further treatment is required.
Vitamin K-responsive coagulopathies have
been reported in cats with malabsorption due
to inflammatory bowel disease or exocrine
pancreatic insufficiency.
Methimazole, used in the treatment of
hyperthyroidism, has been reported to affect
activation of vitamin K-dependent factors
although one retrospective study found evidence
to support this in only one of 20 methimazole-
treated cats (Randolph, et al 2000).
DIC arises due to the systemic activation of
haemostasis as a result of underlying disease
processes in the body. Platelets and factors
are involved in widespread clot formation
and fibrinolysis is activated. This results in a
thrombocytopenia, factor depletion (prolonged
PT and APTT), low antithrombin, and increased
D-dimers from breakdown of cross-linked
fibrin. Cases present with haemorrhage and/
or thrombosis. In cats DIC is most commonly
associated with neoplasia, liver disease and FIP
(Peterson, et al 1995).
FIV infection has been associated with
prolongation of the APTT due to an intrinsic
pathway problem although the cause of this has
not been identified (Hart and Nolte 1994).
Back to contents
Fe
REFERENCES
Brooks, M. & DeWilde, L. (2006) Feline Factor
XII Deficiency. Compendium on Continuing
Education for the Practicing Veterinarian, 28,
148-155.
Center, S.A., Warner, K., Corbett, J., Randolph,
J.F. & Erb, H.N. (2000) Proteins invoked by
vitamin K absence and clotting times in clinically
ill cats. Journal of Veterinary Internal Medicine,
14, 292-297.
Hart, S.W. & Nolte, I. (1994) Hemostatic disorders
in feline immunodeficiency virus-seropositive
cats. Journal of Veterinary Internal Medicine, 8,
355-362.
Kohn, B., Weingart, C. & Giger, U. (2003)
Haemorrhage in seven cats with suspected
anticoagulant rodenticide intoxication. Journal
of Feline Medicine and Surgery, 5, 295-304.
Lisciandro, S.C., Hohenhaus, A. & Brooks, M.
(1998) Coagulation abnormalities in 22 cats
with naturally occurring liver disease. Journal of
Veterinary Internal Medicine, 12, 71-75.
Peterson, J.L., Couto, C.G. & Wellman,
M.L. (1995) Hemostatic disorders in cats: a
retrospective study and review of the literature.
Journal of Veterinary Internal Medicine, 9, 298-
303.
Randolph, J.F., DeMarco, J., Center, S.A.,
Kantrowitz, L., Crawford, M.A., Scarlett, J.M. &
Brooks, M. (2000) Prothrombin, activated partial
thromboplastin, and proteins induced by vitamin
K absence or antagonists clotting times in 20
hyperthyroid cats before and after methimazole
treatment. Journal of Veterinary Internal
Medicine, 14, 56-59.
Stokol, T. (2005) Disorders of haemostasis. In:
BSAVA Manual of Canine and Feline Clinical
Pathology (ed. by E. Villiers & L. Blackwood),
pp. 83-98. BSAVA, Gloucester.
2006 World Congress WSAVA/FECAVA/CSAVA
367
Fe
Fe - Feline Medicine
FELINE BLOOD TYPING AND TRANSFUSION – A PRACTICAL
APPROACH
Barbara Kohn, Prof. Dr. med.vet.,
Dipl ECVIM-CA
Clinic for Small Animals
Free University of Berlin
Oertzenweg 19b
14163 Berlin
kohn@vetmed.fu-berlin.de
The most common reason for blood transfusions
in the cat are anemias due to blood loss (mostly
acute, rarely chronic), intra- or extramedullary
mediated ineffective erythropoiesis or hemolysis.
The decision whether a blood transfusion is
indicated depends on the hematocrit (Hct). A
RBC transfusion is recommended for critically
ill cats if the Hct falls below 10-15%. However,
even more important is the general condition of
the patient: parameters like tachycardia, weak
pulse, prolonged capillary refill time, lethargy,
and weakness are indicators for the need of a
transfusion. In cases of acute anemia or if the
animal needs surgery, blood transfusions are
given at higher Hct values. Cats with a chronic
anemia tolerate a low Hct better than those with
an acute anemia.
The most important blood group system in cats
is the AB system with the blood groups A, B,
and AB which is biochemically not related to the
human AB0 system. Recently, another erythrocyte
antigen has been described in a Domestic shorthair
cat, the so-called Mik antigen.
In European and American short- and longhair
cats the blood group A is dominating. The
2006 World Congress WSAVA/FECAVA/CSAVA
percentage of cats with this blood group varies
geographically between 73.7 and 100%. In
purebred cats the frequency of blood group B
varies. There are breeds in which type B cats have
not been reported (Siamese, Burmese, Russian
Blue, Tonkinese) or have been found between
1-10% (Maine Coone, Norwegian forest cat),
11-20% (Abyssinian, Birman, Persian, Somali,
Sphinx, Scottish Fold), and 20-45% (Exotic and
British shorthair, Cornish and Devon rex). The
third blood group AB is very rare in pedigree and
non-pedigree cats (e.g. in Germany 0.7%).
Cats possess, unlike dogs, naturally occurring
antibodies (alloantibodies) against the blood
group they are lacking. Cats of blood type B have
strong hemagglutinating antibodies of the IgM
type against type A cells, and cats of blood type
A have weak hemolysin and hemagglutinating
368
Back to contents
Christiane Weingart, Dr. med. vet.
Clinic for Small Animals
Free University of Berlin
Oertzenweg 19b
14163 Berlin
antibodies of the IgM and IgG type against type
B cells. Kittens of both blood groups have no
antibodies against other blood groups during
the first weeks of life. Plasma of type AB cats
of all ages does not contain anti-A or anti-B
antibodies.
Prior to blood transfusion in cats blood typing
of donor and recipient is strongly recommended
since naturally occurring alloantibodies can
lead to incompatibility reactions in case of
incompatible transfusions. Cats with blood type
B which receive type A blood may develop a
severe acute hemolytic transfusion reaction
with clinical signs such as lethargy, bradycardia,
dyspnea, cardiac arrhythmia, salivation, vomitus,
defecation and urination, and neurological
disorders. Death might occur during this phase.
If the cats survive they develop tachycardia,
tachypnea, hemoglobinemia, and hemoglobinuria.
Receive type A cats blood of type B cats, only
mild incompatibility reactions like restlessness,
tachycardia, and tachypnea can be observed.
However, the transfusion is not efficient due to a
rapid destruction of erythrocytes. Therefore, type
A cats may only receive type A blood and type B
cats only type B blood. Type AB cats, which have
no antibodies, may be transfused with blood of
the blood types AB or A.
These alloantibodies are also important for
breeders since type A kittens born to a type B
queen are at risk for neonatal isoerythrolysis.
For blood typing a test card method suitable for
practice (Rapid Vet®H Feline, DMS laboratories,
Flemington, NJ) has been developed. In case
of spontaneous agglutination of the patient’s
erythrocytes, blood typing is only possible if the
agglutination is not persisting after washing the
RBC with physiological saline. Recently, a new
gel containing tube system for the identification
of blood types has been introduced (DiaMed-
VET®, Cressier Morat, Switzerland).
If blood type B is suspected the so-called “back
typing” can be performed for confirmation:

EDTA blood of the proband is being centrifuged
at 1000 g for 2 minutes; 30 µl of the plasma is
mixed with 15 µl EDTA whole blood of a type
A cat on a glass slide. Agglutination confirms
blood type B.
If blood typing is not possible, a blood
crossmatching (BCM) can be performed in case
of emergency. While blood typing tells which
type of antigens are on a red cell, BCM detects
the donor and recipient antibody compatibility
or incompatibility. The major CM tests the
recipient plasma against the donor cells, while
the minor CM tests the donor plasma against
the recipient cells. If there is agglutination, then
the two individuals are incompatible. In case
of autoagglutination a crossmatch can not be
performed. BCM does not prevent sensitization
to RBC antigens, which may result in a hemolytic
reaction during future transfusions, because it
detects only antibodies that are currently present
in the donor or recipient.
If cat plasma is administered it should be the
same blood type as the recipient.
In case of an identical AB blood type of donor
and recipient the BCM should turn out negative.
However, especially for cats which had been
transfused several times incompatibilities have
been described despite AB compatibility. A BCM
is recommended in these (multiple) transfused
cats.
BCM procedure: After gentle centrifugation
(1000 g, 2 min) plasma and RBC of donor and
recipient are separated. Plasma and the RBC
suspension are mixed on glass slides according
to the following scheme: major – 50 µl (2 drops)
recipient plasma + 25 µl donor RBC; minor – 50 µl
donor plasma + 25 µl recipient RBC; recipient
control for autoagglutination – 50 µl recipient
plasma + 25 µl recipient RBC.
Donor cats should be healthy, adult, large, with a
pleasant disposition, no history of a former blood
transfusion, and slender so that the jugular veins
are easily accessible. The cats must have an Hct
> 30%, best > 35%. After a clinical examination,
a CBC and clinical chemistry (mainly renal and
liver parameters) should be performed before
blood donation. In order to ensure the absence
of infectious agents such as FeLV, FIV, and
hemotrophic mycoplasma, the tested blood
donors should be owned by the clinic or in the
case of “voluntary” donors should solely kept
indoors. Control of ectoparasites is important
in donor cats. Testing for Bartonella henselae,
Cytauxzoon felis, ehrlichia and babesia should be
considered if cats have been in endemic areas.
The entire blood volume of the (slender) cat
amounts to approx. 66 ml/kg and 10% of the blood
volume can be collected from healthy cats without
Back to contents
Fe
side effects. After blood donation, the cats should
be monitored and infused subcutaneously (approx.
20 ml/kg Ringer’s lactate) or intravenously
(especially if larger amounts of blood have been
taken). If cats donate regularly every 3-4 weeks,
an oral iron supplementation is recommended.
Taking blood from cats is best performed from
the jugular vein after clipping and disinfection.
Sedation is necessary in most cases (e.g. ketamine
5-6 ml/kg body weight mixed with midazolame
0.5 mg per cat IM). Blood can be taken via plastic
syringes which contain 1 ml 3.13% sodium citrate
per 9 ml of blood and which are connected with
a 19-gauge butterfly needle (“open system”). The
blood should preferably not be stored for longer
than 24 hours in the refridgerator if collected by
an “open system”.
If the blood is needed for transfusion immediately
or within 8 hours, sodium citrate can be used as
anticoagulant. For longer storage CPDA-1 (1.2 ml
CPDA-1 per 8.8 ml blood) withdrawn from a
blood bag port using a syringe should be used as
anticoagulant.
The principle of component therapy consists in
dividing whole blood into its single elements by
centrifugation. The small blood volume collected
and the difficulties in separation of blood
elements make fresh whole blood transfusions
the norm in feline patients. Clinically significant
disorders of primary and secondary hemostasis
and hypoalbuminemia are rarer in cats than in
dogs and, therefore, the need for plasma and
platelet products is significantly smaller.
Transfusion: Blood which is collected in syringes
can be transferred into 150 ml transfer bags or in
empty physiological saline infusion bottles. The
transfusion is being administered with a special
transfusion set with an incorporated micro filter
(sizes of pores approx. 170 µm).
Initially, the blood should be transfused very
slowly (2-3 ml over 5 minutes); the patient
needs to be monitored for signs of incompatibility.
2006 World Congress WSAVA/FECAVA/CSAVA
Subsequently, depending on the status of the recipient
the transfusion rate is increased. Normovolemic cats
can receive up to 10 ml/kg/hour, cats with cardiac
insufficiency have to be transfused very slowly
(1-4 ml/kg/hour). In massive hemorrhage, the
transfusion should be given as rapidly as possible.
The transfusion should be completed within
4 hours of initiation because of the risk of bacterial
growth. To dilute the blood and thus regulating
the velocity of transfusion more exactly and in
order to wash the small amount of blood entirely
out of the bag only physiological saline can be
used.
The transfusion volume depends on the Hct and the
general condition of the patient, in cats, however,
it often depends on the amount of blood which
369
Fe
is available. Based on a donor’s Hct of 37%, the
Hct of the recipient can be increased by approx.
1% with a transfusion of 3 ml whole blood per kg
body weight, provided that no further blood loss
exists. Cats with coagulopathy receive plasma at
a dosage of about 10 ml/kg.
Transfusion reactions (TR) mostly appear during
or shortly after the transfusion and can be caused
by every component of the blood. However,
altogether they are rare (1.2% of 163 whole blood
transfusions at the Clinic for Small Animals,
FU Berlin) and often mild. By following the
transfusion guidelines with reference to donor
selection, blood typing, blood storage, and
administration, most transfusion reactions can be
prevented.
TR can be divided into acute immunologic (acute
hemolytic reaction, febrile nonhemolytic reaction,
urticaria, head edema), acute nonimmunologic
(electrolyte disturbances – hypocalcemia
due to citrate intoxication, hyperkalemia,
hypomagnesemia; embolism; endotoxic shock;
circulatory overload; contamination of blood
– bacteria, protozoa, spirochetes; physical
damage – freezing, overheating; hypothermia;
vomitus), delayed immunologic (delayed
hemolytic reaction, posttransfusion purpura),
delayed nonimmunologic (infectious disease
transmission – e. g. FeLV, FIP, FIV, bartonellosis,
hemotrophic mycoplasma). Acute TR occur
during or within a few hours after a transfusion,
and delayed reactions occur after completion
of the transfusion. The delay may be months to
years, delayed reactions have not been reported
in the cat.
If TR occur, the transfusion should be
stopped. The serum and urine of the patient
should be examined for hemoglobinemia and
hemoglobinuria. A sample of the erythrocyte
product should be examined for signs of in
vitro hemolysis and a microbiological analysis
2006 World Congress WSAVA/FECAVA/CSAVA
should be performed. Repeating the blood
typing of donor and recipient and repeating
the crossmatching might be indicated. Severe
transfusion reactions with signs of shock should
370
Back to contents
be treated with intensive fluid therapy and with
glucocorticoids (e.g. methylprednisolone succinate
20 mg/kg IV, once). High fever can be treated
with cooling and antipyretics (e.g. metamizol
20 mg/kg slowly IV). In case of erythema or
urticaria antihistaminergic drugs (diphenhydramine
2 mg/kg IV) and / or anti-inflammatory doses of
glucocorticoids (prednisolone 0.5 mg/kg) should
be applied. In the case of vomitus antiemetics
are recommended. Do the transfusion reactions
subside and no hemolysis exists, the transfusion
may be restarted at a slower rate and the recipient
observed carefully.
An alternative for RBC transfusion is the
application of a hemoglobin-based oxygen-
carrying (HBOC) fluid, Oxyglobin® (Biopure
Corporation, Cambridge, USA). This is an
ultrapurified polymerized hemoglobin of bovine
origin in a modified Ringer’s lactate solution
which is licensed for dogs in Germany but not yet
for cats. The small size of the molecules produces
an equal distribution within the vascular system,
yet also a fast passage of the renal glomeruli so
that the plasma half-life only lasts 30-40 hours.
Blood typing and crossmatching is not necessary
because the RBC membrane, which is the major
cause of transfusion incompatibility, has been
removed during the manufacturing process.
A further advantage compared to blood is the
storage time of 3 years at room temperature. We
recommend for cats a dosage of 5-7.5 ml/kg, the
infusion rate should not exceed 5 ml/kg/hour.
Especially in cats with cardiopulmonary disease,
overexpansion of the vascular volume can lead
to pulmonary edema and pleural effusion. Other
possible side effects are a discoloration of the
mucous membranes, sclera, urine and skin,
vomitus, and neurological signs. Moreover,
a dark red discoloration of urine and plasma
leads to invalidity of colorimetric laboratory
measurements. While the concentration of plasma
hemoglobin rises, the Hct may be decreased after
the infusion due to hemodilution and cannot
be used as parameter to monitor course of the
anemia.

Fe - Feline Medicine
PROTEINURIA AND MICROALBUMINURIA IN CATS
Dr Andrew H. Sparkes BVetMed
PhD DipECVIM-CA MRCVS
Animal Health Trust
Newmarket, Suffolk, UK
Andy.sparkes@dsl.pipex.com
Urine produced by a healthy kidney contains little
protein, as these molecules are largely retained at
the level of the glomerulus due to their size and/
or charge. Small proteins or amino acids that do
pass through the normal glomerulus are mostly
reabsorbed by renal tubules, or degraded by tubular
epithelial cells. Persistently increased proteinuria
is an abnormal finding, and in the absence of
lower urinary tract disease may reflect either
altered glomerular permeability, reduced tubular
re-absorption; increased secretion of proteins
from tubular epithelial cells or, less commonly,
overflow from the circulation if there is raised
serum levels of low-molecular weight proteins).
Alterations in glomerular permeability may occur
in primary glomerular disease (amyloidosis,
immune-mediated glomerulonephritis, hereditary
glomerulonephropathies) or as a result of
glomerular capillary hypertension, or endothelial
cell dysfunction.
Proteinuria (in the absence of lower urinary tract
disease) is therefore usually a marker of renal
damage or dysfunction (glomerular or tubular),
although this may result from either primary or
secondary renal disease. In human beings, most
cases of renal failure occur secondary to diabetes
mellitus or essential hypertension, and there
is considerable interest in the potential role of
proteinuria as a cause, as well as an indicator,
of progressive renal damage. Proteinuria may
be measured quantitatively over 24 hours,
or more simply by a random urine protein to
creatinine (UPC) ratio (the two showing a close
correlation in both humans and cats). However,
evidence in humans suggests that early increases
in albuminuria (microalbuminuria, MA) reflect
glomerular damage undetectable by the traditional
UPC ratio, and may serve as both a negative
prognostic marker and also potentially contribute
to renal damage in cases of renal failure, although
MA may also be found in conditions affecting
glomerular function other than renal failure. In
man, MA is defined as an albumin to creatinine
ratio (expressed as mg albumin/g creatinine)
in the range 30-300, which equates to urinary
Back to contents
Fe
Ellie J. Mardell MA VetMB
CertSAM MRCVS
Animal Health Trust
Newmarket, Suffolk, UK
albumin loss of 20-200 µg/min. Smaller losses
are within normal ranges and greater losses are
detectable by the UPC ratio (overt proteinuria).
Monitoring for MA is encouraged in patients
at risk of renal disease in order to allow early
therapeutic intervention.
In the veterinary field, significant renal-origin
proteinuria has been demonstrated in association
with a variety of underlying conditions in dogs,
and there is evidence to suggest that in cases
of canine chronic renal failure, proteinuria is a
negative prognostic indicator, with a number of
recent studies also evaluating MA in dogs. In the
cat, a UPC ratio >0.4-0.5 is accepted as abnormal
proteinuria. Proteinuria has been shown to occur in
cats with immune-mediated glomerulonephritis,
multiple myeloma, acute renal failure, chronic
renal failure, hyperthyroidism acute pancreatitis,
drug reactions and hypertension. There is also
preliminary evidence that higher levels of
proteinuria correlate with reduced survival times
in cats with or without renal failure.
Much less is known about the occurrence
and significance of MA in the cat though. A
commercial semi-quantitative ELISA-based test
for the measurement of feline MA is available,
but normal urine albumin concentrations have
not been well established for feline patients. 2006 World Congress WSAVA/FECAVA/CSAVA
One brief report suggests that healthy cats may
have an age-related increase in urinary albumin
concentrations, and that cats with a wide range
of medical conditions may also have elevated
MA measurements. However, the fact that
tubulointerstitial disease (rather than glomerular
disease) tends to dominate in feline renal failure
raises important doubts over any assumptions that
the interpretation of MA in cats will necessarily
be the same as in humans.
In this study, proteinuria was assessed in 100
randomly selected sick cats and 22 healthy cats
by means of the urine protein:creatinine ratio,
a traditional urine ‘dipstick’ and a commercial
ELISA-based dipstick designed to detect
microalbuminuria (MA) semi-quantitatively. In
addition the repeatability and reproducibility of
371
Fe
the MA test was assessed by comparing results of
five replicate tests of 26 urine samples, interpreted
by two different readers. Discrepancies existed
in the replicate test results in 23% and 27% of the
samples examined by reader 1 and 2 respectively,
and on several occasions this discrepancy was
between whether the sample was ‘positive’ or
‘negative’ for MA. The inter-reader agreement
was good (κ=0.75), but again discrepancies were
noted and part of the reason for these problems
appeared to be the necessity for subjective
interpretation of colour changes when reading test
results. Proteinuria was significantly (P≤0.014)
more prevalent in the sick than the healthy cats
with 36% and 9% respectively having detectable
MA, 34% and 5% respectively having a UPC
ratio >0.5, and 84% and 9% respectively having
2006 World Congress WSAVA/FECAVA/CSAVA
372
Back to contents
positive urine protein dipstick analysis. There
was a moderate significant correlation between
UPC ratio and MA concentrations (rs=0.68,
P<0.0001). While 13/87 cats with a UPC ratio≤
≤0.5 had positive MA results, 10/84 cats with
negative MA results had a UPC ratio >0.5, and
none of these had evidence of lower urinary
tract disease. This study confirmed that MA and
proteinuria are commonly seen in cats with a
variety of diseases, but they are not necessarily
both elevated, and the UPC ratio can be elevated
with negative MA results. Furthermore, some
repeatability problems were demonstrated with
the semi-quantitative MA test. These findings
demonstrate that the semi-quantitative MA test
should not be relied on as the sole determinant
of proteinuria.

Fe - Feline Medicine
THROMBOCYTOPENIA IN CATS
Barbara Kohn, Prof. Dr. med.vet.,
Dipl ECVIM-CA
Clinic for Small Animals
Free University of Berlin
Oertzenweg 19b
14163 Berlin
kohn@vetmed.fu-berlin.de
Hemostasis is a complex interaction between
platelets, blood vessels and the coagulation
cascade. The goal of hemostasis is to form a
clot. Effective primary hemostasis depends
on adequate platelet numbers, adequate
platelet function, vessel wall integrity, and von
Willebrand factor. Bleeding disorders related to
primary hemostasis are mainly related to platelets
and rarely to vessels. Platelet disorders may be
quantitative (thrombocytopenia) or qualitative
(thrombopathia). Thrombocytopenia is the most
common primary hemostatic defect.
In cats, decreased platelet counts are a common
laboratory finding. However, this is often a so-
called pseudothrombocytopenia (incorrect low
platelet values) which can occur with automated
counting of platelets. It is related to the tendency
for feline platelets to aggregate and the size of
some of the platelets that in this species can be
similar to the size of red blood cells. Therefore,
manual counting (e.g. using Thrombo Plus®-
tubes, Sarstedt and a Neubauer counting
chamber) or slide evaluation must always be
done to confirm whether the thrombocytopenia
is real or artifactual. For blood sampling it is
advisable to collect the initial 1-2 ml of blood for
clinical chemistry. The following blood is then
collected in K-EDTA tubes for hematological
evaluation. The EDTA- tubes should be carefully
checked for small blood clots and the counting
of thrombocytes should be completed within
30 minutes, if possible. Studies have shown that
estimation of platelet numbers on stained blood
smears is reliable over a wide range of platelet
counts in cats. Each platelet per oil immersion
field represents a circulating platelet count of
approximately 20,000/µl. Obvious platelet
clumps in the blood smear, however, prevent
accurate determination of the platelet number per
oil immersion field.
A reduced production, increased destruction or
increased utilization of platelets, sequestration
in the spleen, or a combination of these
pathomechanisms can cause thrombocytopenia.
Back to contents
Fe
Clinical studies evaluating the causes for
thrombocytopenia in cats are infrequently found
in the literature.
The prevalence of feline thrombocytopenia
(< 200,000 platelets/µl) at North Carolina
State University from 1985 to 1990 was 1.2%
(41/3300). Cats were divided into six categories
based on clinical diagnoses: 29% had infectious
disease (e.g. FeLV, FIV, FIP), 20% had neoplasia
(e.g. leukemia, lymphoma, hemangiosarcoma),
7% had cardiac disease, 2% had primary
immune-mediated disease, 22% had multiple
diseases (e.g. FeLV, lymphoma, leukemia), and
20% had disorders of unknown etiology. The
mean platelet count for all thrombocytopenic
cats was 52,000/µl with a range of 1000-190,000/µl.
No significant differences were found between
groups with respect to platelet count. Disseminated
intravascular coagulopathy was diagnosed in
12% of the cats.
In a study performed at the Clinic for Small
Animals, FU Berlin, the following diagnoses were
established in 63 cats with thrombocytopenia
(platelet counts 10,000 – 179,000/µl, median
83,000): 17 cats had viral infections (7 FIP,
3 FeLV, 4 FIV, 3 feline rhinitis), 16 had
aseptic inflammation (4 fat necrosis, 4 trauma,
2 pancreatitis, 2 FLUTD, 2 hepatitis, 1 nasal polyp,
2006 World Congress WSAVA/FECAVA/CSAVA
1 gastric ulcer), 10 had neoplasia (6 lymphoma,
2 leukemia, 1 fibrosarcoma, 1 hemangiosarcoma),
6 had bacterial infections (2 pneumonia, 1 cystitis,
1 pyelonephritis, 1 abscess, 1 pyometra), 3 had bone
marrow disease (aplasia), 3 immune-mediated
disease (1 immune-mediated hemolytic anemia,
1 primary immune-mediated thrombocytopenia,
1 Evans’ syndrome), 4 cats had other diseases
(1 renal failure, 1 hyperthyroidism/ cardiomyopathy,
2 hepatopathy), and 4 were random findings
(routine check-up).
Other reasons for feline thrombocytopenia
mentioned in the literature are drugs, e.g.
propylthiouracil, methimazole, griseofulvin,
albendazole, chloramphenicol, cytotoxic drugs
(doxorubicin, carboplatin, azathioprin etc.) and
373
Fe
infections with parvovirus, Ehrlichia risticii,
Anaplasma phagocytophilum, Babesia felis,
Mycoplasma spp., Cytauxzoon felis, Histoplasma
capsulatum.
Based on these data one of the main causes
of thrombocytopenia in cats are viral
infections. The mechanisms associated with
thrombocytopenia during a viral infection may
be multifactorial and vary with the agent. Virus
induced thrombocytopenia may be caused
by inhabiting precursor cells, thus reducing
megakaryocytopoiesis, direct platelet damage
or lysis by the virus itself, removal of platelets
by the mononuclear phagocytic system, or by
disseminated intravascular coagulation (DIC).
Immune-mediated destruction of the platelets can
be a contributing factor.
Inflammatory diseases are another important
cause for decreased platelet counts in cats. In
inflammatory disease states interactions of
platelets with altered or damaged endothelial
surfaces cause extensive platelet activation,
clumping, and removal of platelets by the
mononuclear phagocytic system. Platelet
destruction in bacterial infections can occur as
a result of platelet adherence or aggregation to
activated monocytes or neutrophils. Exotoxins
may directly damage platelets and contribute to
thrombocytopenia. Immune-mediated destruction
might contribute to thrombocytopenia in different
infectious diseases.
In neoplastic disease there is a wide variety
of pathomechanisms that may cause
thrombocytopenia: Platelets may be sequestered
in the spleen, liver, or the tumor as such;
consumption of platelets may be increased (e.g.,
due to DIC); they may be destroyed by immune
reactions, and production may be reduced due to
bone marrow involvement.
In cats primary or secondary immune-mediated
thrombocytopenia have rarely been described
2006 World Congress WSAVA/FECAVA/CSAVA
or characterized. ITP occurs as a primary or
idiopathic (pITP) and as a secondary (sITP)
form In sITP, infections, other immune-mediated
diseases (e.g., systemic Lupus erythematosus),
drugs, neoplasias, blood transfusions, or
vaccination may trigger an increased production
of antibodies which may adhere to or cross react
with platelet receptors causing an increased
destruction of platelets by the mononuclear
phagocytic system. The diagnosis of a primary
ITP in cats is based as in other species on the
exclusion of underlying diseases, the presence of
a mostly severe thrombocytopenia, the response
to immunosuppressive therapy, and the presence
of platelet-bound antibodies (PBA). For cats,
little information is available on the application of
direct or indirect methods to detect platelet-bound
374
Back to contents
or anti-megakaryocytic antibodies to evaluate
immunological factors in the pathogenesis of
thrombocytopenia. Recently we have described
flow cytometry for evaluation of PBA in cats.
The advantage of flow cytometry over other
methodologies is the small amount of blood
required and even in severely thrombocytopenic
animals enough platelets can be recovered
for reliable evaluation. Little denaturation of
antigens and antibodies on the platelet membrane
occurs as there is minimal sample handling and
manipulation.
Platelet-bound antibodies may be antiplatelet
auto-antibodies, but could also represent
‘secondary’ antibodies. The latter include
immune complexes, which are bound to platelet
Fc receptors, antibodies against platelet antigens,
which are formed by modification of the antigen
(e.g., caused by disease), or antibodies which
bind to antigens, which were adsorbed by the
surface of thrombocytes (e.g., tumor antigens,
drug metabolites).
Direct PBA testing was performed in
42 thrombocytopenic cats (platelet counts
60,000-179,000/µl, median 56,000/µl). Of
these 42 cats, 19 had positive PBA test results,
17 of which were considered to have secondary
immune-mediated thrombocytopenia (sITP).
Underlying diseases included fat necroses (4), FIP
(3), FeLV (2) or FIV (2) infections, lymphoma
(2), leukemia (1), hepatitis (1), pyelonephritis
(1), or hyperthyroidism/cardiomyopathy (1). In
2 cats, no underlying disease was found suggesting
a primary immune-mediated thrombocytopenia
(pITP). The PBA test was negative in 23 cats
diagnosed with varying underlying diseases and
in 47 healthy control cats with platelet values
within the reference range. These data suggested
that immune-mediated destruction of platelets
might be an important pathologic mechanism
for feline thrombocytopenia caused by various
underlying diseases.
In humans and small animals, spontaneous
bleeding occurs rarely at platelet values >
> 20 – 30,000/µl if they do not suffer from
thrombocytopathia or a coagulopathy in addition.
In a study 7 out of 63 cats with thrombocytopenia
displayed spontaneous bleeding. Platelet
counts in these bleeding cats ranged from
10,000 – 57,000/µl, median 34,000/µl. 13 of
63 cats had platelet counts < 30,000/µl, 10 of these
13 cats displayed no clinical signs of hemorrhage.
The 7 bleeding cats exhibited mainly surface
bleeding: bleeding of the gums (4), petechiation
(4), epistaxis (1), retinal and scleral hemorrhage
(1). Two cats had hematomas, and one cat had
abdominal bleeding. The diagnoses in these 7 cats
were FIV (3), primary ITP (1), Evans’ syndrome (1),

leukemia (1), megakaryocytic/erythrocytic aplasia
of unknown cause (1). Of the 7 cats suffering
from spontaneous bleeding examined in our
study, 5 resulted PBA test positive; 3 of 5 had
platelet counts > 30,000/µl. It was shown in
humans, that PBA may alter the shape, volume,
and morphology of thrombocytes, which may
interfere with their function.
In another study, 9 out of 41 cats showed
spontaneous hemorrhage. Bleeding was related to
platelet values below 30,000/µl, and occurred in
cats suffering from neoplasia (n = 5), infections
with FeLV (2), pITP (1), or associated to an
Eisenmenger’s syndrome (1).
If bleeding occurs or not is not only dependent
of the number of platelets but also of their age
and functionality and of the vascular integrity.
Cats might be able to tolerate very low platelet
counts without showing spontaneous bleeding.
This could be explained by thrombocytes of cats
being activated more easily than those of dogs.
Feline platelets are stimulated more readily
by aggregation inductors, such as collagen or
thrombin, than those of dogs. Activation of
thrombocytes results in the release of serotonin.
It was shown that dense-granules of cats contain
3 or 1.5 times the amount of serotonin compared
to dense-granules of humans or dogs, respectively.
Serotonin is a potent vasoconstrictor and induces
primary aggregation of platelets. In addition,
serotonin will potentiate the aggregation effect of
other agonists.
Therapeutic approach in cats with
thrombocytopenia depends on the underlying
disease. Patients with severe thrombocytopenia
should always be closely monitored for critical
bleeding. Transfusion of platelets is most
beneficial in thrombocytopenia caused by
decreased platelet production, where the platelet
life span is normal. It is less beneficial with
increased consumption and sequestration and least
beneficial in ITP, where transfused platelets may
be rapidly destroyed. A review of transfusions at
the author’s clinic revealed that of 91 transfused
cats four were transfused because of blood
loss due to severe thrombocytopenia (Evans’
syndrome, ITP, FIV infection, leukemia). In cats
with acute hemorrhage due to thrombocytopenia
or if surgery is necessary transfusions with fresh
whole blood are recommended. If fresh whole
blood is used, a rule of thumb is to transfuse
10 ml/kg, although resources may dictate a smaller
dose. This amount will raise the recipient platelet
count by a maximum of approx. 10,000/µl.
Back to contents
Fe
References
Abrams-Ogg ACG (2003) Triggers for prophylactic
use of platelet transfusions and optimal platelet
dosing in thrombocytopenic dogs and cats. Vet
Clin North Am Small Anim Pract 33, 1401-
1418.
Hart S, Nolte I (1991) ZurThrombozytenaggregation
bei der Katze. Tierärztl Prax 19, 413-418.
Jordan HL, Grindem CB, Breitschwerdt EB
(1993) Thrombocytopenia in cats: a retrospective
study of 41 cases. J Vet Intern Med 7, 261-265.
Kohn B, Linden T, Leibold W (2006) Platelet-
bound antibodies detected by a flow cytometric
assay in cats with thrombocytopenia. J Feline
Med Surg (in press)
Linden T (2004) Thrombozytopenie bei der
Katze unter besonderer Berücksichtigung der
immunvermittelten Thrombozytopenie – eine
prospective Studie (Januar 1999 – Juni 2000). Vet
Med Dissertation, Free University of Berlin.
Meyers KM, Holmsen H, Seachord CL (1982)
Comparative study of platelet dense granule
constituents. Am J Phys 243, 454-461.
MoritzA, Hoffmann C (1997) Thrombozytenzählung
bei der Katze. Tierärztl Prax 25, 695-700.
Severine T, Cripps PJ, Mackin AJ (1999)
Estimation of platelet counts on feline blood
smears. Vet Clin Pathol 28, 42-45.
Weingart C, Giger U, Kohn B (2004) Whole blood
transfusions in 91 cats: a clinical evaluation. J Fel
Med Surg 6, 139-148.
Zelmanovic D, Hetherington EJ (1998) Automated
analysis of feline platelets in whole blood,
including platelet count, mean platelet volume,
and activation state. Vet Clin Pathol 27, 2-9.
2006 World Congress WSAVA/FECAVA/CSAVA
375
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

GG
Gastroenterology
stroe

Back to contents

INVITED LECTURES - FULL PAPERS
G – Gastroenterology
THE GROWING PROBLEM OF OBESITY IN DOGS AND CATS
Dr. Alex German
Department of Veterinary Clinical
Science
University of Liverpool
Small Animal Hospitál
Crown Street
Liverpool
L7 7EX
United Kingdom
ajgerman@liv.ac.uk
Obesity is defined as an accumulation of
excessive amounts of adipose tissue in the body,
and has been defined as a greater than 15%
increase above the ideal body weight for the
individual. In humans, strict definitions of the
degree of adiposity based upon relative mortality
risk and risk of developing associated diseases.
Although data from companion animals are more
limited, some studies do suggest and increase in
morbidity when animals are both underweight
and overweight. This presentation will summarise
the current knowledge on obesity and its co-
morbidities in companion animals.
Measurement of obesity in companion animals
All measures of adiposity involve defining body
composition, which is the ‘relative amounts of
the various biological components of the body’.
The main conceptual division of importance is
between fat mass (FM; the triglyceride component
in adipose tissue) and lean body mass (LBM).
The various techniques differ in applicability
to research, referral veterinary practice and
first-opinion practice. Whatever method is
used, investigators should be aware of both the
precision and accuracy of the chosen method.
Ideally, a test which is both accurate and precise
should be chosen; however, many tests for body
composition are precise but not accurate, whilst
some are neither! Other important aspects of a
test are cost, ease of use, acceptance by veterinary
surgeons and clients, and invasiveness. At the
current time, there is no method which cannot be
criticised and, therefore, the perfect method for
analysis does not yet exist.
Potential research techniques include chemical
analysis, densitometry, total body water
measurement, absorptiometry (including
dual-energy X-ray absorptiometry – DEXA),
ultrasonography, electrical conductance, and
advanced imaging techniques (CT and MRI).
Back to contents
G
In the clinical setting there is more of a need
for quick, cheap and non-invasive methods
of body composition measurement. The most
widely adopted quantitative procedures include
measurement of body weight and morphometry.
Morphometry is defined as the measurement
of ‘form’ and, in relation to body composition
analysis, refers to a variety of measured parameters
that are used to estimate body composition.
The three main approaches are measurement
of skinfold thickness, dimensional evaluations
(where various measures of stature are combined
with weight) and body condition scores.
Dimensional evaluations are usually performed
by tape measure, and a number have been
reported in dogs and cats. Body condition
scoring is a subjective, semi-quantitative method
of evaluating body composition. A number of
schemes have been devised, with 9-point scheme
being the most widely accepted. All systems
assess visual and palpable characteristics which
correlate subcutaneous fat, abdominal fat and
superficial musculature (e.g. ribcage, dorsal
spinous processes, and waist). Unfortunately,
despite their apparent ease of use, these systems
2006 World Congress WSAVA/FECAVA/CSAVA
are used all too uncommonly in companion
animal practice.
Prevalence of Obesity in Companion Animals
We are all now well-aware of the ever-growing
problem of obesity in people, with current
estimates in the UK suggesting that over 55%
of adults are overweight and a further 22% are
obese. As in humans, obesity is one of the most
important medical problems in the pet population.
Studies, from various parts of the world, have
estimated the prevalence of obesity in the pet
population to be between 22% and 40%. The
most recently published data comes from a large
study in Australia, where 33.5% of dogs were
classed as overweight, whilst 7.6% were judged
377
G
to be obese. These figures are similar to recent
data from a study in France.
Causes of obesity
Although some diseases (e.g. hypothyroidism and
hyperadrenocortism in dogs), pharmaceuticals
(e.g. drug-induced polyphagia caused by
glucocorticoids and anti-convulsant drugs) and
rare genetic defects (in humans) can cause obesity,
the main reason for development of obesity is
getting the ‘energy balance equation’ wrong. In
this respect, either excessive dietary intake or
inadequate energy utilisation can lead to a state
of positive energy balance; numerous factors
may be involved including genetics, amount of
physical activity, and the calorific content of the
diet.
The effect of genetics is illustrated by recognised
breed associations (e.g. Labrador retriever, Cairn
terrier, cavalier King Charles spaniel, Scottish
terrier, cocker spaniel for dogs; domestic shorthair
for cats). Neutering is an important risk factor
in both species, whilst gender is a predisposing
factor in some canine studies, with females over-
represented. Other recognised associations in
dogs include indoor lifestyle, inactivity, middle
age, neutering, have all been associated with
obesity in dogs. In cats, middle age, male gender,
neutering, and apartment dwelling are possible
risk factors.
Dietary factors can also lead to the development
of obesity in both species. For instance, in dogs,
the number of meals and snacks fed, the feeding
of table scraps, and the animal being present when
owners prepared or ate their own meal. However,
the price of the pet food does have a significant
effect, where obese dogs are more likely to have
been fed cheaper rather than premium brand
foods. Behavioural factors may also play a part;
the development of obesity in cats may be caused
by anxiety, depression, failure to establish a
2006 World Congress WSAVA/FECAVA/CSAVA
normal feeding behaviour, and failure to develop
control of satiety.
The pathological importance of obesity
In humans, the medical importance of obesity
lies in the effect on mortality and morbidity of
associated diseases. Obese humans, on average,
do not live as long, and are more likely to
suffer from diseases such as type II diabetes
mellitus, hypertension, coronary heart disease,
certain cancers (e.g. breast, ovarian, prostate),
osteoarthritis, respiratory disease, and reproductive
disorders. Similarly, obesity has detrimental
378
Back to contents
effects on health and longevity of dogs and cats.
Problems to which obese companion animals
may be predisposed include orthopaedic disease,
diabetes mellitus, abnormalities in circulating
lipid profiles, cardiorespiratory disease, urinary
disorders, reproductive disorders, neoplasia
(mammary tumours, transitional cell carcinoma),
dermatological diseases, and anaesthetic
complications.
Treatment of obesity
In humans, current therapeutic options for
obesity include dietary management, exercise,
psychological and behavioural modification,
drug therapy, and surgery. Many of these
options are available for companion animals,
although it is not ethically justifiable to consider
surgical approaches. Further, no pharmaceutical
compounds have, as of yet, been licensed for
weight loss in dogs and cats.
Dietary therapy forms the cornerstone to weight
management in dogs and cats, and will be
covered in detail in another lecture. Increasing
exercise and behavioural management form
useful adjuncts. Increasing physical activity may
only increase energy expenditure by a modest
amount it has other benefits such as promoting
fatty acid oxidation and preserving lean tissue
during weight loss. The exact programme must
be tailored to the individual, and take account
of any concurrent medical concerns. Suitable
exercise strategies in dogs include lead walking,
swimming, hydrotherapy, and treadmills.
Exercise in cats can be encouraged by increasing
play activity, using cat toys (e.g. fishing rod toys),
motorised units and feeding toys. Cats can also
be encouraged to ‘work’ for their food by moving
the food bowl between rooms prior to feeding, or
by the use of feeding toys.
In addition to the above strategies, it is essential
that the whole weight reduction regime be
supervised. This is labour intensive, requires
some degree or expertise and training in owner
counselling, and often requires a dedicated
member of staff. Nevertheless, in the author’s
opinion, this is the single most important
component to the weight loss strategy. A recent
study has demonstrated that weight loss is more
successful if an organised strategy is followed,
which includes owner education.
References
References available on request.

G – Gastroenterology
NUTRITIONAL MANAGEMENT OF CANINE OBESITY
Denise Elliott BVSc (Hons) PhD
Dipl ACVIM Dipl ACVN
Director of Scientific
Communications
Royal Canin USA
500 Fountain Lakes BLVD, Suite
100
St Charles, Missouri, 63301
USA
denise.elliott@royalcanin.us
Introduction
Obesity is a clinical syndrome that refers to
the excess accumulation of body fat. Obesity
is considered to be the most common form of
malnutrition in small animal practice. It has been
suggested that as many as 40% of pets are obese.
The significance of obesity pertains to its role in
the pathogenesis of a variety of diseases and the
ability to exacerbate pre-existing disease. Obesity
has been associated with an increased incidence
of arthritis, cardiorespiratory problems, diabetes
mellitus, constipation, dermatitis, anesthetic risk,
and reduced life-expectancy.
Causes of Obesity
Obesity develops when energy intake consistently
exceeds daily energy expenditure. Undoubtedly
there are numerous environmental and social
factors that contribute to the formation of obesity.
These include decreased daily exercise as a result
of confinement to the house and overfeeding of
the pet by the client. Ad-libitum feeding of highly
palatable diets may predispose to overeating.
Snacks and treats contribute to excess daily
caloric intake. Breeds including the Labrador
Retriever, Cairn Terrie, Collie, and Basset hound
seem to have an increased likelihood of obesity.
Additional risk factors for obesity include age
(increased risk with aging), sex (females have
higher risk), and neutering.
Obesity is less likely to result from a disease
process or drug. Endocrine abnormalities
associated with obesity such as hypothyroidism
and hyperadrenocorticism. Drugs such as
the progesterones, used for contraceptive
management, have been associated with the
development of obesity.
Techniques to Determine Obesity
Obesity is defined by an excess accumulation
of body fat. Techniques to assess the degree of
body fat include morphometric measurements,
Back to contents
G
dilutional techniques, bioelectrical impedance
analysis, dual energy x-ray absorptiometry,
densitometry, computed tomography, magnetic
resonance imaging, total body electrical
conductivity, total body potassium, and neutron
activation analysis. Unfortunately, many of these
techniques are not clinically applicable.
Body weight is the simplest technique available
and should be included in the examination of
every patient. It provides a rough measure of
total body energy stores and changes in weight
parallel energy and protein balance. However,
edema and ascites may mask losses in body fat or
muscle mass. Likewise, massive tumor growth or
organomegaly can mask loss in fat or lean tissues
such as skeletal muscle.
Body condition scoring (BCS) provides a quick
and simple subjective assessment of body
condition. Different scoring systems have been
described but the most common scoring system
used is a 5-point system where a BCS of 3 is
considered ideal or a 9-point system where a
BCS of 5 is considered ideal. The technique of
body condition scoring does depend on operator
interpretation and does not provide any precise 2006 World Congress WSAVA/FECAVA/CSAVA
quantitative information.
Management of Obesity
The management of obesity requires clinical
identification of either those dogs that are obese
or, just as importantly, those dogs that are at
risk of obesity. Once this has been determined,
a thorough dietary history should be obtained.
Information that should be gathered includes
● The name, manufacture and type (i.e. canned
versus dry) of the current diet
● The amount of diet that is fed each day (can
versus cups of food)
● The method of feeding (ad-libitum versus meal fed)
● The person responsible for feeding the dog
● Additional persons that may fed the dog (especially
children, elderly parents or friendly neighbors)
379
G
● The number and type of snacks or human foods
given each day
● Access to foods for other pets
This dietary information should be used to
calculate the daily caloric intake of the dog. The
dog’s current body weight should be recorded,
and the target body weight of the dog should be
calculated. Ideally, the initial target body weight
should be 15% of the current body weight. It
is very important to set realistic and obtainable
goals for weight loss in order to maintain client
compliance. New target body weights can be
selected once the current target body weight has
been achieved until the dog has an ideal body
weight. The amount of calories to feed the dog is
determined on the basis of the target body weight.
If the amount of calories to achieve weight loss
is actually less than the current daily caloric
intake, the dietary history should be re-evaluated
to search for additional calories. If no additional
daily calories are identified, then the daily caloric
intake of the dog should be reduced by 15%.
Once the daily caloric requirement to achieve 15%
body weight has been calculated, consideration
should be given to the type of diet to feed.
There are essentially two main dietary options,
either feed a reduced amount of the regular
maintenance diet, or feed a diet that has been
specifically formulated for weight reduction. It
is not advisable to feed less of the regular diet
because this was the diet that lead to the problem
in the first place. However more importantly,
feeding a maintenance diet increases the risk
of nutrient deficiency and unhealthy weight
loss. Canine maintenance diets are formulated
according to energy intake. This means that if
a dog eats its daily energy requirement, it will
automatically consume the required amounts
of additional essential nutrients such as amino
acids, vitamins and minerals. By feeding less of
2006 World Congress WSAVA/FECAVA/CSAVA
the maintenance diet, you are not only reducing
the amount of energy, but also are reducing the
amount of protein, vitamins and minerals, and
thereby may risk malnutrition. Conversely, diets
that have been specifically formulated for weight
reduction have been formulated such that they
contain more essential nutrients relative to the
energy content of the diet. This means that they
will receive the required amounts of proteins,
vitamins, and minerals, even thought they are
ingesting less energy.
Diets formulated specifically for weight reduction
will vary according to the fiber and protein
content. High fiber diets have been suggested for
weight loss because fiber may provide a satiating
effect. High dietary fiber content will reduce the
digestibility of the diet, increases the amount
380
Back to contents
of fecal material and increases the amount of
water lost into the feces. High protein diets have
been reported to increase the proportion of fat
loss while preserving or indeed increasing the
lean body mass. The lean body mass is the most
metabolically active portion of the body and
includes skeletal muscle tissues. Preservation
of lean body mass has been shown to facilitate
successful long term maintenance of ideal body
weight once weight loss has been achieved.
Carnitine is an amino acid that is vital for energy
metabolism. Carnitine facilitates the movement
of long chain fatty acids across the mitochondrial
membrane were the long chain fatty acids
can be used for energy production. Carnitine
supplementation may facilitate fat loss and
maintain lean body mass.
Ideally, the dog should be meal fed rather then fed
ad libitum. The number of feedings per day can be
selected to suit the clients’ schedule, but 2-4 meals
per day is adequate. One member of the household
should be selected to feed the dog. This will reduce
inadvertent over feeding by additional family
members. The owner should be instructed to either
eliminate treats completely, or if this is met with
resistance, instructed to limit the number of treats
to less than 10% of the daily caloric intake. Ideally,
low calorie treats should be selected. The behavior
of the owner should also be altered by not allowing
the dog into the kitchen or dining room during meal
preparation or eating. This will reduce the likeliness
that the client will give the dog human snacks
which are generally high in calories. In addition,
the client should inform and enlist the support of
both family members and neighbors to the weight
reduction program so that they do not unknowingly
give the dog additional calories. In some cases, it
may be useful for the client to utilize a food diary to
record the amount of food and snacks fed each day.
For other clients, this technique is often met with
resistance and should not be considered.
In addition to reducing the daily caloric intake, every
effort should be made to increase the daily energy
expenditure by encouraging exercise. This could be
in the form of walks or, if the dog has concurrent
arthritis, swimming.
Dogs on weight reduction programs should
be reevaluated every two to four weeks. Body
weight, and body condition score should be
recorded. The dietary history should be reviewed.
Ideally, the dog should achieve about 1-3% body
weight loss per week.
Prevention of Obesity
The key to obesity management is prevention.
Energy requirements decrease when the animal is
spayed or castrated. Therefore, prevention should
begin at the time of neutering. Owners should

be counseled about the risk factors of obesity
(age, sex, breed, life-style, inappropriate feeding
practices), and the consequences of obesity.
Importantly, owners should be instructed on
both how to feed their dog, and how to regularly
determine body condition such that they can
maintain ideal body condition of their dog. The
importance of optimal body weight control should
be reinforced at each annual health examination.
References
Bierer TL, Bui LM. High-protein low carbohydrate
diets enhance weight loss in dogs. J Nutr 2004:
134: 2087S-2089S
Burkholder WJ, Bauer J: Foods and techniques
for managing obesity in companion animals, J
Am Vet Med Assoc 212: 658-662, 1998.
Diez M, Nguyen P, Jeusette I, et al. Weight loss
in obese dogs: evaluation of a high-protein, low
carbohydrate diet. J. Nutr 2002, 1685s-1687s.
Diez M, Michaux C, Jeusette I et al. Evaluation
of blood parameters during weight loss in
Back to contents
G
experimental obese beagle dogs. J Anim Physiol
Anim Nutr 3004; 88(3-4): 166-71
Diez M, Nguyen P, Jeusette I et al. Weight loss
in obese dogs: evaluation of a high-protein, low-
carbohydrate diet. J Nutr 2002; 132[6 Suppl 2]:
1685S-7S
Edney ATB, Smith PM. Study of obesity in
dogs visiting veterinary practices in the United
Kingdom. Vet Rec 1986; 118: 391-396
Elliott DA, Metabolic and Electrolyte Disorders.
In: Nelson RW, Couto G (ed). Small Animal
Medicine. 3rd edition. St Louis: Mosby 2003, p
816-827
Markwell PJ, Butterwick RF, Wills JM, et al.
Clinical studies in the management of obesity
in dogs and cats. Int J Obes Relat Metab Disord
1994; 18: S39-S43
Mason E: Obesity in pet dogs, Vet Rec 86: 612-6,
1970
2006 World Congress WSAVA/FECAVA/CSAVA
381
G
G – Gastroenterology
UPDATE ON PANCREATITIS IN DOGS
Kenneth W Simpson BVM&S,
PhD, MRCVS, DipACVIM,
DipECVIM
College of Veterinary Medicine
Cornell University
kws5@cornell.edu

From a clinical perspective pancreatitis can be
broadly categorized as acute, recurrent acute or
chronic. It can be further classified according to
its effect on the patient as mild or severe, non-
fatal or fatal, and also by the presence of sequela
such as abscess formation. Histologically, acute
pancreatitis is characterized by findings that
range from pancreatic edema to necrosis, variable
infiltrates of mononuclear and polymorphonuclear
cells, and local changes such as peri-pancreatic
fat necrosis and thrombosis. Acute pancreatitis
may resolve or persist and can be complicated
by secondary infection and pseudocyst or abscess
formation. It is tempting to equate mild acute
pancreatitis with pancreatic edema, and severe
or fatal pancreatitis with pancreatic necrosis, but
this relationship has not been critically examined
in patients with naturally occurring pancreatitis.
Chronic pancreatitis is characterized by fibrosis
and low grade mononuclear inflammation and
may be a sequela of recurrent acute pancreatitis
or a subclinical disease process that may present
as diabetes mellitus or exocrine pancreatic
insufficiency (EPI).
Etiology and Pathogenenesis
The etiology and pathogenesis of spontaneous
pancreatitis is poorly understood. The major
factors which have been implicated (by
association) as causes of acute pancreatitis in the
dog and the experimental evidence to support
their involvement are summarized as follows:

Potential aetiology Clinical Experimental

Hyperlipidemia Lipemia High fat diet
Abnormal lipid profiles IV Free Fatty Acids
Lipodystrophy
Diet Diet indiscretion Fat >>protein diet
Obesity Ethionine supplementation
2006 World Congress WSAVA/FECAVA/CSAVA

Bile reflux Concomitant biliary Bile infusion

Hypercalcemia
Corticosteroids
Drug/toxin related
Ischemia/reperfusion
Hereditary predisposition
Endocrinopathies
disease (?cats)
Ca infusion Ca infusion
? Hyperparathyroidism
? Hyperadrenocorticism Increased CCK sensitivity
? + Disc surgery? Pancreatic duct hyperplasia
Organophosphates Organophosphates
L-asparaginase
Azathioprine, sulphonamides
Potassium bromide and Phenobarbital
Zinc
Post-GDV Ex-vivo pancreas
? Miniature Schnauzer, Min. poodle,
Terriers, non-sporting dogs
? Hypothyroidism, diabetes mellitus

382
Back to contents

Irrespective of the initiating cause pancreatitis
is generally believed to occur when digestive
enzymes are activated prematurely within the
pancreas. In the normal pancreas safeguards are
present to ensure that harmful pancreatic enzymes
are not activated until they reach the intestinal
lumen. Enzymes are stored in zymogen granules
within the acinar cell in the presence of pancreatic
secretory trypsin inhibitor (PSTI) and are released
at the apical surface directly into the duct system.
They are only activated in the intestine, by trypsin,
following the cleavage of trypsin activation
peptide (TAP) from trypsinogen by enterokinase.
Potential sites for the intrapancreatic activation
of pancreatic enzymes can therefore logically be
divided into interstitial (within the duct system
and interstitium) and intracellular (within the
acinar cell). Experimental studies suggest that
bile and enteric reflux, and intravenous free fatty
acid (FFA) infusion initiate pancreatitis by an
interstitial mechanism whereas hyperstimulation
with caerulein or organophosphates, pancreatic
duct obstruction and choline deficient ethionine
supplemented diet (CDE diet) result in
intracellular activation. Experimental pancreatic
hyperstimulation with cholecystokinin (CCK: or
its analogue cerulein), dietary supplementation
with ethionine, and obstruction of the pancreatic
duct lead to the formation of large intracellular
vacuoles in acinar cells. Vacuole formation is
thought to be a consequence of the uncoupling
of exocytosis of zymogens and abnormal
intracellular trafficking of digestive and
lysosomal enzymes. These subcellular alterations
are considered to precipitate the intracellular
activation of digestive enzymes. Pancreatic
hyperstimulation may be of direct relevance to
naturally occurring pancreatitis in dogs. CCK is
normally released by cells in the duodenum in
response to intraluminal fat and amino acids and
coordinates and stimulates pancreatic secretion
and gallbladder contraction during digestion. It
is possible that high fat diets exert their effects
via the excessive release of cholecystokinin
and that hypercalcemia, organophosphates and
high levels of circulating glucocorticoids also
facilitate (potentially by changing pancreatic
sensitivity to hyperstimulation), or cause
pancreatic hyperstimulation; however, this is
not proven. Edematous pancreatitis induced by
CCK hyperstimulation in dogs is characterized
by a rapid but self-limiting, burst of trypsinogen
activation suggesting that the pancreas has a
feedback mechanism to limiting trypsinogen
synthesis and activation (see nutritional
management). This concept of pancreatic
down regulation is important when considering
nutritional intervention in acute pancreatitis.
Back to contents
G
Often pancreatic inflammation is a self-limiting
process, but in some animals reduced pancreatic
blood flow and leukocyte and platelet migration
into the inflamed pancreas may cause progression to
pancreatic necrosis. Secondary infection may arise
by bacterial translocation from the intestine. Release
of active pancreatic enzymes and inflammatory
mediators from the inflamed pancreas, such as Tumor
Necrosis Factor-α (TNF-α) interleukin-1 (IL-1)
and phospholipid platelet activating factor
(PAF), amplifies the severity of pancreatic
inflammation, and adversely affects the function
of many organs (systemic inflammatory
response), and cause derangement in fluid,
electrolyte and acid-base balance. It is the
development of multisystemic abnormalities
that separates mild from severe, potentially
fatal pancreatitis.
Diagnosis and Treatment
There is currently no single specific test for
pancreatitis in dogs and diagnosis is based
on a combination of compatible clinical,
clinicopathological and imaging findings.
Surgical biopsy may be required to confirm a
diagnosis, and to distinguish inflammation from
neoplasia.
Clinical findings
Signalment and History: Midlle aged to old
dogs (>5yrs years old) who are overweight
appear at higher risk. Miniature Schnauzers,
Yorkshire and Silky Terriers, non-sporting
breeds and perhaps miniature poodles may be at
increased risk of developing pancreatitis. There
is no clear sex predisposition. Endocrinopathies
such as hypothyroidism, diabetes mellitus and
hyperadrenocorticism may also be risk factors.
Thirteen percent of 221 dogs with diabetes mellitus
had histological evidence of acute pancreatitis.
Hyperlipidemia is another potential risk factor.
The history may reveal a recent episode of
2006 World Congress WSAVA/FECAVA/CSAVA
dietary indiscretion, toxin ingestion or drug
administration. Common clinical signs include
lethargy, anorexia, hunched stance, vomiting (±
blood), diarrhea (± blood), increased respiratory
rate and enlarged abdomen. Some dogs have a
history of icterus preceded by vomiting. Polyuria
and polydipsia may be present in dogs with
diabetes mellitus and pancreatitis.
Physical Examination: hysical findings in dogs
with acute pancreatitis are variable and range
from depression, to mild dehydration with signs
of abdominal pain, to acute abdominal crisis with
shock (tachycardia, prolonged capillary refill
time, tacky mucous membranes, hypothermia),
petechiation, icterus and ascites. An abdominal
mass is palpated in some dogs.
383
G
Diagnostic approach and differential diagnosis
The differential diagnosis of acute pancreatitis
in dogs is usually centered round the problems
of vomiting and abdominal pain.
In vomiting dogs the initial approach is to
distinguish self-limiting from more severe
causes of vomiting on the basis of physical
findings and a minimum database (e.g. Packed
cell volume, total protein, azostick, urinalysis,
plasma concentrations of sodium and potassium).
Where vomiting is associated with systemic
signs of illness, or is persistent, the clinician
has to differentiate metabolic, polysystemic
infectious, toxic and neurologic causes from
intra-abdominal causes. This is usually achieved
on the basis of combined historical and clinical
findings coupled with a minimum database
and the evaluation of hematology and serum
chemistry profile, urinalysis and abdominal
radiography. Measurement of serum amylase
or lipase is often reported on routine serum
chemistry profile. Additional procedures such
as ultrasonography, abdominal paracentesis
or assay of trypsin-like immunoreactivity,
TAP or immunoreactive canine pancreatic
lipase are usually performed on the basis of
these initial test results and help to distinguish
pancreatitis from other intra-abdominal causes
of vomiting.
Where abdominal pain is the major finding
localizing abnormalities such as abdominal
distension are rapidly pursued with radiography,
ultrasonography and paracentesis while providing
supportive treatment on the basis of physical
findings and a minimum data base and awaiting
the results of hematology, serum chemistry profile
and urinalysis. Abdominal pain can arise from
any intra-abdominal structure. Musculoskeletal
disorders such as discospondylitis and prolapsed
discs can be hard to distinguish from abdominal
causes of pain.
2006 World Congress WSAVA/FECAVA/CSAVA
Diarrhea, which was bloody in some cases, is
reported as a more frequent sign than vomiting in
dogs with experimental acute pancreatitis. Acute
pancreatitis and its complications (infection,
pseudocyst or abscess formation) should also
be considered in the differential diagnosis of
icterus and pyrexia. Some dogs with pancreatitis
exhibit few localizing clinical signs. Diagnosis in
these animals requires a high index of suspicion
and use of versatile diagnostic tests such as
ultrasonography.
Clinicopathological findings
Hematology: Extremely variable, ranging
from mild neutrophilia and slightly increased
haematocrit, through marked leukocytosis with
or without a left shift, to thrombocytopenia,
384
Back to contents
anemia and neutropenia with a degenerative left
shift. Thrombocytopenia in dogs with pancreatitis
is often associated with DIC and additional tests
of hemostasis (OSPT, APTT, FDP or D-dimer,
fibrinogen, antithrombin III) are performed to
determine if DIC or other coagulopathies are
present.
Serum biochemistry: Serum biochemical
abnormalities include azotemia (pre-renal and
renal), increased liver enzymes (ALT, AST, AP),
hyperbilirubinemia, lipemia, hyperglycemia,
hypoproteinemia, hypocalcemia, metabolic
acidosis and variable abnormalities (usually
decreased) in sodium, potassium and chloride.
Urinalysis: Enables azotemia to be characterized
as renal or pre-renal. Proteinuria occurs in some
dogs with acute pancreatitis and is usually
transient. The presence of glucose or ketonuria
should prompt consideration of diabetes
mellitus.
Pancreas specific enzymes: Classically, elevations
in serum amylase and lipase activity have been
used as indicators of pancreatic inflammation in
dogs. However these enzymes can be increased in
non-pancreatic disease, and dogs with confirmed
pancreatitis may also have normal amylase
and lipase activity. For example, in dogs with
histologically confirmed pancreatitis, lipase is
normal in 28 to 61% of dogs, and amylase is
normal in 31 to 47% of dogs. These limitations
have led to the development of assays for
enzymes or markers considered pancreatic in
origin such as trypsin-like immunoreactivity
(TLI), trypsinogen activation peptide (TAP),
and pancreatic lipase immunoreactivity (PLI).
Experimental studies have documented high
concentrations of TLI, TAP and PLI in dogs with
experimental acute pancreatitis. The utility of
TLI, TAP and PLI for the diagnosis spontaneous
pancreatitis in dogs has not been thoroughly
evaluated. Normal, subnormal and increased
concentrations of TLI have been observed in dogs
with confirmed pancreatitis. Elevations of TAP
have been observed in the serum and urine (TAP:
creatinine) of dogs with severe pancreatitis, and
TAP may be a better prognostic than a diagnostic
indicator of pancreatic inflammation. Experience
with PLI is even more limited, though it appears
more promising than TLI, as serum elevations of
PLI seem more substantial and prolonged than
TLI. Diseases such as renal disease can increase
TLI, TAP and PLI.
Radiography: Radiographic findings in dogs with
acute pancreatitis are generally non-specific and
include loss of serosal detail, increased opacity
in the right cranial quadrant of the abdomen,
displacement of the duodenum ventrally and/
or to the right, dilated hypomotile duodenum

and caudal displacement of the transverse
large intestine. Punctate calcification may
occasionally be identified in dogs with long-
standing pancreatitis; it indicates saponification
of mesenteric fat around the pancreas.
Thoracic radiographs may enable the detection of
pleural fluid, edema or pneumonia which has been
associated with pancreatitis in dogs and cats.
Ultrasonography: Ultrasonographic findings
include enlarged, hypoechoic pancreas, cavitary
lesions such as abscess or pseudocyst, dilated
pancreatic duct, swollen hypomotile duodenum,
biliary dilatation and peritoneal fluid. One study
of dogs with fatal acute pancreatitis indicated that
ultrasound supported a diagnosis of pancreatitis
in 23/34 dogs. Disorders other than pancreatitis
e.g. pancreatic neoplasia, pancreatic edema
(associated with hypoproteinemia or portal
hypertension) and enlarged peri-pancreatic
structures, can have identical ultrasonographic
appearance to pancreatitis. Fine needle aspirates
of cavitary lesions may be useful to distinguish
abscess from pseudocyst.
Abdominal paracentesis: Examination of peritoneal
fluid may aid the detection of various causes
of acute abdominal signs such as pancreatitis,
gastrointestinal perforation or ruptured bile duct.
Prognostic indicators
Stratifying the severity of pancreatitis is useful
when deciding how aggressive to be with
medical and nutritional support, and in offering a
prognosis. Severe pancreatitis requires aggressive
support and carries a guarded prognosis, whereas
mild pancreatitis often responds to short term
symptomatic therapy and has agood prognosis.
Clinical and clinicopathological criteria can be
used to predict the severity of acute pancreatitis.
The presence of shock or abnormalities such as
oliguria, azotaemia, icterus, markedly elevated
transaminases, hypocalcaemia, hypoglycaemia,
hypoproteinaemia, acidosis, leukocytosis,
falling haematocrit, thrombocytopaenia and DIC
should be considered likely indicators of severe
pancreatitis in the dog and cat.
The measurement of components of the systemic
inflammatory response such as TNF-α and
C-reactive protein, and IL-6 may also yield
information about the severity of pancreatitis that
in the future might lead to the administration of
specific antagonists of this response.
Potentially useful prognostic indicators that are
pancreas specific include assay of trypsinogen
activation peptide (TAP), trypsin complexed with
inhibitors, and phospholipase A2. Trypsinogen
activation peptide has been shown to accurately
predict severity in humans with pancreatitis. This
Back to contents
G
peptide is released when trypsinogen, a pancreas-
specific enzyme, is converted to its active form
and rapidly accumulates in the urine and plasma
of dogs with experimental acute pancreatitis. In
spontaneous pancreatitis. Plasma and urinary
TAP concentrations, as well as urinary TAP to
creatinine ratio, were all increased in dogs that
died with necrotising pancreatitis. Values were
not increased in mild, interstitial pancreatitis.
Increased plasma TAP concentrations were
also present in dogs with severe renal disease.
Phospholipase A2 is elevated in dogs with severe
pancreatitis.
Morphologic assesment of severity is accomplished
in humans by use of contrast enhanced computed
tomography (CE-CT). Where lack of pancreatic
perfusion is encountered i.e. necrosis, fine needle
aspiration is used to distinguish infected from
sterile necrosis. Substantially reduced mortality
has been achieved by the detection and surgical
treatment of people with infected necrosis.
CE-CT has recently been reported in 2 dogs
with pancreatitis. Contrast-enhanced computed
tomography (CT) findings in both dogs were
compatible with pancreatic necrosis. In one dog
managed medically for 11 days the follow-up
CT scan disclosed decreased pancreatic size and
increased contrast enhancement compatible with
partial resolution of pancreatitis.
Treatment
Medical treatment is based on maintaining
or restoring adequate tissue perfusion,
limiting bacterial translocation and inhibiting
inflammatory mediators and pancreatic enzymes;
surgical treatment consists principally of restoring
biliary outflow, removing infected necrotic
pancreatic tissue, or coping with sequela such as
pseudocysts. No studies have critically evaluated
treatment modalities in dogs or cats with naturally
occurring pancreatitis.
Initial management: The initial medical
2006 World Congress WSAVA/FECAVA/CSAVA
management of dogs with acute pancreatitis
is based on the presenting clinical findings and
the results of an initial database. Dehydration
or hypovolemia are supported with intravenous
fluid therapy e.g. LRS or 0.9% NaCl. Potassium
and glucose should be supplemented where
necessary. The type of fluid is tailored on the basis
of electrolyte and pH measurements to restore
normal electrolytes and acid-base balance. E.g.
vomiting and mild dehydration are usually given
crystalloids such as lactated Ringer’s solution at
a rate that will provide maintenance and replace
both deficits and ongoing losses over a 24h
period. Dogs with signs of shock require more
aggressive support. The volume deficit can
be replaced with crystalloids at an initial rate
385
G
of of 60-90ml/kg/h, then tailored to maintain
tissue perfusion and hydration. Plasma (20ml/
kg i.v.) or colloids (eg. Hetastarch, Dextran 70:
10-20 ml/kg/day i.v.). may be indicated in the
presence of hypoproteinemia or shock. Colloids
such as dextran 70 and hetastarch may also have
antithrombotic effects that help maintain the
microcirculation.
Insulin therapy is initiated in diabetic patients.
Where vomiting is a problem, antiemetics
(metoclopramide or chlorpromazine) and antacids
(e.g. famotidine) can be prescribed.
Prophylactic broad-spectrum antibiotics (e.g.
amoxicillin ± enrofloxacin depending on severity)
may be warranted in patients with shock, fever,
diabetes mellitus or evidence of breakdowm of
the GI barrier.
Analgesia can be provided using buprenorphine
(0.005-0.01mg/kg SC q6-12hrs) or oxymorphone
(0.1-0.2 mg/kg dogs IM, SC Q 1-3hrs). It may be
necessary to administer low dose sedation with
acepromazine (0.01mg/kg IM) to patients who
become dysphoric after opioids. Buprenorphine
is a partial agonist and may antagonise the
administarion of more potent analgesics in
animals with severe pain. A transdermal fentanyl
patch (Duragesic, Janssen) applied to a clipped
clean area of skin provides a longer duration
of analgesia in dogs (10-20kg, 50µg/hr patch q
72hrs). Adequate fentanyl levels are not attained
for between 6-48 hrs after application, so another
analgesic should be administered in the short
term. The author avoids using non-steroidal
analgesics in patients with acute pancreatitis due
to concerns for GI ulceration, renal failure and
potentially hepatotoxicity.
Specific therapy: Many dogs with acute
pancreatitis respond to fluid therapy and nothing
by mouth for 48h. Hence, specific therapy is
usually reserved for dogs that do not respond to
fluid therapy or those with signs of multiorgan
2006 World Congress WSAVA/FECAVA/CSAVA
system involvement or DIC.
The specific treatment of pancreatitis has evolved
along two paths, 1. Stopping further pancreatitis
from occurring, and 2. Limiting the local and
systemic consequences of pancreatitis.
Therapies aimed at inhibiting pancreatic secretion
(e.g. glucagon, somatostatin) or the intracellular
activation of proteases (e.g. gabexate mesilate)
which have been of benefit in ameliorating
the severity of experimental pancreatitis have
shown little benefit in the treatment of patients
with spontaneous pancreatitis, unless they are
given before pancreatitis is induced (e.g. before
ERCP). The lack of success with inhibiting the
progression of spontaneous pancreatitis has led
to increased emphasis on damage limitation;
ameliorating the effects of inflammatory
386
Back to contents
mediators or pancreatic enzymes on the patient
and maintaining pancreatic perfusion.
Where a coagulopathy e.g. DIC, or hypoproteinemia
are present, or the patient with pancreatitis is
deteriorating, fresh frozen plasma (10-20ml/kg)
may be beneficial in alleviating the coagulopathy,
hypoproteinemia and restoring a more normal
protease-antiprotease balance. Heparin (75-150IU/
kg TID) may be potentially useful in ameliorating
DIC, promoting adequate microcirculation in
the pancreas and clearing lipemic serum. In
experimental pancreatitis isovolemic rehydration
with dextran has also been shown to promote
pancreatic microcirculation in dogs. Therapy to
abrogate the systemic inflammatory response
with antagonists of PAF (e.g lexipafant), IL-1 and
TNF-α holds promise for the future.
Oral pancreatic enzyme extracts have been
reported to reduce pain in humans with chronic
pancreatitis, though this is controversial. They
are less likely to be effective in dogs as they do
not appear to have a protease mediated negative
feedback system.
Nutritional support
The intial aim is to identify and prevent, or treat,
nutritional factors associated with pancreatitis:
Where obesity, hyperlipidemia and dietary
indiscretion are reported it would seem prudent
to address their underlying cause in an attempt to
prevent future bouts of pancreatitis.
Precise recommendations for the dietary
management of acute pancreatitis in dogs are
hampered by the absence of controlled studies,
and are often based on empirical wisdom and a
best guess least harm approach.
The dilemma between feeding and stimulating
the pancreas: Pancreatic secretion in healthy
dogs occurs in response to ingested nutrients,
particularly fats and amino acids delivered into
the duodenum. Pancreatic secretion in response
to food is mediated by hormones such as CCK
and secretin, parasympathetic stimulation, and
duodenopancreatic nerves. Restricting oral intake,
or providing nutrients intravenously, does not
stimulate pancreatic secretion. Thus it has been
largely accepted that to provide “pancreatic rest”
oral intake should be withheld until clinical signs
resolve, or when signs persist for 72-96hrs that
parenteral nutrition is introduced. This dogma is
still prevalent in veterinary and human medicine.
However, there is growing evidence in people,
and animals, that enteral nutrition is superior
to parenteral nutrition in the treatment of acute
pancreatitis. Jejunal feeding (distal to the site of
pancreatic stimulation) does not exacerbate acute
pancreatitis in people or experimental animals.
People with acute pancreatitis fed via jejunostomy
tubes (these can be oral transpyloric tubes), have

lower morbidity, shorter hospital stays and
less cost than those treated with TPN. As it is
now feasible to place jejunostomy tubes non-
surgically in dogs, through the nose, esophagus
or stomach, clinical application of this feeding
strategy is not restricted by a surgical procedure.
However, it remains open whether dogs with
acute pancreatitis really require jejunal delivery
of nutrients. There is evidence that the pancreas
of dogs with acute experimental pancreatitis,
and people with naturally occurring severe
pancreatitis, is not as amenable to stimulation
as the normal pancreas. Dogs recovering from
naturally occurring pancreatitis have also been
shown to have subnormal circulating TLI
concentrations suggesting that pancreatic enzyme
synthesis is downregulated. In addition, it appears
that the major benefits of enteral support in acute
pancreatitis in people and experimental dogs are
due to reductions in the systemic inflammatory
response and the translocation of enteric bacteria
rather than a reduction in pancreatic stimulation.
Intestinal permeability and morbidity in dogs with
parvovirus are positively impacted by feeding a
liquid diet (41%protein, 18% fat, 3%CF) through
a nasoesophageal tube supporting the concept
that enteral feeding in general, rather than jejunal
delivery, is the reason for the beneficial effects of
EN, though this needs to be critically evaluated.
Resistance to enteral feeding of dogs with
pancreatitis is anticipated, despite evidence of a
beneficial effect. One common argument used to
promote PN in dogs with pancreatitis is that they
vomit too frequently to be fed enterally. However,
recent studies in dogs with parvovirus should
also help to allay this fear as these dogs tolerated
nosesophageal feeding despite severe vomiting
and diarrhea, with enterally fed dogs showing
faster recovery rates, greater body weight gains
and lower intestinal permeability than dogs that
were held NPO.
This is not meant to imply that parenteral
nutrition should be discarded, but it’s use
be restricted to patients that really need it,
for instance those in whom caloric intake is
severely and persistently impaired by persistent
vomiting. When parenteral nutrition is indicated
a choice has to be made between total and partial
parenteral nutrition. Partial parenteral nutrition
(PPN) is a more practical and manageable
procedure than TPN in most settings and has
been shown to be a safe and effective way of
providing nutrition to dogs with pancreatitis
and gastrointestinal disease. Interestingly dogs
that received a combination of enteral and PPN
survived more often than those receiving PPN
exclusively.
Back to contents
G
What diet should be fed to dogs recovering from
pancreatitis?
Free choice feeding is usually resumed
when the appetite returns and vomiting and
abdominal pain have subsided. Fat is frequently
regarded as the major stimulus for CCK release
and pancreatic secretion. However amino
acids are also potent stimulators of pancreatic
enzyme secretion and they are not restricted.
Perhaps a more rational basis for fat restriction
(?<15%DM) is the presence of hyperlipidemia.
Avoidance of other dietary factors associated
with pancreatitis, such as high fat diets, and
high fat protein restricted diets designed for
struvite dissolution, that have a nutrient profile
similar to diest known to induce pancreatitis in
dogs, is also reasonable. Obesity, a risk factor
for pancreatitis, should be controlled with a
balanced nutritional approach. Elemental diets
cause a similar degree of pancreatic stimulation
as normal diets.
Patient Monitoring
Minimal monitoring for stable patients
includes regular assessment of vital signs and
fluid and electrolyte balance. In those with
systemic abnormalities, monitoring should be
more aggressive and may include vital signs,
weight, haematocrit, total protein, fluid intake
and output, blood pressure (central venous
and arterial), electrolytes and glucose, acid-
base status, platelets and coagulation status.
Monitoring pancreas specific markers and
clinical signs on a sequential basis should
help to support resolution or progression of
pancreatic inflammation.
Ultrasound-guided fine needle aspiration of
the pancreas may enable infected pancreatic
necrosis to be detected. Ultrasonography may
also enable detection of delayed consequences
of acute pancreatitis such as pancreatic
abscessation, pseudocyst formation and biliary
2006 World Congress WSAVA/FECAVA/CSAVA
obstruction.
Surgical intervention
Surgery is potentially indicated to remove
devititalized tissue in patients with infected
pancreatic necrosis and to investigate and relieve
persistent biliary obstruction. The removal or
drainage of abscesses is another indication
for surgery. Resection or surgical drainage of
pancreatic pseudocysts is not always necessary
as these can resolve spontaneously or following
percutaneous drainage. Pancreatitis that is
recurrent or is unresponsive to treatment may
also require surgery to confirm a diagnosis and to
exclude pancreatic cancer.
387
G
Prognosis
The prognosis for dogs with mild acute pancreatitis
is good. Severe or recurrent pancreatitis is
associated with a guarded prognosis.
References and Suggested Reading
Chan DL, Freeman LM, Labato MA, Rush JE.
Retrospective evaluation of partial parenteral
nutrition in dogs and cats. J Vet Intern Med. 2002,
16(4): 440-5
Duerksen DR, Bector S, Parry D, Yaffe C,
Vajcner A, Lipschitz J. A comparison of the effect
of elemental and immune enhanceing polymeric
jejunal feeding on exocrine pancreatic function.
JPEN J Parenter Enteral Nutr 2002; 26: 205-8
Harmoinen J, Saari S, Rinkinen M, Westermarck
E.Evaluation of pancreatic forceps biopsy by
laparoscopy in healthy beagles.Vet Ther. 2002
Spring; 3(1): 31-6.
Hess RS, Kass PH, Shofer FS, Van Winkle TJ,
Washabau RJ (1999). Evaluation of risk factors
for fatal acute pancreatitis in dogs. Journal of the
American Veterinary Medical Association 214:
46-51.
Hess RS, Saunders HM, Van Winkle TJ, Shofer FS,
Washabau RJ (1998). Clinical, clinicopathologic,
radiographic, and ultrasonographic abnormalities
in dogs with fatal acute pancreatitis: 70 cases
(1986-1995). Journal of the American Veterinary
Medical Association 213: 665-668.
Jaeger JQ, Mattoon JS, Bateman SW, Morandi F.
Combined use of ultrasonography and contrast
enhanced computed tomography to evaluate
acute necrotizing pancreatitis in two dogs. Vet
Radiol Ultrasound. 2003, 44(1): 72-9
Johnson GB, Brunn GJ, Platt JL. Cutting edge: an
endogenous pathway to systemic inflammatory
response syndrome (SIRS)-like reactions through
Toll-like receptor 4.J Immunol. 2004, 172(1): 20-4.
2006 World Congress WSAVA/FECAVA/CSAVA
Mansfield CS, Jones BR, Spillman T. Assessing
the severity of canine pancreatitis. Res Vet Sci.
2003; 74(2): 137-44.
Mansfield CS, Jones BR. Plasma and urinary
trypsinogen activation peptide in healthy dogs,
dogs with pancreatitis and dogs with other
systemic diseases.Aust Vet J. 2000 Jun; 78(6):
416-22.
McClave SA, Greene LM, Snider HL, Makk LJ,
Cheadle WG, Owens NA, et al. Comparison of
the safety of early enteral vs parenteral nutrition
in mild acute pancreatitis. JPEN J Parenter Enteral
Nutr 1997; 21: 14-20.
Mentula P, Kylanpaa ML, Kemppainen E,
Jansson SE, Sarna S, Puolakkainen P, Haapiainen
R, Repo H.Plasma anti-inflammatory cytokines
388
Back to contents
and monocyte human leucocyte antigen-DR
expression in patients with acute pancreatitis.
Scand J Gastroenterol. 2004 Feb; 39(2): 178-87.
Mohr AJ, Leisewitz AL, Jacobson LS, Steiner JM,
Ruaux CG, Williams DA. Effect of early enteral
nutrition on intestinal permeability, intestinal
protein loss, and outcome in dogs with severe
parvoviral enteritis. J Vet Intern Med. 2003 Nov-
Dec; 17(6): 791-8.
Olah A, Belagyi T, Issekutz A, Gamal ME,
Bengmark S. Randomized clinical trial of specific
lactobacillus and fibre supplement to early enteral
nutrition in patients with acute pancreatitis. Br J
Surg 2002; 89: 1103-07.
Oruc N, Ozutemiz AO, Yukselen V, Nart D,
Celik HA, Yuce G, Batur Y. Infliximab: a new
therapeutic agent in acute pancreatitis? Pancreas.
2004 Jan; 28(1): e1-8.
Paraskeva C, Smailis D, Priovolos A, Sofianou
K, Lytras D, Avgerinos C, et al. Early enteral
nutrition reduces the need for surgery in Severe
Acute Pancreatitis. Pancreatology 2001; 1: 372.
Powell JJ, Murchison JT, Fearon KC, Ross JA,
Siriwardena AK. Randomized controlled trial of
the effect of early enteral nutrition on markers of
the inflammatory response in predicted severe
acute pancreatitis. Br J Surg 2000; 87: 1357-81
Pupelis G, Austrums E, Jansone A, Sprucs R,
Wehbi H. Randomised trial of safety and efficacy
of postoperative enteral feeding in patients with
severe pancreatitis: preliminary report. Eur J Surg
2000; 166:383.
Qin HL, Su ZD, Gao Q, Lin QT.Early intrajejunal
nutrition: bacterial translocation and gut barrier
function of severe acute pancreatitis in dogs.
Hepatobiliary Pancreat Dis Int. 2002 Feb; 1(1):
150-4.
Qin HL, Su ZD, Hu LG, Ding ZX, Lin
QT.Parenteral versus early intrajejunal nutrition:
effect on pancreatitic natural course, entero-
hormones release and its efficacy on dogs with
acute pancreatitis. World J Gastroenterol. 2003
Oct; 9(10): 2270-3
Raraty MG, Connor S, Criddle DN, Sutton R,
Neoptolemos JP.Acute pancreatitis and organ
failure: pathophysiology, natural history, and
management strategies.Curr Gastroenterol Rep.
2004 Apr; 6(2): 99-103.
Ruaux CG, Atwell RB. (1999). Levels of
total alpha-macroglobulin and trypsin-like
immunoreactivity are poor indicators of clinical
severity in spontaneous canine acute pancreatitis.
Research in Veterinary Science 67: 83-87.
Ruaux CG, Pennington HL, Worrall S, Atwell
RB (1999). Tumor necrosis factor-alpha at

presentation in 60 cases of spontaneous canine
acute pancreatitis. Veterinary Immunology and
Immunopathology 72: 369-376.
Saunders HM (1991) Ultrasonography of the
pancreas. In Problems in Veterinary Medicine Vol
3, Ultrasound. Ed PM Kaplan. Philadelphia, WB
Saunders p 583.
Simpson K.W., Beechey-Newman N., Lamb C.R.,
Smyth J.B.A., Hughes G., Coombe K., Sumar
Back to contents
G
N., Hermon-Taylor J. (1995). Cholecystokinin-
8 induces edematous pancreatitis in dogs which
is associated with a short burst of trypsinogen
activation. Digestive Diseases and Sciences 40,
2152-2161
Zyromski N, Murr MM. Evolving concepts in the
pathophysiology of acute pancreatitis. Surgery.
2003 Mar; 133(3): 235-7.
2006 World Congress WSAVA/FECAVA/CSAVA
389
G
G – Gastroenterology
NUTRITIONAL MANAGEMENT OF CANINE PANCREATITIS
Denise Elliott BVSc (Hons) PhD
Dipl ACVIM Dipl ACVN
Director of Scientific
Communications
Royal Canin USA
500 Fountain Lakes BLVD,
Suite 100
St Charles, Missouri, 63301
USA
denise.elliott@royalcanin.us
Introduction
Pancreatitis is an inflammatory condition of the
pancreas that occurs when proteolytic enzymes
are activated and autodigestion of the pancreas
occurs. The underlying cause of pancreatitis is
often unclear, but a number of factors have been
implicated, including obesity, the consumption of
high fat diets, hyperlipidemia (either idiopathic
or dietary), drugs (e.g. phenobarbitol and
potassium bromide therapy, azothioprin), toxins
(zinc, cholinesterase-inhibitor insecticides,
uremic toxins), hypercalcemia, pancreatic duct
obstruction, trauma, ischemia/reperfusion injury,
and concurrent disease (e.g., hepatobiliary,
hyperadrenocorticism, or diabetes mellitus).
Pancreatitis is most common in middle aged to
older dogs. The clinical signs vary from mild
and or subclinical to severe, necrotizing acute
pancreatitis. Chronic or recurrent pancreatitis
may ultimately result in exocrine pancreatitic
insufficiency and/or diabetes mellitus. Most
patients that present with pancreatitis have a
history of anorexia, depression, lethargy, vomiting
and occasional diarrhea. Vomiting and abdominal
pain are the most consistent signs in dogs.
2006 World Congress WSAVA/FECAVA/CSAVA
Traditional Management
The medical management of pancreatitis involves
decreasing pancreatic autodigestion by decreasing
pancreatic enzyme release, maintaining or
restoring adequate tissue perfusion, and correcting
electrolyte and acid-base imbalances. A key
requirement for the management of pancreatitis
is to minimize pancreatic enzyme release, and
yet provide adequate nutritional support to the
patients to minimize protein calorie malnutrition
and optimize healing and recovery. To some,
these two goals are diabolically apposed hence
traditional therapy has focused on nil per os until
the clinical sign of vomiting has resolve.
Once the vomiting has resolved, water, particularly
in the form of ice cubes is reintroduced. If the
390
Back to contents
patient is able to tolerate oral water, then small
amounts of “bland” highly digestible diets,
offered multiple times per day, are gradually
reintroduced. Pancreatic enzyme secretion is
triggered by several gastrointestinal hormones
including gastrin, secretin, and cholecystokinin
(CCK). CCK is the most potent stimulator of
pancreatic secretions. The release of CCK is
triggered by long chain fatty acids, amino acids,
and hydrogen ions. Carbohydrates appear to
have a weak to negligible effect on stimulating
CCK release. Therefore, reintroducing a highly
digestible carbohydrate source such as rice may
be prudent when refeeding the patient. If tolerated,
small amounts of high biological value protein
such as low fat cottage cheese or boiled skinless
chicken breast can be gradually introduced.
At all stages of refeeding, diets or ingredients
that are high in fat should be avoided, since fat
is the most potent stimulator of CCK secretion.
In addition, feeding high fat diets - either
commercial or table foods – has been anecdotally
associated with pancreatitis. However, what
constitutes a restricted fat diet varies considerably.
Nutritionists consider a restricted fat diet to be
one that contains less than 18% of the energy
from fat. Using this recommendation, it is clear
that many diets formulated for the management
of gastrointestinal disease are not actually low
fat diets, and would be inappropriate for the
management of pancreatitis.
Enteral versus Parenteral Nutrition
Nil per os therapy can only be instituted for
1-3 days. Patients that have persistent vomiting
or severe pancreatitis for longer than 3 days
will require nutritional support. There are three
modes of nutritional therapy that will minimize
pancreatic secretions; partial parenteral nutrition,
total parenteral nutrition and jejunostomy tube
feeding.
Parenteral nutrition involves the administration

of essential nutrients by intravenous infusion.
Parenteral nutrition should be used only when
enteral feeding is not possible. Parenteral
nutrition is complicated, more expensive and
is associated with a high risk of infection and
villous atrophy of the small intestine, which may
increase the risk of bacterial translocation and
sepsis. Total parenteral nutrition solutions are
very hypertonic (>1500 mOsm/L) and must be
administered into a large central vein to minimize
the incidence of phlebitis and thrombosis. Partial
parenteral solutions are generally formulated
with an osmolality less than 600 mOsm/L and
hence may be administered into a peripheral vein.
However, because of the dilute nature of PPN, the
total daily caloric intake can not be achieved. At
best PPN solutions deliver only 50% of the daily
illness energy requirement.
Parenteral nutrition solutions are generally
formulated with 3-6 grams of protein per 100
kcal, with the energy provided by a ratio of fat
(intralipid) to dextrose. There is no evidence to
date to suggest that high lipid parenteral nutrition
solutions are detrimental in the management
of canine pancreatitis. In general, fat-soluble
vitamins and trace elements do not need to be
added if parenteral nutrition is conducted for less
than 1-2 weeks. Vitamin K should not be added
to the parenteral nutrient solution, but should be
administered subcutaneously once weekly.
The nutrient-rich parenteral solutions provide
an ideal growth media for bacteria. To minimize
complications with infections, the solutions
must be prepared and administered under
sterile conditions through a dedicated catheter.
Parenteral solutions should always be mixed in
the following manner – dextrose, amino acids,
and lipid, and refrigerated until use. Parenteral
nutrition solutions should be administered for
a maximum of 2 days before discarding. It has
been recommended to cover the solution with a
bag or aluminum foil to protect the amino acids
and lipids from light degradation.
Enteral feeding is considered more physiologically
sound than intravenous feeding, as it maintains the
health of the gastrointestinal tract, and prevents
bacterial translocation. In addition, recent studies
in humans suggest that enteral feeding is superior
to parenteral feeding with lower morbidity and
shorter hospitalization. Studies in dogs have
clearly demonstrated that jejunal feeding does not
exacerbate acute pancreatitis.
Jejunal feeding requires the placement of a feeding
tube into the jejunum. This is most commonly
achieved via surgical placement. However,
there are newer techniques described whereby
the jejunum tube is placed transpylorically via a
Back to contents
G
gastrostomy tube. Feeding through a jejunostomy
tube must be by a continuous infusion pump due
to the narrow diameter of the tube and the volume
necessary to meet energy demands. Theoretically,
low fat, highly digestible elemental liquid diets
would be the first choice for feeding the pancreatic
patient with a jejunostomy tube. However,
veterinary diets with these specifications are not
available. Such diets are available for humans,
but care must be given to ensure that these diets
provide adequate protein, taurine, and arachidonic
acid for feline patients.
Nutritional Management Post-hospitalization
Significant risk factors for the development
of pancreatitis in dogs include obesity,
hyperlipidemia and dietary indiscretion.
Therefore, it is necessary to provide nutritional
counsel to the client to reinforce the necessity
to remain on a fat-restricted diet, and to avoid
high fat foods, including human foods. Hess et al
reported that 43% of dogs with acute pancreatitis
were overweight or obese. Therefore, prevention
of obesity by maintaining optimal body condition
should help to reduce the likelihood of pancreatitis.
For those patients that are overweight or obese, a
weight management plan incorporating nutrition,
exercise and behavior modification should be
implemented.
References
Chan DL, Freeman LM, Labato MA et al.
Retrospective evaluation of partial parenteral
nutrition in dogs and cats. J Vet Intern Med 2002;
16: 440-5
Hess RS, Saunders HM, Van Winkle TJ, et al.
Clinical, clinicopathologic, radiographic, and
ultrasonographic abnormalities in dogs with fatal
acute pancreatitis: 70 cases (1986-1995). J Am
Vet Med Assoc 1998; 213: 665-670.
Hess R, Kass P, Shofer F, et al. Evaluation of risk 2006 World Congress WSAVA/FECAVA/CSAVA
factors for fatal acute pancreatitis in dogs. J Am
Vet Med Assoc 1999; 214(1): 46-51.
Kalfarentzos F, Kehagias J, Mead N et al. Enteral
nutrition is superior to parenteral nutrition in
severe acute pancreatitis: results of a randomized
prospective trial. Br J Surg 1997; 84: 1665-9.
Qin HL, Su ZD, Gao Q et al. Early intrajejunal
nutrition: bacterial translocation and gut barrier
function of severe acute pancreatitis in dogs.
Hepatobiliary Pancreat Dis Int 2002: 1: 150-4.
Qin HL, Su ZD, Hu LD, et al. Parenteral versus
early intrajejunal nutrition:effect on pancreatic
natural course, entero-hormones release and its
efficacy on dogs with acute pancreatitis. World J
Gastroenterol 2003; 9: 2270-3.
391
G
G – Gastroenterology
CHRONIC GASTRITIS IN COMPANION ANIMALS
Kenneth W Simpson BVM&S,
PhD, MRCVS, DipACVIM,
DipECVIM
College of Veterinary Medicine
Cornell University
kws5@cornell.edu
Gastritis is a common finding in dogs,
with 35% of dogs investigated for chronic
vomiting and 26- 48% of asymptomatic dogs
affected. The prevalence in cats has not been
determined. The diagnosis of chronic gastritis
is based on the histological examination of
gastric biopsies and it is usually sub-classified
according to histopathological changes and
aetiology.
Histopathological features of gastritis
Gastritis in dogs and cats is usually classified
according to:
The predominant cellular infiltrate (eosinophilic,
lymphocytic, plasmacytic, granulomatous,
lymphoid follicular)
The presence of architectural abnormalities
(atrophy, hypertrophy, fibrosis, edema, ulceration,
metaplasia)
Its subjective severity (mild, moderate, severe).
A standardized visual grading scheme has been
proposed by Happonen et al (1998) and has been
adapted for pathologists (Wiinberg, 2005).
The most common form of gastritis in dogs
and cats is mild to moderate superficial
2006 World Congress WSAVA/FECAVA/CSAVA
lymphoplasmacytic gastritis with concomitant
lymphoid follicle hyperplasia.
Aetiology
Despite the high prevalence of gastritis an
underlying cause is rarely identified and in
the absence of systemic disease, ulcerogenic
or irritant drugs, gastric foreign objects,
parasites (Physaloptera, Ollulanus) or, in
rare instances, fungal infections (Pythium
insidiosum, Histoplasma), it is usually
attributed to dietary allergy or intolerance,
occult parasitism, or a reaction to bacterial
antigens, or unknown pathogens. Treatment
is often empirical but can serve to define
the cause of gastritis e.g. diet-responsive,
antibiotic-responsive, steroid-responsive or
parasitic.
392
Back to contents
Clinical findings
The major clinical sign of chronic gastritis is
vomiting of food or bile. Decreased appetite,
weight loss, melaena or haematemesis are
variably encountered.
The concurrent presence of dermatological and
gastrointestinal signs raises the likelihood of
dietary sensitivity.
Access to toxins, medications, foreign bodies, and
dietary practices should be thoroughly reviewed.
The patient details should not be overlooked as it
may increase the probability that chronic gastritis
is the cause of vomiting, e.g.: Hypertrophy of the
fundic mucosa is frequently associated with a
severe enteropathy in Basenjis and stomatocytosis,
haemolytic anaemia, icterus and polyneuropathy
in Drentse Patrijshond. Hypertrophy of the pyloric
mucosa is observed in small brachycephalic
dogs such as Lhasa Apso and is associated with
gastric outflow obstruction (see disorders of
gastric emptying). Atrophy of the gastric mucosa
that may progress to adenocarcinoma has been
reported in Lundehunds with protein losing
gastroenteropathy.Young, large breed, male
dogs in the Gulf States of the USA may have
granulomatous gastritis caused by Pythium spp.
with infection more prevalent in autumn (fall),
winter and spring.
Physical examination is often unremarkable in
patients with chronic gastritis.
Abdominal distension may be related to delayed
gastric emptying caused by obstruction or defective
propulsion. Abdominal masses, lymphadenopathy
or ocular changes may be encountered in dogs
with gastric fungal infections.
Clinicopathological testing
Clinicopathological tests are often normal in
patients with chronic gastritis.
A biochemical profile, complete blood count,
urinalysis and T4 (cats) should be performed as a
basic screen for metabolic, endocrine, infectious,
and other non-GI causes of vomiting, as well as

the acid base and electrolyte changes associated
with vomiting, outflow obstruction or acid
hypersecretion.
Eosinophilia may prompt the consideration of
gastritis associated with dietary hypersensitivity,
endoparasites, or mast cell tumours.
Hyperglobulinaemia and hypoalbuminaemia
may be present in Basenjis with gastropathy/
enteropathy, or dogs with gastric pythiosis.
Panhypoproteinaemia is a feature of
gastroenteropathy in Lundehunds, moderate to
severe generalized inflammatory bowel disease,
GI lymphoma and GI histoplasmosis. More
specific testing such as an ACTH stimulation test,
or serology for Pythium insidiosum are performed
on the basis of these initial test. Determination of
food specific IgE has not been shown to be useful
in the diagnosis of dietary sensitivity in dogs or
cats. The utility of non-invasive tests, such as
serum pepsinogen and gastric permeability to
sucrose, used to diagnose gastritis in people has
not been determined in dogs and cats.
Diagnostic imaging
Survey abdominal radiographs are frequently
normal in dogs and cats with gastritis but
may show gastric distention or delayed gastric
emptying (food retained >12hrs after a meal).
Contrast radiography may reveal ulcers or
thickening of the gastric rugae or wall but has
largely been supersceded by the combination of
ultrasonography to detect mural abnormalities
and endoscopy to observe and sample the gastric
mucosa.
Endoscopic examination enables the
visualization of foreign bodies, erosions,
ulceration, haemorrhage, rugal thickening,
lymphoid follicle hyperplasia (evident as mucosal
pock marks), increased mucus or fluid (clear or
bile stained) and increased or decreased mucosal
friability.
Discreet focal or multifocal mucosal nodules may
be observed with Ollulanus infection. Parasites
such as Physaloptera may be observed as 1-4cm
worms.
Gastric phycomycosis can be associated with
irregular masses in the pyloric outflow tract
and may prompt serological testing by ELISA,
Western blotting, and culture of fresh gastric
biopsies.
Large amounts of bile stained fluid is suggestive
of duodenogastric reflux associated gastritis,
whereas lots of clear fluid may indicate
hypersecretion of gastric acid.
Gastric fluid can be aspirated for cytology
(Helicobacter, parasite ova or larvae) and pH
measurement. Impression smears of gastric
biopsies are an effective way of looking for
Back to contents
G
Helicobacter spp. (5-12 µm spirals) and are more
sensitive than the biopsy urease test (Helicobacter
spp. produce urease).
Serum gastrin should be measured in the face
of unexplained gastric erosions, ulcers, fluid
accumulation or mucosal hypertrophy.
Gastroscopic food sensitivity testing (GFST),
the endoscopic procedure of dribbling dietary
antigens onto the gastric mucosa to ascertain the
presence of food allergy has not been useful in
dogs or cats. GFST is highly subjective, detects
only immediate hypersensitivity, and does not
correlate with the results of dietary elimination
trials.
The stomach should be biopsied even when it
looks grossly normal (usually 3 biopsies from
each region- pylorus, fundus and cardia).
Thickened rugae may require multiple biopsies,
and a full thickness biopsy is often required to
differentiate gastritis from neoplasia or fungal
infection, and to diagnose submucosal or
muscular hypertrophy.
Examination of gastric biopsies:
The interpretation of gastric biopsies has important
implications for patient care as biopsy findings
are often used to guide treatment e.g. moderate
lymphoplasmacytic gastritis without Helicobacter
is often treated with corticosteroids, whereas
mild lymphoplasmacytic gastritis may be treated
with a change in diet. As the histopathological
evaluation of gastric biopsies has not been
standardized the prudent clinician should carefully
review histological sections to get a feel for their
pathologist’s interpretation. Even with optimum
evaluation similar histological changes can be
observed in patients with different underlying
aetiologies so well structured treatment trials often
form the basis of an aetiological diagnosis.
Gastric sections should be stained with H&E for
evaluation of cellularity and architecture, and
modified Steiner stain for gastric spiral Further
2006 World Congress WSAVA/FECAVA/CSAVA
special stains e.g. Gomori’s methenamine silver
are indicated to detect fungi if pyogranulomatous
inflammation is present.
Treatment
Treatment of chronic gastritis initially centres
on the detection and treatment of underlying
metabolic disorders and the removal of drugs,
toxins, foreign bodies, parasites and fungal
infections.
Parasitic gastritis
Ollulanus tricuspis is a microscopic worm (0.7-
1mm lon, 0.04mm wide) infecting the feline
stomach. Mucosal abnormalities range from
none, to rugal hyperplasia, and nodular (2-
393
G
3mm) gastritis. Histological findings include
lymphoplasmacytic infiltrates, lymphoid folicular
hyperplasia, fibrosis and up to 100/hpf globular
leukocytes. Ollulanus is not detectd by faecal
examination, and requires evaluation of gastric
juice, vomitus or histological sections for larvae
or worms. Gastric lavage and xylazine induced
emesis have been described to aid diagnosis.
Treatment with fenbendazole 10mg/kg PO SID
for 2d may be effective.
Physaloptera species are 2 to 6 cm long worms
that are sporadiaclly detected in the stomachs
of dogs and cats. Diagnosis is difficult as worm
burden is often low and the eggs are transparent
and difficult to see in sugar floatation. Treatment
with pyrantel pamoate (5mg/kg PO: dogs single
dose; cats two doses 14d apart) may be effective.
Control of infection may be difficult due to
the ingestion of intermediate hosts such as
cockroaches and beetles and paratenic hosts such
as lizards and hedgehogs.
Given the diffculty of diagnosing Ollulanus
and Physaloptera empirical therapy with an
anthelminthic such as fenbendazole may be
warranted in dogs and cats with unexplained
gastritis.
Gastric pythiosis
The presence of transmural thickening of the
gastric outflow tract and histology indicating
pyogranulomatous inflammation raise the
possibility of infection with fungi such as
Pythium insidiosum. Special staining (Gomori’s
methenamine silver), culture, serology and PCR
of infected tissues can be used to help confirm
the diagnosis. Treatment consists of aggressive
surgical resection combined with itraconazole
(10mg/kg PO SID) and terbinafine (5-10mg/kg
PO SID) for 2-3 months post-surgery. ELISA
titres of pre- and post-treatment samples may
show a marked drop during successful treatment
2006 World Congress WSAVA/FECAVA/CSAVA
and drugs can be stopped. Medical therapy is
continued for another 2-3months if titres remain
elevated. The prognosis is poor and only <25%
are cured with medical therapy alone.
Helicobacter associated gastritis
An uncontrolled treatment trial of dogs and cats
with gastritis and Helicobacter infection showed
that clinical signs in 90% of 63 dogs and cats
responded to treatment with a combination of
metronidazole, amoxicillin and famotidine,
and that 14 of the 19 animals re-endoscoped
had resolution of gastritis and no evidence of
Helicobacter in gastric biopsies.
Controlled clinical trials have been hampered
by a much higher apparent recrudescence or re-
infection rate than the 1-2%/yr observed after
treatment of H. pylori infected people.
394
Back to contents
Only symptomatic patients with biopsy
confirmed Helicobacter infection and gastritis
should be treated.
The combination of amoxicillin (20mg/kg PO
BID), clarithromycin (7.5mg/kg PO BID) and
metronidazole (10mg/kg PO BID) for 14days
may be effective.
Ideally eradication should be confirmed by the
evaluation of gastric juice or biopsies 1 month
after stopping treatment, and non-responsive
patients should be evaluated for resistant
infections.
Chronic gastritis of unknown cause
Lymphocytic plasmacytic gastritis of unknown
cause is common in dogs and cats. It may be
associated with similar infiltrates in the intestines,
particularly in cats (who should also be eveluated
for the presence of pancreatic and biliary disease).
The cellular infiltrate varies widely in severity
and it may be accompanied by mucosal atrophy
or fibrosis, and less commonly hyperplasia.
Mild lymphoplasmacytic gastritis is initially
treated with diet.
The diet is usually restricted in antigens to which
the patient has been previously exposed e.g. a lamb
based diet if the patient has previously been fed
chicken and beef, or contains hydrolyzed proteins
(usually chicken or soy) that may be less allergenic
than intact proteins. The test diet is fed exclusively
for a period of about 1-2 weeks while vomiting
episodes are recorded. If vomiting is improved
a challenge with the original diet is required to
confirm a diagnosis of dietary sensitivity. The
introduction of a specific dietary component to the
test diet, e.g. beef, is required to confirm dietary
sensitivity. If vomiting is unresponsive the patient
may be placed on a different diet for another 1-
2 weeks, usually the limit of client tolerance,
or started on prednisolone (1-2mg/kg/day PO,
tapered to every other day at the lowest dose that
maintains remission over 8-12 weeks).
Moderate to severe lymphoplasmacytic
gastritis is usually treated with a combination of
a test diet and prednisolone. If the patient goes
into remission they are maintained on the test diet
while prednisolone is tapered, and potentially
discontinued.
Antacids and mucosal protectants are added to
the therapeutic regimen if ulcers or erosions are
detected at endoscopy or if haematemesis or
melaena are noted. If gastritis is unresponsive
to diet, prednisolone, and antacids, the
diagnosis should be re-evaluated prior to
aggressive immunosuppression. In dogs
immunosuppression is usually increased with
azathioprine (PO 2mg/kg SID for 5d then EOD, on
alternating days with prednisolone). Chlorambucil

may be a safer alternative to azathioprine in cats
(PO) and has been successfuly employed in the
management of inflammatory bowel disease
and small cell lymphoma. Prokinetic agents e.g
metoclopramide, cisapride, erythromycin can
be used as an adjunct where delayed gastric
emptying is present and are discussed below.
Diffuse eosinophilic gastritis of undefined
aetiology is usually approached in a similar
fashion to lymphoplasmacytic gastritis.
Atrophic gastritis
Atrophic gastritis has been infrequently described
in dogs and cats but is often associated with
a marked cellular infiltrate. Atrophy has also
been associated with gastric adenocarcinoma in
Lundehunds and in dogs with lymphoplasmacytic
gastritis of undetermined cause atrophy correlates
with the expression of mRNA for IL-1b and IL-
10 and the presence of neutrophils. There is no
clear evidence that lymphoplasmacytic gastritis
progresses to atrophy and gastric cancer in dogs
or cats, and the role of Helicobacter or antigastric
antibodies in the development of atrophy in
dogs and cats remains to be determined.Dogs
and cats with atrophic gastritis have not been
reported to develop cobalamin deficiency, unlike
Back to contents
G
in man. This is probably because the pancreas,
rather than the stomach, is the main source of
intrinsic factor in these species. Achlorhydria
has been described in dogs, and may enable the
proliferation of bacteria in the stomach and upper
small intestine, though this has not been proven.
The treatment of atrophic gastritis has received
limited attention, but Helicobacter eradication
and immunosuppression have been effective in
people.
Hypertrophic gastritis
Hypertrophy of the fundic mucosa is uncommon
and is often part of the breed specific gastropathies
or gastroenteropathies mentioned above.
Concurrent hypergastrinaemia should prompt
consideration of underlying hepatic or renal
disease, achlorhydria, or gastrin producing
tumors, which should be pursued appropriately.
Basenji gastoenteropathy is variably associated
with fasting hypergastrinaemia and exaggerated
secretin stimulated gastrin, and anecdotal reports
suggest that affected Basenjis may respond to
antimicrobial therapy. Antral hypertrophy of
brachycephalic dogs causes outflow obstruction
and is treated with surgery.
2006 World Congress WSAVA/FECAVA/CSAVA
395
G
G – Gastroenterology
NUTRITIONAL CONSIDERATIONS FOR THE VOMITING PATIENT
Denise Elliott BVSc (Hons) PhD
Dipl ACVIM Dipl ACVN
Director of Scientific
Communications
Royal Canin USA
500 Fountain Lakes BLVD, Suite
100
St Charles, Missouri, 63301
USA
denise.elliott@royalcanin.us
The differential diagnosis list for the vomiting
patient is exhaustive and includes both
gastrointestinal and non-gastointestinal disorders.
Therefore the nutritional management of the
vomiting patient will depend on the ultimate
diagnosis. For example patients that are vomiting
secondary to a systemic disease such as renal
failure are most appropriately managed by
nutrient alterations designed to minimize uremic
toxins. This lecture will confine the discussion
of nutritional considerations for the vomiting
patient to those patients whose vomiting is due
to a gastric cause.
Gastric causes of vomiting can be broadly
classified into gastric outflow obstruction and
disruption of the mucosal barrier (gastritis).
Causes of gastric outflow obstruction can be
divided into functional (i.e. motility disorders)
and physiological obstruction. Most disturbances
of gastric motor activity delay gastric emptying.
Delayed Gastric Emptying
A brief review of gastric motility will help
understand the nutritional effects that can be
employed to facilitate gastric emptying. The
2006 World Congress WSAVA/FECAVA/CSAVA
proximal stomach receives and stores boluses
of food from the esophagus. Contractions of
the proximal stomach are regulated by neural,
hormonal (stimulated by motilin; inhibited
by CCK, gastrin, secretin, GIP, glucagon,
and somatostatin) and paracrine (histamine,
serotonin) inputs. The proximal stomach is
responsible for facilitating receptive relaxation,
so that with the onset of deglutition and before the
arrival of the bolus of food from the esophagus,
the pressure within the lumen of the proximal
stomach decreases to allow the stomach to fill
without large increases in intra-gastric pressure.
Accommodation allows the stomach to be
distended to a large size with little or no change
in intragastric pressure.
The slow sustained contractions of the proximal
stomach gradually press the ingested contents
396
Back to contents
toward the distal stomach and duodenum. The
steady pressure exerted on the gastric content
by the sustained contractions of the proximal
stomach has a major role in controlling gastric
emptying of liquids. Increasing the strength of
the contractions increase intragastric pressure
and speed gastric emptying of liquids.
The distal stomach refers to the distal two thirds
of corpus, antrum, and gastroduodenal junction.
The primary role of the distal stomach is
retention and trituration (grinding) of solids and
prevention of duodenogastric reflux. Contractions
in the distal stomach are triggered by distension
and involve neural, hormonal (stimulated by
gastrin, CCK, motilin; inhibited by secretin,
VIP, glucagon, GIP, somatostatin) and paracrine
(histamine, serotonin, substance P) effects. The
peristaltic waves of the distal stomach aid in the
aboral propulsion of the contents and mix it with
gastric juice. The liquids in chyme are permitted
to pass readily through into the duodenum, but
solids are retained by the terminal antrum and
gastroduodenal junction. Powerful terminal antral
contractions grind the solids into particles about
0.1mm in size, which then become suspended
in the liquid phase of the gastric chime and are
then emptied from the stomach with the liquids.
Once gastric content has been emptied into the
duodenum, the gastroduodenal junction prevents
its reflux back into the stomach. The rate of gastric
emptying is carefully controlled by feedback
from small intestinal receptors so that the rate
is commensurate with digestion and absorption
in the small intestine. In contrast to the liquids
and digestible solids in chyme, indigestible solids
larger than about 1 mm are held in the stomach
throughout the postprandial period, after which
they are emptied by cyclically recurring bursts of
interdigestive gastric contractions.
The rate of emptying of solutions that are colder
or warmer than body temperature is slower than
that of fluids at body temperature. The rate of
emptying of liquids is faster when larger volumes

are ingested, however the rate of emptying of
gastric solids does not vary greatly with the
volume ingested. Carbohydrates generally empty
faster than proteins, which in turn empty faster
than fats, however, isocaloric amounts of fat,
protein, and carbohydrate empty at similar rates.
Gastric contents at pH 7.0 empty more rapidly
than those that are more acidic. The viscosity
of gastric chyme has little influence on its rate
of emptying. As the osmolality of a solution
increased the rate of its emptying is decreased.
Acidic solutions empty more slowly form the
stomach than neutral solutions because of the
presence of small intestinal receptors sensitive to
acid. The receptors detect the acids and activate
mechanisms which in turn slow gastric emptying.
Intestinal receptors sensitive to osmolarity of
the just emptied gastric chyme also influence
gastric emptying. The osmoreceptors are
postulated to act in response to a change in their
volume brought about by the osmotically active
particles. In general, the more hyperosmolar the
solution, the slower is gastric emptying. A model
postulates that when chyme is hyperosmolar,
the osmoreceptors shrink in size and thereby
activate mechanisms designed to slow gastric
emptying. In contrast, with hypoosmolar chyme
the receptor increases in size which speeds
gastric emptying. Small intestinal receptors
sensitive to fatty acids as well as to mono and
diglycerides are also present. Unsaturated fats
slow emptying more than saturated fats. The fatty
acid chain length is also important. The greatest
slowing of gastric emptying is brought about by
fatty acids with chain lengths of 14 carbon atoms.
Receptors sensitive to L-tryptophan are able to
detect physiologic concentrations of this amino
acid in chyme and activate an inhibitory feedback
mechanism that slows gastric emptying.
Studies on the nutritional management of delayed
gastric empting are lacking in dogs, however,
by reviewing the physiology, it seems logical
to consider frequent feedings of small volumes
of highly digestible, isocaloric, liquid, low fat
foods that are low in soluble fiber. Small frequent
feedings attempt to compensate for conditions
of impaired ability of the stomach to distend in
response to a meal. The food should be fed at body
temperature. The osmolality can be decreased by
diluting or blending the food with water. Feeding
liquid diets will facilitate gastric emptying.
Accelerated Gastric Emptying
Accelerated gastric empting is rarely diagnosed
in dogs. In humans, accelerated gastric
emptying is termed the dumping syndrome.
Accelerated gastric emptying overloads the
neutralizing, digestive and absorptive capacities
Back to contents
G
of the intestinal and causes duodenal ulceration.
Management techniques include frequent feeding
of low osmolality meals that are high in soluble
fiber. Soluble fiber such as psyllium husks attract
water and for gels which slows gastric emptying.
Ideally, patients should be fed dry food, and water
with the meal should be avoided.
Gastritis
Acute gastritis is typically managed by NPO
for 12-36 hours as food increases the release
of HCL which in turn, may increase mucosal
damage. Although NPO has been the traditional
management technique for patients that are
vomiting, recent evidence suggests that the
presence of food in the GIT provides trophic signals
in addition to direct nutrition to the enterocytes.
The trophic signals increase mesenteric blood
flow, stimulate the release of digestive enzymes
and enterohormones which influence intestinal
cell proliferation, differentiation, and the rate
of mucosal cell turnover. Studies in piglets
have suggested that small bowel atrophy begins
within days of nil per os. The signs of atrophy
that have been noted include decreased villus
height, decreased absorption and a reduction in
brush border enzymes. These changes ultimately
compromise the intestinal barrier. Enteral feeding
has been shown to be a powerful mechanism to
prevent gastrointestinal atrophy in piglets.
A recent randomized controlled clinical trial
investigated the effect of enteral nutrition on
intestinal permeability, intestinal protein loss
and outcome in dogs with parvo-viral enteritis,
compared to nil per os. Enteral nutrition was
associated with a shorter time to recovery,
increased body weight gain, and improved gut
barrier function. This study suggests that feeding,
rather than dietary rest should be considered for
some patients with gastrointestinal disease.
When feeding the patient with gastritis, small
frequent quantities of highly digestible, low fat,
2006 World Congress WSAVA/FECAVA/CSAVA
moderate protein, isocaloric diets are appropriate.
Frequent small quantities are imperative as
distension of an acutely inflamed stomach can
trigger the vomiting reflex. High digestibility
decreases the production of HCl, and increases
the rate at which the gastric contents are emptied
from the stomach. Low dietary fat concentration is
important to increase the rate of gastric emptying.
Amino acids are the most potent stimulators of
gastrin and HCl secretion hence the protein
content of the diet should be adequate, but not
excessive. Compared to protein and fat, CHO
provides the least stimulation of HCl, hence an
easily digestible starch such as rice is appropriate
for the patient with gastritis.
397
G
G – Gastroenterology
CHRONIC DIARRHEA IN DOGS – DIAGNOSTIC APPROACH
Frédéric Gaschen, Dr.med.vet.,
Dr. habil., DACVIM,
DECVIM-CA
School of Veterinary Medicine
Louisiana State University
Baton Rouge
Louisiana
USA
fgaschen@vetmed.lsu.edu
In the dog, diarrhea represents a significant
proportion of all visits to veterinary clinics. Acute-
onset diarrhea usually responds well to treatment
against intestinal parasites, dietary modification
and/or symptomatic therapy, however successful
approach of chronic diarrhea is usually more
challenging. Affected dogs often receive
treatment with different diets, antimicrobials
or anti-inflammatory drugs without success. A
systematic approach is required to narrow down
the list of possible differential diagnoses. Finally,
close cooperation between the veterinarian and
the dog’s owners is a pre-requisite to optimize
treatment success.
Diagnostic approach
The causes of chronic diarrhea in dogs are
multiple, multiple factors are involved, and
the prevalence of different diseases can vary
depending on the geographical location. Some
diseases can generally be ruled out using
relatively simple exams (e.g. intestinal parasites).
However, the diagnostic approach other diseases
may require therapeutic trials (e.g. adverse
reaction to food) or more detailed investigations.
2006 World Congress WSAVA/FECAVA/CSAVA
In severely sick animals (with obvious systemic
signs), it is preferable to immediately adopt a
more aggressive, global approach involving
blood tests, diagnostic imaging, and possible
endoscopy or laparotomy with sampling of
mucosal biopsies.
Parasite infestation: it is essential to rule out the
presence of intestinal parasites. Fecal shedding
of parasite ova or cysts is not continuous,
therefore a single negative parasitological fecal
analysis may not truly rule out the possibility of
parasite infestation. Moreover, several protozoan
parasites may be difficult to detect (e.g. Giardia
spp. for which ELISA testing is more sensitive
than direct fecal smears or fecal floatation).
However, after analyzing 3 successive fecal
samples, negative results confirm the absence of
intestinal parasites. A «practical» alternative to
398
Back to contents
multiple fecal exams consists in systematically
administering a broad spectrum anthelminthic
drug to treat locally prevalent endoparasites
(e.g. fenbendazole 50 mg/kg p.o. daily during
5 days).
Diet: when parasites have been ruled out, dietary
problems are probably the most frequent cause of
chronic diarrhea in dogs. In a recent clinical study
including 65 adult dogs referred to the University
of Bern, Switzerland for further workup of chronic
diarrhea, clinical signs resolved in 2/3 of patients
following a dietary elimination trial of 7-10 days
(consisting of exclusive feeding of a novel protein
diet). Excellent compliance of the dogs’ owners
was likely an essential component for the success
of dietary therapy. Many of them had decided
that they would participate in the study as a last
resort before giving up on controlling their dog’s
problem, and were therefore very motivated.
Food can elicit gastrointestinal inflammation
in several ways: in genuine food allergy an
immunological reaction against one of the dietary
components (allergen) is at the origin of the
problem. In such cases, it is recommended to feed
the dog during several weeks with a diet consisting
of nutrients to which it had no previous contact
(individually tailored hypoallergenic diet). To
confirm the diagnosis and find out what exactly
the dog is allergic to, it is necessary to perform a
dietary challenge with different allergens which
were part of the original diet (e.g. beef, chicken,
lamb, etc.) and to wait for the recurrence of
clinical signs. Most of the dogs in the Bern study
that responded to dietary elimination probably
suffered from food intolerance. Their clinical
signs disappeared with 7-10 days after they were
fed exclusively the hypoallergenic diet. However,
dietary challenge did not elicit recurrence of
clinical signs in most of those which underwent
that test. Food intolerance is not due to an
immulogical phenomenon. It could be caused
by the inability to adequately digest some of the

dietary components or to substances added to the
diet during industrial food processing.
It is therefore recommendable to prescribe
a hypoallergic diet to all dogs which did not
respond to treatment against GI parasites. Strict
complicance from the owners is essential. In
our experience, most dogs respond within 7-
10 days with a significant improvement of
stool consistency and clinical status (although
some of them may require more time). The diet
change must occur progressively. Many suitable
hypoallergenic diets are available from the main
pet food manufacturers. At this time there is no
published evidence that diets based on hydrolyzed
proteins are superior to novel protein diets. When
the clinical signs have subsided, it is advisable to
maintain a strict diet to avoid recurrences.
What to do if parasiticide treatment and
elimination diet fail?
In cases of large bowel diarrhea (colitis with typical
clinical presentation), a therapeutic trial can be
initiated with metronidazole (20-25 mg/kg p.o. BID
during 5-10 days), and addition of fiber to the diet.
However, sampling of mucosal biopsies prior to
further treatment may be the best course of action.
The existence of the syndrome of idiopathic
small intestinal bacterial overgrowth (SIBO)
is currently questioned by most veterinary
gastroenterologists. However, all agree that a
number of dogs with chronic intestinal disease
respond well to antimicrobial treatment (antibiotic
responsive diarrhea or ARD). The etiology of
ARD is unknown, and a bacterial infection with
unidentified bacteria cannot be ruled out at this
time. German shepherd dogs may be predisposed
to that disease due to insufficient production of
immunoglobulins A (IgA). Clinical signs may
vary considerably: chronic, recurring, mostly
small intestinal diarrhea is frequent (although
large intestinal signs may also occur). Additional
signs include borborygmi, flatulence, decreased
appetite and weight loss. Once parasite treatment
followed by 3-4 weeks elimination diet have been
attempted without success, many small animal
gastroenterologists consider ARD a possible
diagnosis and recommend oral antimicrobial
treatment with metronidazole (10-20 mg/kg BID),
tylosine (10-20 mg/kg once daily or BID) or
tetracycline (10-20 mg/kg TID). Interestingly all
3 substances may also exert immunomodulating
or even anti-inflammatory effects on the intestinal
mucosa in addition to their antimicrobial
properties.
In dogs presented with chronic diarrhea and
systemic signs including lethargy, a global
approach must be adopted, and the approach must
be more aggressive. A detailed clinical exam
Back to contents
G
followed by CBC and chemistry panel with all
the usual parameters including total protein and
albumin, and urinalysis (particularly checking
for proteinuria) are necessary. The possibility of
exocrine pancreatic insufficiency must be ruled
out. (serum trypsin-like immunoreactivity or
TLI). Rectal cytology is a simple test that may
be very useful for the diagnosis of intestinal
infections (especially fungal infections).
Abdominal ultrasonography is recommended as
it may show disruption of the typical architecture
of the intestinal wall. However, ultrasonographic
findings, which may also include intestinal wall
thickening and enlargement of mesenteric lymph
nodes, are not specific for a particular disease,
with the possible exception of lymphangiectasia.
They may just confirm the presence of intestinal
inflammation. If no clear diagnosis can be made
at that time, sampling of mucosal biopsies is
generally necessary. Gastrointestinal endoscopy is
the least invasive method, however it only allows
sampling of specific segments of the intestine,
and the biopsies may be quite superficial. This
is why a more invasive, surgical approach with
collection of transmural biopsies may be preferred
in some cases. Several studies have shown that
proper interpretation of intestinal biopsies is not
easy, and requires good communication between
clinician and pathologist.
Specific laboratory tests of interest in dogs with
chronic diarrhea
Serum albumin concentration: although serum
albumin may be mildly to moderately decreased
with many intestinal diseases with involvement of
the small intestine, severe decreases (< 20 g/l) are
usually associated with a syndrome called protein-
losing enteropathy, and are often associated with
panhypoproteinemia. Possible causes include
IBD or lymphangiectasia. Patients with severe
hypoproteinemia are usually severely affected
and may present with ascites, hydrothorax, and/or
2006 World Congress WSAVA/FECAVA/CSAVA
subcutaneous edema. They usually require more
aggressive and intensive treatment.
Serum acute phase proteins: C-reactive protein
(CRP) serum concentration has been shown to
increase in parallel to clinical activity of disease,
and may be a useful parameter to monitor the
evolution of disease and/or assess response to
treatment in difficult patients. However, it lacks
specificity for intestinal diseases as inflammatory
disorders from most organ systems may elicit an
increase in CRP
Serum cobalamin: decreased serum concentration
of cobalamin may be present in distal small
intestinal dysfunction, however its sensitivity is
low.
Fecal alpha1-proteinase inhibitor can be a
399
G
useful early marker of intestinal protein loss.
In patients with protein-losing enteropathy,
it may also be used for monitoring the
evolution of disease and/or assess response to
treatment.
Fecal culture: it can be useful if specific bacteria
are suspected (e.g. Campylobacter spp.), but
can be difficult to interpret (is the identified
bacterium at thye origin of the problem or does
it just represent an opportunistic growth in the
inflamed intestine?)
2006 World Congress WSAVA/FECAVA/CSAVA
400
Back to contents
Conclusion
Due to the multiple causes of chronic diarrhea in
dogs, a systematic approach is necessary to narrow
down the list of differential diagnoses and initiate a
successful treatment. In spite of these efforts, some
complicated cases may not show the expected
response to treatment and lead to frustrations for
dog owner and veterinarian. However, such cases
are the exception and not the rule...
A list of references can be obtained by sending an
e-mail request to the author.

G – Gastroenterology
SMALL INTESTINAL DIARRHEA – CAUSES AND TREATMENT
Frédéric Gaschen, Dr.med.vet.,
Dr. habil., DACVIM,
DECVIM-CA
School of Veterinary Medicine
Louisiana State University
Baton Rouge
Louisiana
USA
fgaschen@vetmed.lsu.edu
When presented with a dog or a cat with
diarrhea, it is useful attempt to identify which
segment of the intestine is affected. Although
many animals with small intestinal involvement
will at some time show signs of large bowel
diarrhea, the presence of large bowel diarrhea
alone is associated with a different approach and,
possibly, a better prognosis. A table summarizing
the clinical signs associated with small and large
bowel diarrhea can be found in the summary of
the lecture on large intestinal diarrhea.
Small intestinal disease will ultimately lead to
decreased absorption of nutrients through the
small intestinal mucosa and to severe systemic
consequences leading to malnutrition and weight
loss. Dogs and cats with diarrhea of small
intestinal origin are usually presented with a
variety of associated clinical signs, reflecting
the secondary involvement of numerous organ
systems. On the other hand, small intestinal
diarrhea may also occur secondary to a variety
of non-gastrointestinal diseases such as
polysystemic infections, endocrine diseases (e.g.
hypoadrenocorticism in dogs or hyperthyroidism
in cats), renal disease, various toxins and drugs,
etc. This is why, once parasitism has been ruled
out, a broad-based diagnostic approach including
blood analyses and abdominal imaging (and any
other test deemed appropriate for the affected
animal) is always recommendable in severely
affected dogs and cats with small intestinal
disease.
This presentation will focus on describing the
most frequent small intestinal diseases. Systemic
diseases with secondary involvement of the
gastrointestinal (GI) tract will not be further
discussed. The veterinarian should first attempt
to rule out the presence of any GI parasites
using the appropriate parasitological test. Then,
a precise dietary history should be available:
dietary indiscretion is a frequent problem leading
to acute diarrhea in young but also in adult dogs.
Back to contents
G
In fact, many cases come with a previous history
of similar problems, or have been seen ingesting
potentially harmful food. In chronic cases, food
intolerance (including food allergy) is a very
frequent problem that needs to be ruled out early
in the work-up.
Anomalies: the most frequent anomaly associated
with the digestive tract and leading to diarrhea is
exocrine pancreatic insufficiency. The clinical
signs are quite specific (production of large
amounts of yellowish or grey feces of decreased
consistency, weight loss, and flatulence, often
associated with a ravenous appetite). Diagnosis is
easily confirmed by evaluating the serum trypsin-
like immunoreactivity (cTLI). Treatment consists
of enzyme replacement often with dietary
modification with a low fat, easily digestible
diet.
Infections: viral infections such as parvovirosis
(dogs) and panleukopenia (cats) typically cause
severe, acute small intestinal disease in non
vaccinated young animals. Currently, feline
panleukopenia is less frequently encountered
than canine parvovirosis. The viruses attack the
small intestinal crypt cells and severely damage 2006 World Congress WSAVA/FECAVA/CSAVA
the intestinal epithelium. Treatment is mostly
symptomatic with aggressive fluid therapy, broad
spectrum systemic antimicrobials, antiemetics
and analgesia. Secondary electrolyte disorders
such as hypokalemia should be prevented, and
animals watched for the occurrence of secondary
intussusception. Early refeeding (small amounts,
naso-gastric feeding tube) is recommended as
soon as vomiting has subsided.
With few exceptions, bacterial infections appear
to be a rare cause of small intestinal disease in
dogs and cats. The small intestinal lumen naturally
harbors a variety of bacteria in limited numbers.
This resident bacterial flora has important
functions in preserving anatomical structures
and enhancing physiological processes necessary
for the proper digestion and absorption of food.
401
G
The small intestinal flora also plays a role in
preventing colonization by pathogenic bacteria,
and enhances the development of the enteric
immune system. Enteric bacterial infections have
been documented in small animals. Responsible
enteropathogens include Campylobacter spp.,
Clostridium perfringens and difficile, Salmonella
spp., Yersenia spp., and some strains of E. coli.
However, some of these bacterial species have
not only been isolated in feces of dogs and cats
with diarrhea, but also in healthy animals. To
further complicate matters, pathogenic bacteria
may just be “opportunists” in small animals
with intestinal diseases due to an unrelated
cause. If enteropathogenic bacteria are not the
actual source of the animal’s problems or if they
represent an incidental finding, indiscriminate
use of antibiotics is not recommended as it may
lead to development of resistant strains with
possible public health relevance. Even though the
pathogenicity of many of these bacteria is subject
to controversy, a risk for the transmission of
zoonotic infections to humans exists after contact
with sick dogs and cats, but more importantly
also after contact with healthy animals shedding
such enteropathogens. These important facts have
contributed to a sometimes confusing situation
making diagnostic and therapeutic decisions
difficult. Additional research is needed to more
clearly establish the role of enteric pathogens in
canine or feline intestinal diseases.
Numerous reports have shown that C. jejuni, C.
upsaliensis, and other enteric Campylobacter
spp. may be present in the feces of healthy and
diarrheic dogs and cats. Campylobacter infections
appear to be less frequent in cats than in dogs.
In Sweden, Campylobacter spp. were isolated
in 76% of young healthy dogs < 12 months of
age, but only in 39% of adult and older healthy
dogs. Campylobacter spp. can also infect human
beings, and cause abdominal discomfort, fever
2006 World Congress WSAVA/FECAVA/CSAVA
and diarrhea which may be bloody. Recovery
occurs frequently spontaneously but antibiotic
treatment may be required. Based on recent
studies, risk factors for human infection include
eating poultry that was cooked at home, drinking
water from a well or from a lake/river, and daily
contact with a dog. Therefore, fecal shedding
of Campylobacter spp. by healthy pets seems
to represent an important source of infections
in people. The therapeutic approach of dogs
with proven fecal shedding of Campylobacter
spp. depends on the health status of the patient
(i.e., healthy vs. showing gastrointestinal signs).
Among healthy dogs, those sharing home with
immune-compromised people or with infants
should probably be treated. In dogs showing
diarrhea, vomiting, and/or other signs compatible
402
Back to contents
with small intestinal disease, appropriate antibiotic
therapy is recommended, even though the causal
relationship of Campylobacter spp. infection and
the clinical signs may be difficult to establish.
The antibiotics of choice are erythromycin
(in dogs 20 mg/kg p.o. BID for 2-3 weeks) or
fluoroquinolones (e.g. enrofloxacin 5 mg/kg p.o.
BID for 7-10 days) at the usual dosages. The
prognosis for full recovery is generally good. If
the infection is secondary to another underlying
intestinal condition, recovery may also depend on
identification and treatment of that condition
Idiopathic inflammatory bowel diseases (IBD):
In small animal gastroenterology, the term IBD
groups various chronic intestinal diseases of
unknown etiology leading to chronic enteropathies.
These diseases may be further differentiated on
the basis of the histological appearance of the
inflammatory infiltrate: lymphocytic-plasmocytic,
eosinophilic, neutrophilic or granulomatous. The
clinical signs are characterized by chronic small
and/or large bowel diarrhea. The diagnosis is
made by elimination of all other identifiable
causes of diarrhea including food intolerance and
ARD.
In dogs, severe IBD could lead to protein-
losing enteropathies. Affected dogs can be
presented because of diarrhea associated
with the consequences of hypoproteinemia
(strong hypoalbuminemia, often with
panhypoproteinemia) causing effusions
and edema. Often, histological exam of the
intestinal mucosa reveals lymphangiectasia with
inflammatory infiltration. Even though it has
been reported to occur specifically in certain
breeds (Soft Coated Wheaton Terrier, Norwegian
Lundehund, possibly also Yorkshire Terrier etc.),
the cause of this syndrome remains unknown.
Generally, treatment consists of feeding the
dog with a highly digestible diet with low fat
content together with treatment of IBD (see
under). In severely affected dogs, intensive care
with aggressive fluid therapy aiming at restoring
adequate oncotic pressure may be necessary. The
prognosis is generally guarded to poor when
severe systemic clinical signs are present.
Current treatment protocols for canine IBD most
often involve the use of immunosuppressive
doses of corticosteroids (CS) for several weeks
followed by slow tapering to reduce the intestinal
mucosal inflammation and achieve clinical
remission. The usual protocols for predniso(lo)ne
usage recommend dosages of 1-2 mg/kg BID for
approximately 2-4 weeks, followed by a slow
tapering period over weeks to months. However, a
number of dogs treated with immune suppressive
doses of CS will show either no response at
all to the drug or will relapse after weeks to

months of treatment. At high dosages, CS have
numerous side-effects such as PU-PD which may
become unbearable for the owners, especially in
large breed dogs. In difficult cases that require
prolonged CS therapy but are sensitive to its side-
effects, the more expensive drug budesonide has
been used with good anecdotical success (3.0
mg/m2, resp. 0.5-3.0 mg per dog, depending on
body weight, once daily or every other day). In
humans, budesonide undergoes a first pass hepatic
extraction of approximately 80-90%. Therefore,
only a fraction of the absorbed compound reaches
the systemic circulation, theoretically decreasing
the side-effects. It has been documented that
budesonide suppresses the hypothalamic-
pituitary-adrenal axis in dogs with IBD
Other immunosuppressive agents such as
azathioprine, chlorambucil, cyclophosphamide at
the usual dosages are used alone or in combination
with CS. They may (a) decrease the required
dosage of CS and the associated side-effects, or
(b) allow the dogs to be weaned off CS as soon
as possible. Moreover, these drugs are also used
cases of steroid-refractory canine IBD. However,
they may have a delayed onset of action (weeks
to months until maximal effect). Recently, we
described the use of cyclosporine A (5mg/kg once
daily) in CS-refractory dogs with IBD, leading to
clinical improvement in 12/14 dogs.
As is the case in dogs, IBD in cats is an
exclusion diagnosis. Other causes of chronic
enteropathies have to be systematically ruled
out, and a compatible infiltrate has to be present
in the intestinal mucosa. The most common
inflammatory infiltrates include lymphocytes,
plasma cells, or eosinophils. Contrarily to what
is observed in dogs, diarrhea may not be the
most common clinical signs associated with
feline IBD. Initially, cats may show loss of
appetite/anorexia and/or chronic vomiting with
weight loss. In severe cases, cats are emaciated
or cachectic, and abdominal palpation reveals
rigid intestinal loops and/or presence of
enlarged lymph nodes. The diagnostic approach
is similar to that of dogs. Treatment may occur
in several steps: in mild cases start with a diet
change to a novel protein (“hypoallergenic”)
diet. Metronidazole may be administered
simultaneously (62,5 mg/cat 1x daily during
10-20 days). Resistant cats or those with severe
disease are given immunosuppressive doses of
prednisolone (1-2 mg/kg initially BID). Cats
are usually less sensitive to side-effects of
Back to contents
G
corticosteroids than dogs (exception: diabetic
cats). If the treatment using high doses of
prednisolone is successful after 10-15 days, the
doses are decreased stepwise until the minimal
effective dose can be reached (total duration
approx. 3 months). Resistant cats can benefit
from the addition of other immunosupressants to
the protocol (e.g. chlorambucil 2mg p.o. every 4
days).
It is important to know that most cats with chronic
intestinal disease are likely to develop cobalamin
deficiency due to intestinal malabsorption.
Cobalamin has important functions in virtually
all body cells, and chronic deficiency can lead
to a variety of non-specific clinical signs. This
is why parenteral supplementation is usually
recommended in chronic feline enteropathies,
particularly if serum cobalamin concentration
is lower than 300 ng/l. Injections of vitamin B
complex are not sufficient due to low cobalamin
concentration. Injectable cobalamin is available
in 1 mg/ml strength, and should be administered
s.c. at a dose of 0.25 mg weekly to cats up to 5 kg
for 6 weeks, then every other week for 6 weeks,
finally monthly for 2 months.
Neoplasia: Gastrointestinal lymphoma diffusely
infiltrates the intestinal mucosa, and preferably
affects older cats (generally > 7 years old). In
the last years GI lymphoma has become the
most prevalent form of feline lymphoma in
many areas. According to a recent study, 54% of
feline lymphomas affect the abdomen, and 75%
of those involve the gut. However, 10 to 46% of
affected cats do not show any gastrointestinal
signs (they essentially present with decreased
appetite or anorexia, and weight loss). Chronic
diarrhea however remains a frequent reason for
presenting the cat to a veterinarian. Diagnosis
may require “full thickness” intestinal biopsies, as
the histological differentiation between IBD ansd
small cell lymphoma can be very challenging
for the pathologist. Well differentiated tumors
2006 World Congress WSAVA/FECAVA/CSAVA
seem to respond well to “simple” chemotherapy
protocols during numerous months, but blast
forms are more difficult to treat. Generally, the
prognosis depends on the tumor response during
the first weeks of chemotherapy. If only a partial
or no remission is achieved, the success chances
of chemotherapy are compromised.
A list of references can be obtained by sending an
e-mail request to the author.
403
G
G – Gastroenterology
LARGE INTESTINAL DIARRHEA – CAUSES AND TREATMENT
Frédéric Gaschen, Dr.med.vet.,
Dr. habil., DACVIM,
DECVIM-CA
School of Veterinary
Medicine
Louisiana State University
Baton Rouge
Louisiana
USA
fgaschen@vetmed.lsu.edu

The large intestine plays an important role in
the digestion, however it is not involved in
the active absorption of nutrients. Electrolyte
transport, water absorption, mucus secretion,
bacterial fermentation of fiber to easily absorbed
short-chain fatty acids, immune surveillance,
and motility are the main physiological events
associated with the large bowel.
The prevalence of large bowel diarrhea in small
animals affected with chronic diarrhea may
differ according to geographic location and the
environment of the animal. In cats, diseases
affecting exclusively the large intestine occur
less frequently than those involving the small
bowel or the whole length of the intestine. The
associated clinical signs are typical for that
segment of the intestine, and reflect the failure of
water extraction and defecation control. In most
cases, they can be easily differentiated from those
resulting from small intestinal disease, as shown
in the following table.

Clinical sign Small intestinal disease Large intestinal disease

Frequency of defecation Normal or only slightly increased Moderately to severely increased
Fecal volume per defecation Normal to increased Often decreased
Presence of mucus No Frequent
Presence of blood Melena (digested blood) Hematochezia (fresh blood)
Possibly hematemesis
Tenesmus No Yes
Urgency No Yes
2006 World Congress WSAVA/FECAVA/CSAVA

Flatulence Possible Uncommon

General condition May be decreased (lethargy) Generally unaltered
Appetite Inappetence, anorexia frequent Alteration uncommon
Abdominal discomfort Possible Possible
Vomiting Rel. common Possible
Weight loss Frequent (if chronic) No

As is the case in small bowel disease, intestinal special test for protozoa, and fecal smears). It
parasites (especially whipworms) are the most is important to remember that three consecutive
common reason for large bowel diarrhea. fecal samples must be negative for parasite ova
Therefore, parasitological analysis of the feces is or cysts in order to rule out parasite infestation.
the first diagnostic test to apply (e.g. fecal flotation, Alternatively, a broad spectrum anthelmintic can
preferably using a centrifugation technique, be admininstered to eliminate most endoparasites
404
Back to contents

(e.g. fenbendazole, 50 mg/kg p.o. daily during
5 days). Beside parasite infestation, causes of large
bowel diarrhea include idiopathic inflammatory
bowel diseases (IBD), food intolerance, histiocytic
ulcerative colitis (HUC), clostridial infections, and
a disease similar irritable bowel syndrome (IBS) in
humans.
For a discussion of food intolerance and IBD,
the reader is referred to the lectures on small
intestinal diarrhea and chronic diarrhea. It is
noteworthy that endoscopy of the large intestine
requires appropriate preparation with prolonged
fasting (24-48 hrs), administration of electrolyte
solutions with osmotic laxative effects, and
possibly enemas. Rigid proctoscopy can be
performed in sedated dogs, however a full exam
of rectum, colon and cecum is only possible using
flexible endoscopes under general anesthesia. In
many instances, mucosal biopsies of the ileum
can be sampled during the procedure.
In recent years, the pathogenesis of HUC in
the dog has been at least partially elucidated.
This rare disease seems to affect mainly
brachycephalic breeds, even though it has been
diagnosed in other breeds as well. For many
years HUC was thought to be an immune-
mediated disorder, and was treated with
immune-suppressive doses of corticosteroids
without success. However, recently the disease
was shown to respond to enrofloxacin therapy
at usual doses. Additional research made
it possible to detect a deep-seated mucosal
infection with E. coli in dogs with HUC.
Clostridia are large Gram-positive, strict
anaerobic bacteria. Some clostridia are part of
the normal intestinal microbial flora. However,
Clostridium perfringens type A as well as
Clostridium difficile may produce gastrointestinal
disease and enterotoxemia in dogs.
Clostridium perfringens is widespread in the
environment and can be present in feces of
healthy animals. C. perfringens type A produces
enterotoxin (also called C. perfringens enterotoxin
or CPE). Enterotoxigenic C. perfringens are
commonly associated with food poisoning in
humans. CPE can be detected in fecal samples
using immunoassays such as ELISA. Although
C. perfringens could be cultivated from canine
fecal samples in 76-86% of healthy and 71-75%
of diarrheic dogs, only 5-14% of isolates from
healthy dogs and 15-34% of those from dogs with
diarrhea were enterotoxigenic. Enterotoxigenic
strains have been associated with nosocomial
canine diarrhea, hemorrhagic enteritis, and acute
or chronic large and/or small bowel diarrhea.
Isolation of C. perfringens in canine feces is not
sufficient for the diagnosis of C. perfringens-
associated disease. Endospore counts performed
Back to contents
G
on fecal smears are also unreliable. Moreover, the
clinical value of CPE assay as an accurate marker
of pathogenicity of C. perfringens remains to
be determined: fecal CPE was detected in non-
diarrheic dogs, however it was more prevalent
among in diarrheic dogs. The following antibiotics
are reported efficacious against C. perfringens: in
acute cases metronidazole (10 mg/kg BID for 7
days), amoxicillin (10-20 mg/kg BID to TID for
7 days), in chronic cases with intermittent signs
long-term tylosin (10-20 mg/kg BID) may be
preferable.
Clostridium difficile produces two major toxins
(toxins A and B), and is a common cause of
nosocomial and antimicrobial-associated enteric
infections in humans that may lead to potentially
fatal pseudomembranous colitis. In various
studies, C. difficile was cultured from the feces
of healthy puppies and their dams, healthy
adult dogs and cats, and diarrheic dogs and cats
presented to veterinary clinics. C. difficile was
also isolated from feces of dogs with nosocomial
diarrhea. Production of toxins A and/or B
was detected significantly more frequently in
diarrheic pets than in healthy pets. Therefore, a
causal relationship between enterocolitis and C.
difficile should only be suspected if toxins A and/
or B can be detected in a fecal sample. C. difficile
infections are best treated with metronidazole at
usual dosages.
In some dogs showing large bowel diarrhea no
diagnosis can be made in spite of a comprehensive
diagnostic workup including colonoscopy and
histological evaluation of mucosal biopsies. By
analogy to a syndrome known in humans, irritable
bowel syndrome (IBS) is suspected in these dogs.
The etiology has not been elucidated, but recurring
diarrheic episodes may be associated with stressful
events, and psychological factors are believed to
play a role (nervous dogs, dogs with abnormal
behavioral traits). The diagnosis is based on a
history of chronic recurring large bowel diarrhea, 2006 World Congress WSAVA/FECAVA/CSAVA
commonly with hematochezia, occasionally
with bloating and abdominal pain, and possible
behavioral problems after other known causes
of large bowel diarrhea could be ruled out.
Symptomatic treatment includes the addition of
fiber to the diet (e.g. psyllium). Dogs that respond
to fiber supplementation alone have an excellent
prognosis. However, additional therapy is usually
necessary, and a combination of antispasmodics
and sedatives is given [Librax® (Roche) –
suggestive dosage: 0.1-0.25 mg/kg clinidium BID
to TID to be given at the time of stressful events,
or when the first clinical signs of an episode are
noticed]. Although IBS does not resolve in dogs
requiring this combination treatment, the syndrome
can be kept under control with appropriate and
timely medication.
405
G
Symptomatic treatment of colitis includes
dietary manipulations and drug therapy. The
administration of an easily digestible diet is
recommended. Because food intolerance and
food allergy may be involved in the pathogenesis
of colitis, administration of a hypoallergenic diet
based on a novel protein source or hydrolyzed
peptides is a logical choice. Most hypoallergenic
diets manufactured by the pet food industry have
an optimized ratio of n6 to n3 polyunsaturated
fatty acids which can be beneficial to decrease
the inflammatory response. Supplementation
with fermentable fiber plays a central role in
the treatment of colitis, and exerts numerous
positive effects on the colonic mucosa. It also
favorably influences the composition of the large
intestinal bacterial flora. While some commercial
diets with increased fiber content are available,
supplementation of the diet with psyllium
(approximately 1-1.5 g/kg daily with food) is
also effective. Metrononidazole (10 mg/kg BID)
is often the first line agent for drug therapy.
2006 World Congress WSAVA/FECAVA/CSAVA
406
Back to contents
Sulfasalazine liberates 5-amino-salycilic acid in
the colon, and is widely used in the treatment of
dogs with colitis (10-25 mg/kg p.o. BID to TID,
can be increased up to 50 mg/kg TID, not to exceed
a total dose of 3 g/day). The duration of treatment
may be brief in mild cases (7-14 days), while
moderate to sever case with a chronic recurring
colitis may need to be treated for months to year.
In such cases, the lowest effective dose should
be determined by progressively decreasing the
dosage. Keratoconjuctivitis sicca is a possible
complication of sulfasalzine therapy, and it is
advisable to check tear production regularly,
especially in dogs receiving long term treatment.
In cats, administration of immune-suppressive
doses of corticosteroids is preferred and often
successful.
A list of references can be obtained by sending an
e-mail request to the author.

G – Gastroenterology
CHRONIC ENTEROPATHIES IN DOGS – WHICH DIET WHEN?
Denise Elliott BVSc (Hons) PhD
Dipl ACVIM Dipl ACVN
Director of Scientific
Communications
Royal Canin USA
500 Fountain Lakes BLVD, Suite
100
St Charles, Missouri, 63301
USA
denise.elliott@royalcanin.us
Dietary therapy is an important aspect of
the management of intestinal disease in
dogs. Therapeutic recommendations have
classically focused on dietary rest followed by
implementation of a highly digestible or “bland”
diet. However, as our understanding of the
pathophysiology of intestinal disease unfolds,
it is clear that that no single diet is likely to be
effective for every patient. The overall objectives
of dietary modification are to enhance digestion
and absorption of nutrients, support the mucosal
barrier function, promote normal intestinal
motility and function, decrease inflammation,
and incorporate nutrients that have a positive
effect on the small intestine and intestinal flora. In
addition to these key objectives, dietary therapy
for intestinal disease can be divided into four key
strategies:
● Diseases that respond to novel or hydrolyzed
protein diets
● Diseases that respond to high energy, high
dietary fat
● Diseases that respond to low levels of dietary fat
● Diseases that respond to high levels of dietary
fiber
Novel or Hydrolyzed Protein
Novel or Hydrolyzed protein diets are indicated
for dogs with a diagnosis of dietary sensitivity or
inflammatory bowel disease. Dietary sensitivity,
an adverse reaction to food, is a term used
to describe a clinically abnormal response to
the ingestion of a particular food. The reason
an immunological response against a specific
protein (or food allergen) is mounted in certain
individuals is not fully understood. Genetics, age,
poor digestibility of proteins, a defective mucosal
barrier, defective oral tolerance, and increased
mucosal permeability are all predisposing factors
for food allergy.
Highly digestible diets typically have digestibility
values that exceed 85%. A highly digestible diet
Back to contents
G
requires less gastric, pancreatic, biliary and
intestinal secretions for digestion. This results in
almost complete digestion and absorption in the
upper small intestine so that minimal residue is
presented to the lower bowel. Proteins that are
incompletely digested have more potential to
incite an immune response to the residual antigenic
proteins and large polypeptides. Conversely,
highly digestible proteins are completely digested
to free amino acids and small peptides, which
have less potential to elicit an allergic response.
Therefore highly digestible protein should be
selected for patients with intestinal disease.
Elimination diets and subsequent re-challenge
with the original diet are the only way to confirm
a diagnosis of food allergy in pets. The aim is to
feed a complete and balanced diet while strictly
feeding a protein and carbohydrate source to
which the pet has never been previously exposed.
Gluten sensitivity is a specific example of food
hypersensitivity which has been documented in
Irish Setters.
The antigenicity of dietary proteins can be
minimized by enzymatic hydrolysis to produce
low molecular weight protein hydrolysates.
Decreasing the size of the proteins that are ingested
2006 World Congress WSAVA/FECAVA/CSAVA
reduces the chances of immunoglobulin cross-
linking and subsequent mast cell degranulation.
Hypoallergenic diets have been recommended
for both the diagnosis and management of food
hypersensitivity and inflammatory bowel disease
in dogs. Dossin et al fed a soy isolate hydrolysate
diet to eight dogs with biopsy confirmed
inflammatory bowel disease. Within 4 weeks of
feeding the diet, fecal scores improved in all 8
dogs, intestinal movements normalized in 6 of
the 8 dogs, and the infiltration of the intestinal
mucosa reduced in 2 of the 8 dogs.
Nelson et al reported that clinical signs resolved
in 13 dogs with lymphocytic, plasmocytic
idiopathic chronic colitis when they were fed
a cottage cheese and rice diet. In 11 dogs, two
407
G
commercial diets not previously fed to these dogs
were successfully substituted for the initial test
diet, without causing recurrence of signs. Only
two of these 11 dogs subsequently tolerated a
switch to diets that had been fed at the time of
onset of signs of colitis. Patterson et al reported
that 20 dogs that exhibited both a non-seasonal
puritus and gastrointestinal signs had either
improvement or complete resolution when fed
either a homemade fish and potato or commercial
fish and soy based diet. Nineteen of the dogs
were subsequently maintained successfully on
the commercial food. Simpson et al evaluated the
effect of a selected protein chicken and rice diet
for the management of idiopathic chronic colitis.
Within one month, clinical signs of straining,
fecal blood, fecal mucus and fecal consistency
were significantly improved. Within two months
of dietary therapy, 90% of 11 dogs were stabilized
and did not require drug therapy to control clinical
signs of disease.
Fat
The selection of a diet with a high or low fat
concentration depends on the origin of the
intestinal disorder and the patient’s clinical
status. Fat is the most highly digestible of all
the nutrients, with digestibility values exceeding
90%. High fat diets are energy dense, reducing
the volume of food consumed at each feeding.
Fat will slow gastric emptying and prolong
digestion, which can be beneficial for some
forms of intestinal disease. Twelve dogs with a
confirmed diagnosis of chronic intestinal disease
(exocrine pancreatic insufficiency, inflammatory
bowel disease, bacterial overgrowth, acute or
chronic gastritis) were fed a diet containing a
high concentration of fat. The benefits of the high
fat diet were readily apparent with improvements
in appetite, weight gain, and resolution of clinical
signs of vomiting and diarrhea noted at 15 and 30
2006 World Congress WSAVA/FECAVA/CSAVA
days following institution of dietary therapy.
Of the energy-providing nutrients, fat digestion
requires the interplay between the intestine, liver
and pancreas. A deficiency of pancreatic enzymes
impairs digestion and results in malabsorption
of dietary nutrients. Bacteria in the intestinal
tract can metabolize undigested fat to hydroxy-
fatty acids which leads to secretory diarrhea in
the large intestine. Bacteria also deconjugate
bile acids further impairing fat digestion and
absorption. For this reason, fat restriction is
beneficial for conditions where fat may become
available for microbial metabolism, for example
in malabsorption syndrome, small intestinal
bacterial overgrowth, or bile acid deficiency.
Unlike amino acids and monosaccharides which
are absorbed directly into the blood stream, fat
408
Back to contents
is discharged from enterocytes into lacteals and
is transported to the systemic circulation via
mesenteric lymph vessels and the thoracic duct.
Lymphangiectasia, a disorder characterized by
congestion and/or dilatation of lymphatic vessels,
will impair fat transport. Therefore, restriction of
dietary fat is clearly indicated for the management
of some intestinal disorders.
A clinical study with 48 dogs with chronic diarrhea
(exocrine pancreatic insufficiency, small intestinal
bacterial overgrowth, malabsorption syndrome,
colitis and idiopathic diarrhea) was conducted at
the University of Edinburgh. All dogs had chronic
diarrhea despite aggressive drug and dietary
management. All dogs were transitioned to a low
fat diet and 14 parameters of GI function were
measured monthly for 5 months. A significant
improvement in body weight, appetite, drinking
habits, demeanor, coat condition, skin condition,
fecal appearance, consistency and frequency
of defecation, and a reduction in vomiting and
copraphagia were reported.
Polyunsaturated fatty acids are essential for
the maintenance of membrane integrity as
constituents of membrane phospholipids and the
provision of substrates for eicosanoid synthesis
(prostaglandins, thromboxanes, and leukotrienes).
Long chain ω fatty acids such as eicosapentaenoic
acid and docosahexaenoic acid, directly compete
with arachidonic acid for the lipoxygenase and
cycloxygenase enzymes. Subsequent metabolism
of eicosapentaenoic acid generates less
inflammatory mediators such as LTB5, and PGE3
compared to the metabolism of arachidonic acid.
In addition, the metabolism of eicosapentaenoic
acid produces hydroxy-fatty acids that block the
production of LTB4, a potent chemotatic factor,
from arachidonic acid. Therefore, in general, ω
fatty acids are anti-inflammatory compared with
the derivatives of ω fatty acids. Fish oils have
been suggested to improve the clinical status
of human patients with ulcerative colitis and
Crohn’s disease. Indeed, many diets formulated
for the management of gastrointestinal disease in
pets have been enhanced with ω fatty acids.
Dietary Fiber
Fiber, which is the non digestible carbohydrate
of plants, can be classified according to solubility
or fermentability. Soluble fibers form a gel in
water which delays gastric emptying and inhibits
absorption in the small intestine. Insoluble
fibers such as cellulose and oat fiber increase
fecal bulk, fecal water content, absorb toxins
and normalize both segmental and propulsive
motility. Both insoluble and soluble dietary fiber
may be beneficial in the symptomatic treatment
of certain large bowel diarrheas since fiber helps

to normalize transit time and increase fecal water
content. By normalizing intestinal transit time,
insoluble fibers are often recommended for
patients with constipation.
Fermentable fibers such as beet pulp, pectin, guar
gum, gum arabic, and fructo-oligosaccharides
may have a positive effective on the mucosal
barrier by stimulating the growth of intestinal
bacteria such as lactobacilii and bifidobacter.
These bacterial species have been shown to be
beneficial to intestinal health by decreasing the
growth of pathogens such as Clostridia and E.coli.
In addition, they produce the short chain fatty acids
butyrate, acetate and propionate, which provide
fuel for the colonocytes. Short chain fatty acids
enhance sodium and water absorption, increase
mucosal blood flow and increase gastrointestinal
hormone release. These mechanisms contribute
to the trophic role that short chain fatty acids have
on the intestinal mucosa, stimulating enterocyte
and colonocyte proliferation.
Leib et al reviewed the medical records of 37 dogs
diagnosed with chronic idiopathic large-bowel
diarrhea. Twenty three of 27 dogs were classified
as having a very good to excellent response to a
soluble fiber supplementation. Diarrhea returned
in 6 of 11 dogs when fiber supplementation was
withdrawn.
Additional Nutrients of Interest
Mucosal atrophy typically leads to a decreased
availability of disacchardases and carbohydrate
malabsorption. Bacterial overgrowth and
decreased transport of monsaccharides by
malfunctioning enterocytes can also contribute
to carbohydrate malabsorption. Regardless of
the mechanism, malabsorption of carbohydrates
contributes to osmotic diarrhea. Therefore,
diets formulated for pets with intestinal disease
should use reduced quantities of highly digestible
carbohydrate. Rice has long been considered the
ideal carbohydrate of intestinal disease. White
rice is highly digestible, gluten free, and has
rarely been implicated in food hypersensitivity.
Glutamine long considered a non-essential
amino acid, has been suggested to be particularly
beneficial for intestinal health. Glutamine
preserves the intestinal barrier function, increases
brush border enzyme activity, promotes protein
synthesis and aids recovery from intestinal
injury. Glutamine is the preferred fuel source
for enterocytes. It is also used as a substrate
for denovo synthesis of purine and pyrimidine
nucleotides for DNA and RNA synthesis. GIT
epithelial have very high turnover rate, therefore
glutamine now appears to be conditionally
essential nutrient for optimal GIT function in
starvation and stress. Glutamine supplementation
Back to contents
G
has been reported to improve nitrogen balance,
decreased mucosal atrophy, decrease bacterial
translocation, and stimulate the immune system
in humans and laboratory species.
The gastrointestinal tract provides a home
to a diverse population of bacterial. Recent
research is focusing on methods to manipulate
the gastrointestinal bacterial population
to improve health. Prebiotics are dietary
substances, such as fructooligosaccharides
(FOS), mannanoligosaccharides (MOS), inulin,
resistant starch, or arabinogalactans (AG) that
promote the health of beneficial bacteria in the
gut and deter the growth of pathogenic bacteria,
such as E. coli, Salmonella and Campylobacter.
Williard et al evaluated the effect of 1% fructo-
oligosaccharides in 16 IgA-deficient German
Shepherd Dogs with small intestinal bacterial
overgrowth. FOS supplementation resulted in
significantly lower aerobic/facultative anaerobic
bacterial colony-forming unites in the small
intestine. The results of this study indicated that
FOS can affect the population of bacteria in
the small intestine in dogs with small intestinal
bacterial overgrowth. Swanson et al reported
that supplemental fructooligosaccharides (FOS)
and (or) mannanoligosaccharides (MOS) have
beneficial effects on colonic health and immune
status of dogs.
Probiotics are live microbial feed supplements
that are administered to improve the
microbiological balance in the intestine. Baillon
et al reported the ability of a probiotic strain
to survive transit through the canine intestinal
tract. Potential health promoting effects of the
probiotic noted included increased phagocytic
capability of neutrophils, a substantial reduction
in serum endotoxin levels, and a lowering
of erythrocyte fragility indices. Furthermore
there was a significant decrease in the number
of Clostridia reflecting a change in the colonic
microflora towards a healthier balance. These
2006 World Congress WSAVA/FECAVA/CSAVA
changes are indicative of beneficial changes in
immune function and intestinal barrier integrity,
suggesting the possibility that probiotics could
play an important role in protecting from
disease.
Zeolite, or sodium silico aluminate, a tetrahedral
clay, is capable of absorbing bacterial toxins,
bile acids, and gases. By forming a protective
film on the intestinal mucosa, zeolite helps
to enhance the intestinal mucosal barrier.
Grandjean et al reported that the addition of
clays to food decreased the duration and the
severity of diarrhea in sled dogs. Clays have
also been shown by Fioramonti et al to reduce
diarrhea induced by experimental cholera toxin,
in dogs.
409
G
References
Baillon, M.-L., Z. Marshall Jones, et al.
Lactobacillus acidophilus Ds 13241 Promotes
Beneficial Gastrointestinal And Systemic Effects
In Healthy Dogs. J Vet Intern Med 2003; 17:
417.
Benyacoub, J., G. L. Czarnecki-Maulden, et al.
Supplementation of food with Enterococcus
faecium (SF68) stimulates immune functions in
young dogs. J Nutr 2003; 133(4): 1158-62.
Biourge, V., C. Vallet, et al. The use of probiotics
in the diet of dogs. J Nutr 128; 1998: 2730S-
2732S.
Fioramonti, J. and M. Droy-Lefaiz. Changes in
gastrointestinal motility induced by cholera toxin
and experimental osmotic diarrhea in dogs: effect
of treatment with an argillaceous compound.”
Digestion 1987; 36: 230-237.
Granjean, D. and F. Crepin (1992). “Interet de la
smectite dans les diarrhees aigues du cheine de
traineau.” Rec Med Vet 168(5): 323-329.
Leib, M. S. (2000). “Treatment of chronic
idiopathic large-bowel diarrhea in dogs with
a highly digestible diet and soluble fiber: a
retrospective review of 37 cases.” Journal of
Veterinary Internal Medicine 14(1): 27-32.
Marks, S. L., D. P. Laflamme, et al. (2002).
“Dietary trial using a commercial hypoallergenic
2006 World Congress WSAVA/FECAVA/CSAVA
410
Back to contents
diet containing hydrolyzed protein for dogs with
inflammatory bowel disease.” Vet Ther 3: 109-118.
Nelson, R. W., L. J. Stookey, et al. (1988).
“Nutritional management of idiopathic chronic
colitis in the dog.” Journal of Veterinary Internal
Medicine 2(3): 133-7.
Paterson, S. (1995). “Food hypersensitivity in
20 dogs with skin and gastrointestinal signs.” J
Small Anim Pract 36(12): 529-34.
Simpson, J. W., I. E. Maskell, et al. (1994). “Use
of a restricted antigen diet in the management of
idiopathic canine colitis.” J Small Anim Pract 35:
233-238.
Swanson, K. S., C. M. Grieshop, et al. (2002).
“Supplemental fructooligosaccharides and
mannanoligosaccharides influence immune
function, ileal and total tract nutrient digestibilities,
microbial populations and concentrations of
protein catabolites in the large bowel of dogs.” J
Nutr 132(5): 980-9.
Willard, M. D., R. B. Simpson, et al. Effects of
dietary supplementation of fructo-oligosaccharides
on small intestinal bacterial overgrowth in dogs.
Am J Vet Res 1994; 55(5): 654-9.
Zentek, J., B. Marquart, et al. Intestinal
effects of mannanoligosaccharides,
transgalactooligosaccharides, lactose and
lactulose in dogs. J Nutr 2000; 132: 1682S-4S

G – Gastroenterology
HELICOBACTER IN DOGS AND CATS - WHAT’S NEW?
Kenneth W Simpson BVM&S,
PhD, MRCVS, DipACVIM,
DipECVIM
College of Veterinary Medicine
Cornell University
kws5@cornell.edu
Gastric Helicobacter
The discovery of the association of Helicobacter
pylori with gastritis, peptic ulcers, and gastric
neoplasia has led to fundamental changes in
the understanding of gastric disease in humans.
Investigation of the relationship of gastric disease
to Helicobacter spp. in other animals has resulted
in the discovery of H. mustelae in ferrets with
gastritis and peptic ulcers, H. acinonychis in
cheetahs with severe gastritis, and H. Heilmannii
in pigs with gastric ulcers. The presence of
gastric Helicobacter-like organisms (HLO) in the
stomachs of dogs and cats has been known for
many years but the relationship of those organisms
to gastric disease remains controversial.
Helicobacter spp. infecting the stomachs of dogs
and cats
Helicobacter are spiral-shaped or curved, or
sometimes coccoid Gram negative bacteria that
inhabit the glands, parietal cells and mucus
of the stomach. The large gastric HLO are
morphologically indistinguishable by light
microscopy, in which they are seen as large,
5-12µ long spirals. They have been classified
into several Helicobacter spp. on the basis of
16s rRNA sequencing, DNA hybridization, and
electron microscopic appearance. H. felis, “H.
heilmannii”, H. bizzozeronii, and H. pametensis
have been detected in the gastric mucosa of
pet cats. H. pylori has been isolated from the
stomachs of a group of colony housed cats, but
not pet cats. H. bizzozeronii, H. heilmannii, H.
felii, H. salomonis, F. rappini and H. bilis have
been identified in dogs.
How common is infection with gastric
Helicobacter spp.?
There is a high prevalence of gastric Helicobacter
infection: HLO have been observed in gastric
biopsies from 41-100% of clinically healthy
Back to contents
G
and 57-100% of vomiting cats. The prevalence
of individual Helicobacter spp. has not been
thoroughly investigated, as it requires specialized
techniques. H.felis has been cultured from 3/21
Helicobacter infected cats in Finland, whereas
“H. heilmannii” was identified by PCR in
38/49 Swiss cats. PCR studies in Helicobacter
infected cats in the USA have identified 18/36
with “H. heilmannii”, 6/36 with H. felis (4/36
coinfected with H. felis and “H. heilmannii”),
2/36 H. bizzozeronii and 10 cats with unclassified
Helicobacter spp. Broadly similar results have
been observed in 50 German cats, though H.
bizzozeronii infected up to 30% of cats. Electron
microscopic examination of gastric biopsies from
infected cats has demonstrated co-infection with
spiral organisms of differing morphology-H.
felis, H. Heilmannii, H. bizzozeronii, and other
large gastric spiral organisms.
H. pylori infection has been reported in a group
of laboratory cats in the USA, but has not been
reported in pet cats in the USA or Europe to
date. It has been proposed that H. pylori is an
anthroponosis - an animal infection with a human
pathogen. 2006 World Congress WSAVA/FECAVA/CSAVA
Several studies have shown that gastric
Helicobacter are common in dogs, with a
prevalence ranging from 67-100% in healthy pet
dogs, 74-90% in dogs presented with vomiting
and 100% in laboratory beagles. In dogs H.
bizzozeronii is the most prevalent species followed
by “H. heilmannii” and H.salomonis, with H.
felis less common. Coinfection with one or more
spp, usually H. bizzozeronii and H. heilmannii, is
apparent in about 15-20% of dogs. H.pylori has
not been found in pet dogs.
Are cats and dogs a zoonotic risk?
“H. heilmannii”, the predominant species in pet
cats, and 20-40% of pet dogs, is also found in the
mucosa of 0.4-4% of people. H. heilmannii type
411
G
1 is the principal subtype in people and is thought
to be acquired by zoonotic transmission from
dogs, cats or pigs which are commonly infected
with H. heilmannii-like organisms (HHLO).
To provide a more informed estimate of the
zoonotic potential of cats, gastric DNA from
cats (45 American and German) infected with
H. heilmannii, was amplified with primers against
H. heilmannii ureB and 16s rDNA genes and
sequenced. Fluorescence in situ hybridization
(FISH) with eubacterial and H. heilmannii
specific probes was employed to directly visualise
H. heilmannii subtypes and their intragastric
distribution (Priestnall et al). ureB sequences
of H. heilmannii amplicons clustered with
human and feline isolates of H. heilmannii and
were distinct from the Helicobacter heilmannii-
like organisms, H. felis, H. salomonis and
H. bizzozeronii. 16S rDNA sequences in cats
and dogs were not consistent with H. heilmanii
Type 1 and clustered predominantly with types
2 and 4. No obvious differences in sequences
were observed between cats from different
countries. FISH failed to definitively characterize
H. heilmannii subtypes present in 14 of 15 cats.
As H. heilmannii type 1 is the dominant species
in infected people, the zoonotic risk posed by cats
and dogs is likely small.
In another study (Van den Bulck et al) gastric
biopsy samples from humans with histological
evidence of non-Helicobacter pylori spiral
bacteria (n = 123) and samples from the gastric
antrum, corpus, and cardia from dogs (n = 110)
and cats (n = 43) were subjected to a multiplex
PCR, enabling the identification of Helicobacter
felis, Helicobacter bizzozeronii, Helicobacter
salomonis, and “Candidatus Helicobacter suis.”
Single infections with “Candidatus Helicobacter
suis,” H. felis, H. bizzozeronii, H. salomonis, a
hitherto unknown genotype of a non-H. pylori
spiral organism (Helicobacter-like organism
2006 World Congress WSAVA/FECAVA/CSAVA
135 [HLO135]), and H. pylori were identified in
30.9%, 8.9%, 2.4%, 11.4%, 7.3%, and 8.9% of
the human biopsy samples, respectively. Mixed
infections (16.3%) with two or even three of
these were also found. Although the majority of
human non-H. pylori organisms are Helicobacter
species naturally occurring in the stomachs of
pigs, cats, and dogs, the frequent identification of
H. salomonis in human gastric biopsy samples is
in contrast to its rare identification in pet carnivore
samples, suggests other sources of infection.
Do Helicobacter spp cause gastric disease?
The cause of gastritis in cats and dogs is seldom
determined and is usually been attributed to
dietary allergy or intolerance, parasites, or a
reaction to bacterial antigens. The association
412
Back to contents
of Helicobacter infection with gastric disease in
humans, ferrets, cheetahs, pigs and experimentally
infected laboratory animals suggests that spiral
organisms may have a role in the pathogenesis of
gastritis in cats. The results of studies of cats and
dogs with naturally acquired gastric Helicobacter
Infection can be summarized as follows:
The relationship of infection to clinical signs
The high prevalence of gastric colonization with
HLO in healthy and sick cats indicates that there
is no simple “infection = disease” relationship.
An uncontrolled treatment trial of dogs and
cats with gastritis and Helicobacter infection
showed that clinical signs in 90% of 63 dogs and
cats responded to treatment with a combination
of metronidazole, amoxicillin and famotidine,
and that 74% of 19 animals re-endoscoped had
no evidence of Helicobacter in gastric biopsies.
Controlled clinical trials are required to confirm
these observations (see treatment).
The relationship of infection to gastric
histopathology
The majority of studies in cats and dogs with
naturally acquired Helicobacter infections
demonstrate that the fundus and cardia are more
densely colonized with bacteria than the pylorus.
Large HLO colonize the superficial mucus
and gastric glands, and may also be observed
intracellularly. Degeneration of gastric glands,
with vacuolation, pyknosis and necrosis of
parietal cells is more common in infected than
uninfected dogs and cats.
The gastric mucosal inflammation present in
Helicobacter infected dogs and cats is generally
mononuclear, and ranges from mild to moderate
in severity. A correlation between the presence of
HLO and the extent of histopathological changes
in the gastric corpus has been demonstrated
in cats. The paucity of uninfected animals has
hampered most investigations.
We have analyzed cytokines in gastric mucosa
from 8 uninfected and 20 infected cats. Infected
cats have upregulation of IL-8 (P=0.001) and IL-
1ß (P=0.01), but not IFN-γ or IL-10.The evaluation
of cytokines complements histopathology and
should be useful when evaluating grading systems
for inflammation. Gastric lymphoid hyperplasia is
more common and more extensive in Helicobacter
infected, than uninfected cats. Studies in cats that
have examined full thickness gastric biopsies
have demonstrated a strong association between
infection and lymphoid follicle hyperplasia. In
addition to this local immune response, a systemic
immune response characterized by circulating
anti-Helicobacter IgG has been detected in sera
from naturally infected cats. To date there has

been no association made between Helicobacter
infection and gastrointestinal ulcers or gastric
neoplasia in cats. However the relatively low
prevalence of these diseases coupled with the
small number of animals evaluated to date means
that such a relationship cannot be discounted.
Studies of the immune and inflammatory changes
in 30 dogs with naturally acquired gastritis
have shown that mucosal pathology is related
to cytokine mRNA expression (neutrophils to
IL-8 and IFN-γ, macrophages and lymphocytes
to IFN-γ, and fibrosis to IL-1ß) (Wiinberg et al).
Gastritis was categorized as lymphoplasmacytic
in all dogs, and its histological severity correlated
with atrophy, infiltration with lymphocytes and
macrophages, and the expression of IL-10 and
IFN-γ. Helicobacter spp infection was associated
with increased expression of TGF-ß, and fibrosis.
Macrophages, T-cells, and epithelial metaplasia
were more frequent in uninfected than infected
dogs. Circulating anti-Helicobacter IgG was
higher in uninfected than infected dogs. Studies
in Korea have also failed to show a relationship
of Helicobacter infection to pro-inflammatory
cytokine upregulation (Hwang et al).
Further defining the pathogenicity of individual
Helicobacter species
Studying the effects of Helicobacter on the gastric
mucosa of cats presenting with spontaneous
disease is limited by the variability in the host
makeup and the infecting Helicobacter species
(and possible strain variation too). In contrast
to humans, in whom H. pylori infection
predominates, the investigation of pathogenicity
in cats is complicated by the fact that they can be
colonized by a variety of Helicobacter spp., and
simultaneous colonization with multiple species
has been frequently observed. To overcome
some of these difficulties and improve our
understanding of cat-Helicobacter interactions
we have employed experimental infections with
H. felis and H. pylori.
Studies of the pathogenicity of H. felis in laboratory
cats have demonstrated gastritis, lymphoid
follicular hyperplasia and seroconversion.
H. pylori infection in cats is associated with a
moderately severe to severe gastritis yet clinical
signs associated with gastritis, such as inappetance
and vomiting, are generaly absent. It serves as a
model for investigating feline gastric mucosal
responses and the mechanisms of Helicobacter
pylori colonization, persistence and disease.
Analyses of gastric juice and biopsies from
kittens in an H. pylori-infected cat colony, using
rapid urease tests, ureB PCR and histopathology
demonstrated H. pylori in nine of 17 kittens
by eight weeks and in 16 of of these same
Back to contents
G
17 kittens by 14 weeks of age. UreB RLP patterns
and sequences of PCR products from gastric
mucosa were identical in mothers and kittens.
Bacterial densities were similar in the pylorus,
fundus and cardia. Infection was associated with
circulating anti-Helicobacter IgG antibodies and
significant (P<0.05) gastric inflammation and
lymphoid follicles; the pathology resembled that
often seen in infected human infants.
In more chronically infected cats we sought to
measure the development of host inflammatory
and immune responses, and their relationship
to the putative bacterial virulence factors cag
pathogenicity island (cagPAI), vacA allele and
oipA in combination with bacterial colonization
density in a feline model of the early stages of
H. pylori infection (Straubinger et al). Infecting
H. pylori strains were positive for vacAs1 but
lacked the cagPAI and an active oipA gene.
Colonization density was uniform throughout
the stomach. Up-regulation of IFN-γ, IL-1α,
IL-1ß, IL-8, and increased severity of inflammatory
infiltrates and fibrosis were observed in infected
cats. The median number and total area of
lymphoid aggregates were five and ten times
greater, respectively, in the stomachs of infected
than uninfected cats. Secondary lymphoid
follicles in uninfected cats were rare and positive
for BLA.36 and B220 but negative for CD3
and CD79α, whereas in infected cats they were
frequent and positive for BLA.36, CD79α, and
CD3 but negative for B220. Cats infected with H.
pylori can also develop antigastric antibodies that
cross-react with Helicobacter antigens. Changes
in gastric acid secretion and serum gastrin which
are known to occur in humans with H. pylori
infection have recently been demonstrated in cats
with experimental H. pylori infection.
These findings have implications for the
development of gastric inflammation and possibly
GI Lymphoma. The methods developed to study
these research cats are now being employed to
2006 World Congress WSAVA/FECAVA/CSAVA
evaluate cast with spontaneous gastritis. Further
studies are ongoing to try to determine the
genetic attributes of H. pylori that impact the host
response.
Eradicating Helicobacter spp in cats and dogs
The general lack of knowledge of the pathogenicity
of gastric Helicobacter spp. has meant that
veterinarians are faced with the dilemma of either
treating, or ignoring, spiral bacteria observed in
biopsies from patients with chronic vomiting
and gastritis. Eradication of H. pylori infection
in symptomatic humans has been associated
with resolution of symptoms and gastric
abnormalities. In light of their pathogenicity in
man and other animals it would seem reasonable
413
G
that eradication of gastric Helicobacter spp.
is considered prior to initiating treatment with
immunosuppressive agents to control gastritis.
An uncontrolled treatment trial of dogs and cats
with gastritis and Helicobacter infection lends
support to this approach. Clinical signs in 90%
of 63 dogs and cats responded to treatment with
a combination of metronidazole, amoxicillin
and famotidine, and 74% of 19 animals re-
endoscoped had no evidence of Helicobacter in
gastric biopsies. However, controlled therapeutic
studies in asymptomatic cats suggest that it is
difficult to eradicate gastric Helicobacter spp.
in cats with azithromycin, tinidazole, bismuth
and ranitidine, or clarithromycin, metronidazole,
bismuth and ranitidine for four or seven days.
After three weeks of amoxicillin, metronidazole
and omeprazole, cats with H. pylori infection
were culture negative, but five out of six cats
were positive in a species specific PCR in dental
plaque, saliva and/or gastric fluid samples.
Amoxicillin and metronidazole does not appear
to be an effective treatment in dogs either, with a
high failure rate 1 month after antibiotics.
It is unclear if in most studies antibiotic failure
was due to reinfection or recrudescence, although
the persistence of Helicobacter by PCR suggests
recrudescence is likely. These findings contrast
markedly with studies in H. pylori infected people
where 80% cure rates with 1%/yr reinfection are
observed.
We have recently performed a study in H.
pylori infected cats to determine if differences
in H.pylori genotype, and antibiotic sensitivity
explain the difficulty in eradicating Helicobacter
in cats: DNA sequences of a variety of genes
from H. pylori isolated from cat strains
matched those of H. pylori strains of human
origin. Isolates from different cats differed in
growth rate in culture, intrinsic susceptibility
to metronidazole and their ability to colonize
2006 World Congress WSAVA/FECAVA/CSAVA
stomachs of H. pylori-free cats. The pattern
of metronidazole sensitivity and the role of
genes metabolizing metronidazole were similar
in strains from people and cats. Further tests
showed that chronically infected cats could be
cured of resident H. pylori with amoxicillin
(20mg/kg PO BID 14days), metronidazole (10-
15mg/kg PO BID) and clarithromycin (7.5mg/
kg PO BID). This yielded 100% eradication in
12/12 cats 1 month post treatment.
Non- gastric Helicobacter spp.
Cholangiohepatitis / cholangitis complex in
cats is an ill-defined inflammatory disorder of
the hepatobiliary tree, that is one of the most
common hepatic disorders in cats .It has been sub-
categorized as suppurative and non-suppurative
414
Back to contents
to reflect the relative proportions of neutrophils
to lymphocytes and plasma cells, and the degree
of bile duct hyperplasia and fibrosis. Suppurative
cholangiohepatitis is often associated with a short
duration of illness, moderate elevations of liver
enzymes, jaundice, fever, neutrophilia and being
male. Non-suppurative cholangiohepatitis is
similarly characterized by jaundice and elevated
hepatic enzymes, but a longer duration of clinical
signs, hepatomegaly and a protein rich abdominal
effusion, hyperglobulinemia and lymphocytosis
are observed more frequently than in cats with
suppurative cholangiohepatitis.
Bacterial infections, most frequently enteric
species, have been implicated in acute
cholangiohepatitis, and a clinical response to
antimicrobial therapy has been observed in a cat
with Enterobacter associated cholangiohepatitis.
Concurrent pancreatic or intestinal inflammation
and cholestasis (intra- or extrahepatic) are also
frequently diagnosed in cats with both suppurative
and non-suppurative cholangiohepatitis and may
facilitate bacterial colonization, possibly by
ascending infection of the biliary tree. However,
a cause and effect relationship of these potential
etiologies to cholangiohepatitis has yet to be
demonstrated.
In people, rodents and dogs there is evidence
that inflammation and/or neoplasia of the liver
and biliary tract are associated with infection
with Helicobacter spp. Helicobacter DNA or
organisms, have been identified in the liver,
bile or gallbladder of people with chronic
cholecystitis, cholestatic liver disease and
hepatobiliary carcinoma and cirrhosis. In mice
H. hepaticus have been associated with hepatitis,
hepatocellular carcinoma,and inflammatory bowel
disease and Helicobacter bilis with hepatitis and
typhlitis. H. cholecystus has been cultured from
the gallbladders and pancreas of hamsters with
cholangiohepatitis and pancreatitis.H. canis has
been cultured from the liver of a young dog
with hepatitis. To date there are no reports of
Helicobacter spp associated liver disease in cats.
However, as cats, like humans and other species,
harbor Helicobacter in their stomachs i.e. H. felis,
H. heilmanii and H. bizzozzeronii, and H. Canis,
bilis, cinaedi and Flexispira have been cultured
from feces it is possible that Helicobacter species
have a role in hepatic disease in cats.
It is against this background that we
examined the role of Helicobacter spp. in
cholangiohepatitis in cats, by evaluating
archived hepatic tissue samples from cats with
and without cholangiohepatitis for the presence
or absence of Helicobacter spp using PCR,
immunocytochemistry and silver staining.
Tissue blocks from 32 cats with cholangiohepatitis

were identified in the pathology database for
the period 1992-2001 (Greiter-Wilke et al).
Tissue blocks from a group of 13 cats with non-
inflammatory liver disease, and 4 with normal
hepatic histlogy served as a control group.
Positive PCR results of liver samples were
obtained from 2 cats with cholangiohepatitis,
and 1 cat with PSVA. Sequence analysis
indicated homology with H. nemestrinae / pylori
in one Ch cat, and H. bilis in the PSVA cat.
Two amplicons of different sizes persistently
detected in the third cat, were consistent with H
nemestrinae / pylori and H. fenelliae/cinaedii.
PCR of gastric tissue samples yielded sequences
with close homology to gastric Helicobacter
spp e.g.H. heilmannii. No Helicobacter-like
organims were identified in hepatic tissue by
Steiner stain or immunocytochemistry. FISH
using a eubacterial probe identified a semicurved
bacterium in the intrahepatic bile duct of one cat
with cholangiohepatitis.
Recent studies of cats with lymphocytic
cholangitis (Boomkens et al) detected H. pylori
like sequences in the bile of 4/15cats with
lymphocytic cholangits, 8/51 cats with non-LC
cholangitis and 7/12 healthy cats.
The Helicobacter sequences identified in thee
studies are consistent with those associated with
liver disease in other species. Further, prospective
studies are warranted to elucidate the role of
Helicobacter and other infectious agents in liver
disease in cats.
Acknowledgements
Dr. Simpson is supported by a grant from the US
public health service (DK 002938). I gratefully
acknowledge the generous support provided
by numerous graduate students, post-docs,
technicians and external collaborators- some of
whom are mentioned in the refrences below!
Back to contents
G
References
Boomkens SY, Kusters JG, Hoffmann G, Pot RG,
Spee B, Penning LC, Egberink HF, van den Ingh
TS, Rothuizen J.Detection of Helicobacter pylori
in bile of cats. FEMS Immunol Med Microbiol.
2004 Nov 1;42(3):307-11
Greiter-Wilke,A, E. Scanziani, S. Soldati,
P.L. McDonough, S.A.Center, M.Rishniw
K.W.Simpson. Evaluation of the association of
Helicobacter with feline cholangiohepatitis JVIM
2006,In press.
Hwang CY, Han HR, Youn HY.Prevalence and
clinical characterization of gastric Helicobacter
species infection of dogs and cats in Korea.J Vet
Sci. 2002 Jun;3(2):123-33.
Priestnall SL, Wiinberg B, Spohr A, Neuhaus
B, Kuffer M, Wiedmann M, Simpson KW.
Evaluation of “Helicobacter heilmannii” subtypes
in the gastric mucosas of cats and dogs.J Clin
Microbiol. 2004 May;42(5):2144-51.
Straubinger RK, Greiter A, McDonough SP,
Gerold A, Scanziani E, Soldati S, Dailidiene
D, Dailide G, Berg DE, Simpson KW.
Quantitative evaluation of inflammatory
and immune responses in the early stages of
chronic Helicobacter pylori infection.Infect
Immun. 2003 May;71(5):2693-703.
Van den Bulck K, Decostere A, Baele M,
Driessen A, Debongnie JC, Burette A, Stolte
M, Ducatelle R, Haesebrouck F.Identification
of non-Helicobacter pylori spiral organisms in
gastric samples from humans, dogs, and cats.J
Clin Microbiol. 2005 May;43(5):2256-60.
Wiinberg B, Spohr A, Dietz HH, Egelund T,
Greiter-Wilke A, McDonough SP, Olsen J,
Priestnall S, Chang YF, Simpson KW.Quantitative
analysis of inflammatory and immune responses
in dogs with gastritis and their relationship to
Helicobacter spp. infection. J Vet Intern Med.
2005 Jan-Feb;19(1):4-14. 2006 World Congress WSAVA/FECAVA/CSAVA
415
G
G – Gastroenterology
HISTIOCYTIC ULCERATIVE COLITIS: INFECTIOUS OR IMMUNE
MEDIATED?
Kenneth W Simpson BVM&S,
PhD, MRCVS, DipACVIM,
DipECVIM
College of Veterinary Medicine
Cornell University
kws5@cornell.edu
The development of culture independent
techniques for determining the presence of
infectious agents has revolutionized the approach
to detecting both suspected and unsuspected
pathogens. For example: PCR with broad range
primers has led to the identification of Bartonella
henselae as the agent of cat scratch fever and
peliosis hepatis. PCR with pathogen specific
primers has enabled the accurate differentiation
of a growing number of Ehlichial associated
diseases. The development of labeled DNA
probes against bacterial 16- or 23s rRNA not
only facilitates specific identification of bacterial
pathogens, but also their localization within
tissues and cells, and antimcrobial resistance e.g.
associated with 23s mutations - clarithromycin.
This presentation focuses on the application of
culture independent techniques to Histiocytic
Ulcerative Colitis.
Canine Histiocytic Ulcerative Colitis
(HUC: also known as Granulomatous Colitis
2006 World Congress WSAVA/FECAVA/CSAVA
of Boxer Dogs) is a severe disease of unknown
etiology that typically affects Boxer dogs.
Clinically it is characterized by frequent, bloody,
mucoid stools,ulceration and inflammation of
the colon, anemia, hypoalbuminemia and weight
loss. The dominant histological features are an
accumulation of lymphocytes and plasma cells,
and large numbers of PAS positive macrophages
containing inclusions (similar to Whipple’s
disease) and the loss of colonic epithelium and
goblet cells. Immunopathological studies describe
an increase in IgG3 and IgG4 plasma cells, and
PAS+ positive macrophages and CD3-T cells, L1
and MHCII positive cells, with HUC likened
to human ulcerative colitis. Several studies
have described bacteria within a proportion of
macrophages in the mucosa of HUC affected dogs.
Ultrastructural studies suggest active phagocytosis
416
Back to contents
of bacteria that in some instances resemble
Chlamydia. Known invasive enteropathogens
such as Salmonella, Campylobacter Yersinia, and
Shigella have not been isolated from dogs with
HUC. Mycoplasma have been isolated from the
colon and regional lymph nodes of 4 boxer dogs
but an attempt to reproduce granulomatous colitis
with Mycoplasma was unsuccessful. This failure
to identify or isolate an infectious agent has lead
to HUC being considered a chronic immune
mediated disease. The outcome of treatment with
empirical combinations of diet, antimicrobials
and immunosuppression is variable, with perhaps
the most favorable outcome described in dogs
receiving antibiotics such as chloramphenicol
and tylosin. Recent reports indicate resolution of
clinical signs and histological lesions, including
the disappearance of PAS infiltrates in response
to enrofloxacin alone or in combination with
amoxicillin and metronidazole, re-awakening
the possibility that HUC may indeed have an
infectious etiology.
Colonic biopsies from affected dogs (13 Boxers
with HUC) and controls (27 non-HUC, 11 normal
histology) were examined by fluorescent in situ
hybridization (FISH) with a eubacterial 16srRNA
probe. Culture, 16s rDNA sequencing, and
histochemistry were used further to define the
invasive flora, and guide subsequent FISH. HUC-
associated E.coli were evaluated for their ability
to invade and persist in cultured epithelial cells
and macrophages, serotype, overall genotype,
phylogenetic group, and presence of virulence
genes.
Intramucosal bacteria, predominantly Gram-
negative coccobacilli, were present in 100% of
GCB, but none of the control samples. Culture
and 16srDNA sequencing yielded mostly
Enterobacteriaceae, and invasive bacteria
hybridized with FISH probes to E.coli. HUC-

associated E. coli isolates adhered to, invaded,
and persisted within cultured epithelial cells.
Invasion triggered a “splash”-type response, was
decreased (P<0.05) by cytochalasin-D, genistein,
colchicine and wortmannin, and paralleled the
behavior of Crohn’s disease-associated E. coli
LF-82. HUC-associated E.coli isolates and LF-82
were diverse in serotype and overall genotype, but
similar in phylogeny (B2 and D), and virulence
gene profiles (fyuA, irp1, irp2, chuA, fepC,
ibeA, kpsM-II, iss). HUC-associated E.coli that
displayed an adherent and invasive phenotype in
cell culture and LF82 were larger in genome size
than commensal E.coli, and belonged to novel
MLST clonal groups.
Thus HUC of Boxer dogs is associated
with selective intramucosal colonization by
Escherichia coli. E. coli strains associated with
HUC and Crohn’s disease have an adherent and
invasive phenotype, and resemble extraintestinal
pathogenic E. coli in phylogeny and virulence
genes. These findings support the thesis that
IBD is a consequence of mucosal colonization
by a restricted subset of the luminal microflora
in a susceptible individual, and point to the
association of E.coli resembling extraintestinal
pathogenic strains in genotype with chronic
intestinal inflammation. As HUC is largely
confined to Boxer dogs, it is tempting to speculate
that a defect in host defense, perhaps analagous
to those identified in some patients with Crohn’s
disease e.g. NOD2/CARD 15, TLR4, is present
in Boxer dogs and linked to bacterial invasion
and inflammation.
Further reading
Darfeuille-Michaud A, et al. High prevalence of
adherent-invasive Escherichia coli associated with
ileal mucosa in Crohn’s disease. Gastroenterology.
2004, 127: 412-21
Franchimont D et al. The toll-like receptor
(TLR)-4 Asp299gly polymorphism is associated
with Crohn’s disease and ulcerative colitis. Gut.
2004, 53: 987-92.
Harmsen HJ, et al. Extensive set of 16S rRNA-
based probes for detection of bacteria in human
feces. Appl Environ Microbiol. 2002,68:2982-
90.
Hostutler R et al.Antibiotic-responsive histiocytic
ulcerative colitis in 9 dogs.J Vet Intern Med.
2004,18:499-504.
Kleessen B, et al. Mucosal and invading bacteria
in patients with inflammatory bowel disease
compared with controls. Scand J Gastroenterol.
2002,37:1034-41
Liu Y et al Immunocytochemical evidence of
Listeria, Escherichia coli, and Streptococcus
Back to contents
G
antigens in Crohn’s disease. Gastroenterology.
1995,108,1396-404.
Martin HM, et al .Enhanced Escherichia coli
adherence and invasion in Crohn’s disease and
colon cancer. Gastroenterology. 2004,127:80-93.
Mow WS et al. High-level serum antibodies to
bacterial antigens are associated with antibiotic-
induced clinical remission in Crohn’s disease: a
pilot study. Dig Dis Sci. 2004, 49:1280-6.
Priestnall SL et al .Evaluation of “Helicobacter
heilmannii” subtypes in the gastric mucosa of cats
and dogs. J Clin Microbiol. 2004,42:2144-51.
Ryan P, et al.Bacterial DNA within granulomas
of patients with Crohn’s disease--detection by
laser capture microdissection and PCR. Am J
Gastroenterol. 2004,99:1539-43
Sartor RB Therapeutic manipulation of the
enteric microflora in inflammatory bowel
diseases: antibiotics, probiotics, and prebiotics.
Gastroenterology. 2004,126:1620-33.
Schuppler M, et al.An abundance of Escherichia
coli is harbored by the mucosa-associated
bacterial flora of interleukin-2-deficient mice.
Infect Immun. 2004,72:1983-90
Seksik et alAlterations of the dominant faecal
bacterial groups in patients with Crohn’s disease
of the colon. Gut. 2003,52:237-42.
Swidsinski A et al Mucosal flora in inflammatory
bowel disease. Gastroenterology. 2002,122:44-54.
Van Kruiningen, H. J., I. C. Civco, and R. W.
Cartun. 2005. The comparative importance of
E. coli antigen in granulomatous colitis of Boxer
dogs. Apmis 113:420-425.
Van Kruiningen, H. J., R. J. Montali, J. D.
Strandberg, and R. W. Kirk. 1965. A granulomatous
colitis of dogs with histologic resemblance to
Whipple’s disease. Pathol Vet 2:521-544.
Watanabe T et al. NOD2 is a negative regulator 2006 World Congress WSAVA/FECAVA/CSAVA
of Toll-like receptor 2-mediated T helper type 1
responses. Nat Immunol. 2004,5,800-8.
Acknowledgements: Dr. Simpson is supported
by a grant from the US public health service
(DK 002938). The author is grateful to Sean
McDonough, Mark Rishniw, Belgin Dogan,
Richard Goldstein, Patrick McDonough, Alex
German, Robin Yates, David Russell, Yung-Fu
Chang, Raghavan Palanappian, Martin Weidman,
Kendra Nightingale, Roger Hostutler, Jennifer
Chaitman, Susan Johnson, Ynte Schukken,
Francis Davies, Pat Fisher and Douglas Berg
for their input and collaboration on the studies
described above
417
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

HH
Hepatology
epatol

Back to contents

INVITED LECTURES - FULL PAPERS
H – Hepatology
HEPATIC VASCULAR DISORDERS IN SMALL BREED DOGS
Sharon A. Center, DVM, Dipl
ACVIM
College of Veterinary Medicine
Cornell University
Ithaca
New York
USA
14853
Sac6@cornell.edu
Hepatic Vascular Disorders: What Do We Mean?
A number of hepatic vascular disorders are
described in small breed dogs, most involving
abnormal development of the portal vein. While
extrahepatic congenital portosystemic vascular
anomalies (PSVA) have received the most
attention, the most common congenital vascular
abnormality is microvascular dysplasia (MVD).
Histologically, MVD is indistinguishable from
PSVA, yet MVD encompasses a number of
histologic peculiarities in addition to diminished
portal venous perfusion. Along with PSVA,
MVD appears to be an inherited abnormality in
certain terrier-type dogs. Portal atresia describes
a congenital absence of perfuseable extrahepatic
or intrahepatic portal vasculature. A veno-
occlusive lesion associated with MVD/PSVA is
recognized in some breeds. Non-cirrhotic portal
hypertension, histologically indistinguishable
from PSVA and MVD, occurs more commonly
in large breed dogs, and is associated with portal
hypertension and APSS. This lesion has at times
been mislabeled hepatoportal fibrosis. Hepatic
arteriovenous fistulas are bizarre malformations
representing the merging of branches of the
hepatic artery and portal vein. This lecture will
present a synopsis of diagnostic and clinical
features of vascular syndromes in small breed
dogs as well as their managerial approaches and
treatment successes.
Portosystemic Vascular Anomalies (PSVA)
Without question, this disorder is the most common
hepatic topic in the veterinary literature from both
a diagnostic and therapeutic perspective.
Typical Historical & Clinicopathologic Features:
Dogs with a symptomatic PSVA usually present
during the first 2 years of life. Many are stunted
Back to contents
H
and intermittently display neuroencephalopathic
signs consistent with hepatic encephalopathy
(HE), polyuria / polydipsia, episodic inappetence
or pica, or vague gastrointestinal signs. Some
dogs present only for development of ammonium
biurate urolithiasis. However, not all dogs are
overtly symptomatic. Some are discovered later
in life when liver function tests or abdominal
ultrasonography “discover” and abnormality.
We really do not know how many PSVA dogs
are asymptomatic. Current work suggests that at
least 20% of dogs may lack clinical signs notable
by an owner. Some PSVA bitches(unligated) have
repeatedly produced litters. The most common
routine clinicopathologic features include RBC
microcytosis, a borderline anemia, a low BUN
and creatinine, low glucose (very young toy
breed dogs), normal or modestly increased (up
to 3-fold) liver enzymes, normal or modestly
reduced albumin, hypocholesterolemia, low urine
specific gravity (Pu/Pd) and ammonium biurate 2006 World Congress WSAVA/FECAVA/CSAVA
crystalluria. Urine sediments from at least 3 urine
samples collected at different times of the day
(especially several hours after eating) are needed
to rule out ammonium biurate crystalluria. No
routine hematologic, biochemical, or urine
assessments are abnormal in every case.
Liver Function Test: Most dogs with PSVA are
initially identified with high serum bile acid
(SBA)or blood ammonia concentrations. Paired
SBA (12-hr fasted AND 2-hr postprandial
(PSBA)) have a 100% sensitivity for PSVA
detection. SBA are considered the most clinically
convenient and sensitive liver function assessment
(reflect abnormal perfusion or cholestasis)
that can be routinely managed and mailed for
analysis. Blood ammonia concentrations also
have high sensitivity for detecting PSVA but
419
H
samples must be immediately stored on ice, and
rapidly analyzed. In some cases, a provocative
ammonia challenge (NH4Cl, ammonia tolerance
test, (ATT)) is necessary to demonstrate ammonia
intolerance. Both fasting ammonia and fasting or
“random” SBA concentrations have each failed
to detect some PSVA dogs; provocative testing
with either test (PSBA, ATT) produces abnormal
values. A recently developed urine bile acid test is
now being used to screen high risk dogs for PSVA
and MVD (urine collected 4-8 hrs after feeding).
Improved differentiation of PSVA from MVD
can be achieved inexpensively and noninvasively
by measurement of Protein C; low values are
found in dogs with “severe” shunting (MVD dogs
usually have normal values.)
Liver Histology: Histologic lesions in PSVA
include hepatic lobular atrophy, juvenile portal
triads, portal triad arteriolarization (increased
arterial cross sections), lymphatic distention
in portal triad adventitia and surrounding large
hepatic venules, inconspicuous portal venules,
and prominent smooth “throttling” hepatic venule
musculatur. These features also are associated
with MVD. Histopathologic features are difficult
to identify in small hepatic core biopsies. Liver
biopsy is not definitive for syndrome classification
and must be combined with imaging studies or
Protein C. Biopsy rules out acquired liver disease
as an underlying cause.
Definitive Imaging: Until recently, the definitive
gold standard for PSVA diagnosis was portovenous
venography, with portography completed in right
and left lateral and ventrodorsal recumbency.
PSVA have been missed when only a single
lateral or VD image was recorded.
Ultrasonography: Ultrasonography can detect
“classic” features: small liver, hypovascular
intrahepatic portal system, large kidneys,
uroliths, and in 60 to 90% of cases (depending on
ultrasonographer skill) identification of an aberrant
2006 World Congress WSAVA/FECAVA/CSAVA
shunting vessel. Doppler color flow interrogation
identifies PSVA associated turbulence in the vena
cava. Otherwise, a slow, tedious, systematic
search of the portal vasculature is required.
Nuclear Scintigraphy Studies: Noninvasive
detection of PSS is achieved with colorectal
scintigraphy; a small amount of technicium
pertechnetate (99m) is placed in the colon with
portal uptake/delivery (liver:heart) recorded
in real-time with a gamma camera. A shunt
fraction (high operator variability) usually
> 50% (normal < 15%). A more quantitative
but invasive procedure involves injection of
99m
Tc-macroaggregates in a splenic vein (US
guidance).
Multisector CT Imaging of the Portal Vasculature:
definitively distinguishes PSVA (exact position of
420
Back to contents
aberrant vasculature) and APSS. Images can be
obtained in heavily sedated animals in less than 2
minutes, with vascular structures distinguished by
peripherally administered nonionic iodinated contrast.
PSVA Treatment: Medical & Surgical: According
to the veterinary literature, surgical attenuation
of PSVA is the treatment of choice. However,
depending on the procedure used and surgical
expertise, a 15% to 30% mortality may be
realized with persistent shunting in up to 50-
60% of cases. A variety of methods have been
investigated including partial or complete
PSVA occlusion using: silk ligation, ameroid
constrictors, cellophane banding, and thrombotic
coils. Outcome studies are difficult to compare
owing to different surgical procedures, follow-up
intervals, and tests. What is clear is that despite
an impression of complete surgical ligation,
many dogs continue to shunt, that incomplete
ligation can remarkably improve symptomatic
dogs, and that SBA concentrations inconsistently
normalize. While there is an impression that
PSVA cannot be managed medically, we have
managed a number of minimally symptomatic
dogs long term with a prescription veterinary diet
formulated for dogs with hepatic insufficiency.
Combination of dietary management with
lactulose (dosed to achieve several soft stools per
day), lactose (similar effect to lactulose in some
dogs), or low dose metronidazole (7.5 mg/kg PO
BID) is routinely recommended before surgical
intervention. While ameroid banding is lauded for
its low immediate post-operative complications,
some dog breeds (especially Yorkshire Terriers,
Maltese) may develop portal hypertension when
complete ligation is realized (days, weeks,
months). Some surgeons now purposely place a
larger size ameroid constrictor than indicated for
complete ligation, on dogs intolerant to complete
occlusion at surgery. Acquired PSS secondary to
portal hypertension develops as early as 2 months
in intolerant dogs that are totally ligated. Recent
review of cellulose band ligation of extrahepatic
PSVA documented this phenomenon. Clearly
we still cannot predict which dogs will tolerate
complete PSVA ligation and who should have
surgery. There is no data even yet that the
hepatic portal vasculature undergoes an adaptive
accommodation to “forced” perfusion induced
by PSVA ligation beyond the initial filling
phenomonenon. Lastly, many clinicians remain
naïve to the fact that asymptomatic PSVA have
been recognized in dogs as old as 13 yrs!
Indications for PSVA Ligation: episodic
neurobehavioral signs of HE, severe PU/Pd that
restricts pet ownership, recurrent development of
ammonium biurate crystalluria despite optimal
medical management. Male dogs ligated to their

tolerance that continue to develop ammonium biurate
urolithiasis are given permanent urethrostomies.
Microvascular Dysplasia (MVD)
A congenital aberration of the hepatic
microvasculature disturbing portal-sinusoidal
perfusion and associated with attenuated tertiary
portal branches, abnormal positioning of hepatic
venules within portal triads, and an abnormal
appearance or perfusion of hepatic venules. MVD
occurs in kindreds with increased prevalence of
PSVA where it appears to be a linked-inherited
abnormality. In fact, dogs with MVD outnumber
dogs with PSVA in certain terrier kindreds by 5:1 or
more. MVD dogs typically DO NOT demonstrate
routine hematologic, biochemical, or clinical
changes consistent with PSVA although they
have abnormal SBA concentrations that overlap.
Most MVD dogs are discovered by routine
screening for PSVA. However, MVD also may
be serendipitously identified later in life when a
SBA test is performed for the first time during an
illness. Screening puppies from high risk breeds
(SBA or UBA) is encouraged to eliminate such
diagnostic confusion later in life. Most MVD dogs
do not develop hyperammonemia or ammonium
biurate crystalluria and most DO NOT require
medical therapy or even a reduction in protein
intake. In rare symptomatic cases, clinical signs
are controlled with medical management as for
PSVA. However, in the author’s experience, most
symptomatic MVD dogs have a PSVA and were
erroneously labeled as MVD or have another
liver syndrome. Some dogs with MVD develop a
progressive veno-occlusive lesion.
Portal Hypoplasia vs Portal Hypoperfusion
Portal hypoplasia is used by some pathologists
to describe attenuated intrahepatic portal
vasculature. Unfortunately, this terminology
implies a congenital abnormality. Any disorder
that diminishes portal venous perfusion (e.g.
portal venous thrombus, portal venous stenosis,
surgical creation of an Eck fistula), imparts
a similar histologic pattern (lobular atrophy,
inconspicuous portal venules, lymphatic
distention, and physiologic adaptation of the
hepatic artery to increase blood flow). Arteries
subjected to higher flow / pressure become
tortuous causing an increase in their cross
sectional profiles (arteriolarization). Histologic
features in dogs with surgically created PSS
cannot be differentiated from dogs with PSVA,
MVD or non-cirrhotic portal hypertension.
The literal definition of portal hypoplasia is
underdevelopment, incomplete or arrested
development of the portal vein. Portal venous
hypoperfusion, is a more appropriate descriptive
term.
Back to contents
H
Portal Vein Atresia
Atresia indicates the congenital absence of a
passageway. Portal atresia is diagnosed when the
extrahepatic portal vein is judged to be very small
or absent or when there is no tolerance to occlusion
of a single PSVA. Eventually this abnormality is
associated with multiple APSS and ascites. There
is no treatment except medical management of
HE and ascites. Without multisector CT imaging,
these dogs are commonly operated with the
expectation of finding a single PSVA.
Non-Cirrhotic Portal Hypertension (NCPH)
This syndrome is impossible to clearly distinguish
from portal vein hypoplasia and constitutes an
overlap syndrome that has confused retrospective
case studies. At times, NCPH has been mislabeled
as hepatoportal fibrosis. A curious disorder
histologically indistinguishable from PSVA and
MVD, NCPH involves diminished perfusion of
the tertiary portal branches and is associated with
portal hypertension, multiple APSS, and ascites
(variably). Affected dogs range in age from 3
mths to 8 yrs (most < 4 yrs) at initial diagnosis.
NCPH has been diagnosed in 12 Doberman
Pinchers, 7 Cocker Spaniels, 5 Rottweilers,
and multiple other breeds. It also has been
documented in littermates (Dobermans, Cocker
Spaniels, Standard Schnauzers). A several week
history (or longer) of clinical illness precedes
initial presentation. Historical features include:
abdominal enlargement (ascites), gastrointestinal
signs (vomiting, diarrhea), polydipsia, HE, and
melena. Physical findings include: poor body
condition and small stature. Common clinicopatho-
logic features include: RBC microcytosis (60%),
high serum ALP and ALT activites (3-5 fold,
respectively, 60%), hypoalbuminemia (76%),
low BUN (40%),low urine SG (69%). Abdominal
effusion is a pure transudate. Abdominal US
discloses microhepatica, abdominal effusion,
and multiple APSS. Extrahepatic portal venous
2006 World Congress WSAVA/FECAVA/CSAVA
thrombi have been identified in some dogs.
Hepatic parenchyma may appear hyper-, hypo, or
heterogeneously echoic or normal. Liver function
assessment by SBA is always abnormal. Dogs
are inconsistently hyperammonemic and may
not demonstrate ammonium biurate crystalluria.
Diagnosis requires liver biopsy to rule out acquired
necroinflammatory or fibrosing liver syndromes
as an underlying cause of APSS. Liver biopsy
by laparoscopy is recommended owing to the
healing problems created by ascites. Treatment
is symptomatic for HE and to control ascites
(sodium restriction, diuretic therapy, usually
combination of furosemide and spironolactone).
Some dogs live a normal life span, some require
lifelong medical management for HE and ascites,
421
H
and some live well only on a prescription diet
manufactured for dogs with hepatic insufficiency,
and some have done well without treatment after
initial medical management. Hypoalbuminemic
dogs may have a concurrent intestinal lesion
(e.g. inflammatory bowel disease). A severe
bout of hemorrhagic gastroenteritis historically
precedes development of NCPH in many dogs.
This syndrome resembles a disorder in humans
NCPH) associated with poor socioeconomic
conditions (high incidence of enteric bacterial
and parasitic infections). A similar lesion can
be induced in rabbits and dogs by intraportal
injection of killed nonpathogenic Escherichia
coli. In man, individuals with NCPH have a better
2006 World Congress WSAVA/FECAVA/CSAVA
prognosis than individuals with APSS secondary
to cirrhosis, similar to the situation in dogs.
Affected people may live a relatively normal
lifespan similar to some dogs with NCPH.
Hepatic Arteriovenous Fistula
An uncommon, usually congenital malformation.
Arteriolization of the portal circulation leads
to portal hypertension, APSS, and abdominal
effusion. Hepatic vascular abnormalities distant
to the primary fistula are common. Despite fistula
resection or occlusion, many dogs are not cured.

422
Back to contents

H – Hepatology
ANTIOXIDANTS IN LIVER DISEASE: A FOCUS ON THIOL
SUPPLEMENTATION
Sharon A. Center, DVM, Dipl
ACVIM
College of Veterinary Medicine
Cornell University
Ithaca
New York
USA
14853
Sac6@cornell.edu
Hepatic Antioxidant System
The pivotal involvement of the liver in cleansing
blood from the gut (considered to be the richest
source of oxidants and toxins in the body), it’s
central role in intermediary metabolism and
detoxification processes, its large active Kupffer
cell (macrophage) population, imposes high risk
for exposure to injurious substances, infectious
agents, toxic adducts, and oxidizing substrates.
Consequently, the liver is endowed with diverse
antioxidant/detoxification mechanisms. Many of
the non-enzymatic antioxidants can be directly
supplemented. Since glutathione (GSH) is
involved in many antioxidant processes, there is
tremendous interest in thiol (GSH) donors such as
s-adenosyl-methionine(SAMe). SAMe functions
in this capacity as well as participating in a large
number of other critical cellular processes and
biochemical pathways). An additional group of
extracellular selenoproteins, thioredoxins, also
possess antioxidant activity.
Antioxidative enzymes provide first line defense
and whether or not these can be sufficiently
Back to contents
H
supplemented remains controversial. Enzymatic
antioxidants are localized in specific subcellular
compartments where radicals are frequently
generated (mitochondria, peroxisomes or
microbodies, cell cytosol) or are present in the
systemic circulation. Examples include superoxide
dismutase (SOD), catalase, and GSH peroxidases
(GSH-Px) a family of cytosolic, mitochondrial,
and extracellular enzymes that detoxify lipid
hydroperoxides and H2O2 by oxidizing GSH to
GSSG. Several GSH-Px’s require selenium. GSH
reductase (requires riboflavin as a co-factor)
regenerates reduced-GSH from its oxidized
disulfide(GSSG).
There is great interdependence among the
antioxidants such that supplementation with only a
single agent may not provide an optimal response.
At present, no one knows what “cocktail” is
ideal for dogs or cats. Since nutritional balance
is an important variable influencing antioxidant
availability (e.g. vitamin E, trace metals, cysteine
for GSH), nutritional support is essential in liver
disease along with antioxidant supplementation.
2006 World Congress WSAVA/FECAVA/CSAVA
423
H
Protection by protein binding of toxic adducts
or transition metals (copper or iron) to
albumin, transferrin, ferritin, ceruloplasmin or
metallothionein, provides another rapid venue
for detoxication (liver and systemic circulation).
While these cannot be directly supplemented
(except albumin), their synthesis can be enhanced
through nutritional support. Supplementing with
supraphysiologic doses of single agents can
produce oxidant injury. Examine the diagram
above and note that excessive administration of
vitamin C (ascorbate) or vitamin E (tochoperol)
can result in accumulation of their respective
oxidant radicals.
Combination Therapy: Antioxidant Agents with
Immunomodulatory / Antifibrotic Medications
Advantageous combination therapy in
necroinflammatory and cholestatic liver
disorders may include glucocorticoids, other
immunomodulatory or anti-inflammatory
prescription drugs combined with various
antioxidants. Since glucocorticoids are known
to mediate inhibition of NF-kB (benefically
modulated by certain antioxidants such as thiols),
adjunctive therapy with an effective thiol donor
(e.g. NAC or SAMe) and vitamin E may optimize
control of inflammatory mediator release and cell
response as compared to pure immunomodulatory
treatment or therapy limited to antioxidants. It
is reasonable to expect, given the complexity
of disease pathomechanisms, that a mixture of
antioxidants (an antioxidant “cocktail” so to
speak) will eventually be used in combination
with other anti-inflammatory / antifibrotic agents
for different types of liver disease and will
necessitate unique recommendations for different
species.
2006 World Congress WSAVA/FECAVA/CSAVA
424
Back to contents
Thiols
Thiols play a central yet cooperative role in
the antioxidant network. (Figure adapted from:
Sen CK, Packer L: Thiol homeostasis and
supplements in physical exercise. Am J Clin
Nutr 2000; 72(suppl): 653S-669S). Substances
containing S-H bonds, HS-SH disulfide that have
central importance in many biochemical and
pharmacological reactions. Reduction of only a
few essential SH-SH bonds in a biologic reactant
can remarkably change its molecular properties.
Thus, it is important that a system exists to
protect against damage to these vulnerable
bonds. Most thiols act as reducing agents (absorb
emitted electrons in oxidant processes, thiol
is lost). The importance for conserving thiol
bonds is evident when one understands that
incorporation of a cysteine moiety influences
the tertiary structure of proteins (e.g. molecule
configuration, folding) and can influence effects
of certain drugs (e.g. insulin). A significant
number of proteins involved in signaling have
critical thiols (e.g. cell receptors, ubiquitinylation
proteins, protein kinases, and some transcription
factors). Metallothionein, the only known protein
implicated in cellular zinc distribution, binds
7 zinc atoms via thiolated ligands. Binding sites
lose function with oxidation of the thiol group;
dogs with copper storage hepatopathy may benefit
from antioxidants that preserve these bonds
allowing zinc transport. Cysteine residues are
among the most easily metabolized compounds,
being easily oxidized by transition metals
and participating in thiol-disulfide exchange
reactions. The most important non-protein thiol
source in intermediary metabolism is glutathione
(GSH, containing a single cysteine moiety) and
the small protein thioredoxin (containing two
redox-active half-cysteine residues; a ubiquitous

protein, important for gene expression) that we
will not discuss. Each of these play important
roles in antioxidant defense, protein folding, and
signal transduction. In vivo, reductases recycle
disulfides to thiols using cellular-reducing
equivalents (e.g. NADH or NADPH) maintaining
a favorable oxidoreductive (or redox) state in the
cell and thiol conservation.
Hepatic GSH in Liver Disease
Low hepatic GSH concentrations develop
in dogs and cats with substantial liver injury
(necroinflammatory, cholestatic disorders).
Contributing factors include: reduced nutritional
intake (proteins, essential amino acids,
competition between amino acid transporters,
vitamin insufficiency [riboflavin: GSSG
reductase, nicotinic acid: NADPH, pyridoxine
(B6): SAMe pathway], mitochondrial dysfunction:
ATP deficiency, down regulation SAMe synthase,
oxidation of SAMe pathway enzymes, enhanced
GSH utilization: conjugation reactions (toxins,
drugs), and overwhelming oxidative challenge.
GSH Supplementation
N-Acetylcysteine (NAC), S-Adenosylmethionine
(SAMe), Whey Protein Extract:(limited scientific
evidence of efficacy), Lipoic Acid: (lethal feline
toxicity proven)
Back to contents
H
N-Acetylcysteine (NAC)
An acetylated variant of L-cysteine can provide
SH groups. A direct thiol donor given IV when
supplementa-tion urgent (e.g. oxidant challenge
/ fulminant hepatic failure). Metabolized into
products that stimulate GSH synthesis and
promote detoxification pathways. Functions
directly as a free radical scavenger (circulation).
Dose: severe oxidant injury / hepato-toxicosis,
IV administration of saline diluted NAC
(1:2 for 10% or 1:4 for 20% NAC solution).
Administer via non-pyrogenic filter. Protocol
as for acetaminophen toxicity: 140 mg/kg IV
initially: slow bolus NOT constant rate infusion
(ŕ ammonia toxicity) then 70 mg/kg IV or PO x
3-6 (or more) treatments given at 8 to 12 hour
intervals. Treatment tailored to condition urgency/
severity. Chronic PO treatment provided with
SAMe. NAC Toxicity: Oral dose LD50 approxi-
mates 6-8 gm/kg in rodents. Infrequent allergic
reactions (IV administration) in humans and
dogs (rash, pruritus, facial swelling, tachycardia,
gastrointestinal signs). NOTE: doses as low as
1.2 g daily in humans might confer a pro-oxidant
effect, lowering GSH and increasing the GSH/
GSSG ratio.
S-Adenosyl-L-Methionine (SAMe)
Plays a complex role in metabolism, functioning
as a methyl group donor (transmethylation
2006 World Congress WSAVA/FECAVA/CSAVA
425
H
reactions), precursor of sulphur-containing
compounds (transsulfuration pathway), and
in production of polyamines. Note important
products of the transmethylation pathway and
transsulfuration pathway shown. The polyamine
pathway influences cell replication / regeneration,
DNA synthesis, and apoptosis and yields an
important metabolite methylthioadenosine (plays
a pivotal role in hepatocyte function and gene
transcription). Since 85% of transmethylation
reactions and up to 48% of methionine metabolism
occurs in the liver, hepatic SAMe availability is
essential. SAMe has been shown to provide a
benefit in a variety of liver disorders (modeled in
experimental animals, in humans, and in dogs and
cats), the molecular basis of SAMe’s protective
effects have been demonstrated in vitro using
hepatocyte cell cultures. Oral SAMe in cirrhotic
humans replenishes hepatic GSH and improves
resistance against free radical / reperfusion injury.
By sustaining appropriate DNA methylation,
SAMe has a broad range of potential effects
on cell repair, inflammatory mediator release,
and the pathobiology of ongoing immune-
mediated liver injury. Studies in dogs with
glucocorticoid induced vacuolar hepatopathy,
cats with spontaneous liver disorders, and
healthy cats, has proven both hepatic and RBC
protective effects. We documented bioavailability
and biologic effects of a stable salt of SAMe
(1,4-butanedisulfonate salt, Nutramax Laboratories,
Nutramax Laboratories, USA) in healthy cats,
2006 World Congress WSAVA/FECAVA/CSAVA
426
Back to contents
cats with asymptomatic cholangiohepatitis,
and dogs with glucocorticoid-induced vacuolar
hepatopathy. In each circumstance, this stable
SAMe salt was absorbed, significantly increased
plasma SAMe concentrations, hepatic GSH
concentrations, and improved tissue redox status.
Beneficial effects on RBCs also were shown. How
SAMe accesses hepatocytes has not been clarified
but it is proven to become rapidly incorporated
within cell membrane phospholipids, to influence
intracellular SAMe pathways and products and to
readily cross into mitochondria.
Dose: 17-20 mg/kg is advised for dogs and of 200
mg/day in cats using bioavailable enteric coated
tablets given on an empty stomach. We only use
a form of SAMe proven to be bioavailable that
contains an excess of the biologically active
S’S SAMe isomer. Selecting an appropriate
SAMe product depends on specific information
provided by the manufacturer regarding shelf-
life, bioavailability, and S’S isomer content.
Toxicity: Adverse effects to SAMe are rare but
may include inappetence, vomiting, lethargy, and
agitation after initial treatment. Effects may self-
resolve, or abate with a reduced dose, gradually
increasing back to the therapeutic target. In
rodents, a single dose LD50 > 4.6 gm/kg SAMe
exits. Chronic studies in rats given 200 mg/kg
body weight per day for 104 weeks, dogs given
20 mg/kg PO x 84 days, cats given 40-65 mg/kg
for 118 days did not produce any signs of toxicity
(blood testing, liver histology).

H – Hepatology
COPPER STORAGE DISEASES IN DOGS
Jan Rothuizen, Professor
of Internal Medicine
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine,
University Utrecht
j.rothuizen@vet.uu.nl
An abnormal copper metabolism can cause
hepatic copper accumulation and subsequently
an increase in oxidative stress. We therefore
analyzed the copper metabolism pathways and
(non)- enzymatic defenses against ROS in three
different forms of chronic liver failure in the dog.
Chronic hepatitis caused by inherited copper
toxicosis (Copper toxicosis, CT) was compared
to chronic hepatitis of unknown etiology (CH).
These two were compared to liver failure due to
chronic extrahepatic bile duct obstruction (extra
hepatic cholestasis, EC). Copper metabolism was
analyzed using histochemical staining (copper
levels) and quantitative PCR (Q-PCR) on copper
excretory and storage gene products (ATOX1,
COX17, ATP7A, ATP7B, CP, MT1A, MURR1,
XIAP). Oxidative stress and cellular homeostasis
was measured with Q-PCR (SOD1, CAT, GSS,
GPX1, CCS, p27KIP, Bcl-2) as well as GSH and
GSSG levels.
Results showed massive accumulation of hepatic
copper (5+) in CT. In EC and CH no or only slight
copper accumulation (1-2+) was observed. Most
gene products for copper metabolism remained
at control levels. Three clear exceptions were
observed in CT; 3-fold mRNA increase of ATP7A
and XIAP and complete absence of MURR1.
Only quantitative differences between CH, CT,
and EC were observed regarding oxidative stress
and cellular homeostasis. This was confirmed
with GSH/GSSG ratio measurements, were the
strongest reduced ratio was seen in CT (8-fold),
the least in CH (5-fold). In conclusion, cholestasis
and inflammation do not or not significantly
increase copper accumulation. All three diseases
have reduced protection against oxidative stress,
opening a rationale to use anti-oxidants as
possible therapy.
Copper is an integral part of many important
enzymes involved in several vital biological
processes.1 In humans the only copper storage
disease of which the molecular background
Back to contents
H
is resolved is Wilson’s disease. A major
pathogenetic pathway is that accumulated copper
catalyzes the formation of highly reactive oxygen
species (ROS), like hydroxyl radicals. In dogs
like in man, hepatic copper accumulation may
cause hepatitis which ultimately causes cirrhosis.
Copper associated hepatitis has been described
in dog breeds such as Bedlington terriers,
Doberman pinschers, Sky terriers, Dalmatians,
Anatolian shepherds, and Labrador retrievers.
Copper Toxicosis (CT) in Bedlington terriers
is an autosomal recessive disorder causing
impaired biliary copper excretion. The resulting
progressive lysosomal accumulation of copper
becomes histologically evident at one year of
age. The genetic defect in Bedlington terriers is
caused by a deletion of exon 2 of the MURR1
(COMMD1) gene. In all other dog breeds the
molecular background of the disease is unknown.
Cholestasis is a sequel of most parenchymal liver
diseases, and may cause a reduced biliary copper
excretion and secondary copper accumulation.
For understanding the primary or secondary
role of copper it is important to evaluate copper
trafficking pathways, oxidative stress, and 2006 World Congress WSAVA/FECAVA/CSAVA
cholestasis.
Copper is intracellularly bound to specific
proteins. Small copper-binding proteins, denoted
copper chaperones, distribute copper to specific
intracellular destinations. ATOX1 for instance,
delivers copper to the ATPases, CCS distributes
copper to Cu/Zn superoxide dismutase (SOD1),
COX17 delivers the copper to the cytochrome
c oxidase in the mitochondria, and MURR1 is
implicated in the lysosomal storage of copper as
well as the excretion into bile. The ATPases ATP7A
and ATP7B transport copper to the cuproenzymes
and ameliorate excretion of excess copper.
Ceruloplasmin (CP) is a metalloprotein which
binds copper during synthesis and is secreted into
serum. Metallothionein 1A (MT1A) is a small
intracellular protein capable of chelating several
427
H
metal ions, including copper. XIAP is an X-
linked inhibitor of apoptosis recently associated
with MURR1.
Excess copper can induce oxidative stress which
could lead to cell death and chronic inflammation.
The enzymatic defense against oxidative stress
consists of several tightly regulated proteins
such as superoxide dismutase (SOD1) and
Catalase (CAT). Non-enzymatic defenses are
exerted by molecules such as alpha-tocopherol,
beta-carotene, ascorbate, and a ubiquitous
low molecular thiol component, Glutathione.
The synthesis of Glutathione from glutamate,
cysteine, and glycine is catalyzed by two
cytosolic enzymes, γ-glutamilcysteine synthetase
(GCS) and GSH synthetase (GSS). The redox
status of GSH depends on the relative amounts
of the reduced and oxidized forms of glutathione
(GSH/GSSG).
We have investigated the presence of copper and
its possible role in inflammatory and cholestatic
chronic liver diseases. To study the effect of
cholestasis, we examined dogs with the chronic
extrahepatic cholestasis. In comparison we
analysed idiopathic chronic hepatitis (CH) in
breeds not associated with copper accumulation,
and the only proven inherited form of copper
toxicosis in dogs, CT in Bedlington terriers.
Observations on the histological grading of copper
showed a marked diffuse copper accumulation
in the hepatocytes and focally in macrophages in
Bedlington terriers with CT, in agreement with
earlier reports. On the other hand, in extrahepatic
cholestasis and chronic idiopathic hepatitis there
were no copper granules detectable in 33% and
50% of the cases, respectively. In the other cases
there was only a slight to moderate degree of copper
staining. This implies that copper accumulation is
not a consistent feature and never exceeds slightly
increased levels of copper in dogs with cholestasis
and idiopathic hepatitis. Copper may thus be of
2006 World Congress WSAVA/FECAVA/CSAVA
minor importance in these diseases.
428
Back to contents
Comparing the differential mRNA expression
profiles showed only significant differences
between the three diseasesfor ATP7A and XIAP.
The large increase in XIAP and ATP7A (which
is the extracellular transport of copper through
the trans-Golgi network) in Bedlington terriers
lacking functional MURR1 is most likely a
compensatory effect to overcome complete
absence of the MURR1 pathway. In the EC and
CH-group no significant changes were found
in ATP7A, CP, and MURR1. Perhaps only the
decrease in mRNA for ATP7B has had an effect
to produce slight accumulation of copper in the
EC and CH-group.
With respect to the defence against oxidative
stress the dogs with EC and CH were similar.
Cholestasis and inflammation caused reduced
expression of mRNA for SOD1 and CAT.
However, however, these reductions were greater
in the CT-group. We conclude that, although
copper is a major trigger for oxidative stress,
diseases with primary copper accumulation
cannot be distinguished from primary cholestatic
or inflammatory diseases based on their reaction
profile to exposure to ROS.
GSH/GSSG ratios were decreased in all diseases
with the highest reduction in the CT-group.
The use of anti-oxidants or GSH esters may
be effective in treating these liver pathologies.
Furthermore, the use of SAM-e in a cirrhotic rat
model has shown to have an inhibiting effect on
Collagen-I production which could ameliorate
liver fibrosis. Because of the decrease in oxidative
stress defenses (enzymatic and non-enzymatic),
the use of SAM-e could be considered in dogs
with CT, but also in other inflammatory and/or
cholestatic liver diseases.
Results clearly showed that cholestasis and
inflammation cause no or only minimal copper
accumulation, and that the only gene in the copper
metabolic pathways which is affected by

H – Hepatology
REGENERATION AND FIBROSIS IN CANINE HEPATITIS AND
CIRRHOSIS
Jan Rothuizen, Professor
of Internal Medicine
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine,
University Utrecht
j.rothuizen@vet.uu.nl
Chronic hepatitis is characterized by hepatocellular
apoptosis or necrosis, inflammation, and fibrosis.
Fibrosis is the major factor causing morbidity and
mortality due to the development of cirrhosis We
have studied different forms of hepatitis: Acute
Hepatitis (AH) without fibrosis, Chronic Hepatitis
(CH), and cirrhosis (CIRR), including Lobular
Dissecting Hepatitis (LDH). The last disease is a
specific form of cirrhosis with severe fibrosis and
complete disruption of the lobular architecture.
It has already been established that a transient
increase of transforming growth factor β1 (TGF-
β1) in the liver promotes fibrosis with the formation
of extracellular matrix (ECM) components and
suppresses hepatocyte proliferation. The major
components of the ECM are interstitial collagens
(types I and III), membrane collagen (type IV),
and non-collagenous glycoproteins, such as
laminin and fibronectin.
We analyzed liver fibrosis using several
molecular and biochemical techniques
(Q-PCR, Western blotting, and semi-quantitative
immunohistochemistry on ECM proteins).
Prolonged overexpression of TGF-β1 suppresses
cell proliferation, is pro-apoptotic, and induces a
deposition of ECM proteins, resulting in fibrosis
in major organs such as the liver.
In fibrotic diseases (CH, LDH, and CIRR) the
TGF-β1 pathway was activated. There was an
Back to contents
H
increase in mRNA levels of the TGF-β1 ligand
and the two receptors. uPA, the activator of TGF-
β1, was expressed at a higher level. Western
blotting confirmed increased TGF-β1 in these
diseases. In summary, increased levels of TGF-β1
signalling may very well explain the activation
of Smad-2 and subsequently the formation of
collagens (Fig. 3, 4, 5).
Immunostaining against collagen I and III on
normal liver tissues showed normal staining
of the collagens in portal tracts, around the
hepatic veins, as well as in the perisinoidal space
(particularly centrolobular). The corresponding
results of mRNA levels and immunostaining in
LDH can be explained by the rapid clinical course
of the disease in LDH. In CCl4-induced rodent
models of liver fibrosis, TGF-β1 and procollagen
mRNAs were increased, including procollagen I,
III, and IV.
The mechanisms underlying progressive fibrosis
are unknown, but hypoxia is a known fibrogenic
stimulus. On the other hand, it is conceivable that
increased collagen deposition leads to reduced
oxygen levels in the surrounding tissue and
consequently up regulates HIF-1α. Indeed, the
two major fibrotic diseases, LDH and CIRR,
2006 World Congress WSAVA/FECAVA/CSAVA
clearly showed an induction of HIF-1α mRNA
levels of 3- and 7-fold, respectively.
429
H
H – Hepatology
TREATMENT FOR SEVERE FELINE HEPATIC LIPIDOSIS

Sharon A. Center, DVM, Dipl

ACVIM
College of Veterinary Medicine
Cornell University
Ithaca
New York
USA
14853
Sac6@cornell.edu

The feline hepatic lipidosis syndrome (HL)
is a potentially lethal intrahepatic cholestatic
syndrome observed in over conditioned (obese)
cats associated with anorexia and catabolism.
This circumstance commonly complicates other
liver disorders in the cat and a thorough approach
to its management entertains therapeutic
maneuvers thought to have benefit in many
jaundiced cats. Successful recovery from feline
liver disorders improves with early diagnosis and
requires a committed effort to provide nutritional
and metabolic support. Since cats have a unique
propensity for accumulation of lipid vacuoles in
their hepatocytes, there has been confusion in some
cases where the HL syndrome was diagnosed in
an individual having only minor to moderate cell
vacuolation (histopathology or cytology). In the
HL syndrome > 80% of hepatocytes are involved;
in health, only 5% of hepatic weight is attributed
to triglyceride. The disorder is best considered a
syndrome as it has a multifactoral pathogenesis
leading to malnutrition. The old term “idiopathic”
associated with this condition is obsolete since in
most cases ( > 85% in the author’s clinic) a more
primary disease condition can be identified as the
underlying problem.

Disorders Associated with Secondary Feline Hepatic Lipidosis Syndrome

Other liver disorders: Small intestinal diseases
Cholangiohepatitis Eosinophilic enteritis
Choledochitis Lymphocytic/plasmacytic enteritis
extrahepatic bile duct obstruction Chronic bowel obstruction
2006 World Congress WSAVA/FECAVA/CSAVA

Chronic suppurative hepatitis Salmonella enteritis

Portosystemic vascular anomaly
Bile duct adenocarcinoma Renal disorders:
Hepatic lymphosarcoma Chronic FUS
Neoplasia (non-hepatic): Pyelonephritis
Urinary bladder Chronic interstitial nephritis
transitional cell carcinoma Hyperthyroidism
Metastatic carcinoma Severe Anemia
Intestinal adenocarcinoma Pyometra
Intestinal lymphosarcoma Cardiomyopathy
Pancreatitis Central neurologic disease
Diabetes mellitus

430
Back to contents

Confirming the Diagnosis of Hepatic Lipidosis:
DON’T be in a hurry to acquire tissue if hepatic
lipidosis is a primary consideration.
USE CYTOLOGY & CLINICOPATHOLOGIC
FEATURES to make a Presumptive Diagnosis.
During the initial few days of therapy / rescue,
these animals have high risk for anesthetic /
surgical complications.
We have observed heinz body hemolysis after:
etomidate and diazepam sedation (propylene
glycol carrier), and after propofol anesthesia
(phenol derivative). Usually, the heinz body crisis
hits about 12-hours after drug administration.
EARLY Liver BIOPSY MAY LEAD TO DEATH:
related with failure to recover from anesthesia or
bleeding.
A Presumptive Diagnosis of HL is Made on the
Basis of: Signalment, physical examination,
clinicopathologic data, and abdominal ultrasound.
This justifies hepatic needle aspiration for
cytology. However, this procedure is only done
after vitamin K1 response. Liver biopsy is
really not necessary to diagnose HL, however
it IS NECESSARY to diagnose cholangitis
/ cholangiohepatitis (suppurative or non-
suppurative) and other liver disorders. Make
sure that > 80% of hepatocytes are vacuolated
on aspiration cytology and that hepatocytes were
sampled, not just omental / falciform fat.
When to Pursue a Liver Biopsy ? if poor response:
feeding attempts fail, bilirubin does not decline,
clinical illness persists at a severe level AFTER
7-10 days of critical supportive care.
Fluid & Treatments Routinely Used in Rescuing
Cats with Hepatic Lipidosis
Fluids: Avoid lactate containing and dextrose
supplemented fluids. High lactate associated with
HL. Dextrose supplementation may thwart
adaptation to fatty acid oxidation; carbohydrates
poorly handled in stressed cats.
KCl Supplementation: according to the
conventional sliding scale. Do not exceed
0.5 mEq/kg/hr KCl. If concurrently supplementing
H
K phosphate, reduce KCl dose by amount of K in
K phosphate.
Potassium Phosphate Supplementation: Phosphate
concentrations decline after initial feeding
(refeeding phenomenon). Initial dose of 0.01 to
0.03 mmol/kg/hr Usually use the high dose rate,
even if initial phosphate is not low, upon refeeding
hypophosphatemia frequently developes.
Monitor serum phosphate concentrations every
3 to 6 hours (during and immediately after
discontinued supplementation). Discontinue
phosphate infusion when serum phosphorus > 2
mg/dl. Complications: Too much phosphate can
result in hypocalcemia and soft tissue calcium-
phosphate deposition. Calcium-phosphorus
product > 58 mg/dl = mineralization. Iatrogenic
hyperkalemia: failure to appropriately reduce
KCl infusion rate. Parenteral requirements
resolve once alimentation established.
Vitamin K: 0.5 to 1.5 mg/kg PO at 12 hour
intervals parenterally, NOT IV and NOT PO, 2-3
doses only.
Vitamin E: 10 IU/ kg PO per day until convinced
of recovery
Water Soluble Vitamins: 1 - 2 ml B Soluble
vitamins per liter, keep covered from light.
Thiamine (B1): 100 mg orally, use B-soluble
vitamins in fluids NOT SQ or IM injection ŕ
collapse (rare).
B12-Cobalamin: B-soluble vitamin supplementation
in fluids and commercially available critical care
diets
(commercial pet foods are supplemented with
stable, pharmaceutical grade vitamin B12) can
provide therapeutic B12 for many patients.
However, those with severe inflammatory bowel
disease or malabsorption due to infiltrative
bowel disease (including lymphoma) may
require parental “loading” and protracted therapy
with parenterally administered B12 (1 mg IM).
Frequency of dose administration is determined
based on sequential plasma B12 concentrations
2006 World Congress WSAVA/FECAVA/CSAVA
(5 -7 day intervals to once monthly have been
determined in individual cats). B12 insufficiency
may augment development of hepatic lipidosis.

Contents of a Fortified B-Vitamin Complex Used in Crystalloid Fluids in Cats with FHL
Thiamine hydrochloride (Vitamin B1): 50 mg
Riboflavin 5’ Phosphate sodium (Vitamin B2): 2.0-2.5 mg
Niacinamide (Vitamin B3): 50-100 mg
d-panthenol (Vitamin B5): 5-10 mg
Pyridoxine HCl (Vitamin B6): 2-5 mg
Cyanocobalamin (Vitamin B12): variable 0.4 to 50 mcg
(Low B12 values necessitate additional supplementation in deficient cats, IM)
Benzyl alcohol (preservative): 1.5% (no adverse consequences noted in FHL cats)

431
Back to contents
H
l-Carnitine: 250 mg PO / day has been used as
a routine supplement in the author’s hospital
for the theoretical reason of promoting fatty
acid oxidation, increasing loss of CN-ester fatty
acids in urine, and retention of lean body mass.
Metabolic response to l-CN has recently been
proven in obese healthy cats undergoing weight
loss. Synthesis of l-carnitine may be enhanced by
SAMe supplementation.
GSH donors: Markedly low hepatic GSH has
been demonstrated in liver tissue from cats with
HL.
May promote RBC hemolysis not
attributable to electrolyte aberrations (severe
hypophosphatemia), and may be associated
with RBC heinz bodies and adverse response
to oxidative drugs (e.g. too much vitamin K,
propofol anesthesia, injectable diazepam or
etomidate contain propylene glycol).
N-acetylcysteine: 140 mg/kg IV, then 70 mg/kg
IV at 12 hour intervals.
Dilute 10% NAC (Mucomyst®) with saline 1: 4,
administer IV using a 0.25 micron filter.
s- Adenosylmethionine (SAMe; Denosyl-SD4):
use source providing S’S stereioisomer =
biologically active form ONLY. 20 mg/kg PO
BID. Follow NAC as PO thiol (GSH) donor.
Since SAMe is given with food
in the HL cat which is on continuous nutritional
support and since the presence of food reduces
SAMe bioavailability, we have empirically
increased the total dose by BID administration.
NutritionalSupport:ESSENTIALCORNERSTONE
OF THERAPY for JAUNDICED CATS
Initial Feeding: Use oral feeding or nasogastric
(NG) tube. Avoid food aversion response, DO
NOT anesthetize for feeding tube insertion
until electrolytes, hydration, and vitamin K
supplementation have been established (usually
2006 World Congress WSAVA/FECAVA/CSAVA
48 to 72 hours). Initial feeding best accomplished
using an NG tube. STOP oral feeding if salivation,
nausea or struggling to get away from the food.
After a few days of rehydration, corrected
electrolytes, improved vitality, response to
vitamin K, you have an optimal situation for
placing an E-tube.
Feeding Tubes: Nasogastric / Nasoesophageal
tube initially, followed by placement of an E-tube
(preferred).
General Tips for Feeding Tube Care: Maintenance
of tube hygiene is essential. Flush with warm water
after each feeding with enough volume to cleanse
the tube yet not fill stomach. Avoid putting pill
form of medications that can cause concretions
(some ground up medications congeal in liquid
form) into narrow feeding tubes; may cause tube
occlusion.
432
Back to contents
If G-Tube: Aspirate tube before feeding to
evaluate gastric emptying: > 10 ml = gastric
hypokinesia that may reflect either electrolyte
derangements or pain derived from gastrostomy
tube (site infection, leakage, insertion causing
mechanical restriction of gastric motility.
Check Ostomy Site: 1-2x daily for the first 10
days. Perform cytology on ANY discharge. Avoid
infection as this complicates recovery. Visually
inspect the anchoring sutures.
If Persistent Vomiting: CHECK ELECTROLYTES:
rule out severe hypokalemia or hypophoshatemia
ensure that feeding tube is not causing gastric
outflow obstruction
radiographic contrast injection (RenografinŇ) or
by use of ultrasound (US).
Provide some modest exercise: may stimulate
enteric motility
Antiemetics:
Metoclopramide:
0.01-0.02 mg/kg/hr IV constant rate infusion / 24 hours
0.2 - 0.4 mg/kg SQ 20 min. before meal
Ondansetron:
5 HT3 receptor antagonist (expensive, oral only)
0.1-1.0 mg/kg q 12-24 hrs
Trickle Feed: Slow rate / 24 hours continuous
feeding of a liquefied diet through an infusion
pump. Running feeding line through a warm
water bath (bowl of warm water) may assist food
flow through small tube lumen. Re-new food q
4-6 hours to avoid bacterial contamination.
IF Still Persistent Vomiting: Double check tube
for problems (contrast radiography, US)
If Tube occlusion: Problem typically restricted
to G-tubes, use solutions that can digest food:
Coca Cola, papaya juice, or pancreatic enzymes.
Let dwell 20 to 40 minutes; then flush well
with lukewarm water. Do Not Attempt to Clear
Tube with a Solid Stilette: may penetrate tube
or patient. Radiographically re-evaluate tube
patency/position.
Diet to Feed: DO NOT restrict protein UNLESS
signs of hepatic encephalopathy.
Feed maximum calorie balanced feline foods.
How Much to Feed: 60-90 kcal/kg body wt per
day. Start with a liquid diet through NG tube.
Initially administer 5 ml of lukewarm water at 2-hr
intervals 2-to 3-times to determine the likelihood
of emesis & gastric atony. Food is progressively
introduced over a 2 to 4 day interval to achieve
intake of between 250 to 400 kcal per day for the
average sized cat. If G-tube used, initial feeding
is delayed for 24-36 hours after tube insertion
to allow return of gastric motility and to permit
formation of an initial wound seal around the
insertion site. Feeding through an E-tube may be
initiated after full recovery from the anesthetic
restraint.

AVOID RELIANCE ON APPETITE MODIFIERS
Diazepam, Oxazepam, Cyproheptadine: DO
NOT ENSURE ADEQUATE NUTRITIONAL
INTAKE.
Diazepam and Oxazepam are benzodiazepines
which are considered hepatoencephalogenic
toxins. These require hepatic biotransformation
and conjugation for elimination (the HL cat is
presumably deficient in these processes).
If Neck Ventroflexion: Consider electrolyte or
thiamine insufficiency. In these cats be sure to
monitor electrolytes (K, P, Mg) and to correct
any insufficiencies. Cats with HL may waste
potassium in urine. Those with hypokalemia
that is difficult to correct may be magnesium
deficient. Since there is no single test that rules
out thiamine deficiniency as a cause of neck
ventroflexion (and also neurologic signs confused
with hepatic encephalopathy) you should
administer thiamine: 100 mg in fluids (B-soluble
vitamins given slowly with crystalloid fluids) and
supplement with 100 mg via enteric route daily.
Parenteral administration of injectable thiamine
Back to contents
H
(intramuscular thiamine HCl may rarely cause
vasovagal collapse and neuromuscular paralysis;
mechanism unknown).
Predicting Recovery from Hepatic Lipidosis
Cats making a successful clinical recovery
from HL demonstrate a gradual reduction in
serum enzyme activities and total bilirubin
concentrations over time. Generally, within 10
days the total bilirubin concentration declines
by > 50% while serum enzyme activity may
remain near values documented at the time of
case admission. Cats with severe HL making a
successful recovery required 10 days (median)
of hospitalization; those that died did so by day
7 (median). Surviving cats my require up to 21
days of hospital care, depending on the owner’s
nursing skill and desire to participate in the cat’s
care. Treatment with l-carnitine and the regimen
outlined above has not reduced the length of
hospitalization of cats in our clinic. However, a
chance of recovery > 85% can be estimated in our
hospital if an individual cat survives the initial 96
hours.
2006 World Congress WSAVA/FECAVA/CSAVA
433
H
Survival in Cats with Severe Hepatic Lipidosis Receiving Balanced Nutritional Support
And Supplements Described in these Notes or Without Supplements
2006 World Congress WSAVA/FECAVA/CSAVA

434
Back to contents

H – Hepatology
CHOLANGITIS IN CATS – A REVIEW
Jan Rothuizen, Professor
of Internal Medicine
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine,
University Utrecht
j.rothuizen@vet.uu.nl
Cholangitis in cats is a complex of diseases,
about which there has been much controversy.
There are several names in use, which are in part
overlapping. The WSAVA liver standardization
group has judged that at present there is no ground
to define more than three inflammatory biliary
diseases in cats: (1) neutrophilic cholangitis,
(2) lymphocytic cholangitis, and (3) liver fluke
infection.
Neutrophilic cholangitis
This is an inflammation of the biliary tree (intra-
and extrahepatic bile ducts and the gall bladder)
characterized by presence of neutrophils in the
bile, but often also within the epithelial cells
lining the bile ducts.
Neutrophilic cholangitis is essentially a septic
inflammatory disease. In nearly all untreated cases
it is possible isolate bacteria from the bile. By far
the most common bacterium associated with this
disease is E. coli, but occasionally Pseudomonas
or other species can be identified. The most likely
route of infection is believed to be ascending from
the duodenum. The disease may be favoured by
pre-existing gall stones, lymphocytic cholangitis,
liver flukes, or pancreatitis. However, in the vast
majority of the cases no predisposition can be
identified. The disease is typically an acute septic
disease, with leucocytosis. The disease may
cause cholestasis, but jaundice is not present in
all cases. Most cats with neutrophilic cholangitis
have elevated plasma bile acid concentrations
and alkaline phosphatase, but there are also cats
without any obvious clinical or biochemical
sign of hepatobiliary disease. The disease may
become more chronic and the originally pure
neutrophilic inflammation may then become
a mixed inflammatory cell inflammation with
neutrophils, plasma cells and lymphocytes.
Chronic cases may also develop some fibrosis in
the portal areas, and the chronic cholestasis may
result in proliferation of bile ductules.
Symptoms: Clinical signs are general malaise,
and usually increased body temperature. The
Back to contents
H
bile ducts have a rich autonomic innervation, and
these cats have therefore nausea with more or less
pronounced anorexia and/or vomiting. Reduced
appetite and vomiting are present in virtually all
cats with neutrophilic cholangitis. Cholestasis
may be variable and although most of these cats
have yellow mucous membranes, some don’t
show icterus.
Diagnosis: Clinicopathological features usually
include leucocytosis, increased plasma bile acids,
ALT and AP, and often hyperbilirubinaemia. These
liver-specific parameters are not specific and are
thus not diagnostic. Ultrasonography often shows
no abnormalities of the biliary tract or the liver. In
rare chronic cases the lumen of the common bile
duct may be dilated. Ultrasound-guided puncture
of the gall bladder with a thin needle (22G) is
diagnostic. Bile should be examined cytologically
and by culture. Cytology reveals the presence of
neutrophils, whereas normal bile contains no
cells whatsoever. Bacterial may also be found
cytologically, but culture is needed to identify
and specify the infection, and to allow sensitivity
testing. In most cases the colour of the bile, which
is normally dark brown, becomes dark green. The
diagnosis may be completed with histopathology
of the liver. Histopathological lesions may be 2006 World Congress WSAVA/FECAVA/CSAVA
variable of intensity and irregularly distributed in
milder cases. Therefore histopathology does not
always permit to make a definite diagnosis
Treatment and prognosis: Neutrophilic cholangitis
should be treated with antibiotics, preferably
based on sensitivity testing after culture. In
most cases routine choices like amoxicillin are
effective. A three weeks’ course is adequate.
These cats have a good prognosis, provided the
absence of complicating factors.
Lymphocytic cholangitis
Lymphocytic cholangitis is characterized
by infiltration of the portal tracts with small
lymphocytes. These lymphocytes may also be
present in the lumen and epithelial cells of the bile
ductules. This is a chronic disease and there may
435
H
be pronounced fibrosis in the portal areas. Fibrous
connections between portal areas (bridging
fibrosis) may be called biliary cirrhosis. This
disease is common but the symptoms are so non-
specific that it may be easily overlooked.
The disease progresses slowly and affects the
entire biliary tree. Inflammation of the bile
ducts causes irregular dilatations and fibrosis
of the bile ducts. The liver lesions are confined
to pure lymphocytic inflammation of the portal
tracts, chronic cases develop portal fibrosis and
proliferation of bile ductules. There is usually
no severe portal hypertension or associated
symptoms like ascites or hepatic encephalopathy.
Nearly all cats have very high gamma globulin
levels which would be better compatible with
activation of plasma cells than with the presence
of only lymphocytes. In most textbooks the
advised therapy is with immunosuppressive
drugs, such as prenisone or metothrexate. The
underlying assumption is that lymphocytic
cholangitis is an immune-mediated disease,
and that immunomodulation may stop the
progression. There are no documented reports
that this treatment is indeed effective.
Symptoms: This is often a very chronic disease.
Cats may be sick for many months or even
years. Nausea is the most prominent sign. Signs
are relatively mild and cats with lymphocytic
cholangitis just have decreased, variable
appetite, and occasional vomiting. As a result
gradual weight loss is what the owners report.
Only some 60-70% is clinically icteric (Utrecht
University hospital population).
Diagnosis: Clinicopathological findings may
include high plasma bile acids and liver enzyme
activities (ALT, AP). However, increased gamma
globulin is the most consistent finding (95% of the
cats). Leucocytosis is absent in the majority of the
2006 World Congress WSAVA/FECAVA/CSAVA
cases. Ultrasonography is very abnormal in most
cats with lymphocytic cholangitis. The chronic
inflammation causes dilatations and strictures of
the bile ducts inside and outside the liver. The
irregular, fibrous bile ducts with dilatations and
strictures have a striking resemblance the ducts
of humans with primary sclerosing cholangitis.
Cytological evaluation of bile is usually not
informative. Culture of bile is typically negative.
Lymphocytic cholangitis is much more common
in cats than bile duct obstruction. However, with
the typical ultrasound findings the only differential
diagnosis is extrahepatic cholestasis. Therefore,
it is important to complete the diagnosis by
taking a large core liver biopsy sample (16G
biopsy needle). It is very important to use careful
436
Back to contents
ultrasound guidance, since the liver may be filled
with wide irregular bile ducts which should be
avoided.
Treatment: Reviewing our case records of cats
that were treated with 2 mg prednisone/kg/day
for long periods (six weeks to six months)
and evaluated with repeated ultrasonography
and liver biopsies, we have found that this
medication had no significant effect on the
course of the disease. In some cases there
was a slight temporary improvement, but we
have never seen permanent recovery. It is
therefore hard to believe that the pathogenesis
is predominantly immune-mediated. In recent
series of cases we have treated these cats
with ursodeoxycholic acid tablets (UrsocholR,
15 mg/kg/day), and found a much better response
than with corticosteroid medication.
Cholangitis due to liver fluke infection
Chronic cholangitis associated with liver
fluke infestation is regularly observed in cats
in endemic areas. Infections are caused by
members of the family Opisthorchiidae. These
liver flukes require snails and sweet water fish
as intermediary hosts. Cats become infected
by eating raw sweet water fish in which
metacercariae are encysted. Young liver flukes
migrate from the small intestines to the liver
via the bile ducts and cause inflammation of
the common bile duct and the large extra- and
intraheptic bile ducts. This chronic inflammation
results in malformation and irregular dilatation
of these ducts. An inflammation of the smaller
bile ductules in the portal areas is visible in
liver histology; there is mixed cell inflammation
with neutrophils, lymphocytes and plasma cells.
Eosinophils are indicative for this disease but
they are usually only present in limited numbers.
Occasionally the typical eggs are seen in liver
biopsy samples within the bile ductuli.
Diagnosis: The disease gives lesions which
are very similar to those in lymphocytic
cholangitis. The chronic course, the clinical
signs, the biochemical and haematological
abnormalities found in blood examination, and
the ultrasonographic abnormalities of the biliary
tree are more or less identical. Histologically, the
more mixed type of inflammation and if present
the eosinophilic component of inflammary
reaction are indications of liver fluke infection.
Careful histologic evaluation may reveal liver
fluke eggs, which are of course diagnostic. It
is important to realise that eating raw sweet
water fish is the mode of infection and if this

can be excluded, this pleas strongly against this
diagnosis. Careful anamnesis is thus important to
permit exclusion or inclusion of this differential
diagnosis.
Treatment: Treatment is with praziquantel given at
a single daily dose of 20 mg/kg orally, given three
Back to contents
H
consecutive days. If culture of the bile reveals
bacteria, treatment with antibiotics for 3-6 weeks
is important (see neutrophilic cholangitis). Cats
may improve well clinically, but the malformed
bile ducts will remain and make the cat sensitive
to recurrent bacterial infections.
2006 World Congress WSAVA/FECAVA/CSAVA
437
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

He
Haery & Genetic
Hereditary
eredit
Diseases - FECAVA
Symposium

Back to contents

INVITED LECTURES - FULL PAPERS
He – Hereditary & Genetic Diseases - FECAVA Symposium
HEALTHY DOG BREEDING – THE VALUE OF BREEDING
PROGRAMMES
Astrid Indrebo, DVM, PhD
Scientific Director of the
Norwegian Kennel Club
Norwegian School of Veterinary
Science
Department of Companion
Animal Clinical Science
PO Box 8146 Dep.
N-0033 Oslo, Norway
astrid.indrebo@nkk.no
The last 10-15 years there have been major
development in veterinary medicine, giving us the
knowledge, equipment and medicine to diagnose
and treat a large number of diseases. Moore dogs
are diagnosed and treated – giving the impression
that dogs are more diseased than a decade ago.
Has all our effort in regulating breeding through
screening, breeding programmes and advices
failed? On the other hand, advanced treatment
allows even diseased dogs to live a longer and
happier life, so maybe breeding programmes
are less important than they used to be? But
again, on the other hand, advanced possibility
for diagnosis should give us a great tool in
preventing hereditary diseases and diseases with
genetic disposition that are provoked by the
environment. This can partly be done through
screening programmes, but they have obvious
limitations. Screening programmes are available
only for a small number of diseases, and these are
not necessary the most important diseases for the
dogs’ functional health. And for diseases like hip
dysplasia (HD) and elbow dysplasia (ED), where
the environment plays a major role in forming
the dogs’ phenotype, the screening result of a dog
does not necessary tell the truth about the dogs
genotype. Index based breeding will hopefully be
a valuable tool in the future breeding programmes
on polygenetic diseases, as an index is based not
only on the dog’s own screening result and the
result of offspring, but also on a large number of
ancestors and relatives.
A unique tool in future breeding would be a test
showing the dogs’ genotype. At the moment such
DNA tests are available for some monogenetic
diseases, and more tests will be available in the
future. But there will probably always be a lot of
important health issues that cannot be measured
Back to contents
He
by DNA tests or screening results. Nevertheless,
these health issues must still play an important
role in breeding programmes.
Indexes and DNA results must not replace other
aspects in breeding programmes or the use of
common sense, but should be supplements to
reach the common goal: Functionally healthy
dogs with a construction and a mentality typical
to the breed.
What is a breeding programme?
A breeding programme should be a guideline for
dog breeders. Some ethical aspects should be the
same for every breed, in addition to important
breed specific health issues. The programme
should consist of both basic demands that must
be fulfilled in order to register puppies, and
recommendations on how to breed, how to
select dogs for breeding and how to do the right
combinations. Eradication of genetic diseases
and breeding only genetically healthy dogs is a
totally unrealistic goal. Too strict regulations and 2006 World Congress WSAVA/FECAVA/CSAVA
demands in breeding programmes could have the
opposite effect, as it will exclude too many dogs,
reducing the breeding population and result in
inbreeding.
Education of dog breeders is basic in order
to succeed with a breeding programme. The
breeders have a large responsibility, both to the
dogs, the owners and the society. Both kennel
clubs and breed clubs must play an important
role in educating breeders; knowledge is vital to
succeed.
Another key word to success is cooperation to the
benefit of dogs’ health. There must be cooperation
between kennel clubs, breed clubs and scientists.
For cooperation to succeed, we must respect and
trust each other; honesty is vital for success.
439
He
Reliable statistics based on screening is an
important tool. So are the DNA tests. The results
of both screening and DNA tests should be
registered in a kennel club register, open to the
public. True identification, microchip or tattoo,
is vital to any breeding programme. A national
disease register based on veterinary diagnosis
linked to the identification of the dog would be
very beneficial to breeding programmes.
A breeding programme based on knowledge,
cooperation, honesty, reliable results from
screening and DNA-test, and hopefully in the
future also from a national disease register,
combined with other important health issues,
including mental health, should have every
possibility to be beneficial for breeding healthy
dogs.
Basic rules and recommendations for breeding
healthy dogs
1.The breeding programme should not exclude
more than 50% of the breed; the breeding
stock must be selected from the best half of the
population.
2.Only functionally, clinically healthy dogs
should be used for breeding; dogs with chronic
diseases should never be bred unless we know
for sure that heritability plays no role in causing
the disease. If a dog suffers from a disease that is
suspected, but not proven, to be inherited, the dog
should not be used for breeding. If close relatives
of such a dog are used for breeding, they should
be mated to dogs from bloodlines with low or no
occurrence of the same disease.
3. Avoid matador breeding. A basic recommendation
should be that no dog should have more offspring
than equivalent to 5% of the number of puppies
registered in the breed during a five year period.
4. A bitch that is unable to have normal birth,
due to anatomy or inherited inertia, should be
excluded from breeding – no matter the breed.
2006 World Congress WSAVA/FECAVA/CSAVA
5. A bitch that is unable to take care of the
newborn puppies, due to mentality or inherited to
agalactia, should not be used for breeding.
6. Dogs with a mentality atypical for the
breed, aggressive dogs, should not be used for
breeding.
7. Screening results for polygenetic diseases
should be used for preparation of an individual
index, based on both national and international
screening results. The breeding combination
should have an index better than the average for
the breed.
8. Results from DNA tests should be use to
avoid breeding diseased dogs, not necessarily to
eradicate the disease.
9. The raising of puppies, with correct feeding,
environmental exposure, stimulation by their
440
Back to contents
mother, breeder and others to develop social sense
and response, must be basic in every breeding.
If these simple basic rules and recommendations
are implied in a breeding programme, we would
attain considerable improvement of dogs’ health.
Breed specific health issues should be added in
order to make an even greater improvement of
the health.
National health committees
Each kennel club should have their own health
committee, giving advice to breed clubs on health
issues. The Norwegian Kennel Club (NKC) has
only few registration restrictions and gives the
breed clubs more responsibility for the details in
the breeding programmes. We put a lot of effort
in educating the breed clubs and the breeders. It is
our true believe that it is better to include as many
breeders as possible in organized in the kennel
club work and to educate them on how to breed
healthy dogs, instead of excluding too many dogs
and to many breeders due to heavy restrictions.
We can only influence the breeders that cooperate
with the kennel club. In Norway a large majority
of pure bred dogs are registered in the kennel
club, in some breeds close to 100%.
The Nordic Kennel Union (NKU)
The Scandinavian countries cooperate in health
issues through the NKU Scientific Committee. The
members are mainly scientists who are appointed
by their kennel club. Subcommittees are working
with DNA-tests and HD-index. NKU has an HD/
EA panel, consisting of the veterinarians that are
responsible for reading radiographs for official
HD and ED diagnose in each country.
DNA-tests
The number of DNA-tests is rapidly increasing.
To be beneficial for healthy dog breeding, the
DNA test must represent a disease that is harmful
for the dog; we must test our dogs due to a health
problem – not mainly because there is a test
available. All the results must be available to the
breeders; there must be a reliable register for the
result of every dog that is tested, not only the dogs
that are free of the specific gene causing disease.
The dog must be identified with microchip or
tattoo.
In Norway the veterinarians employed by the
NKC decides, together with the breed club, which
DNA-test that are important for the breed and
then make an agreement with a laboratory that
do the testing. A specific form can be obtained
from the NKC database; the dog owner fill in the
registration number of the dog, and a complete
form containing all the dogs’ data from the data
base, including the ID-number, is then sent

immediately by e-mail to the owner. By signing
this form, the owner allows the test result to be
public in the database. The veterinarian checks
and states the dog’s identity. The sample must be
mailed by the veterinarian, not by the owner. The
test result is sent from the laboratory both to NKC
and to the owner.
The results of DNA-tests can contribute to healthy
dog breeding as part of a breeding program. We
will know whether a dog is a free of the gene
causing a recessive disease, a carrier or if it will
develop the disease. Through selective breeding,
we can assure that at least one parent of a litter is
free of the gene causing the disease, resulting in
puppies which will not develop the disease. We
do not have to exclude the carriers from breeding.
This is basic in NKC breeding policy.
Screening for hip and elbow dysplasia
To be useful in international breeding programmes,
the score from screening for HD or ED should
be the same for the same dog, no matter where
the dog is diagnosed. Minimum age, position of
the dog when radiographed, technical demands,
depth of sedation and reading the result should be
uniform in every country.
Figure 1 shows the screening results of Bernese
Mountain Dogs registered in NKC from 1986-
2005. 64% of dogs registered in this period have
an official ED result. In the period ’86-’97, 66%
were diagnosed as free. The average ED score was
0.53. In 1999, there is an obvious improvement of
the ED status. From ‘99-‘05, 82% are diagnosed
as free, and the average ED score is 0.27. Is this
the result of the breeding programme? Probably
it is not due to genetics. From 01.01.2000 the
minimum age for official ED status was lowered
from 18 to 12 months, due to Scandinavian
harmonization. As the ED score is based mainly
on arthrosis, it is not surprising that the score is
improving when dogs are examined at lower age.
This shows the importance of early harmonization;
if the protocol differs between countries, the
screening results will not be compatible, and
preparation of international indexes would not be
reliable.
The main issue of NKU HD/ED Panel is to
harmonize the protocol for screening for these
Back to contents
He
diseases in Scandinavia, and hopefully the same
harmonization will be valid also in other FCI
countries and the rest of the dog world.
Screening for inherited eye diseases
The same disease should have the same diagnose
in every country. This is an important issue for
European College of Veterinary Ophthalmologists
(ECVO) and for the European Eye Group,
consisting of both eye panellists and kennel club
representatives. To succeed in harmonization, it
is important to have common education for eye
panellists, and a common international form for
diagnosing and reporting the results of an eye
examination to the national register. The ECVO
form will hopefully be used by an increasing
number of countries in near future.
The kennel club database open to the public
Access to information about the individual
dog, its ancestors and offspring is important
in breeding programmes. The NKC database
contains every available information on any
dog registered the last 30 years. To be useful
in breeding programmes, these data must be
available to the public. The NKC database is
open to all members of the NKC, breed clubs and
veterinarians. Pedigree, screening results, DNA
results and results from dog shows and other
competitions like obedience, hunting etc can be
obtained from the database.
Summary
Breeding programmes can be valuable for
breeding functionally healthy dogs. These should
be guidelines and not contain too stringent
demands. Every dog should be identified with
chip or tattoo. The protocol for screening results
should be the same for all countries, and national
and international indexes should be performed
for polygenetic diseases. Results of DNA-tests
should be used to avoid breeding diseased dogs.
2006 World Congress WSAVA/FECAVA/CSAVA
When selecting dogs for breeding, the dog and
the breed should be looked upon in its entirety.
The goal should be functionally healthy dogs
with a construction and a mentality typical to the
breed.
441
He
Figure 1. The prevalence of elbow dysplasia in Bernese Mountain Dogs in Norway 1986-2005, based
on radiographic screening. Total number of dogs of this breed registered in this period is 5818, of which
3743 (64%) were examined. (Data from the Norwegian Kennel Club, May 2006, www.nkk.no)
2006 World Congress WSAVA/FECAVA/CSAVA

442
Back to contents

He – Hereditary & Genetic Diseases - FECAVA Symposium
SEGREGATION ANALYSIS TO DETERMINE THE MODE OF INHE-
RITANCE
Ottmar Distl, Prof. Dr. med.
vet. Dr. habil.
Institute for Animal Breeding and
Genetics
University of Veterinary
Medicine Hannover
Bünteweg 17p
30559 Hannover
Germany
ottmar.distl@tiho-hannover.de
Introduction
Many disorders in animals are observed more
frequently in certain breeds and within breeds
more often in the same families. Familiarity
is assumed for a disorder when families are
observed with more than one affected family
member. Familial disorders may have a genetic
contribution. The same is often claimed for
disorders which show a breed disposition. On
the other hand, genetically caused diseases
may not necessarily lead to breed differences in
incidence but will contribute to variation among
families within breeds. A useful starting point
for answering the question whether a disorder is
inherited is by drawing pedigrees to provide an
initial impression of the distribution of affected
and non-affected animals and how frequently the
disorder is transmitted from one generation to the
next. General evidence for genetic contribution to
a disorder is given when environmental factors
can be excluded as the only responsible causes
for a disorder and a significant proportion of
the phenotypic variation of a disorder can be
explained by genetic models. With increasing
molecular genetic data, the type of gene action
based on known DNA sequence variation can be
characterized by individual genes and the nature
of complex genetic traits can be understood much
better.
The presentation will give an overview on the
model components included in estimation of the
mode of inheritance based on phenotypic data
and further developments for incorporation of
molecular genetic data into the analyses.
Segregation analysis
Segregation analysis is employed to determine
whether familial data for particular disorders or
Back to contents
He
other traits are compatible with specific modes
of inheritance. Modes of inheritance tested
in segregation analyses include monogenic
(Mendelian), digenic or polygenic models. In
addition, age of onset, sex effects and sampling
scheme can be taken into account besides the
specific genetic hypothesis under consideration.
Simple segregation analysis tests the segregation
parameter θ under a specified sampling scheme
and mating type. Pedigrees used for segregation
analysis may be from specifically planned matings
or randomly sampled pedigrees with arbitrary
structure or sampled through ascertained cases in
clinics or veterinary practice. Arranged matings
among animals can be more easily tested for
specific modes of inheritance than pedigrees with
arbitrary structure, missing data and many inbred
animals. In the case of a rare disease and an
autosomal dominant hypothesis, the segregation
ratio θ is assumed to be 0.5 as families segregating
for the trait are most likely composed by matings
of heterozygous affecteds and homozygous non-
carriers. As far as the segregation ratio is not 2006 World Congress WSAVA/FECAVA/CSAVA
significantly different from θ = 0.5, this mode
of inheritance is accepted. Different methods for
estimating θ have been developed and are easily
applied (Singles Method, Weinberg’s General
Proband Method). These simple approaches to
segregation analyses often encounter problems
when different mating types have to be
considered and several hypotheses are more or
less likely. Complex segregation analyses have
been developed to allow for more factors to vary
and to reduce the restrictions on assumptions
to be made for the model tested. Methods used
to solve the likelihood functions are based on
maximum likelihood or Markov chain Monte
Carlo approaches (Gibbs sampling).
443
He
Complex segregation analysis
Complex segregation analysis is based on a
mathematical model that incorporates several,
functionally independent components to
accommodate for arbitrary mating types,
different modes of monogenic or oligogenic
inheritance (major genes), to allow for polygenic
variation and non-genetic variation in addition
to major genes and different data types such
as binary, categorical and continous data. In
addition, age of onset of a disease and sampling
scheme (random pedigrees versus non-randomly
selected pedigrees) can be modelled. The basic
model as formulated in the Elston-Stewart
algorithm was the basis for the more complex
models. The Elston-Stewart algorithm included
a component describing the joint distribution
of genotypes of mating individuals whereby
these genotypic distributions stem from a single
locus with two alleles (monogenotype), a few
loci with each two alleles (oligogenotype)
or from a polygenotypic distribution with an
infinite number of genotypes (polygenotype).
The second component of the Elston-Stewart
algorithm specified the relationship between the
genotypes and phenotypes, separately for each
genotype (penetrance function). Mathematically,
the phenotype investigated is modelled as
a conditional probability on the genotype
underlying the model used. The simplest genetic
model for a dichotomous trait and a monogenic
autosomal inheritance of two alleles is then
completely defined by the following genotype
to phenotype relationships: gAA(1) = gAa(1) =
1, gaa(1) = 0 and gAA(0) = gAa(0) = 0, gaa(0) =
1, where the conditional probability equals
unity when for the genotypes AA and Aa the
phenotypic outcome is affected (=1) and for the
genotype aa the phenotypic status is unaffected
(=0). Similarly, if a completely penetrant
recessive trait is assumed, we have the following
2006 World Congress WSAVA/FECAVA/CSAVA
conditional distributions: gaa(1) = 1, gAa(1) =
gAA(1) = 0, gaa(0) = 0, gAa(0) = gAA(0) = 1. Two-
or three-locus models give raise to much more
models (phenogrammes) how the oligogenotype
is related with the phenotype. If we do not wish
to assume complete penetrance we can introduce
for each distinct genotype or groups of genotypes
a specific penetrance. For X-linked loci, the
conditional distributions of phenotypes have
to be defined for males and females separately.
Furthermore, traits only expressed in males or
females can be modelled via the penetrance
parameter allowing fully expressed traits only for
one sex. Just as the phenotypic distribution may
be sex-dependent, so the disorder considered has
a variable age of onset and thus the observation
whether the disorder is expressed, depends upon
444
Back to contents
the age at examination of each individual. Then
the probability that an individual with a genotype
AA, Aa or aa is affected by a specific age depends
of the age-related susceptibility of the genotype
to the disorder. When we turn to polygenotypes,
we use normal distribution functions. In the case
of a binary or categorical phenotype, this model
corresponds to the threshold or liability model.
The polygenotypes are normally distributed with
genetic variance σ2G and residual variance σ2E. An
individual is affected or mildly/severely affected
whose liability is greater than the threshold. The
threshold may also depend upon the genotype
of an additional monogenic locus.
The mode of inheritance can be described
how the genetic variability is passed on from
one generation to the next and is summarized
mathematically by the genotypic distributions
of the offspring in dependence upon the parental
genotypes. Let us assume that an individual has
parents with genotypes s and t, then the conditional
probabilities for the genotypes of this individual
can be viewed as elements of a stochastic matrix
called the genetic transition matrix, probability
(P) for the individual genotype given genotypes of
parents s and t, P(gi|gF,gM). All types of monogenic
and oligogenic inheritance can be parameterized
in terms of transmission probabilities. In the
autosomal monogenic model with alleles A and B,
the transmission probabilities are the probabilities
that an individual with genotype AA, AB or BB
transmits the allele A to offspring. Using the
definitions for the transmission probabilities
τAA=1, τAB=0.5 and τBB=0, the probabilities for
the genotype AA of the individual with parents
s and t are equal to τsτt, the probabilities for
the genotype AB with parents s and t are equal
to τs(1-τt) + τt(1-τs) and the probabilities for
the genotype BB with parents s and t are equal
to (1-τs)(1-τt). Extension to several unlinked
loci and linked loci is straightforward. Linked
loci require recombination rates among loci as
further parameters. Polygenic inheritance using
an additive model can be modelled through the
transmission of the gametic values being 0.5 for
any polygenotype. The polygenotypes of offspring
are produced by the mid-parents´ values of their
polygenotypic effects with variance σ2G/2.
Sampling scheme describes the way how
individuals were selected from the population for
study. Random sampling means that we take a
random sample of individuals from a population
and then augment this sample by including all or a
random sample of relatives up to a certain degree
of relatedeness. When well designed recording
schemes are introduced, random samples of
progeny or sibships with their ancestors can be
collected. These samples can be collected in a

specific geographic area which is not critical as
long as individuals outside this area are not selected
according to their phenotype or genotype. Rare
conditions are hardly studied in random samples
hence many uninformative families are collected.
Typically for this situation, families are included
in the study because at least one member of the
family is affected. The kind of the non-random
sampling procedure is characterized by the type of
ascertainment. Complete ascertainment is given
when a sibship enters the sample independently
of the number of additional affected members.
The opposite extreme to complete ascertainment
is single ascertainment. The probability for an
affected individual tends to be zero to be brought
into the study when there is not more than one
affected family member. Incomplete multiple
ascertainment is the situation between single
and complete ascertainment. To ensure a valid
segregation analysis, the kind of ascertainment
should be identified. Methods of estimation of the
segregation ratio depend on how the families have
been brought into the study. A likelihood function
based on the components of the segregation
analysis model can be derived and maximized for
the data observed. Since the likelihood function
includes the different types of genetic models
as well non-genetic factors, submodels can be
tested against the most general model. Inferences
can be performed for both continuously and
categorically distributed data and genetic models
that include monogenic, digenic, polygenic and
mixtures of monogenic and polygenic as well
as oligogenic and polygenic models. A genetic
background of a trait analysed is given when
the model explaining only non-genetic factors
can be rejected and models including genetic
components explain a significant proportion of
the phenotypic variation.
A likelihood ratio test statistic is used to compare
a specific null hypothesis (H0) defined by a
specific model (restricted model) against a most
general (not restricted) model. The test statistic
Back to contents
He
asymptotically follows a χ2-distribution, and
significance levels can be obtained by using this
distribution. Degrees of freedom are given by the
difference of independently estimated parameters
for the models compared. The information
criterion of Akaike (AIC) can be used as an
additional measure to choose the sparsest model
with the best fit to the data. The model with the
smallest AIC fits the data best with a minimum
number of parameters but all hypotheses that
cannot be rejected against the most general
model using the likelihood ratio test must also be
considered as possible. The AIC criterion cannot
be used to exclude a hypothesis if this model was
not rejected against the most general model by
using the likelihood ratio test.
Conclusions
Complex segregation analysis is a powerful
tool to detect major gene variation. Quantitative
genetic models rely on the assumption of
many (infinite) loci with very small and equal
effects. This model is severely compromised
in the presence of segregation of major genes.
Extensions and improvements of algorithms
made to the simple segregation models allow to
estimate major genotype effects in the framework
of the methodology developed for quantitative
genetic analysis. Gibbs sampling can be employed
to estimate non-genetic effects, genotype
frequencies and their associated genotypic effects
and quantitative genetic variation including all
relationships of the animals. When information
for genetic markers in population-wide linkage
disequilibrium or mutations of genes associated
with trait variation can be included in the
analysis, the genotypic distributions need no
longer to be estimated and inferences on the
genotypic effects are much more precise. Such
genetic polymorphisms enable us to model the
gene actions and their interactions in networks
for complex genetic traits.
2006 World Congress WSAVA/FECAVA/CSAVA
445
He
He – Hereditary & Genetic Diseases - FECAVA Symposium
BREEDING FOR IMPROVED HEALTH IN SWEDISH DOGS
Sofia Malm
MSc in Animal Science
Swedish University of
Agricultural Sciences
Department of Animal Breeding
and Genetics
Box 7023
S-75007 Uppsala
Sweden
sofia.malm@hgen.slu.se
INTRODUCTION
In Sweden there are about 950 000 dogs, 85%
of which are purebred and registered in the
Swedish Kennel Club (SKC). Furthermore, a
large proportion of Swedish dogs have a health
insurance. Thanks to the extensive registration
and insurance of dogs in Sweden, large amounts
of data regarding morbidity, mortality, and
ancestral background are being collected and
made available to breeders and scientists. These
databases are valuable tools for breeders and
breed clubs in selection of breeding stock and
in breeding planning. They also offer unique
possibilities for both epidemiological and genetic
studies on different diseases in dogs.
GENETIC HEALTH PROGRAMMES
The SKC started to develop genetic health
programmes more than 25 years ago. Records
from these programmes are stored in the SKC
database and are freely accessible through the
SKC web site. The first programmes concerned
hip and elbow dysplasia (HD and ED). Today,
2006 World Congress WSAVA/FECAVA/CSAVA
numerous breeds are included in a genetic health
programme for HD or ED, implying that hip or
elbow status of both the sire and the dam should
be known for the offspring to be registered in the
SKC. In many breeds, an additional requirement
is that dogs should be free from HD to be accepted
for breeding.
In addition to HD and ED, genetic health
programmes for other inherited conditions, such
as hereditary eye diseases, have been developed.
These are based on breed-specific needs and have
been introduced on request from the breed clubs.
Besides physical health, the SKC has developed
programmes with respect to mental health and
management of genetic variation. Since 2002,
all breeds belonging to the Swedish Working
Dog Association are obliged to undergo a
446
Back to contents
standardised behavioural test (dog mentality
assessment), describing the mental status of the
dog, before being used in breeding. Furthermore,
Border Collies need to undergo a working test for
evaluation of their herding skills if the progeny
are to be registered in the SKC.
Management of genetic variation is important to
avoid loss of genetic diversity, manifestation of
recessive defects and inbreeding depression. In
some Swedish breeds, limitations for the maximum
number of offspring allowed for a single male
have been introduced to avoid extensive use of
popular sires. Also, programmes for out-crossing
with individuals from closely related breeds have
been developed in order to increase the effective
population size and improve health traits.
In conclusion, the genetic health programmes
currently operated by the SKC aim at improved
physical and mental health, as well as maintained
possibilities for a sustainable breeding with
respect to genetic variation. However, so far
genetic health programmes for physical health
have been developed only for diseases with well
defined and validated methods for examination
and diagnosis. Many breeds have other, less
well defined, inherited conditions that may
have a larger impact on the dogs’ health. It is
therefore important not to put too much focus
on one or a few diseases only because they are
easy to diagnose and to record. Because genetic
health programmes only cover some aspects of
mentality and functionality, most breed clubs
have additional recommendations or restrictions
in their breeding policies.
NEW TOOLS
Development of breeding strategies
Breeding of dogs is regulated both on international
and national levels. In addition to breed specific

genetic health programmes, all members of the
SKC are obliged to follow the general regulations
and breeding policy set up by the SKC. These
documents give general restrictions, guidelines,
and goals for breeding of dogs. However, there
are almost 300 different breeds in Sweden and
each breed has its own specific conditions that are
important to consider in the breeding programme.
Therefore, in 2001 the SKC decided that each
breed should have their own breeding strategy,
taking into account all aspects relevant in the
breeding goal for that specific breed. Thus, the
breeding strategy should consider and prioritize
between aspects of both physical and mental
health, also taking the population structure and
genetic variation into account. Breed-specific
goals and strategies to achieve these goals should
be included, constituting an overall plan for the
breed. The responsibility for developing these
strategies was given to the breed clubs, and at
present more than 140 clubs have submitted a
breeding strategy to the SKC.
Breeding value prediction
Despite efforts to reduce the frequency of HD and
ED by means of genetic health programmes, based
on radiographic examination of the phenotype
and subsequent mass selection, the improvement
has been disappointing in several breeds. Low or
no improvement in HD has been reported also by
other countries (Lingaas and Heim, 1987; Willis,
1997; Leppänen and Saloniemi, 1999).
In grading systems for HD and ED there are
limited possibilities for measuring differences
among phenotypically normal dogs. In some
breeds, a large proportion of the dogs are free
from dysplasia which makes selection based on
the phenotypic value alone inefficient. In addition,
the phenotype is affected by various systematic
environmental factors, e.g., age at screening (Distl
et al., 1991; Swenson et al., 1997a, b; Mäki et al.,
2000). Also the type of chemical restraint, used
for sedation during radiographic examination of
HD, has an impact on the diagnosis of hip status
(Malm et al., 2006a). The effect of different
environmental factors on evaluation of hip and
elbow status implies that the individual’s own
screening result alone may be inaccurate for
selection purposes.
Genetic evaluation using mixed linear models
(often called BLUP) for prediction of breeding
values have been used extensively in breeding of
cattle, horses, poultry and swine for several years.
However, in dog breeding this methodology has
been used only to a limited extent. Prediction
of breeding values for HD and ED would
enable a more accurate comparison of genetic
merit of dogs. The BLUP method makes use
Back to contents
He
of all available information about relatives and
simultaneously adjusts for environmental effects.
Selection against HD and ED based on predicted
breeding values has already been introduced
in some countries, e.g. Finland and Germany.
In Sweden, the SKC is planning to implement
breeding value prediction for HD and ED as a
routine for a number of breeds during 2007.
A genetic study of HD and ED has been conducted
in two breeds, Rottweiler and Bernese Mountain
Dog, to estimate the amount of genetic variation
in HD and ED, and to assess genetic trends (Malm
et al., 2006b). Based on these results, a statistical
model for routine prediction of breeding values
for HD and ED in Swedish dogs was suggested.
The next step will be to evaluate the model also
for other breeds.
The genetic evaluations of HD and ED in Sweden
will be managed by the SKC and breeding values
will most likely be updated once a week. Only
dogs with an own screening record will get their
breeding value published, together with the
accuracy of the prediction.
A strategy for implementation of the breeding
values in the overall breeding programme for
each breed is needed. Other traits included the
breeding strategy need to be considered relative
to HD or ED. Besides, the relationship between
individuals selected for breeding must be
considered to avoid increased inbreeding due to
selection of close relatives.
Breeding value prediction can be a useful tool for
genetic evaluation of traits other than HD and ED.
Genetic improvement not only of other diseases,
but also behavioural and functional traits, could
probably be enhanced by selection on breeding
values instead of phenotypes.
DNA tests for canine disorders
Advances in molecular genetic studies of the
dog and the availability of the canine genome
sequence imply that an increasing number of genes
2006 World Congress WSAVA/FECAVA/CSAVA
underlying diseases in dogs are being revealed.
The development of DNA tests for different
gene mutations makes it possible to accurately
predict the genotype of an individual dog with
respect to a specific disease, i.e. to identify
genetically normal, carrier and affected animals.
The possibility to identify carriers of a defective
allele enables a more subtle management of
breeding programmes to decrease the frequency
of a particular disease gene without unnecessary
reduction of the overall gene pool.
The SKC currently records results from DNA
tests for canine leukocyte adhesion deficiency
(CLAD) in the Irish Setter, congenital stationary
night blindness (CSNB) in the Briard, von
Willebrand disease in the Kooikerhondje and one
447
He
type of progressive retinal atrophy (prcd-PRA) in
a number of breeds. All results are published on
the SKC web site for anyone to access and genetic
health programmes based on the DNA testing are
developed for each breed individually.
Internet based breeding statistics
The SKC has recently developed an internet based
service including breeding statistics for both
individual dogs and for each breed as a whole.
The statistics are based on results from genetic
health programmes, the dog mentality assessment,
official competitions, and dog shows, as well
as pedigree information. For individual dogs,
own records as well as statistics for littermates,
full-sibs and offspring are available. Also, the
pedigree and coefficient of inbreeding is shown
for each dog. The population-wide information
for each breed includes statistics on number of
registrations, health traits, mental status, breeding
animals (regarding number of offspring and
grandchildren per sire or dam, litter size, and
age at breeding) and average levels of inbreeding
by birth year. Furthermore, the service contains
an option to calculate the expected inbreeding
coefficient for offspring resulting from a planned
mating.
This tool is available to anyone through the SKC
web site and is very useful to breeders for genetic
evaluation and selection of breeding animals.
It also facilitates for breed clubs to assess the
overall situation in the breed.
CONCLUSION
Dog breeding is of concern not only to individual
breeders, but also to breed clubs, kennel clubs,
geneticists, veterinarians, and authorities.
Sustainable breeding of healthy dogs is facilitated
by cooperation between the different parties and
agreement about the breeding goals. In addition,
genetic evaluation and selection must be based
2006 World Congress WSAVA/FECAVA/CSAVA
on accurate information about the individual
animals and the breed as a whole. Recording of
traits considered to be of importance is therefore
essential, as well as pedigree information to
enable evaluation of population structure and
studies of the mode of inheritance for different
traits. Consequently, the access to information
and tools that enhance genetic evaluation is of
great value. The development of breed-specific
448
Back to contents
breeding strategies constitutes a solid basis
for a comprehensive and long-term breeding
programme.
REFERENCES
Distl, O., Grussler, W., Schwarz, J., Krausslich,
H., 1991. Analysis of Environmental and Genetic
Influences on the Frequency of Hip Dysplasia in
German Shepherd Dogs. J. Vet. Med. A. 38, 460-
471.
Leppänen, M., Saloniemi, H., 1999. Controlling
canine hip dysplasia in Finland. Prev. Vet. Med.
42, 121-131.
Lingaas, F., Heim, P., 1987. En genetisk
undersøkelse av hofteleddsdysplasi i norske
hunderaser [Genetic investigation on hip
dysplasia in Norwegian dog breeds]. Norsk
Veterinærtidsskrift 99, 617-623.
Malm, S., Danell, B., Audell, L., Strandberg,
E., Swenson, L., Hedhammar, Å. 2006a. Impact
of sedation method on the diagnosis of hip and
elbow dysplasia in Swedish dogs. Prev. Vet. Med.
Submitted.
Malm, S., Strandberg, E., Fikse, W.F., Danell,
B., 2006b. Genetic Variation in Hip and Elbow
Dysplasia in Swedish Rottweiler and Bernese
Mountain Dog. In preparation.
Mäki, K., Liinamo, A.E., Ojala, M., 2000.
Estimates of genetic parameters for hip and
elbow dysplasia in Finish Rottweilers. J. Anim.
Sci. 78, 1141-1148.
Swenson, L., Audell, L., Hedhammar, Å. 1997a.
Prevalence and inheritance of and selection for
elbow arthrosis in Bernese Mountain Dogs and
Rottweilers in Sweden and benefit:cost analysis
of a screening and
control program. J. Am. Vet. Med. Assoc. 210,
215-221.
Swenson, L., Audell, L., Hedhammar, Å. 1997b.
Prevalence and inheritance of and selection for
hip dysplasia in seven breeds of dogs in Sweden
and benefit:cost analysis of a screening and
control program. J. Am. Vet. Med. Assoc. 210,
207-214.
Willis, M.B., 1997. A review of the progress in
canine hip dysplasia control in Britain. J. Am.
Vet. Med. Assoc. 210, 1480-1482.
Back to contents
2006 World Congress WSAVA/FECAVA/CSAVA
He

449
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

II Immunology
Clinical
ini

Back to contents

INVITED LECTURES - FULL PAPERS
I - Clinical Immunology
WHY IS THIS DISEASE IMMUNE?
Professor Michael J. Day
Division of Veterinary Pathology,
Infection and Immunity
School of Clinical Veterinary
Science
University of Bristol
Langford BS40 5DU
United Kingdom
m.j.day@bristol.ac.uk
What is an immune-mediated disease?
There is a spectrum of immune-mediated disease
that may be considered on a number of different
levels. Clinically, four major subtypes of immune
system abnormality are recognized: (1) primary
congenital immunodeficiency, (2) allergy, (3)
autoimmunity and (4) immune system neoplasia.
On another level, immune-mediated disease
might be considered to be primary or secondary in
nature. Finally, many types of immune-mediated
diseases might be considered mechanistically
– using the Gel and Coombs classification of
hypersensitivity reactions.
What are the general characteristics of immune-
mediated disease?
•A strong genetic basis.
•Particular age predispositions.
•Non-specific clinical signs.
•A waxing and waning clinical course.
•Absence of underlying disease or recognized
trigger factors.
•Response to immunomodulatory therapy.
Back to contents
I
What are the laboratory hallmarks of immune-
mediated disease?
•Many animals with immune-mediated disease will
have serum polyclonal hypergammaglobulinaemia
and elevation in serum concentrations of IgG,
IgM or IgA.
•Leukocytosis, in particular neutrophilia, is often
a hallmark of immune-mediated disease.
•Lymphadenopathy is a common feature of
immune-mediated disease and is a reflection of
immune system activation.
•All cats with suspected immune-mediated
disease should be screened for retroviral infection
(FeLV, FIV).
•The serological changes compatible with
immune-mediated disease are often very specific
for the disease process. By contrast, some
serological changes are less disease specific
•The revolution in molecular diagnostics has
ready applicability to diagnosis of immune-
mediated disease.
2006 World Congress WSAVA/FECAVA/CSAVA
451
I
I - Clinical Immunology
UPDATE OF LABORATORY DIAGNOSTIC METHODS IN CLINICAL
IMMUNOLOGY
Miroslav Toman, Prof.
MVDr., CSc.
Veterinary Research Institute
Hudcova70
62100 Brno
Czech Republic
toman@vri.cz
Immunological tests should be preceded by a
thorough evaluation of anamnestic data and clinical
examination results, as many symptoms may
signalise potential immune-mediated diseases.
Also standard laboratory tests, biochemical,
haematological, cytological or histological
analyses and visualisation (radiography) methods
may be of a great value for an immune-mediated
disease diagnosis. Accordingly, immunological
tests should be only performed in the case of an
adequate indication, with respect to their costs and
cogency. Diagnostic criteria have been established
for various immune-mediated diseases, with
laboratory analysis playing major or minor roles,
according to their diagnostic value.
Immunological laboratory diagnostic methods
can be classified from several aspects:
I.Based on a group of diseases that facilitate
diagnosis
•Immunological profile tests for the detection
of immunodeficiency
•Hypersensitivity tests
•Autoimmunity tests
2006 World Congress WSAVA/FECAVA/CSAVA
II. Based on availability of the methods
•Methods performed in a surgery
•Methods included in haematological or
biochemical analysis, and histological
or visualisation methods that provide
valuable information for immunological
diagnosis
•A group of basic methods conducted in a
specialised immunological laboratory
•Advanced immunological methods above
all, used in clinical research
Whereas laboratory diagnosis of allergic and
autoimmune diseases is based on serological
examination and the tests are usually available
as commercially produced kits, technically
demanding methods are necessary for the detection
of immunodeficiency or immunosuppression
disorders.
452
Back to contents
Martin Faldyna,
MVDr., PhD.
Veterinary Research Institute
Hudcova70
62100 Brno
Czech Republic
Basic laboratory examinations
Leukocyte count and differential leukocyte count,
i.e. standard haematological parameters should
be included in basic laboratory examinations,
commonly available in any small animal
practice. Cytology and histology of various
samples obtained from biopsies are also of great
value for immunological diagnosis. Preliminary
methods selected for humoural immunity testing
involve the assessment of total immunoglobulins
using a simple precipitation method or
serum electrophoresis. Among inflammatory
parameters, the C-reactive protein test is available
as a commercial kit in dogs however it is not
commonly used, due to its cost versus diagnostic
value.
Allergy tests
Practical veterinary surgeons have available
in their consulting rooms the hypersensitivity
skin tests for allergy diagnosis, including tests
for the detection of a particular allergen. These
tests produce quite reliable results especially
in canine atopy. Allergens are commercially
available and tests are usually used in practice
for the detection of hypersensitivity type I.
Nevertheless, hypersensitivity type IV detection
is also relevant.
Nowadays, the diagnostic value of intradermal
skin tests is comparable with that of serological
detection of specific IgE antibodies against
respective allergens using commercially available
ELISA kits.
Detection of autoantibodies
Detection of autoantibodies is an important
diagnostic tool for diagnosis of autoimmune
diseases. Despite the fact that their occurrence
is not quite specific for a respective disease, it
may considerably facilitate the diagnosis. Human
immunological laboratories have available a wide

range of commercial tests, whereas the offer in
veterinary medicine is somewhat limited.
Analysis of circulating immune complexes by
their non-specific precipitation in sera with
polyethyleneglycol is an auxiliary method for
the detection of hypersensitivity type III status.
However, elevated concentration of circulating
immune complexes is also usually detected
during chronic infectious processes and due to
this fact, the result of the analysis does not lead to
a specific conclusion.
Antinuclear antibodies (ANA) are characteristic
for systemic autoimmune diseases, above all:
systemic lupus erythematosus (SLE). They are
detected by indirect immunofluorescence, in
sera. A significant level of antibodies (titre
80 - 100) and characteristic localisation (granular
or homogenous fluorescence of the nucleus) is
a precursor for obtaining a positive result in the
test. The diagnostic value of the test is relatively
high.
Rheumatoid factor (RF) is the antibody against
Fc fragment of immunoglobulin, in dogs this is
usually against IgG, the RF isotype being IgM, or
IgA. Rheumatoid factor detection is performed by
various tests: conventional Rose-Waaler test, or
most recently by turbidimetry or ELISA methods.
The diagnostic value of RF detection that should
be characteristic of rheumatoid arthritis is low,
because rheumatoid factor is also found in serum
during other autoimmune diseases, chronic
inflammatory responses and even in the serum of
normal (especially older) animals.
Immune-mediated anaemia is characterised
by the presence of autoantibodies and/or the
C3 component of complement proteins on the
surface of erythrocytes from a patient. Direct
antiglobulin (Coombs) test is most convenient for
their detection, as it reveals when autoantibodies
or complement proteins are bound to the surface
of a patient’s erythrocytes. A positive reaction
of agglutination signalises an immune-mediated
cause of anaemia, but the primary (idiopathic)
I
autoimmune haemolytic anaemia (AIHA)
cannot be distinguished from secondary immune
mediated anaemia (IMHA) using this test, which
is caused by microbial agents or drugs.
A comparable direct test for the detection of
antibodies against thrombocytes in patients
with idiopathic thrombocytopenia has also been
developed, however it is not commonly available
for routine diagnosis.
Tests for the detection of other antibodies, such as
antibodies against the acetylcholine receptor, for
the diagnosis of myasthenia gravis, or antibodies
against thyroglobulin and thyroid peroxidase for
diagnosis of autoimmune hypothyroidism, are
not commonly available.
Immunohistochemistry techniques are very
useful methods for the detection of free or
immune complex-bound autoantibodies in
biopsy specimens. Those are usually used for
the detection of skin autoantibodies, which can
distinguish between various types of pemphigus
complexes. The use of these methods for the
detection of various types of glomerulonephritis,
or inflammatory bowel disease, is less common
but likewise significant.
A non-specific immunological profile testing
Laboratory assessment of primary or secondary
immunodeficiency is demanding for both
methodical background and financial costs and
especially tests of cell activities are offered
only by specialised laboratories that are
usually associated with universities or research
institutions. Immunological laboratories have
different validated methods available (Tab. 1);
nevertheless, it is always necessary to perform a
set of immunological examinations. An isolated
finding of a decrease in one of the immunological
parameters determined, does not necessarily
give evidence of immunodeficiency. Also, if the
values of one or more parameters are changed,
it is recommended to repeat the examination to
2006 World Congress WSAVA/FECAVA/CSAVA
confirm persistent immunodeficiency.

Table 1: Methods of immunological profile

Parameter Methods
Phagocytosis migration and che motaxis under agarose, test of synthetic particles
or microbes ingestion,chemiluminiscence, detection of respiratory
burst, microbicidity test
Lymhocyte subsets flow cytometry, immunohistochemistry
Lymphocyte activity lymphocyte transformation test, mixed lymphocyte reaction
Cytokines bioassay, ELISA, PCR
Immunoglobulin levels single radial immunodifudion RID, ELISA
Complement haemolytic activity, ELISA
CRP, lysosyme and other ELISA, turbidimetry
humoural factors
453
Back to contents
I
Cell counts and activity detection follow up the
haematological analysis of total and differential
leukocyte counts. It occurs in the assessment
of functional activity of phagocytic cells and
lymphocytes, and sometimes also in lymphocyte
subset identification (see below). Phagocytic
activity may be studied by means of a number of
tests (tab.1); however, their diagnostic values vary.
The lymphocyte transformation test (LTT) which
monitors capability of lymphocyte stimulation,
by non-specific mitogens for cell proliferation, is
most valuable, however technically demanding.
The most common findings in immunosuppression
of animals are lymphopenia, together with
dysbalance of lymphocyte subsets and a decreased
activity of lymphocytes in LTT. These changes
were detected in primary immunodeficiencies
(e.g. severe combine immunodeficiency disease)
and also in German shepherd deep pyoderma,
demodicosis, distemper, parvovirosis, in cats in
FIV, FeLV and FIP infections, and also in chronic
renal failure.
Among the tests of humoural factors, the
detection of total concentration of antibody
isotypes is crucial. The radial immunodiffusion
test is simple and available as a commercial
kit. It is mostly used for the assessment of
isotypes present in serum in high concentrations
(IgG, IgM), whilst the ELISA method is
preferred for the detection of isotypes present
in serum in low concentrations (IgA, IgE).
Reduced concentrations of immunoglobulins
indicate humoural immunodeficiency, which
may be primary (selective IgA deficiency is
most common) or secondary (occurs after
some infectious diseases, commonly of viral
origin). Decreased levels are sometimes found
in newborns with non-sufficient colostrum
supply. Elevated levels of immunoglobulins
are found in chronic inflammatory processes
and infections. Extremely high levels of serum
2006 World Congress WSAVA/FECAVA/CSAVA
immunoglobulins are detected in myeloma and
occasionally in some infectious diseases.
Table 2: Lymphocyte subsets in dogs
Subtype Fenotypic molecules
T helper cells (Th) CD3, CD4, TCRαβ, (CD2, CD5)
T cytotoxic cells (Tc) CD3, CD8, TCRαβ, (CD2, CD5)
B lymphocytes CD19, CD21, sIgM
±
γδ T cells CD3, CD8 , TCRγδ
double positive T cells CD3, CD4, CD8
454
Back to contents
Level or activity of complement proteins are a
significant immunological parameter too. It is
assessed by the test of haemolysis of sensitised
erythrocytes, or immunochemical serological
analysis of the respective components,
particularly C3.
Advanced methods in immunology
Similarly, as in related fields, knowledge in
the field of immunology has been enormously
extended by application of methods monitoring
events in the cell at molecular levels, using the
methods of genomics and proteomics. Some
of these methods have already been applied to
clinical immunology, usually as newly obtained
knowledge from clinical and experimental
studies. However, due to the fact that they are
technically demanding and thus expensive, they
are only rarely used for direct diagnosis.
Flow cytometry is the most commonly and
recent method used, for the determination of
lymphocyte subsets. Lymphocytes appear to be in
a uniform population when viewed by microscopy.
However, they are divided functionally into
a series of subpopulations, which undertake
various functions (Tab. 2). Monoclonal antibodies
against phenotypic surface molecules are used
for distinguishing between respective subtypes
of lymphocytes. Changes in T and B lymphocyte
ratios and changes in the ratios of helper (Th) and
cytotoxic (Tc) T lymphocytes have been studied
intensively. Changes in the ratios of these cells
have been found to be indicative of SLE, GSP-
associated immunodeficieny or leishmaniosis.
More recently, other minority subsets (γδ T cells,
NK cells), are studied in dogs in connection
with immune diseases. Flow cytometry is also
exploited, such as when detecting cytoplasm
proteins including cytokines, distinguishing
between apoptosis and necrosis and determining
cell cycle stages, which is a test used in oncology
diagnoses.
Range in blood
30 – 48 %
15 – 25 %
12 – 25%
1–2%
0–1%

Methods of molecular biology and genomics
are even more noteworthy. Detection of gene
expressions based on polymerase chain reaction
techniques (at present it is above all reverse
transcription-PCR, real-time PCR) are used in
clinical immunology, above all for the cytokines
detection. The most commonly detected cytokines
are inflammatory cytokines (IL-1, IL-6, TNFα),
regulating cytokines (Th1 cytokines – IL-2, IFNγ,
Th2 cytokines – IL-4, IL-5, IL-10 and others) and
chemokines. So far, the detection of cytokine in
mRNA levels has been used in cells or tissues in
dogs with various diseases including immune-
mediated.
These methods have been also applied in
immunogenetics. Damaged genes that cause primary
immunodeficiency may be detected in the case of
Severe combined X-linked immunodeficiency
disease (SCID) of bassets; C3 deficiency and
canine leukocyte adherence deficiency (CLAD).
The significance of MHC allotyping is gradually
increasing; given its association with a number of
immune-mediated diseases, in both animals and
humans. The association of a particular type of
MHC allotype has been confirmed in thyroidism
and diabetes mellitus to date.
Back to contents
I
References
Chabanne, L., Bonnefont C, Bernaud J, Rigal
D.Clinical applications of flow cytometry and
cell immunophenotyping to companion animals
(dog and cat). Methods Cell Sci. 22, 2000, 199-
207.
Day M.J.: Clinical immunology of the dog and
cat. Manson publishing, London, 1999, 288p.
Hegemann N, Wondimu A, Kohn B, Brunnberg
L, Schmidt MF.: Cytokine profile in canine
immune-mediated polyarthritis and osteoarthritis.
Vet Comp. Orthop. Traumatol. 18, 2005, 67-72
Kennedy, L.J, Huson, H.J., Leonard J., Angles,
J.M., Fox, L.E., Wojciechowski, J.W., Yuncker, C,
Happ, G.M.: Association of hypothyroid disease
in Doberman Pincher dogs with rare major
histocompatibility DLA complex II haplotype.
Tissue antigens, 67, 2006, 53-56
Toman, M., Svoboda, M., Rybnicek, J., Krejci,
J., Svobodova, V.: Secondary immunodefficiency
in dogs with enteric, dermatologic, infectious or
parasitic diseases. J. Vet. Med. (B), 45, 1998,
321-334
2006 World Congress WSAVA/FECAVA/CSAVA
455
I
I - Clinical Immunology
IMMUNE-MEDIATED HEMOLYTIC ANEMIA IN THE DOG
Luc Chabanne, DVM, PhD,
Assistant Professor
(Small Animal Internal Medicine)
École Nationale Vétérinaire de
Lyon
Small Animal Department
1, avenue Bourgelat
69280 Marcy L’Etoile - France
l.chabanne@vet-lyon.fr
Immune-mediated hemolytic anemia (IMHA) is
a common cause of anemia in dogs and a primary
idiopathic or autoimmune form of the disease
is considered to be the most frequent form of
IMHA in this species. Anemia may be severe
and recurrent, with a mortality rate up to 70%
according to certain publications. Diagnostic trail,
appropriate treatment and potential prognosis
depend on an understanding of the underlying
mechanisms of the disease.
IMMUNOPATHOGENESIS
Immune-mediated hemolytic anemia is a type II
immune reaction in which circulating red blood
cells’ (RBC) destruction is antibody-mediated
(cytotoxic). Antibody attachment to erythrocyte
surface depends on two main causes:
• In the autoimmune form of the disease, antibodies
(auto-antibodies) recognize a self-antigen of the
erythrocyte membrane. Autoimmune hemolytic
anemia (AIHA) may occur as a single clinical
entity (idiopathic AIHA), may be recognized
2006 World Congress WSAVA/FECAVA/CSAVA
concurrently with autoimmune thrombocytopenia
(Evans’ syndrome), or may be part of a
multisystemic autoimmune disease like systemic
lupus erythematosus (SLE). The development of
autoimmunity results from a failure of the normal
control mechanisms of the immune system.
Autoimmune diseases are multifactorial disorders
in which clinical expression relies on the presence
of an optimum array of predisposing factors.
Genetic factors are key determinants of disease
susceptibility that explain breed or familial
predispositions. Other predisposing factors
must be important: hormonal background, age,
environmental factors (infectious agents, drugs
and chemicals, etc.). The aim in the treatment
of AIHA as with all autoimmune diseases is to
manipulate (to down regulate or suppress) the
456
Back to contents
immune response that causes the disease so that
the process is reduced or abolished.
• In secondary IMHA, antibodies have a
specificity for a foreign antigen (an infectious
agent or a drug) that is associated with the RBC
surface, or for a neo-antigen, which is an RBC
determinant modified by a drug, an infectious
agent or secondary to a neoplastic phenomenon.
Immune-complexes can also be adsorbed at the
RBC surface. In this case, RBC destruction is due
to bystander hemolysis as the causative antibody
is not specific to the normal RBC. The prognosis
of secondary IMHA is more closely related to the
underlying disorder than the hemolytic anemia.
Therapy should be directed to the control of this
disease, and the management of the hemolytic
process itself.
In literature, the use of the subsequent
denominations: idiopathic, primary, autoimmune
or secondary IMHA is sometimes confusing:
• Primary or idiopathic IMHA is used when there
is no underlying disease or evidence of recent
drug administration and is frequently used as a
synonym of autoimmune while the presence of
true autoantibodies is not verified.
• Secondary IMHA is used when an underlying
disease is present (or drug administration), even
if anemia is due to true autoantibodies, like
in systemic autoimmune disease like SLE, in
some neoplasia (especially lymphoproliferative
diseases), or after the administration of some
drugs (such as α-methyldopa in humans).
Antibody attachment to cell membranes triggers
RBC destruction by a number of different
mechanisms. This is influenced by many factors
including the nature of the antibody itself (IgM,
IgG and IgG subclasses), the concentration of
antigen sites, complement, and macrophage
activity. Cell destruction may be intravascular or
extravascular:

• In the presence of a potent complement-
fixing antibody and a large number of antigen
sites, the complement cascade may proceed
to its full amplification with the formation of
the destructive terminal attack complex, with
resulting intravascular cell lysis.
• More frequently, the surface immunoglobulin
and complement interact with immunoglobulin
heavy chain (Fc) and complement receptors
expressed by macrophages. The macrophages
attempt to remove the abnormal protein; the
RBC are subjected to destruction by immune
phagocytosis in extravascular sites such as
the spleen or liver (extravascular hemolysis).
During the process, some of the bound cells, now
membrane depleted, become detached and re-
enter the circulation often as spherocytes. These
are then exposed to either mechanical destruction
in the circulation or more importantly premature
death in the adverse metabolic and osmotic
environment of the splenic sinusoids.
• Typically, IMHA is caused by antibodies
directed against circulating, mature RBC, with
bone marrow mounting a healthy regenerative
response (peripheral phenomenon). However,
in some dogs (up to about one third), antibodies
target erythroid precursors at any stage in their
development in the bone marrow instead of,
or in addition to, circulating RBC, resulting in
defective or ineffective erythropoiesis, and pure
red cell aplasia.
DIAGNOSIS
Basic hematological data and prognosis factors
Hematology in patients with IMHA typically
reveals a moderate to severe anemia, which is
most commonly regenerative, with anisocytosis,
polychromasia, a high reticulocyte count (> 120
G/L) and, sometimes, increased numbers of
nucleated RBC. Reticulocyte counts can however
sometimes be inappropriately low, either because
anemia is peracute (since it takes 3 to 5 days for
the bone marrow to mount a strong regenerative
response), or because antibodies are also
directed against RBC precursors. Additionally
hematology can often reveal clues that suggest an
immunologic mechanism:
• Agglutination: An autoagglutination can be
observed in the collection tube containing
anticoagulated blood, by placement of a drop
of blood onto a slide, or on the blood smear.
Autoagglutniation may only occur at +4°C, so
blood should be refrigerated before making
this assessment. True autoagglutination may be
grossly distinguished from rouleaux formation
by the addition of an equal volume of saline to
the drop of blood. Rouleaux is dispersed by this
Back to contents
I
procedure. A positive slide agglutination result is
highly suggestive of IMHA diagnosis, and also
suggests that the condition is likely to be acute
and severe. A negative slide agglutination does not
rule out IMHA: incomplete (non-agglutinating,
non-hemolytic) antibodies are reported to be
the most common antibodies in small animals
with IMHA. Recent clinical studies however,
report a much higher incidence of positive slide
agglutination, perhaps reflecting a referral bias as
the result of practionners tending to refer only the
most severe cases.
• Spherocytosis: Spherocytes are small spherical
erythrocytes that, when present in high numbers,
strongly suggest an IMHA diagnosis.
IMHA patients are at risk for developing
thromboembolism and disseminated intravascular
coagulation (DIC). Platelet count and a more
complete investigation of the coagulation cascade
should be considered. Thrombocytopenia is
associated with a poor survival prognosis.
A consensus seems to be for two other
clinicopathological parameters: high serum total
bilirubin concentration and leukocytosis (with
neutrophilic left shift and toxic changes).
Immunological testing
Specific immunological testing can be used to
support a tentative diagnosis of IMHA, and the
definitive diagnostic procedure of IMHA remains
the direct Coombs’ test.
Direct Coombs’ test (direct antiglobulin test,
DAT): A full Coombs’ test is performed with a
polyvalent antiglobulin (a mix of antibodies
directed against canine IgG, IgM and
complement), and the test should be performed at
body temperature (+37°C) and at +4°C. The titer
of each positive reaction should be determined.
No clear association between the titer of
RBC-bound antibody and disease severity exists,
although low-titered reactions are more consistent 2006 World Congress WSAVA/FECAVA/CSAVA
with secondary IMHA than AHAI. Moreover, the
titer should be used for disease follow-up and
treatment monitoring.
Alternate technologies for antiglobulin tests: Most
of them have been designed to either increase the
sensitivity of the test or to lessen the subjectivity
associated with the assessment of the degree of
agglutination (enzyme-linked antoglobulin test,
immunofluorescent test and gel test). Gel test is
a form of a column agglutination assay, where
RBC agglutinates can be trapped by a specific
type of matrix. Gel tests were first developed at
the Blood center of Lyon (Établissement Français
du Sang, Lyon, France), then commercially by
DiaMed AG (Cressier, Switzerland), and have
provided an innovative approach to blood group
serology and antiglobulin testing.
457
I
Autoantibodies: Autoantibodies eluted from
the surface of patient RBC or present in serum
(circulating autoantibodies) may be detected
using an indirect Coombs’ test by incubation
with normal erythrocytes. Antinuclear
antibodies, and platelet autoantibodies in
case of concurrent thrombocytopenia (Evans’
syndrome), should be requested in the
investigation of primary idiopathic IMHA,
presumably autoimmune.
Identification of the underlying disease
Since IMHA can be secondary, confirmation
of a diagnosis of IMHA is not necessarily the
end of the diagnostic trail. Primary IMHA can
only be diagnosed with absolute certainty once
potential underlying causes have been thoroughly
investigated! The influence of secondary factors
is now more widely recognized. This reflects
the availability of more advanced diagnostic
means for detecting the underlying disease, the
geographic extension of particular underlying
infectious diseases, and the recognition of new
trigger factors. Unfortunately, this presents
practitioners with a dilemma: although IMHA is
unlikely to be a treat unless the underlying causes
have been identified and eliminated, a complete
search for such causes can be time consuming,
expensive, potentially invasive and, in the case of
primary IMHA, ultimately fruitless. Therefore a
justification for a better characterization of AHMI
and rigorous diagnosis based upon the detection
of autoantibodies is needed.
Bone marrow analysis
Bone marrow analysis (aspiration cytology) is
also indicated in patients suspected to have the
non-regenerative forms of IMHA. In pure red
cell aplasia, bone marrow evaluation indicates
an erythroid maturation arrest (a relative or
complete lack of RBC precursors within the
2006 World Congress WSAVA/FECAVA/CSAVA
marrow). Phagocytosis of erythrocytes and RBC
precursors is frequently seen.
Treatment
The imprecision of the diagnosis, the lack of
prospective treatment efficacy studies, the
poor prognosis associated with the disease, and
the high cost of treatment and supportive care
contribute to a frustrating task for choosing a
treatment regimen for dogs.
Supportive/Ancillary therapy
Patients with severe anemia will benefit from
reducing oxygen demand (cage rest). Severely
compromised dogs may require transfusion or
oxygen-carrying support (Oxyglobin®), yet
the use of this type of supportive therapy has
been controversial. Since patients are prone to
458
Back to contents
thromboembolism and DIC, particularly those
with severe anemia and autoagglutination,
preventive therapy could be recommended. A
poor response to the prophylactic administration
of heparin (unfrationated) as an antithrombotic
strategy has been reported. An ultralow-dose
aspirin regimen (0.5 mg/kg/day for 2 days) is
promising.
Initial immunosuppressive therapy
High glucorticoid doses are the first line of
treatment for arresting RBC hemolysis in
IMHA patients. We use an initial infusion of
methylpredinosolone (2 to 4 mg/kg, once or
twice a day at admission) followed by oral
prednisone or prednisolone (1 to 2 mg/kg twice
daily) for a minimum of 7 to 10 days. IMHA
patient should be monitored at least weekly until
the anemia resolves. Once hematological and
immunological signs are improved (hematocrit
above 30% and negative DAT), the dose is then
tapered by 50 % every two weeks over a three-
month period depending on the initial dosage,
hematocrit and severity of side effects.
Specific treatment
Immunosuppressive therapy: In dogs that have
severe, acute-onset intravascular hemolysis or
in the case of persistent or relapsing-remitting
AHMI, azathioprine (2 mg/kg orally once
daily) should be added to glucocorticoids.
Azathioprine is relatively inexpensive and
usually well tolerated. Potential side effects are
rare, and idiosyncratic severe myelosuppression
(within a few weeks of commencing therapy)
should be reversible if leucopenia is promptly
detected. Other approaches to therapy are
documented. The benefit of cyclophophasmide
is controversial. Cyclosporine is costly, but
has been used successfully to treat dogs with
refractory IMHA. Another expensive, but
promising drug is leflunomide. This inhibitor of
pyrimidine biosynthesis is very well tolerated
in dogs (4 mg/kg/day). We use also danazol
(5 mg/kg orally t.i.d), an impeded androgen,
as an adjunctive therapy with glucocorticoids
in non-regenerative forms of IMHA in order
to reduce the dose of steroid that is needed for
long-term therapy.
Other treatment: Since arguably rickettsial agent
and related organisms (Bartonella, haemoplasma,
etc.) may predispose the animal to secondary
IMHA, a treatment based on doxycycline
(10 mg/kg/day for 28 days) might be indicated
in endemic areas.

Selected recent publications
Carr AP, Panceira DL, Kidd L. Prognostic
factors for mortality and thromboembolism in
canine immune-mediated hemolytic anemia:
a retrospective study of 72 dogs. J. Vet. Intern.
Med., 2002, 16: 504-509.
Day MJ. Immune-mediated hemolytic anemia.
In Feldman BF, Zinkl JG, Jain NC. Schalm’s
veterinary hematology, 5th ed. Lippincott,
Williams & Wilkins, Philadelphia. 2000, pp. 799-
806.
Miller SA, Hohenhaus AE, Hale AS. Case-control
study of blood type, breed, sex, and bacteremia in
dogs with immune-mediated hemolytic anemia.
J. Am. Vet. Med. Ass., 2004, 224: 232-235.
Back to contents
I
Thompson MF, Scott-Moncrieff JC, Brooks
MB. Effect of a single plasma transfusion on
thromboembolism in 13 dogs with primary
immune-mediated hemolytic anemia. J. Am.
Anim. Hosp. Assoc., 2004, 40: 446-454.
Wardrop KJ. The Coombs’ test in veterinary
medicine: past, present, future. Vet. Clin. Path.
2005, 34: 325-334.
Weinkle TK, Center SA, Randolph JF, Warner
KL, Barr SC, Hollis NE. Evaluation of prognostic
factors, survival rates, and treatment protocols for
immune-mediated hemolytic anemia in dogs: 151
cases (1993-2002). J. Am. Vet. Med. Ass., 2005,
226: 1869-1880.
2006 World Congress WSAVA/FECAVA/CSAVA
459
I
I - Clinical Immunology
HYPERGAMMAGLOBULINAEMIA IN THE DOG AND CAT

Professor Michael J. Day

Division of Veterinary Pathology,
Infection and Immunity
School of Clinical Veterinary
Science
University of Bristol
Langford BS40 5DU
United Kingdom
m.j.day@bristol.ac.uk

One of the most common laboratory diagnostic
procedures performed in veterinary medicine is
the serum biochemistry profile which generally
includes data on serum globulin concentration.
Identification of elevated serum globulin in a
patient should trigger further investigation of this
phenomenon by serum protein electrophoresis.
Protein electrophoresis gels, whether examined
qualitatively or subject to densitometric
scanning, provide information on the nature
of elevated globulins – in particular whether
these are primarily of the alpha, beta or gamma
class. The majority of alpha and beta globulins
comprise an assortment of proinflammatory
proteins, and elevations of these molecules
should be expected in any disease state involving
2006 World Congress WSAVA/FECAVA/CSAVA
an inflammatory process. A number of studies
have examined correlations between disease
state and concentration of these proteins (in
particular C-reactive protein which migrates in
the gamma globulin region), but such findings
can only be regarded as non-specific indicators
of inflammation. Elevation of gamma globulins
indicates immune system reactivity and may be
polyclonal or monoclonal in nature. By contrast,
hypogammaglobulinaemia in an animal with
inflammatory or infectious disease might
suggest failure of the immunological response
(primary or secondary immunodeficiency) and
trigger further investigation of this phenomenon.
This presentation reviews the causes for
hypergammaglobulinaemia in the dog and cat.

460
Back to contents

I - Clinical Immunology
CHARACTERIZATION OF CANINE DENDRITIC CELLS AND THEIR
POTENTIAL THERAPEUTIC USE
Catherine Bonnefont-Rebeix
École Nationale Vétérinaire de Lyon
Small Animal Department
1, avenue Bourgelat
69280 Marcy L’Etoile - France
Jeanine Bernaud
Immunology Department
Établissement Français du Sang de
Lyon
1 à 3, rue du Vercors
69364 Lyon 07 - France
Thierry Marchal, DVM, PhD,
Assistant Professor (pathology)
École Nationale Vétérinaire de Lyon
Small Animal Department
1, avenue Bourgelat
69280 Marcy L’Etoile - France
Dentritic cells are the most potent antigen-
presenting cells, and play a key role in the
regulation of the immune system since they are
the only cells capable of priming naive T cells.
Their potency in antigen presentation has led
several investigators to use them as vaccine
adjuvants in therapy against tumors.
Since dogs are considered as a very interesting
experimental model for immune-mediated
diseases, graft rejections and cancers, a better
characterization of canine dendritic cells (caDC)
is required. caDC can be derived from monocytes
(Mo) in the presence of canine GM-CSF (caGM-
CSF) and canine IL-4 (caIL-4) in a 7 day culture.
To date, no specific marker of caMo-DC has been
described in contrast to human Mo-DC, for which
several markers are available for characterizing
the different subsets of DC and the different steps
of differentiation and maturation.
The first part of our study consisted in the
development of an elutriation technique to
obtain large quantities of pure canine monocytes.
Canine peripheral blood mononuclear cells were
isolated from whole blood by Ficoll gradient,
then separated by an elutriation process. We
demonstrated that these techniques allow the
isolation of canine peripheral blood monocytes
with a purity of 64%±7.9 when labelled with
anti-CD14 antibody. This purity increased to
83%±2.2 by the use of magnetic anti-CD14
Back to contents
I
Dominique Rigal, MD, PhD
Immunology Department
Établissement Français du Sang
de Lyon
1 à 3, rue du Vercors
69364 Lyon 07 - France
Luc Chabanne, DVM, PhD,
Assistant Professor
(small animal internal medicine)
École Nationale Vétérinaire
de Lyon
Small Animal Department
1, avenue Bourgelat
69280 Marcy L’Etoile -
France
l.chabanne@vet-lyon.fr
microbeads after elutriation. Cell viability was
more than 95% and apoptosis was less than 10%.
The monocytes purified by these methods were
functionally active in a mixed leukocyte reaction
(MLR).
In the second part, we demonstrated that caMo-DC
were labelled with three anti-human costimulatory
molecule CD86 (FUN-1, BU63 and IT2.2
clones), while resting and activated lymphocytes
or monocytes were not stained. CD86 expression
was induced by caIL-4 and was upregulated
during the differentiation of the caMo-DC, with a
maximum at day 7. Furthermore, caMo-DC were
very potent even in low numbers as stimulator 2006 World Congress WSAVA/FECAVA/CSAVA
cells in allogeneic MLR, and BU63 monoclonal
antibody (mAb) was able to completely block the
caMo-DC-induced proliferation in MLR. We also
observed that caMo-DC highly expressed MHC
class II and CD32, but we failed to determine their
maturation state due to the lack of commercially
available canine markers.
In the third part, we investigated the expression
of toll-like receptor 3 (TLR3), which was shown
to be specifically expressed in human DC. TLR
is a family of functionally important receptors
for recognition of pathogen-associated molecular
pattern, since they trigger the pro-inflammatory
response and upregulation of costimulatory
molecules. We demonstrated the cross-reactivity
of three TLR3 mAb (619F7, 722E2 and 713E4
461
I
clones, Dendritics, Lyon, France) towards canine
PBMC and caMo-DC. Using flow cytometry,
TLR3 expression was low to moderate in caMo
and lymphocytes depending on the anti-TLR3
clone used, with the 722E2 clone remaining
always more intense. After culture of caMo
in the presence of caGM-CSF and caIL-4 for
7 days, the non-adherent caMo-DC obtained
strongly expressed TLR3 with the 3 anti-TLR3
clones. These results slightly differ from those in
human, where TLR3 was shown to be exclusively
expressed in DC but absent in precursor
monocytes, by means of total RNA extraction and
northern blot analysis.
Indeed, the caMo-DC we generated in the
presence of caGM-CSF and caIL-4 could have
already initiated their maturation since they were
found to express CD86 and to be competent to
stimulate lymphocyte proliferation in MLR, but
we do not have enough criteria, such as CD83
and the DC-Lamp in humans, to define if these
caMo-DC are mature or immature.
At least this first approach of canine TLR3 protein
expression could be useful to investigate canine
innate immune defence and its role in adaptative
immunity. However, since there is a lack of canine
specific markers, these results will contribute to a
better characterization of canine dendritic cells,
and could perhaps advance the use of caMo-DC
in immunotherapy.
To date, canine DC have been studied as models
for graft rejection and for their role in the
presentation of minor histocompatibility antigens.
Canine DC were also produced from CD34+
bone marrow progenitor cells and generated from
PBMC from dogs with oral malignant melanoma.
Recently, bone marrow-derived DC were used to
vaccinate dogs with stage I and III oral melanoma
after surgical excision and treatment with
radiation therapy (Gyorffy et al., 2005). Among
the 3 dogs receiving 3 subcutaneous vaccinations
2006 World Congress WSAVA/FECAVA/CSAVA
over a 4-month period, one dog has displayed no
clinical signs of recurrent melanoma 48 months
after initial DC injection, and another relapsed
462
Back to contents
22 months after vaccination. Although this
therapeutic approach warrant some additional
investigation, ex vivo DC expansion seems
feasible for immunotherapy of spontaneous
cancers in outbred dogs.
Selected publications:
Catchpole, B., Stell, A.J., Dobson, J.M., 2002.
Generation of blood-derived dendritic cells in
dogs with oral malignant melanoma. J. Comp.
Pathol. 126, 238-241.
Deeg, H.J., Aprile, J., Storb, R., Graham, T.C.,
Hackman, R., Appelbaum, F.R., Schuening, F.,
1988. Functional dendritic cells are required
for transfusion-induced sensitization in canine
marrow graft recipients. Blood 71, 1138-1140.
Gyorffy, S., Rodriguez-Lecompte, J.C., Woods,
J.P., Foley, R., Kruth, S., Liaw, P.C.Y., Gauldie,
J., 2005. Bone-marrow-derived dendritic cell
vaccination of dogs with naturally occurring
Melanoma by using human gp100 antigen. J. Vet.
Med. 19, 56-63.
Hagglund, H.G., McSweeney, P.A., Mathioudakis,
G., Bruno, B., Georges, G.E., Gass, M.J., Moore,
P., Sale, G.E., Storb, R., Nash, R.A., 2000. Ex vivo
expansion of canine dendritic cells from CD34+
bone marrow progenitor cells. Transplantation 70
(10), 1437-1742.
Kalhs, P., White, J.S., Gervassi, A., Storb,
R., Bean, M.A., 1995. In vitro recall of
proliferative and cytolytic responses to minor
histocompatibility antigens by dendritic cell
enriched canine peripheral blood mononuclear
cells. Transplantation 59 (1), 112-118.
Storb, R., Thomas, E.D., 1985. Graft-versus-host
disease in dog and man: the Seattle experience.
Immunol. Rev. 88, 215-238.
Weber, M., Lange, C., Gunther, W., Franz,
M., Kremmer, E., Kolb, H.J., 2003. Minor
histocompatibility antigens on canine hemopoietic
progenitor cells. J. Immunol. 170 (12), 5861-5868.
 I
I - Clinical Immunology
AN UPDATE: IMMUNOPATHOGENESIS OF GERMAN SHEPHERD
ANTIBIOTIC RESPONSIVE DIARRHOEA
Professor Michael J. Day
Division of Veterinary Pathology,
Infection and Immunity
School of Clinical Veterinary
Science
University of Bristol
Langford BS40 5DU
United Kingdom
m.j.day@bristol.ac.uk

The German shepherd dog (GSD) has clear
breed predisposition to inflammatory bowel
disease (IBD) and antibiotic responsive diarrhoea
(ARD). Both of these enteropathies are likely to
involve an abnormal interaction of the intestinal
immune system with antigens derived from
the luminal microflora, and as such a good
candidate mechanism to explain the strong breed
association would be defective mucosal IgA
production. Insufficiency of luminal IgA would
contribute to reduced barrier function in affected
small intestine, thus resulting in greater exposure
to causative antigen. The nature of the intestinal
inflammatory response in these disorders has now
been well characterized in terms of the phenotype
of lamina propria and intraepithelial lymphocytes
and cytokine mRNA expression, although the
most recent investigations of the latter area have
failed to confirm earlier observations suggesting
elevation of transcription of genes encoding pro-
inflammatory and Th1-related cytokines.

2006 World Congress WSAVA/FECAVA/CSAVA

463
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Ip
p
Ip
Infectious
fectiou & Parasitic
Diseases

Back to contents

INVITED LECTURES - FULL PAPERS
Ip - Infectious & Parasitic Diseases
INFECTION OF CATS WITH H5N1 AVIAN INFLUENZA VIRUS
Prof. emer. Marian C. Horzinek
Veterinary Research Consult
Bithoven
The Netherlands
horzinek@planet.nl
This document has been compiled by Etienne
Thiry (Liege/B), with the assistance of Diane
Addie (Glasgow/UK), Herman Egberink (Utrecht/
NL), Katrin Hartmann (Munich/D), Hans Lutz
(Zurich/CH) and Hervé Poulet (Lyon/F). It is
published under the authority of the Advisory
Board on Cat Diseases (ABCD), a committee
dedicated to developing and issueing guidelines
for the prevention and management of feline
infectious disease. The initiative is supported by
animal health care company Merial.
Introduction
The H5N1 subtype of Avian Influenza Virus
type A, a member of the Orthomyxoviridae
family, occurs primarily in birds. Transmission
to mammals happens sporadically, and the
infection then may cause disease with a high
morbidity and a high number of deaths among ill
animals. Humans, primates, rodents, lagomorphs,
mustelids and felids, including the domestic cat
may be infected and may succumb to the disease.
A listing of susceptible species is given at
http://www.nwhc.usgs.gov/disease_information/
avian_influenza/affected_species_chart.jsp.
Infection of cats
Felids can be naturally and experimentally
infected with H5N1 virus. In February 2004,
infection of household cats was reported from
Thailand (WHO, 2004); also from that country,
two outbreaks of fatal disease in tigers and
leopards have been published (Keawcharoen
et al., 2004; Thanawongnuwech et al., 2005).
In February/March 2006, three cats were found
dead on the island of Rügen, Germany and
infection with H5N1 virus was established by
laboratory tests. Also in March 2006, three cats
were found infected but alive in an animal shelter in
Graz, Austria. - First experimental evidence for the
pathogenicity of H5N1 avian influenza virus for the
Back to contents
Ip
Prof. Etienne Thiry
Université de Liège
Faculté de Médicine Vétérinaire
20 Blvd. Colonster bâtiment B43b
4000 Liège
Belgium
etienne.thiry@ulg.ac.be
domestic cat was obtained by Kuiken et al. (2004).
A statement from the WHO (28th February
2006) reads: “There is no present evidence that
domestic cats play a role in the transmission
cycle of H5N1 viruses. To date, no human case
has been linked to exposure to a diseased cat. No
outbreaks in domestic cats have been reported.
Unlike the case in domestic and wild birds, there
is no evidence that domestic cats are a reservoir
of the virus. All available evidence indicates that
cat infections occur in association with H5N1
outbreaks in domestic or wild birds.”
The following data have been obtained from
experimental infections (Kuiken et al., 2004;
Rimmelzwaan et al., 2006); they reflect the
current state of knowledge and will have to be
revised and expanded, as additional information
becomes available:
•cats can be infected via the intratracheal and oral
routes, and by feeding them infected chickens;
•infection can occur through contact with infected
birds;
•infected cats can transmit the virus to in-contact
cats; 2006 World Congress WSAVA/FECAVA/CSAVA
•moderate amounts of virus are sufficient to infect
a cat;
•the virus is shed with nasal secretions and in
faeces; nasal excretion starts 3 days after infection
and continues for 4 days or longer;
• the incubation period in experimental infections
is about 2 days;
•clinical signs are fever, lethargy/depression,
dyspnoea, conjunctivitis; when clinical signs occur,
the outcome of the disease is mostly fatal within one
week. Also icterus has been observed.
•at necropsy, multifocal lung lesions and petechial
haemorrhages in the tonsils, mandibular and
retropharyngeal lymph nodes, and the liver are seen;
•histologically, inflammatory and necrotic lesions
are seen in the lungs, heart, brain, kidneys, liver
and adrenal glands. Lesions in the small intestine
465
Ip
are observed in cats that had been fed infected
chickens.
Risk considerations – questions and answers
1. How may a cat become infected after contacts
with birds or poultry products?
•Precondition is that the cat lives in a region
where one or more H5N1 virus infected birds
have been identified by laboratory tests; if this
condition applies, the following risk factors must
be considered:
•the cat lives in an environment where aquatic
birds are present;
•the cat has access to outdoors;
•the cat has contact with free ranging or indoor
poultry;
•the cat has been fed uncooked poultry meat.
2. How may a cat be infected by another cat?
•close contact with an H5N1 infected, sick cat
is required at least during the first seven days of
infection; although inapparent infection might
occur for a limited period, persistent H5N1 virus
infections have not been reported.
3. How may a cat transmit the infection to a
person?
To date (March 2006), virus transmission from a
cat to a person has not been reported.
However,
•a H5N1 virus which had infected a cat is already
adapted to a mammalian species; viruses isolated
from humans exhibited increased virulence for
mammals (Maines et al., 2005);
•this virus is excreted by the respiratory route and
in the faeces;
•the level of excretion is high enough to allow
in-contact cats to become infected;
•in view of the habitual close contacts between
2006 World Congress WSAVA/FECAVA/CSAVA
cats and their owners, an infected cat can probably
infect a human;
•the risk of infection and disease for humans can
presently not be estimated.
4.When should a veterinary practitioner suspect
an ill cat to be infected with H5N1 virus?
•Before expressing a suspicion, the potential risk
must be evaluated according to the answers to the
anamnestic questions above;
•if a risk is assumed, a clinical assessment must
be performed and clinical signs as given above
should be observed: fever, lethargy/depression,
dyspnoea, conjunctivitis, rapid death; also
neuroligical signs have been reported;
•the differential diagnosis should exclude other
infections leading to similar systemic and
respiratory signs, as caused by feline herpesvirus
466
Back to contents
and calicivirus and by bacteria (Bordetella
bronchiseptica, Chlamydophila felis, also
mycoplasma);
•clinical signs can only result in a probability
diagnosis, which must be confirmed by laboratory
testing.
5. How should samples for laboratory diagnosis
be taken and handled?
The authorities must be notified as specified
by the national regulations and the diagnostic
laboratory is contacted for detailed instructions.
There are some general rules:
To take oropharyngeal, nasal, and rectal swabs or
faecal samples:
•plastic tubes should be labelled using an alcohol-
proof ink marker;
•the samples are transferred to the tubes, which
are tightly closed;
•the outside of the tubes is swabbed with ethyl
alcohol to reduce the risk of infection for the
receiving personal;
•the material safely enclosed in plastic bags
is shipped to the national reference laboratory
according to procedures defined by the
authorities;
Post mortem samples of lung and mediastinal
lymph nodes should be kept and shipped in 10%
formol saline.
It is not recommended to perform an in-house
influenza detection test.
6. Which measures must be taken by the veterinary
practitioner when a case of H5N1 virus infection in
a cat is suspected?
For own protection:
• physical contact with the cat must be minimized,
scratching and biting avoided;
•gloves, mask and goggles (protective eyewear)
should be worn when the cat is manipulated;
•sedation of the cat is recommended before taking
samples;
•for surface decontamination, a standard medical
disinfectant is used.
For protection of attending personnel and other
animals:
•in the veterinary clinic, the suspected cat is kept
in isolation in a cage.
For protection of owners and relatives:
•in the owner’s house, the cat has to be kept in a
separate room;
•physical contact with the cat must be minimized,
scratching and biting avoided;
•litter trays, bowls, baskets and other potentially
contaminated objects must be disinfected using a
hypochloride solution (bleech);
•rooms where the cat had access before the visit

to the veterinarian should be thoroughly cleaned
using a household detergent (which is expected to
inactivate influenza virus).
7.What can owners do to minimize the risk of an
H5N1 avian influenza virus infection?
•the development of the epidemic must be
followed in the national and local media;
•feeding of uncooked poultry meat to cats must
be avoided;
•if many deaths occur amongst wild birds, cats
should be kept indoors until further information
about the cause is available.
References
Keawcharoen et al., Avian influenza H5N1 in
tigers and leopards. Emerg. Infect. Dis., 2004,
10, 2189-2191.
Kuiken et al. Avian H5N1 influenza in cats.
Science, 2004, 306, 241.
Maines et al. Avian influenza (H5N1) viruses
isolated from humans in Asia in 2004 exhibit
Back to contents
Ip
increased virulence in mammals. J. Virol., 2005,
79, 11788-11800.
Rimmelzwaan et al. Influenza A virus (H5N1)
infection in cats causes systemic disease with
potential novel routes of virus spread within and
between hosts. Am. J. Pathol., 2006, 168, 176-
183.
Thanawongnuwech et al., Probable tiger-to-tiger
transmission of avian influenza H5N1. Emerg.
Infect. Dis., 2005, 11, 699-701.
WHO, Avian influenza A (H5N1) – update 28:
reports of infection in domestic cats, 20 February
2004.
Relevant web sites
World Health Organisation: http://www.who.int/en/
World Organisation for Animal Health: http://
www.oie.int
European Commission, Animal Health and
Welfare: http://europa.eu.int/comm/food/animal/
2006 World Congress WSAVA/FECAVA/CSAVA
467
Ip
Ip - Infectious & Parasitic Diseases
INFECTIOUS DISEASES OF THE RESPIRATORY TRACT
Remo Lobetti BVSc, MMedVet
(Med), PhD, Dipl. ECVIM
(Internal Medicine)
Bryanston Veterinary Hospital
PO Box 67092
Bryanston
2021
South Africa
rlobetti@mweb.co.za
Infectious diseases affecting the respiratory
tract of the dog and cat include viral, bacterial,
protozoal, and fungal. Upper respiratory tract
infections are more common in the cat, whereas
lower respiratory tract infections are more
common in the dog.
Feline Upper Respiratory Infections
Several viral and bacterial entities comprise feline
upper respiratory infections. These organisms are
present in saliva, nasal and ocular discharges and
are mainly spread by direct contact, via fomites
and by aerosol inhalation and ingestion. Infections
can be more severe if there is concurrent FeLV
or FIV infection. Although infections are usually
limited to the upper respiratory tract they may be
complicated by bronchial infection or pneumonia.
Infections are more severe in kittens and elderly
cats.
Feline Viral Rhinotracheitis
Feline viral rhinotracheitis is an upper respiratory
infection caused by feline herpesvirus-1 and
characterized by sudden onset sneezing, fever,
2006 World Congress WSAVA/FECAVA/CSAVA
copious mucoid nasal discharge and lacrimation.
Ocular disease can be severe, with keratitis,
conjunctivitis and panophthalmitis. There may
also be ulcers on the tongue and necrosis of the
turbinates. In kittens mortality can be very high.
This virus causes about one-half of respiratory
disease in cats and many cats become latent
carriers. In the latter, various stresses may trigger
the excretion of the virus with recurrence of
clinical disease.
Feline Calicivirus
Feline calicivirus infection is an upper respiratory
disease characterized by fever, rhinitis,
conjunctivitis, palatine and/or glossal ulcerations
and nasal discharge. When bronchopneumonia
develops, the mortality rate may exceed 30%.
Lameness occurs following infection with some
468
Back to contents
strains of calicivirus. Infected cats may become
carriers and the virus can be shed continuously
from the pharynx and tonsils for months and
sometimes years.
Feline Pneumonitis (Feline Chlamydiosis)
Feline pneumonitis is caused by the bacterium
Chlamydophila felis (previously Chlamydia
psittaci) and characterized mainly by a chronic
follicular conjunctivitis with an ocular discharge
that may become purulent. The ocular form is
seen most commonly in 5 - 12 week old kittens.
Pneumonitis is an infrequent feature of the
disease.
Feline Mycoplasma
Mycoplasma felis causes an infrequent
upper respiratory infection characterized by
conjunctivitis and unilateral or bilateral rhinitis.
The infection can resolve spontaneously in 2 - 4
weeks. There is some question as to whether M.
felis has a primary or secondary role. M. gatae and
M. feliminutum are occasionally recovered from
the respiratory tract, but they are not considered
to be pathogenic.
Feline Bordetella
Bordetella bronchiseptica is an important cause,
either primary or secondary to respiratory viruses,
of upper respiratory tract infections in cats. It
has also been implicated as an infrequent cause
of pneumonia. Serious outbreaks have occurred
in laboratory cats and in breeding colonies with
bronchopneumonia and deaths. The disease is
most severe in young cats.
Canine Infectious Tracheobronchitis
Infectious tracheobronchitis is a highly
contagious, non-life threatening respiratory
disease of dogs characterized by paroxysms
of cough that usually persist for several days
or rarely for several weeks. Viral infections

damage the upper respiratory mucosa and pave
the way for secondary infection with bacteria
such as Bordetella bronchiseptica. A variety of
other bacteria can become involved as end-stage
organisms in canine infectious tracheobronchitis,
e.g. Staphylococci, Streptococci, Pseudomonas
and coliforms. Infectious tracheobronchitis is
therefore a clinical syndrome with multiple and
sometimes combined aetiologies. Clinically,
the syndrome is defined as being mild, upper
respiratory in nature, and self limiting. Infection
with multiple agents results in more severe
clinical signs, but is only life threatening when
a virulent agent such as canine distemper virus
is involved.
Canine Parainfluenzavirus (CPIV)
CPIV is frequently isolated from dogs with an
acute dry cough. CPIV only affects the surface
epithelium of the upper and lower respiratory
tract and does not appear to persist in the dog.
CPIV produces an acute inflammatory reaction in
the upper and lower respiratory tract and regional
lymph nodes. Clinical signs are mild and include
an acute disease with coughing, tonsillitis,
and nasal discharge. With secondary bacterial
infection, severe disease may develop.
Type 2 Canine Adenovirus (CAV-2)
CAV 2 is commonly isolated from the more severe
cases of infectious tracheobronchitis and usually
occurs in unvaccinated dogs and in pups that
have lost their maternal antibody protection. CAV
2 can induce a very mild disease, or can produce
a fatal bronchopneumonia. Clinical signs usually
include fever and lethargy, and a dry cough of
tracheal origin persisting for 10 15 days. In
contrast to CPIV, CAV 2 seems to persist for long
periods of time. Like CPIV, CAV 2 can cause a
severe tracheobronchitis with mycoplasmas and
secondary bacterial infections.
Distemper virus
Canine distemper virus can infect epithelial
tissues throughout the body, resulting in signs
due to respiratory, gastro-intestinal, neurologic,
or ophthalmologic involvement. Respiratory
system involvement is usually identified with
severe disease, and bacterial pneumonia is a
common complication. Mild transient signs are
often mistaken for infectious tracheobronchitis.
Canine Herpesvirus
In contrast to newborn pups in which this
virus causes generalized disease, herpes virus
infection in older dogs appears to be restricted
to the upper respiratory tract causing mild
disease. In comparison to CPIV and CAV 2,
Back to contents
Ip
herpesvirus is often not associated with infectious
tracheobronchitis. It does not spread as rapidly
from dog to dog as CPIV or CAV 2 and infected
dogs remain permanent carriers.
Canine Reovirus
Reovirus infection lesions are mild and confined to
the lungs which show exudation of macrophages
into alveolar spaces and diffuse thickening of
alveolar septa. After experimental inoculation
dogs develop a mucoid nasal discharge, fever
and sometimes a mild cough. Reovirus is not
a significant etiological agent of infectious
tracheobronchitis.
Bacterial Pneumonia
Bacterial pneumonia is common in the dog and
relatively uncommon in the cat. It can be a primary
disease or, more frequently as a complication to
other pulmonary disease processes. Dogs with
bacterial pneumonias should be thoroughly
investigated for underlying disease, especially
if cases are unresponsive to treatment. Primary
bacterial pneumonia can occur due to B.
bronchiseptica and Streptococcus zooepidemicus.
Secondary bacterial pneumonias can involve both
gram-negative organisms (E. coli, Klebsiella,
Pasteurella multocida, B. bronchiseptica,
Pseudomonas aeruginosa) and gram-positive
cocci (Staphylococcus and Streptococcus spp).
Mycoplasmas can also play a role but are usually
secondary to bacterial infections. Clinical signs
usually include fever, nasal discharge, dyspnoea,
congested or cyanotic mucous membranes, and
abnormal lung sounds (moist crackles).
Lung Abscessation
This is an uncommon condition, occurring more
frequently in cats, secondary to foreign bodies,
chronic lung infection, penetrating wounds, and
neoplasia. Clinically these cases manifest with
chronic debilitating disease, coughing, variable
2006 World Congress WSAVA/FECAVA/CSAVA
respiratory distress, fever and leukocytosis.
Diagnosis is based on history, clinical signs, and
radiographic signs of focal increased lung density
and/or pleural effusion. Initial treatment involves
appropriate antibiotic therapy, chest irrigation and
drainage. Only after concerted medical treatment
has failed should a thoracotomy with partial or
total lung lobectomy be considered.
Protozoal Pneumonia
Toxoplasma gondii or Pneumocystis carinii may
on rare occasions be responsible for protozoal
pneumonia in immunosuppressed animals.
Animals with toxoplasmosis may show acute
or chronic disease and often have multiple
organ involvement (lung, liver, lymph nodes,
469
Ip
muscles, CNS, uterus, eye) whereas those with
pneumocystosis usually only present with
chronic pneumonia. Pneumocystosis has a high
prevalence in young miniature Dachshunds.
Clinical signs, radiography, and haematology
are of little diagnostic value. The diagnosis is
confirmed on demonstration of organisms in
tracheal wash or broncho-alveolar lavage fluid
or lung aspirate cytology. Faecal examinations
and serum antibody titres may be useful in the
diagnosis of T. gondii. If possible, the underlying
immunosuppressive state should be identified
and corrected (distemper, Ehrlichia canis,
FIP, FeLV, FIV, Cushing’s disease, exogenous
immunosuppressive agents).
Mycotic Pneumonia
Mycotic pneumonia can be caused by Histoplasma
capsulatum, Blastomyces dermatitides,
Coccidioides immitis, Aspergillus fumigatus,
or Cryptococcus neoformans. Animals may be
asymptomatic or show signs of severe lower
respiratory disease including a diffuse miliary
interstitial pattern and hilar lymphadenopathy.
Cytological identification of organisms in
macrophages on tracheal wash or broncho-
alveolar lavage fluid or lung and peripheral
lymph node cytology is the preferred method of
diagnosis. Fungal culture and serology may be
used as adjuncts in the diagnosis.
Granulomatous Pulmonary Disease
There are a number of diseases that produce an
inflammatory interstitial process within the lung
resulting in an accumulation of inflammatory
cells within the pulmonary interstitium. The
pulmonary parenchyma is predominantly
2006 World Congress WSAVA/FECAVA/CSAVA
470
Back to contents
infiltrated with mononuclear inflammatory cells
(macrophages, lymphocytes and plasma cells).
Lymphomatoid granulomatosis, eosinophilic
granulomatosis, SLE, FIP, mycobacterial
infections (Mycobacterium tuberculosis and M.
bovis), foreign body reactions, mycotic infections,
neoplasia, and external allergic alveolitis have all
been reported to cause granulomatous reactions
within the lung. A lung biopsy is often required to
make the diagnosis.
Parapneumonic Effusion
A parapneumonic effusion is the accumulation
of an uninfected effusion (modified transudate
to exudate) that is associated with primary
pulmonary infection and inflammation. This
effusion clears with antibiotic therapy for the
primary pulmonary disease and does not require
chest drainage.
Pyothorax
This is the accumulation of a purulent, often foul
smelling, septic exudate within the pleural space
as a result of bacterial or fungal infection. The
routes of infection include penetrating thoracic
wounds (especially bite wounds in cats), extension
from bacterial pneumonia, migrating foreign
bodies, oesophageal perforation (associated
with mediastinitis) and haematogenous spread.
Anaerobes and Nocardia asteroides are most
frequently isolated in dogs, while anaerobes and
Pasteurella multocida are the most common
isolates in cats.
References
Available by contacting the author by email.

Ip - Infectious & Parasitic Diseases
INFECTIOUS DISEASES OF THE GI TRACT
Remo Lobetti BVSc, MMedVet
(Med), PhD, Dipl. ECVIM
(Internal Medicine)
Bryanston Veterinary Hospital
PO Box 67092
Bryanston
2021
South Africa
rlobetti@mweb.co.za
Infectious diseases affecting the gastro-intestinal
tract of the dog and cat include viral, bacterial,
protozoal, and fungal. In the dog and cat, infectious
diseases, especially in chronic cases can often be
overlooked as the cause of the GI tract problem.
Feline Astrovirus
Astrovirus can cause sub-clinical infections and
also diarrhoea, particularly in kittens that may last
as long as two weeks.
Feline Coronavirus
Feline coronaviruses are divided into two
groups: The pathogenic strains that cause feline
infectious peritonitis (FIP) and those feline enteric
coronaviruses (FECV) that cause a sub-clinical
or mild enteric infection. Viruses of these two
categories are closely related.
Feline Panleukopenia
Feline panleukopenia virus, a parvovirus, is a
highly contagious, frequently fatal, viral disease
of cats. The disease is seen most frequently in cats
3 - 5 months of age and is associated with high
mortality. The virus is present in nasal secretions,
faeces and urine and is transmitted by contact with
infected animals via fomites. Infection of kittens in
utero or within a few days of birth leads to cerebellar
ataxia. Clinical signs include pyrexia, anorexia,
depression, weakness, sternal recumbency, nasal
discharge, conjunctivitis, vomiting, and diarrheic.
Canine Parvovirus
Canine parvovirus infection is a contagious disease
of dogs caused by canine parvovirus 2, which is
closely related to the parvovirus causing feline
panleukopenia. The disease is seen in household
dogs and may involve whole litters and kennels.
Young and elderly dogs and Doberman pinschers
and rottweilers are most susceptible. Clinical
signs include vomiting, haemorrhagic diarrhoea,
fever, dehydration, and marked leukopenia.
Back to contents
Ip
Canine Parvovirus 1
Canine parvovirus 1 causes infrequent enteric
and respiratory infections in young puppies. A
number of puppies in a litter may be infected
and the outcome may be fatal. Clinical signs
include dullness, anorexia, diarrhoea, vomiting
and dyspnoea. Unless a particular cell line
(Walter Reed canine cell line) is employed for
isolation or special immunological reagents
are used, laboratory diagnosis is usually
unsuccessful.
Canine Coronavirus
Canine coronavirus infection is a relatively mild
enteric disease of mainly young dogs although all
ages may be infected. The virus is relatively labile
and can survive outside the animal for 1 - 2 days.
Clinical signs are anorexia, depression vomiting,
and diarrhoea.
Rotavirus
Rotavirus occurs widely in the intestine of dogs
but infections are generally sub-clinical. Feline
rotaviruses can cause sub-clinical infections and
occasionally mild enteritis in kittens, but not the
severe infection seen in the young animals of 2006 World Congress WSAVA/FECAVA/CSAVA
other domestic species. Rotavirus can be detected
in faeces with electron microscopy.
Salmon Poisoning Complex
Salmon poisoning complex is a rickettsial disease
of dogs contracted from eating fluke-encysted
salmon and occasionally other fish. It is an acute,
febrile disease with mortality reaching as high as
90% if untreated. The intermediate hosts of the
rickettsia are snails and fish. The disease is caused
by Neorickettsia helminthoeca, which is present in
the liver fluke Nanophyetus salmincola, the cysts
of which occur in salmon. Clinical signs include
diarrhoea, hemorrhagic enteritis, vomiting, and
dehydration.
471
Ip
Campylobacteriosis
Campylobacteriosis is a contagious disease caused
by Campylobacter jejuni and characterized by
enteritis and diarrhoea of variable duration and
severity, although dogs and cats can carry and
shed C. jejuni, without showing clinical signs. C.
jejuni is a small, fragile, gram-negative rod. Dogs
less than six months of age are more severely
affected and there is some question as to whether
this organism causes enteritis and diarrhoea in
normal cats other than kittens. Debilitated cats
and those with parasitic or microbial infections
are more susceptible. Although C. coli and C.
upsaliensis can occasionally be recovered from
the faeces of cats, their significance is not clear.
Canine Haemorrhagic Gastroenteritis
This infrequent, sporadic, noncontagious disease
is characterized by rapid onset and course with
severe bloody diarrhoea. Toy, miniature breeds
and young dogs are particularly susceptible.
Although the aetiology is not known, the
presence of Clostridium perfringens in large
numbers in the faeces is suggestive of clostridial
enterotoxaemia, although the increase in bowel
permeability in the absence of inflammation and
necrosis is indicative of a type I hypersensitivity
reaction. Possible contributing factors are stress
and dietary change. The cardinal clinical sign is
copious bloody diarrhoea of rapid onset. There
is usually also vomiting, anorexia, and profound
depression.
Helicobacter Infection
At least 14 species of these gram-negative,
spiral-shaped bacteria are included in the genus
Helicobacter. In man the most significant is H.
pylori, which causes gastritis and peptic ulcers,
which may progress to gastric carcinoma. A
number of Helicobacter species have been
isolated from the stomachs of dogs and cats
2006 World Congress WSAVA/FECAVA/CSAVA
including H. felis, H. heilmannii, and H. pylori.
There has, however, been much debate about the
pathogenic significance of these organisms in dogs
and cats. Clinical signs attributed to Helicobacter
infections include vomiting, regurgitation,
abdominal pain, diarrhoea, anorexia, weight loss,
and poor condition.
Salmonellosis
Salmonellosis is a contagious disease of animals
and humans caused by many varieties of the
enteric gram-negative bacterium Salmonella.
Over 2000 serotypes of Salmonella have been
implicated as causes of salmonellosis. The most
common serotype recovered from dogs and cats is
S. typhimurium. Concurrent enteric infection and
immunosuppression may predispose to clinical
472
Back to contents
salmonellosis. Salmonellosis is manifested by one
of the following three syndromes: septicaemia,
acute enteritis and chronic enteritis. Young
animals most frequently develop the septicaemic
form, whereas acute and chronic enteritis is seen
most commonly in adult animals. Cats are highly
resistant to salmonellosis but there are reports
of outbreaks in kittens and infrequent clinical
disease in adult cats. A considerable number of
dogs and cats are carriers. Clinical signs vary
with the severity of the infection and include
acute to chronic gastroenteritis, episodes of fever,
vomiting, depression, occasionally pneumonia and
sometimes abscesses in lymph nodes and liver.
Tyzzer’s Disease
Tyzzer’s disease is a severe, frequently fatal,
bacterial infection characterized by a focal
necrotic hepatitis. The cause is Clostridium
piliforme, which is a large, spore forming,
gram-positive, anaerobic rod that is part of the
normal intestinal flora of many rodents. The
disease is characterized by enteritis and focal,
necrotic hepatitis. Most animals are found dead
or in a coma, without showing premonitory
signs. Clinical signs include fever, icterus and
sometimes diarrhoea.
Coccidiosis
Several species of Isospora have been associated
with diarrhoea in dogs and cats, particularly in
puppies and kittens; however, most infections
are sub-clinical. Infection is by ingestion of
sporulated oocysts found in faeces contaminated
feed, water, and soil. Dogs and cats usually
become infected before one year of age and may
remain sub-clinically infected for long periods.
Overcrowding, poor sanitation, poor nutrition,
impaired immunity, and other stresses predispose
to clinical coccidiosis. Among the clinical signs
is intermittent diarrhoea for several days with
bloodstained faeces.
Cryptosporidiosis
This is a widespread, worldwide infection of
humans and domestic animals, caused by the
coccidian parasite, Cryptosporidium parvum.
Infection is by the oral-faecal route. Most
infections are sub-clinical with clinical disease
rare in dogs and cats. Kittens and puppies are
most susceptible. When it occurs there may be
predisposing underlying disease, e.g., FeLV
or FIV infections. The organism invades the
microvillous border resulting in mild to severe
villous atrophy. Both the intestine and colon
are affected. Clinical signs are mild to severe
diarrhoea.

Giardiasis
Giardiasis is a protozoal intestinal infection,
caused by Giardia duodenalis. This flagellated
protozoan inhabits the lumen of the small intestine
where it produces microscopic lesions on villi.
Transmission takes place when cysts are passed
in faeces and ingested. Contaminated food and
water are frequently the source of infection. Cysts
are resistant and can survive for long periods
outside the host. Infections in adult dogs and cats
are usually sub-clinical but clinical disease is also
seen. Acute and chronic diarrhoea occurs mainly
in kittens and puppies. Clinical signs include soft
to diarrheic faeces, poor hair coat, flatulence, and
loss of or failure to gain weight.
Toxoplasmosis
This is a widespread, frequently sub-clinical,
protozoal disease of many warm-blooded animals
and humans throughout the world. Toxoplasma
gondii, a coccidia-like protozoan, completes its
life cycle in epithelial cells of the intestine of the
cat. Cats are the definitive host and serve as the
main reservoir. Clinical disease may develop as a
result of stress, impaired immunity and concurrent
disease. In cats intestinal infections are usually
sub-clinical with mild diarrhoea infrequently
seen. Cysts in tissues do not usually result in
clinical signs; however, they can cause diarrhoea,
vomiting, fever, anorexia, dyspnoea, icterus,
ocular disease, and neurological dysfunction. In
dogs infections are acquired from eating uncooked
meat and ingesting faecal contaminated food and
water. Infections are usually asymptomatic. Some
of the conditions attributed to toxoplasmosis are
neurological infections with abnormal reflexes,
ataxia, paralysis; infections of the myocardium
and skeletal muscle; pneumonia; and hepatitis.
Fungal infections
Fungal infections of the GI tract include
zygomycosis, pythiosis, candidiasis, and
histoplasmosis. In general disease is uncommon
Back to contents
Ip
and often associated with immune suppression.
Fungi of the genera Mucor, Absidia, Rhizopus
and Mortierella, all of which are widespread in
nature, cause Zygomycosis.
Pythiosis is caused by Pythium insidiosum,
which can cause primary intestinal infection.
The disease is contracted by the ingestion of
zoospore-contaminated water and often seen
in dogs working in swamp-like environments.
Clinical signs include anorexia, vomition, and
progressive weight loss.
Candidiasis is caused by the yeast-like fungus
Candida albicans and characterized most
frequently by infection of the skin and mucous
membrane of the alimentary tract and occasionally
the genital tract. Young and debilitated animals
are most often affected. Prolonged antibiotic
treatment and immunodeficiency may predispose
animals to candidiasis, particularly the systemic
form. The infrequent disseminated form may
involve the lungs, heart, kidneys, and placenta.
The oral form of the disease with ulcerative
pseudomembranous inflammation of the mouth,
extending sometimes to the oesophagus and
stomach is seen infrequently in dogs and cats.
Histoplasmosis is caused by Histoplasma
capsulatum. The route of infection is mainly
respiratory, although primary intestinal infection
has been reported. The disease is characterized by
the formation of tubercle-like granulomas in the
lungs, intestine, lymph nodes, and other internal
organs depending upon the form. Sub-clinical
infections are by far the most common. The chronic
form is mainly seen in either a predominantly
pulmonary or intestinal form. Clinical signs
will depend upon the form of the disease and its
extent. They include fever, depression, loss of
weight and condition, dyspnoea, hepatomegaly,
lameness osteomyelitis), diarrhoea and evidence
of ocular involvement.
References
2006 World Congress WSAVA/FECAVA/CSAVA
Available by contacting the author by email.
473
Ip
Ip - Infectious & Parasitic Diseases
USE OF SEROLOGY FOR THE PREDICTION OF CANINE AND FELI-
NE CORE VACCINE NEEDS
Michael R. Lappin, DVM,
PhD, DACVIM
Professor
Department of Clinical Sciences
Colorado State University
Fort Collins
Colorado 80523
USA
mlappin@colostate.edu
Feline vaccine serology
Feline vaccines occasionally induce side-effects
including an association with formation of
soft tissue sarcomas. Adjuvanted rabies virus
and feline leukemia virus vaccines cause the
most inflammation and have been linked most
frequently to tumor production but soft tissue
sarcomas have also developed at the site of
subcutaneous inoculation with modified live or
killed feline herpesvirus 1 (FHV-1), calicivirus
(FCV), and panleukopenia virus (FPV) vaccines
(FVRCP). Recently, administration of FVRCP
vaccines arentally has been linked to the
production of antibodies against the cell line used
to grow some vaccine viruses. In some cats, those
antibodies cross react with renal and other tissues.
While a disease association has not been shown,
it is another factor to consider when determining
an optimal vaccination protocol for an individual
cat.
The duration of immunity for some feline vaccine
antigens is known to be > 3 years. Thus, the
American Association of Feline Practitioners/
2006 World Congress WSAVA/FECAVA/CSAVA
Academy of Feline Medicine (AAFP/AFM)
and others have questioned the need for annual
vaccination with FVRCP products after the
1 year booster immunization. It is unknown to
what extent humoral or cell-mediated immunity
is responsible for the protection elicited by FPV,
FHV, or FCV vaccination. The humoral immune
response to FCV, FHV-1, and FPV vaccines
can be readily measured by the detection of
virus-specific antibodies. Quantification of cell-
mediated immune responses is difficult and is
not typically performed on a routine diagnostic
basis. In general, presence of serum antibodies
indirectly suggests that cell-mediated immune
responses are also intact as B lymphocytes
(humoral) require T lymphocyte (cell-mediated)
help to maintain antibody production. Regardless
whether humoral immunity is responsible for
474
Back to contents
protection, if the presence of virus-specific
antibody correlated with protection from
challenge with FPV, FCV, and FHV-1, serologic
screening of individual vaccinated cats could be
used to predict vaccine needs. In one study, serum
antibodies against FHV-1, FCV, and FPV could
be detected in 100% of c ats inoculated twice
with a killed FVRCP product 3 years previously.
When these cats were challenged with virulent
virus 7.5 years after vaccination, the cats were
100% protected against FPV (Scott et al, 1999).
When challenged with virulent FHV-1 and FCV,
clinical signs of disease in the vaccinated cats
were decreased 52% and 63%, respectively, when
compared to unvaccinated controls.
Virus neutralization (FHV-1, FCV) and
hemagglutination inhibition (FPV) assays
have classically been used to assess antibody
responses to FVRCP vaccines. These assays are
labor intensive, are only available in specialized
laboratories, and are usually not standardized
between laboratories. There are now other
techniques on the world market for detection
of antibodies. For example, enzyme-linked
immunosorbent assays (ELISAs) using whole
virus or virus infected cell preparations have been
used for detection of antibodies specific for FCV
and FHV-1 and are potentially more sensitive
than virus neutralization techniques. In addition,
ELISAs are technically less complicated, can be
standardized for use in multiple laboratories, and
can be adapted for use in the veterinary clinic.
In one study, serum antibody responses to feline
panleukopenia virus (FPV), feline herpesvirus
1 (FHV-1), and feline calicivirus (FCV) were
compared to resistance to challenge with the
respective virulent viruses in experimental cats.
In total, 72 laboratory-reared cats were used and
then adopted to private homes. In 4 separate
experiments, cats were either vaccinated against
FPV, FHV-1, and FCV using an intranasal

vaccine or one of two subcutaneous vaccines
or maintained as unvaccinated controls.
Between 9 and 36 months after vaccination,
the cats were challenged with virulent viruses
using USDA protocols for vaccine approval.
ELISAs for detection of FPV, FHV-1, and FCV
antibodies were developed (HESKA Diagnostic
Laboratory, Fort Collins, CO). Serum antibody
levels as determined by ELISAs as well as
hemagglutination inhibition (HI) for FPV
and serum neutralization (SN) for FHV-1 and
FCV (New York State Veterinary Diagnostic
Laboratory) were correlated to resistance to
viral challenge.
When used with vaccinated cats, the positive
predictive value of FPV, FHV-1, and FCV
antibodies as detected by ELISAs were 100%,
90.5%, and 100%, respectively. When used
with vaccinated cats, the positive predictive
value of FPV, FHV-1, and FCV antibodies as
detected by HI or SN were 100%, 91.3%, and
100%, respectively. The ELISAs were also
applied to sera from 276 client-owned cats. The
seroprevalences for FPV, FHV-1, and FCV were
68.5%, 70.7%, and 92.4%, respectively. It was
concluded that when used with vaccinated cats,
positive antibody tests for FPV, FHV-1, FCV
correlate to resistance to challenge in most cats
regardless of vaccine type or interval. Whether
use of serum antibodies to predict resistance to
infection with FPV, FCV, and FHV-1 would be
affected by route of vaccine administration or
vaccination interval was previously unknown
since only a single long term study using one
product was reported. In the study described,
two FPV and FHV-1 vaccines and 3 FCV
vaccines were assessed. Additionally, interval
between vaccination and challenge varied from
9 months to 31 months for FHV-1 and FPV and
from 9 months to 36 months for FCV. Positive
predictive values of the serum antibody tests
were similar regardless of the vaccine or vaccine
interval.
Since the majority of client-owned cats are
seropositive for these agents with antibody
titers that predict resistance to infection, use of
arbitrary vaccination intervals is likely to lead
to unnecessary vaccination of some cats. If
validated assays are available, serological testing
for prediction of FVRCP antigen needs appears
to be appropriate for use in lieu of arbitrary
vaccination intervals.
It is possible that in the future, serological tests
could be used to predict vaccine needs for other
antigens, potentially feline leukemia virus and
rabies virus. However, at this time, information
concerning use of serological tests for other feline
vaccine antigens is largely unavailable and is not
recommended.
Back to contents
Ip
Canine vaccine serology
Like cats, vaccine associated side-effects in dogs
are rare. However, over-vaccination occasionally
causes problems and so if a vaccine antigen is
not needed, it should not be given. For dogs in
the United States, core vaccines include canine
distemper virus, parainfluenza, adenovirus 2,
parvovirus, and rabies. Puppies are generally
vaccinated every 3-4 weeks with distemper,
parvovirus, and adenovirus 2 vaccines until 14-16
weeks of age. At one year of age or one year later
the dog should return for a booster vaccination.
After one year of age, risk of infection by canine
distemper virus, parainfluenza, adenovirus 2,
and parvovirus should be assessed yearly while
performing a physical examination and checking
for enteric parasites.
In several studies, canine distemper virus titers
and canine parvovirus titers suggestive of
resistance were detected in >95% of the dogs
tested, respectively. Canine parvovirus vaccines
may provide life-long immunity and distemper
virus titers are detected for up to 10 years in
many dogs. Thus, in low risk dogs, modified
live DA2PP vaccines should be administered no
more often than every third year. In addition to
serological studies, challenge studies from several
vaccine manufacturers have shown at least 36-
57 week duration of immunity to infectious
canine adenovirus, distemper, and parvovirus on
challenge.
Positive serologic tests for canine distemper
virus, canine adenovirus 1, and canine parvovirus
are predictive of resistance. If validated assays
are available, serological testing for prediction
of these vaccine antigen needs appears to be
appropriate for use in lieu of arbitrary vaccination
intervals.
For some vaccine antigens, serology is not
predictive. For example, some dogs with
serological responses to Borrelia burgdorferi
and leptospires can still be infected with the
2006 World Congress WSAVA/FECAVA/CSAVA
organism. For other vaccine antigens, information
or validated assays are not currently available.
SUGGESTED READINGS
1. Lappin MR, et al. Prediction of resistance to
feline parvovirus, feline herpesvirus 1 and feline
calicivirus challenge utilizing serology. J Am Vet
Med Assoc 2002; 220: 38-42.
2. Lappin MR, et al. Investigation of the induction
of antibodies against Crandell-Rees feline kidney
cell lysates and feline renal cell lysates after
parenteral administration of vaccines against
feline viral rhinotracheitis, calicivirus, and
panleukopenia in cats. Am J Vet Res 2005; 66:
506-511.
475
Ip
3. Mouzin DE, et al. Duration of serologic
response to three viral antigens in cats. J Am Vet
Med Assoc 2004; 224: 61-66.
4. Mouzin DE, et al. Duration of serologic
response to five viral antigens in dogs. J Am Vet
Med Assoc 2004; 224: 55-60.
5. Paul MA, et al. 2006 AAHA Canine Vaccine
Guidelines. J Am Anim Hosp Assoc 2006; 42:
80-89.
6. Richards J, et al. Feline vaccine selection and
administration. Compend Cont Ed Pract Vet
2001; 23: 71-80.
7. Schultz RD. Duration of immunity for canine
and feline vaccines: A review. Vet Microbiol 2006
April 18, Epub ahead of print.
8. Scott FW, Geissinger C. Duration of immunity
in cats vaccinated with an inactivated feline
Ip - Infectious & Parasitic Diseases
UPDATE ON THE FLEA-ASSOCIATED AGENTS OF CATS; BARTONELLA
SPP., HEMOPLASMA SPP., AND RICKETTSIA FELIS
Michael R. Lappin, DVM,
PhD, DACVIM
Professor
Department of Clinical Sciences
Colorado State University
Fort Collins
Colorado 80523
USA
mlappin@colostate.edu
2006 World Congress WSAVA/FECAVA/CSAVA
Bartonella spp.
Bartonella henselae is a gram negative organism
that replicates within erythrocytes and endothelial
cells. The organism is the most common cause
of cat scratch disease as well as bacillary
angiomatosis, and bacillary peliosis, common
disorders in humans with AIDS. Humans with
cat scratch disease develop a variety of clinical
signs such as lymphadenopathy, fever, malaise,
weight loss, myalgia, headache, conjunctivitis,
skin eruptions, and arthralgia. Most cases of
cat scratch disease are self-limiting but may
take several months to completely resolve. Cats
can also be infected with B. clarridgeiae, an
organism that has also been associated with cat
476
Back to contents
panleukopenia, herpesvirus, and calicivirus
vaccine. Fel Pract 1997; 25: 12-19.
9. Scott FW, Geissinger CM. Long term immunity
in cats vaccinated with an inactivated trivalent
vaccine. Am J Vet Res 1999; 60: 652-658.
10. Scott-Moncrieff JC, et al. Evaluation of
antithyroglobulin antibodies after routine
vaccination in pet and research dogs. J Am Vet
Med Assoc 2002; 221: 515-521.
11. Tizard I, Ni Y. Use of serologic testing to
assess immune status of companion animals. J
Am Vet Med Assoc 1998; 213: 54-60.
12. Twark L, Dodds WJ. Clinical use of serum
parvovirus and distemper virus antibody titers for
determining revaccination strategies in healthy
dogs. J Am Vet Med Assoc 2000; 217: 1021-
1024.
scratch disease. It is currently unknown whether
other Bartonella spp. that infect cats are common
or associated with human or feline disease.
Bartonella henselae is transmitted between cats
by fleas. Based on seroprevalence studies in cats,
exposure to Bartonella spp. varies by region
around the world but exposure is very common.
The prevalence rates for B. henselae in blood
of cats and fleas collected off their bodies were
34.8% and 22.8%, respectively. The prevalence
rates for B. clarridgeiae in cats and their fleas
were 20.7% and 19.6%, respectively. Bartonella
henselae survives in flea feces for days after
passed by infected C. felis. Thus, cat claws and
teeth may be contaminated with the organism by

ingesting fleas or flea feces during grooming and
then transmit the organisms to people by bites.
Most seropositive, blood culture positive, or PCR
positive cats are clinically normal. However,
Bartonella spp. infection of cats has also been
associated directly or indirectly with a variety
of clinical manifestations like fever, lethargy,
lymphadenopathy, uveitis, gingivitis, and
neurological diseases. How often cats become
ill from Bartonella spp. infections is unknown
and more information is needed. However, it
can be difficult to determine which cats have
been exposed and which cats are diseased. For
example, in recent studies of stomatitis, seizures,
and uveitis in cats, the prevalence rates for
Bartonella spp. antibodies in feline sera were not
significantly different for cats with and without
disease. It is also still also still unclear as to
why some cats develop Bartonella associated
illness and others do not. Immune suppression or
pathogenic strains are possible explanations.
Blood culture, PCR assay on blood, and
serologic testing can be used to assess individual
cats for Bartonella infection. However, there
is no positive result that correlates to clinical
illness. Cats that are culture-negative or PCR-
negative and antibody-negative and cats that are
culture-negative or PCR-negative and antibody-
positive are probably not a source of flea, cat, or
human infection. However, bacteremia can be
intermittent and false-negative culture or PCR
results can occur, limiting the predictive value
of a single battery of tests. With PCR, false
positive results can occur and positive results
do not necessarily indicate that the organism
is alive. While serologic testing can be used to
determine whether an individual cat has been
exposed, both seropositive and seronegative
cats can be bacteremic, limiting the diagnostic
utility of serologic testing. Thus, testing healthy
cats for Bartonella spp. infection is not currently
recommended in most situations. Testing should
be reserved for cats with suspected clinical
bartonellosis. If the results of Bartonella tests
are negative in a clinically ill cat, the organism
is not likely the cause of the clinical syndrome
unless the infection was peracute and serological
testing was used as the diagnostic test. If the
results of Bartonella tests are positive, the agent
remains on the differential list, but other causes
of the clinical syndrome must also be excluded.
If no other cause of the clinical syndrome can
be determined, a therapeutic trial with a drug
with presumed anti-Bartonella activity could
be started. Administration of doxycycline,
amoxicillin-clavulanate, erythromycin, or
fluoroquinolones can limit bacteremia but does
not cure infection in all cats and has not been
Back to contents
Ip
shown to lessen the risk of cat scratch disease.
Thus, treatment is generally recommended for
clinically ill cats. Doxycycline at 10 mg/kg, PO,
daily, formulated into a flavored suspension (to
avoid esophageal strictures) for 7 days is the first
drug of choice. If a positive response is achieved,
continue treatment for 2 weeks past clinical
resolution of disease or for a minimum of 28
days. If a poor response is noted and bartonellosis
is a differential diagnosis, azithromycin or a
fluoroquinolones are considered appropriate
choices. Difficulty in treatment may relate to the
intracellular location of the organism. Cats with
uveitis thought to be from bartonellosis should be
topically with glucocorticoids to attempt to lessen
inflammation and subsequent glaucoma.
To lessen the likelihood of acquiring a Bartonella
spp. infection from a cat, the following were
adapted from what is recommended to HIV-
infected people and other cat owners by the
Centers for Disease Control and the American
Association of Feline Practitioners:
1. Flea control should be maintained;
2. If a family member is immunosuppressed
and a new cat is to be acquired, adopt a healthy
cat > 1 year;
3. Declawing is generally not advised, but
immunosuppressed people should avoid bites and
scratches;
4. Cat-associated wounds should be washed
promptly and medical advice sought; and
5. Cats should not be allowed to lick open wounds
on immunosuppressed people.
Hemoplasma spp.
There are three epi-erythrocytic hemoplasmas
of cats that are currently recognized;
Mycoplasma haemofelis (Mhf), ‘Candidatus M.
haemominutum’ (Mhm), and ‘Candidatus M.
turicensis’. These organisms were previously
called Haemobartonella felis. The organisms 2006 World Congress WSAVA/FECAVA/CSAVA
are likely worldwide. Mycoplasma haemofelis
appears to be the most pathogenic species. In
prevalence studies performed with assays capable
of amplifying both Mhf and Mhm, both organisms
have been detected and Mhm infection is most
common. In a recent study, we collected fleas
from cats and attempted to amplify hemoplasma
DNA from flea digests as well as the blood of
the cat. The prevalence rates for Mhf in cats and
their fleas were 7.6% and 2.2%, respectively.
The prevalence rates for Mhm in cats and their
fleas were 20.7% and 23.9%, respectively. In
addition, fleas ingest Mhm and Mhf from infected
cats when feeding. Hemoplasmas have been
transmitted experimentally by IV, IP, and oral
inoculation of blood. Transmission by biting has
been hypothesized. Red blood cell destruction is
477
Ip
due primarily to immune-mediated events; direct
injury to red blood cells induced by the organism
is thought to be minimal.
Clinical signs of disease depend on the degree of
anemia, the stage of infection, and the immune
status of infected cats. Pale mucous membranes,
depression, inappetence, weakness, and
occasionally, icterus and splenomegaly are most
common. Fever occurs in some acutely infected
cats and may be intermittent in chronically
infected cats. Evidence of coexisting disease may
be present. Weight loss is common in chronically
infected cats. Cats in the chronic phase can be
subclinically infected only to have recurrence of
clinical disease following periods of stress. Fever
has been associated with chronic infections.
Diagnosis is based on demonstration of the
organism on the surface of erythrocytes on
examination of a thin blood film or amplification
of microbial DNA by PCR assay. Organism
numbers fluctuate and so blood film examination
can be falsely negative up to 50% of the time. The
organism may be difficult to find cytologically,
particularly in the chronic phase. Real time PCR
to quantify hemoplasma DNA has now been
titrated and can be used to monitor response to
treatment.
Doxycycline has less side effects than other
tetracyclines in cats and so is preferred.
Doxycycline is administered as a flavored
suspension (to avoid esophageal strictures)
at 10 mg/kg, PO, every 24 hours for 7 days.
If there is a positive response and the cat is
tolerating the drug, treatment is continued for a
total of 28 days if possible. If autoagglutination
is evident, prednisolone at 1 mg/kg, PO, every
12 hours is given for the first 7 days or until
autoagglutination is no longer evident. In
cats intolerant of doxycycline, enrofloxacin
(5 mg/kg, PO, daily), marbofloxacin (1.25 mg/lb,
PO, daily), or imidocarb (5 mg/kg, SQ or IM, every
2006 World Congress WSAVA/FECAVA/CSAVA
14 days) may be effective. Azithromycin was not
effective for the treatment of hemoplasmosis in
one study. Blood transfusion should be given if
clinically indicated. Treatment does not always
eliminate infection and re-infection can occur. To
attempt to prevent feline hemoplasma infections,
478
Back to contents
flea control should be maintained. Cats should
be housed indoors to avoid vectors and fighting.
Clinic blood donor cats should be screened for
both Mycoplasma spp. by PCR prior to use. There
are currently no known human health risks.
Rickettsia felis
Rickettsia felis is a spotted fever group organism
occasionally associated with fever, headache,
myalgia, and macular rash in people. It has been
detected in Ctenocephalides felis, C. canis, and
Pulex irritans; these fleas have a worldwide
distribution. Rickettsia felis has been determined
in C. felis collected from cats in several countries
around the world. In a study recently completed
in my laboratory, 67.4% of fleas collected from
92 cats were PCR positive for R. felis DNA.
Rickettsia spp. antibodies are commonly detected
in cats in the United States; it is likely the cats are
exposed to R. felis because C. felis is common.
However, we failed to detect R. felis DNA in cats
with fever in the United States. Thus, further data
is needed to determine whether the organism
induces illness in cats.
Summary
Because Bartonella spp., Hemoplasma spp.,
and R. felis infections of fleas are so common
and because significant illness can occur in cats
(Bartonella spp. and hemoplasmas) and people
(Bartonella and R. felis), flea control is now
recommended for all cats in the United States.
ADDITIONAL REFERENCES AVAILABLE
UPON REQUEST
1. Boulouis HJ, et al. Factors associated with
the rapid emergence of zoonotic Bartonella
infections. Vet Res 2005; 36: 383-410.
2. Comer JA, et al. Urban zoonoses caused by
Bartonella, Coxiella, Ehrlichia, and Rickettsia
species. Vector Borne Zoo Dis 2001; 1: 91-118.
3. Tasker S, Lappin MR. Haemobartonella felis:
recent developments in diagnosis and treatment.
J Fel Med Surg 2002; 4: 3-11.
Webpages: aafponline.org; capcvet.org; cdc.gov

Ip - Infectious & Parasitic Diseases
CANINE EHRLICHIOSIS – A SILENT KILLER
Dr. Gad Baneth, DVM, PhD,
Dipl. ECVCP
Professor of Veterinary Medicine
School of Veterinary Medicine
Hebrew University
P.O. Box 12
Rehovot 76100
Izrael
baneth@agri.huji.ac.il
Introduction
Ehrlichial organisms are obligatory intracellular
bacteria of the order Rickettsiales. Recently,
the nomeclature of organisms in this order was
revised. Ehrlichioses are caused by organisms
of the genera Ehrlichia, Anaplasma and
Neorickettsia. Ehrlichia canis and E. chaffeensis
infect monocytes, Anaplasma phagocytophilum
and E. ewingii infect granulocytes, and A.
platys infects platelets. The significance of
the ehrlichioses has been highlighted since
the discovery and emergence of the human
ehrlichioses caused by E. chaffeensis, E. ewingii,
and A. phagocytophilum. Most ehrlichioses are
tick borne diseases.
Etiology of canine monocytic ehrlichiosis
Ehrlichia canis, the etiologic agent of canine
monocytic ehrlichiosis, has been recognized
worldwide as an important canine infectious
agent. Ehrlihcia canis infection has been
reported from Africa, Asia, America, and
Europe. Autochtonous (non-imported)
cases of Ehrlichia canis in Europe have
been reported mostly from Spain, Portugal,
Southern France, Corsica, Italy including
Sardinia, and Greece.
Ehrlichia canis morulae found in monocytes and
macrophages are a “microcolony” of bacteria
surrounded by a membranous vacuole. Morulae
may contain 100 or more ehrlichiae resembling
elementary bodies of chlamydiae. E. canis is
transmitted by the three-host tick Rhipicephalus
sanguineus. The pathogenesis of the disease
involves an incubation period of 8-20 days,
followed by 3 consecutive phases: an acute phase
which lasts 1-4 weeks, a subclinical phase which
may last from months to years, and a chronic phase.
Not all infected dogs develop the chronic severe
form of the disease and the conditions that lead to
the development of this stage are unknown.
Back to contents
Ip
Clinical findings
The clinical presentation of the disease caused
by E. canis may vary, and the clinical signs
most frequently reported are depression,
lethargy, anorexia, fever, lymphadenomegaly,
splenomegaly and hemorrhages (mainly
petechiae, ecchymoses and epistaxis). Ocular
manifestations of canine ehrlichisosis include
anterior uveitis, keratoconjuctivitis, hyphema,
glaucoma, chorioretinitis and retinal detachment.
Polyarthritis and polymyositis have been
described in E. canis infection. The neurological
abnormalities found in canine ehrlichiosis are
associated with vasculitis, meningoencephalitis,
lymphocytic infiltration of the central and
peripheral nervous system or hemorrhages.
Renal pathology has been associated with
canine ehrlichiosis due to immune-complex
glomerulonephritis.
Ehrlichia canis infection has been termed by
some clinicians as the “silent killer”. It is often
inapparent during the early and sub-clinical
stages of infection. When the disease is diagnosed
in the chronic stage, it may be too late to save the 2006 World Congress WSAVA/FECAVA/CSAVA
canine patient as treatment may not be helpful in
reversing the severe pancytopenia and immune
mediated phenomena associated with this
disease.
Laboratory findings
Laboratory abnormalities in canine monocytic
enrlichiosis include hematologic and serum
biochemistry changes. Thrombocytopenia is
the most frequent hematological abnormality
occurring in more than 90% of cases. Anemia,
usually non-regenerative normocytic and
normochromic, is another common finding in this
disease. In addition, mild to severe leucopenia
is a frequent abnormality. Hyperglobulinemia,
hypoalbuminemia and mild elevation of alkaline
phosphatase (ALP) and alanine aminotransferase
479
Ip
(ALT) activities are frequently reported in
ehrlichiosis. Dogs in the chronic severe stage
of the disease may develop severe pancytopenia
as their bone marrow becomes hypocellular. The
prognosis of these chronically ill dogs is grave.
Immune-mediated responses play a major
role in the pathogenesis of E. canis infection.
Anti-platelets antibodies (APA) have been
demonstrated less than a week after experimental
E. canis infection of dogs. Platelet aggregation
abnormalities, anti-nuclear antibodies (ANA),
RBC autoagglutination with positive coombs’
test, and circulating immune-complexes have
been shown in infected dogs and are associated
with the disease process.
The decrease in platelets during canine ehrlichiosis
is probably a result of several mechanisms. These
mechanisms include increased consumption with
vascular endothelial changes, platelet sequestration
and pooling in the spleen, thrombophagocytosis
with immunological destruction, a decrease in the
half life time of circulating platelets possibly due
to opsinization with antibodies, and production
impairment due to bone marrow destruction and
hypocellularity. In addition to the decrease in
circulating platelet number, platelets dysfunction
(thrombocytopathy) has also been implicating as
an additional factor contributing to lack of platelet
functionality in canine monocytic ehrlichiosis.
Co-infections with hemoparasites or other
infectious agents are often detected in conjunction
with canine ehrlichiosis. Hepatozoon canis and
Babesia canis vogeli are transmitted by the same
vector tick, R. sanguineus. In addition, Leishmania
infantum is another common co-infecting
protozoal pathogen whose vector, phlebotomine
sand flies are often found in the same sub-tropical
climate conditions and ecological niches, as R.
sanguineus ticks transmitting E. canis infection.
Diagnosis
2006 World Congress WSAVA/FECAVA/CSAVA
The laboratory diagnosis of E. canis infection
includes evaluation of the hemogram and serum
biochemistry panel. The detection of morulae in
monocytes in stained blood smears is rare and
can not serve as a main diagnostic option.
Anti-E. canis antibodies can be detected in dogs
infected with this pathogen and persist long after
recovery from the disease. Serum antibodies are
thought not to be protective or play an important
role in eliminating this intracellular infection.
Serology is indicative of exposure to E. canis and
may often be helpful in ruling out progressive
infection. Antibodies may not be detectable
during the early stage of infection. However,
seropositive dogs with previous exposure to the
pathogen may also present due to other urgent
disease conditions. Several commercial “in
480
Back to contents
house” test kits are available for E. canis infection
in addition to the laboratory indirect fluorescent
antibody test (IFAT) which is often considered
the golden standard for serology. Some serologic
cross-reactivity between different Ehrlichia
species may occur. Anti-E. canis antibodies have
been reported to cross-react with E. chaffeensis,
A. phagocytophilum & E. ewingii but not with
A. platys.
Detection of the presence of E. canis DNA by
the polymerase chain reaction (PCR) is highly
sensitive and specific and has become a popular
assay in research of this disease as well as in its
clinical diagnosis.
Treatment and prevention
Ehrlichial organisms are susceptible to
tetracyclines, and doxycycline is most widely
used for treatment of infection. Doxycycline is
very efficient in clearing rickettsemia in acute
cases of E. canis infection. Clinical recovery is
noticed within 48-72 hours, yet treatment should
be commenced for 3 weeks, as some dogs may
remain carriers when shorter treatments are
applied.
Treatment with the injectable drug imidocarb
dipropionate has been shown to be ineffective in
eliminating E. canis in some cases. However, it is
often used in combination with doxycyline when
Babesia co-infection is suspected.
The control of tick infestation by topical treatment
with acaricidals and environemental eradication
of ticks is recommended for the prevention of E.
canis infection.
References
Baneth, G., Waner, T., Koplah, A., Weinstein,
S., Keysary, A. 1996. Survey of Ehrlichia canis
antibodies among dogs in Israel. Vet. Rec. 138:
257-259.
Frank, J.R., Breitschwerdt, E.B. 1999. A
retrospective study of ehrlichiosis in 62 dogs
from North Carolina and Virginia. J. Vet. Intern.
Med. 13: 194-201.
Dumler, J.S., Barbet, A.F., Bekker, C.P.J., Dasch,
G.A., Palmer, G.H., Ray, S.C., Rikihisa, Y.,
Rurangwira, F.R. 2001. Reorganization of genera
in the families Rickettsiacea and Anaplasmatacea
in the order Rickettsiales: unification of some
species of Ehrlichia with Anaplasma, Cowdria
with Ehrlichia and Ehrlichia with Neorickettsia,
description of six new species combinations and
designation of Ehrlichia equi and “HGE agent” as
subjective synonyms of Ehrlichia phagocytophilum.
Int. J. Syst. Evol. Microbiol. 51: 2145-2165.
Harrus, S., Kass, P.H., Klement, E., Waner. T. 1997.
Canine monocytic ehrlichiosis: a retropsective

study of 100 cases, and an epidemiological
investigation of prognostic indicators for the
disease. Vet. Rec. 141: 360-363.
Harrus. S., Kenny, M., Miara, L., Aizenberg,
I., Waner, T., Shaw, S. 2004. Comparison of
simultaneous splenic sample PCR with blood
sample PCR for diagnosis and treatment
of experimental Ehrlichia canis infection.
Antimicrob. Agents Chemother. 42: 362-68.
Ip - Infectious & Parasitic Diseases
TWO CAUSES OF CANINE AND FELINE DIROFILARIASIS
Dr. Gad Baneth, DVM, PhD,
Dipl. ECVCP
Professor of Veterinary Medicine
School of Veterinary Medicine
Hebrew University
P.O. Box 12
Rehovot 76100
Izrael
baneth@agri.huji.ac.il
Filariasis in dogs and cats can be caused by a
number of species that vary from one geographic
region to another. At least 8 different filarial
spp. have been described to cause persistent
microfilaremia in dogs. Some of the filarial
species can be highly pathogenic and cause a
life-threatening disease, whereas other species
are associated with asymptomatic infection.
Dirofilaria immitis and Dirofilaria repens are two
filarial species infecting dogs and cats that are
often found in the same area but cause different
clinical syndromes.
Dirofilaria repens infection
Filariasis caused by Dirofilaria repens is prevalent
in several regions in the world including: the
Mediterranean basin, southeastern Europe,
Africa and southeast Asia. Due to the recent
elevation in the number of human infections in
Spain and Italy, it is considered an emerging
zoonosis in these countries. Dogs, foxes and cats
are the reservoir for this infection and people
are accidental “dead end” hosts in which the life
cycle is not completed.
The mosquito vectors of D. repens vary in
different geographic regions and include species
belonging to the genera Culex, Anopheles and
Aedes. Microfilariae taken up in the blood meal by
Back to contents
Ip
Mylonakis, M.E., Koutinas A.F., Breitschwerdt,
E.B., Hegarty, B.C., Billinis, C.D., Leontides,
L.S., Kontos, V.S. 2004. Chronic Canine
Ehrlichiosis (Ehrlichia canis): A Retrospective
Study of 19 Natural Cases. J. Am. Anim. Hosp.
Assoc. 40: 174-184.
Ae. aegpyti mosquitoes migrate to the malphigian
tubules where they develop to stage 3 (L3) larvae
that reach the proboscis. Larvae injected during
the mosquito bite into the skin of the dog migrate
through the subcutaneous tissues, develop to L4, L5
and adult worms and shed microfilariae in the blood.
Canine infection is often an incidental hematological
finding, or accompanied by mild clinical signs
including skin swelling, hyperpigmentation or
subcutaneous granulomas containing adult worms.
In humans, immature D. repens migrate in 2006 World Congress WSAVA/FECAVA/CSAVA
connective tissues and elicit an inflammatory
response resulting in the formation of nodules
around the worms that are frequently confused
with tumors and treated by surgical excision. The
manifestations of D. repens infection in people are
associated with nodules that have been described
from the lung, subcutaneous tissues, epididymis,
spermatic cord, omentum, conjuctiva, and the
breast. Infections have been recorded to persist
for 8 years and can be detected in tourists that
have visited endemic areas.
Heartworm disease
In contrast to the relatively non-pathogenic D.
repens, D. immtis is a major pathogen in many
parts of the world. Dirofilaria immitis causes
heartworm disease in domestic and wild canine
481
Ip
and feline spp. in warm and temperate regions.
It is present in southern Europe, North and South
America, Africa, Asia and Australia. The life
cycle of D. immitis is basically similar to that of
D. repens. The main difference is that the larvae
injected into the skin migrate through the muscles
to the lung blood vessels reaching the pulmonary
arteries where they continue to mature. Adult
worms are found primarily in the pulmonary
arteries and in severe infections also in the right
side of the heart and occasionally in the vena
cava. The pre-patent period, e.g. the time from
infection to the appearance of microfilaremia, is
approximately 6-7 months and the life expectancy
of the worm in the dog is approximately 5 years.
Chronic heartworm disease results from
progressive proliferative endarteritis and
thromboembolism of the pulmonary artery caused
mostly by adult worms, and not by juvenile
migrating worms. The progressive vascular
changes lead to pulmonary hypertension, right
ventricular hypertrophy or dilation and cor
pulmonale. The first clinical signs of disease
typically include exercise intolerance and cough.
This is followed by signs of chronic right heart
failure including ascites, hepatomegaly, syncope
and respiratory signs such as dyspnea, tachypnea,
cough and hemoptysis. More acute heartworm
disease with a heavy worm burden causes vena
caval syndrome with erythrocyte membrane
disruption and a hemolytic crisis. Humans can
become infected with D. immitis but the worm
does not complete its life cycle in people.
Wolbachia and dirofilariasis
Wolbachia are Gram-negative bacterial
endosymbionts of arthropods and filarial worms.
Wolbachia have been demonstrated to be
transovarially transmitted in the human filarial
pathogens Onchocerca volvulus and Brugia
malayi. Hosts with filarial infection come into
2006 World Congress WSAVA/FECAVA/CSAVA
contact with Wolbachia following the death of
the filarial parasite. Dogs infected with D. immitis
have been shown to mount a specific immune
response to Wolbachia antigens.
Diagnosis of dirofilariasis
The diagnosis of dirofilariasis can be achieved
by detection of microfilaremia with microscopic
examination of blood smears when microfilaremia
is high. The Knott’s concentration method allows
detection of lower numbers of microfilaria.
Failure to detect circulating microfilariae does not
rule out infection. There are several D. immitis
ELISA tests employing monoclonal antibodies
for the detection of circulating D. immitis antigen
useful also for the detection of occult infection.
Serology for infection of cats is usually aimed at
the detection of anti-D. immitis antibodies.
482
Back to contents
The filarial species that have been reported to
cause persistent microfilaremia in dogs include D.
immitis, D. repens, Acantocheilonema reconditum
(formerly Dipetalonema), Acantocheilonema
dracunculoides, Brugia malayi, Brugia
ceylonensis, Brugia phangi and Cercopithifilaria
grassi. The geographic distribution of some
fliarial spp. is limited and therefore some spp.
can be expected to be found only in certain
parts of the world. PCR diagnosis of filariasis in
canine blood is available in several laboratories.
A recent publication has described an assay that
can discriminate between 6 species of canine
microfilariae by a single PCR.
Treatment and prevention
Treatment of infected dogs usually includes
the adulticide drug melarsomine hydrochloride
injected intramuscularly on two consecutive
days followed by microfilaricidal treatment with
ivermectin or a related drug.
There are several prophylactic drug formulations
for the prevention of infection. These include
preparations of ivermectin, moxidectin,
milbemcycin, spot on selamectin and more.
References
Anyanwu, I.N., Agbede, R.I.S., Ajanusi,
O.J., Umoh, J.U., Ibrahim, N.D.G. 2000. The
incrimination of Aedes (stegomyia) aegypti as the
vector of Dirofilaria repens in Nigeria. Veterinary
Parasitololgy 92: 319-327.
Baneth, G.,Volanski, Z., Anug, Y, Favia, G., Bain,
O., Goldstein, G, Harrus, S. 2002. Dirofilaria
repens infection in a dog: diagnosis and treatment
with melarsomine and doramectin. Veterinary
Parasitology 105: 173-178.
Bredal, W.P., Gjerde, B., Eberhard, M.L.,
Aleksandersen, M., Wilhelmsen, D.K. and
Mansfield, L.S. 1998. J. Sm. Anim. Prac. 39:
595-597.
Cancrini G, Allende E, Favia G, Baornay F,
Anton F, Simon F. 2000. Canine dirofilariosis in
two cities of southeastern Spain. Vet Parasitol 92:
81-86.
Kamalu, B.P., 1986. Canine filariasis in
southeastern Nigeria. Bull. Anim. Hlt. Prod. Afr.
34: 203-205.
Kamalu, B.P., 1991.Canine filariasis caused by
Dirofilaria repens in southeastern Nigeria. Vet.
Parasitol. 40: 335-338.
Ferasin L. 2004.Disease risks for the traveling
pet: Heartworm disease. In Practice July/August
2004 350-355.
Gardiner CH, Oberdorfer CE, Reyes JE, Pinkus

WH, 1978. Infection of man by Dirofilaria repens.
Am J Trop Med Hyg 27: 1279-1281
Kramer, L., Simon, F., Tamarozzi, F., Genchi, M.,
Bazzocchi, C. 2005. Is Wolbachia complicating
the pathological effects of Dirofilaria immitis
infections? Vet. Parasitol. 133: 133-136.
Orihel, T.C., Helentjaris, D., Alger, J. 1997.
Subcutaneous dirofilariasis: single inoculum,
multiple worms. Am J Trop Med Hyg 56: 452-
455
Pampiglione, S., Rivasi, F. and Canestri Trotti,
G. 1984. Human pulmonary dirofilariasis in Italy.
Lancet Feb. 11: 333.
Pampiglione, S. and Fedeli, F. 1991. Dirofilariasi
polmonare umana: aspetti parassitologici del
secondo caso segnalato in Italia. Parassitologia.
33: 153-157.
Pampiglione, S., Rivasi, F., Boldorini, R.,
Incenasti, R.M., Pastomerlo, M., Pavesi, M.,
Back to contents
Ip
Ramponi, A. 2001. Dirofilariasis due to Dirofilaria
repens in Italy, an emergant zoonosis: report of
60 new cases. Histopathology. 38: 344-354.
Rishniw, M., Barr, S.C., Simpson, K.W.,
Frongillo, M.F., Franz, M., Dominguez Alpizar
J.L. 2006. Discrimination between six species of
canine microfilariae by a single polymerase chain
reaction. Vet. Parasitol. 135: 303-14.
Tarello, W. 1999. La dirofilariose sous-cutanee
a Dirofilaria (Nochtiella) repens chez la chien.
Revue bibliographique et cas clinique. Revue.
Med. Vet. 150: 691-702.
Vakalis, N.C. and Himonas, C.A., 1997. Human
and canine dirofilariasis in Greece. Parassitologia.
39: 389-391.
Wieslaw, J.K. 2005. What is new in the
Wolbachia/Dirofilaria interaction. Vet. Parasitol.
133:127-32.
2006 World Congress WSAVA/FECAVA/CSAVA
483
Ip
Ip - Infectious & Parasitic Diseases
UPDATE ON THE COMPLICATIONS AND MANAGEMENT OF
CANINE BABESIOSIS
Remo Lobetti BVSc, MMedVet
(Med), PhD, Dipl. ECVIM
(Internal Medicine)
Bryanston Veterinary Hospital
PO Box 67092
Bryanston
2021
South Africa
rlobetti@mweb.co.za
Babesia canis and B. gibsoni are responsible for
canine babesiosis throughout the world. Babesia
canis consists of a group of three biologically
different subspecies, namely B. c. canis, B.
c. vogeli, and B. c. rossi. Babesia gibsoni is
subdivided into 2 subspecies: the North American
and Asian subspecies. Babesia c. canis is found
in Europe, B. c. vogeli in northern Africa, North
America and South Africa and B. c. rossi in
southern Africa. The pear-shaped trophozoite of
B. canis measures 4-5 μm long and is usually
found in pairs within the erythrocyte, but up to
eight or more may be present. In comparison,
B. gibsoni is much smaller; is round to oval
in shape; measures 3 μm long; and is found in
Asia, Australia, North America and northern and
eastern Africa.
The more commonly encountered complications
of canine babesiosis are acute renal failure,
cerebral babesiosis, coagulopathy, icterus and
hepatopathy, immune-mediated haemolytic
anaemia (IMHA), peracute babesiosis,
2006 World Congress WSAVA/FECAVA/CSAVA
ARDS, haemoconcentration, hypotension,
myocardial pathology, pancreatitis, and shock.
Rare complications include gastrointestinal
disturbances, myalagia, ocular involvement, upper
respiratory signs, necrosis of the extremities, fluid
accumulation, and chronic disease. Different
complications can overlap. The more recently
reported complications: hypotension, myocardial
changes, pancreatitis, hypoglycaemia, acid-base
changes, and multiple organ dysfunction, will be
discussed in this paper.
Hypotension
Dogs with severe and complicated babesiosis
are frequently presented in a state of collapse
and clinical shock. Shock in these animals
can resemble the hyperdynamic phase of
septic shock. Collapsed dogs with babesiosis
484
Back to contents
may, however, not display the classic signs
of shock syndrome, partially because of the
haemodynamics of haemolytic anaemia. The
pulse may be bounding or weak; temperature
elevated or subnormal; and mucous membranes
pale, icteric or congested (haemoconcentration).
Babesial shock, like endotoxic shock, may
pass through a hyperdynamic stage followed
by a hypotensive stage. Hypotension occurs
frequently in babesiosis and that the presence and
severity of hypotension increases with increased
disease severity. The presence of hypotension
in a large proportion of dogs with complicated
babesiosis is consistent with the hypothesis that
inflammatory mechanisms play a major role
in this disease, and can result in a sepsis-like
state. It is likely that hypotension in babesiosis
is a combination of vasodilation, reduced
vascular volume due to increased vascular
permeability and/or dehydration, and myocardial
depression. Hypotension can play a role in the
pathophysiology of the disease as it has been
hypothesized to facilitate parasite sequestration.
Acute pancreatitis
Gastrointestinal disturbances have generally
been considered a rare complication of
babesiosis; however, the aetiology of the reported
gastrointestinal disturbances may have been acute
pancreatitis. Digestive system abnormalities
reported as a complication of canine babesiosis
have included vomiting, diarrhoea, abdominal
pain, gastritis, enteritis, and enterorrhagia. A
recent study documented 23 dogs that developed
pancreatitis as a complication of babesiosis, which
was an incidence of 1.8% amongst hospitalised
babesiosis cases. Median time of diagnosis based
on serum amylase and lipase activities was 3
days post-admission. No sex predilection was
identified, with primarily young, sexually intact

dogs being affected. The severity of anaemia
did not correlate with the severity or incidence
of pancreatitis. The most common clinical signs
of acute pancreatitis were anorexia, vomiting,
melaena, and abdominal pain. Hypokalaemia was
commonly identified, especially in icteric dogs.
Early identification of these clinical signs in a dog
with babesiosis should increase the clinician’s
index of suspicion for acute pancreatitis, with
timeous diagnostic procedures and therapeutic
intervention instituted.
Cardiac changes
Cardiac dysfunction in canine babesiosis has
traditionally been regarded as a rare complication,
with the majority of lesions reported as incidental
findings at post-mortem examination. Recent
studies have, however, demonstrated cardiac
lesions in canine babesiosis. Cardiac troponins,
especially troponin I, are sensitive markers of
myocardial injury in canine babesiosis, and
the magnitude of elevation of plasma troponin
I concentrations appears to be proportional to
the severity of the disease. ECG changes in
babesiosis are similar to the pattern described
for myocarditis and myocardial ischaemia, and
together with histopathological findings indicate
that the heart suffers from the same pathological
processes described in other organs in canine
babesiosis, namely inflammation and hypoxia.
The clinical application of the ECG appears to be
limited and thus cardiovascular assessment should
be based on functional monitoring rather than an
ECG tracing. On cardiac histopathology from
dogs that succumbed to babesiosis, haemorrhage,
necrosis, inflammation and fibrin microthrombi
in the myocardium were documented, all of
which would have resulted in ECG changes
and elevations in cardiac troponin. Myocardial
damage causes left ventricular failure, which will
result in hypotension and an expansion of the
plasma volume due to homeostatic mechanisms.
Hypoglycaemia
Hypoglycaemia is a common complication
of virulent canine babesiosis. In a study were
plasma glucose concentration was measured
at presentation in 250 dogs with babesiosis,
the prevalence of hypoglycaemia (< 3.3 mmol/
l) was 9%. Twenty-two hypoglycaemic dogs
required admission, making the prevalence of
hypoglycaemia in admitted dogs 19.8%. Sixteen
dogs had severe hypoglycaemia (<2.2 mmol/l),
of which 5 had glucose < 1 mmol/l. Risk factors
for hypoglycaemia were collapsed state, severe
anaemia, icterus, under 6 months of age, and
vomiting. Toy breeds and pregnant bitches were
not at higher risk for hypoglycaemia than other
Back to contents
Ip
dogs. Blood glucose concentration should ideally
be measured in all dogs with babesiosis but is
mandatory in collapsed dogs; puppies; and dogs
with severe anaemia, vomiting, or icterus. In the
past many dogs have probably been misdiagnosed
with cerebral babesiosis, and thus hypoglycaemia
should be suspected in any dog with coma or
other neurological signs.
Multiple organ involvement
In a study in dogs with babesiosis 52%
demonstrated organ damage in one organ and
48% had multiple organ damage. In the cases
with single organ involvement, the liver was
most commonly involved (34%), followed
by kidneys (24%), lungs (17%), CNS (17%),
and muscle (7%). In double organ damage the
organs involved were liver (61%), lungs (46%),
muscle (46%), kidneys (38%), and CNS (8%).
The organ combinations were liver/lungs (31%),
liver/kidneys (23%), liver/muscle (15%), muscle/
kidney (15%), muscle/ lungs (8%) and muscle/
CNS (8%). In cases of triple organ damage,
the liver was involved in 92%, muscle in 83%,
kidneys in 58%, lungs in 50% and CNS in 17%.
The organ combinations were liver/muscle/
kidney in 33%, liver/muscle/lungs in 25%, liver/
kidneys/lungs in 17%, liver/muscle/CNS in 17%,
and muscle/kidneys/lungs in 8%. Outcome was
not affected by whether one or multiple organs
showed evidence of damage. However, the
specific organ involved significantly affected
outcome: CNS involvement and renal dysfunction
had a 57-fold and 5-fold increased risk of death,
respectively. Liver or muscle damage did not
affect the outcome.
Acid-Base Disturbances
The most commonly reported acid-base disturbance
in dogs with babesiosis and severe anaemia is
metabolic acidosis. However, more recent studies
suggest that a mixed acid-base disturbance is
2006 World Congress WSAVA/FECAVA/CSAVA
present in many cases, which would reflect a
more complex pathophysiology than previously
assumed. Dogs with severe canine babesiosis
showed a combination of abnormalities, including
hyperchloraemic (low SID) metabolic acidosis;
high anion gap (probably due to hyperlactataemia)
metabolic acidosis; hypoalbuminaemic alkalosis;
hyperphosphataemic acidosis, dilutional acidosis,
and respiratory alkalosis. Respiratory alkalosis
was as common as metabolic acidosis and arterial
blood pH was a poor indicator of the complexity
of the pathology.
Therapy
The three drugs that are recognized and
recommended for the treatment of B. canis are
485
Ip
diminazene aceturate, imidocarb, and trypan
blue. Other drugs that have been used include
amicarbalide, euflavine, quinoronium sulphate
and chloroquine; however, because of poor
efficacy and severe adverse effects, they are no
longer recommended and are used infrequently.
The antimalarial drug atovaquone combined with
azithromycin has been shown to be effective in
treating B. gibsoni.
Curdlan sulphate, an anti-HIV drug, has been
shown to have a significant inhibitory effect on
B. bigemina parasites both in vitro and in a mouse
model.
Blood transfusions are based on the magnitude of
anaemia. In cases of babesiosis, however, factors
such as acuteness of onset, clinical signs, degree
of erythrocyte regeneration, and presence of
concurrent cardiac or respiratory disease must be
considered. Dogs with babesiosis are considered
candidates for transfusion when the haematocrit
is 15% or lower. Blood is almost invariably
administered at a haematocrit below 10%. Blood
transfusions are also given when a clinical need
such as dyspnoea or tachypnoea is apparent. The
degree of parasitaemia is not an important factor
because it often bears little relation to the degree
of anaemia.
Packed erythrocytes are the component of choice
2006 World Congress WSAVA/FECAVA/CSAVA
486
Back to contents
for treating haemolytic anaemia. Administering
the plasma component of whole blood is usually
unnecessary and can place the patient at risk of
volume overload. If rehydration is required,
crystalloid replacement solutions are preferable.
Fresh whole blood has a favourable effect on
oxygen status and acid-base balance and replaces
sub-functional haemoglobin with functional
haemoglobin.
A vaccine against a specific, less virulent canine
babesiosis strain is available in France; however,
cross-immunity between the different Babesia
strains apparently does not occur with this
vaccine. A recent study has shown that protective
immunity to a virulent strain can occur if the
infection is not sterilized; therefore, vaccines
from different strains of the parasite are feasible.
Pre-immunity has been recognized as important
in controlling clinical signs of the virulent
form of babesiosis in endemic areas. Complete
eradication of parasites from infected animals
therefore may not be advantageous in these areas,
and the use of drugs to sterilize the infection may
be undesirable. The role of pre-immunity in areas
with less virulent strains is unknown.
References
Available by contacting the author by email.

Ip - Infectious & Parasitic Diseases
RELAPSING FEVER BORRELIOSIS IN PETS
Dr. Gad Baneth, DVM, PhD,
Dipl. ECVCP
Professor of Veterinary Medicine
School of Veterinary Medicine
Hebrew University
P.O. Box 12
Rehovot 76100
Izrael
baneth@agri.huji.ac.il
Introduction
Borrelia are spirochete bacteria transmitted by
arthropod vectors. The Borrelia species can
be divided into 2 major groups, Lyme Disease
Borrelia which include Borrelia burgdorferi
and other closely related species, and Relapsing
Fever (RF) Borrelia. RF in humans is an acute
infectious disease. It is characterized by recurrent
episodes of fever which often concur with
spirochetemia. The RF borrelioses can be grouped
into two forms: louse-borne epidemic RF caused
by B. recurrentis and tick-borne endemic RF
transmitted by Argasid soft ticks and caused by
several Borrelia spp. including B. crocidurae, B.
duttoni, B. hermsii, B. hispanica and B. persica.
Infection of humans with B. persica in the
Middle East is known as Persian RF and has been
reported also from Iran, Egypt, Kashmir, parts of
the former USSR, and western China. B. persica
is transmitted by the soft tick Ornithodoros
tholozoni, whose distribution includes the Middle
East, central Asia and northern India. O. tholozani
feeds on warm-blooded animals and commonly
lives in caves, rock crevices and man-made
shelters, where livestock is housed.
Clinical findings
Microscopic examination of blood smears
from two cats and a dog whose blood was
submitted for a complete blood count (CBC)
to a veterinary diagnostic laboratory in Israel
during 2003 revealed spirochetemia. EDTA-
anticoagulated blood samples from these animals
were further analyzed by molecular genotyping.
A one-year-old male and a two-year-old female
domestic shorthair cats from the Jerusalem area
were admitted to veterinary care by separate
owners and at different dates due to lethargy
and loss of appetite. Both of them had normal
body temperatures, however, CBC revealed
thrombocytopenia and severe anemia with
Back to contents
Ip
hematocrits of 17.0% and 20.8%, respectively.
Heparinized blood from the male cat was sent
to the University of Leipzig in Germany in
attempt to cultivate Borrelia. This cat died on the
evening of admission despite antibiotic therapy
with an amoxicillin-clauvolonic acid injection,
whereas the female cat recovered with clearance
of spirochetemia one day following treatment
with the same antibiotic. A one-year-old Siberian
Husky dog from a village in northern Israel was
examined because of lethargy and loss of appetite.
The dog was febrile with a body temperature of
40.8ºC (canine normal range 37.5-39.5ºC), had
thrombocytopenia and anemia with a hemtoctrit
of 27.1% (canine reference range 35-55%). It
recovered following oral antibiotic treatment
with ciprofloxacin for 5 days.
Blood samples from 6 febrile human RF patients
that were laboratory-confirmed with Borrelia
spirochetemia by microscopy of thick blood
smears were collected for molecular diagnosis
and genotyping. All these patients recovered
following treatment with doxycycline.
Molecular biologic analyses and isolation 2006 World Congress WSAVA/FECAVA/CSAVA
Polymerase chain reaction (PCR) for a fragment
of the Borrelia 16S rRNA gene was positive in the
blood samples of all animals and of the 6 infected
humans. Partial sequencing and phylogenetic
analysis of the 16S rRNA sequences indicated
that they were most closely related to the 16S
rRNA of B. persica originating from an O.
tholozani tick in Iran (GenBank accession number
U42297). Additional PCR amplifications of the
Borrelia flagellin (fla) and glycerophosphodiester
phosphodiesterase (GlpQ) genes yielded partial
gene sequences with a high degree of similarity
to the canine, feline and human samples. The
GlpQ gene is specific for RF Borrelia spp. and is
not found in Lyme disease Borrelia.
Culture of the male cat’s blood was successful
487
Ip
with motile dividing organisms observed 9
days after seeding of the sample. Isolates were
cryopreserved and passaged multiple times.
Analysis of a fragment of its 16S rRNA gene
indicated that it was closely related to B. persica
(GenBank accession no. U42297). Isolation and
in-vitro maintenance of B. presica has not been
reported from vertebrates to date.
Conclusions
This study provides evidence that RF occurs in
domestic pets in the Middle East. Interestingly,
a different Borrelia sp. in North America, B.
turicatae, is a causative agent of human RF that
was recently described as a pathogen of dogs
in Florida and Texas. These findings highlight
the pathogenic potential of RF Borrelia spp. in
animals.
The high identity scores and the close clustering
of the 16S rRNA DNA sequences from the
humans and animals in Israel with the Iranian B.
persica sequence strongly support the hypothesis
that B. persica is the cause of infection. However,
this does not preclude the possibility that more
than one RF spp. may be present in Israel or
neighboring Middle Eastern countries. Since this
is the first report of suspected B. persica RF in
domestic animals, these findings indicate that this
RF infection found in humans and animals in the
same region fits the term zoonosis which relates
to a disease of animals transmissible to humans or
in a broader sense, any disease shared by humans
and other vertebrate animals.
Although Lyme borreliosis is not endemic to
Israel or the Middle East, 10% of the dogs
naturally exposed to ticks were serologically
positive to B. burgdorferi antigen in a study from
Israel. Western blot analysis of the sera indicated
that these infections cannot be attributed to B.
2006 World Congress WSAVA/FECAVA/CSAVA
488
Back to contents
burgdorferi sensu lato sp. but to a different cross-
reactive Borrelia spp., which might have been
a RF Borrelia. Further research is warranted
to further elucidate the epidemiology of this
infection.
REFERENCES
Baneth, G., Breitschwerdt, E.B., Hegarty, B.C.,
Pappalardo, B. and Ryan, J. A., 1998. Survey
of tickborne bacteria and protozoa in naturally
exposed dogs from Israel. Vet. Parasitol.74, 133-
42.
Breitschwerdt, E.B., Nicholson W,L., Kiehl,
A.R., Steers, C, Meuten, D.J., Levine, J.F., 1994.
J. Clin. Microbiol. 32, 352-7.
MacCall, P.J., Tick-borne relapsing fever. In:
Service MW, ed., 2001. The encyclopedia of
arthropod-transmitted infections. Oxon: CABI
Publishing, 513-16.
Parola, P., Raoult, D., 2001. Ticks and tickborne
bacterial diseases in humans: an emerging
infectious threat. Clin. Infec. Dis. 32, 897-928.
Ras, N.M., Lascola, B., Postic, D., Cutler, S.J.,
Rodhain, F., Baranton, G., and Raoult, D., 1996.
Phylogenesis of relapsing fever Borrelia spp. Int.
J. Syst. Bacteriol. 46, 859-65.
Schwan, T.G., Raffel, S.J., Schrumpf, M.E.,
Policastro, P.F., Rawlings, J.A., Lane, R.S.,
Breitschwerdt, E.B., Porcella, S.F., 2005.
Phylogenetic analysis of the spirochetes Borrelia
parkeri and Borrelia turicatae and the potential
for tick-borne relapsing fever in Florida. J. Clin.
Microbiol. 43, 3851-59.
Sidi. G., Davidovitch, N., Balicer, R.D., Anis, E.,
Grotto, I., Schwartz, E., 2005. Emerg. Infect. Dis.
11, 1784-6.
Back to contents
Ip

2006 World Congress WSAVA/FECAVA/CSAVA

489
Ip

2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

M
M of Veterinary
Management
anagem
Practice

Back to contents

INVITED LECTURES - FULL PAPERS
M - Management of Veterinary Practice
PROMOTING SERVICES WITHOUT “SELLING” THEM
Lowell Ackerman DVM
DACVD MBA MPA
Bizvet, Inc., and Tufts
University Cummings School
of Veterinary Medicine
525 South Street
Walpole
Massachusetts
USA
www.bizvet.com
Lowell.Ackerman@tufts.edu
Introduction
Marketing is the process of planning and
executing the development, pricing, promotion
and distribution of goods and services, with
the purpose of achieving practice goals. By
anticipating and satisfying the wants and needs
of the consumer, products and services flow from
the practice to the pet owner.
Marketing sometimes gets a bad reputation
amongst veterinarians, but there is nothing
immoral or unethical about meeting the health
care needs of patients. In fact, in these days of
heightened awareness of compliance, it might
well be considered unethical for practices not to
make their clients aware of products and services
for which their pets may benefit.
Marketing is not about selling unwanted services,
but is a method of meeting the needs of clients
by informing them of what they should be doing
for their pets and how the veterinary hospital can
help meet those needs. Today’s marketing is about
developing long-term productive relationships
with clients. It is a client-oriented business
philosophy that stresses customer satisfaction as
the key to achieving practice goals.
Internal Marketing
Internal marketing directs marketing efforts
towards existing clients, while external marketing
efforts target new clientele. To be effective, a
marketing plan must address both concerns.
Future growth in veterinary practices comes
from increased utilization of services from those
existing clients as well as the entry of new clients to
the practice (which must at least offset the regular
attrition of clients in the practice). Dramatic
gains can be made in many practices simply by
providing needed information to the public and to
Back to contents
M
existing clients. Traditional “selling” need not be
part of a professional marketing plan.
Internal marketing deals with promoting services
to existing clients. Existing clients are already
a well-defined population whose healthcare
predilections are easily accessible. Compliance
studies have shown that existing clients are rarely
following existing protocols for most veterinary
hospitals, so marketing to existing clients is both
medically necessary and cost effective.
The Need for Internal Marketing
Organized veterinary medicine is failing the
vast majority of clients that are already using
veterinarians for their pets’ health care needs. The
failure is not one of medical incompetence, but of
limited information sharing. Seeing veterinarians
on a once-a-year basis means that pet owners are
getting information from other potentially less-
informed sources the remainder of the time.
Internal marketing is not about selling; it is about 2006 World Congress WSAVA/FECAVA/CSAVA
educating. Veterinarians need to inform clients
about the proper ways of caring for their pets. The
more complete the picture provided, the more
likely there is to be compliance and good choices
made by clients. Similarly, the more often clients
hear the same message from different individuals
from within the hospital, the more likely they are
to act on it.
Database Management
Effective internal marketing requires knowledge
of the pets being served by the practice, contact
information for owners, and some way to measure
compliance. Whether the system is computerized
or manual, if the information is not available in
the records, then it is hard to use it productively
for internal marketing efforts.
491
M
The practice must be able to track this information
and direct client educational materials to those
owners who have been notified but have not
yet acted. The information of what services are
outstanding for any individual animals must be
available as a central resource, not just buried in
the medical records.
Personalized Pet Care
As a profession, veterinarians have tended to
make generalized rules for patient care, but
in the age of the Internet, clients are expecting
customized solutions and deserve such. Is the
medical care of a Labrador retriever really that
similar to the needs of a Shih Tzu? Groomers
certainly appreciate the differences, as do boarding
facilities, but veterinarians for the most part still
embrace a one-size-fits-all healthcare philosophy.
The profession is just coming to terms with the
frequency of vaccine administration as a general
ruling but have yet to address similar concerns -
should a Chihuahua receive the same vaccine dose
as a Great Dane? Should a Doberman pinscher
receive vaccinations on the same recommended
interval as a Shetland sheepdog? Are all pets
considered senior (geriatric) at 7 years of age?
Each breed has its own risk factors for diseases,
and veterinarians would be well served to
understand these differences when developing
internal marketing efforts1. Similarly, protocols
should be established for monitoring patients on
therapeutic or preventive regimens. Sometimes,
delivering doses of medications on a monthly
basis to owners is superior to selling them
a year’s supply if they are prone to missing
doses. Animals on most medications should be
monitored periodically for therapeutic benefits
as well as for adverse effects. All animals require
some form of periodic monitoring, even if they
are otherwise healthy and just on preventive
medicine regimens.
2006 World Congress WSAVA/FECAVA/CSAVA
Personalized pet care requires more effort, but it is
infinitely more responsive to the needs of clients
and pets. This is even more significant when it
comes to disease screening. Each breed has its
own risk factors for diseases, and veterinarians
would be well served to understand these
differences when developing internal marketing
efforts.
Reminder Systems
Along with having systematic documentation of
patient needs that are easily accessible, it is also
important to have functional reminder systems.
At the end of every client visit, there should be a
reminder generated for the next visit. Logically,
pets should be seen at least twice a year, but even
if the practice adheres to a once-yearly evaluation,
a reminder should be generated in the system.
492
Back to contents
Give the client several options for reminders,
and most clients who lead hectic lives will not
consider this an intrusion. Some options include
e-mail, text messaging on cell phones, mail, and
telephone calls.
Since mailings are the most expensive and
sometimes the most neglected forms of contact
(by recipients), having the other options available
are convenient for both client and practice. If all
reminders have been sent and the client has still
not responded, the practice should send one final
notification that it is assuming that the client is
not interested in continued veterinary care at the
practice and that unless it hears otherwise, the
patient’s medical record will be removed from
the active medical files. If veterinary care is
being provided elsewhere, then the practice offers
to forward relevant medical information to that
practice, upon notification by the owner. Above
all, the message should be that if the pet is not
receiving care at the practice, it is the hope that
the pet is receiving its needed care elsewhere.
If clients do not respond to this message, there is
no point in sending additional reminders. If the
client does respond, the staff should schedule the
needed appointment and then inquire as to the
form of reminder notification preferred by the
client.
External Marketing
External marketing deals with increasing the
exposure of the practice to new clientele. In
contradistinction, internal marketing deals with
promoting services to existing clients. Attracting
new clients to a practice depends of creating value
within the practice, differentiating the practice
from others in the area, and then promoting this
value to the public.
External marketing is important, because it is a
necessary growth strategy for practices. Clients
will be naturally lost to attrition over time and
new clients are needed not only to fill the lost
client positions, but for the practice to thrive and
grow.
Miscellaneous
Internal marketing should not involve selling
clients services that lack intrinsic value. For most
veterinary practices, internal marketing should
focus on delivering those services, which the
hospital team already believes is valuable, but
which is not currently being delivered in a reliable
fashion. Consultants refer to this as “low-hanging
fruit”. Whereas veterinarians may be tempted to
buy expensive equipment that can be marketed to
clients, there are so many routine services that are
not being consistently delivered and that warrant
increased attention by practices.

Pet owners are at a disadvantage compared to
parents of children, who tend to have a variety of
resources at their disposal for the anticipated care
and expenses of dependents. Armed with this
knowledge, emphasis is placed on routine medical
visits, preventive care, proper socialization,
education, and insurance to mitigate the costs of
medical care.
For too many years, pet owners have been trained
to expect that a one-time neutering surgery and
occasional vaccination is all that is needed unless
an animal is ill. Compliance studies support the
notion that clients do not appreciate the level of
care they should be receiving, and veterinarians
overestimate the care that is being provided on
the basis of their instructions.
Today’s clients are value shoppers, and it is
critical that veterinary practices invest in future
growth through effective marketing campaigns.
In this competitive environment, it is important to
differentiate one practice from another, and one
must be able to demonstrate how one’s practice
provides value relative to its differentiation.
Back to contents
M
Recommended Reading
Ackerman, L: Business Basics for Veterinarians,
ASJA Press, New York, 2002
Ackerman, L: Management Basics for
Veterinarians, ASJA Press, New York, 2003
Ackerman, L: Five-Minute Veterinary Practice
Management Consult, Blackwell Publishing,
2006
Stowe, JD; Ackerman LJ: The Effective Veterinary
Practice, Lifelearn, Inc., Guelph Ontario, 2004
[No part of this material may be reproduced or
copied in any manner without express written
consent of author. Some of this material has
been abstracted from Management Basics for
Veterinarians, with permission]
2006 World Congress WSAVA/FECAVA/CSAVA
493
M
M - Management of Veterinary Practice
WINNING WEB SITE STRATEGIES
Lowell Ackerman DVM
DACVD MBA MPA
Bizvet, Inc., and Tufts
University Cummings School
of Veterinary Medicine
525 South Street
Walpole
Massachusetts
USA
www.bizvet.com
Lowell.Ackerman@tufts.edu
Web sites provide both internal and external
marketing opportunities, and are available 24
hours a day, 7 days a week. Web sites are among
the most economical forms of advertising and
should be created, maintained, and actively
utilized by all veterinary hospitals.
The Internet is a global medium, but our target
market is local, so appropriate strategies must be
utilized. Internal and external marketing using
the Internet can be efficient and cost-effective
Effective internet marketing should be an
extension of effective client service initiatives
The World Wide Web (WWW) is a feature on
the Internet that brings all of the audiovisual
qualities of television right into your computer
with one major advantage. Sites on the WWW
are typically “linked” with similar sites so you
can start at one point and leapfrog along to a
variety of sites that might be of interest. This
is what is commonly referred to as ‘surfing the
net.’ One of the other features of the WWW
is that there are a variety of “search engines”
to help you find what you’re looking for. The
search engines are superior to printed indexes
2006 World Congress WSAVA/FECAVA/CSAVA
because, when you see a site of interest, you
just need to click on it (not even plug in an
address) and you’re instantly there.
Veterinarians not only like to ‘surf the net’ but
many are making a presence on the Web with
their own Web pages. With new software and
online server options now available, web pages
can be created without specific knowledge of
HTML, the computer language of the Web, just
as current word processors have icons to replace
basic DOS and ASCII commands. There are also
several sites at which you can register your own
domain name or process it through your current
Internet provider. For the economy-minded, it’s
also possible to piggy-back your web site on other
sites without incurring any major expense.
Creating a practice web site has never been
494
Back to contents
simpler, or more economical. However, the goal
of such an endeavor is not just to have a presence
in cyberspace. The goal must be to provide an
enhanced customer service experience that not
only serves the needs of existing clients, but
attracts new ones as well.
Web Site Creation
There are now many options available for
creating a web site, regardless of who actually
does the design work. The most important aspect
of creating the site is to design the content that
will appear on the site. This cannot be delegated
to a “webmaster”, but can be assigned if the
content design is being done by a company that
also deals with veterinary marketing. There are
three major options for web site creation: Host
the site yourself; use onsite hosting, or; use a
company-supported site. All have advantages and
disadvantages.
Select a URL
The Uniform Resource Locator (URL) is the
practice’s address on the World Wide Web. It is a
sequence of numbers and periods, but for people
to be able to find the site, it is assigned a domain
name. The process of selecting a name is neither
difficult nor expensive, but it does take some
flexibility since many veterinary-related domain
names have already been assigned.
The domain name should be selected with great
care, since it is the means by which the practice
will be identified on the Internet. Avoid long and
complicated names, in favor of those that are
short, descriptive, and easy to remember.
To properly utilize the domain name so that when
a client accesses the site they see the appropriate
content, the server must link the domain name
with the IP address provided by the hosting
service.

Content
It is important to realize that a web site should
be a portal for pet owners, not a one-time visit,
so content must reflect this strategy. When
practices invest in a showpiece web site with lots
of technological gimmickry, they might impress
a client on a first-time visit, but they do not, on
their own, entice the viewer to return with any
regularity.
There are several features that need to be
addressed to keep web sites effective as
marketing tools and not just glorified banner
advertisements. Provide useful health-related
content, preferably with illustrations, that will
help clients learn about health care topics. Provide
detailed information about the hospital and its
staff. In many veterinary hospitals, the client
never gets to see any of the hospital beyond the
examination rooms and reception areas. The web
site can serve as a valuable resource for touring
the facility (including treatment areas, imaging,
surgery, intensive care, boarding, grooming, etc.)
as well as giving clients the opportunity to better
appreciate the staff. The content on any site must
be fresh if it is to entice viewers to come back
on a regular basis. This can be done by regularly
adding content to the site, refreshing existing
content, and by using technology (such that some
new content rotates onto the site every time an
existing viewer returns). Make content on the
site easy to find. Clients lose patience if it takes
more than 3 hyperlinks to find the information
they are seeking. Either keep the site content tabs
manageable, or create a site search engine for
clients.
Make site easy to find
The Internet is global, but a good marketing
program is local, so it is important to make the
practice easy to find by consumers likely to use
it. While it might be gratifying for pet owners
around the world to visit the site for their
healthcare information, this is unlikely to result
in increased client traffic or enhanced revenues
for the practice.
Use the web address on all marketing pieces,
including business cards, client education
materials, newsletters, e-newsletters, etc. This
information will be used by clients, and perhaps
shared with friends and family in the practice
trade area. It is a good strategy to use abridged
topic information in these pieces and direct clients
to the web site for more complete information.
Create a local network of businesses that cater
to the same client base, including groomers,
boarding kennels, pet supply outlets, veterinary
associations and even other veterinary practices.
Shared links not only increases the likelihood
Back to contents
M
of increased client exposure, but it increases the
relative page rank of the site, which in turn raises
the site in the listings of search engines.
Consider advertising on local search engines,
which only charge on a click-through basis.
That means that charges only apply if consumers
actually click on the hyperlink that takes them to
the practice web site.
Strategies for Getting Noticed
Web sites must be optimized so they will be
included in search engines, and so clients will be
able to find the site if they don’t already know
about its existence. Creating a beautiful site is
only half the battle. If clients can’t find the site,
and if pet owners don’t find the practice by routine
web searches, then the web site is failing.
Keywords
It is important to optimize the site for keywords,
depending on how you think your potential clients
might be trying to find you on search engines.
They might be searching for any of the following:
Vet, veterinarian, veterinarians, veterinary clinic,
veterinary hospital, animal clinic, animal hospital,
location, etc.
Meta-Tags are pieces of information that are
provided on a web site, but not visible to viewers.
They are incredibly important in helping a practice
be ranked highly on a search engine. There are
several important meta-tags that can be utilized
for search engine optimization, such as:
•Title Tag
•Description Tag
•Keyword Tag
•<ALT> Text
•Robot Text
Each of these has opportunities and limitations,
but must be part of a strategy for getting noticed
on the Internet. For example, Keyword tags used
to be more important, but since many web owners 2006 World Congress WSAVA/FECAVA/CSAVA
abused the process by “salting” their sites with
keywords and trick effects, this has become less
important in the ranking of web sites. However,
it is a mistake to ignore keywords simply because
they are less important in the ranking system than
they once were.
Other Strategies
Search engine optimization also is enhanced by
links to the site, links within the site, and using
keywords and optimization strategies to help the
site rank highly on internet searches.
Miscellaneous
The World Wide Web is a global network of
computer networks, but the promotional needs of
495
M
most veterinary practices are decidedly local. It
is important to concentrate on marketing efforts
that will attract clients from the local trade area,
and this often requires the participation of an
experienced web-marketing consultant rather
than a technically sophisticated “webmaster”
When creating a web site, design it with the notion
that some clients that access the site will not have
broadband Internet connections, and may not have
the latest and fastest home computers. It is best to
keep the resolution of graphic images at about 72
dpi so that the file sizes are small enough to be
easily and quickly loaded. Since the web cannot
currently handle resolutions higher than this,
larger image files are a waste of bandwidth, and
frustrating for owners trying to access content.
Similarly, consider whether the site really needs
special effects, such as Flash animation. While
this is an impressive use of technology, it greatly
increases the cost of web site development with
no evidence that it translates into selection of
veterinary services by the consumer.
2006 World Congress WSAVA/FECAVA/CSAVA
496
Back to contents
Finally, devote the most effort to search engine
optimization, improving the chances that the
practice will be found on web searches. After all,
a web site does not good for the practice if it does
not attract business to the practice.
Recommended Reading
Ackerman, L: Business Basics for Veterinarians,
ASJA Press, New York, 2002
Ackerman, L: Management Basics for
Veterinarians, ASJA Press, New York, 2003
Ackerman, L: Five-Minute Veterinary Practice
Management Consult, Blackwell Publishing
2006
Bizvet. www.bizvet.com
[No part of this material may be reproduced or
copied in any manner without express written
consent of author. Some of this material has
been abstracted from Management Basics for
Veterinarians, with permission]

M - Management of Veterinary Practice
INCREASING PRACTICE PROFITS
Lowell Ackerman DVM
DACVD MBA MPA
Bizvet, Inc., and Tufts
University Cummings School
of Veterinary Medicine
525 South Street
Walpole
Massachusetts
USA
www.bizvet.com
Lowell.Ackerman@tufts.edu
Profit is an elusive term for many veterinarians.
For many, the very simplest of definitions for
profit is any surplus remaining when all expenses
are deducted from all revenues. The problem is
that some veterinarians may not pay themselves
a reasonable salary commensurate with their
time and expertise, and keep the difference
between revenues and costs as their reward,
calling it a “profit”. The problem is that this does
not recognize their inherent value in delivering
veterinary services, managing the practice etc.
The best way to understand profit is to imagine
that the practice owner needs to pay others a
going wage for doing all jobs within the practice
as though the owner was an absentee landlord.
When this exercise is performed, many veterinary
practices are only marginally profitable, and
some are actually losing money. The situation is
even more complicated when veterinarians own
the practice real estate rather than lease. In many
instances, the value of the land is worth more for
purposes other than a veterinary hospital. When
this “opportunity cost” is factored in, profit for
veterinary hospitals becomes even more elusive.
For these reasons, and many others, veterinary
hospitals need to concentrate on profit. Without
profit, there is no possibility for the practice to
survive and advance, to pay its staff reasonable
salaries and benefits, to buy new equipment, and
to be able to eventually sell the practice for a
reasonable price that would reflect all the effort
that went into it. Follow these guidelines to better
understand and appreciate profit within your
practice.
•Pay yourself first
•Understand Where the Money Goes
•Grow the Top Line
•Leverage staff
•Develop profit centers
•Perform Value Analysis on Equipment
Purchases
•Set prices reasonably
Back to contents
M
•Data Mining and Compliance
•Benchmark and Respond
•Develop strategic planning protocols
1. Pay Yourself First
While this seems simple, many veterinarians
actually pay themselves … last. There seems to be
this illusion that whatever is left when everything
and everybody else is paid is profit, and this is the
entitlement of ownership. Of course, this is not
true. If you didn’t own the hospital and you were
working as an associate elsewhere, what type of
salary would you command based on the number
of hours worked, or the amount of client revenue
derived? Whatever this salary is, pay it, on the
same schedule as the other employees. If you
suddenly find that cash flow is tight, this might
be the first realization that the practice is not as
profitable as originally suspected, and this is a
worthwhile realization. If the practice owner also
does management duties, this also needs to be
reflected in salary, since if the owner doesn’t do it,
someone else would need to do this task. Having
a spouse do it without any compensation is not a
reasonable expectation. It is not unusual for 3% 2006 World Congress WSAVA/FECAVA/CSAVA
of total revenues to be needed to compensate for
management duties.
Understand Where the Money Goes
Veterinarians practice medicine, but veterinary
hospitals are businesses, and they must be
generating profits if they are to continue as
worthwhile investments. For every hospital, there
is a finite amount of money to be spent, based on
the revenues collected from services provided and
products sold. This is somewhat variable based
on the country in which the practice operates and
the type of practice.
Staffing is by far the largest practice expense.
It includes compensation and benefits for all
doctors in the practice, paraprofessional staff,
administrative staff, and other personnel. Materials
497
M
and supplies are used in the practice of medicine,
and include all pharmaceuticals, diets, laboratory
supplies, radiographic supplies, surgical supplies,
etc. General and administrative expenses include
rent, mortgage or lease payments, utilities,
telephone, insurance, administrative supplies and
other things needed to run a veterinary practice.
Grow the Top Line (Revenues)
After considering the expense of running a
veterinary practice, the temptation is to try to
increase profit by cutting costs. This approach
almost never solves the problem. The most likely
way to increase profit is by increasing the “top
line” of financial statements – revenues. The
reason is that most expenses in a veterinary
practice are fixed – such as rent, staff salaries,
utilities, and many more. A smaller percentage of
expenses are variable; they vary with the amount
of business being conducted. Other than the
standard stock of radiographic film and supplies,
more is only purchased if the existing stock is
being used by taking (and hopefully charging for)
radiographs.
Because so much of a practice’s expenses
are fixed, increasing revenues tends to only
marginally affect costs. So, if a practice went from
taking 40 radiographs a week to 60 radiographs a
week, the revenue would increase by 50% (from
40 to 60) but the cost would only increase by
much less, only the expense of the films and their
development (perhaps 5%), for a solid net gain in
profits. This net gain cannot be achieved by cost-
cutting.
Leverage staff
In many small veterinary practices, veterinarians
not only see clients and order diagnostic tests and
treatments, but are often active participants in
collecting laboratory samples, taking radiographs,
placing catheters, etc. When a practice isn’t busy
2006 World Congress WSAVA/FECAVA/CSAVA
and there is “overcapacity” (i.e., appointment
slots open and no client demand to fill them),
then this may be a productive and cost-saving
use of veterinary talent. However, as the practice
becomes busier, using veterinarians to perform
tasks that could just as competently be performed
by lower-paid paraprofessional staff is inherently
inefficient and robs the practice of additional
revenue generation.
In general, veterinary technicians and assistants
receive salaries much less than that of
veterinarians, so leveraging staff is important
in being able to increase revenues on a per-
doctor basis. If veterinarians can see additional
appointments, or perform additional procedures
for which only they are qualified, while
paraprofessionals are performing duties for
498
Back to contents
which they are qualified, then revenues climb at a
rate higher than expenses. In most efficient small
animal hospitals, there can be 3-4 non-veterinary
staff leveraged across every veterinarian. In very
busy high revenue-generating practices, there
may be 10 or more non-veterinary staff for every
veterinarian in the practice.
Veterinarians are often the bottlenecks in
revenue generation. In very basic veterinary
hospital models, revenue is only generated by
the veterinarian. If the veterinarian is performing
surgery, no medical appointments are being seen.
If the veterinarian is seeing medical appointments,
no surgeries are being performed. The practice is
still paying fixed expenses for both, which leads
to inefficiency and loss of revenue generation.
Leveraging staff allows revenue to continue to
flow from many fronts, even when the veterinarian
is personally engaged in only one task.
Develop Profit Centers
Most veterinary hospitals are full-service,
providing clinical visits, surgery, imaging,
laboratory testing, hospitalization and other
services. In the end, the profit is often a composite
of all of these services. However, in human
medicine, they have long ago learned that it is
not cost-effective for doctors to provide all of
these services. No doubt, the same will occur in
veterinary medicine. If veterinarians are to offer a
variety of services, they must be able to determine
which of these services is profitably offered and
which ones actually lose the practice money. This
is accomplished by establishing profit centers
within the hospital.
Profit centers are established to determine the
profitability of individual services within a
hospital, spreading the expenses of the hospital
across each profit center. While the number of
profit centers varies somewhat from hospital to
hospital, some common profit centers include
examinations, anesthesia & surgery, laboratory
testing, hospitalization, imaging, pharmacy, diets
& retail, medical treatment, dentistry, boarding,
grooming, etc.
As part of the profit center assessment, assign all
profit-center specific expenses (e.g., equipment
leases, materials used solely by profit center) to
the particular profit center, and then divide all of
the hospital expenses (staff, overhead, general
materials) by a fair method which allocates a
relative proportion of total expenses to each
profit center. In so doing, it usually becomes
apparent that some services within a hospital are
being “carried” by others, not being profitable
on their own merits. This allows the hospital to
understand and appreciate their most profitable
services and to make changes to services that are

only marginally profitable, or may be actually
losing money for the practice.
Use Value Analysis for Equipment Purchases
Along with profit center analysis, it is important
to develop policies in which new profit centers,
or new expenses related to equipment are only
approved if a clear value to the practice can
be determined. Reinvestment in the practice
is important, but asset acquisition should be
evaluated in light of its potential to improve
practice profits. New equipment must either
provide medical value-added qualities that allow
a higher quality of medicine to be performed
and have value to the practice, or client value-
added qualities that are immediately appreciated
by clients and they would be willing to pay
for services utilizing that equipment. Here are
examples of some equipment that usually justifies
their expense.
Dental prophylaxis equipment is of modest
expense and allows thorough cleaning of pets’
teeth. This is increasingly recognized by both
veterinarians and clients as not just a cosmetic
tool, but one that can improve the overall health
of animals. Since about 85% of all pets over 4
years of age have some degree of periodontal
disease, there is potentially wide application of
this technology.
Radiowave surgery (e.g., ellman Surgitron)
uses high-frequency radiowaves to both cut and
coagulate tissues. Much cheaper and typically
more versatile than a laser, it provides cutting
and coagulating, with applications including soft-
tissue surgeries, and uses in dermatology, dentistry,
ophthalmology, neurology, and oncology. It also
provides almost bloodless surgery in birds and
exotics.
Photographic capability is a powerful marketing
tool in veterinary practices. This not only provides
owners with images of problems they can’t easily
see themselves, but also provides a valuable
addition to the medical record.
Other valuable equipment than can be profitable
but warrants value analysis for each individual
practice includes in-hospital laboratory
equipment, blood pressure monitors, tonometry,
etc.
Set Prices Reasonably
While veterinary practices are small business, pricing
is often a reflection of charges by other veterinary
hospitals in a community, and not necessarily based
on the costs of offering those services. While it may
be necessary to price some services on the basis of
community expectations, veterinary practices would
be well advised to use a more objective measure of
setting fees, such as cost-plus pricing.
Back to contents
M
In most industries, cost-plus pricing is the fairest
way to set fees, since it is a composite of actual
costs, not guesswork. For any service provided in
a veterinary hospital, a fair fee can be determined
if labor, overhead, and materials are considered,
as well as a desired profit margin. To keep
the calculations simple, it is best to calculate
overhead and labor rates on a per-minute basis,
and materials have both a direct and an indirect
cost. Finally, creating a final price to the client
requires using an appropriate formula to calculate
profit “off the top”. Using a “mark up” is not the
same as a profit margin. The appropriate formula
is:
P = TC + (P),
where P = Price to the client, TC = total costs,
and = profit desired, expressed as a decimal or
percentage.
Data Mining & Compliance
Effective internal marketing requires knowledge
of the pets being served by the practice, contact
information for owners, and some way to measure
compliance. Whether the system is computerized
or manual, if the information is not available in
the records, then it is hard to use it productively
for internal marketing efforts.
The practice must be able to track this information
and direct client educational materials to those
owners who have been notified but have not
yet acted. The information of what services are
outstanding for any individual animals must be
available as a central resource, not just buried in
the medical records.
Benchmarking
Benchmarking is becoming more and more
popular in veterinary medicine, as more practices
start to embrace more standardized methods of
reporting. There now several excellent resources
for benchmarking income and expense elements, 2006 World Congress WSAVA/FECAVA/CSAVA
veterinary fees, and compensation and benefits,
but these are not universally available in all
countries. In the United States, there is a free
online resource for benchmarking provided by the
National Commission on Veterinary Economic
Issues.
For countries that have not established
benchmarks, or fee schedules, it is worthwhile for
veterinarians to work collectively to produce such
standards. In too many instances, veterinarians
compete against one another forcing prices down,
rather than working collaboratively to ensure that
all make a decent living. The goal is not collusion
or price-fixing but to work together for fair pricing
and reasonable expectations.
499
M
Develop Strategic Planning Protocols
Creating an organizational plan for a practice
to experience significant financial improvement
requires forward-thinking strategic initiatives.
Improving existing operations will likely lead
to improved circumstances, but substantial
improvement (typically greater than 25%)
typically requires changes in hospital processes
themselves. Whereas examination of financial
reports can tell a practice what it has done over
the recent and distant past, it cannot provide a
“roadmap” for substantial improvement going
forward. This is the job of strategic profit
planning.
Future success is better defined by incorporating
staff and business process changes that are likely
to be responsive to client needs, and to do soon
relatively short notice. One of the best ways
to encourage this process is to use established
2006 World Congress WSAVA/FECAVA/CSAVA
500
Back to contents
strategic planning tools. There have been several
such approaches used in industry, including the
Balanced Scorecard. The Business Assessment
Report Kard (BARКSM) was developed by Dr.
Lowell Ackerman as a strategic planning model
specifically designed for veterinary practices.
Recommended Reading
Ackerman, L: Business Basics for Veterinarians.
ASJA Press, 2002
Ackerman, L: Management Basics for
Veterinarians. ASJA Press, 2003
Ackerman, L: Five-Minute Veterinary Practice
Management Consult. Blackwell Publishing,
2006
Stowe, JD; Ackerman, LJ: Effective Veterinary
Practice. Lifelearn, 2004

M - Management of Veterinary Practice
COMMUNICATION TOOLS THAT SELL YOUR SERVICES
Philippe Moreau, DVM, MS,
DECVIN, DECVIM-CA
Medi-Productions
rue Pierre Brossolette
87000 Limoges
France
pmoreau@mediproductions.
com
Introduction
We know that communication represents much
more than the simple linear relationship between
two individuals. On the contrary, it relies on an
interrelated system, of reports and exchange,
a perpetually moving system that generates
reactions. Communicating is transmitting,
revealing, sharing knowledge and information.
For some, to communicate it is also to please and
to seduce.
Development of practical supports
These supports are today essential means for
efficient communication. One of the primary
principles for good communication is to make
sure that the same message is repeated in time
and space. In addition veterinarians and staff
cannot afford to tell clients all they need to
know at all times on all topics related to their
pet’s wellness. We mentioned the limitations of
human resources, and therefore an important
place remains for communication tools. It is also
true that willingness to communicate with our
clients directly can vary with time and with our
“mood”. As a colleague practitioner once told
me:”my ability to communicate with clients will
drastically change if it is Monday morning and
the appointment book is empty, or if it is Friday
evening and the waiting room is full”.
How can we handle this dilemma concerning
our lack of availability and willingness to serve
our clients at times? First, by forcing ourselves
to adhere to our schedule and time we devote to
each person. True. But secondly we can also use
tools that will help us to be consistent, that will
save us time, that will please our clients because
they appreciate these kind of documents. Today,
the more a practice grows, the more there is a
need for high quality services, the less human
resources are available and the more these forms
of communication relays toward our clients are
useful or even indispensable.
Back to contents
M
The concept of message relay: To increase service
value it should be accompanied by a tangible
and objective feature because the service is now
substantiated and reinforced.
The intangibility of services: The fundamental
feature of a service is that it is intangible. It
cannot be palpated. And yet these are the services
we sell. In addition most of these services are
consumed as they are produced. Finally another
important feature of service is that it cannot be
stocked and kept for later use. What we failed to
provide today is lost… It is important to generate
documents that would transform our services into
tangible products.
This is the role of most communication tools. The
classical example of this concept is the invoice
(which we should use at all times). Other common
examples are the vaccination booklet, examination
forms, post surgical forms, prescriptions, surgical
reports, lab reports, hospitalisation forms, the
patient medical file & data, etc. in other words all
documents that quantify and materialize services.
Communication tools for the reception area
I like to say that “veterinarians are not selling,
they are helping their clients to buy”. There 2006 World Congress WSAVA/FECAVA/CSAVA
is a clear nuance and this should help most
practitioners that are sometimes reluctant to act
in a commercial manner.
Most of these promotional table posters or displays
are very often given by drug companies that are
obviously interested in promoting their products
on the practice counter, simply because it will
increase their sales by 20%, 30% and sometimes
much more… The purpose of an SPP is triple:
● to Remind : this is a reminder of some communication
elements given elsewhere in the practice (the
consultation room, the waiting zone, etc.)
● to Inform : about the specific product or service,
and its features, for example its price or its use
(i.e. for old dogs) etc.
501
M
● to Stimulate: this is part of the “impulse purchase”
concept
In Europe according to “Consumer buying habits
study” (CB News n°407, 2002), 20 to 55% of
purchases are “impulse purchases” (65% in the
USA). In that study it was interesting to note that
the mean reading time of a consumer in front of
an SPP is 7 seconds… This is not long at all and
yet quite sufficient. This is why there is no need
to have long messages on “information message
displays”. Be concise and efficient…
Most clinics today use part of their reception area
to display products including and for the most part
nutrition products. Today it is no longer possible
to simply install products on a shelf. There are
specific techniques, dedicated furniture and an
entire set of concepts, including specialised
professionals (merchandisers) from a marketing
division or specialty called merchandising.
The waiting area
The “waiting-room concept: One should no
longer call it “the waiting room”! Who wants to
wait nowadays? This word is no longer adapted to
a client service because it implies a “waiting time”.
Consumers do not care to wait, so let’s decrease the
perception of a waiting time by all means. I suggest
using the term “reception area”, or “welcome area”
no longer care to sit in a closed room (historically
“the waiting room”) as in the past.
Consumers should actively participate in the
service and feel part of the community that
delivers that service. This is the reason why walls
and doors should be removed between clients and
staff in the reception area. Today the “waiting
zone” should be integrated within the reception
area. People should ideally be in contact with
one another (staff vs clients). This form of
environment is seen in many different businesses
where clients see, and participate in the action.
2006 World Congress WSAVA/FECAVA/CSAVA
Internal communication tools (placed and used
within the practice itself):
It is helpful to differentiate communication tools
that are available and consulted by clients within
the waiting and reception area from those that
clients may take home and use at distance. Both
internal and external communication should be
used concomitantly and be synergetic.
a) posters: Veterinarians receive nice posters from
drug companies, wholesalers and other pet-food
distributors… Some of these posters are generic
(no products are mentioned) or directly linked to
a product.
b) brochures and leaflets: Drug and pet-food
companies are inundating veterinarians with
different sort of brochures and leaflets on products
and services. The purpose of these documents
502
Back to contents
is to inform and educate clients about their
pets’ needs and to contribute to the veterinary
communication.
c) magazines and newspapers: As a rule, clients
will not read while in the practice. Should we
place magazines and newsletters? If you should
decide to place a people publication in your
practice, remember that the most successful item
remains the local daily newspaper
d) small ads panel board: Your clients belong
to a community: your practice. Help them to
communicate between themselves by installing
a board that they can use to place small ads and
announcements. Such panels or boards contribute
to the “community” bond and help clients to
identify with it.
e) pictures of human resources: It is a nice way to
highlight the practice team and to include a frame
with pictures of the veterinarians as well as of the
staff.
f) guided picture tour of the clinic: Most clients
enjoy visiting the “back-stage” of the practice.
This is not always possible. Therefore taking some
nice action pictures of the “back office”, showing
your equipments and services, are valuable.
g) practice photo album: All veterinarians receive
pictures and thank you notes from happy clients.
Why not use these testimonials from clients and
place them in a “practice photo album”?
h) multimedia concepts and products: In a
veterinary practice the environment is particularly
favourable because the clients have a certain
waiting time, they are sitting at least part of that
time and they are concerned about their pet’s
health. One of the objectives of visual supports
is to entertain while people are waiting. The
program should therefore be attractive, amusing,
and yet informative.
Today dedicated cartoons or animated movies
are the ideal form of programs for veterinary
practices. It is also interesting to notice that
people identify better when watching a cartoon
instead of a movie with real animals in action,
probably because the animal actors in these
movies are always different from their own pets.
On a cartoon this is not a issue…
i) computer with an Internet access: Some
veterinarians have produced their own web site
and offer these new media to their clients to learn
about additional services. It would be logical for
those who have a personal Internet site to offer
a computer station in the practice with Internet
access, including a direct presentation of the
clinic web site.
Conclusion
Communication today is an integral part of so
called “total customer management” (TCM)

that places the client as an actor in the service
activity. The challenge is no longer to prescribe
or sell a high quality product and service. Today,
this is a “given” feature of veterinary medicine
services, but to include these products and
services in global client management. This is
where communication becomes essential and
contributes to client satisfaction that makes the
difference.
The emergence of new technologies will influence
M - Management of Veterinary Practice
HOW TO DEVELOP A SENIOR PET PROGRAM
Philippe Moreau, DVM, MS,
DECVIN, DECVIM-CA
Medi-Productions
rue Pierre Brossolette
87000 Limoges
France
pmoreau@mediproductions.
com
Importance and value of a service
Offering services adapted to clients needs and
expectations and then provide excellence in the
delivery of these services, here is one of the
key of success in a veterinary practice. Such
development of services requires preparation,
management, marketing and communications
tools, training, internal set-up, and a proper
launch. It is not enough to offer a service, it is
needed to study the manner it will be perceived
and accepted by clients. It is crucial to study the
value that will be associated with the reception of
the service by the client, as well as the return on
investment for the practice.
For example a senior check-up service will
only satisfy a demand from clients if it is well
documented and explained to clients. By the
same way, such a service will only be valuable
if it generates sufficient revenues for the practice
and is worth the time and efforts.
Back to contents
M
the use of communication and the tools that are
associated with it.
Additional References
Philippe Moreau : Les outils de la communication:
pourquoi faire ?, La Dépèche Vétérinaire, 2002
Philippe Moreau, Christophe Buhot : Manuel
de Practice Management : la communication du
cabinet vétérinaire, 2004
Setting-up a new service
People don’t buy a service as they buy a product.
It is necessary to point out the value of the service
for the client (and for his or her pet). For a product
it is easier because it is tangible, a service has less 2006 World Congress WSAVA/FECAVA/CSAVA
objective value and you need to communicate on
such important value. It is the case of course for
all services. The example of a senior program
(including a check-up) is easy to understand. I
have seen veterinarians that are embarrassed when
the results are normal! It should be the opposite!
Remember we are taking care of a normal animal,
not a sick or injured patient. We are dealing here
with a form of preventive medicine…
TO best present the value of a service to a client,
one should detail and list the features of the
service (various aspects of the check-up, including
a complete physical examination, some essential
blood work that will allow to survey most internal
organ functions, thoracic radiographs, etc…).
Once the features are listed, or at the time they
are detailed, one should explain the benefits that
503
M
each of these tests will bring to diagnose possible
anomalies in a elderly patient for example…
In parallel to these explanations, it is always a
good idea to show through documents, images,
the various aspects of the service. For example
show the documents, forms, folders, etc… that
will accompany the service. All these documents
bring an important feature to the service: these
documents transform what was intangible
and subjective in a action that now is tangible
(through the reports and documents) even if these
brochures, these reports look basic to you, they
add crucial value to the perception of the service.
It is also important to go over the materialistic
aspects of the service (how much it will cost,
how the pet will be handled and what would be
required from the owner practically…). When
approaching cost, it is our advise to present
the price as a benefit because of the “package”
format of the service. Another important feature
of a service and a real value, is to point out that
all preventive diagnosis will contribute to detect
abnormalities at the early age and therefore will
allow to treat sooner and often better and for a
reduced cost. Better results, better prices…
Examples of services to propose to pet owners
There are several services that would contribute
to a better medicine and at the same time
would contribute to practice growth. Some of
these services would also correspond to clients
expectations. It is the case for example for a
“senior pet “ management program. The human-
animal bond is such that there is a deeper affection
for older pets, and a true need and demand from
clients to keep them happy, with no pain nor
suffering, and as long as possible…
A senior pet management program
A senior pet management program is an important
service to place in your practice routine. If you
2006 World Congress WSAVA/FECAVA/CSAVA
haven’t done yet, consider it today! If you start
such a program, you should talk to all clients,
even those who have a young animal, even if it
is just quickly mentioning it…, because they will
become adult and soon senior pets before you
know… and such a program will therefore be a
natural and normal step and the annual follow-up
f their pet…
The efforts that pet owners are willing to take to
help their older dog or cat to feel better, to live
happier and longer, are often immense. A survey
by Idexx in 1997, showed that pet-owners in the
USA were spending 184$ /year for their dog less
than 10 years, and 277$ for pets over 10 years of
age. Another study from the AVMA, showed, as
in man, that the pet population was getting older
and that 25% of pets were older than 8 years.
504
Back to contents
Some practical aspects of a senior pet management
service
Once you plan to set up a senior pet management
service, it is crucial that the entire clinic team,
the veterinarians, the technicians, the staff, the
receptionists, become part of the service and
adopt it. The clinic team should understand and
communicate around the value of such a service
for the pet, for the owner. Such communication
should be part of the daily messages to clients
and it should obviously start before pets enter
the “senior category”. Why? Simply because if
you explain and make the clients understand that
their pet, once reached a certain age, will require
different sort of preventive management and
check-up”, it is natural that these services will be
applied almost instinctively at that time. It is often
the clients that will even remind you that time
has come to enter the “senior pet management”
program. You set the senior program, and it
becomes a natural and normal step in the lifetime
follow-up of the pet. The various “check-up” and
services associated with the program do no longer
require any deep and detailed explanation and
convincing communication. This is the reason
why it is important to communicate early about
a service and as a team with the same energy and
conviction.
The senior pet program and the annual health
examination
An efficient method to set-up a “senior pet
management program” consist to start with the
annual visit, often referred as “the vaccines” and
try to reinvent such a consultation. We all know
that annual vaccines protocols are getting more
and more controversial and that these common
annual vaccines may change as less and less
boosting of these immune protection will be
expected in the future.
This is the reason why it is important to start today
to present the annual visit as the “annual health
check of the pet” (during which some vaccines
may be given as needed) instead of the ”annual
vaccinations”. The entire communication should
change and reinforce and focus on the annual
examination of the pet instead of the vaccines.
This include the reminder cards or letters that
are sent to clients and should emphasize the
clinical examination vs the vaccines. Once such
system is progressively put into place, with the
annual examination placed into the center of the
service, focusing on the clinical examination
and associated services, it is natural, once the
pet becomes a senior, that such annual visit will
include additional clinical tests, associated with
the pet’s age.

The financial return of a « senior pet program
Not only following closely a senior pet is a
good medical practice, it is clear that such a
preventive program generate a positive financial
return. Some would even call it a good “return
on investment”. Indeed pets are often “senior”
for several years and these years are important
to manage well. There is a significant difference
with the services that are developed for pets
during their growth, which is a short period of
their life. Think of the time and efforts that are
developed to communicate with clients about
their pet’s growth needs, nutritional, behavior,
external and internal parasites, pet’s vaccines
etc…all these aspects of pet care during the first
10 to 12 months of their life are important and
require several period of time. Think that when
it comes to a senior pet, the follow-up services
related to the senior will be needed much longer,
usually several years.
The various steps to start a new service
To set-up a new service for example a senior pet
program, one could adopt the following steps:
1. be convinced of the service, its value for the
pet, the client, and the practice…
Back to contents
M
2. make sure that the entire team is convinced
as well…to consolidate the coherence of the
communication about the service…
3. define who are the clients that you will select
and target for the service…
4. develop the appropriate communication tools
that will be needed to market the service
5. prepare the launch of the service…(date,
practical details, logistic, tools, staff meeting,
etc.)
6. initiate the communication toward your clients,
starting with your “fan club”
7. establish a developmental strategy for the
service (where is it going to be in 5 years and
what do you need to do to get there…?)
8. associate the service to others and try to bundle
the offers into “packages” that add value for the
clients…
9. start the program and make sure every details
are covered prior to launch
10. evaluate results (surveys) and make
appropriate changes as time go by
2006 World Congress WSAVA/FECAVA/CSAVA
505
Ip

2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

NN
Nursing
ursin

Back to contents

INVITED LECTURES - FULL PAPERS
N - Nursing
KEEPING THE CLIENT INFORMED: THE MANAGEMENT OF THE
SURGICAL CASE FROM ADMISSION TO DISCHARGE
Ray Butcher MA Vet MB
MRCVS
The Wylie Veterinary Centre
UK
ray.butcher31@tiscali.co.uk
Introduction
Throughout the world we are faced with the same
type of clinical cases, which respond to similar
therapeutic options. However, as a veterinary
clinic we are also a service provider and the way
we organise our clinic and staff will reflect local
economic and cultural differences.
For the sake of this presentation I will presume
that we are trying to offer a good quality service
for which the client will hopefully pay extra.
The clinic team
I will also assume that the clinic works as a team
involving vets, nurses and receptionists. Each
group has an important role to play and each
group requires special qualities. Nurses are key
members of the team in their own right – they are
not mini – vets, nor indeed do vets make good
nurses.
The hospitalised surgical case
However routine the procedure, we must
remember that this is a very stressful time for
the owner. We all have a fear of the unknown,
and so the owner’s stress can be reduced by good
communication. Nurses have an important role
here.
Back to contents
N
The stages involved in the management of the
surgical case are:
• Booking the procedure
• Sending information sheets prior to admission
• Admission to the clinic
• The clinical procedure
• Aftercare
• In-patient enquiries (by telephone)
• In-patient enquiries (in person)
• Discharge of the patient
Each of these stages will be considered. Each
offers an opportunity for the nurse to communicate
to the client in a way that enhances the service
to the client. We should all aim to have happy
clients that have confidence in the quality of the
service provided.
Building client confidence
Each interaction of the client with the clinic staff
is an opportunity to develop the clinic/client
bond. However, true confidence is something that
is cumulative and built up over time. Therefore
events such as open days, open evenings or puppy 2006 World Congress WSAVA/FECAVA/CSAVA
parties are important to encourage bonding and
form a basis on which further trust can be built.
Nurses, too, have a role to play in such events.
507
N
N - Nursing
NUTRITIONAL SUPPORT OF THE SURGICAL PATIENT - THE NEED
TO FEED
Dr. Terry Lake
Animal Health Technology,
Thompson Rivers University
Kamloops, Canada
tlake@tru.ca
“The need to feed” is becoming a well-known term
in veterinary practice these days as we recognize
that hospitalized patients do far better with proper
nutritional support. This is particularly true for
patients undergoing surgery in which tissue repair
and resistance to infection are paramount.
Tissue synthesis and wound healing depend on
local and whole body nutrition. Amino acids
and carbohydrates are needed for collagen and
ground substance synthesis while fibroblasts
require energy to synthesize RNA, DNA and
ATP necessary for proteins. The liver and bone
marrow require energy and protein for glucose,
complement, platelet, leukocyte and monocyte
production. Studies show that post operative
patients that are fed demonstrate a much higher
rate of protein synthesis versus protein degradation
while those that are not fed demonstrate higher
protein degradation.
The immune system is particularly susceptible
to the effects of poor nutrition and post surgical
patients depend on a healthy immune system to
ward off infection. In people, decreased protein-
calorie intake is the most common cause of
secondary immunodeficiency and animals are
2006 World Congress WSAVA/FECAVA/CSAVA
likely similar.
There are other factors that make adequate
nutrition following surgery even more critical
and these are in response to the injury itself.
Following trauma, metabolic and physiologic
changes occur in response to the release of
catecholamines, adrenocorticoids, glucagon,
and a number of other hormones associated with
the “fight or flight” response. The result of this
hormonal hurricane is:
• Suppression of insulin secretion
• Hyperglycemia
• Increased proteolysis
• Increased cardiac output
This metabolic alteration must be met with a
nutritional plan that matches the needs of the
body.
508
Back to contents
Nutritional needs
The resting energy requirement of a non-fasted
patient in a cage in a thermoneutral environment
can be calculated using the formula RER = 70 +
+ (30 x Body weight). For a 20 Kg dog this would
be 670 kcal. For patients recovering from surgery
or other trauma the RER should be multiplied by
1.25 or in the case of our 20 Kg dog this would
mean feeding about 840 kcal per day.
Once the number of calories is determined we
must ensure the correct balance of nutrients is
present to maximize healing and prevent problems
associated with the patient’s stress response. We
have seen that protein requirements are increased
due to the rate of tissue and immune component
synthesis that must take place. This protein
must be of high quality so that it is biologically
available to the patient.
Since surgical patients often will not eat as
much as normal, the food must be calorie
dense. Fat can provide 2.5 times the energy
of protein or carbohydrate and unless there are
contraindications such as pancreatic disease, fat
should be utilized as an energy source. Vitamins,
particularly B vitamins, are critical to liver
function and can be supplemented in IV fluids as
well as delivered in the diet. Most pet foods will
deliver enough vitamins and minerals providing
the patient is receiving adequate quantities of
food.
How to feed
Many non-injured patients do not eat well in the
hospital so those recovering from surgery may
be even more challenging due to factors such as
anesthetic effects and pain. Proper attention to
analgesia and comfort will make your patients
more likely to regain their appetite. Depending
on the type of surgery, in most cases you will
want to start feeding your patients as soon as the
noticeable effects of anesthesia have worn off. It
is best to select a food with high palatability and
it may be necessary to warm the food above room

temperature to increase its attractiveness. Hand
feeding may be required in some cases combined
with some tender loving care (TLC). This seems
to be particularly important with cats who we all
know can be extremely finicky when it comes to
food.
If the patient does not respond within 24 hours
of surgery it is time to consider some assisted
feeding techniques which can range from simple
to quite complicated. Some pharmacological
agents will increase appetite in cats and can
be tried before physical intervention. These
include cyprohepatadine (2-4 mg per cat) and
diazepam(dosage varies).
Forced feeding involves using a syringe to place
a semi-solid food into the pharyngeal area to
stimulate the swallowing reflex. This can be met
with resistance and care must be taken to avoid
injury to the patient or the nurse. In dogs, it is best
to place the syringe between the cheek and the
molars with the head held in a normal position.
For cats the syringe is placed between the four
canine teeth. Some animals will refuse to swallow
a bolus of food and you must be careful not to be
too aggressive or aspiration may result.
The next level of intervention is the use of an
orogastric tube and should only be used on
cooperative patients that require such feeding
for 2-3 days. A lubricated soft rubber tube is pre-
measured to the ninth rib and introduced gently
with the head held in the normal position. Once
the patient swallows, pass the tube to the pre-
measured mark and instill some sterile water to
ensure proper placement before feeding. There
are some mouth gags designed to prevent the
patient from chewing on the tube.
For patients that require assisted feeding for a
prolonged period it is best to place a fixed feeding
tube as this will reduce the stress on the patient
and ensure proper delivery.
Nasoesophageal tubes
Nasoesophageal tubes can be left in place for
prolonged periods of time (usually 1-2 weeks) and
are generally well tolerated if properly inserted.
As noted by the term, these tubes are best placed
in the distal esophagus rather than the stomach to
prevent reflux. A number of different tube types
can be used and vary in size from 5-Fr for cats
to 8-Fr for most dogs. These tubes can be placed
without anesthesia or sedation (in most cases)
and are thus preferable for patients considered
anesthetic risks. After some drops of local
anesthesia, the tube is directed ventromedially
Back to contents
N
to avoid the ethmoturbinate bones and advanced
to the pre-measured mark once the swallowing
reflex is initiated. Sterile water should be used to
ensure proper placement and the tube can be fixed
to the skin with a couple of sutures or tissue glue
followed by a protective buster collar.
Pharyngostomy/esophagostomy tubes
For patients with oral trauma or for those that
need a longer term of tube placement (weeks
to months), pharyngosotomy or esophagostomy
tubes can be used. These procedures require
anesthetic and complications include infection,
hemorrhage and aspiration. Owners can maintain
these tubes at home and due to their larger size
(8-16 Fr) they can tolerate a wider range of food
types than nasogastric tubes.
Gastrostomy tubes
Gastrostomy tubes have become more popular
for enteral feeding now that different placement
techniques have been developed. The most
common method employs an endoscope but there
are blind methods that can be used and special
kits that make this much easier. Food is placed
directly into the stomach and as in the other tube
techniques, the patient is able to eat on its own if
it desires.
What to feed
As mentioned previously, a patient recovering
from surgery requires protein and calories at
a higher level than its normal resting energy
requirement. This can be supplied in many forms
but the easiest way is to use one of the many
veterinary critical care diets available. Hills
Prescription Diet a/d is a syringable diet high
in fat, low in carbohydrate (to combat insulin
resistance) and high in omega fatty acids, amino
acids and glutamine. The diet is very palatable
and well received by many patients. There are
several other veterinary diets available and home
2006 World Congress WSAVA/FECAVA/CSAVA
made diets can also be formulated.
It is important to remember that some patients,
especially cats, may develop food aversions.
When forced to eat a food when in pain or
unwell, the patient may refuse to eat the same
food once forced feeding is discontinued. Always
offer other alternatives so that the patient can
resume eating on its own as soon as possible. It is
important to remember that a successful surgical
outcome depends heavily on post operative care
and nutrition is one of the key components.
509
N
N - Nursing
THE TPLO TECHNIQUE AND PHYSIOTHERAPY OF CRUCIATE
INJURIES
Dr. Terry Lake
Animal Health Technology,
Thompson Rivers University
Kamloops, Canada
tlake@tru.ca

The cranial cruciate ligament (CCL) is a critical

stabilizing structure in the canine stifle joint
and rupture of this ligament is one of the most
common orthopedic injuries in large breed dogs.
The CCL (number 4 on diagram) counters the
tendency of the tibia to move forward (tibial
thrust). Unlike humans, dogs walk on their toes
with their heel elevated off of the ground and
their knee bent forward. These results in forces
applied down through the femur to the tibial
plateau which is sloped backwards. If the slope
is too great the CCL is put under too much stress
and can rupture, either partially or fully, resulting
in lameness.

For many years various techniques were

devised to repair the CCL and stabilize the other
structures around the stifle joint. While many
have been successful, results have not always
been satisfactory. The Tibial Plateau Levelling
Osteotomy (TPLO) was devised by Dr. Barclay
Slocum in 1993 and has grown in popularity in
the last few years. Unlike traditional approaches
to cruciate rupture, the TPLO does not rely
on repair of the ligament but instead relies
2006 World Congress WSAVA/FECAVA/CSAVA

upon correcting the slope of the tibial plateau.

This prevents the femur from sliding down
the plateau and tibial thrust is eliminated. The
technique involves a curved cut in the tibia
and reattachment with a special plate after
forward rotation thus reducing the angle of the
tibial slope. The “drawer sign”, the movement
of the tibia in a cranial direction noted after
cruciate rupture, is still present after the TPLO
technique and is not a sign of failure. The
TPLO was patented by Dr. Slocum and initially
only available to those who were accredited to
perform the procedure. This patent has expired
leading to more widespread use of the technique
but it does require specialized training and
equipment.

510
Back to contents

Recovery from CCL surgery
The recovery from CCL surgery is similar with
all techniques but veterinarians can be notorious
for failing to impress upon owners the importance
of the recovery phase. While designing a
rehabilitation program, remember the importance
of nutrition following any kind of surgery. The
goals of the rehabilitation program are:
1. Reduce swelling
2. Regain functional control of motion in hip,
stifle and hock
3. Encourage early controlled weight bearing
4. Increase muscle strength to aid in joint
stability
5. Prevent re-injury
During the rehabilitation the dog should not be
allowed to jump onto or off of furniture, in or out
of vehicles, run, play roughly, climb stairs, and
precautions must be taken against slipping.
Day 1-10
Ice the area for 10-15 minutes 2-3 times a day.
For the first three days use only ice. After three
days, heat can be alternated with ice but always
start and end with ice.
Begin passive range of motion (ROM) exercises
gently gliding the limb. This involves flexing and
extending the hip, stifle and hock. Some muscle
massage is also helpful.
Short, very controlled leash walks on a flat
surface with good traction for five minutes 3-4
times a day.
Day 10 to week 4
Continue ROM exercises and increase walks to
10 minutes but remain on flat ground with good
traction.
Back to contents
N
Begin static weight bearing exercises for 3-5
seconds at a time. These include offering a treat
from the opposite hip, lifting the sound leg,
lifting the sound leg and the opposite front leg,
and rocking forward, back, and side to side.
Week 4-6
Increase leash walks to 15-20 minutes and add
very small hills. Increase weight bearing exercises
to 10 seconds and add chest raises.
Week 6-8
Increase leash walks to 25 minutes and add
moderate inclines. Lead the dog in figure eight
patterns and add some low barriers to walk over.
Swimming can be started.
Week 8-12
Start to increase active exercises including
walking in circles in both directions and climbing
small staircases (5-6 stairs). Start slow jogging
but always on a leash.
Each patient will progress at its own rate but
pushing too hard or failing to properly supervise
the dog may result in breakdown of the surgical
repair or at the very least, increase the recovery
time.
There are more and more veterinary nurses
learning about physiotherapy and also many
human physiotherapists taking an active interest
in veterinary patients. It is important to remember
that the success of the surgical repair is often
determin
ed by the post operative care.
2006 World Congress WSAVA/FECAVA/CSAVA
511
N
N - Nursing
FLUID THERAPY IN HOSPITAL PATIENTS (TRAUMA MODEL)
Luis H. Tello. DVM, MS
Clinica Veterinaria Las
Condes
Geronimo De Alderete 1567
- Vitacura
Santiago De Chile
ltello@uchile.cl
Fluid therapy is one of the cornerstones in the
trauma patients. Shock and hemorrhage, fluid
shift from the vascular to the interstitial space,
decreased blood pressure and the organic
peripheral vasoconstriction are the main targets
in the fluid therapy, because all of them are
primarily cause of death in that patients.
Body fluid distribution
The total body water ranges from 55 – 70% of the
lean body weight. In the average adult dog the
total body water is about 60%. Thus in a 15 Kg
dog the total body water will equal about 9 liters.
Total body water is distributed into 2 main
compartments:
A)the intracellular fluid space, and
B)the extracellular fluid space.
About 66% of the total body water reside in
the intracellular fluid space and 33% in the
extracellular fluid space.
The extracellular fluid space is further subdivided
into two fluid containing compartments:
1) the interstitial space (containing 75% of the
extracellular fluid space water) and
2) the intravascular space (containing 25% of the
2006 World Congress WSAVA/FECAVA/CSAVA
extracellular fluid space water).
When water is added to one compartment, it
distributes evenly across the total body water and the
amount of volume added to any given compartment,
is proportional to its fractional representation of the
total body water. Thus, if one liter of free water is
placed in the intravascular space, there will be a
minimal increase in the intravascular volume after
equilibrium takes place. In fact, approximately 30
minutes after rapid volume infusion of free water,
only 1/10th of the volume infused remains in the
intravascular space.
TRAUMA AND BLOOD LOSS
Blood loss is one the most common consequences
in a trauma patients, therefore it is not well
tolerated in the animal. Although loss of 80% of
512
Back to contents
the adrenals and liver, 75% of the kidneys an red
cell mass, and loss of several lobes of lung do
not result in the demise of an animal, loss of 35%
of the blood volume can be fatal. The dangers
of hemorrhage are related to a cardiovascular
system that operated whit a small volume and
steep Frank – Starling curve, (volume sensitive
ventricle) for which the purpose may be to limit
cardiac work and conserve energy.
In a healthy animal, a 15% loss of blood volume
does not require intervention with intravenous
fluids. With a loss of this volume, there is a
three phase compensatory response to mild
hemorrhage:
Phase I.
Within one hour of mild hemorrhage, interstitial
fluid begins to move into the capillaries. This
fluid shift continues for 36 – 40 hours. The egress
of fluid from the interstitial space leaves an
interstitial fluid deficit.
Phase II.
The loss of blood volume activates the renin/
angiotensin/aldosterone system, which promotes
sodium conservation by the kidneys. Because
sodium distributes primarily in the interstitial
space (80% of sodium is extravascular), the
retained sodium replenishes the fluid deficit in
the interstitial space. About the PVC, when any
plasma expander, including cristalloids, is infused.
a immediate fall in PVC can be expected. As the
intravenous resuscitation fluids redistribute, the
PVC again rises.
Total serum protein shows similar changes
to PVC. Endogenous restoration of depleted
intravascular volume occurs through the
movement of interstitial fluids into the
intravascular space. Catecholamines mediate
arteriolar vasoconstriction which diminishes
capillary bed hydrostatic pressure favoring influx
of interstitial fluid into the vascular tree distal
to the arteriolar constriction. Subsequently, the

lymphatic flow pattern returns the plasma proteins
to the intravascular space. Increases in interstitial
pressures caused by crystalloid distribution into
the interstitial space may augment lymphatic
flow thus the “protein - refill” mechanism.
This process combined with increased albumin
synthesis and spontaneous diuresis secondary
to volume repletion explains the return of serum
protein levels after crystalloid resuscitation.
Phase III.
Within a few hours after mild hemorrhage, the
bone marrow begins to increase production of
erythrocytes. Unfortunately, their replacement
is slow with only 15 - 20 ml of cell volume
being produced daily and complete replacement
requiring a couple of months.
CRYSTALLOID FLUIDS FOR
RESUSCITATION
Crystalloid fluids are mixtures of sodium chloride
and other physiologically active solutes. They are
generally isotonic with plasma and have sodium
as their major osmotically active particle. The
Table I. Electrolyte concentrations of crystalloid solutions
Plasma 0.9% Saline
Na 145 154
Cl 103 154
K 4-5 - 4
Ca/Mg 3/0
Buffer HCO3 (22) - Lactate (28)
pH 7.4 5.7
Osmolality 290 308
(mOsm/Kg)
HYPERTONIC CRYSTALLOIDS
The use of concentrate crystalloid solutions is
appealing because of the reduced volumes of
fluid required, decreasing the risks of pulmonary
edema and the need for specialized equipment for
delivery of very large volumes of fluids.
Hypertonic saline (1.7%, 3%, 5%, 7.5%) is
used in hypovolemic and traumatic shock with
or without hyperoncotic substances. Adding the
hyperoncotic solutions, the duration of effect is
prolonged over their very short action. These
solutions are effective and provide prompt
volume expansion with significantly less volume
than necessary with conventional crystalloids.
Additionally, a decrease in the intracranial
Back to contents
N
distribution of sodium determines the distribution
of infused crystalloid fluids. Sodium is the major
solute in the extravascular space and 75% of the
extracellular space is extravascular. Therefore,
infused sodium will reside primarily outside the
vascular compartment.
During phase I there is an interstitial fluid deficit
which needs to be replaced during early fluid
therapy. In fact, the goal of fluid therapy for mild
hemorrhage is to fill the interstitial space, not the
vascular space. This is the rationale for using
crystalloid (sodium - containing) fluids for the
resuscitation of mild hemorrhage.
Sodium - containing fluids are well suited for
the replacement of extracellular fluid losses
(dehydration) and for replacement of blood
volume. Their use is directed to replacement of the
interstitial fluid deficits seen in hemorrhage. The
significance of the deficit has been questioned.
Nevertheless, crystalloid solutions have proven
to be effective in the resuscitation of animals with
acute hemorrhage and they continue to be popular
resuscitation fluids for trauma victims.
Ringer’s Lactate Normasol - R
130 140
109 98
5
0/3
Acetate (27)
Gluconate (23)
6.7 7.4
273 295
2006 World Congress WSAVA/FECAVA/CSAVA
pressure has been observed in trauma patients.
Experimental studies show hypertonic saline
solutions will improve microcirculatory flow,
possibly by reducing shock - induced endothelial
swelling. With endotoxic shock models,
hypertonic saline is more effective than isotonic
crystalloids in proving cardiac output and oxygen
transport but only very transiently. In another
study no benefit was seen. Controlled trials in
human beings nor veterinary medicine are not
available.
The major drawback of hypertonic saline
resuscitation is the very short duration of response.
Combining hypertonic saline with something like
6% dexytran - 70 will prolong the response. Other
513
N
concerns regarding the use of hypertonic saline
include producing a hypertonic state, the prompt
movement of sodium to the interstitial space, the
water shifts from the interstitium and intracellular
space, and the potential for a rebound interstitial
edema.
COLLOID FLUIDS
Colloids are large molecular weight substances
that do not readily pass across capillary walls.
The particles retained in the vascular space will
exert an osmotic force that keeps fluid in the
blood vessels.
Hypovolemia represents the most life - threatening
aspect of acute hemorrhage. Because colloids are
more effective than crystalloids for increasing
vascular volume, colloid resuscitation should be
more useful with severe bleeding.
COLLOID OR CRISTALLOID
A recent review of 8 randomized (human)
clinical trials comparing the effects of colloid
versus crystalloid solutions on survival showed
a 5.7% relative difference in mortality in favor of
crystalloid therapy. However, a 12.3% difference
in mortality rate was found in trauma patients in
favor of colloids. The confidence intervals for
these studies were large and one must question
whether the studies were appropriately assigned
to trauma or no trauma groups.
Head trauma with hemorrhage is one of the severe
restrictions in the use of colloids by the risk to
colloids leaving the vascular can draw additional
fluid to the area, worsening the cerebral edema
and total cerebral contain of water.
In a more recent analysis of these trials the pooled
date demonstrated a 13.4% mortality rate for
crystalloid - treated human patients and a 21,25%
mortality rate for colloid - treated patients (not
statistically significant at a p= 0.01 level). In
this same study, when the trials were subdivided
2006 World Congress WSAVA/FECAVA/CSAVA
into the apparent severity of the underlying
processes, again no statistically significant
difference was noted between the two treatment
groups, although there was a tendency to a higher
mortality in colloid - treated patients with more
severe illness.
Although mortality is but one factor in assessing
colloids versus crystalloids, the following
recommendations have been made:
- Prompt and adequate fluid therapy is the
mainstay of treatment of septic shock
- Colloid and crystalloid fluids lower hemoglobin
concentration, oxygen carrying capacity and
whole blood viscosity. The optimum hematocrit
in septic shock has not been defined but a value
of 30 - 35% seem acceptable
- The choice of fluid should take into account its
514
Back to contents
effect on plasma oncotic pressure (COP). Severe
decreases in COP should be avoided
- Volume treatment should be individualized and
titrated to individual needs
HEMODYNAMIC EFFICACY IN TRAUMA
PATIENTS
There is no doubt that both, crystalloids and
colloids will adequately resuscitate shock patients.
With crystalloids the amount of fluid necessary
to reach the same hemodynamic endpoint is
usually 2 - 4 times higher with crystalloids than
with colloids. This results in significant changes
in body weight and induces the risk of systemic
edema.
There is convincing evidence that colloid
- containing fluids act more promptly than
crystalloid solutions in restoring hemodynamic
stability. In a study of 600 hypotensive human
patients, the mean resuscitation time was shorter
with colloids. a similar finding in traumatized
humans showed for a given volume of fluids
infused, colloid solutions expand the plasma
volume to a greater extent than crystalloid
solutions.
Hemodynamic and oxygen transport variables
with colloids are more pronounced than with
crystalloids. In a study of postoperative patients,
plasma volumes before and after infusion of 1L
of colloid, shows the advantage clearly to the
colloids.
PULMONARY FUNCTION
One of the core issues in the colloid - crystalloid
controversy is the potential difference of inducing
pulmonary edema with these fluids. Infusion
of crystalloids does result in a significant and
prolonged decline in serum albumin concentration
and colloid oncotic pressure (COP). Colloids
maintain or even increase COP. A low COP can
promote the development of pulmonary edema
microvascular hydrostatic pressure increases
above normal. However, increases in hydrostatic
pressure are more likely to result in pulmonary
edema than comparable decreases in COP.
Therefore, hydrostatic pressure is more important
in fluid exchange in the lung than COP.
Colloid advocates have long argued that
crystalloids alone, dilute the plasma proteins,
thereby reducing plasma COP, and thus sets the
stage for development of pulmonary edema. On
the other hand, colloids by maintaining plasma
oncotic pressure, could aid in the retention of
fluid in the intravascular compartment and limit
the magnitude of edema formation, even in
presence of permeability defect. Colloid infusion
then could promote a transmicrovascular fluid
composed of colloid resulting in an almost

parallel increase in intra - and - extravascular
COP, thereby worsening the severity of edema.
Experimental studies in models with increased
pulmonary have yielded conflicting results.
The IV is the preferred way to deliver fluid in
trauma patients. Short large catheter, 18 – 20
gauge for small dogs and cats and 14 – 16 g for
dogs with 10 Kg or more.
The classic rate of 90 ml/Kg/hour, could be no
Back to contents
N
good for many trauma patients due to the fact of
endothelial damage, cardiovascular compromise
and hemorrhage, so frequent small volumes looks
work better in that patients.
Blood substitute call Oxyglobin® should provide
advantages to animals with reduced oxygen
carrying capacity, but not many trials has been
evaluated.
2006 World Congress WSAVA/FECAVA/CSAVA
515
N
N - Nursing
FELINE AS IN HOSPITAL PATIENT: TRAUMA MODEL
Luis H. Tello. DVM, MS
Clinica Veterinaria Las Condes
Geronimo De Alderete 1567 - Vitacura
Santiago De Chile
ltello@uchile.cl
Many people think that domestic feline cat, are
really a home “introduced” species. Cats have
independent, mysterious and unpredictable
personalities, but this is not the only way that
cats are unique. Their response to disease and
medical therapy represents a challenge in the
veterinary medicine practice, making clear the
famous sentence: “cat is not a dog in emergency
or critical care”
Despite the fact that dogs and cats have the same
clinical entities in emergency, they frequently do
not show the same symptoms and clinical signs.
Cats are very sensitive to hypotension and they
are very difficult to resuscitate from hypotensive
shock. The response to hypotension in cats is very
different because they have vagal fibers close to
sympathetic fibers and hypotension can stimulate
both, showing a normal or slow heart rate, instead
of the tachycardia showed by other species like
dogs. In a research with hypotensive cats (blood
pressure less than 80 mmHg systolic), 100% of
cats were found to have normal or slow heart rates.
As cardiac output is the result of contractility and
rate, the fact of have normal or slow cardiac rate,
diminish the cat patient compensatory response
to shock, aimed at the goal of maintaining oxygen
delivery to the tissues and hemodynamic stability
2006 World Congress WSAVA/FECAVA/CSAVA
like blood pressure and capillary blood flow.
The hyperdynamic signs of shock, commonly seen
in dogs are rarely seen in the cat. Shock in the cat
is most commonly decompensatory, evidence by
normal or slow heart rate, severe hypothermia, weak
or non palpable peripheral pulses and profound
mental depression. The mucous membranes are
gray or white and capillary refill is not evident.
The bradycardia and low cardiac output leads to
hypothermia, and hypothermia accentuates the
bradycardia. There are many aspects of critical
care that are unique for the cat.
Organic response
The very unique physiology of the domestic
cat patient, facing a trauma episode deserve
special consideration. Is well known that the
516
Back to contents
magnitude of the inflammatory response to
trauma is directly proportional to the exchange
of energy and the extent of injury. Cat suffering
severe multiple trauma is at much higher risk
for the development of a significant systemic
inflammatory response, any trauma will incite
the same series of events, including the release
of many different inflammatory mediators.
In the dog, in cases of massive bleeding,
sympathetic response leads to splenic
contraction, releasing of up to 30% of their
volume but in cats the spleen does not react in
the same way.
Shock due to trauma results when organic
response is no longer able to compensate,
leading to maldistribution of blood and
impairment of oxygen delivery. The response to
a traumatic insult also involves the production
of acute phase proteins by the liver like Protein
C and many others cytokines who are involved
in control the inflammatory response, inhibiting
enzymes and modulating coagulation. Feline
endothelium cells has a very important role in
modifying and regulating the body’s response
to injury and is particularly susceptible to
hypoxic injury.
The increased nutritional demands plus a
generalized catabolic state can quickly lead
to negative balance of nitrogen, leading the
patient to malnutrition, that is very important
in cats, as they are at a higher risk for hepatic
lipidosis and more likely to refuse to eat in a
hospital environment.
Tissue hypoxia causes an increase in
intracellular calcium that is cytotoxic, impairs
inmmune celular function, and begin the
production and release of oxygen-free radicals.
In severe case of trauma with a massive
inflammatory response, endothelial disruption
activates the coagulation cascade resulting
in a procoagulant status in the feline trauma
patient. However, Disseminated Intravascular
Coagulation is a very rare syndrome in cats
compare with traumatized dogs.

Approach to the feline trauma patient
The goal of treatment in feline trauma patients
is the same as any critically ill patient: Optimize
perfusion and oxygen delivery to the tissues.
The initial approach should be focused on
major body systems examination, with specail
atention to respiratory and cardiovascular
systems. Stabilization should begin with the
classic ABC: Airway, Breathing, Circulation (or
Cardiovascular). Extra attention should be paid
to the neurologic and renal systems as damage
are common in cats and both can result in life
threatening injuries.
Treatment goal in the feline trauma patient is to
maximize oxygen delivery. The oxygen content in
the blood is a significant determinant of oxygen
delivery. Many sequelae of trauma in the cat
can lead to pulmonary complications that result
in decreased hemoglobin saturation as well as
decreased PaO2.
The initial assessment of the respiratory system
should begin with observation of the cat avoiding
any stress during handling. Evaluation of the
rate, effort and pattern of breathing prior to
any additional stress is important. Panting cat
means the possibility of severe respiratory tract
condition. Always supplemental oxygen should
be provided in a traumatized cat.
Airway is commonly affected by traumatic
injuries in cats. Jaw fractures, skull fractures
are commonly seen in vehicle accidents, while
tracheal avulsion, or direct injury to the laryngeal/
pharyngeal area are common in dogs-cats or cat-
cat fights. If the airway is not patent, tracheostomy
should be considered.
Physical exam and auscultation may reveal
clinical evidence of pulmonary contusions,
pneumothorax or hemothorax. If pleural space
conditions needs to be rule out, do no lead the
patient for radiographs, thoracocentesis should be
performed. In the author experience complications
are rare when is done correctly.
Assessment of pulmonary function by arterial
blood gas analysis is not common in practice,
but another methods like pulse oximetry is
more doable. However, this test can lead to
numerous mistakes and care must be taken in the
interpretation of the results. Hypothermia, very
common in the post trauma cats, poor capillary
perfusion, anemia, movement and pigmented
mucosa can lead to inaccurate results.
Thoracic radiographs should be delay until cat
is stable. Pulmonary contusions, rib fractures,
diaphragmatic hernia, as well as pleural space
disease can be diagnosed by X ray examination,
but also stress of restraint can be life threatening
in an unstable cat. Many thoracic injuries are
commonly seen in the trauma cat: penetrating chest
Back to contents
N
wounds, hemothorax, pneumothorax, pulmonary
contusions and tension pneumothorax.
Cat lungs are very sensitive to hypoxemia due
to poor perfusion, leading to increased capillary
leak and inflammatory lung disease secondary
to severe trauma, so much attention should be
paid to the respiratory status of any cat after any
significant trauma, even in cases where there was
no direct thoracic trauma.
Cardiac output is another important determinant
of oxygen delivery, and is commonly diminished
in the trauma patient. Hemorrhage, arrhythmias,
direct cardiac injury and myocardial dysfunction
can all lead to impairment of adequate cardiac
output. Initial evaluation includes assessment of
heart rate and rhythm, mucous membrane color,
capillary refill time, pulse rate and pulse quality.
Assessment of blood pressure can be difficult
in cats. Direct blood pressure is not common
in practice: excessive handling, pain, need to
anesthesia or sedation, and side effects are the main
reason. Indirect determination of arterial blood
pressure can be done by doppler measurement,
but studies done in healthy cats have shown that
these measurements underestimate the systolic
blood pressure. However there are no studies
about the accuracy of doppler measurements in
sick cats.
The cardiovascular response to poor tissue
perfusion and impaired oxygen delivery in the
dog is tachycardia, but this is not the case in cat
patients, where low heart rates are common in
critical care cats.
This response seems to be unique to the feline
species, and still there is no explanation about the
mechanism. Theory goes to cytokine-associated
myocardial depression which may play a role.
Hypothermia which is very common in critically
ill cats has been suggested as responsible for the
bradycardia, but no research has demonstrate a
correlation.
Cardiac arrhythmias should be investigate in
2006 World Congress WSAVA/FECAVA/CSAVA
any trauma injured cat with evidence of poor
tissue perfusion (tachycardia or bradycardia, pale
mucous membranes, prolonged capillary refill
time, weak pulses) by regular ECG assessment.
Treatment begins with fluid administration,
always starting with isotonic crystalloids. In
cats, bolus of 30-50 ml/kg of crystalloids plus
5-10 ml/kg of colloids. Care should be taken
when administering fluids to injures cats as
fluid overload is common: pulmonary edema
and pleural effusion are common in this patient
population. Cats on inflammatory conditions
has increased vascular permeability, myocardial
dysfunction and decreased colloid oncotic
pressure due to hypoalbuminemia.
It is recommended start with small boluses of
517
N
10 – 20 ml/kg and monitor the effect of this
volume like blood pressure normalization No
matter is the cat patient is hypothermic, always
warm fluids before the administration. Therefore
external warming should be used with air heating,
circulating water blankets, or incubator. Always
monitore temperature
Consider that may be possible that cats have a
previous anemia (FeLV - FIV infections) leading
to low hemoglobin, decrease oxygen delivery and
add the consideration of decreased ability of the
feline spleen to contract, if so, blood transfusion
should be administered. But remember that cats
can have naturally occurring antibodies, leading
to transfusion reactions, even in those cats that
never previously received a blood transfusion.
Neurologic damage in the trauma patient can
occur through direct trauma to the brain tissue or
secondary to hypoxic tissue damage from poor
perfusion to the CNS. A complete neurologic
evaluation should be done after initial resuscitation
to determine any necessary therapeutics and
establish a baseline for further monitoring.
Additional details on therapy for patients with
head trauma will be discussed below.
In general, maintenance of adequate perfusion
to the CNS is imperative in both treating and
preventing neurologic damage. Renal Signs of
damage to the renal system are often not evident
on initial presentation of the trauma patient.
These manifestations may not be detected for
several hours and require close monitoring after
the traumatic incident. Abnormalities such as an
uroabdomen, uroretroperitoneum, direct renal
trauma or urethral damage can be life threatening.
Close monitoring of the urine output, BUN,
creatinine and potassium should be done in any
cat in which renal system damage is suspected.
2006 World Congress WSAVA/FECAVA/CSAVA
518
Back to contents
Additional diagnostics such as abdominal
radiographs, abdominal ultrasound or intravenous
contrast studies may be necessary in some cats.
Neurologic trauma considerations
Head trauma is commonly seen in cats vehicle
accident or cats falling due to high rise syndrome.
The primary goal in the treatment of head trauma
is optimizing tissue perfusion and maintaining
cerebral perfusion pressure (CPP). Supplemental
oxygen, elevation of the head 30º, avoidance of
any neck twist position or occlusion of the jugular
veins should be insured.
The goal of maintain CPP is made by strict control
on mean arterial blood pressure and intracranial
pressure. Keep an eye on mean arterial pressure is
imperative in these cats, and aggressive treatment
for any intracranial hypertension is necessary. A
well discussed issue in hypotensive head trauma
cats is using hypertonic saline at a dose of 3 – 5
ml/kg. Still there is no clear information about it,
but some evidence show that hypertonic fluids
improves intravascular volume and helps decrease
intracranial pressure. If there is clinical evidence
suggesting cerebral edema and increased ICP,
mannitol at 0.5 – 1 g/kg iv should be given over
30 – 60 minutes.
Nursery
After first aid and stabilization and assessment of
the major body systems, additional considerations
include clipping, flushing and cleaning of any
wounds as well as stabilization of any fractures
prior to definitive surgery. Evaluation of the oral
cavity for any fractures, dislocations or pain is
important in the cat, as any trauma that may lead
to anorexia must be addressed.
Back to contents
N

2006 World Congress WSAVA/FECAVA/CSAVA

519
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Ne
Noegy
Neurology
eurol

Back to contents

INVITED LECTURES - FULL PAPERS
Ne - Neurology
FELINE NEU ROMUSCULAR DISORDERS
Richard A. LeCouteur, BVSc,
PhD, Diplomate ACVIM
(Neurology), Diplomate ECVN
University of Kalifornia
Davis CA 95616
USA
ralecouteur@ucdaviss.edu
Feline neuromuscular diseases may be
classified according to their location as those
involving peripheral nerves and/or nerve roots,
those involving the neuromuscular junction,
and those that involve muscle (1). Each of
these neuromuscular diseases will produce
lower motor neuron (LMN) disease, however
significant variations in clinical signs may occur.
Peripheral nerve and muscle diseases result
in varying degrees of paresis, muscle atrophy,
hyporeflexia, and hypotonia. Hyporeflexia,
hypotonia, ataxia and proprioceptive positioning
deficits are most characteristic of peripheral
nerve disease. Some primary muscle disorders
may be characterised by muscle hypertrophy
rather than atrophy. Neuromuscular junction
disorders (“junctionopathies”) result in a variety
of clinical signs, that range from flaccid paralysis
to exercise-induced weakness.
Cervical ventroflexion is a dramatic sign of
generalised neuromuscular weakness in cats. The
chin usually rests near the thoracic inlet, with the
eyes positioned dorsally to maintain a straight-
ahead gaze. Other common physical examination
findings are a slight protrusion of the dorsal
aspects of the scapulae when weight is placed
on thoracic limbs, and a stiff thoracic limb gait.
A crouched, wide-based stance is often seen in
pelvic limbs.
Megaoesophagus rarely has been reported in
cats, although a predisposition has been noted
in Siamese and Siamese-related breeds. In most
cats the cause of acquired megaoesophagus is
unknown.
NEURONOPATHIES
Feline Dysautonomia: A generalised disorder
of autonomic ganglia. There is no age or breed
predilection for this disease. The disorder is a
Back to contents
Ne
neuronal disorder; however, clinical signs relate
more to autonomic dysfunction, and are largely
gastrointestinal in nature. The most common
signs are depression, anorexia, constipation,
dry external nares and oral mucosa, reduced
tear production, regurgitation, protrusion of the
membrana nictitans, mydriasis, and bradycardia.
Tetanus: The Clostridium tetani exotoxin
interferes with release of neurotransmitters from
inhibitory interneurons in the spinal cord. Local
tetanus has been reported in cats.
Feline Motor Neuron Diseases: A group of
disorders characterized by degeneration and loss
of motor neurons.
INHERITED POLYNEUROPATHIES
Sphingomyelinase-deficiency polyneuropathy’
hyperchylomicronemia-associated neuropathy,
hyperoxaluric peripheral neuropathy,
hypertrophic polyneuropathy, and Birman cat
distal polyneuropathy are examples of inherited
polyneuropathies.
2006 World Congress WSAVA/FECAVA/CSAVA
ACQUIRED POLYNEUROPATHIES
Diabetic Polyneuropathy: A distal polyneuropathy
has been reported in cats with uncontrolled or
poorly controlled diabetes mellitus. Neurological
abnormalities include a plantigrade stance,
progressive paraparesis, muscle atrophy, and
patellar hyporeflexia.
Ischemic Neuromyopathy: Occurs in cats with
cardiomyopathy, subsequent to thrombosis of the
caudal aorta or its principal branches.
Trauma: Brachial plexus avulsion produced by
severe thoracic limb abduction with secondary
stretching or tearing of nerve roots is a commonly
occurring peripheral nerve injury of cats.
Sacroiliac fracture/dislocation, sacral fracture, or
caudal vertebral fracture/luxation may result in
521
Ne
damage to the sixth and seventh lumbar and first
2 sacral nerve roots. Mononeuropathies of radial
nerve and sciatic nerve occur in cats following
mechanical blows, gunshot wounds, fractures,
pressure and stretching.
Neoplasia: Feline malignant lymphoma may
involve nerve roots or peripheral nerves. Other
primary peripheral nerve neoplasms rarely are
seen in cats.
Toxic Neuropathies: Drug-induced neuropathies
are not well defined in cats.
Laryngeal Paralysis: Acute laryngeal paralysis
may be diagnosed in cats with signs of upper
airway obstruction, including dysphonia, absence
of purring, and progressive inspiratory dyspnea.
Miscellaneous Peripheral Polyneuropathies:
Single case reports exist of a variety of
peripheral neuropathies in cats. These include:
inflammatory polyneuropathy (a chronic relapsing
polyradiculoneuritis) and an acute polyneuritis,
an idiopathic chronic relapsing polyneuropathy
responsive to immunosuppressive glucocorticoid
therapy, and an acute brachial plexus neuropathy
with a suspected relationship to a previous
vaccination.
“JUNCTIONOPATHIES”
Myasthenia Gravis: Myasthenia gravis is a
condition that results from either an inherited or
an acquired reduction of acetylcholine receptors
of neuromuscular junctions. The most consistent
signs in cats include tremors, initial stiffness with
progression to generalised weakness on exercise,
cervical ventroflexion, dysphagia, dysphonia,
ptyalism, facial weakness, and dyspnea. Overt
megaesophagus or esophageal hypomotility are
common.
Miscellaneous “Junctionopathies”: Abnormalities
in neuromuscular junction function also may
result from tick paralysis, administration of certain
drugs, selected toxins, or from envenomation.
2006 World Congress WSAVA/FECAVA/CSAVA
Botulism has not been reported as a clinical
entity in cats, however, it may be produced
experimentally in cats.
INHERITED MYOPATHIES
Muscular Dystrophy: Muscular dystrophy-like
disorders of cats have been. Clinical signs may
first be seen in cats at 5-6 months of age, and
include generalised skeletal muscle hypertrophy,
522
Back to contents
excessive salivation, reduced exercise tolerance,
stiff gait and “bunny-hopping” when running,
difficulty in jumping, adducted hocks, cervical
rigidity, vomiting/regurgitation, and partial
protrusion of the tongue.
Miscellaneous Inherited Myopathies; Myotonia
comgenota, nemaline myopathy, myositis
ossificans, and glycogen storage diseases (or
glycogenoses) have been reported in cats.
ACQUIRED MYOPATHIES
Infectious Polymyositis: Infectious myositis may
occur in association with bacterial infection,
migrating parasites, or protozoan disease.
Polymyositis: Polymyositis occurs sporadically in
cats, occasionally in association with thymoma.
Clinical signs are characterised by a persistent
cervical ventroflexion, appendicular weakness,
painful muscles, and exercise intolerance.
Serum levels of creatine kinase and aldolase are
elevated.
Potassium-depletion Polymyopathy: This acute
feline polymyopathy, resulting from a severe total
body potassium depletion, is usually secondary to
a reduced potassium intake and increases in the
fractional excretion of potassium in urine (due to
renal dysfunction). Clinical signs include muscle
weakness, cervical ventroflexion, stiff and stilted
gait, and muscle pain. A similar syndrome with a
suspected hereditary basis has been reported to
occur in Burmese cats.
Miscellaneous Myopathies: There are a number
of case reports of muscle-related diseases of cats
(e.g., nutritional myopathy secondary to vitamin
E deficiency, myositis secondary to Clostridium
chauvoei and Clostridium septicum infections,
fibrotic myopathy of the semitendinosus muscle,
quadriceps contracture secondary to trauma, and
hypernatraemic myopathy).
REFERENCES
1. Dickinson PD, LeCouteur RA. Muscle and
nerve biopsy. Veterinary Clinics of North America
Small Animal Practice 2002; 32: 63-102.
2. Dickinson PD, LeCouteur RA. Feline
Neuromuscular Disorders. Veterinary Clinics
of North America Small Animal Practice 2004;
1307-1360.

Ne - Neurology
USE OF MRI IN THE DIAGNOSIS OF DISC DISEASE IN THE DOG
Simon R. Platt BVM&S
MRCVS Dipl. ACVIM
(Neurology) Dipl. ECVN
RCVS Specialist in
Veterinary Neurology Head
of Neurology / Neurosurgery
Unit
Centre for Small Animal
Studies
The Animal Health Trust
Lanwades Park
Kentford, Newmarket
Suffolk CB8 7UU
England
simon.platt@aht.org.uk
The science behind Magnetic Resonance Imaging
(MRI): The nucleus of an atom must contain
an uneven number of protons in order to be
affected by a magnetic field. The simplest atom
to contain an odd number of protons is hydrogen,
which contains just one proton. Presently, all
clinical applications of MRI utilize the hydrogen
nucleus. Hydrogen protons are abundant in
the body. When located in a random direction,
each proton’s magnetic field will cancel each
other out. However, when a patient is placed in
a magnetic field, the proton becomes orientated
either parallel or anti-parallel to the magnetic
field. Parallel creates a low energy state and
anti-parallel creates a high-energy state. When
stimulated by a pulsation of radiofrequency waves
from a transmitter coil, the protons flip their
orientation 90° and start to rotate or resonate at a
characteristic frequency, the resonant frequency.
The magnetic fields of the resonating protons
induce a voltage in a receiver coil, producing a
signal. Immediately after the pulse, the spin starts
to move out of the transverse position and start
rotating out of phase, causing the signal to decay.
Because the hydrogen protons of various tissues
in the body are held together differently, the rates
of relaxation will be different and characteristic
for that tissue. These differences can then be
measured and exploited to provide tissue contrast
to the image.
The unique advantage of MRI is the ability
to image in different planes. These planes are
defined by using the three-dimensional Cartesian
Coordinate System (x, y & z axes). Generally
the operating factors controlling the appearance
of a regular x-ray or CT (as well as ultrasound
or nuclear medicine) are limited. With MRI,
Back to contents
Ne
however, there are literally hundreds of ways
to perform an exam. Depending on which pulse
sequence is used, tissues will show up as black,
white, and everything in between. For example,
pure water such as CSF will appear black on the
T1 image and white on the T2 image.
T1-Weighted Images: A radio frequency (RF) is
sent in and displaces the longitudinally aligned
proton by 90 degrees in the transverse plane.
When the RF pulse is turned off, the protons will
want to straighten themselves in the longitudinal
direction, where they were in the first place. The
faster they return to their original position aligned
with the main magnet, the stronger the signal and
the brighter the visualized structure. It is crucial
to measure the emitted signal early so as to
differentiate it from those sent out by the various
tissues as eventually the protons will all realign
and show no differentiation. The sampling time
is known as TR and to maximise T1 contrast one 2006 World Congress WSAVA/FECAVA/CSAVA
must use a short TR sampling time.
T2 Weighted images: T2 contrast relates to
transverse magnetization. In addition to the
realignment in the longitudinal plane, turning
off the RF signal results in what is called a
‘dephasing’ in the transverse plane, i.e; while
in the transverse plane when the RF pulse was
on, the protons were all resonating in phase.
When the RF pulse was turned off they started
to dephase at different rates. At this time, a
follow up180° RF pulse is given which puts the
dephasing protons back in phase. As time passes,
these protons again become out of phase and
the signal decreases. Tissues which have a long
T2 remain in phase for a lengthy period of time
and emit a stronger signal. Since all tissues are
initially in phase, maximum T2 contrast can
523
Ne
be obtained by delaying the sampling time in
the transverse plane (a time designated as TE).
Therefore for maximum T2 contrast, a long TE is
desired. If we negate the T1 contrast by using a
long TR and then use a short TE to negate the T2
contrast, we will be left with an image that has a
contrast only different in the proton density. This
image is called the proton density image.
Tissues that have minimal hydrogen protons
(air, bone, and calcification) will have no signal,
and therefore will appear as a signal void or
black. Because the spins of flowing blood do
not stay in a slice long enough to be affected by
the 180° pulse, they rapidly dephase and lose
signal; thus they also appear as a signal void
on spin echo images. Because fats have short
T1 and T2 relaxation times ( ie, they recover
and decay quickly), they will appear relatively
hyperintense with T1 weighting (short TR)
and hypointense with T2 weighting (long TE)
on spin echo images. Because pure liquids such
as CSF have long relaxation times, they appear
hyperintense with T2 weighting and hypointense
with T1 weighting. Impure liquids such as the
brain have intermediate intensity normally, but
have a tendency to become more hyperintense
with T2 weighting and either hypointense or
isointense with T1 weighting when affected by
inflammation or neoplasia.
Contrast Enhancement with MRI: On MR
images, distribution of a paramagnetic agent
(eg, gadolinium-DTPA (Gd-DTPA)) will appear
bright on T1 because of its ability to shorten
the relaxation time of nearby hydrogen protons.
Contrast medium is used to identify blood vessels,
to monitor blood flow, and to enhance lesions and
normal tissue such as the parenchyma of organs.
With brain imaging, contrast medium normally
enhances the meninges and choroid plexus and
the pituitary gland because their capillaries are
fenestrated and permit passive diffusion of contrast
2006 World Congress WSAVA/FECAVA/CSAVA
medium into their interstitium. Contrast medium
does not normally enter the brain parenchyma
because of the blood-brain-barrier. When this
barrier breaks down, substantial leakage of
proteinaceous plasma filtrate into the extracellular
space of the brain from the diseased or damaged
capillaries results in vasogenic oedema. This
oedema migrates along the white matter fire tracts
and usually does not enter the tightly integrated
cortical grey matter. The abnormal signals from
lesions can be differentiated from the vasogenic
fluid that intially saturates the perilesional space
by the process of contrast enhancement. On T1-
weighted images, the Gd-enhanced lesion will
appear hyperintense and may be surrounded by
hypointense perilesional edema.
524
Back to contents
SPINAL MRI
The spatial resolution of MRI generally is not
as good as CT for spinal imaging but the greater
contrast resolution that is provided by MRI ensures
great anatomic detail. This especially pertains
to the structure of the disc and the spinal cord
itself. The image sequencing used determines
the appearance of the normal spine. With
T1-weighted images (T1W), intervertebral discs
are of nearly uniform medium signal intensity,
slightly greater than that of the spinal cord. The
spinal cord and nerve roots are isointense, with
slightly less intensity than the disc. Epidural fat has
a short T1 relaxation time and so is hyperintense
providing great contrast with the surrounding
structures. Cortical bone of the vertebrae appears
as a black shell in all imaging sequences owing
to its relative lack of hydrogen. It is difficult to
define the longitudinal and interarcuate ligaments
except over the disc spaces.
On T2-weighted (T2W), normal intervertebral
discs are characterized by a high-signal central
area surrounded by a medium-signal area. This
is due to the varying content of ground substance
within the structure of the disc. The ground
substance is composed of hyaluronic acid and
glycosaminoglycans that have a strong negative
charge therefore attract and hold water. Epidural
fat has medium signal intensity, considerably
lower than that seen on T1W images. Heavily
T2W images show an area of high signal intensity
surrounding the spinal cord, creating a natural
myelogram effect. As with the T1 images, cortical
bone and the ligaments of the spine are of low
signal intensity and cannot be resolved.
Disc Disease
MRI is becoming the imaging modality of choice
for the evaluation of degenerative spinal disease
in centres that have this facility. This is because
MRI has a high sensitivity for the evaluation of
disc degeneration. Most reports in veterinary
medicine are limited to the study of LS disease in
dogs. Disc degeneration is best seen on sagittal
T2W images as partial or complete loss of the
normal high signal within the nucleus pulposus
and inner annular portions of the disc. This again
is due to the variations in the content of ground
substance in the disc (decreased in the dehydrated
degenerative disc). The presence of a normal
signal within a disc on T2W images can help rule
out disc degeneration.
Anatomic detail is best seen on T1W images
because of high signal-to-noise ratio and sharp
contrast between high signal epidural fat.
The intervertebral disc protrusion can be seen
as a dorsal displacement of the disc into the
spinal canal, loss of the normal shape of the

disc and displacement of the epidural fat on
sagittal images. The images can also define a
lateralized disc by virtue of its occlusion of the
intervertebral foramen and its subsequent affect
on the periradicular fat. Transverse images can
be helpful with the assessment of the degree of
narrowing of the vertebral canal by permitting
the visualization of the cross-sectional area of the
vertebral canal.
T1W contrast medium such as gadolinium-DTPA
has two major applications in the evaluation
of degenerative spinal disease. Firstly, the
Back to contents
Ne
differentiation of a lateral disc herniation from
a nerve root tumour, the latter enhancing with
contrast administration. This is only possible if the
images are taken immediately after the contrast
administration as the disc material will contrast
enhance after time. Secondly, the use of contrast
to differentiate recurrent disc herniation from
scar formation at the site of a previous surgery
has been described. A scar will typically enhance
uniformly, whereas herniated disc material will
not do this immediately.
2006 World Congress WSAVA/FECAVA/CSAVA
525
Ne
Ne - Neurology
THE PARALYSED CAT
Dr. Simon. Wheeler BVSc PhD
DiplECVN DiplMgmt FRCVS
Veterinary Neurology LTD
Hertfordshire
UK
Simon.wheeler@mac.com
As all clinicians well know, cats are not just small
dogs! Whereas the basic principles of history
taking, physical examination, neurological
examination etc. apply in both species, the
diseases that lead to neurological signs differ.
Clinicians must be aware of these differences
when approaching a case and discussing
interventions with owners.
SPINE
Tetraparesis and tetraplegia
A cat with neurological deficits in all four
limbs may have a lesion at any of the following
locations:
• intracranial
• cervical spine (C1-C5)
• cervicothoracic spine (C6-T2)
• generalized neuromuscular
• multiple lesions
Differentiation is based on the findings of the
neurological examination.
Paraparesis and paraplegia
There are several conditions that must be
2006 World Congress WSAVA/FECAVA/CSAVA
considered in the acutely paralyzed cat. Trauma,
ischaemic neuromyopathy (aortic embolism) and
neoplasia are the most important. In more chronic
cases, neoplasia and disc-related conditions are
more likely. Disc disease is being recognized
more frequently.
Trauma usually results from road accidents.
Most cases are readily recognized by historical
or physical information, but accurate client
information regarding trauma is relatively less
common in cats than in dogs. Radiography will
confirm the diagnosis. Many cats respond well to
conservative treatment by cage rest or application
of a body cast. Surgical intervention may be
appropriate if there is myelographic evidence of
cord compression, the fracture is unstable or the
cat is in severe pain.
526
Back to contents
Ischaemic neuromyopathy (aortic thromboembolism)
is a common cause of acute paraplegia in cats. Acute
paraplegia, areflexia, absent pain sensation, cold
limbs, absent femoral pulses and swollen painful
gastrocnemius muscles are the most common
features. Affected cats have cold extremities in
the hindlimbs, with cyanotic nail beds and toes
that do not bleed with needle prick. Occasional
cats have signs referable to renal, gastrointestinal
or other dysfunction. Diagnosis is based on
the characteristic clinical signs. Preexisting
cardiomyopathy underlies the thromboembolic
episode, but the presence of a thrombus does not
entirely explain the clinical signs. There appears
to be a failure of collateral circulation because of
release of vasoactive substances from the area of
the thrombus.
Neoplasms of the spinal cord and associated
structures are common in cats. Lymphosarcoma
is the most prevalent; vertebral tumors are rare.
Most cases of spinal lymphosarcoma occur in cats
less than 3 years old, and the progression of the
clinical signs is relatively acute. Thus, neoplasia
must be considered in all cats, regardless of age
or acuteness of signs. Thoracic and lumbar tumors
are most common, causing neurological signs in
the hindlimbs.
Diagnosis of spinal tumors in cats depends largely
on myelography. Plain radiographic abnormalities
are unusual. Occasional tumors involve the
vertebrae. In some cases of lymphosarcoma, a
soft tissue mass is visible in the thorax, ventral
to the area of the spine involved. Cerebrospinal
fluid may be abnormal but is unlikely to provide
definitive information. In spinal lymphosarcoma,
systemic signs are usually not apparent, but the
vast majority of these cats are FeLV-positive.
Disc disease and discospondylitis - disc protrusions
occur frequently in cats, but clinical signs related
to spinal cord compression are comparatively rare.
Cats with myelographic evidence of spinal cord
compression should have decompressive surgery.
Discospondylitis is rare in cats and is generally

seen with other manifestations of infection, for
example, subcutaneous abscesses.
Congenital spinal deformities - spina bifida is
seen occasionally in cats, particularly in the
Manx breed.
Ischaemic myelopathy causing peracute,
asymmetrical neurological deficits is rare in
cats. The diagnosis is based on the absence of a
compressive lesion on myelography. Conservative
treatment is indicated.
PERIPHERAL NERVE, NEUROMUSCULAR
JUNCTION AND MUSCLE
Peripheral polyneuropathy
Diabetic neuropathy occurs in some cats with
diabetes mellitus. Affected cats are paraparetic
with a plantigrade stance. Definitive diagnosis
of polyneuropathy requires electrophysiological
evaluation.
Inherited hyperchylomicronaemia causes peripheral
neuropathy. Peripheral nerves are compressed by
the lipid granulomas that develop. The condition
may improve if the hyperchylomicronaemia is
reduced.
Ischaemic neuromyopathy is the most common
peripheral neuropathy in cats, but the clinical
signs of acute paraplegia are initially more
suggestive of spinal disease - see above.
Neuromuscular junction disorders
Myasthenia gravis may cause typical episodic
weakness related to exercise, regurgitation,
muscle tremors, dysphonia and neck flexion.
Aspiration pneumonia may develop with
megaoesophagus. Both congenital and acquired
forms of the disease are seen, and Abyssinian
and related breeds may have a relatively high
incidence. The diagnosis is based on the clinical
signs and may be confirmed by the intravenous
administration of edrophonium hydrochloride
(0.25-0.5 mg I.V.) - “the edrophonium response
test.” Here, cats with acquired myasthenia gravis
Back to contents
Ne
rapidly become normal for a period of several
minutes. The disease is immune-mediated, with
antibodies directed against the acetylcholine
receptor. Treatment with pyridostigmine
hydrochloride (0.5-3.0 mg/kg/per day by mouth)
and corticosteroids is indicated.
Myopathy
Potassium-depletion myopathy is the most
commonly recognized muscle disease of cats
reported during recent years. Affected cats show
acute muscle weakness with a typical posture of
neck flexion and the head carried low. The gait is
stilted and the cats are reluctant to walk. Muscles
may be painful on palpation and exercise induces
collapse.
Differential diagnosis includes myasthenia gravis,
polymyositis and generalized polyneuropathy. The
diagnosis is confirmed by demonstrating a low
serum potassium (less than 3.0 mEq/l) in a clinically
affected cat. Other causes of hypokalemia, for
example, alkalosis, hyperinsulinaemia or recent
fluid therapy, must be eliminated. Creatine kinase
concentrations are usually elevated.
Treatment depends on the severity of the
clinical signs. Severely affected cats require
aggressive intervention but care must be taken.
Administration of fluids can cause a rapid decline
in the condition and even result in respiratory
paralysis. Careful intravenous potassium
supplementation is required. When the crisis
is resolved, or in less severely affected cats,
oral potassium supplementation is adequate
with potassium gluconate. If renal insufficiency
if present, oral potassium supplementation is
required for life. The prognosis for recovery of
muscle function is good.
Polymyositis is rare in cats. Typical clinical signs
of stiffness, weakness and painful muscles may be
seen in Toxoplasmosis or in cats with idiopathic
polymyositis. 2006 World Congress WSAVA/FECAVA/CSAVA
527
Ne
Ne - Neurology
NON-ORTHOPAEDIC LAMENESS; CHECK OUT THE NERVOUS
SYSTEM
Dr. Simon. Wheeler BVSc PhD
DiplECVN DiplMgmt FRCVS
Veterinary Neurology LTD
Hertfordshire
UK
Simon.wheeler@mac.com
It can be a challenge for the clinician to unravel
the various factors influencing a gait abnormality
in a patient. Particular situations leading to
difficulties are:
• Where lameness is caused by an occult
neurological problem, with or without concurrent
orthopaedic disease.
Case example – a seven-year-old Retriever with
progressive forelimb lameness over several
months, with mild osteoarthritis of the elbow.
Eventual diagnosis is of brachial plexus tumour.
• Where lameness is the presenting sign in a
nervous system disease that usually manifests
itself with clear neurological deficits
Case example – German shorthaired pointer
with intermittent hindlimb lameness caused by a
lumbosaral disc protrusion
• Where neurological disease co-exists with
orthopaedic disease and the significance of either
is not clear.
Case example – German shepherd dog with severe
coxofemoral osteoarthritis being considered for
total hip replacement, but also with degenerative
myelopathy.
2006 World Congress WSAVA/FECAVA/CSAVA
It can be very difficult to differentiate between
orthopaedic and neurological causes of lameness,
and in rare situations, vascular disease can
underlie the problem. Of course, there is also the
occasional case of a soft tissue lesion causing
lameness. Some patients may have problems with
several body systems. For this reason, it is vital
that each patient be approached in a thorough and
methodical manner. The clinician must complete
a complete orthopaedic, neurological and soft
tissue assessment on each case, which must start
with a careful history.
THORACIC LIMB
Neoplasia
Most nerve tumours in dogs and cats occur close
to the spinal cord, although they may come to
528
Back to contents
involve the brachial plexus. Any mature animal
with a chronic forelimb lameness for which
no orthopaedic cause can be found should be
evaluated for the possible presence of a brachial
plexus tumour. Pain in the axilla, muscle atrophy,
loss of the panniculus reflex and Horner’s
syndrome all are indicative of a brachial plexus
tumour. Clinical signs include lameness, paralysis
distal to the lesion and pain or thickening on
palpation. Surgical exploration, biopsy and
resection are indicated in solitary tumours.
Infraspinatus Contracture
Working dogs seem prone to fibrotic myopathy of
the infraspinatus muscle. This leads to forelimb
lameness with a characteristic outward rotation of
the distal limb.
PELVIC LIMB
The most common neurological causes of
monoparesis and monoplegia lie in the nerves and
spinal cord segments of the lumbo-sacral region.
Deficits of the femoral innervation manifest as
loss of the patellar reflex. There may also be
sensory loss on the medial aspect of the limb.
The animal is unable to extend the stifle, thus it
cannot bear weight. Sciatic deficits lead to lack of
the withdrawal reflex, often seen as an inability
to flex the hock.
UMN vs. LMN
Upper motor neurone (UMN) lesions causing
hindlimb neurological problems include:
• Ischaemic myelopathy
• Disc herniation
• Neoplasms
Lower motor neuron (LMN) deficits can be
caused by:
• Disc herniation
• Degenerative myelopathy
• Ischaemic myelopathy and neoplasia as
mentioned above.

• Focal tetanus
• Lumbosacral disease
• Discospondylitis
Pelvic Trauma
This is a major cause of neurological damage to
the hindlimbs. It can be very difficult to determine
whether there are neurological complications of
pelvic fractures because of the severe pain that
many dogs suffer and the lack of mobility, which
restricts neurological assessment. It is wise to
attempt some sort of neurological examination
in all patients with pelvic fractures, even if it is
restricted to reflex evaluation and assessment of
pain perception. Loss of sciatic reflexes and / or
deep pain complicate the picture and may indicate
a poor prognosis.
Injections
Intramuscular injections in the caudal thigh carry
a significant risk of damaging the sciatic nerve.
For this reason, other injection sites are preferable.
Intrafascicular injection can result in severe nerve
damage with permanent disability, particularly
with certain preparations, for example, penicillin/
streptomycin and anthelmintics. Other drugs,
for example, soluble corticosteroids, seem to
be less irritant. Treatment depends to a large
degree on the progression of the patient. Any
improvement, whether monitored clinically or
electrophysiologically, is an indication not to
interfere surgically. Remembering that nerve fibres
regrow at approximately 1cm per week, adequate
time must be given for recovery. If after such
Back to contents
Ne
time significant improvement has not occurred,
surgical exploration is indicated. Recovery after
nerve injection, either spontaneous or following
surgical intervention, is unlikely to be complete.
Surgical Injury
There are several situations where nerve injury
is commonly seen following orthopaedic or other
procedures.
Sciatic nerve injury may occur following retrograde
intramedullary pin placement in the proximal
fragment in femoral fracture repair. Similar
lesions can occur if a femoral intramedullary
pin migrates proximally. The initial clinical
sign is severe pain on walking and on palpation
over the greater trochanter. Apparently severely
affected sciatic nerves can recover to a marked
degree following this type of injury, and surgical
intervention should be cautious, particularly
when considering grafting. Other orthopaedic
procedures likely to cause nerve injury are repair
of distal humeral fractures via a medial approach
(radial nerve); cranial cruciate repair by “over-
the-top” techniques (peroneal nerve); and ileal
shaft fractures (lumbosacral trunk).
Perineal hernia repair using sutures through the
sacrotuberous ligament is particularly hazardous
to the sciatic nerve, Sutures should be passed
through this ligament, not around it. If following
surgery the dog is lame, painful or has sciatic
paralysis, the sutures on the affected site must be
removed immediately and an alternative method
used.
2006 World Congress WSAVA/FECAVA/CSAVA
529
Ne
Ne - Neurology
CANINE BRAIN TUMORS
Richard A. LeCouteur, BVSc,
PhD, Diplomate ACVIM
(Neurology), Diplomate ECVN
University of Kalifornia
Davis CA 95616
USA
ralecouteur@ucdaviss.edu
In dogs, meningiomas and gliomas appear to occur
most frequently. Most primary brain tumors are
solitary, but multiple primary brain tumors have
been reported. Secondary or metastatic tumors
appear to be less common and may result from
local extension (e.g. nasal adenocarcinoma) or
metastases from primary tumors elsewhere. Skull
tumors may affect the brain by local extension.
Although brain tumors occur in dogs of all breeds,
either sex, and any age, the incidence increases
over 5 years of age, and with certain breeds. Glial
cell tumors and pituitary tumors occur commonly
in brachycephalic breeds, whereas meningiomas
occur most frequently in dolichocephalic breeds.
Pathology
Primary brain tumors originate from cells
normally found within the brain and meninges.
Secondary tumors are metastasis from a primary
tumor located outside the nervous system, or
occur by local invasion from adjacent non- neural
tissues (e.g., bone). Pituitary gland neoplasms and
tumors arising from cranial nerves are considered
secondary brain tumors.
Brain tumors cause cerebral dysfunction through
2006 World Congress WSAVA/FECAVA/CSAVA
infiltration of normal brain tissue, compression
of adjacent structures, disruption of cerebral
circulation, and local necrosis. Secondary effects
of brain tumors include hydrocephalus, increased
intracranial pressure (ICP), cerebral edema,
and brain herniation. Primary brain tumors
often are slow growing and the brain adapts to
the slow increase in ICP. During this period of
compensation there may be a history of vague
signs and subtle behavior changes. Even with
a slowly progressive tumor, clinical signs may
progress rapidly when compensatory mechanisms
have been exhausted. Rapidly growing tumors do
not permit the same degree of compensation and
a sudden onset of severe neurological dysfunction
may occur in the absence of premonitory signs.
530
Back to contents
History and Clinical Signs
Neurological signs resulting from a brain tumor
depend primarily on the location, size, and rate
of growth of the mass. Many dogs or cats will
have a long history of “vague” signs, such as not
wishing to be handled, hiding during the day,
decreased frequency of purring, or diminished
activity levels. Frequently focal or generalized
seizures occur.
Focal neurological signs usually are indicative
of a fairly well developed mass lesion.
Neoplasms involving the brain stem may result
in cranial nerve deficits. Weakness and sensory
abnormalities often are seen with a lesion in the
cerebral frontoparietal regions or their deeper
pathways. Visual deficits may accompany masses
that involve the visual pathways from the occipital
lobe of the cerebrum to the optic nerve. Hearing
loss involves the cerebellomedullary region, the
brain stem, or temporal lobes of the cerebrum.
Decreased ability to smell may be seen with
lesions of the cribriform plate or olfactory bulbs,
or other rhinencephalic connections. Difficulties
with balance or gait suggest cerebellar or
vestibular involvement.
Secondary effects of brain tumors include
increased ICP and cerebral edema. Clinical signs
include alterations in behavior (e.g., lethargy,
irritability), circling, head pressing, compulsive
walking, altered states of consciousness, or
associated locomotor disturbances. The majority
of cats or dogs with a brain tumor will be
presented to a veterinarian with problems related
to the secondary effects of a tumor.
Diagnostic Techniques
On the basis of signalment, history, and the
results of complete physical and neurological
examinations, it is possible to localize a problem
to the brain and, in some cases, to determine
the approximate location. Signs resulting from
disease in a given location in the nervous system

will be similar regardless of the exact cause. In
order to eliminate other categories of disease it
is essential to follow a logical diagnostic plan.
A minimum data base for these patients should
include a hemogram, serum chemistry panel,
urinalysis, survey radiographs of the thorax,
and abdominal ultrasound. Although plain
skull radiographs are of limited value in the
diagnosis of a primary brain tumor, their use
may facilitate detection of skull or nasal cavity
neoplasms. Occasionally, lysis or hyperostosis
of the skull may accompany a primary brain
tumor (e.g., meningioma of cats), or there may
be radiographically visible mineralization within
a neoplasm. General anesthesia is necessary for
precise positioning of the skull for radiographs.
Analysis of cerebrospinal fluid (CSF) is
recommended as the results may help to rule
out inflammatory diseases, and may support a
diagnosis of a brain tumor. Care should be used
in the collection of CSF, because frequently ICP
is increased and pressure changes associated
with CSF drainage may lead to brain herniation.
Hyperventilation of the patient or administration
of mannitol prior to CSF collection will help to
decrease intracranial pressure. Increased CSF
protein content and a normal to increased CSF
white blood cell count are considered “typical”
of a brain neoplasm although often CSF may be
normal. Neoplastic cells may be present in CSF,
particularly when sedimentation techniques are
used for analysis.
Computed tomography (CT) and magnetic
resonance (MR) imaging provide accurate
information about the presence, location and size
of intracranial neoplasms. MR images are superior
to those of CT in certain brain regions (e.g., the
brainstem). Meningiomas may be difficult to detect
on MR images, without contrast administration.
A meningioma may have a “mottled” appearance
and an interface is often visible between the
tumor and the surrounding brain on T1- and T2-
weighted images. This hypointense signal may
indicate a compressed arachnoid plane between
the tumor and the brain, and also compression of
the draining venous plexus. Hypointense areas
within the meningioma may indicate intratumoral
mineralization. The “dural tail” sign, while not
necessarily specific for a meningioma, is often
associated with either neoplastic infiltration of
meninges beyond the margin of the meningioma
or hypervascularity of the dura mater. Ideally, an
intracranial lesion should be biopsied prior to
the institution of therapy, however biopsy is not
always attempted for practical reasons such as
cost and morbidity.
Non-neoplastic space-occupying lesions may
mimic the CT or MR imaging appearance of a
Back to contents
Ne
neoplasm and occasionally a metastasis may
resemble a primary brain tumor. Currently, biopsy
is the only method available for the definitive
diagnosis of brain tumor type. Biopsy methods
described include ultrasound-guided biopsy, and
CT-guided biopsy. CT-guided stereotactic biopsy
systems provide a relatively non-invasive, rapid,
and extremely accurate means of tumor biopsy,
with a low rate of complications.
Cytological evaluation of brain tumor biopsy
specimens may be done within minutes of biopsy
collection by means of crush preparations. Tissue
samples are rapidly fixed in 95% alcohol and
stained with hematoxylin and eosin. Accurate
information using this rapid technique generally
is available from both primary and metastatic
nervous system tumors, and from non-neoplastic
lesions. Air-dried slides of crush preparations
also may be stained with Wright’s stain and
counter stained with Giemsa to provide additional
information regarding cell types present in a
mass.
Therapy
The aims of therapy for a brain tumor are to
eliminate the tumor (or reduce its size) and to
control secondary effects (e.g., increased ICP or
cerebral edema). Palliative therapy for animals
with a brain tumor consists of glucocorticoids
for edema reduction and, in some cases (e.g.,
lymphoma), for retardation of tumor growth.
Should seizure therapy be needed, phenobarbital
is the drug best suited for the control of generalized
seizures.
Surgery has become an essential consideration in
the management of intracranial neoplasms of cats
or dogs. The precise location, size, and type of a
neoplasm, determine the extent of removal that is
possible. Meningiomas, particularly those located
over the frontal lobes of the cerebrum, often
may be completely removed, especially in cats.
In contrast, there is a significant morbidity and
2006 World Congress WSAVA/FECAVA/CSAVA
mortality associated with the surgical removal
of caudal fossa and brainstem neoplasms. Partial
removal of a brain neoplasm may relieve signs
of cerebral dysfunction, provide a histological
diagnosis, and may make an animal a better
candidate for other therapy such as radiation.
Surgical biopsy of a tumor must be approached
with care to avoid seeding of tumor cells to
normal tissue.
The use of radiation therapy for the treatment
of primary brain tumors of dogs and cats is well
established and it may be used either alone or
in combination with other treatments. External
beam, megavoltage irradiation currently is
recommended for the therapy of brain tumors
in dogs or cats. Although orthovoltage radiation
531
Ne
has been used it is not optimal because of poor
beam penetration, profile, and limited field
configuration. Careful treatment planning by a
radiation therapist is essential. The selection of
a radiation dose is based on considerations such
as tumor type, location, and tolerance of the
surrounding normal tissues.

Ne - Neurology
INFLAMMATORY CENTRAL NERVOUS SYSTEM DISEASE OF THE
DOG
Simon R. Platt BVM&S
MRCVS Dipl. ACVIM
(Neurology) Dipl. ECVN
RCVS Specialist in
Veterinary Neurology Head
of Neurology / Neurosurgery
Unit
Centre for Small Animal
Studies
The Animal Health Trust
Lanwades Park
Kentford, Newmarket
Suffolk CB8 7UU
England
simon.platt@aht.org.uk

The hallmark of CNS inflammation is infiltration infected following stress, immunosuppression,

of peripheral blood leukocytes into the
neuroparenchyma and its coverings, resulting in
various types of encephalitis and/or meningitis,
and sometimes associated with altered vascular
integrity that leads to oedema. The aetiologies
of inflammatory disease of the CNS are very
diverse. Simplistically, they can be classed as
pathogenic and non-pathogenic, with the latter
being potentially related to immune-system
dysfunction. Infectious causes may be viral,
protozoal, bacterial, rickettsial, or fungal.
2006 World Congress WSAVA/FECAVA/CSAVA
or contact with diseased animals. Fifty to 75%
of susceptible dogs are subclinically infected
but clear the virus from the body. Factors
predisposing to development of clinical disease
are multifactorial, including age, vaccination
status, breed, and viral virulence.
Virus replication initially begins in lymphoid
tissues. The initial systemic phase of infection
by this virus is marked by immunosuppression.
Virus reaches the CNS approximately 1 week
after infection by virus-infected lymphocytes,

monocytes, and platelets associated with immune

Canine Distemper Encephalomyelitis
Canine distemper encephalomyelitis (CDE) is
caused by a paramyxovirus (genus Moribillivirus)
closely related to measles virus of man. Although
the incidence is decreasing, CDE is still a
common CNS disorder in the dog, primarily
in unvaccinated dogs but also occasionally in
those dogs with a vaccinal history. Young dogs
are especially susceptible to infection, although
older dogs are also at risk. While there are several
different strains of the virus, there is only one
serotype which means that exposure to one strain
protects dogs against any subsequent challenge.
The virus is most commonly spread by aerosol
exposure, although rarely, the virus may be spread
transplacentally. Dogs that are not immunized
regularly may lose their protection and become
532
Back to contents
complexes. Spread of virus through cerebrospinal
fluid pathways may explain the frequent. A rapid
and high-titered viral antibody response to CDV
is crucial for recovery from viral infection with
minimal or no clinical signs. Dogs unable to
mount an adequate response develop a rapidly
progressive disease and die. Dogs that mount a
delayed or intermediate response tend to develop
chronic neurological disease.
Lesions may be found in gray and white matter.
The earliest changes seen in the CNS are
degenerative and appear to be the result of viral
replication in glial cells, especially astrocytes,
followed by viral-induced demyelination, while
a non-suppurative inflammatory component
occurs later, perhaps as viral immunosuppression
is declining, and becomes superimposed on the

degenerative lesion, although both may be seen
together.
Canine Distemper Encephalomyelitis in Immature
Dogs: This is the most common form of distemper
virus infection and is often initially characterized
by systemic evidence of gastrointestinal and
respiratory disturbances: vomiting, diarrhoea,
coughing, and seromucopurulent oculonasal
discharges. Hyperkeratosis of the footpad may
be seen. Additionally, many animals have
conjunctivitis and chorioretinitis. However, in
one clinical report, only one third of the canine
distemper cases had extraneural involvement.
These systemic signs may precede, or occur
simultaneously with, neurological signs.
Neurological signs are quite varied, often
asymmetrical, and usually suggest a multifocal
distribution of lesions. Cortical and subcortical
signs include generalized seizures and sometimes
personality changes, such as depression and
disorientation. Signs of localization in the brain
stem include incoordination, hypermetria,
falling, head tilt, and nystagmus. Occasionally,
monoplegia and paraplegia are observed. A sign
that is characteristic of distemper encephalitis is
myoclonus (generalized or localized), or more
correctly, flexor spasm. Appendicular flexor
muscles, abdominal muscles, and the cervical
musculature are most frequently involved.
Sometimes the masseteric, temporalis, and
periorbital muscles are affected. These rhythmic
contractions are not necessarily associated with
limb paresis or paralysis and usually persist during
sleep. The movements are temporarily abolished
by intravenous injection of local anesthetic
agents. An abnormality in the motor neuron-
interneuron pool in the spinal cord is thought to
cause the muscle contractions. Contractions are
not dependent on sensory nerves or descending
pathways from the brain. Acute visual impairment
(optic neuritis), typically accompanied by dilated,
unresponsive pupils, may be the only clinical sign
in some dogs. Canine distemper virus is a common
cause of convulsions in dogs less than six months
of age. Olfactory dysfunction has been reported
in affected dogs. Neonatal infection prior to
eruption of permanent dentition can cause enamel
hypoplasia. Cell-mediated immunosuppression
can occur with CDV, predisposing affected
animals to other infectious agents, including
Toxoplasma gondii and Neospora caninum.
Multifocal Distemper Encephalomyelitis in
Mature Dogs: In mature dogs between the ages of
4 and 8 years, canine distemper virus can produce
a type of multifocal encephalomyelitis (MDE)
that is characterized by a chronic course. It is
not unusual for an animal to be presented with
a history of neurological signs that have been
Back to contents
Ne
present for 12 months or more. The incidence of
this disease is relatively low and does not appear
to be related to breed or sex. Animals that have
received vaccinations against distemper virus
may be affected. This disease is not preceded
by, nor is it coincident with, the systemic signs
that are seen in younger dogs. Furthermore, it is
not unusual for this slowly progressive disease
to remain clinically and pathologically static.
The initial neurological signs that are commonly
seen in mature dogs with MDE include weakness
of the pelvic limbs, generalized incoordination,
and occasional falling. These signs frequently
progress to tetraplegia. Generalized seizures
or personality changes are not features of this
disease and affected animals maintain a normal
mental state. Many dogs will have unilateral or
bilateral menace deficits, with normal or abnormal
pupillary reflexes. Some animals will have signs
of facial paralysis, head tilt, and nystagmus.
Although head tremors may be seen, myoclonic
movements or flexor spasms are usually not
observed.
The diagnosis of canine distemper encephalomyelitis
(in young dogs, especially) is usually based
on history and clinical signs. The index of
suspicion is higher in affected dogs that have
not been vaccinated. Positive diagnosis may
be made through use of immunofluorescent or
immunocytochemical techniques to detect canine
distemper viral antigen in brain sections and other
tissues (e.g., mononuclear cells in blood smears,
conjunctival or tracheal washes, or footpad
biopsies).
Hematological and biochemical data are non-
specific, although many affected dogs will be
lymphopenic during the acute phase of illness.
CSF analysis may reveal a moderate pleocytosis
(15 to 60 WBCs/μl) of mononuclear cells
(lymphocytes and macrophages), and elevated
gamma globulins, although during the acute
demyelinating stage of the disease, inflammatory
2006 World Congress WSAVA/FECAVA/CSAVA
reactions may be limited or lacking and CSF
protein/cell count may be normal. Detection of
CDV in urine using polymerase chain reaction
(PCR) amplification has been recently reported
as a useful routine screen for dogs with suspected
distemper encephalomyelitis.
Prognosis is guarded. Seizures are an unfavorable
prognostic sign. There is no treatment for CDE,
except supportive, and dogs with progressive
neurological signs leading to incapacitation need
to be euthanized. The prognosis is better in dogs
with non-progressive neurological complications,
such as intermittent seizures, myoclonus, and
visual impairment, although only seizures may
respond to medication.
533
Ne
Post-vaccinal Canine Distemper Encephalitis: Post-
vaccinal canine distemper encephalitis occurs
in young animals, especially those less than six
months of age. It has been recognized as a disease
entity for a number of years and is believed to be
associated with vaccination using live virus. The
pathogenesis of this disease is unclear.
Granulomatous Meningoencephalomyelitis
Granulomatous meningoencephalomyelitis (GME)
is a sporadic, idiopathic, inflammatory disease of
the CNS of dogs. This disease appears to have
a worldwide distribution, with recent reports
coming from the USA, Australia, New Zealand,
and Europe. The cause of GME is unknown.
Most cases of GME occur in small breed dogs,
and commonly in terrier and toy breeds and
Poodles, although any breed may be affected.
The majority of confirmed cases occur in young
to middle-aged dogs, with a mean age around 5
years (ranging from 6 months to 12 years). GME
occurs in both sexes; however, there appears
to be a higher prevalence in females. A lack of
obvious correlation between clinical signs and the
course of the disease has been reported. Clinical
signs usually reflect several (i.e. multifocal)
syndromes, e.g., cerebral, brain stem, and spinal
cord syndromes, as a result of the scattered
distribution of lesions. However, focal signs have
been reported in up to 50% of cases. Common
signs include incoordination, ataxia and falling,
cervical hyperesthesia, head tilt, nystagmus, facial
and/or trigeminal nerve paralysis, circling, visual
deficits, seizures, depression, and tetanic spasms.
Occasionally, fever, peripheral neutrophilia,
and excess non-segmented neutrophils will
accompany the clinical neurological signs. An
infrequently reported ocular form of GME appears
to be related to lesions localized in optic nerves
and optic chiasm resulting in visual impairment
and abnormal pupillary reflexes.
2006 World Congress WSAVA/FECAVA/CSAVA
A tentative diagnosis of GME may be suggested
by signalment data, the clinical course of the
disease, and clinical signs. Haematology, serum
chemistry, and urinalysis studies are usually
normal and electroencephalographic recordings
are frequently non-specific. Rarely, an intrathecal
filling-defect may be detected myelographically
in dogs possibly due to focal cord swelling or
subarachnoid granulomas. The most useful
diagnostic aid is CSF analysis. In most dogs,
CSF is abnormal with mild to pronounced
pleocytosis, ranging from 50 to 900 WBCs/μl.
Cells are predominantly mononuclear, including
lymphocytes (60 - 90%), monocytes (10 -
20%), and variable numbers of large anaplastic
mononuclear cells with abundant lacy cytoplasm.
While neutrophils typically comprise from 1
534
Back to contents
- 20% of the cell type differential, they may be
the predominant cell type on rare occasions.
Occasionally, protein is elevated without
pleocytosis. In one retrospective study of dogs
with GME, lumbar-derived CSF contained fewer
cells and less protein than CSF derived from
cisternal puncture. CSF protein and cellularity
is not necessarily influenced by the degree of
meningeal involvement or the extent of necrosis
within the granulomatous lesions. A combination
of CSF and MRI findings may also be useful, the
latter being characterized by isointense lesions
on T1-weighted images. Pial/dural meningeal
enhancement may be found with MRI. Although
infrequently performed, brain biopsy can be a
very useful diagnostic test in animals with focal
lesions.
Prognosis for permanent recovery is poor. Some
dogs die from inhalation pneumonia secondary
to megaesophagus. Shortest survival periods,
ranging from several days to weeks, are seen
with the disseminated and ocular forms. Longer
survival periods of from 3 to 6 months, or
longer, are more suggestive of a focal lesion. In
one retrospective study of 42 dogs with GME ,
median survival time for dogs with focal versus
disseminated disease was 114 and 14 days,
respectively, and dogs with focal forebrain signs
(e.g., seizures) had significantly longer survival
times (>395 days) than did dogs with focal signs
in other areas of the CNS (59 days). Long-term
therapy is generally unsatisfactory, although
temporary remission of signs is often achieved
with corticosteroid administration, such as
oral prednisone, 1 to 2 mg/kg/day initially for
several days, then reducing the dosage to 2.5 -
5 mg on alternate days. Most dogs will require
continued therapy to prevent recurrences of signs.
Improvement may last for several days, weeks or
months, although most will eventually succumb
to the disease. Part of the temporary improvement
may be related to a reduction of mast cell function
in dogs receiving glucocorticoid medication.
Cessation of glucocorticoid therapy is invariably
associated with rapid and dramatic clinical
deterioration. Results of a recent retrospective
study suggested that radiation therapy (e.g.,
total doses ranging from 40 to 49.5 Gy, divided
in 2.4- to 4.0-Gy fractions) may be an effective
treatment for dogs with GME, particularly those
with clinical signs suggesting focal involvement.
Promising clinical, CT, and CSF results following
use of cytosine arabinoside (at 50 mg/m2, SQ, bid
x 2 days, repeat q 3 weeks) in an 8 year old Shih
Tzu, suggests that this potent anti-inflammatory
drug may be an effective sole therapy for the
long-term treatment of GME in dogs.

Steroid Responsive Meningitis-Arteritis
A severe form of steroid responsive meningitis-
arteritis (SRMA) has been reported in Beagles,
Bernese Mountain Dogs, Boxers, German Short-
Haired Pointers, and sporadically in other breeds.
This condition has a worldwide distribution and
represents one of the most important inflammatory
diseases of the canine CNS. Beagles, especially
but not exclusively those in laboratory-
bred colonies, appear at risk. In the Beagles,
the condition has been termed Beagle pain
syndrome, necrotizing vasculitis, polyarteritis,
panarteritis, juvenile polyarteritis syndrome,
and primary periarteritis. In other breeds, this
condition previously appears under the terms
necrotizing vasculitis, corticosteroid-responsive
meningitis, aseptic suppurative meningitis, and
corticosteroid-responsive meningomyelitis.
This plethora of terminology reflects not only
the dearth of knowledge about this condition
but also highlights important clinical signs such
as pain, improvement following corticosteroid
medication, and histologic involvement of the
meninges and blood vessels.
Affected animals usually are most commonly
young adults between 8 and 18 months of age,
although the age range may extend from 4
months to 7 years. The clinical course is typically
acute with recurrences. A more protracted form
of the disease may be seen following relapses and
inadequate treatment. Signs include recurring
fever, hyperesthesia, cervical rigidity, and
anorexia. There may be a creeping gait, arching
of the back with head held down, and crouched
posture. Some dogs with protracted disease may
show clinical signs of parenchymal involvement
such as ataxia, paresis, tetraparesis or paraplegia.
Hematological studies often reveal a peripheral
neutrophilia with a left shift, increased erythrocyte
sedimentation rate, and in some cases, an elevated
α2-globulin fraction. CSF studies indicate
increased protein and neutrophilic pleocytosis
(in some dogs as high as 12,600 WBCs/μm).
Dogs with chronic disease may have a normal or
mildly increased CSF protein content and a mild
to moderate, mixed cell pleocytosis. In acute
and chronic forms of the disease, the majority
of affected dogs show elevated IgA levels
in CSF and serum, presumably as a result of
dysregulation of the immune system. CT imaging
may help localize changes in the CNS (meninges,
spinal cord, and brain) and assist in the efficacy
of therapy.
The cause of SRMA remains unknown. To date,
no bacterial or viral infectious agents have been
identified, although activated T cells have been
found in some dogs indicating these cells have
had contact with some unidentified antigen.
Back to contents
Ne
The prognosis is guarded to favorable,
especially in dogs with acute disease that are
treated promptly using immunosuppressive
doses of corticosteroids. Untreated dogs tend to
have a remitting and relapsing course. Tipold
recommends the following long-term therapy
(e.g., for at least 6 months), especially in any
dog that has had a relapse: prednisolone at
4 mg/kg/day, PO or IV initially. After 2 days, the
dose is reduced to 2 mg/kg daily for 1 to 2 weeks,
followed by 1 mg/kg daily. Dogs are re-examined,
including CSF analysis and hematology, every
4 to 6 weeks. When signs and CSF are normal,
the dose can be reduced to half of the previous
dosage until a dosage of 0.5 mg/kg every 48 to 72
hours is attained. Treatment is stopped 6 months
after clinical examination, CSF, and blood
profiles are normal. In refractory cases, other
immunosuppressive drugs such as azathioprine
(at 1.5 mg/kg PO every 48 hours) may be used in
combination with steroids (e.g., alternating each
drug every other day). Antibiotics are ineffective.
Results of a long-term treatment protocol (up to
20 months) involving 10 dogs with SRMA have
been recently published. Eight of the 10 dogs
were without clinical signs up to 29 months
after the treatment was terminated. Long-term
glucocorticosteroid treatment resulted only
in mild clinical side effects, such as polyuria/
polydipsia, polyphagia and weight gain, which
were reversible after the therapy was discontinued.
It was noted that elevated serum and CSF IgA
levels did not decrease to normal values during
prednisolone treatment and were still slightly
increased after the therapy was discontinued.
Monitoring of CSF cell count in dogs with this
condition was a sensitive indicator of success of
treatment. In addition, older dogs with high IgA
levels in the CSF and frequent relapses seemed to
require a longer duration of therapy and had a less
favorable prognosis long term.
Note that Akitas, Bernese Mountain dogs, and
2006 World Congress WSAVA/FECAVA/CSAVA
other breeds with immune-mediated polyarthritis
may show similar clinical signs as animals with
SRMA and have concurrent meningitis.
Bacterial Meningitis
Bacterial meningitis is a rarely reported condition
in dogs and cats. Animals of any age may be
affected, although most affected dogs are adult,
with a mean age around 5 years. Bacterial
infections of the CNS most often occur via
haematogenous spread from distant foci within
the body (e.g., lung or splenic abscess, vegetative
endocarditis, pleuritis, and urinary tract
infections), by direct extension from sinuses, ears
and eyes, as a result of trauma (e.g., bite wound),
meningeal spread with entry along nerve roots,
535
Ne
or from contaminated surgical instruments (e.g.,
spinal needle). Organisms usually disseminate
via CSF pathways and produce cerebrospinal
meningitis, often associated with microabscess
formation of brain and spinal cord. A plethora
of organisms have been cultured from dogs
with bacterial meningitis including Pasteurella
sp (e.g., P. multocida), Staphylococcus aureus,
Staphylococcus epidermidis, Staphylococcus
albus, Actinomyces sp, Nocardia sp, Escherichia
coli, Streptococcus sp (e.g., S. pneumoniae) and
Klebsiella sp.
Irrespective of the etiologic agent, bacterial
meningitis usually is acute in onset and tends to
be characterized by a group of clinical signs that
include hyperesthesia, fever, cervical pain, and
frequently, cervical rigidity. In addition, vomiting,
bradycardia, anorexia, occasional cranial nerve
deficits, and seizures may be observed. Seizures
may be caused by high fever, hypoglycemia,
brain edema, or inflammation, while vomiting
may result from increased intracranial pressure
or from direct effects on the vomiting center.
In some animals, clinical signs may develop
that suggest parenchymal involvement. The
clinical diagnosis of bacterial meningitis is
supported by the finding of highly pleocytic CSF
(500 to 1000+ WBCs/μl) with a high proportion
of neutrophil cells. The protein content of the CSF
is usually increased as well (100 to 1000+ mg/dl).
Low CSF glucose, relative to plasma glucose
values, are typical. Organisms may be seen on
CSF cytology. Neutrophilia may be present in
blood samples and there may be evidence of shock,
hypotension, and disseminated intravascular
coagulation Thrombocytopenia, abnormal liver
enzymes, electrolyte imbalance, abnormal anion
gap, and uremia have been reported in some
cases [278]. Electroencephalographic traces
may demonstrate high voltage (30 - 70μv), fast
(20 - 35 Hz) or slow (5 - 10 Hz) wave activity.
2006 World Congress WSAVA/FECAVA/CSAVA
Definitive diagnosis is made by bacterial culture
of CSF (both aerobic and anaerobic). Blood and
urine cultures may incriminate a pathogenic
organism when CSF cultures are negative (which
is usually the case in our experience). Meningeal
inflammation, ventriculitis, and possibly brain
edema can be detected using MRI or CT scans.
Pathological findings that are characteristic of
bacterial meningitis include diffuse infiltration of
inflammatory cells (by both polymorphonuclear
and mononuclear cells) into the leptomeninges.
Frequently, inflammation is found throughout the
entire subarachnoid space of the brain and spinal
cord. Vasculitis is often pronounced. Bacterial
invasion of CNS parenchyma is characterized
by mononuclear and polymorphonuclear
inflammatory infiltration and extensive
536
Back to contents
perivascular cuffing. Necrosis of gray and white
matter, sometimes associated with vascular
thrombosis, may be observed with infiltration of
macrophages, neutrophils and plasma cells.
Prognosis is guarded since death is common even
if appropriate therapy is administered, and relapses
are frequently encountered. Appropriate use of
antibiotics, according to the culture results, is
basic to successful therapy of bacterial meningitis
(encephalomyelitis). Antibiotic therapy should be
maintained for several weeks after clinical signs
have resolved. Chloramphenicol (up to 50 mg/kg,
IV, IM, or SC, bid), metronidazole (10 - 15 mg/kg,
PO, tid), trimethoprim-sulfonamide (from 30 to
60 mg/kg, PO, daily; note that complications
may include sulfonamide urolithiasis in dogs
and nephrotoxicity in cats) penetrate the CNS
in therapeutic concentration. Ampicillin and
penicillin enter the CNS only with meningeal
irritation. Aminoglycosides and cephalosporins
reportedly do not adequately penetrate the CNS,
even when inflammation exists. Intrathecal
administration of antibiotics should only be
considered in refractory cases. Corticosteroids,
in general, are contraindicated in the treatment of
bacterial meningitis . It has been suggested that
Staphylococcus sp. should be assumed when the
organism involved is not known [277]. Ampicillin,
5 - 10 mg/kg, IV, every 6 hours is recommended.
Diazepam or other anticonvulsants can be used
for seizures if they occur. Osmotic diuretics
may be useful for treating increased intracranial
pressure secondary to brain oedema.
Note that it may be very difficult to differentiate
between bacterial meningitis and steroid
responsive meningitis-arteritis (SRMA). The
latter is more common and probably should be
at the top of the differential list. Analysis of CSF
for elevated levels of IgA should be diagnostic
for SRMA.
Mycotic Diseases of the CNS
Mycotic agents sporadically produce a
granulomatous meningoencephalomyelitis in
dogs and cats. The more common mycotic
infections of the CNS are caused by Cryptococcus
neoformans, Blastomyces dermatitidis,
Histoplasma capsulatum and Coccidioides
immitis. Each agent has a particular geographic
distribution in the USA. The pathogenesis is
similar for blastomycosis, histoplasmosis and
coccidioidomycosis. The organism is present
in the soil, producing mycelia and airborne
spores. The coccidia of spores are probably
inhaled, deposited in the alveoli, phagocytosed
and converted into the spherical parasitic, yeast
form. This form is disseminated via lymphatics
producing local hilar lymphadenopathy and there

is hematogenous spread to other organs. The fate
of the infected host is believed to be dependent
upon time and ability to develop cellular immunity
to fungal antigens. Unlike other mycotic diseases,
C. neoformans exists only in the yeast form and
has a worldwide distribution. Endemic areas
have not been identified. Infection is probably
acquired from the environment rather than from
animals. Cryptococcosis infection often occurs in
mature dogs and cats that are immunodepressed
(e.g., cats with feline leukemia virus or
feline immunodeficiency virus, or dogs with
ehrlichiosis), and infection may be accelerated or
worsened by glucocorticoid therapy. Cats contract
the disease more frequently than dogs. The natural
route of infection is generally believed to be the
respiratory tract, with subsequent hematogenous
and lymphogenous dissemination to other areas
of the body. As with bacteria, mycotic infections
also may reach brain and spinal cord by direct
spread from an adjacent infection, e.g., from the
nasal chambers, tooth alveolus and sinuses, outer
ear, eustachian tube, middle/inner ear, petrous
temporal bone, and basilar bone.
While the overall incidence of CNS involvement
by mycotic diseases is low, C. neoformans may
be more likely to be incriminated than the other
organisms in dogs. Neurological signs will vary
according to lesion location and severity. The
signs may reflect either a focal mass lesion or a
diffuse multifocal disease process. Neurological
signs may include seizures, depression,
disorientation, circling, ataxia, falling, pelvic
limb paresis, paraplegia, anisocoria, pupillary
dilatation and blindness. Deficits of one or
several of cranial nerves 5 to 12 are often present.
Note that these signs may be seen with any of
the mycotic infections. Radiographic evidence of
diffuse miliary to nodular interstitial pulmonary
infiltrates may be seen with blastomycosis,
histoplasmosis, and coccidioidomycosis. Gross
lesions may include thickening of the meninges,
which sometimes have a gelatinous, cloudy
appearance. On sectioning of the brain, cystic
spaces may be seen within the parenchyma. These
spaces reflect expanded perivascular spaces and
are frequently filled with crytococcal organisms
having a round/ovoid cell body and surrounded by
a halo-like capsule that stains strongly with PAS
or Mayer’s mucicarmine. In cats, only a minimal
or mild nonsuppurative inflammatory response
may be present. In affected dogs, the cellular
response is more granulomatous with epithelioid
macrophages, lymphocytes, and plasma cells.
The organism may be found as free hyphae or
yeast form some of which may be budding. The
yeast form is often present within macrophages.
Back to contents
Ne
Ocular lesions associated with a cell-mediated
chorioretinitis may also be observed.
Pyogranulomatous encephalitis has been reported
occasionally in dogs and cats in association with
blastomycosis. Neurological disease associated
with histoplasmosis and coccidioidomycosis is
rare or quite uncommon, although granulomatous
meningitis attributable to C. immitis was
diagnosed on postmortem examination in a
4 year old Border Collie by demonstration of
coccidioides endospores in brain tissue. There are
a few reports of CNS infection in dogs and cats
associated with uncommon opportunistic fungi,
such as phaeohyphomycoses, in which the agents
involved are almost always Cladosporidium
species, and usually C. bantianum. CNS disease
is usually due to localized brain abscess or to
multiple large pyogranulomatous lesions in
the cerebrum and meninges, sometimes with
multifocal malacic foci, and is invariably fatal.
Diagnosis of mycotic infection is based on
demonstration of the organisms in tissue sections
using immunofluorescent procedures or in
material taken from aspirates or impression
smears, culture, and serology. A commercial
latex agglutination test is available for detecting
cryptococcal capsular antigen in serum, urine, or
cerebrospinal fluid. Inflammatory mycotic lesions
may be detected using MRI.
Prognosis of mycotic infection is always guarded,
especially in the disseminated form and with CNS
involvement. Most of the organisms are sensitive
to treatment with amphotericin B (AMB), e.g.,
using a dosage of 0.1 to 0.5 mg/kg body weight,
IV, three times weekly, in dogs and cats. The
treatment of choice for cryptococcosis still appears
to be AMB and flucytosine (FCY), although toxic
epidermal necrolysis may sometimes be seen as
a side-effect. A recommended dosage for FCY
is 120 mg/kg body weight, divided into 4 equal
doses daily. Due to the inability of AMB and FCY
to cross the blood-CNS barrier, it is recommended
2006 World Congress WSAVA/FECAVA/CSAVA
that these drugs be used in combination with other
antifungal agents such as itraconazole (ITZ, at
5 - 10 mg/kg, PO, bid) or fluconazole (FCZ, at
5 - 15 mg/kg, PO, bid) in animals with CNS disease.
It would seem that the same recommendation
would apply to other fungal diseases having
CNS involvement, e.g., itraconazole at 10
mg/kg, PO, daily is suggested for dogs with
blastomycosis/brain involvement. In a recent
report of cryptococcosis in 19 cats, treatment with
ketoconazole (KTZ), was unrewarding in cases
with CNS involvement, although KTZ and ITZ
(both at 10 mg/kg, PO, daily) successfully treated
a small number of experimentally-infected cats,
including some with CNS disease.
537
Ne
Protozoan Encephalitis-encephalomyelitis
Toxoplasma, Neospora, and Sarcocystis are three
genera of the phylum Apicomplexa that cause
encephalomyelitis in dogs and cats.
Toxoplasmosis and Neosporosis: Toxoplasmosis
is an infectious condition caused by the protozoal
parasite Toxoplasma gondii and occurs in acquired
and congenital forms in man and animals. Cats
are the definitive host for this parasite. The three
known infective stages of Toxoplasma gondii are
bradyzoites, tachyzoites and sporozoites. The
three modes of transmission are carnivorism
(ingestion of encysted bradyzoites), fecal
contamination, and in utero infection. These
modes of transmission involve the different
infective stages as follows: carnivorous ingestion
of encysted bradyzoites, tachyzoites or both;
contamination with feline feces containing
sporozoites of sporulated oocysts; transplacental
infection of the fetus with tachyzoites after
ingestion of encysted bradyzoites or sporulated
oocysts by the mother. Humans, sheep, pigs, dogs
and (rarely) cats are known to transmit T. gondii
transplacentally. In humans, congenital infection
occurs when a woman becomes infected during
pregnancy. Toxoplasma oocysts are shed in feline
feces unsporulated and are not infective until
sporulated (1 - 5 days). Sporulated oocysts can
survive in soil for several months. Land snails,
earthworms, flies and cockroaches may serve
as transport hosts for oocysts. Most mammals
become intermediate hosts through ingestion of
oocysts. Following the acute systemic infection
in intermediate hosts in which the organism can
be disseminated to many body organs (this phase
may be subclinical), tissue cysts form, most
commonly in the CNS, skeletal muscle, and heart
muscle. This conversion is related to development
of the host humoral and cellular immune response.
The parasites are mainly intracellular and
subclinical infection may persist for the life of
2006 World Congress WSAVA/FECAVA/CSAVA
the host. Activation of toxoplasmosis may occur
in association with severe immunosuppressive
disorders. The condition is often associated
with canine distemper or other infections such,
as ehrlichiosis, or with glucocorticoid therapy.
Clinical toxoplasmosis is most commonly seen
in young dogs less than 1 year of age or in
immunocompromised older dogs. Note that many
disorders previously ascribed to toxoplasmosis
in dogs have now been found to be cases of
neosporosis caused by Neospora caninum, an
apicomplexan protozoan parasite that can infect
puppies in the neonatal period. Dogs are the
only proven definitive host for N. caninum. Its
life cycle is unknown, although transplacental
transmission has been shown in dogs. It has a
wide host range, but its zoonotic potential is
538
Back to contents
unknown. Older dogs may also be affected. Fatal
neosporosis has been documented throughout the
world and Neospora caninum has been isolated
in the USA and in several European countries.
These isolates may have significant biological
and genetic differences. Because many cases of
neurological disease previously diagnosed as
toxoplasmosis are now turning out to be examples
of neosporosis, the acronym TX-NS will be used
in the following discussion to encompass both
protozoa.
TX-NS in dogs resulting in a systemic infection
will typically affect most organs, and the CNS,
in particular. Neurological signs associated with
TX-NS encephalomyelitis are variable and may
reflect a focal or multifocal disease process. In
dogs, signs include hyperexcitability, depression,
intention tremor, paresis, paralysis, head tilt, and
seizures.
In the diagnosis of TX-NS neurological disease,
abnormal hematological parameters may
include non-regenerative anemia, neutrophilic
leukocytosis, lymphocyosis, and eosinophilia.
Serum alanine aminotransferase and aspartate
aminotransferase levels may be increased,
especially in dogs with acute hepatic and muscle
necrosis. Results of CSF may be abnormal,
with elevated protein content and a mixed
monocytic-polymorphonuclear pleocytosis.
An eosinophilic pleocytosis was found in
2 dogs with a granulomatous encephalomyelitis
due to protozoan infection. Xanthochromia
will be present if hemorrhage has occurred.
Electromyographic testing may reveal fibrillation
potentials, positive sharp waves, bizarre
high-frequency potentials, and myotonic-like
discharges. Nerve conduction velocities may
be decreased. Serum creatine kinase levels are
often increased. Protozoan meningoencephalitis
has been detected using MRI scans. The close
resemblance between T. gondii and N. caninum
tachyzoites and tissue cysts prevents definitive
diagnosis by histopathology, and the clinical
syndromes appear to be identical. Differentiation
between the two protozoan organisms can be made
using assays for circulating antibodies, by tissue
immunocytochemistry, and ultrastructural studies.
Sensitive polymerase chain reaction assays have
been reported for the detection of both Neospora
caninum DNA and Toxoplasma gondii DNA in
biological samples. Muscle biopsy of appropriate
muscles (as suggested by the clinical signs)
may also provide the possibility of a definitive
premortem diagnosis using the aforementioned
techniques. Prognosis is poor when signs of
pelvic limb spasticity are observed and is guarded
in any animal with signs of CNS disease. In
one study involving 27 cases of neosporosis,

recovery was less likely in peracute cases with
severe clinical signs, and when treatment was
delayed [535]. Many animals with myositis-
polyradiculoneuritis have concomitant lesions in
the CNS. A 4 to 8 week regimen of trimethoprim-
sulfonamide (at 15 - 20 mg/kg combined dose,
PO, bid) and pyrimethamine (at 1 mg/kg, PO,
daily) has successfully treated animals with TX-
NS-induced encephalomyelitis and myositis-
polyradiculoneuritis [378,411]. Clindamycin is
Back to contents
Ne
considered to be the drug of choice for treating
canine and feline toxoplasmosis, at a dose of 10
to 40 mg/kg/day, PO or IM, divided bid to tid.
This dose can also be used for treating dogs with
neosporosis. Clindamycin crosses the blood-
brain barrier. Oral and parenteral dosages are
similar because of the good intestinal absorption
of clindamycin. Oral clindamycin can cause
anorexia, vomiting, or diarrhoea in dogs and
cats.
2006 World Congress WSAVA/FECAVA/CSAVA
539
Ne
Ne - Neurology
BRAIN BIOPSY TECHNIQUES FOR DOGS & CATS
Richard A. LeCouteur, BVSc,
PhD, Diplomate ACVIM
(Neurology), Diplomate ECVN
University of Kalifornia
Davis CA 95616
USA
ralecouteur@ucdaviss.edu
The detection, localization and characterization
of brain lesions has been greatly improved
through the use of computed tomography (CT)
and magnetic resonance (MR) imaging, however
in most cases appearance alone provides only
a broad list of differential diagnoses for these
lesions. There remains a need to obtain an
intraoperative neuropathological diagnosis
from tissue samples of the lesion. In people
the intraoperative cytological evaluation of
smear preparations of brain lesions has become
a routine procedure, providing a rapid, highly
accurate diagnosis. In addition, future therapies
may involve intralesional administration of
drugs, following results of a brain biopsy. The
need to obtain biopsy material for diagnosis and/
or to deliver therapeutic agents with precision
and without an invasive surgical procedure has
stimulated the development and refinement of
image-guided brain biopsy.
For a number of reasons stereotactic brain biopsy
has been slower to develop in dogs and cats
as compared to people where it is viewed as a
routine procedure. Most commercially available
2006 World Congress WSAVA/FECAVA/CSAVA
systems use a cumbersome head-frame, designed
specifically for the human skull, and require
dedicated, expensive computer software for the
planning phase. More recently several different
techniques of image-guided brain biopsy have
been studied in dogs.
CT-Guided Free-Hand Needle Biopsy
CT-guided, free-hand needle biopsy of brain
tumors has been reported in a series of eight
dogs with intracranial lesions. The procedure
was performed in order to obtain a histological
diagnosis prior to initiation of treatment. Results
of the study indicated that although free-hand CT-
guided needle biopsy was a safe procedure, the
diagnostic yield was low, and incorrect (normal
tissue) samples were obtained in five of eight dogs.
540
Back to contents
In one dog in which a meningioma was diagnosed
by biopsy, necropsy results showed that the tumor
was in fact an oligodendroglioma. Error was
attributed to an inadequate amount of tissue being
obtained on biopsy. The low diagnostic yield was
especially disappointing considering the fact that
the investigators obtained four tissue samples
(each 1-2 mm in diameter) from each dog.
Pelorus Mark III Stereotactic Biopsy System
More recently modifications of the human CT-
guided Pelorus Mark III Stereotactic Systema
have allowed this system to be used very
successfully in obtaining biopsies of brain lesions
in dogs and cats. This system has been promoted
as being relatively inexpensive, mechanically
less complex, and easier to use than other
commercially available stereotactic systems.
The Pelorus Mark III Stereotactic System differs
from other devices in two important aspects
that have allowed its adaptation for use in dogs
and cats. It employs a simple metal ring as a
base plate to attach various imaging and biopsy
devices to the patient’s skull. Other systems
employ a large ring that encircles the patient’s
head like a crown. Secondly the translation of
the target coordinates from CT space to biopsy
frame space is accomplished mechanically on a
special phantom frame, and does not require any
propriety computer software.
Modifications of the human system are necessary
to accommodate the 90% shift in orientation of
the canine head as compared to the human head
during CT imaging, and to facilitate other phases
of the biopsy procedure that are affected by the
uneven and variable size and shape of canine and
feline skulls. This is accomplished by the addition
of a plastic adaptor skull ring to the system. This
adaptor ring, by having more screw holes, is more
easily attached to the dogs skull than the Pelorus
aluminum skull ring used in people. Placement of

AO spiked washers between the plastic adaptor
ring and the skull helped to secure the ring, which
is especially important in smaller patients.
The safe and accurate use of this device to
perform CT-guided stereotactic brain biopsies
in 50 dogs with intracranial lesions has been
reported by the author. Since that time it has
been used successfully in an additional 70 dogs
and cats. In the 50 dogs reported the stereotactic
brain biopsy diagnosis was compared with the
diagnosis obtained from surgical resection, or
necropsy in 22 animals. The stereotactic biopsy
provided a correct diagnosis in 20 dogs for an
overall diagnostic yield of 91%. This is similar to
the diagnostic yield reported in people.
Using this system, brain biopsies were most
easily performed on rostral fossa lesions. This
is related to the ease of attaching the plastic
adaptor ring over the relatively flat surface of
the frontal sinuses, and of drilling the biopsy
access hole through the skull when the biopsy
needle trajectory is nearly perpendicular to the
calvarial surface. Biopsy needle placement error
was significantly affected by lesion location, with
error being largest for caudal fossa lesions, and
intermediate for middle fossa lesions.
Intraoperative Diagnosis Using the Smear
Technique
The rapid cytological evaluation of a brain
lesion from a biopsy sample can provide crucial
information on operative management, medical
management, chemotherapy, or radiation therapy.
In people intraoperative cytological evaluation of
smear preparations of brain tumors, supported by
frozen and paraffin-embedded tissue, has become
a routine procedure, and cytological profiles of
smears of various types of human brain tumors
have been well described. Smear preparations are
generally wet fixed in 95% alcohol and stained
with hematoxylin and eosin although toluidine
blue, geimsa, or Papanicolaou’s stain may also
be used.
In a recent study, tissue samples were obtained
from lesions either by CT-guided stereotactic
brain biopsy (44 samples) or intraoperatively
during craniotomy (49 samples) and the results
from the smear technique compared with those
from sections of paraffin-embedded tissue.
The overall diagnostic accuracy from samples
obtained by both craniotomy and stereobiopsy
was about 80%. This compares favorably with
the 69-94% accuracy reported in some large
series of human cases. The main advantages of
this method of intraoperative diagnosis are speed,
ease of preparation, technical simplicity, need for
minimal equipment, high degree of cytological
resolution compared to frozen preparations, low
Back to contents
Ne
cost and small sample size required. A limitation
of this system is that it is difficult to prepare
adequate smear preparations in certain tough and
coherent tumors (e.g., schwannomas, fibrillary
astrocytomas, and some meningiomas). Smear
preparations provide excellent cytologic detail,
however these differ from the conventional
histologic appearance of HE-stained paraffin-
embedded tissue. Experience is required in the
correct interpretation of smear preparations.
a
Pelorus Mark III Stereotactic System, Ohio
Medical Instrument Company, Cincinnati, OH.
References
Harari J, Moore MM, Leathers CW, Roberts
GD, Gavin PR: Computed tomographic-guided,
free-hand needle biopsy of brain tumors in dogs.
Progress in Veterinary Neurology 1992, 4: 41-
44.
Koblik PD, LeCouteur RA, Higgins RJ, Bollen
AW, Vernau KM, Kortz GD, Ilkiw, JE: CT-guided
brain biopsy using a modified Pelorus Mark III
stereotactic system: Experience with 50 dogs.
Veterinary Radiology & Ultrasound 1999, 40:
434-440.
Koblik PD, LeCouteur RA, Higgins RJ, Fick J,
Kortz GD. Sturges BK, Pascoe PJ: Modification
and application of a Pelorus Mark III Stereotactic
system for CT-guided brain biopsy in 50 dogs.
Veterinary Radiology & Ultrasound 1999, 40:
424-433.
Moissonnier P, Bordeau W, Devauchelle P, Delisle
F, Doliger S: CT-guided stereotaxic biopsy of
intracranial lesions. Presented at the 7th Annual
Scientific Meeting of the European College of
Veterinary Surgeons, Poertschah, Austria, June,
1998. Vet Surg 1998, 27: 293 (abstr).
Moissonnier P, Blot S, Devauchelle P, Delisle F,
Beuvon F, Boulouha L, Colle M-A, 2006 World Congress WSAVA/FECAVA/CSAVA
Lefrançois T: Stereotactic CT-guided brain
biopsy in the dog: Cytological and histological
diagnosis and early complications in 23 dogs.
Presented at the 10th Annual Scientific Meeting
of the European College of Veterinary Surgeons,
Velbert, Germany, July 2001. Vet Surg 30: 296
(abstr).
Vernau KM, Higgins RJ, Bollen AW, Jiminez
DF, Anderson JV, Koblik PD, LeCouteur RA:
Primary canine and feline nervous system
tumors: Intraoperative diagnosis using the smear
technique. Vet Pathol 2001, 38: 47-57.
541
Ne
Ne - Neurology
CEREBROVASCULAR DISEASE IN DOGS
Simon R. Platt BVM&S
MRCVS Dipl. ACVIM
(Neurology) Dipl. ECVN
RCVS Specialist in
Veterinary Neurology Head
of Neurology / Neurosurgery
Unit
Centre for Small Animal
Studies
The Animal Health Trust
Lanwades Park
Kentford, Newmarket
Suffolk CB8 7UU
England
simon.platt@aht.org.uk
Cerebrovascular accidents (CVA) are one of the
major causes of disability among human adults.
Previously considered uncommon, CVA are
increasingly recognized in dogs or cats with the
advances of neuro-imaging. Most types of CVA
that are seen in humans have been documented in
dogs.1 Recovery from cerebrovascular disorders
in animals is probably more spectacular than in
humans because animals have a less prominent
pyramidal system.2 A ‘stroke’ is a suddenly
developing focal neurological deficit resulting
from a cerebrovascular accident.3 The causes of
strokes can be divided into two basic groups:
(1) obstruction of the blood vessels leading to
ischemia, and (2) rupture of blood vessel walls
leading to hemorrhage.4
The central nervous system (CNS) requires a
continuous supply of glucose and oxygen to sustain
its high expenditure of energy. The transportation
of these fuel molecules requires sufficient
2006 World Congress WSAVA/FECAVA/CSAVA
blood flow through a cerebral vasculature with
adequate capacity. In the dog, blood supply to the
brain arises from the basilar and internal carotid
arteries, which join at the base to form the arterial
circle of Willis.5 The cerebrum is supplied by
three pairs of cerebral arteries arising from this
arterial circle, with each one responsible for
the perfusion of large but overlapping areas of
the cerebrum.5 Any diseases which affect the
cerebral blood vessels will cause disturbances
of the cerebral blood flow (CBF) which in turn
can lead to tissue damage. The metabolism of the
brain is solely aerobic and without any significant
energy reserves. The exceptionally high demand
for circulating blood and oxygen is reflected is
reflected in the disproportionately high rate of
CBF compared with flow to other parts of the
542
Back to contents
body, comprising 20% of the cardiac output and
15% of oxygen consumption when the body is at
rest, even though the brain makes up only 2% of
the body weight.4
Cerebral ischemia is the reduction, although
not necessarily the cessation, of blood flow
to a level incompatible with normal function;
the impairment may be global or regional.4, 6
Ischemia, viewed simplistically as hypoxia plus
hypoglycemia, will affect the most sensitive
elements in the tissue, and if severe, persistent,
or both, perturb all components. In its mildest
form, impaired regional CBF causes a transient
ischemic attack (TIA). TIA has an abrupt onset
but is a rapidly diminishing neurological deficit
of vascular origin, which lasts for less than 24
hours.4, 5 This is well documented in humans but
has not been studied in dogs, although the authors
do believe that this occurs in dogs, occasionally
as a historical precursor to an infarction.
Severe ischemia, which in the CNS would
produce necrosis of the neurons and glial
elements, results in an area of dead tissue termed
an infarct.6 Severe arterial hypotension produces
bilateral infarction in the boundary or watershed
zones between major arterial territories.4 The
critical threshold values of CBF needed for
the maintenance of functional and structural
integrity of the brain has been determined to
be approximately 40% of the normal value (i.e.
approx. 20 ml/100 g per minute).4 From about
40% to 30%, increasing numbers of neurons are
unable to produce sufficient energy to maintain
the functions needed for the transmission of nerve
impulses, and at about 30% of normal blood flow
transmission ceases completely although the
cells can stay alive, as in a TIA. If regional CBF

further diminishes below about 15% of normal
(10-12 ml/100 g per minute), there is absolute
membrane failure resulting in an irreversible
nerve cell injury, as in an infarct.4 These levels
can be higher in an already compromised brain.
In humans, there are regions of vulnerability within
the brain where neurons are prone to be injured
by global hypoxia-ischemia and hypoxia. These
areas are the cerebral cortex, the hippocampus,
the amygdala, several basal and thalamic nuclei,
and the cerebellar cortical purkinje cells.6
Infarction can result from arterial obstruction or
venous thrombosis; arterial infarction can be due
to either obstruction from thrombosis or embolism
or to occlusion from blood vessel abnormalities
such as vasculitis.5 A number of classification
systems for ischemic stroke have been proposed
in humans. The most commonly used clinical
systems divide ischemic stroke into three major
stroke subtypes: large artery or atherosclerotic
infarctions, cardioembolic infarctions and small
vessel or lacunar infarctions.7 Atherosclerotic
infarctions are the most common subtype
documented in people.7 Although the frequency
of the three different subtypes is as yet unknown
in dogs, atherosclerosis has been reported in
dogs; it is especially seen in older dogs, dogs with
hypothyroidism, and Miniature Schnauzers with
idiopathic hyperlipoproteinemia.5 Other diseases
associated with infarction in dogs include
sepsis, coagulopathy, neoplasia and heartworm
infections.5 The use of MR with techniques such
as diffusion weighted imaging and angiography
may well help to define the subtype of infarction
in the future. Because of abundant venous
anastomoses, venous infarction is uncommon
in dogs; as arterial blood flow is preserved,
hemorrhage and edema tend to be more severe in
venous infarction than in arterial infarction.8
Cerebrovascular accidents can on occasion result
from hemorrhage.5 This can occur within or
around the brain and may result in rapid cerebral
dysfunction often by alteration in cerebral
volume (mass effect). It is classified as epidural,
subdural, subarachnoid, intraparenchymal
(primary or secondary), or intraventricular.5
When the bleeding is substantial enough to
form an excessive additional volume within the
CNS, the results can be fatal. The presence of a
hematoma initiates edema and neuronal damage in
surrounding parenchyma.9 Fluid begins to collect
immediately in the region around the hematoma,
and edema usually persists for up-to 5 days,9 and
in some cases as much as 2 weeks.10 Early edema
around the hematoma results from the release
and accumulation of osmotically active serum
proteins from the clot.9 Vasogenic edema and
cytotoxic edema subsequently follow owing to the
Back to contents
Ne
disruption of the blood-brain barrier, the failure of
the sodium pump, and the death of neurons.11 The
delay in the breakdown of the blood-brain barrier
and the development of cerebral edema after
intracerebral hemorrhage suggest that there may
be secondary mediators of both neural injury and
edema. It had been thought that cerebral ischemia
occurred as a result of mechanical compression
in the region surrounding the hematoma, but
recent studies in animals and humans have not
confirmed this.12 It is currently thought that blood
and plasma products mediate most secondary
processes that are initiated after an intracerebral
haemorrhage.12 Neuronal death in the region
around the haematoma is predominantly necrotic,
with recent evidence also suggesting the presence
of programmed cell death (apoptosis).12
The source of primary intraparenchymal
hemorrhage is incompletely understood but
human patients often have systemic hypertension
with concurrent fibrinoid degeneration of
arteries in the brain.13 Hypertension in dogs
may be primary or secondary to disorders such
as renal disease, and hyperadrenocorticism;
these animals may be predisposed to intracranial
hemorrhage.14 A variety of secondary causes
of hemorrhage exist in dogs. Dogs with brain
infarction can have associated hemorrhage, as
can dogs with intracranial tumors, vasculitis or
coagulopathies.5
Clinical signs: CVA are characterised clinically by
a peracute or acute onset of focal, asymmetrical
and non-progressive brain dysfunction.5
Worsening of edema (associated with secondary
injury phenomenon) can result in progression
of neurological signs for a short period of 24-
72 hours. Hemorrhage may be an exception to
this description and be presented with a more
progressive onset. Clinical signs usually regress
after 24-72 hours; this is attributable to diminution
of the mass effect secondary to hemorrhage
and reorganisation or edema resorption.15
With brainstem involvement, neurological 2006 World Congress WSAVA/FECAVA/CSAVA
examination of the cranial nerves will define the
exact location and extension of the lesion. With
forebrain lesion, the clinical sign may vary from
simple disorientation to death. A unilateral lesion
will induce ipsilateral circling, hemi-inattention
syndrome, contralateral central blindness, as
well as contralateral ataxia and proprioception
deficits. Seizures are reported to be very common
in association with CVA in dogs.16
Diagnosis
Blood and urine analysis is indicated to identify
the possible underlying causes described above.
Thyroid function (FT4, TT4 and endogenous
cTSH levels), a coagulation profile (including
a buccal mucosal bleeding time, a prothrombin
543
Ne
time, a partial thromboplastin time and fibrinogen
degradation products), and if possible multiple
systolic blood pressures and an ECG, should be
evaluated in any animal suspected of CVA. A
fecal analysis should be performed to rule out
parasitic infestation. Blood and urine cultures
are indicated in case of sepsis. Cerebrospinal
fluid analysis is unlikely to confirm a diagnosis
of CVA but may help to rule-out inflammatory
CNS disease or may on occasion reveal recent
haemorrhage (xanthochromia), normal to
increased protein and a mild neutrophilic or
mononuclear pleocytosis.5 Imaging studies of the
brain (computed tomography {CT} or magnetic
resonance imaging {MRI}) are necessary to
confirm the clinical neurolocalisation, re-enforce
the suspicion of CVA, identify associated mass
effect and rule-out other causes of focal brain
disorders (trauma, tumor, inflammation). CT
also allows rapid image acquisition, in addition
to the fact that changes associated with ischemia/
infarction can be detected as early as 3 to 6 hours
after the onset.7 Enhancement usually appears
after 24-48 hours and is most evident after 1
or 2 weeks especially in the periphery where
neovascularistion exists.17
MR imaging is more sensitive than is CT in
early infarction, with changes seen within an
hour if onset.18 Magnetic resonance imaging
is more sensitive in the detection of edema,
provides multiplanar views, and lacks beam-
hardening artifact when compared with CT.7
The conventional imaging findings in evolving
cerebral infarction are well characterized and
follow a temporal evolution similar in many
ways to that seen on CT.18 These changes seen
in ischemic parenchyma rely on an increase in
tissue water content.7 Gradually, during the acute
stage, the T2-weighted image becomes more
hyperintense in the ischemic region, particularly
over the first 24 hours 7 These signal changes seen
2006 World Congress WSAVA/FECAVA/CSAVA
in the first 24-hours are best appreciated in grey
matter and are well visualised in deep grey matter
structures such as the thalamus or basal ganglia,
in addition to cortical grey matter. Gadolinium
enhances infarcts because of vascular rupture but
does not enhance ischemia or edema.
Computed tomography is very sensitive for
acute hemorrhage, with a linear relationship
demonstrated between CT attenuation and
hematocrit.19 In a patient with a normal
hematocrit, acute hemorrhage is seen as an area
of increased attenuation, which tends to increase
for the first 72 hours and then slowly decreases to
isodensity at about 1 month post-hemorrhage.19
The periphery of the lesion may enhance from
approximately 6 days to 6 weeks after onset, on
a CT scan.
544
Back to contents
The initial MRI appearance of haemorrhage is
dependent on the age of the hematoma, among
other determinants, which determines its unique
signal intensity patterns.20 Localization of
hemorrhage to the parenchyma or ‘extra-axial’
space is central to assessing the etiology and
the initiation of treatment.20 In dogs, it is more
common to see intraparenchymal than ‘extra-
axial’ hemorrhage, the latter of which is typically
subdural in location.
Other imaging modalities which may be utilised to
investigate CVAs include; cerebral angiography,
to demonstrate vascular malformations; cerebral
scintigraphy as a non-specific way to identify
a brain lesion; Doppler ultrasonography to
analyse cerebral blood flow; and single photon
emission computed tomography (SPECT) to
analyse regional blood flow. These modalities
are not frequently used now as the advances
possible with MR technology mean that blood
vessel abnormalities and regional blood flow can
be assessed in conjunction with the structural
abnormalities suggestive of a CVA.
Treatment and prognosis
There is no specific treatment for infarctions and
the majority of intraparenchymal hemorrhages.
The treatment of any type of CVA focuses
on maintaining cerebral perfusion, through
maintenance of systemic blood pressure, and
subsequent tissue oxygenation, as well as the
management of secondary neurologic sequelae
such as seizures, and the treatment of any
underlying diseases. The outcome of dogs with
CVA depends on the size of the lesion, the
location of the lesion and the severity of the
clinical signs. Many cases of cerebral infarctions
can improve dramatically over a few days to
weeks; however, these cases are at risk of multiple
events. Intraparenchymal hemorrhage may also
cause reversible signs but the severity of both the
clinical signs and the underlying diseases may
often be more severe.
References
1. Frankhauser R, Luginbuhl H, McGrath JT.
Cerebrovascular disease in various animal
species. Ann N Y Acad Sci 1965; 127: 817-859.
2. DeLahunta A, ed. Veterinary Neuroanatomy
and Clinical Neurology. Philadelphia: W B
Saunders Co. 1983: 130-155.
3. Garcia JH. The evolution of brain infarcts: a
review. J Neuropathol Exp Neurol 1992; 51: 387-
393.
4. Kalimo H, Kaste M, Haltia M. Vascular
diseases. In: Graham DI, Lantos PL, eds.
Greenfield’s neuropathology. London: Arnold,
2002: 281-355.

5. Thomas WB. Cerebrovascular disease. Vet Clin
N Am: Small Anim Pract 1996; 26: 925-943.
6. Summers BA, Cummings JF, de Lahunta
A. eds. Veterinary Neuropathology. St. Louis:
Mosby. 1995: 208-350.
7. Marks MP. Cerebral ischemia and infarction.
In: Atlas SW, ed. Magnetic imaging of the brain
and spine. Philadelphia: Lippincott Williams
&Wilkins 2002: 919-979.
8. Toole JF, Burrow DD. Pathophysiology and
clinical evaluation of ischemic vascular disease.
In: Youmans JR, ed: Neurological surgery.
Philadelphia: WB Saunders Co 1990: 1463-
1515.
9. Wagner KR, Xi G, Hua Y, et al. Lobar
intracerebral hemorrhage model in pigs: rapid
edema development in perihematomal white
matter. Stroke 1996; 27: 490-497.
10. Zazulia AR, Diringer MN, Derdeyn CP,
Powers WJ. Progression of mass effect after
intracerebral hemorrhage. Stroke 1999; 30: 1167-
1173.
11. Wagner KR, Xi G, Hua Y, Kleinholz M, de
Courten-Myers GM, Myers RE. Early metabolic
alterations in edematous perihematomal brain
regions following experimental intracerebral
hemorrhage. J Neurosurg 1998; 88: 1058-1065.
12. Qureshi AI, Tuhrim S, Broderick JP, Batjer
HH, Hondo H, Hanley DF. Spontaneous
intracerebral hemorrhage. N Engl J Med 2001;
344: 1450-1460.
Classes & Causes of Cerebral Infarction
Class of Infarction
(i) Arterial Obstruction
Thrombosis
Embolism
(ii) Arterial Occlusion
(iii) Venous Thrombosis
Back to contents
Ne
13. Castel JP, Kissel P. Spontaneous intracerebral
and infratentorial hemorrhage. In: Youmans JR,
ed: Neurological surgery. Philadelphia: WB
Saunders Co 1990: 1890-1917.
14. Dukes J. Hypertension: A review of the
mechanisms, manifestations, and management. J
Small Anim Pract 1992; 33: 119-129.
15. Kazui S, Naritomi H, Yamamoto H, Sawada
T, Yamaguchi T. Enlargement of spontaneous
intracerebral hemorrhage. Incidence and time
course. Stroke 1996; 27: 1783-1787.
16. Shores A, Cooper TG, Gartrell CL, et al.
Clinical characteristics of cerebrovascular
disease in small animals. In, Proceedings of the
9th American College of Veterinary Internal
Medicine Forum 1991: 777-778.
17. Inoue Y, Takemoto K, Miyamoto T, et al.
Sequential computed tomography scans in acute
cerebral infarction. Radiology 1980; 135: 655-
662.
18. Brant-Zawadzki M, Periera B, Weinstein P, et
al. MR imaging of acute experimental ischemia
in cats. Am J Neuroradiol 1986; 7: 7-11.
19. Grossman RI. Intracranial hemorrhage. In,
Latchaw RE, ed. MR and CT imaging of the
head, neck, and spine. St. Louis: Mosby Year-
Book, 1991: 171-202.
20. Atlas SW, Thulborn KR. Intracranial
hemorrhage. In: Atlas SW, ed. Magnetic imaging
of the brain and spine. Philadelphia: Lippincott
Williams &Wilkins, 2002: 773-832.
Causes of Infarction
2006 World Congress WSAVA/FECAVA/CSAVA
• Atherosclerosis (Hypothyroidism /
hyperlipoproteinemia / idiopathic)
• Extension of CNS infection
• Sepsis
• Neoplasia
• Dirofilaria immitis
• Heart disease
• Vasculitis
• Arteriosclerosis
• Inflammation
• Neoplasia
545
Ne

Classes & Causes of Cerebral Hemorrhage

Class of Hemorrhage Cause of Hemorrhage
(i) Primary • Hypertension
(ii) Secondary • Hemorrhagic infarction·
• Cerebral amyloid angiopathy
• Vascular malformation
• Neoplasia
• Vasculitis
• Coagulopathy

Time Course of Evolving Infarction on Computed Tomography

Time after Infarction CT Characteristics
0 – 24 hours Normal or subtle hypodensity +/- sulca effacement
1 – 7 days Mass effect (peaks at 3-4 days)
Days to months / years Hypodensity
1-8 weeks Contrast enhancement
Weeks to years Atrophy

Acute infarction: Conventional Magnetic Resonance Findings

1. Lesion in arterial distribution
2. High intensity on proton density / fluid attenuated inversion
3. Gyri swollen, sulci effaced
4. Subcortical white matter hypointensity
5. Intravascular contrast enhancement
2006 World Congress WSAVA/FECAVA/CSAVA

Physiologic factors influencing magnetic resonance appearence of hematomas

Age of hemorrhage (Table 4b.)
Site of hemorrhage
Size of hemorrhage
Local partial pressure of oxygen
Local pH
Hematocrit
Blood-brain barrier integrity
Presence of underlying lesion

546
Back to contents
 Ne
Physiologic factors influencing magnetic resonance appearance of hematomas
Effect of Age of Hematoma on its Magnetic Resonance Imaging Charateristics

Biochemical Clinical Approximate Time Intensity* Intensity*

Form Stage of Appearance on T1- on T2-
weighted weighted
Image Image
OxyHb in RBCs Peracute Immediate to first ≈ ↑
several hours
DeoxyHb in RBCs Acute Hours to days ≈↓ ↓↓
MetHb in RBCs Subacute First several days ↑↑ ↓↓
Extracellular MetHb Subacute to Chronic Days to months ↑↑ ↑↑
Ferritin & Hemosiderin Chronic Days to indefinite ≈↓ ↓↓

* Signal intensity is relative to normal brain parenchyma

2006 World Congress WSAVA/FECAVA/CSAVA

547
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

O
O
Oncology
ncolog

Back to contents

O – Oncology
SARCOMAS OF SOFT TISSUES
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
INTRODUCTION
Sarcomas of soft tissues (STS) are common
in companion animals and pose a therapeutic
and diagnostic challenge for the practising
veterinarian. STS is defined as a malignant
tumour of the extraskeletal connective tissues.
These tissues, all of mesoderm origin, surround,
support or connect other anatomic structures and
are present in any part of the body. Because soft
tissues are estimated at 40% proportional body
weight, it is not surprising that numerous soft
tissue tumours arise with regularity. STS form
an assembly of tumours of different histogenetic
origin, with ubiquitous localisation possibilities,
and variation in biological behaviour. Still, STS
are often grouped together because of their
shared mesodermal origin, similarities in clinical
presentation, and communality in diagnostic and
therapeutic approach.
In general, STS are fleshy (the Greek word
‘Ѕαρκομα’ or ‘sarkoma’ is often translated as
flesh-like mass), infiltrative and locally aggressive
tumours that have a variable metastatic potential.
This chapter will describe the common STS in
dogs and cats. Visceral and other organ-specific
STS (e.g., splenic hemangiosarcoma) will be
discussed in the representative chapters.
INCIDENCE
STS are common tumours and comprise from 15%
(skin and subcutaneous tissues) to 35% (spleen)
of all canine tumours, dependent on original
tumour location. Cats are afflicted less frequently
(7% reported for skin and subcutaneous tissues).
The annual incidence of STS in the United
States is estimated to be 35/100.000 for dogs
and 17/10000 for cats at risk. These data are not
available for the European countries.
Back to contents
O
EPIDEMIOLOGY
Little is known about the pathogenetic cause of
STS in dogs and cats. Changes in genetic make-
up, chronic trauma, foreign bodies, vaccinations,
parasites and radiation have been associated
with STS in both species. P53 mutations and
MDM2 gene amplification were observed in a
subgroup of canine soft tissue sarcoma; however,
familial predispositions have not been reported.
No sex or breed predilections have been found,
although certain breeds seem to be afflicted
with tumours more commonly than others.
For example, retrievers seem predisposed to
development of soft tissue sarcomas of the head
(oral cavity/mandibular/maxillary region) with
often a low grade histologic appearance but high
aggressiveness. Whether STS predisposition is
caused by a breed-specific genetic abnormality
or by a high inbreeding coefficient due to the
popularity of the breeds, is at present unknown.
In general, most studies report medium to large
breeds to be affected more commonly, with a
overrepresentation of the older animal. Trauma
was associated with the incidence of STS. It is 2006 World Congress WSAVA/FECAVA/CSAVA
unclear if trauma causes an owner to be more
aware of problems in that area or if trauma is an
initiating cause in STS. The presence of foreign
bodies or material (such as vaccinations) may
induce chronic stimulation of the tissues and
promote neoplastic transformation. An example
of this is the parasitic infestation of Spirocerca
Lupi and the incidence of oesophageal cancer.
Radiation has also been associated with sarcoma
formation, although sarcoma formation after
extracorporal therapeutic radiation seems to be
rare.
CLASSIFICATION
All soft tissues are exposed to the risk of benign
or malignant tumour formation. Extensive
549
O
classification schedules are available from
human literature and are simplified to fit into
the companion animal situation (Table 1). Any
classification schedule, however, is complicated
by overlapping patterns of dedifferentiation or
by the inability to recognize the appearance of
the cell of origin. A classification by localisation,
grade and tumour stage seems more logical and
may prove more useful at present. Advances
in histochemical, electron microscopic and
biogenetic markers will improve the ease of
classification in the future. Muscle actin, desmin,
vimentin, factor VIII actigen and lysozyme
are suggested to be useful for the differential
diagnoses of STS, and cytokeratins for synovial
cell sarcomas specifically.
DIAGNOSIS
The diagnostic plan for STS is not essentially
different from any other tumour type. The physical
appearance is noticed depending on the location
of the tumour and, in general, peripherally-
located tumours are more easily detected and
often smaller than more centrally-located STS.
Clinically, STS often are solid masses that seem
well-circumscribed and encapsulated. However,
this is based upon the presence of a pseudocapsule
of atrophic remains of surrounding tissue and
wedged tumour cells, while infiltration through
this pseudocapsule and through fascia leads to
attachment to deeper structures.
Pain is associated with location, pressure of the
tumour or tumour invasion. Some peripheral
nerve sheath tumours have been reported to be
sensitive to the touch. A clinical differentiation
between benign and malignant is not possible, so
additional diagnostics are necessary. Moreover,
rate of growth of the tumour often does not predict
the biologic behaviour correctly. Additional
biopsy specimens should be obtained in all cases.
The easiest method of biopsy is fine needle
2006 World Congress WSAVA/FECAVA/CSAVA
aspiration (FNAB), and this method should be
used as the first step in the diagnosis. Although
many STS are not well-diagnosed by FNAB
because of their limited exfoliative character,
many other tumour types can be excluded as well
as some inflammatory processes; in particular if
infection can be demonstrated while overlying
skin is intact. Chronic traumatic inflammation
as cytologic diagnosis of FNAB should fit with
history and site. In case of any doubt, and in
particular also if cytology indicates mesenchymal
proliferation in absence of an inflammatory
response, this provides a solid indication for
further diagnostic work-up. Incisional, excisional
or thick needle core biopsy (TNCB) specimens
should be obtained. TNCB is the easiest and
fastest method and requires minimal sedation.
550
Back to contents
Multiple core biopsies should be performed and
submitted to the pathologist. Sufficient tissue,
however, is often better acquired by incisional or
excisional biopsies. Excisional biopsies are only
advantageous when adequate margins can be
obtained. In all other cases an incisional biopsy is
preferred. Normal tissue should be incorporated
in the biopsy specimen to evaluate peripheral
infiltration of the tumour. Incisional biopsies
should always be performed in such a manner
that removal of the scar is possible in future
radical excisions or adjunctive radiation therapy
protocols. Adjunctive diagnostic evaluations
should include routine blood work, radiographs
of the local tumour site for possible underlying
bone infiltration, ultrasound of the tumour,
radiographs of the chest for possible metastatic
spread, FNAB of the regional lymph node and
CT or MRI imaging techniques.
In evaluating soft tissues, MRI has many
advantages over CT imaging, however, is often
not available or cost-effective. A pulmonary
CT scan is preferred above plain radiographs.
Although haematogenous spread of STS is more
common, undifferentiated STS may spread to
regional lymph nodes, warranting evaluation of
these lymph nodes. For example, synovial cell
sarcomas are often reported to spread through the
lymphatics. Proper imaging should be performed
of more centrally-located lymph nodes along the
lymphatic tract, in cases of suspected or proven
metastasis to the regional lymph node. For
example, metastasis to regional lymph nodes in
the limb or inguinal area, should be followed by
ultrasound examination of the internal iliac area.
In addition, there are indications that splenic
metastases are not uncommon in cases with
synovial cell sarcomas.
The most important factors in STS evaluation are
the determination of tumour grade and tumour
stage. Tumour grade is determined through
histological evaluation and varies among grade
I (low grade or well differentiated) to grade III
(high grade or poorly differentiated). Tumour
grade is determined by degree of differentiation,
cellular pleiomorphism, cellularity and matrix
formation, as well as mitotic index and amount of
tumour necrosis. Experienced pathologists may
apply a different weight to the respective factors
in different types of STS to assess tumour grade.
In human sarcomas, the tumour grade has a major
impact on tumour staging. Tumour staging is
based on four parameters: histological grade (G),
tumour size (T), regional lymph nodes (N), and
distant metastasis (M) (Table 2). Factors reported
to be of prognostic importance in canine STS are
size, site, grade and presence of local or distant
metastases. The prognostic effect of localisation

of the tumour is most likely dependent on the
difficulty of complete excision. The higher the
stage of the disease, the poorer the prognosis
GENERAL CONSIDERATIONS
STS pose a problem to the veterinarian mainly
because they tend to be locally aggressive.
Complete surgical excision is often impossible
because of localisation or size of the tumour.
Recurrence is common after incomplete resection
and is the primary reason to refer STS to the
Utrecht University Surgical Oncology Service.
Most recurrences will occur within 2 years after
primary tumour removal. Recurrence is caused
because STS tend to spread into deeper or
surrounding tissues by invasion or extension next
to natural anatomic structures. These finger-like
outgrowths of the tumour are often compared to
the tentacles of an octopus. Cutting of the tumour
mass (cf. body of the octopus) leaves these tumour
extensions (cf. tentacles) in the patient. Through
this, the tumour homeostasis is disrupted and fast
growing tumour cells thrive causing fast tumour
regrowth. Early detection and diagnosis of the
original STS will facilitate complete removal and
prevent recurrence. Shelling out STS is the most
common cause for recurrence. Education and
communication should be directed in the future
to achieve these goals of early detection and
complete removal.
Overall metastatic rate is estimated to be 20%.
Among STS subtypes there exists considerable
variation. In part, this appears based on a link
between subtype and frequency distribution
of histologic grade. Low to moderate rate
of metastasis is seen in (mostly low grade)
hemangiopericytoma and the closely related
malignant peripheral nerve sheath tumour.
Similarly, a low to moderate rate of metastasis
is seen in most fibrosarcomas (the subgroup of
oral cavity/mandibular/maxillary fibrosarcomas
is the exception to the rule). Synovial cell
sarcoma and undifferentiated sarcomas are more
frequently of high grade and have a relatively
high rate of metastasis, i.e., 40-60%. Rhabdo or
leiomyosarcomas are relatively less common,
and liposarcomas are rare; these last subtypes
have a moderate rate of metastasis, except for
embryonal rhabdomyosarcoma (high rate).
Metastases spread by haematogenous routes
and lymph node involvement is reported to be
rare. High grade tumours, such as synovial cell
sarcoma and rhabdomyosarcoma have an higher
incidence of lymphatic spread especially in late
stages of the disease.
Back to contents
O
HISTOLOGICAL SUBTYPES
Fibrosarcoma
Fibrosarcoma (FSA) was the most commonly
diagnosed STS. The recent more complete
pathological differentiation in subtypes, however,
will decrease the total number of ‘pure’ FSA in
dogs and cats. For instance, neuroFSA, a diverse
group of tumour types derived from fibroblast
associated with nerves, are currently grouped
under the nomenclature malignant peripheral
nerve sheath tumours (PNST) instead of under
FSA. Per definition, FSA are tumours derived
from the fibrocytes. FSA are relatively more
common in the cat than in the dog and have a
locally-aggressive behaviour. They can occur
anywhere in the body, but are most commonly
seen in the skin and subcutaneous tissues and the
oral cavity. The canine, histologically-low-grade-
and-biologically-high-grade, FSA, located in the
oral cavity, and mandibular and maxillary region,
is a tumour that should be mentioned specifically.
This tumour, most commonly associated with
young dogs, has an aggressive biological
behaviour, whilst diagnostic surgical biopsies
depict a low histological grade. Feline FSA occur
often on the limbs in older animals without a sex
or breed predilection.
Malignant peripheral nerve sheath tumours
(PNST)
Malignant PNST contain a group of tumours with
varying nomenclature. Included in this group are
neurofibrosarcoma and malignant schwannoma.
PNST are locally aggressive and metastasise
rarely (in less than 20% of the dogs). Metastasis
rate is dependent on tumour grade, however. It
is unclear at this moment what the cell of origin
is in these tumours (i.e., fibrocytes or Schwann
cells). PNST can occur anywhere in the peripheral
nerve system. The most common location is the
subcutaneous tissues of the distal extremities in
2006 World Congress WSAVA/FECAVA/CSAVA
de dog. PNST located in the closer proximity
to the vertebrae (including those in the region
of the plexus brachialis) often will cause nerve
compression and signs of pain and neurological
deficit. Invasion of these tumours into the spinal
cord is not uncommon and may be seen in over
half of cases of high histological grade. Before
surgery, a CT-scan (or MRI) of the region is
advised.
Haemangiopericytoma (HPC)
Haemangiopericytomas (HPC) were believed for
long to stem from pericytes (cells with contractile
properties surrounding small blood vessels),
though proof is lacking for this histogenetic
origin. HPCs form a whorl-like growth pattern
551
O
at histological examination without visible
connection with nerves. Biological behaviour
of HPCs is similar to that of PNST, and many
will stain positive for the immunohistochemical
marker S100, indicating peripheral nerve origin.
Therefore, some authors group HPC under PNST.
HPC often have a slow rate of growth, yet are
locally aggressive (infiltrative), but have a low
(<15%) rate of metastasis. Older dogs (with boxers
predisposed) are affected, and HPC consists of
5% of all skin and subcutaneous tumours. Most
HPC’s are located on the extremities.
Myxosarcoma
Myxosarcoma are FSA containing connective
tissue cells that produce intracellular mucin. These
tumours are often soft to the touch, but behave
similarly to other FSA, in which tumour grade is
the most important predictor of behaviour.
Haemangiosarcoma (HAS)
HSA are common tumours that arise from
endothelial cells of blood vessels. HSA commonly
are located in body cavities and are of extreme
aggressiveness (see related chapter). Somewhat
less common, they originate of capillaries in
dermis, subcutis or deep-seated tissues, including
muscle or even bone.
Dermal/subcutaneous HSA have been reported in
certain breeds (Whippet, Saluki, Blood Hound,
pointers) and may be associated with exposure
to ultraviolet light. Predilection sites include
abdomen, prepuce and hind legs. Rupture of bad-
quality, tumourous blood vessels is not rare, and
may lead animals to be presented with haematoma,
with or without knowledge by the owner of a pre-
existing lump in the same area. Behaviour of
extracavitary HSA depends on location and size.
Strictly dermal HSA without invasion have a fair
prognosis, with assessments of less than a 25%
rate of metastasis. High rates of metastasis are
2006 World Congress WSAVA/FECAVA/CSAVA
seen with invasive lesions and with those of deeper
anatomical location. Multifocal manifestation of
HSA is not only seen with visceral forms, but
also sometimes at dermal/subcutaneous sites,
posing a major problem in the therapy. Dermal
(stage I) HSA are small tumours, often located
in the ventral-abdominal or preputial region, and
associated with longer survival times (median
survival 780 days) than the hypodermal (stage II)
and deep muscular (stage III) located tumours.
The deep muscular HSA have a larger size, do not
have an anatomical predilection, and generally
have a shorter survival (median survival 172
and 307 days, respectively). The majority of the
cutaneous HSA, however, are superficial tumours.
There appears to be some influence of hair length
and skin colour. Dogs with short hair coats and
552
Back to contents
lightly pigmented skin have more dermal type of
HSA, less subcutaneous types, and more HSA of
ventral smooth and hairless skin.
Liposarcoma
Liposarcomas are rare, malignant tumours
derived from fat cells. Liposarcomas are observed
in older animals and may be associated with
foreign bodies or obesity. Liposarcomas are often
firmer than ‘normal’ lipomas, are poorly defined
and often occur in the ventral region of the body.
Biological behaviour is characterised by local
infiltration and early metastasis. Infiltrative
lipoma is a form that is described in the dog and
is comparable with the human well-differentiated
liposarcoma. They have an infiltrative behaviour
and are difficult to remove locally because of
their infiltrative nature. Infiltrative lipomas
are often observed in the muscles of the front
and hind legs. Infiltrative lipomas can only be
distinguished from benign lipomas if muscle
invasion is present histologically. Clinically, they
appear more attached to the deeper structures and
less encapsulated.
Lymphangiosarcoma
Lymphangiosarcoma are rare tumours of the
lymph vessels. Although often described in young
animals, they can affect dogs and cats of all ages.
The ventral thorax and abdomen is a predilection
site of the cat. The tumours have a soft and cystic
like appearance and may coincide with peripheral
oedema. Lymph fluid may ‘sweat’ through the
skin of affected sites. Lymphangiosarcomas are
invasive and have a high metastatic potential
Leiomyosarcoma
Malignant transformation of smooth muscle cells
are the origin of leiomyosarcoma. They can occur
in any part of the body, but are described as firm,
lobulated masses most commonly associated
with the digestive tract from oesophagus to
rectum or the urogenital tract. Clinical signs
may relate to obstruction or bleeding due to
ulceration. Transformation of benign leiomyomas
to leimyosarcomas has been suggested but not
scientifically proven. Leiomyosarcomas are
infitrative tumours that metastasise late in the
disease process. Multiple leiomyosarcomas are
possible and warrant thorough examination
of the abdomen before or during the surgery.
Paraneoplastic hypoglycaemia has been
associated with leiomyosarcoma.
Rhabdomyosarcoma
Rhabdomyosarcoma, a tumour from the striated
muscle cells, is relatively rare in the dog. Two
forms have been described: the first occurring in

the urogenital tract of young dogs (mainly bladder)
and is referred to as juvenile-type or botryoid
rabdomyosarcoma. The second form occurs
in the older animal and is described affecting
the tongue, pharynx, myocard and rarely other
skeletal muscle locations Rhabdomyosarcomas
are locally aggressive and metastasise early.
Synovial cell sarcoma
Synovial cell sarcoma (SCS) are tumours that arise
from tenosynovial tissue and are often associated
with lameness. Predilection sites are the stifle and
elbow joint but other locations near joints, tendons
or bursae have been described. Also, in this
tumour type, the origin of the tumour cell is not
clear (synovial cell versus periarticular connective
tissue cell). Histologic typing may divide those
with one-cell population (monophasic) from those
with two-cell populations (biphasic), with either
one being epithelial-like, the other mesenchymal.
Immunohistochemistry often demonstrates a
positive signal for both cytokeratins as well as for
desmin, reflecting the mixed differentiation. Local
invasion of underlying bone is common in later
stages of the disease and is easily recognisable on
routine radiographs by punched-out bone lesions.
The tumour invades the bone at the attachment
of the joint capsule or tendons to the bone. SCS
are locally aggressive and metastasise late in the
disease process. Metastasis rates of up to 50%
have been reported, again depending on tumour
grade. SCS metastasise to lymph nodes, lungs,
spleen and liver.
TREATMENT
Surgery is the primary therapy of STS, with or
without adjunctive therapy. The surgical goal is
to completely remove the STS and, as a result,
a large margin of normal tissue is sacrificed. An
example of this type of surgery is the amputation of
a limb. Limb-sparing surgeries are an alternative,
but can only be performed in combination
with adjunctive therapy modalities such as
radiotherapy, chemotherapy and immunotherapy.
Surgery
Surgery is only successful if large margins of
normal tissue are obtained, with margins of 2-
3 cm normal tissue advocated. The objective
local failure rate for marginal excisions (peel-
out or shelling-out STS) in humans is 86%;
however, these rates, based on large numbers,
are unknown in dogs and cats. Failure rates
after wide local excisions and more radical
excisions (such as amputations) were 49% and
14% in humans, respectively. Extrapolation
from human data is tempting, but should be
interpreted with caution. Recurrence rates of 60-
Back to contents
O
70% are reported in marginally-excised, canine
haemangiopericytomas and STS. Although most
STS tend to recur within a year after surgery,
adequate follow-up of 2 to 3 years is necessary.
Wide surgical excision is often complicated by the
anatomic localisation of the tumour to important
structures. In these cases a more conservative
surgery is planned (eg. limb spare). The owner
should be made aware of the increased chance
of recurrence compared to radical excision. In
general, a repeat surgery is more complicated if the
STS has recurred and failure is more likely. The
first surgery has the largest chance for complete
removal. Recurrence, as of yet, is not associated
with an increased risk of metastases, however.
It is the authors’ opinion that the incidence of
metastases depend more on tumour grade than on
the type of surgery performed. The recurrence rate
decreases when the surgery is performed by more
experienced oncologic surgeon. Experience often
correlates to a more radical surgery, knowledge
of innovative reconstruction techniques and
better understanding of the pathophysiological
properties of the tumour.
Radiation therapy
Conventional techniques of radiation are rarely
successful, while fractionated radiotherapy as a
sole therapy using megavoltage irradiation yields
a one-year control of about 50-60%. Radiation
therapy is associated with acute-onset and with
chronic side effects. Radiation is more effective
with minimal (microscopic) disease than with
more bulky disease. Radiation in combination
with surgery results in increased disease free
intervals. The radiation therapy is used to treat
the microscopic disease left behind after marginal
excision of the tumour bulk, achieving identical
results compared to radical excision (80-90%
at 2 years). Forrest, et al. (J Vet Med Intern
2000) showed a median time to recurrence after
incomplete excision of STS and radiotherapy of
2006 World Congress WSAVA/FECAVA/CSAVA
798 days. Of STS-subtypes, HPC seems relatively
sensitive. Surgical excision and radiotherapy did
not increase median tumour-free and survival
times compared to complete excisions in feline
FSA. Most cats of the first group had incomplete
(dirty) surgical excisions, however.
Radiation has also been used in combination with
local or whole-body hyperthermia. The addition
of whole body hyperthermia was not associated
with a better local tumour control, and most dogs
experienced local failure or metastatic disease.
Two-year recurrence free rates of approximately
30% were described.
Intraoperative radiotherapy has been described
to cause STS formation in approximately 20% of
dogs treated.
553
O
Chemotherapy
Chemotherapy can be used to treat local
and systemic disease. Chemotherapy is used
for palliation in macroscopic and may be of
limited benefit in eliminating miscroscopic
local or metastatic disease in STS. Multidrug
chemotherapy protocols, including anthracyclines
(doxorubicin, mitoxantrone), have been
advocated as the most successful. Combination
therapy of an anthracycline with vincristine
and cyclophosphamide appear more effective
in a limited series of STS. The scientific data
supporting the efficacy of these protocols in
dogs and cats are currently missing, however.
More randomised studies using large populations
evaluating the effect of chemotherapy are
necessary.
Immunotherapy
The treatment of STS with immunotherapy is
under review at Utrecht University. Interleukin-2,
a cytokine and immunostimulant, was combined
2006 World Congress WSAVA/FECAVA/CSAVA
554
Back to contents
with marginal surgery in a pilot study of 17 dogs
with MPNST and is currently tested in a double-
blind prospective study. The initial results from
the pilot study are encouraging. A pilot study in
17 dogs showed a recurrence free percentage at
two years of approximately 70%.
Photodynamic therapy
Photodynamic therapy was used after surgery
in dogs with HPC and appeared to have no
advantage over other forms of therapy in
regards to preventing recurrence. Complications,
including delayed wound healing and infection,
and limited efficacy decrease the applicability of
this therapy type in dogs with STS.
REFERENCE
Kirpensteijn J, Rutteman GR, BSAVA Manual
2003

O – Oncology
RECENT ADVANCES IN MAST CELL TUMORS
Gregory K. Ogilvie, DVM,
Diplomate ACVIM (Specialties
of Internal Medicine, Oncology)
Director, CVS Angel Care
Cancer Center (www.
CVSAngelCare.com)
President, Special
Care Foundation for
Companion Animals (www.
SpecialCareFoundation.org)
100 North Rancho Santa Fe
Rd #100
San Marcos CA 92024 USA
Gogilvie@aol.com
Very few tumors present in such a wide variety
of clinical signs: they are indeed the great
impostors! They can look like anything and
behave differently depending on the histologic
type, location and the extent of the disease. The
following is a brief discussion about these tumors.
Some highlights are as follows:
• Mast cell tumor granules do not stain well with
Diff Quick type stains unless they are “soaked” in
the alcohol for several minutes prior to staining.
• Some important prognostic indicators include
duration of presence, location and histologic type
in the dog.
• Mast cell tumors tend to metastasize to nodes,
liver spleen and bone marrow...rarely to lungs.
• Radiation therapy is extremely effective for
controlling local disease.
• Prednisone and vincristine when used as single
agents induce a remission (partial or complete) in
about 23% of the tumors.
Diagnostics
Diagnosis of mast cell tumors often can be
made by a fine needle aspiration cytology but
excisional biopsy is required if accurate histologic
grading of the tumor is desired. Mast cell tumors
are classified as round cell tumors along with
lymphosarcoma, histiocytomas and transmissible
venereal tumors.
Diagnostic workup of mast cells usually includes
a number of procedures. These include a complete
blood cell count (CBC), serum chemistry
profile, and urinalysis. In addition, fine needle
aspiration of the lesion, regional lymph nodes and
examination of buffy coats or bone marrow helps
to determine the extent of tumor involvement.
A CBC is valuable in assessing animals with
mast cell tumors because those animal patients
Back to contents
O
with systemic mastocytosis occasionally have
peripheral eosinophilia and basophilia in addition
to circulating mast cells. Mastocytemia is a more
common clinical phenomenon in the cat than
in the dog. The CBC may also give evidence
of gastrointestinal bleeding or gastrointestinal
perforation. In general, mastocytosis associated
with primary cutaneous tumors is more easily
detected by examination of the buffy coat or bone
marrow than by examination of peripheral blood.
Care must be exercised in interpreting buffy
coats since mastocytemia has been reported in a
variety of acute inflammatory diseases of the dog
including parvovirus infections. Peripheral mast
cell counts may be high in cats with mastocytosis
and have accounted for up to 25% of the total
white cell count.
Therapy
Surgical considerations include wide surgical
margins with at least 3 cm of normal looking 2006 World Congress WSAVA/FECAVA/CSAVA
skin around the tumor should be removed when
possible. The 3 cm recommendation is a guideline
and might not be feasible when the tumor is
located on the face, lower limbs or in the inguinal
region. It should be remembered that most mast
cells extend laterally to adjacent tissue rather
than deep into underlying muscles. All excised
tumor should be examined histologically for the
completeness of excision. Extension of the tumor
beyond the surgical borders should prompt either
wider excision or radiation therapy of the tumor
bed. Approximately 50% of the mast cell tumors
recur at the surgical site traditionally. Histologic
grade is an important factor in predicting
recurrence at the surgical site. Those that are
undifferentiated tend to have a higher recurrence
rate. Cats with mast cell tumors with splenic
555
O
involvement often will benefit from splenectomy.
Survival times of 10 weeks to 30 months have
been reported following splenectomy, even in
patients with evidence of sytemic mastocytosis.
Seguin et al (J Am Vet Med Assoc 218[7]:1120-
1123 2001) evaluated 60 mast cell tumors that
were surgically excisted with cleanmarings in
55 dogs were included. Median follow-up time
was 540 days. Three mast cell tumors recurred
locally; median time to local recurrence was 62
days. Six dogs developed another mast cell tumor
at a different cutaneous location; median time
to a different location was 240 days. Three dogs
developed metastases; median time to metastasis
was 158 days. The authors concluded that
additional local treatment may not be required
after complete excision of grade-II mast cell
tumors and that most dogs do not require systemic
treatment.
Glucocorticoid therapy frequently results in
partial or occasionally complete remissions in
canine mast cell tumors. However, cats appear
to be less responsive to glucocorticoid treatment.
The effect of glucocorticoids is to reduce markedly
the number of mast cells in the mast cell tumor.
The exact mechanism by which glucocorticoids
exert their cytotoxic effects on mast cell tumors
is unknown although it may be similar to the
effects of glucocorticoids on lymphocytes. The
susceptibility of mast cell tumors might depend on
the presence of intracytoplasmic glucocorticoid
receptor sites. Glucocorticoid receptor sites have
recently been found in the cytoplasm of canine
mast cell tumors. Although sex steroid receptors
for progesterone and estrogen have been recently
described in dogs with canine mast cell tumors,
the role of sex steroids in the treatment of canine
mast cell tumors has yet to be investigated. The
type of glucocorticoids administered appears to
be unimportant but it has been suggested that
intralesional corticosteroid may be more effective
2006 World Congress WSAVA/FECAVA/CSAVA
than systemic therapy for local disease. Fewer
Cushingoid side effects have been seen with
short-acting glucocorticoids such as prednisone
or prednisolone when used in the dog. The usual
dose of prednisone is .5 mg/kg orally administered
once daily and that of triamcinolone is 1 mg for
every cm diameter of tumor intralesionally,
administered every two weeks. Remission times
are usually 10 to 20 weeks. Dogs that are tumor
free after six months however have a low incidence
of recurrence and therefore therapy is usually
discontinued at this time. Tumor resistance may
be caused by the emergence of mast cells with
fewer or ineffective glucocorticoid receptors.
Survival data based on histologic grade correlates
with various chemotherapeutic regimens has not
been reported.
556
Back to contents
Vinblastine and prednisone or CCNU appear
to be the most favored drug protocols for the
treatment of mast cell tumors. The use of these
drugs is always with surgery.
Rassnick and colleagues (J Vet Intern Med
13[6]:601-605 1999) evaluated the efficacy and
toxicity of CCNU in 23 dogs with measurable
mast cell tumors (MCT). Response could be
evaluated in 19 dogs. Eight of the 19 dogs (42%)
had a measurable response to CCNU. One dog
had a durable complete response for 440 days.
Seven dogs had a partial response for a median
and mean duration of 77 days and 109 days,
respectively (range, 21-254 days). The acute
dose-limiting toxicity was neutropenia 7 days
after administration of CCNU.
Thamm et al (J Vet Intern Med 13[5]:491-497
1999) evaluated 41 dogs with mast cell tumors
treated with oral prednisone and vinblastine
both in the adjuvant setting and in dogs with
gross disease. Adverse effects were noted in
20% of the patients, usually after the 1st dosage.
Median survival time (MST) for the entire patient
population was not reached with a median follow-
up of 573 days; however, the MST for dogs with
grade 111 MCT was 331 days, with 45% of dogs
alive at 1 and 2 years.
Ancillary drug therapy is important with
canine mast cells. Animals with mastocytosis
or palpable mast cell disease should receive
H2 antagonists. Cimetidine (Tagamet) reduced
gastric acid reduction by competitive inhibition
of the action of histamine on H2 receptors of the
gastric parietal cells. Ranitidine (Zantac, Glaxo
Inc, Fort Lauderdale, FL), a newer H2 antagonist
that requires less frequent administration, is in
some clinics. The objective of the therapy is to
prevent gastrointestinal ulceration associated with
elevated levels of histamine and to treat ulcers
already present. Some new evidence indicates that
cimetidine may also alter the immune response
to this tumor as well as activation of certain
alkylating agents. Dogs and cats with evidence of
gastrointestinal ulceration and bleeding might also
benefit from sucralfate (Karafate, Marion Labs
Inc, Kansas City, MO) therapy. Sucralfate reacts
with stomach acid to form a highly condensed
viscous adherent paste-like substance that binds
to the surface of both gastric and duodenal ulcer
sites. The barrier formed at the ulcer site protects
the ulcer from potential ulcerogenic properties of
pepsin, acid and bile allowing the ulcer to heal.
Radiotherapy has been used alone or in
combination with other treatment modalities.
Most reports indicate remission rates of 48 to
77%. Doses of 3,000 to 4,000 rads were used in
these studies. Total radiation therapy is usually
fractionated and delivered over a period of

three to four weeks. The use of radiotherapy is
somewhat expensive and is confined to referral
centers. Mast cell tumors in regional lymph nodes
and bone marrow appear to be more resistant to
the effects of radiotherapy than those confined to
the skin. Response of mast cell tumors to radiation
therapy may correlate to histologic grade but has
not been studied.
SUMMARY
Grade 1 Mast Cell Tumors
Dogs with grade 1 MCTs have a high likelihood
of complete tumor control after complete surgical
excision. A recent study showed that all grade
1 MCTs were completely excised with a 1-cm
clinical margin. However, because tumor grading
is performed histologically, not on cytology,
all MCTs for which a grade is as yet uncertain
should be excised for biopsy with wide (2 to 3 cm)
margins.
Grade 2 Mast Cell Tumors
Three recent studies have challenged early
assumptions16,19 that dogs with grade 2 MCTs
have a high likelihood of local recurrence even
after apparently complete excision. These studies
showed that with a more aggressive surgical
technique and histology to examine margins
(rather than the surgeon’s clinical impression),
dogs with grade 2 MCTs have a much lower rate
of local recurrence and longer survival rates than
previously reported. Specifically, between 5%
and 10% of dogs had a local recurrence of MCT
a median of 7 months after surgery (range: 2 to
24 months). More than 30% of these dogs had
an MCT on the limb, for which some limbs were
amputated. On the other hand, many of these dogs
developed another MCT at a distant cutaneous
site. These were considered to be de novo tumors
(rather than cutaneous metastases, which have
not been reported) and were diagnosed from
2 months to 4 years later, with a median time to
diagnosis of about 1 year. Metastasis was rare,
occurring in fewer than 3% of dogs.
Grade 3 Mast Cell Tumors
One study found that grade 3 tumors were more
likely to be incompletely excised and more likely
to metastasize than grade 1 or 2 MCTs. Radiation
therapy is probably warranted (see below), and
chemotherapy should be considered for grade 3
MCTs.
Prognosis
The natural behavior of mast cells suggests
prognosis of this tumor depends on the species,
breed, histologic grade, tumor location, clinical
Back to contents
O
stage and growth rate. In general, cutaneous
mast cell tumors carry a more guarded prognosis
in the dog than in cat. Mast cell tumors in the
boxer are usually of a lower histologic grade than
when found in other breeds. Mast cell tumors in
Siamese are of the less malignant histiocytic type.
Histologic grade has been shown to correlate
with survival following surgical excision by at
least two investigators. The higher the histologic
grade (more undifferentiated tumor), the poorer
the prognosis. This criteria has not had universal
acceptance however, probably due to the
precise nature of histologic grading as well as
tumor heterogeneity. Clinical staging and the
extensiveness of microscopic tumor masses
beyond what might be detected clinically also
plays an important role in the failure of universal
acceptance of the histologic grading system. In
the cat, in addition to the histologic grading
system described for the dog, the histiocytic
mast cell variant tends to carry a better
prognosis than the traditional mast cell. Tumor
location is considered by many investigators
to be an important prognostic feature. Tumors
located in the perineal or preputial area are
likely to metastasize both locally and to deep
lymph nodes. Clinical stage is a clinical means
of assessing tumor spread of the disease
process. The higher the clinical stage, the more
guarded the prognosis. A high histologic grade,
however, should increase the clinical stage at
least one level. Growth rate but not tumor size
is determined also to be an important prognostic
indicator. Growth rate reported by Bostock
indicates that dogs that have tumors that grow
greater than 1 cm per week have only a 25%
chance of living an additional 30 weeks.
Reference
1. Ogilvie GK, Moore AS. Mast Cell Tumors.
In: Managing the Veterinary Cancer Patient: A
Practice Manual. Trenton: Veterinary Learning
2006 World Congress WSAVA/FECAVA/CSAVA
Systems. 1995: 503-514.
2. Rassnick KM, Moore AS, Williams LE, London
CA, et al. Treatment of Canine Mast Cell Tumors
with CCNU (Lomustine) J Vet Intern Med 13[6]:
601-605 1999.
3. Thamm DH, Mauldin EA, Vail DM. Prednisone
and Vinblastine Chemotherapy for Canine Mast
Cell Tumor - 41 Cases (1992-1997) J Vet Intern
Med 13[5]: 491-497 1999
4. Seguin B, Leibman NF, Bregazzi VS, et al.
Clinical Outcome of Dogs with Grade-II Mast
Cell Tumors Treated with Surgery Alone: 55
Cases (1996-1999). J Am Vet Med Assoc 218[7]:
1120-1123 2001.
557
O
O – Oncology
CRITICAL ADVANCES FOR THE MANAGEMENT OF CANINE
LYMPHOMA
Antony Moore, BVSc, MVSc,
Diplomate ACVIM (Oncology)
Direktor
Veterinary Oncology Consultants
379 Lake Innes Drive
Wauchope NSW 2446
Australia
www.vetoncologyconsults.com
voc@vetoncologyconsults.com
Lymphoma is the most common haematopoietic
malignancy in dogs, and is the most responsive
to chemotherapy. Affected dogs are typically
middle-aged. Neither gender nor neutering is a
predisposing factor for developing lymphoma.
In studies of canine lymphoma epidemiology;
boxers, Scottish terriers, German shepherds
and poodles were more often affected, and
recent evidence suggests a high incidence in
golden retrievers. The most common physical
finding in dogs with lymphoma is peripheral
lymphadenopathy, which is usually generalized
but may be localized to a single lymph node
or a region of the body. Involvement of other
organs, such as spleen, liver, or bone marrow is
an indication of advanced disease. Involvement
of other (extranodal) sites is rare in dogs.
Untreated lymphoma progresses rapidly (1–2
months) from presentation to terminal stages.
With chemotherapy, however, considerable
improvement in the duration and quality of the
patient’s life can be expected.
2006 World Congress WSAVA/FECAVA/CSAVA
STAGING AND DIAGNOSIS
Lymphoma is a systemic disease; therefore, it
is important to determine the extent of organ
involvement with lymphoma and to identify
unrelated or secondary conditions that need to be
treated or controlled before instituting appropriate
therapy. Staging carries prognostic significance
and enables the veterinarian and client to make
informed and rational decisions as to the type of
therapy best suited for the patient. Each dog is
clinically staged based on the results of physical
examination, clinical laboratory testing (i.e.,
CBC, biochemical profile, urinalysis, and bone
marrow cytology), and imaging procedures (i.e.,
radiography and ultrasonography).
Cytologic examination of lymph nodes may be
compatible with a diagnosis of lymphoma but
rarely provides a definitive diagnosis. A definitive
558
Back to contents
diagnosis is based on histologic examination of a
surgically resected lymph node. Examination of
nodal architecture enables the pathologist to assign
a grade, which is important for prognosis, and
immunohistochemistry for T and B lymphocyte
markers can be performed. The most accessible,
most easily removed lymph node is the popliteal
lymph node.
PROGNOSTIC FACTORS
Prognostic factors include stage and substage of
disease, histologic type, immunophenotype (B-
cell versus T-cell), presence of hypercalcemia,
response to therapy, pre-treatment steroid therapy,
and possibly gender.
TREATMENT
Once a definitive diagnosis has been obtained and
after the patient has been staged accurately, the
veterinarian should schedule a discussion with
the owner regarding prognosis and treatment.
One of the most important distinctions to make
for the client is between remission and cure.
When toxicities are discussed, the owner should
be given criteria by which to distinguish mild side
effects from those that can be life threatening.
A copy of the protocol to be administered, with
scheduled treatments, rechecks, and blood counts,
will assist owners in remembering much of this
information.
FIRST-LINE THERAPY
Single-Agent Chemotherapy: Most veterinary
oncologists agree that unless palliation rather
than extended remission is the goal of therapy,
single agent treatment of lymphoma should be
avoided.
Combination Protocols
COP Protocol: Much of the information
regarding efficacy of treatment for canine

lymphoma has come from studies using
combinations of cyclophosphamide, vincristine,
and prednisone. COP is a relatively non-toxic
protocol and is relatively inexpensive. Overall,
COP chemotherapy causes complete remission in
about 70% of dogs with lymphoma for a median
of 130 days.
Vincristine, Cyclophosphamide, Prednisone,
Doxorubicin, and L-asparaginase (VELCAP)
Protocols
110 dogs were treated with a sequential
chemotherapy protocol that used the above drugs
(Madison-Wisconsin Protocol or AMC protocol).
Complete remission was achieved in 84% of dogs
for a median of about 9 months. Approximately
50% of the dogs were still alive one year after
starting chemotherapy. Toxicities that required
dose reduction occurred in 40% of the dogs.
Ninety-eight dogs with lymphoma were treated
using the VELCAP-L (Tufts-1) protocol.[1] The
complete remission rate was 69%, with median
remission duration of 13 months. Toxicity was
frequent but rarely fatal.
Because palliation, rather than cure, is a major
goal of chemotherapy in veterinary oncology,
there has been recent interest in developing
protocols that reduce the number of patient visits
as well as cost and toxicity of treatment. The use
of short-term chemotherapy given in pulse doses
may provide similar remission durations to long-
term maintenance chemotherapy. 82 dogs with
lymphoma received a single 15-week course of
chemotherapy after which treatment was ceased
until relapse VELCAP-S (Tufts-2).[2] 68% of
dogs achieved complete remission for a median
first remission duration of 20 weeks. Forty-eight
dogs relapsed, of which 30 repeated the induction
cycle. Dogs received maintenance chemotherapy
when first remission had been short (< 4 months);
the other dogs received 2 or 3 cycles of induction
chemotherapy. Second remission rate for these
dogs was 87%. Overall disease control for the
38 dogs that remained on protocol was 44 weeks
which was not significantly shorter than dogs
treated with VELCAP-L. Delaying maintenance
chemotherapy until after second remission is
achieved does not significantly impact overall
disease control.
Recent reports have documented the efficacy of
lomustine[3] and MOPP[4] (mechlorethamine,
vincristine, procarbazine and prednisone) for
the treatment of relapsed lymphoma. A protocol
that combined VELCAP drugs for induction
and consolidation with lomustine and MOPP
was investigated to see if it would increase the
CR rate and the median duration of first CR of
a discontinuous protocol (VELCAP-SC)[5]. The
Back to contents
O
population was a group of dogs with advanced
disease. 57% were in stage V dogs, 19% stage
IV, 21% stage III; 63% were substage b and
30% had T cell lymphomas. The median overall
survival of 84 dogs was 302 days (range, 5-1447).
The 1 and 2 year survival rates were 44% and
13%, respectively. The only variable that had a
significant negative impact on remission rate in
this high risk group of patients was inappetance at
time of diagnosis, and those negatively affecting
survival time were innappetance at the time of
diagnosis and not requiring a dose reduction for
any drug. This latter finding implies that higher
chemotherapy dosages may be associated with a
better outcome.
High-dose Chemotherapy with Bone Marrow Support:
High-dose chemotherapy with haematopoietic
stem cell (HSC) support, or bone marrow
transplantation (BMT), is important in the
therapy of lymphoma and other malignancies
in humans. Since most chemotherapy drugs
exhibit a dose-response relationship, increased
dose intensity should result in increased efficacy,
and strong clinical evidence in cancer patients
supports this. However, the clinical utility of dose
intensification is limited by the toxicity of the
regimen. Most currently used myeloablative BMT
protocols offer significantly higher cure rates
than those seen with standard therapy, but with
significantly increased toxicity. We are studying
nonmyeloablative stem cell transplantation by
conducting a study with the goal of increasing the
tolerable dose of chemotherapy agents in order
to allow patients to receive the highest possible
chemotherapy dose intensity while still enjoying
the best possible quality of life and lowest
possible risk of complications. Incremental dose
intensification of 500 mg/m2 cyclophosphamide
with autologous bone marrow support at the
end of a 12-week 5 drug combination protocol
is no more toxic than standard-dose therapy.
This protocol provides statistically significant
2006 World Congress WSAVA/FECAVA/CSAVA
lengthening of remission times in dogs with
lymphoma, with a current average remission time
of more than 1 year, compared to 5 months for the
standard-dose 12 week protocol.
559
O
Comparison of different protocols for treatment of canine lymphoma
VELCAP-L Madison-Wisconsin VELCAP-S VELCAP-SC VELCAP-HDC
Number of dogs 98 55
Population typical typical
characteristics
% CR 69 84
Protocol 75 135
duration (weeks)
Median remission 55 36
duration (weeks)
1-year CR % 53 43
2-year CR % 25 25
In summary, the best protocol for lymphoma
currently available for routine clinical use is a “5-
drug protocol” consisting of cyclophosphamide,
vincristine, prednisone, doxorubicin and L-
asparaginase. As long as these drugs are being
used, the exact protocol may not have much of
an overall influence on canine patients. However,
it does seem that using combinations of drugs
wherever possible (rather than single drugs
given sequentially) may be more effective. In
the future, the use of “dose intensification”
such as autologous bone marrow transplant, or
radiation therapy may further improve on these
data, but those techniques are likely to be limited
to specialty practices. In the absence of referral
to a veterinary oncologist, the practitioner is
encouraged to use a protocol that they feel
comfortable with, and make use of expert advice
if problems are encountered during treatment.
The treatment options below are tiered according
to risk of toxicity, cost, and efficacy. First-level
protocols provide a low risk of toxicity at low
2006 World Congress WSAVA/FECAVA/CSAVA
cost but have low efficacy; as the level rises, so
do efficacy, cost, and risk of toxicity.
First Level: For clients who cannot afford or
will not accept a combination chemotherapy
protocol due to the risks of toxicity, a protocol
using prednisolone alone or in combination
with chlorambucil may provide palliation with
few risks of side effects. A CBC should be
collected every 2 to 3 weeks to make sure that
myelosuppression is not occurring.
Second Level: The COP protocol is a relatively
inexpensive chemotherapy protocol with a low
risk of toxicity. Dogs tolerate the treatments,
and veterinarians find the protocol very
manageable. CBCs should be taken 1 week after
each dose of cyclophosphamide to ensure that
myelosuppression (if it occurs) is not severe and
560
Back to contents
82 95 13
typical high-risk typical
68 70 100
15 21 12
44 24 54
36 NR 54
12 NR 31
that doses do not need to be adjusted.
Doxorubicin administered every 3 weeks for five
to eight treatments is the most effective single
chemotherapeutic agent. This treatment regimen
results in a relatively high remission rate with
relatively few serious life-threatening toxicities
(<5%). Because the drug is given every 3 weeks,
this treatment approach is less time intensive
than most chemotherapeutic protocols. A second
remission seems more likely if doxorubicin is used
as first-line therapy and COP is used after relapse
than if COP is used first. Overall remission time
for the two-protocol treatment approach is similar
to that of the COPA protocol.
Third Level: The most effective chemotherapy
protocols use a five-drug combination of L-
asparaginase, vincristine, cyclophosphamide,
doxorubicin, and prednisolone. Similar remission
rates and survival times have been obtained for
the protocols that include these drugs. Although
these protocols require more intense client–
veterinarian communication and monitoring
for toxicity, the overall level of satisfaction for
owners, pets, and veterinarians is high. Most
oncologists now recommend discontinuous
protocols such as VELCAP-S; however, some
clients will not restart chemotherapy when first
remission is over. For such clients less intensive
maintenance schedule may be preferred over
restarting induction treatment at relapse. For
dogs with T-cell lymphoma, protocols that rely
heavily on alkylating agents, such as VELCAP-
SC, should be used.
Fourth Level: The addition of radiation therapy
or, if available, autologous bone marrow support
to allow chemotherapy dose intensification
represents the most aggressive treatment option
for a dog with lymphoma. The potential for long-
term remission and possibly cure is much higher
than with other protocols. Dogs with T-cell

lymphoma may not benefit to the same extent as
those dogs with B-cell lymphoma. Although risks
of toxicity are higher, the addition of radiation
or chemotherapy dose intensification has not
negatively affected the quality of life for treated
dogs.
REFERENCES
1. Zemann B, Moore AS, et al. A combination
chemotherapy protocol (VELCAP-L) for dogs with
lymphoma. J Vet Internal Med 12 465-470, 1998.
2. Moore AS, Cotter SM etal.. Evaluation of a
discontinuous treatment protocol (VELCAP-S)
for canine lymphoma. J Vet Internal Med 15 348-
354, 2001
3. Moore AS, London CA, et al. Lomustine
Back to contents
O
(CCNU) for the treatment of relapsed lymphoma
in dogs. J Vet Internal Med 13 395-398, 1999.
4. Rassnick KM, Mauldin GE, Al-Sarraf R,
Mauldin GN, Moore AS, and Mooney SC.
MOPP chemotherapy for treatment of resistant
lymphoma in dogs: a retrospective study of 117
cases (1989-2000) J Vet Internal Med 16, 576-
580, 2002.
5. Morrison-Collister KE, Rassnick KM, Northrup
NC, Kristal O, Chretin JD, Williams LE, Cotter
SM, Moore AS. A combination chemotherapy
protocol with MOPP and CCNU consolidation
(Tufts VELCAP-SC) for the treatment of
canine lymphoma. Veterinary and Comparative
Oncology 1, 180-190, 2004
2006 World Congress WSAVA/FECAVA/CSAVA
561
O
O – Oncology
ADVANCES IN THE TREATMENT OF MAMMARY NEOPLASIA
Antony Moore, BVSc, MVSc,
Diplomate ACVIM (Oncology)
Direktor
Veterinary Oncology
Consultants
379 Lake Innes Drive
Wauchope NSW 2446
Australia
www.vetoncologyconsults.
com
voc@vetoncologyconsults.com
MALIGNANT MAMMARY TUMORS IN
CATS
Mammary epithelial tumors are the most
common type of feline mammary tumor,
with adenocarcinomas and solid carcinomas
predominating. Mixed mammary tumors and
mammary sarcomas are rare, and sarcomas
appear to be slow to metastasize.
Mammary carcinomas are seen in older cats with
a median age of 10 to 12 years. The risk for a
female cat developing mammary carcinoma
increases steadily with age especially if intact.
The effect of neutering on development of
mammary carcinoma in cats is less clear than it
is for dogs however there is evidence to suggest
that neutering may prevent mammary tumor
development. In one study, the relative risk for a
spayed female developing mammary carcinoma
was approximately half that of an intact cat.
While domestic shorthaired and longhaired cats
are most commonly reported with mammary
carcinoma, only tricolored cats have been shown
2006 World Congress WSAVA/FECAVA/CSAVA
to be about twice the risk for developing the
disease. Even more striking is the increased
incidence of mammary carcinoma in the Siamese
breed accounting for >25% of patients.
The signalment factors shown to be prognostic
for survival after surgical resection of mammary
carcinoma are breed (domestic shorthaired cats
had longer survival times in one study), and age
(older cats having worse survival rates).
Clinical Presentation and History
Mammary carcinomas in cats may remain
undetected by an owner until they become quite
large or ulcerative, even if a previous mass was
detected. Thus, mammary carcinoma is often
advanced by the time a veterinarian is consulted.
Feline mammary carcinoma is an invasive and
often rapidly metastatic tumor. A standard staging
562
Back to contents
protocol involves at least a minimum database
(CBC, biochemical profile, urinalysis, T4 and
FeLV/FIV) and thoracic radiographs. Careful
visual and digital assessments of the extent of the
primary and metastatic tumors are also essential.
Multiple gland involvement may be seen and in
some cats the entire mammary chain is affected
either unilaterally or bilaterally, which probably
indicates lymphatic spread rather than multiple
synchronous primaries. There is frequent
anastamosis between the thoracic and abdominal
lymph drainage in cats, although there does not
appear to be lymphatic anastamosis across the
midline. The most frequently involved regional
lymph nodes are the axillary or inguinal lymph
nodes, although the sternal lymph node may be
enlarged in some cats. In one study, 27% of cats
had histologic evidence of mammary carcinoma
metastases to the lymph nodes.
Pulmonary metastases occur more frequently
than regional lymph node metastases. Pulmonary
metastases usually appear as a miliary pattern on
thoracic radiographs, and may obliterate normal lung.
The clinical factors shown to be independent
predictors of survival for cats after surgery for
mammary carcinoma are; tumor diameter, with
a worse prognosis for larger tumors; cats with
small tumors had both longer remission after
surgery and longer survival times.
Additionally, the finding of lymph node metastasis
at diagnosis was highly associated with poor
survival following surgery. Similarly the finding
of distant metastases was a poor prognostic factor.
Staging of cats according to WHO (World Health
Organization) criteria takes into account the size
of the tumor as well as the presence of lymph
node or distant metastases. WHO staging in one
study also found the presence of metastases to be
a poor prognostic sign for survival after surgery.
 O
Staging and Prognosis
WHO Stage Median Survival (Months) Description
I 29 T < 1 cm, no N
II 12.5 T < 1 cm and N
or T = 1-3 cm + N
III 9 T > 3 cm, or
T < 3 cm + fixed N
IV 1 Any T or N with M

Histologic grading systems rely on subjective cellular reaction and ductular development.
appraisal of nuclear variation, mitotic figures, When used to classify tumors as well, moderately
differentiation of epithelial elements, invasion or poorly differentiated, there appeared to be
of lymphatics or surrounding stroma, lymphoid prognostic value to this system.

Histologic grade and prognosis

Grade Number of cats %of total Percent alive 12 months after surgery
Well-differentiated 7 12.7% 100%
Moderately differentiated 33 60% 54.5%
Poorly differentiated 15 27.3% 0

In another study, the presence of necrosis within
the tumor, and an increasing number of mitotic
figures were associated with shorter survival.
In summary, the clinician should take histologic
findings of mitotic count, nuclear and cellular
pleomorphism into account when looking for
prognostic factors. These criteria when combined
with staging information gained from thoracic
radiographs, abdominal ultrasonography and the
presence or absence of lymph node metastases,
together with tumor size should allow the
veterinarian to assess the prognosis for an
individual cat with mammary carcinoma.
Treatment
Feline mammary carcinomas are invasive and
the high rate of lymphatic involvement mandates
aggressive treatment. The entire affected
mammary chain should be removed with wide
surgical margins, however the efficacy of this
treatment is less clear than would be desired.
Surgical excision alone is unlikely to result in a
cure due to metastatic spread, however, the extent
of surgery appears to play a role in reducing local
recurrence and survival times. Studies that looked
at the effect of conservative surgery (the affected
gland and adjacent tissue) compared to radical
surgery (unilateral or bilateral mastectomy)
found there was no difference in survival
between the two groups. However; the histologic
completeness of resection appears to correlate
with survival.
Due to the high metastatic potential of mammary
carcinoma, chemotherapy would appear to be
the most likely treatment modality to improve
survival as an adjuvant to surgery. At the present
time, doxorubicin appears to be the adjuvant
chemotherapy drug of choice.
Radiation therapy has not been extensively used in
the treatment of mammary carcinoma however, it
may be effective in preventing local recurrence.
Supportive Care
Analgesia is essential during and after surgical
removal of any mammary tumor. Antiemetics
can be helpful at reducing the adverse effects of
chemotherapy, and supplemental feeding methods
and appetite stimulants must be considered in all 2006 World Congress WSAVA/FECAVA/CSAVA
patients to facilitate healing and prevent weight
loss during therapy. In addition, treatment of
underlying secondary problems such as renal or
heart disease is important.
PROGNOSTIC FACTORS FOR DOGS WITH
MAMMARY CARCINOMA
Somewhat surprisingly, the prognosis for dogs
with mammary cancer is not influenced by either
tumor location or number of tumors. Other factors
that are not prognostic are number of pregnancies,
age at first pregnancy and occurrence of
pseudopregnancies. The following are prognostic
factors that have been shown in studies to predict
survival or disease-free interval.

563
Back to contents
O
Stage
Dogs with stage 1 tumors were more likely to
survive longer than dogs with any other stage
Effect of tumor stage on survival.
Stage Percent alive 1 year after surgery
1 97.9
3 75.8
4 13.6
Effect of tumor stage on survival.
Stage Number of dogs
1 8
2 7
3 14
4 6
Tumor Size
This is probably one of the most important
prognostic factors for a dog with a mammary
mass. Dogs with mammary tumors less than 3 cm
in diameter have a significantly better prognosis
than dogs with larger tumors, Tumor size is also
a factor in the staging of mammary tumors, and
stage is also an important prognostic factor.
Metastasis
Metastases to regional lymph nodes has been
associated with an increased risk for tumor
recurrence and for decreased overall survival.
Tumor stage, and specifically the presence of
distant metastases, were found to be prognostically
important in other studies. Those dogs with no
metastases were more than 3 times as likely to
survive one year from diagnosis.
2006 World Congress WSAVA/FECAVA/CSAVA
Age
Older dogs have a worse prognosis in some
studies. It is unclear if this is due to tumor related
factors or competing risks.
Diet and Body Weight
In one study, the effect of diet in the year prior to
diagnosis on survival after surgery showed that
dietary fat and dietary protein together influenced
outcome. When dogs were categorized by the
percent of total calories they derived from fat and
protein, the median survival time for dogs fed a
low fat diet (< 39%) with protein greater than
27%, 23-27%, and less than 23% was 3 years,
1.2 years, and 6 months, respectively. One-year
survival for dogs on a low fat diet with 15%, 25%,
and 35% of total calories derived from protein was
17%, 69%, and 93%, respectively. For dogs fed a
564
Back to contents
tumor. This effect of tumor stage was similar in
other studies and is detailed in the two Tables
below.
Percent alive 2 years after surgery
97.9
66.4
13.6
Median Survival Time (months)
17
14
7
3
high fat diet (> 39%), there was no difference in
survival for the different intake levels of dietary
protein. Dogs that have a mammary carcinoma
may benefit from a low fat, high protein diet after
surgery. These studies do not account for the type
of fat consumed (eg: n-3 vs n-6 long chain fatty
acid content) or for the carbohydrate content of
the diet, all of which may influence outcome.
Degree of Invasion and Ulceration
Dogs with tumors that ulcerate overlying skin
have a worse prognosis (shorter overall survival
times) than dogs with tumors without ulceration.
Rapid and invasive growth correlates with a worse
prognosis, which may be recognized as fixation
of the tumor to the underlying skin. Vascular or
lymphatic invasion is a poor prognostic factor;
dogs with histologic evidence of invasion have a
shorter median survival.
Histopathology
Important factors include histologic classification,
degree of nuclear differentiation, and the presence
of lymphoid accumulation. In general, the more
highly differentiated the tumor, the better the
prognosis. Dogs that have mammary cancer but
no evidence of lymphoid cellular reactivity at
the time of initial mastectomy have a threefold
increased risk of developing recurrence within
two years compared to those with such reactivity.
Dogs with precancerous lesions have a nine-fold
increased risk of developing mammary cancer in
the future. Thus, precancerous lesions should not
be dismissed as benign.
Dogs that have evidence of infiltration into
adjacent tissue, or had permeation into lymphatics
or blood vessels had a worse prognosis.

When reviewing a histopathology report,
the clinician should look for information
regarding completeness of the surgical excision;
invasion into lymphatics or blood vessels, and
differentiation of the tumor.
Hormone-Receptor Activity
Dogs with tumors that are estrogen- and/or
progesterone-receptor positive have a better
prognosis than dogs with tumors that do not have
receptors, with longer disease-free and overall
survival times. Receptor-positive tumors are
likely to be benign.
Proliferative Activity
Dogs with tumors that showed a high proportion of
Ki-67 staining (which is an immunohistochemical
marker for cellular proliferation) were more
likely to develop metastases in three studies.
Additionally Ki-67 staining was inversely related
to survival time.
Ovariectomy Status
In one study dogs that were intact at the time
of surgery for a mammary carcinoma survived
a shorter time (median survival 9.5 months)
Back to contents
O
compared to dogs ovariectomized within
the 2 years before surgery (median survival
25 months). Dogs ovariectomized more than
2 years before mammary tumor surgery did not
benefit to the same extent. In addition, dogs
that were intact had a higher proportion of solid
and anaplastic carcinomas than either group of
ovariectomized dogs (80% solid carcinomas in
intact dogs compared to 20% (<2 years) and 7%
(> 2 years)). In contrast ovariohysterectomy at the
time of tumor removal had no effect on survival
in another study with approximately 60% of dogs
with malignant tumors dying within 2 years of
surgery whether they were spayed at the time or
not.
Extent of Surgery
The extent of surgery influences neither survival
nor disease-free interval but rather the histologic
completeness of surgical margins as assessed by
histopathology has been shown to be prognostic
for survival so the best surgery to achieve
complete margins is the surgery that should be
offered.
2006 World Congress WSAVA/FECAVA/CSAVA
565
O
O – Oncology
TOP TEN ADVANCES IN VETERINARY ONCOLOGY 2005/2006
Gregory K. Ogilvie, DVM, Antony Moore, BVSc, MVSc,
Diplomate ACVIM (Specialties Diplomate ACVIM
of Internal Medicine, Oncology) (Oncology)
Director, CVS Angel Care Director, Veterinary Oncology
Cancer Center Consultants
(www.CVSAngelCare.com) 379 Lake Innes Drive
President, Special Wauchope NSW 2446
Care Foundation for Australia
Companion Animals (www. www.vetoncologyconsults.com
SpecialCareFoundation.org) voc@vetoncologyconsults.com
100 North Rancho Santa Fe
Rd #100
San Marcos CA 92024 USA
Gogilvie@aol.com

Prof. dr. Jolle Kirpensteijn

Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical
Sciences of Companion Animals
Faculty of Veterinary
Medicine
Utrecht University
PO Box 80.154
3508 TD Utrechtj.
kirpensteijn@vet.uu.nl

The popularity of oncology is increasing
dramatically in veterinary medicine in part
because of the many advances in veterinary cancer
diagnostics and therapeutics. The objectives of the
following document are to recognize ten of the
most amazing advances in veterinary oncology
and to:
• Discuss the integration of cancer prevention
2006 World Congress WSAVA/FECAVA/CSAVA
at developing health and wellness programs that
incorporates cancer prevention and screening.
Cancer prevention and early detection and
diagnosis are the key to reducing cancer related
deaths in veterinary medicine. The initiation of
these prevention and screening programs for all
stages of life is not only the right thing to do for
the patient, but it is the correct thing to do for the
concerned client.

into health and wellness programs to increase

cancer cure rates.
• Examine how clients and the veterinary health
care team perceive cancer, dispel the myths
associated with cancer treatment and replace
these myths with accurate concepts about how
dogs and cats with cancer and their caregivers
should be approached, supported and treated.
• Discuss key advances in cancer care including
the management of transitional cell carcinomas,
hemangiosarcoma, transitional cell carcinoma,
and primary lung tumors.
• Briefly review a condition that may be a
debilitating consequence of caring called
‘compassionate fatigue’.
Cancer Prevention
Cancer care will succeed if the profession is active
566
Back to contents
Cancer can be prevented if the known risk
factors are identified. Lifetime obesity is one risk
factor. Eicosapentaenoic and docosahexaenoic
acids have been shown consistently to inhibit
the proliferation of breast and prostate cancer
cell lines in vitro and to reduce the risk and
progression of these tumors in many species (Am
J Epidemiol 141(4): 352-359, 1995).
A lifetime study of restricted daily intake of the
same food was done with Labrador retrievers that
came from seven litters (J Am Vet Med Assoc
220; 1315-1320, 2002). The median life span of
the restricted-fed group was significantly longer.
While the prevalence of cancer between groups
was similar, the mean age due to cancer-related
deaths was 2 years later in the dogs that received
the restricted diet.

Secret #1: Lifetime weight management is
associated with decreased risk of developing
cancer and other diseases such as diabetes
mellitus. DHA and EPA may reduce the risk
of cancer.
Dogs have been shown to have an increased
risk of developing cancer of the respiratory
tract, especially of the lung and nasal cavity,
when exposed to coal and kerosene heaters and
passive tobacco smoke. Mesothelioma is more
common in dogs owned by people who worked
in the asbestos industry. The use of chemicals by
owners, specifically 2,4-dichlorophenoxyacetic
acid, paints, asbestos or solvents, as well as
radiation and electromagnetic field exposure were
associated with increased risk for several types of
cancer in pet dogs. Application of insecticides (but
not in a spot-on formulation) increased the risk
of bladder cancer in Scottish terriers in another
study (Environ Res 32(2): 305-313, 1983).
Secret #2: It is important to eliminate exposure
to environmental carcinogens such as
pesticides, coal or kerosene heaters, herbicides
such as 2,4-dichlorophenoxyacetic acid, passive
tobacco smoke, asbestos, radiation, and strong
electromagnetic field exposure. These steps
may be particularly important for clients of
susceptible breeds (e.g., a Scottish terrier) and
herbicide exposure.
Commandments
Perhaps the greatest barrier to enhanced cure
and control of cancer is that the caregiver, and
the veterinary health care team often have
preconceived notions about cancer and its
treatment. This is true regardless if you are
talking about cancer prevention or treatment. The
first and possibly the most difficult task facing the
veterinary health care team is the dissolution of
the negative myths and misperceptions regarding
cancer and the efficacy and toxicity of cancer
therapy. The first step is to recognize the fears
associated with cancer and to address those head
on. The approaches to the biggest fear about
cancer are called the commandments of cancer
care.
• Do not let them hurt: Providing an active,
preemptive, and ongoing pain management/
prevention program for the dog with cancer is
absolutely imperative. This reassures the caregiver
that quality of life is optimal. Management should
begin with comfort care and then, when needed,
include oral medications (morphine, codeine,
piroxicam (Feldene), carprofen, or others),
transdermal delivery systems (fentanyl patches),
acupuncture or more advanced analgesic
delivery systems (eg: constant rate intravenous
Back to contents
O
infusion, epidural catheters, intrathoracic pleural
analgesia).
• Do not let them vomit or have diarrhea.
Dispensing oral medication such as
metoclopramide to the caregiver each and every
time a potentially nauseating drug is administered,
empowers the caregiver to prevent this symptom
at home. In addition, we must be prepared
to stop nausea and vomiting should it occur,
ensuring that medications and supportive care are
immediately available. Having access to drugs
such as ondansetron hydrochloride and dolasetron
mesylate, although costly, will provide this level
of assurance for all members of the team. Some
believe that tylosin, metronidazol and imodium
can reduce the risk of small and large bowel
diarrhea and often dispense these drugs to their
cancer patients to prevent problems. Enhancing
fiber content can be of great value at enhancing
bowel health.
• Do not let them starve: Nursing care (e.g.,
warming food, providing aromatic foods and
comfortable environments), medicinal appetite
stimulants, and, when needed, assisted feeding
techniques such as esophagostomy, gastrostomy,
or jejunostomy tube placement should be
employed. All of these components of nutritional
care must be available early in the course of
disease, and weight loss must not be tolerated,
particularly in dogs that have fewer reserves due
to their small size. To our caregivers, appetite is a
vital, objective assessment of quality of life that
must not be overlooked or left to chance.
Secret #3: Meeting the medical needs of the
patient and the non-medical needs of the
client can be done by preventing and treating
pain, nausea, vomiting and anorexia early and
often.
Recent Advances in Cancer Care
Gene therapy has been around, at least conceptually
2006 World Congress WSAVA/FECAVA/CSAVA
for forty years, however the technology to
manipulate genes and to deliver them safely
has only recently been realized. In its simplest
definition, gene therapy is the introduction of a
gene or genes into a cell to treat or prevent cancer.
One recently completed trial of xenogeneic DNA
vaccination in canine advanced oral malignant
melanoma using the human tyrosinase gene was
performed (Clin Cancer Res 9(4): 1284-1290,
2003). This novel approach using a gene from
another species elegantly and simply induced
a good immune response against the malignant
melanoma, but not the patient’s own tissue. The
Kaplan-Meier median survival time for all nine
dogs in this study was 389 days with some of the
dogs having stabilization of disease or reduction
567
O
in the size of the cancer. The investigators
concluded that xenogeneic DNA vaccination of
dogs with advanced malignant melanoma is a
safe and potentially therapeutic modality.
Secret #4: Gene therapy provides and exiting
option for cancer control and cure.
Doxorubicin has been shown to improve the
disease free interval in dogs that have had
incompletely excised soft tissue sarcomas
(Selting, Proceedings Vet Cancer Society 2004).
Local lymph node involvement was a significant
negative prognostic factor. Similarly, doxorubicin
has been shown to be of value for the treatment
of surgically resected hemangiosarcoma (J Vet
Intern Med 10(6): 379-84, 1996). A pilot study
by an Australian group (Langova et al) presented
at the Veterinary Cancer Society in 2004 utilizing
alternating carboplatin and doxorubicin with
piroxicam for the treatment of nasal tumors
resulted in a median survival time of 550 days
with 4/8 CR and 2/8 PR.
Secret #5: Doxorubicin is the most effective
agent for the treatment of lymphoma and it has
efficacy for the treatment of hemangiosarcoma,
soft tissue sarcomas and osteosarcoma.
CCNU is an oral alkylating agent that has been
shown to result in a 50% response rate (8.3%
CR) and median survival time of 128 days by
Skorupski et al against histiocytic sarcoma
(Proceedings, Veterinary Cancer Society 2004).
Similarly, this drug has recently been shown
to be helpful for treating mycosis fungoides.
Thrombocytopenia and hypoalbuminemia at
the time of diagnosis were significant negative
prognostic factors. Fifty-seven dogs with MCT
were treated with prednisone and alternating
vinblastine/Lomustine (Hershey); almost all as an
adjuvant to surgery, and about twenty percent for
non-resectable disease. The median DFI is > 375
2006 World Congress WSAVA/FECAVA/CSAVA
days and most dogs had a measurable response.
Secret #6: CCNU is effective for the treatment
of lymphoma, histiocytic sarcoma, mycosis
fungoides, and mast cell tumors.
Piroxicam and possibly other NSAIDs have
been shown to have anticancer effects. Several
studies have been performed confirming that
piroxicam is effective for the treatment of
transitional cell carcinoma and oral squamous
cell carcinoma. Some oncologists favor the
combination of mitoxantrone and piroxicam. In
one study, Forty eight dogs with histologically
convirmed transitional cell carcinoma were
treated with mitoxantrone and piroxicam (Clin
Cancer Res. 2003 Feb; 9(2): 906-11). Forty eight
dogs were treated with the following responses:
568
Back to contents
one complete response, 16 partial responses, 22
with disease stabilization, and 9 with progressive
disease for an overall 35.4% measurable response
rate. Subjective improvement occurred in 75% of
treated dogs. Median time-to-treatment failure
and ST were 194 and 350 days, respectively.
Secret #7: Piroxicam has been shown to be very
effective for the treatment of transitional cell
carcinoma and squamous cell carcinoma in
the dog.
Primary lung tumors have been ineffectively
treated until vinorelbine was shown to be effective
(J Vet Intern Med 18(4):536-9, 2004). The
investigators concluded that The well-tolerated
toxicity profile and clinical activity observed in
dogs with bronchoalveolar carcinoma treated
with vinorelbine warrants further investigation.
Secret #8: Vinorelbine is a promising new agent
for the treatment of pulmonary tumors in dog
and cats.
Inadequately excited mast cell tumors have been
shown to be effectively treated with vinblastine
and prednisone. In one study, 27 dogs with
inadequately excised, cutaneous mast cell tumors
were treated with a vinblastine and prednisolone
chemotherapeutic protocol. Twenty dogs were
available for follow-up examination after 12
months. Over half were disease free after one
year.
Secret #9: Vinblastine is a relatively safe and
effective therapy for mast cell tumors in the
dog.
Compassion Fatigue
When we care for our patients with compassionate
care, we must do so by expressing empathy. The
act of extending empathy as we care for our
patients and their clients can lead to compassion
fatigue. When any member of the veterinary
health care team finds themselves giving more
without allowing themselves to be replentished
emotionally, it is only a matter of time before
there will be a shortage of compassion. Simply
put, compassionate fatigue results when there is
a depletion of emotional resources from within
as we care and provide compassion for others.
This depletion is not a reflection of the character,
professionalism, or even the professional
skill level of the veterinary health care team
member. Rather, the strength and willingness to
be emotionally engaged with another being is
affected. All members of the veterinary health
care team joined the profession to care, from their
minds through medical/surgical/preventative
skills and through their hearts by supporting and

providing for the emotional needs of caregivers.
It is vital to the success of veterinary care to allow
for this level of compassionate care and to support
those individuals who provide it. By appreciating
the issue of Compassion Fatigue and providing
mechanisms within a practice to mitigate its
effects, a practice can thrive by providing the
finest in compassionate care.
Key Points for Prevention:
• Educate the entire veterinary health care team
• Establish weekly debriefing sessions for entire
staff
• Identify and work with professionals within the
community who clearly understand the condition
Back to contents
O
• Define and preserve a ‘comfort room’
• Allow team to have adequate closure at the end
of any patient’s life
• Define and teach team member limits and
boundaries
• Employ humor whenever appropriate
• Find a colleague who understands and share
Secret #10: Recognizing and treating compassion
fatigue is essential to enhance professional,
personal and financial success.
References Available Upon Request
2006 World Congress WSAVA/FECAVA/CSAVA
569
O
O – Oncology
APPROACH TO THE CANCER PATIENT
Antony Moore, BVSc, MVSc,
Diplomate ACVIM
(Oncology)
Director, Veterinary Oncology
Consultants
379 Lake Innes Drive
Wauchope NSW 2446
Australia
www.vetoncologyconsults.com
voc@vetoncologyconsults.com
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical
Sciences of Companion Animals
Faculty of Veterinary
Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
As medical and surgical advances have become
available, recognition of the human-animal
bond, both by clients and veterinarians, has led
to advanced care for pets. This is especially true
of cancer treatment. Within the last 15 years,
tremendous advances have resulted in improved
response rates, disease-free intervals, and survival
times. Despite these strides in veterinary cancer
care, many caregivers and veterinarians are not
2006 World Congress WSAVA/FECAVA/CSAVA
aware that a large percentage of pets with cancer
can be cured or at least rendered free of their
diseases for significant periods. In most situations,
pets undergoing cancer treatment experience
limited or no decrease in the quality of their
life. Advances in supportive care and palliative
therapy have resulted in good quality of life for
cancer patients while they receive treatment.
First obtain a tissue diagnosis: Each tumour is
different and must be identified with a biopsy
and, where appropriate, given a grade by an
experienced, highly trained histopathologist.
Then determine the stage of the tumour: Once
the tumour type is named, it must be staged.
Stage is essentially the extent of the malignancy
locally and at distant sites through the metastatic
process.
Staging often carries prognostic significance
570
Back to contents
Gregory K. Ogilvie, DVM,
Diplomate ACVIM (Specialties
of Internal Medicine, Oncology)
Director, CVS Angel Care
Cancer Center (www.
CVSAngelCare.com)
President, Special
Care Foundation for
Companion Animals (www.
SpecialCareFoundation.org)
100 North Rancho Santa Fe
Rd #100
San Marcos CA 92024 USA
Gogilvie@aol.com
and enables the veterinarian and client to make
informed and rational decisions regarding the
type of therapy best suited to the patient. Most
staging systems are based on assessment of three
major components of the malignant process:
•The size of the primary tumour (T)
•Lymph node metastasis (N)
•Distant metastasis (M)
These components are further modified by the
use of subscript numbers to indicate increase in
tumour size, progressive involvement of regional
lymph nodes, and presence or absence of distant
metastasis.
To obtain this information, ancillary diagnostics
are very important and sophisticated imaging
techniques are often used. Although staging will
vary among tumour types, in general the process
begins with a thorough physical examination to
identify any enlarged lymph nodes or other obvious
areas of cancer spread, a complete blood count,
chemistry profile, urinalysis, thoracic radiographs
(right and left laterals and a ventral-dorsal view),
and abdominal radiographs. In addition, ancillary
diagnostics such as ultrasonography, computerized
tomography, magnetic resonance imaging, or other
more specialized tests may be required.

Next assess the condition of the patient: Any
neoplastic process may result in a number of
paraneoplastic conditions that affect the well
being of the cancer patient. In addition, these pets
are generally geriatric patients, which have the
potential for a number of underlying conditions
that may adversely affect their health and the
potential success of therapy. For example, serum
chemistry profiles are essential to establish the
health of an animal with cancer. When complicated
surgical procedures or multiple radiation therapies
that require repeated or prolonged anesthesia are
planned, acceptable renal and hepatic functions
are vital. In addition, some chemotherapeutic
agents that are metabolized or excreted by the
liver or kidneys may require reduction in dosage
if these organs are functionally compromised. In
many instances, correcting underlying problems
such as renal failure, urinary tract infections,
heart disease, and metabolic disturbances may
significantly improve the overall health of
the patient and thus improve the potential for
successful cancer care.
Finally, treat the patient: Therapies that deal
with the primary tumour are still the mainstay of
veterinary oncology, and surgery is the primary
modality used in veterinary practice.
O
The results of radiotherapy have been largely
based on early studies using low cumulative
doses and coarse fractionation. The low total
doses used in these early studies meant that long-
term tumour control was rare and survival was
short. The treatment schedule was determined
by the difficulties of repeated anesthesia, rather
than by radiobiological necessity. More recently,
safe short-acting anesthetics have allowed more
frequent treatments with smaller doses per
fraction, and the ability to deliver higher total
doses has increased as fraction size has decreased.
With these advances, many of the tumours that
were previously reported as non-responsive
actually may prove to be well controlled by
radiation therapy.
Chemotherapy for pets is a changing field,
and we can expect combination chemotherapy
protocols to become more available for a number
of different cancers. The reader is encouraged
to keep up to date with the literature, as this is a
rapidly advancing field.
Results of treatment with other modalities such as
biological response modifiers (immunotherapy,
anti-angiogenesis) and holistic medicine
approaches are becoming available.

Definitions of Objective Tumour Remissions and Responses Following Anticancer Therapy

Tumour Response Tumour Size

Complete (CR)* Disappearance of all evidence of cancer in all sites for a defined
period of time (e.g., one inter-treatment interval of 3 weeks).
Partial (PR)* Decrease in size of all tumours by 50% or greater as measured by
the sum of the products of two diameters for each tumour. These
diameters should be the largest tumour diameter and the diameter
perpendicular to it. There should be sustained decrease in tumour
size, as defined for CR, and no new tumours should arise.
Stable disease (SD) Decrease of <50% or an increase of <25% in the sum of
2006 World Congress WSAVA/FECAVA/CSAVA
the products of the diameters as measured for PR.
Progressive disease (PD) Increase of 25% or more in the sum of the products of tumour
diameters or the appearance of a new tumour.

*CR + PR = Objective response rate.

The best therapeutic approach for the veterinary cancer patient is yet to be devised. It is clear that

a combination of surgery, radiation therapy, The lecture presented here will outline strategic
chemotherapy and biologic response modifiers, approaches to a pet with cancer.
in addition to supportive care for the relief of pain
and nutritional status, will give the best outcomes.

571
Back to contents
O
O – Oncology
KEY SURGICAL, MEDICAL ADVANCES FOR TREATING
OSTEOSARCOMA
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
Gregory K. Ogilvie, DVM,
Diplomate ACVIM (Specialties
of Internal Medicine, Oncology)
Director, CVS Angel Care Cancer
Center (www.CVSAngelCare.
com)
President, Special
Care Foundation for
Companion Animals (www.
SpecialCareFoundation.org)
100 North Rancho Santa Fe Rd
#100
San Marcos CA 92024 USA
Gogilvie@aol.com
Introduction
Osteosarcoma (OSA) is the most common bone
tumor in dogs and is characterized by a highly
invasive and metastatic behavior. The tumor
is less common in cats. This tumor frequently
affects middle-aged, large breed dogs (less than
5% occur in breeds smaller than 12 kg) and arises
in 75% of cases in the metaphyseal area of bones
2006 World Congress WSAVA/FECAVA/CSAVA
of the appendicular skeleton. The median age
of dogs with OSA is 6-7 years. Males are more
commonly affected than females. A cause for
OSA is unknown although many etiologies have
been stipulated (radiation, microtrauma, genetics,
implants, nutrition). Most cats are older and a
higher number of OS arose from extraskeletal
sites (38%).
Pathology
OSA is a malignant spindle-cell tumor
characterized by direct formation of bone or
osteoid tissue by tumor cells. OSA is an aggressive
tumor with a locally invasive behavior and a
high rate of metastasis and can be subdivided
in chondroblastic, osteoblastic, fibroblastic,
telangiectatic, and mixed type tumors. Common
locations for OSA include the distal radius,
572
Back to contents
Antony Moore, BVSc,
MVSc, Diplomate ACVIM
(Oncology)
Director, Veterinary Oncology
Consultants
379 Lake Innes Drive
Wauchope NSW 2446
Australia
www.vetoncologyconsults.com
voc@vetoncologyconsults.com
proximal humerus, distal femur, proximal tibia,
distal tibia, proximal femur, ulna and scapula.
The remainder of OSA (25%) occurs in the
axial skeleton (mandible, maxilla, vertebrae and
ribs). Multicentric OSA is rare (< 10% of cases).
Fifty-five percent of feline OS occur in the
appendicular skeleton. OS Pulmonary metastases
are present in more than 90% of the patients at
time of initial diagnosis. The prognosis for dogs
with OSA without therapy is poor, less than 5%
will survive longer than one year after diagnosis.
The prognosis for cats seems to be better, but
small numbers have not allowed a good scientific
comparison between groups.
History, clinical signs, and differential diagnosis
Dogs and cats with OS are often presented with an
acute or chronic lameness and a visible swelling
at the affected site. The owner often backdates the
lameness to a minor traumatic incident and pain
can be elicited upon palpation. Muscle atrophy,
a history of progressively decreased weight
bearing, and pathologic fractures may be present.
Differential diagnoses include other primary bone
tumors (fibrosarcoma, chondrosarcoma, etc.),
metastatic tumors (especially in cats), bone cysts
and bacterial or fungal osteomyelitis.

Diagnosis
The presumptive diagnosis of a bone tumor
is easily obtained by regional radiography.
Radiographic changes include a mixed pattern
of osteolysis and bony proliferation and either
change can predominate. Macroscopic pulmonary
metastases (> 5 mm) are evident in 10% of cases
at initial radiographic examination. Metastatic
nodules have the ‘canon-ball’ appearance and are
often located in the periphery. Feline pulmonary
metastases can have a miliairy pattern. The
definite diagnosis is obtained by bone biopsy
and histologic examination. The biopsy can be
performed using a Jamshidi biopsy needle or
Michele bone trephine. Two biopsy specimens,
one obtained from the centre and one from the
tumor-normal tissue transition zone, will allow
proper diagnosis in 92% of cases. Additionally,
scintigraphy may be used to diagnose multicentric
or metastatic OS. However, scintigraphy will
not differentiate benign (non-tumorous) from
malignant lesions, and should be followed by
radiography of regions with increased uptake. CT-
and MRI-scans can be used to estimate the extent
of bony and surrounding soft tissue involvement.
Histology
Evaluation of the histologic characteristics of OS
substantiated the importance of tumor grading.
Dogs with more aggressive tumors (grade III)
had a worse prognosis after multivariate analysis
compared to dogs with lower grade tumors.
Also, preoperative, non-steroid-induced plasma
alkaline phosphatase elevation was associated
with a poor prognosis. Comparisons for cats are
researched at this moment.
Genetic alterations
Canine OS contain genetic alterations comparable
to human OS. P53 mutations were common (42%)
and were associated with poor outcome using
multivariate analysis. Most alterations consisted
of point mutations.
The role of growth hormone (GH) expression
within the tumor is unclear. After we determined
that local GH expression is present in 25% of the
dogs, a large number of dogs were evaluated for
the clinical importance of this finding. Local GH
expression was associated with a poor prognosis.
Local GH production may indicate the presence
of an autocrine phenomenon, in which the tumor
stimulates itself.
Therapy
Successful treatment of OS includes local tumor
control as well as the treatment of systemic tumor
spread. Local marginal resection as sole treatment
will result in high recurrence rates, dysfunction
Back to contents
O
of the leg and undiminished metastatic spread
of tumor and should be avoided if adjunctive
therapy is not available. In dogs, amputation
alone provides good primary local tumor control,
but otherwise does not prolong survival time. A
median survival time of 19 weeks is observed
after amputation. More than 90% of these dogs
will die within a year because of the development
of distant metastases. After amputation, recovery
from surgery and adaptation to three legs is fast.
Most dogs, even the larger breeds, function
extremely well three-legged and most owners
are satisfied with the animal’s quality of life.
Recovery after amputation is faster than many
owners expect. Most dogs are at ease with walking
on three legs within a month and dogs with bone
tumors are able to ambulate well within 7 days.
The owner’s satisfaction with the procedure is
very high and complications are rare. Force plate
analysis of amputees showed significant changes
in ground reaction forces. Dogs with front leg
amputations may have more problems recovering
after the surgery in the beginning because of these
GRF changes. Cats seem to have not problem
with walking on three legs and thus amputation is
the therapy of choice in appendicular OS.
Amputation in combination with chemotherapy
enhances survival in canine OS because it
decreases the occurrence of metastases. The best-
known chemotherapeutic agent, cisplatin, has been
shown to significantly prolong the disease-free
intervals and survival times in dogs, and remains
the drug of choice. Cisplatin is administered
intravenously at 60-70 mg/m2 for 4-6 doses, at
three-week intervals. Cisplatin is associated with
the risk of severe side effects (nephrotoxicity,
gastrointestinal toxicity, myelosuppression, and
ototoxicity) if given as a sole agent. Most side
effects can be prevented by a concurrent 4-hour
saline diuresis protocol; however, mild vomiting
and bone marrow suppression often will occur.
Median survival intervals of dogs treated with
2006 World Congress WSAVA/FECAVA/CSAVA
cisplatin chemotherapy and resection of the
primary tumor is significantly higher than dogs
without chemotherapy. A one-year survival
percentage of 45-55% has been reported. The
median survival interval of dogs treated with
chemotherapy before resection of the primary
tumor compared to postoperative chemotherapy
was not significantly different. Also, the route of
administration (IV versus IA) did not influence
survival. Dogs that receive more than three doses
of cisplatin will survive longer than dogs that
receive two or less. Currently, it is recommended
to give at least four doses of cisplatin.
Other agents, used for canine OS, that have shown
a beneficial effect include doxorubicin, liposome
encapsulated muramyl tripeptides (liposome/
573
O
MTP) and carboplatin. Doxorubicin has been
shown to prolong survival in combination with
cisplatin and as single agent. Dogs treated for OS
with liposome/MTP survived significantly longer
than those treated with placebos. Carboplatin, a
second-generation platinum compound, does not
induce nephrotoxicity and can be given as a 15-
minute bolus injection without saline diuresis.
Carboplatin significantly increased survival
times compared to dogs with amputation alone
and was comparable to cisplatin chemotherapy.
Carboplatin is given intravenously on an every
21-day schedule at 300 mg/m2.
Instead of amputation, local control may also be
obtained by limb-sparing procedures. The goal
of limb sparing is to obtain local tumor control,
while providing a pain-free and functional leg.
The procedure usually involves (marginal) local
surgical excision of the tumor in combination
with chemotherapy or radiation therapy. Common
locations amenable for performing limb sparing
are the distal radius, proximal humerus, scapula
and ulna. OS of the distal radius and proximal
humerus are removed by marginal resection,
replaced by an allograft and affixed to the host
bone using a bone plate. Arthrodesis of the
adjacent joint is often necessary. Recovery after
surgery is often fast with dogs bearing weight
within a week. Eighty percent of dogs return to
normal function after limb-sparing procedures
in 6-8 weeks. OS of the ulna and scapula may
be resected without the use of an allograft.
Ulnectomies distal to the elbow joint and partial
scapulectomies are extremely well tolerated.
Complications associated with limb-sparing
procedures include infection, recurrence and
implant failure. The use of cemented allografts
has decreased the number of complications
associated with allograft failure significantly.
The incidence of local tumor recurrence after
limb sparing varies between 25-50%. Methods
to prevent local recurrence include preoperative
2006 World Congress WSAVA/FECAVA/CSAVA
radiation and preoperative administration of
chemotherapy by intra-arterial route, local
intravenous perfusion, or slow release polymers.
Any of these therapies should be considered in
tumors that have extended through the bony cortex
and have invaded in the surrounding soft tissues.
The use of intravenous, systemic chemotherapy
has been unrewarding in preventing recurrence
after incomplete resection.
In cats, the advantage of adjunctive therapy
after surgical excision is unclear. Some authors
clearly state that feline OS behave comparable
to canine while others debate the effectiveness
of chemotherapy in the cat. One thing is for
sure, however, cats are extremely sensitive for
cisplatin and life-threatening pulmonary edema
occurs after administration of this drug.
574
Back to contents
Metastatic osteosarcoma
OS is a highly metastatic tumor and most
metastases are observed in the lungs. Macroscopic
metastatic disease in canine OS is not responsive
to chemotherapy and the prognosis is often poor.
Surgical resection of pulmonary metastasis is
useful in limited numbers of patients if less than
three nodules are present, if the tumor size has
not doubled in a month, and if the disease-free
interval is longer than 300 days from the initial
date of diagnosis. No data are available for cats
concerning metastatectomy in cats.
References
1.Brodey RS, Abt DA. Results if surgical
treatment in 65 dogs with osteosarcoma. J Am
Vet Med Assoc 1976; 168: 1032.
2.Kirpensteijn J, Straw RC, Withrow SJ, et al.
Partial and total scapulectomy in the dog. J Am
Anim Hosp Assoc 1994; 30: 313.
3.Kirpensteijn J. Current developments in canine
osteosarcoma. Vet Quart 1994; 16s: 31.
4.Kirpensteijn J, van den Bos R, van den Brom,
W, Hazewinkel HAW. Ground reaction force
analysis of large breed dogs when walking after
amputation of a limb. Vet Rec 2000; 146: 155-159.
5.Kirpensteijn J, van den Bos R, Endenburg N.
Adaptation of dogs to the amputation of a limb
and their owner’s satisfaction with the procedure.
Vet Rec 1999; 144: 115-118.
6.Kirpensteijn J, Steinheimer DN, Park RD,
Withrow SJ, Straw RC, Comparison of cemented
and noncemented cortical allografts for limb
sparing procedures in dogs, Vet Comp Orthop
Traumatol 1998; 11: 178-184.
7.Kirpensteijn J. Clinical and pathogenetic
studies in canine osteosarcoma. Thesis Utrecht
University, The Netherlands 1999; 1-174.
8.O’Brien MG, Straw RC, Withrow SJ, et al.
Resection of pulmonary metastases in canine
osteosarcoma: Thirty-one cases. Vet Surg 1993;
22:105.
9.Straw RC, Withrow SJ, Richter SL, et al.
Amputation and cisplatin for treatment of canine
osteosarcoma. J Vet Intern Med 1991; 5: 205.
10.Heldmann E, Anderson MA, Wagner-Mann
C. Feline osteosarcoma: 145 cases (1990-1995).
J Am Anim Hosp Assoc 2000; 36: 518-21.
11.Toxicity and Efficacy of Cisplatin and
Doxorubicin Combination Chemotherapy for
the Treatment of Canine Osteosarcoma. Chun R,
Garrett LD, Henry C, Wall M, Smith A, Azene NM.
J Am Anim Hosp Assoc. 2005; 41(6): 382-38

O – Oncology
NUTRITION AND CANCER: FRONTIERS FOR CURE!
Gregory K. Ogilvie, DVM,
Diplomate ACVIM (Specialties
of Internal Medicine, Oncology)
Director, CVS Angel Care Cancer
Center (www.CVSAngelCare.
com)
President, Special
Care Foundation for
Companion Animals (www.
SpecialCareFoundation.org)
100 North Rancho Santa Fe Rd
#100
San Marcos CA 92024 USA
Gogilvie@aol.com
Using specifically formulated diets or dietary
supplements to prevent and to treat cancer is in its
infancy; however, enough information exists to
begin making some recommendations to prevent
and treat cancer in people and dogs.1–5 In human
medicine, several nutritional factors have been
found to increase the risk and rate of developing
cancer, including3-–5:
•Obesity
•Consumption of nutrient-sparse foods, such as
concentrated sugars and refined flour products
•Low fiber intake
•Inadequate consumption of polyunsaturated
fatty acids of the n-3 series (n-3 PUFAs) and an
increase consumption of PUFAs of the n-6 series
(n-6 PUFAs)
Carbohydrates and Cancer
Evidence is mounting that simple carbohydrates
may be contraindicated for the nutritional
management of cancer in dogs:1,2,6–20
•Dogs with a wide variety of malignant conditions
have elevated resting insulin and lactate levels
compared to control animals.8–11,15 It is unknown
if the elevated insulin levels are a response to
cancer or if they precede and possibly contribute
to the development of cancer via stimulation of
insulin-like growth-factor (IGF) pathways.
•Elevated lactate and glucose levels do not
improve after dogs with cancer are rendered
free of disease with chemotherapy and surgery8
(Figure 31-3). This suggests that the malignancy
causes a fundamental change in metabolism that
persists after all clinical evidence of cancer is
eliminated.
•Elevated lactate levels can result in inefficient
Cori cycle activity to convert lactate back to
glucose; this results in a net energy loss by the
patient.8–11,15
Back to contents
O
•The administration of lactate-containing
parenteral fluids such as lactated Ringer’s solution
has been shown to increase lactate levels in dogs
with lymphoma, suggesting that these types of
fluids may place an additional energy burden on
the host.9
•Before the development of severe malnutrition,
human patients with colon, gastric, sarcoma,
endometrial, prostate, localized head, neck, or lung
cancer have many of the metabolic abnormalities
of type II (non–insulin-dependent) diabetes
mellitus.21,22 These metabolic abnormalities
include glucose intolerance; an increase in hepatic
glucose production, glucose recycling, and
insulin resistance; and an increase in anaerobic
glycolysis causing increased lactate production.
These are essentially the same findings as in dogs
with cancer.1,2,6–20
The metabolic abnormalities noted above are
only important if they affect the patient clinically.
Studies done in human patients suggest that
alterations in carbohydrate metabolism influence
cancer prevention and outcome once cancer is 2006 World Congress WSAVA/FECAVA/CSAVA
diagnosed.23–25 For example, one study evaluated
the hypothesis that glucose, insulin, and IGFs
contribute to breast cancer development in 10,786
women.23 It was concluded in this research that
higher levels of glucose, insulin, and IGF-1 were
associated with a higher risk of developing breast
cancerand a poorer survival after diagnosis.A
second study involving 603 breast cancer patients
was performed to test the hypothesis that excess
insulin and related factors are directly related to
mortality after a diagnosis of breast cancer.24 It
was concluded in that study that high levels of
insulin were associated with poorer survival for
postmenopausal women.
Proteins and Cancer
Dogs with cancer have alterations in protein
575
O
metabolism that are very similar to those observed
in humans and laboratory animals with cancer.1
For example, there is a significant decrease in a
wide variety of amino acids, suggesting that a
high-quality, highly bioavailable protein source
would be beneficial to the animal and to the
tumor. Amino acids of particular importance to
patients with cancer are glutamine, cysteine, and
arginine.
Glutamine supplementation may enhance the
therapeutic index of chemotherapy and radiation
by enhancing the efficacy of these treatments
while reducing adverse effects such as mucositis,
diarrhea, neuropathy, and cardiotoxicity.27,28
Glutamine is conditionally essential for the health
and function of the bowel. At least some of this
amino acid is destroyed in the process of making
many types of dried and canned pet food.
Cysteine is critically important to replenish the
glutathione antioxidant system.29,30 This system
is the principal protective mechanism of the cell
and is a crucial factor in the development of the
immune response. Cysteine supplementation
has been shown to have anticancer activity
via the glutathione pathway, the induction of
p53 protein in cancer cells, and inhibition of
neoangiogenesis.29,30
Arginine is a conditionally essential amino
acid that is necessary during periods of growth
and recovery after injury. Arginine promotes
wound healing, has several immunomodulatory
effects such as stimulating T- and natural-killer
cell activity, and influences proinflammatory
cytokine levels.31 L-Arginine is the sole precursor
for the multifunctional messenger molecule
nitric oxide, which appears to influence tumor
initiation, promotion, and progression; tumor-cell
adhesion; apoptosis angiogenesis; differentiation;
chemosensitivity; radiosensitivity; and tumor-
induced immunosuppression.31 The administration
of arginine to human and veterinary cancer
2006 World Congress WSAVA/FECAVA/CSAVA
patients has resulted in positive outcomes.
Lipids and Cancer
Serum lipid profiles were performed in dogs with
lymphoma before and after they were put into
remission with chemotherapy. These profiles
were compared to those of normal dogs before
and after they were given the same anticancer
drug.11
• The dogs with cancer had significantly
lower levels of high-density lipoproteins. The
total triglyceride levels and very low-density
triglycerides of untreated dogs with lymphoma
were significantly higher than those of untreated
control dogs.11
• After a total of five doses of doxorubicin
576
Back to contents
chemotherapy, the total cholesterol level increased
in dogs with lymphoma but decreased in treated
control dogs.11
• All other parameters remained unchanged
after doxorubicin therapy, suggesting that lipid
abnormalities do not improve significantly, even
after a clinical remission is obtained.11
We tested the hypothesis that diets relatively
high in fat may be beneficial for animals with
cancer compared to diets that are high in simple
carbohydrates, assuming that the protein content,
caloric density, and palatability remain constant.
One study suggested that a high-carbohydrate,
low-fat diet induced elevated lactate and insulin
levels compared to a diet relatively high in fat and
low in carbohydrates.2,12 It also suggested that a
high-fat diet may result in a higher probability
of going into remission with chemotherapy
as well as a longer survival time. The kind of
fat in the diet, rather than the amount, may be
the important factor. For example, n-3 PUFAs
have been shown experimentally to have many
beneficial properties.2,12,16
Emerging Role of PUFAs
For the last decade, investigators have searched
for dietary lipids associated with a delay in cancer
relapse. The use of long-chain polyunsaturated
fatty acids (LC-PUFAs) such as docosahexaenoic
acid (DHA) and eicosapentaenoic acid (EPA)
as adjuvant therapies to enhance the effect of
chemotherapy and radiation therapy shows
promise. LC-PUFAs have been shown to enhance
disease-free interval, survival, and quality of
life after surgery by reducing the rate of cancer
development or incidence. This concept, known
as ‘cancer prevention by delay’ or clinical cancer
chemoprevention, is an important mechanism
behind the successes of several therapeutic agents,
including tamoxifen, retinoids and interferon-alfa,
and nonsteroidal anti-inflammatory drugs.32
Cancer prevention by delay is a valuable clinical
tool until more effective cancer therapeutics can
be developed. Unfortunately, while use of the most
effective cancer therapies (i.e., surgery, radiation,
and chemotherapy) is effective for improving
the disease-free interval of many patients up to
a point, it has not increased the cancer cure rate
or survival time dramatically in the last 10 years.
Therefore, it seems logical to add on relatively
nontoxic therapies that can extend the disease-
free interval, even if the absolute cure rate is not
increased. Tamoxifen, retinoids, and nonsteroidal
anti-inflammatory agents are all recognized to
improve disease-free interval without necessarily
improving the absolute cure rate. Tamoxifen has
been shown to significantly diminish the risk of
human breast cancer; retinoids and interferon-

alfa to reduce the risk of head and neck cancer
in dogs, cats, and humans; and nonsteroidal
anti-inflammatory drugs to delay or reduce the
development of colorectal cancer in humans and
transitional cell and squamous cell carcinomas in
dogs.
Dietary lipids such as DHA and EPA appear to
influence the growth of many types of cancer,
including breast and prostate cancer.33–36 A
group of investigators in France used adipose
tissue sampled during surgery as a biomarker
of past dietary intake of PUFAs in a cohort of
women treated for localized presentations of
breast cancer.37 They found elevated n-3 PUFAs,
especially DHA, to be associated with a higher
metastasis-free survival, suggesting that these
PUFAs could potentially delay metastasis by
decreasing tumor growth or development. Using
a case-control approach comparing the fatty acid
composition of adipose breast tissue obtained at
the time of surgical removal of either malignant or
benign breast tumors, they also found α-linoleic
acid and docosahexaenoic acid to be positively
associated with a decreased risk of having breast
cancer.38
The French group also explored the role of n-3
PUFAs in mammary tumor growth using the
experimental system of N-methylnitrosourea
(NMU)-induced mammary tumors in rats. Because
PUFAs are substrates for lipid peroxidation
processes, the investigators studied the effects of
n-3 PUFAs on tumor growth in interaction with
anti- or pro-oxidant compounds. They found
that dietary n-3 PUFAs, in the form of DHA-
containing fish oil, inhibited tumor development.
This inhibition was most evident in the absence
of the antioxidant vitamin E. Inhibition of tumor
growth was even greater when n-3 PUFAs were
given in the presence of pro-oxidants.340 Such
effects were not found when the lipid diet was
low in PUFAs. These data suggest that oxidized
n-3 PUFAs have an inhibiting effect on tumor
growth and emphasize the importance of the
interaction of anti- and pro-oxidant compounds
with n-3 PUFAs.
There is a growing body of data that suggests
that the presence of n-3 PUFAs such as DHA and
EPA affects several steps of tumor formation. N-3
PUFAs:
• Inhibit tumor vessel formation (angiogenesis)
• Inhibit cell proliferation in several epithelial cell
lines
• Enhance the rate of tumor cell death
• Induce lipid peroxidation, which enhances the
efficacy of radiation- and chemotherapy-induced
cancer cell death; this effect is diminished or
reduced dramatically with vitamin E
• Suppress the expression of cyclooxygenase-2
in tumors, thereby decreasing cancer cell proliferation
Back to contents
O
• Suppress nuclear factor κB activation and BCL-2
expression, thus allowing apoptosis of cancer
cells
Dietary lipids have been shown to modify the
sensitivity of tumors to reactive oxygen species–
generating anticancer drugs. For example, when
dogs with lymphoma were treated with doxorubicin
chemotherapy and a diet supplemented with n-3
PUFAs in the form of fish oils, there was a direct
correlation between the level of DHA in the blood
and improved disease-free interval.18 Another
study, using the same randomized study design,
was used to assess the efficacy of n-3 PUFAs in
combination with doxorubicin chemotherapy to
improve the disease-free interval in dogs with
hemangiosarcoma, a highly metastatic, rapidly
fatal malignancy. There was a statistically
significant positive correlation between the n-
3 PUFAs levels in the serum and disease-free
interval.39 A similar approach was used in rats
bearing autochthonous, NMU-induced mammary
tumors. It was found that dietary supplementation
with fish oil or DHA increased the sensitivity of
mammary tumors to anthracyclines, compared
with dietary supplementation with saturated fatty
acids.39
Because DHA is the most polyunsaturated of the
PUFAs, lipoperoxidation is a likely molecular
mechanism implicated in the enhancement of
the response of cancer cells to cytotoxic drugs.
Addition of vitamin E to the diet provided
to rats with mammary tumors abolished the
enhancing effect of DHA on tumor sensitivity
to anthracyclines.39 In all studies done to date,
there has been no clinically significant toxicity
other than transient gastrointestinal (GI) distress
linked to the dietary change.17,18 Therefore, based
on the safety and efficacy profile of n-3 PUFAs ,
it seems reasonable to further define the efficacy
of n-3 PUFAs, especially DHA, for the treatment
of spontaneously occurring cancer in dogs, with 2006 World Congress WSAVA/FECAVA/CSAVA
the intent to provide evidence for their use in
randomized human clinical trials.
DHA and EPA also augment the efficacy of
chemotherapy and radiation therapy, potentially
enhancing the efficacy of traditional cancer
therapies. Radiation therapy is currently the
most effective treatment for many localized
malignancies. Research is under way to identify
methods to maximize its efficacy while minimizing
the adverse effects associated with it. Among the
agents being evaluated to minimize the damage
to normal tissue are n-3 LC-PUFAs, which
are readily incorporated into cell membranes
and ameliorate inflammation and carbohydrate
dyshomeostasis. In one study, 12 dogs with
histologically confirmed malignant carcinomas
of the nasal cavity were randomized to receive
577
O
isocaloric amounts of a diet supplemented with
menhaden fish oil, including DHA (experimental
diet), or an otherwise identical diet supplemented
with corn oil (control diet). Megavoltage radiation
was delivered to all dogs. The data in this study
suggest that feeding a diet supplemented with
fish oil and arginine is associated with decreased
concentrations of inflammatory mediators
involved with radiation damage in skin and
mucosa and with improved performance scores
in dogs with malignant nasal tumors.41
The ability of PUFAs to sensitize tumors to
radiation has been investigated. Vartak et al42,43
studied the in vitro response of a chemically
induced rat malignant astrocytoma cell line
to radiation after the cell culture medium was
supplemented with g-linoleic acid (GLA) or
n-3 LC-PUFAs. They found that n-3 PUFAs
enhanced radiation-induced cell cytotoxicity. In a
separate study, Colas et al44 documented enhanced
radiosensitivity of rat autochthonous mammary
tumors after administration of dietary DHA.
2006 World Congress WSAVA/FECAVA/CSAVA
578
Back to contents
Whether use of dietary n-3 PUFAs can enhance
sensitivity of tumor tissue in the absence
of a similar increase in the radiosensitivity
of nontumor tissue remains a critical issue.
Several studies have suggested that PUFAs do
not sensitize normal tissue to radiation. For
example, because ionizing radiation generates
reactive oxygen species, we initiated a study to
determine whether dietary DHA might sensitize
mammary tumors to irradiation using a model in
which mammary tumors were induced by NMU
in Sprague-Dawley rats. In the study, we showed
that dietary DHA sensitized mammary tumors
to radiation. The addition of vitamin E inhibited
the beneficial effect of DHA, suggesting that this
effect might be mediated by oxidative damage to
the peroxidizable lipids.44
References
Available Upon Request

O – Oncology
SURGERY OF ORAL TUMORS
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
INTRODUCTION
Canine and feline tumours are relatively common
and often amenable for surgical therapy. Early
recognition and aggressive extirpation may lead
to significant increases in survival times. This
manuscript will discuss the most common oral
neoplasia in dogs and cats and review the surgical
options.
DIAGNOSIS
Diagnosis is obtained using the regular methods
of diagnosing a tumour (see principles of
surgical oncology and biopsy). Use of early
surgical biopsy specimen submission and CT/
MRI scanning are noteworthy in regard to these
types of tumours
ORAL NEOPLASIA
Oral neoplasia are common (up to 6-7% of
all cancers) in dogs but to a lesser extent also
observed in cats (3%?). The most common
canine oral cancers include epulids, malignant
melanoma (MM), fibrosarcoma (FSA) and
squamous cell carcinoma (SCC). In cats, oral
SCC is the most common (in 75% of the cases)
tumour type.
Common types
Malignant melanoma: A frequent tumour of the
gingival, buccal and labial mucosa, palate and
tongue. This tumour of the melanocytes affects
older animals (average age 11 years). The tumour
is locally aggressive and metastasises quickly
to lymph nodes and lungs. The metastatic rate
is dependent on the size (< 2cm is better), site
and tumour grade and is estimated up to 80-90%.
Bone involvement is common. Wide surgical
excision is the therapy of choice for local disease.
Adjunctive therapy is necessary for distant
metastases and in case of incomplete removal of
the primary tumour.
Fibrosarcoma: These are locally aggressive
Back to contents
O
tumours that metastasise in less than 20% of
the cases. Metastatic rate depends mainly on
tumour grade. An exception to this rule is the
histologically low grade-biologically high grade
tumour of the large breed dog. These tumours
tend to be very aggressive, and have a poor
prognosis. Local recurrence is the most common
cause for therapy failure (up to 50%).
Squamous cell carcinoma: This is the easiest
tumour to diagnose. The behaviour is locally
aggressive and the metastasis rate depends on the
location of the tumour. SCC located rostrally are
associated with lower metastatic potential. SCC
are the most common tumours in cats and are rarely
amenable to surgical cure. Photodynamic therapy
cured 8/11 dogs with SCC and is an interesting
alternative to surgery. Other adjunctive therapy
protocols have not been successful so far.
Epulids: Epulids are non metastasising tumours
of the dental tissues. There are four forms: the
fibrous (FE), ossifying (OE), acanthomatous
(AE) and giant cell epulis (GCE). The latter is
more common in cats that in dogs. The GCE and
AE are locally aggressive and can invade bone.
Surgical and radiation results are excellent in 2006 World Congress WSAVA/FECAVA/CSAVA
these types of tumours.
Therapy
Surgery is the first and most important part
of your therapeutic plan. Wide excision of
the local tumour can be performed by several
surgical techniques depending on the location
of the tumour. Surgical excision can include:
partial, rostral or total mandibulectomy, partial,
rostral or caudal maxillectomy, and partial or
total orbitectomy. Cryosurgery is limited to
very superficial tumours and seldom indicated.
Radiation therapy is indicated for tumours that
are sensitive to radiation (AE or SCC) or for
palliation. The use of chemotherapy for MM is
currently under investigation. Carboplatin is
mentioned as chemotherapeutic of choice in MM.
579
O
Immunotherapy is an alternative to chemotherapy,
however, the results are conflicting. Surgical or
adjunctive therapy for oral tumours in cats have
been unrewarding. Surgery in combination with
radiotherapy or immunotherapy is worth further
research.
PHARYNGEAL/LARYNGEAL TUMOURS
The most common pharyngeal tumour is the
tonsillar squamous cell carcinoma. Other tumour
types, such as laryngeal rabdomyosarcomas
are rarely described. A pharyngeal tumour
must not be confused with a middle ear polyp.
These polyps originate in the middle ear and are
attached to the middle ear on a stalk through the
Eustachian tube.
Tonsillar carcinoma
This SCC has a poor prognosis compared with
the rostral oral variant. Systemic spread is present
2006 World Congress WSAVA/FECAVA/CSAVA
580
Back to contents
in 90% of cases but is visible on radiographs in
only 10-20%. Local surgical excision is rarely
possible and in cases of large tumours palliative
radiation is the therapy of choice. Because of the
high metastatic rate most dogs will die within a
year. A significant correlation with urban living
and TSCC may be a clue to pollution as a factor
in this disease.
CONCLUSION
Oral cancer is common in dogs and cats but
tumour behaviour and tumour diagnostics and
therapy are not significantly different compared
to other body locations, making a separate
division of these tumours debatable. Surgery is
often the first step in the therapy protocol and
should often be followed by other adjunctive
therapy modalities.

O – Oncology
RADIATION THERAPY FOR BEGINNERS
Antony Moore, BVSc,
MVSc, Diplomate ACVIM
(Oncology)
Direktor
Veterinary Oncology Consultants
379 Lake Innes Drive
Wauchope NSW 2446
Australia
www.vetoncologyconsults.com
voc@vetoncologyconsults.com
Radiation is becoming widely available to treat
tumors in veterinary patients. Orthovoltage
machines capable of delivering low energy external
beam radiation are less versatile than linear
accelerators and cobalt-60 machines that deliver
megavoltage radiation. In addition, electron beam
capabilities that are available with some linear
accelerators allow more targeted treatment in our
smaller patients. With the increased availability
of computerized treatment planning, and the
delineation of the extent of the disease by CT and
MRI, the beneficial effects of radiation therapy
are bound to increase substantially. The future
of radiation therapy will be tied into the use of
radiobiological and tumor biology information
to enhance the beneficial effects of radiation
therapy. In addition, the combination of radiation
therapy with surgery and chemotherapy may
result in substantial improvement in the efficacy
of this treatment modality.
PALLIATIVE OR DEFINITIVE RADITION
THERAPY
One of the most important decisions is whether
a patient should be treated with curative or
palliative intent. This influences not only the
course of treatment, but expectations of the
caregiver for their pet.
Treatment with curative intent (definitive
therapy) is often complicated, requiring frequent
travel and multiple anesthesias. The total dose
of radiation is usually higher than are required
for palliation and consequently the risks of
unfavorable sequelae are greater. Such treatment
is likely to be prolonged and expensive; however,
for many tumors the chance of long-term tumor-
free survival (> 3 years) is high.
Palliative radiation therapy should have a specific
and often short-term goal, usually to relieve pain
or symptoms of cancer. It is often performed when
a specific site is causing a problem to the patient,
but the rest of the cancer is unlikely to respond
to any treatment (e.g. a painful digital metastasis
Back to contents
O
from a pulmonary tumor that is not causing signs
at any other site). For this reason, palliative
therapy should minimize cost, inconvenience,
discomfort and risk of side effects, and should be
completed in the shortest reasonable time.
TIMING OF RADIATION THERAPY
Radiation is most effective at the periphery of
a tumor where there are small numbers of cells
that are well vascularized. In contrast, surgery is
limited by preservation of normal tissues adjacent
to the tumor and therefore fails microscopically
and peripherally due to residual tumor cells.
Surgery and radiation therapy are therefore
complementary.
Most radiation therapy in veterinary practice
is delivered postoperatively to the residual
microscopic tumor. Postoperative (adjuvant)
radiation therapy has the advantage that it is
possible to histologically identify patients with
residual disease that would benefit most from
radiation therapy. The major disadvantage is
that surgery may reduce tumor vascular supply.
Tumor cells along the surgical scar may survive
radiation therapy because they are protected in
a relatively hypoxic environment. In addition, a
large surgical scar will increase the size of the
2006 World Congress WSAVA/FECAVA/CSAVA
radiation field and hence the risk of side effects.
One study evaluated the effect of starting
radiation therapy the day after surgery compared
to delaying until 1 or 3 weeks after surgery. They
found that the strength of tissues was significantly
less when radiation started immediately after
surgery, but healing was unaffected when the
delay was 1 week or longer.
Preoperative (neoadjuvant) radiation therapy
has the advantage of sterilizing well-oxygenated
cells at the periphery of a tumor before the
vascular supply to these cells is compromised
by surgery. Cells in the periphery that could be
dislodged and seeded at the time of surgery are
also irradiated. Preoperative radiation therapy
may also reduce tumor volume in unresectable
581
O
tumors but this should not be used as a reason
to reduce the size of the surgical field any more
than is absolutely necessary to preserve normal
structures. Disadvantages of preoperative
radiation therapy include a delay of surgery while
acute effects resolve, however, if peripheral cells
are sterilized, this wait is not compromising the
patient. A reduction in gross tumor size may lull
the surgeon into attempting a less aggressive
surgery. Another potential disadvantage is that
fatally irradiated tumor cells may not die until
they attempt mitosis, which can make histologic
interpretation of surgical margins difficult.
Whether radiation is used preoperatively or
postoperatively, irradiation of a large volume of
tissue leads to a poor outcome. When large areas
are irradiated, planning is made more difficult
and a larger volume of normal tissue is irradiated.
This leads to a decreased chance of tumor control
and an increased risk of complications. The
earlier in the course of cancer that radiation is
used, the more likely it is to result in a successful
outcome and the less likely it is to result in severe
toxicity.
CLINICAL OUTCOMES
When comparing results from veterinary studies
that use radiation therapy, the reader should note
not only the median survival times and tumor
control rates but also long-term survival rates
as well as acute and late complication rates.
The low total doses used in early veterinary
studies meant that with few exceptions long-
term tumor control was rare, survival was short
and therefore late effects of radiation were rarely
seen. The treatment schedule was determined
by the difficulties of repeated anesthesia, rather
than by radiobiological necessity and reported
acute effects are relatively mild and short lived.
More recently, safe short-acting anesthetics have
allowed more frequent treatments with smaller
2006 World Congress WSAVA/FECAVA/CSAVA
doses per fraction, and the ability to deliver higher
total doses has increased as fraction size has
decreased. The recent radiation therapy literature
is certainly more encouraging to veterinary
practitioners.
Oral Tumors
The most common oral tumors in dogs are malignant
melanoma, squamous cell carcinoma, fibrosarcoma,
and epulides. Radiation therapy is effective for local
control of many of these oral tumors.
Nasal Tumors
There is little doubt that radiation therapy is the
treatment of choice for dogs with nasal tumors.
There is much variation within the literature
regarding response to therapy. The prognostic
582
Back to contents
factors that may influence response to therapy
include tumor histology, clinical stage, tumor
size, the type of radiation therapy, and the dose of
energy delivered, as well as whether surgery was
performed prior to radiation therapy.
Soft Tissue Sarcomas
Soft tissue sarcomas frequently recur after
incomplete surgical excision because they have
many “fingers” that extend out into surrounding
tissues. Often, the tumor is excised only around
the area that can be palpated, which ensures that
disease will recur. Soft tissue sarcomas (STS)
have been considered to be radiation resistant
however higher total dosages provide long-term
control of this tumor in the majority of dogs.
Mast Cell Tumors
Long-term control is likely for dogs with
incompletely excised grade II mast cell tumors
following radiation therapy. Approximately 90%
of dogs with this tumor treated to a total dose of 48
to 54 Gy in 3 or 4 Gy fractions given three times
a week postoperatively were still alive and tumor
free three years after radiation. This treatment is
clearly the choice for this tumor regardless of the
protocol.
Brain Tumors
Radiation therapy has been delivered to dogs
either alone, or following an incomplete surgical
removal of the tumor. Meningiomas and
hypophyseal macroadenomas appear to be the
most radioresponsive; however, responses have
been seen in dogs with other types of malignant
disease.
Thyroid Tumors
Radiation therapy using 131I has been used to
treat thyroid tumors in dogs even when they are
not actively secreting hormone. External beam
radiation has also been used to treat dogs with
unresectable thyroid carcinomas, and 72% of dogs
were free of disease three years after treatment. In a
compilation of 3 studies, metastases occurred in 14
of 46 dogs (30%) indicating a need for adjunctive
chemotherapy in addition to radiation therapy.
Palliative Therapy
Radiation therapy can be given to alleviate
the pain and discomfort of a wide variety of
malignancies, especially those that involve bone
such as osteosarcoma. The risk of late effects is
acceptable in terminal patients where the chance
of a cure, or even long-term tumor control, is
considered remote, and improvement in quality
of life for a short period outweighs the higher
risks of late effects and tumor recurrence. Despite

the risks of late effects, a German study using RT
to a total dose of 32-48 Gray (Gy) delivered once
a week in 8 Gy fractions found that there were no
significant acute side effects. Late side effects did
O
not occur within the follow-up period and 88%
of the owners were satisfied with this kind of
treatment and would choose it again.

2006 World Congress WSAVA/FECAVA/CSAVA

583
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Op p
Opmo
Ophthalmology
phtha

Back to contents

INVITED LECTURES - FULL PAPERS
Op – Ophthalmology
CLINICAL APPROACH TO THE DOG WITH RED EYE(S)
Ron Ofri, DVM, PhD, DECVO
Koret School of Veterinary
Medicine
Hebrew University of Jerusalem
PO Box 12
Rehovot 76100
ISRAEL
ofri@agri.huji.ac.il
A “red eye” is a common presenting complaint
in veterinary medicine. It is caused by injection
of the conjunctival, episcleral or ciliary blood
vessels. When presented with a red eye, the
clinician should consider three main differential
diagnoses: conjunctivitis, anterior uveitis and
glaucoma. Additional diseases, such as episcleritis
and panophthalmitis, may also cause a red eye,
but are far less frequent.
Several clinical signs should be evaluated
(collectively) to diagnose the cause of the red eye:
• Vision: Vision is not affected in conjunctivitis.
Glaucoma patients, however, frequently present
with severe visual deficits or blindness. Anterior
uveitis does not cause blindness per se, but
corneal edema or opacities of the aqueous humor
(e.g., aqueous flare, hyphema or hypopyon) may
affect vision.
• Globe: The globe may be enlarged in glaucoma
(buphthalmous). It may be enophthalmic
(sunken), causing protrusion of the third eyelid.
The globe is unchanged in conjunctivitis and
anterior uveitis, but severe conjunctivitis of the
third eyelid may cause elevation of the nictitating
membrane.
-The “end stage” of glaucoma and severe
uveitis may be atrophy of the globe (phthisis
bulbi)
• Pain: Acute episodes of glaucoma are very
painful, and may cause blepharospasm and
general depression. Chronic stages of the disease
are also painful, but the behavioral changes are
usually more subtle, and may not be noticed by
the owners. Similarly, acute anterior uveitis may
be moderately painful, but chronic uveitis is not
associated with overt pain signs. Conjunctivitis
may present no pain, or with moderate irritation.
• Secretions: Anterior uveitis and glaucoma may
present with increased lacrimation. Conjunctivitis
may cause serous, mucoid or purulent discharge.
• Conjunctiva: The conjunctiva is thickened,
Back to contents
Op
diffusely hyperemic, and possibly edematous
(chemotic) in conjunctivitis. It is of normal
consistency in glaucoma and anterior uveitis.
• Blood vessels: It is important to determine
if the redness is caused by congestion of the
conjunctival, episcleral or ciliary vessels.
-Mobilizing the conjunctiva with a swab will
cause the conjunctival vessels to move, but
will not affect the deeper vessels. Similarly,
topical phenylepinephrine will cause
immediate blanching of the conjunctival
vessels, but will have a lesser effect on
episcleral and ciliary vessels
-Redness associated with conjunctivitis is
most visible on the palpebral surface and the
fornix. The vessels are typically narrow, and
diffuse congestion is seen.
-Episcleral vessels, which are congested
in glaucoma, are much wider, and are seen
on the bulbar surface, running towards the
limbus.
-Ciliary vessels, which are congested in
uveitis, can not be visualized as they are deep.
They impart a red ciliary flush appearance to
the eye. 2006 World Congress WSAVA/FECAVA/CSAVA
-Note that both glaucoma and anterior uveitis
may also cause conjunctival congestion,
along with the respective episcleral and
ciliary congestion.
• Cornea: It is unaffected in conjunctivitis (though
it is involved in cases of kerato-conjunctivitis).
It is edematous in both glaucoma and anterior
uveitis. Deep corneal vasculariztion may be seen
in both conditions.
• Pupil: The pupil is rarely affected by
conjunctivitis. In glaucoma it is slightly to fully
dilated. Reaction to light may be sluggish or
absent, due to the effects of pressure on the iridal
sphincter. The pupil is miotic in anterior uveitis,
and therefore may show minimal constriction
in response to light. The inflammation is often
585
Op
accompanied by adhesions of the iris to the lens
(posterior synechia), causing the pupil to be
irregular in shape. A complete (annular) synechia
will cause the pupil to be fixed.
• The iris surface is dark, congested and possibly
neovascularized in anterior uveitis. Surface detail
is lost. The iris becomes atrophic and thinner
in chronic glaucoma. The iris is unaffected by
conjunctivitis.
• Lens: It is unaffected in conjunctivitis. Both
glaucoma and anterior uveitis may cause
secondary lens luxation and/or cataracts. It is
noteworthy that the reverse may also be true, as
cataracts may induce anterior uveitis, and lens
luxation may cause secondary glaucoma.
• Intraocular pressure: it is unaffected in
conjunctivitis, elevated in glaucoma, and
decreased in uncomplicated cases of anterior
uveitis.
• Unique signs:
-Lymphatic follicles hypertrophy in conjunctivitis
-Glaucoma may cause striate keratopathy
(“breaks” in Descemet’s membrane),
stretching and thinning of the sclera
(equatorial staphyloma) and atrophy of
the retina and optic nerve head. Cupping
of the optic disc is pathognomonic for
glaucoma.
-Anterior uveitis will be accompanied by
loss of transparency of the aqueous humor.
This may present as aqueous flare, hyphema,
hypopyon or cellular “debris” on the anterior
lens capsule and posterior corneal surface. As
a result, anterior and/or posterior synechia
may form.
-Anterior uveitis may also spread to the more
posterior parts of the eye, causing posterior
uveitis and vitreal inflammation. Severe
cases may cause optic neuritis/atrophy and
endophthalmitis.
2006 World Congress WSAVA/FECAVA/CSAVA
Clinicians should remember that while
glaucoma does not cause uveitis, the reverse
is certainly true, and uveitis frequently causes
secondary glaucoma. The glaucoma may due to
obstruction of the draining irido-corneal angle by
inflammatory cells and debris that are present in
the anterior chamber as part of the inflammatory
response. Formation of adhesions between the
iris and the cornea (anterior synechia) or the lens
capsule (posterior synechia) will likewise impede
the flow of aqueous humor in the eye. The latter
is characterized by elevation of pressure in the
posterior part of the eye, iris bombe.
As glaucoma is discussed elsewhere in these
Proceedings, the following sections will be
devoted to a brief discussion of conjunctivitis and
anterior uveitis. Signs of the two diseases have
already been described.
586
Back to contents
CONJUNCTIVITIS
There is a significant difference in the clinical
approach to canine and feline conjunctivitis. In
the dog, primary pathogens of the conjunctiva are
rare, with the notable exception of the distemper
virus. In most cases the infection is secondary,
and the clinician should direct the efforts to
identifying and treating the primary problem. In
the cat, on the other hand, most cases are caused
by primary pathogens of the conjunctiva, and
treatment should be aimed at these infectious
agents.
Canine conjunctivitis
As noted, infection of the conjunctiva is usually
secondary to an underlying cause. The primary
problem will cause the immune system of
the conjunctiva to be compromised, allowing
overgrowth by the natural flora of the conjunctiva
or by opportunistic agents.
A common primary cause of canine conjunctivitis
is chronic irritation and/or exposure resulting
from anatomical problems of the lids (entropion,
ectropion) or eyelashes (e.g., distichia, trichiasis).
Irritation may also result from nasal folds and
exposure in brachycephalic breeds, as well as
exposure to chemicals, wind and dust. “Dry eye”
(keratoconjunctivitis sicca), allergy, blepharitis
and systemic dermatological diseases are also
common causes of conjunctivitis.
Most of the diagnostic effort should be directed at
identifying the primary cause. Careful inspection
of the eyelid and eyelash conformation, a
dermatological examination and Schirmer
Tear Test may frequently reveal the cause of
the inflammation. As the infection is usually
secondary in nature, bacterial culture is usually
not indicated. A more rewarding diagnostic
approach may be cytology, to determine if the
infection is allergic, bacterial or viral in nature.
After the primary cause has been diagnosed and
treated, most conjunctivitis cases will respond to
a wide-spectrum antibiotic preparation; if needed,
this may be combined with topical steroids.
Feline conjunctivitis
The common primary pathogens of the
feline conjunctiva are Feline Herpes Virus
1, Chlamydiophila felis (Chlamydia psittaci)
and Mycoplsma felis. Corneal involvement is
common with the former, and respiratory disease
may also be present. Diagnosis of the specific
agent may be difficult, as cytology samples can
be unrewarding, and a definitive diagnosis may
require advanced techniques such as PCR or
fluorescence. Furthermore, co-infections are
common. Mycoplasma and Chlamydiophila are
responsive to tetracyclines. The commercially

available anti-viral drugs are frequently
ineffective against feline herpes, and effective
drugs such as idoxuridine may be available
only in compounding pharmacies. Recent
studies suggest that interferon and lysine may
be effective. Because of the possibility of latent
herpes infection, stress, topical steroids and other
cats should be avoided.
UVEITIS
Anterior uveitis is most commonly caused by
an underlying primary problem, which triggers
a secondary inflammatory response of the iris
and ciliary body. It may be caused by virtually
any systemic infectious disease, including viral,
bacterial, fungal, protozoal and rickettsial;
however, it is important to note that in many of
these cases the primary infectious agent does
not reach the eye, which is inflamed, rather
Back to contents
Op
than infected. Non-infectious diseases causing
vasculitis (e.g., toxemia, diabetes, etc.) may also
cause uveitis. Ocular causes of uveitis include
lens induced (an immune response to lenticular
proteins leaking from cataracts), reflex uveitis
triggered by keratitis, and ocular parasites
(e.g., ophthalmomyiasis). Neoplasia should be
considered in any unilateral uveitis in elderly
patients. As in the case of canine conjunctivitis,
the clinician should concentrate on diagnosing
and treating the primary cause. The eye may
be treated symptomatically with topical anti-
inflammatories and with atropine (for cycloplegia
and to reduce the risk of posterior synechia). Sub-
conjunctival and systemic steroids may be added,
depending on the severity of the uveitis and the
patient’s condition. Tissue plasminogen activator
may be injected intraocularly to break fibrin
bands and adhesions.
2006 World Congress WSAVA/FECAVA/CSAVA
587
Op
Op – Ophthalmology
EXAMINATION OF THE BLIND ANIMAL
Ron Ofri, DVM, PhD, DECVO
Koret School of Veterinary
Medicine
Hebrew University of Jerusalem
PO Box 12
Rehovot 76100
ISRAEL
ofri@agri.huji.ac.il
1. History
a)Is the blindness of sudden onset, or gradual
onset?
b)Was deterioration of vision associated with
preferential loss of night vision or day vision?
c)Is the animal healthy? Are there other signs of
illness, besides loss of vision?
2. Localizing the Lesion in the Blind Animal
The blind patient, like all patients, should undergo
a comprehensive physical examination. This is
because in many cases, the cause of blindness
is a systemic disease. Likewise, a neurological
evaluation should be performed to rule neuro-
ophthalmological causes of blindness.
Next, a full ophthalmological examination is
conducted. It is described in detail in a separate part
of these proceedings (“the Ocular Examination”).
Particular attention is paid to methods of
assessing vision (e.g., the menace response and
obstacle course), and to the subcortical tests (e.g.,
the pupillary light reflex, dazzle reflex, etc.).
Additional tests, such as imaging (ultrasound,
CT) or electroretinography (see elsewhere in the
Proceedings) may also be conducted.
Based on the results of the ocular examination and
the pupillary light reflex (PLR), the blind patient may
2006 World Congress WSAVA/FECAVA/CSAVA
be categorized into one of 4 general categories:
a)Abnormal ophthalmic findings combined with
a normal/diminished PLR:
• Opacity of the ocular media: severe
blepharospasm, corneal edema, hyphema/
hypopyon, cataract, vitreal hemorrhage
• Retinal disease – outer retinal degeneration
(PRA), chorioretinitis
b)Abnormal ophthalmic examination and an
absence of PLR:
• Glaucoma
• Retinal detachment
• Optic neuritis involving the proximal
portion of the optic nerve, and causing
papilledema
• Optic nerve hypoplasia/atrophy
588
Back to contents
c)Normal ophthalmic examination and an absence
of PLR:
• Sudden Acquired Retinal Degeneration
(SARD)
• Optic neuritis involving the distal portion
of the optic nerve
• Neoplasia of the optic nerve or neoplasia
compressing the optic nerve or chiasm
• Lesions affecting the contralateral optic
tract, up to the level of the lateral geniculate
nucleus.
d) Normal ophthalmic examination, and normal
PLR: These are usually neurological cases,
caused by central lesions affecting the visual
pathways from the lateral geniculate nucleus to
the contralateral visual cortex.
II. DISCUSSION OF SELECT CAUSES OF
BLINDNESS
Many of the diseases listed above, including
corneal opacities, cataracts, hereditary retinal
diseases and glaucoma, are discussed in other
parts of these Proceedings. Below is a discussion
of the leading causes of acute blindness (other
than glaucoma).
1. Retinal Detachment
Retinal detachment is a separation between the
retina and choroid (more specifically, between
the retina and retinal pigment epithelium).
A result of the separation is ischemia of the
photoreceptors. If the separation is not quickly
resolved, and blood supply restored, cones &
rods will begin dying, leading to irreversible
blindness.
There are 3 types of detachments, depending
on the mechanism of their formation. Serous
detachment is caused by accumulation of fluid
in the subretinal space, between the retina and
choroid. This fluid, which originates in the
choroid, may be blood or exudates. Traction
detachment is caused by a force which pulls
the retina off the choroid. This force may be
generated by forward movement of the vitreous

body (for example, following anterior lens
luxation) or due to traction by fibrin clots.
Rhematogenous detachment is due to penetration
of liquefied vitreous into the subretinal space,
through retinal holes.
Causes of Retinal Detachment
The list of possible causes for retinal detachment
depends on the type of detachment.
• Rhematogenous detachment may be caused
by senile changes, trauma or inflammation (see
below)
• Traction detachment may be caused by lens
luxation, or by inflammation (see below)
• Serous detachments are caused by bleeding or
inflammation.
Causes of exudative (serous) detachment
An inflammation that leads to retinal detachment
is usually one that involves the choroid and retina
(chorioretinitis or retinochorioditis). As is the
case for anterior uveitis, it is conceivable that
any systemic or ocular inflammation will lead to
chorioretinitis. However, chorioretinitis is usually
an inflammation caused by an infectious agent.
These can be viral (distemper in the dog; FIP,
FeLV and FIV in the cat), rickettsia (Ehrlichia
canis), protozoal (Leishmania, Toxoplasma) or
fungal infections.
Causes of hemorrhagic (serous) detachment
Any cause of systemic bleeding could result in a
hemorrhagic retinal detachment. Common causes
include systemic hypertension, thrombocytopenia
(Ehrlichia canis), coagulopathies, hyperviscosity,
anemia and trauma
Clinical Signs Of Retinal Detachment
• Blind eye (no menace response)
• Fixed dilated pupil. A consensual PLR will be
present when stimulating the contralateral eye.
• When performing an ophthalmoscopic
examination, the clinician will find it difficult
to focus on the retina (since it moved from its
natural place). It is possible to see a “sheet”
floating in the posterior part of the eye. This
sheet, which is the retina, may be transparent,
white (i.e., edematous), or hemorrhagic,
depending on the cause of detachment.
Retinal blood vessels may be seen on it
even without the use of an ophthalmoscope.
• Ultrasound. A 10 MHz probe can image the
detached retina. This image is called “the seagull
sign”, because the detached retina usually remains
anchored to the eye in the optic disc and to the ora
serrata. An ultrasound examination is particularly
useful when an ophthalmoscopic examination can
Back to contents
Op
not be conducted due to severe corneal edema,
hyphema, etc.
Treatment of Retinal Detachment
• It is imperative to diagnose the primary cause
of the detachment, and to treat it. Therefore,
systemic workup has to be performed. Depending
on the type of detachment, this workup should be
aimed at diagnosing cardiovascular or infectious
diseases.
• Lens extraction surgery is indicated in when the
detachment is secondary to anterior lens luxation
• Fibrin clots and strands can be dissolved by
injecting tissue plasminogen activator (TPA) into
the eye, thus preventing traction detachments.
• Treatment of exudative serous detachments
involves draining the subretinal fluid. This may
be done using hyperosmotic agents. Systemic
carbonic anhydrase inhibitors should also
be considered. If the cause of the exudate is
inflammatory, systemic steroids should be
considered.
• Specialized referral centers may perform surgery
to re-attach the retina, or to “seal” retinal holes.
2. Sudden Acquired Retinal Degeneration (SARD)
This is an acquired disease of an unknown cause,
typically appearing in middle-aged (female)
dogs. The history provided is one of sudden onset
blindness. The typical patient is “cushinoid”.
In many dogs, owners will report a history of
lethargy, weight gain and PU/PD during the last
few months. Bloodwork is also suggestive of
Cushing’s disease
Examination will reveal a blind eye with a fixed,
dilated pupil. The fundus appears normal during
the first few months. Degenerative changes may
appear at a later stage (few months). The ERG is
flat, indicating lack of retinal activity.
Currently there is no treatment for SARD.
Hopefully, once the cause is identified, treatment 2006 World Congress WSAVA/FECAVA/CSAVA
can be offered.
3. Optic Neuritis
A. Cause
An inflammation of the optic nerve caused by:
• Any cause of meningitis
• Infectious causes – distemper, fungal diseases
(e.g., Cryptococcus), toxoplasma, bacteremia,
etc. In many of the systemic disease, the ocular
signs may be the presenting complaint.
• Neoplasia, trauma or an abscess in regions
where the optic nerve passes (especially at the
optic chiasm!)
• CNS diseases – GME, reticulosis, etc.
• Idiopathic – probably the most common cause
589
Op
B. Diagnosis
• Blind eye with a fixed, dilated pupil
• ERG is normal, since the retina is not affected
(thus distinguishing optic neuritis from SARD)
• The optic disc appears normal or inflamed,
depending on which part of the nerve is involved.
If the proximal part of the optic nerve is involved,
papilledema and vascular congestion of the optic
disc are seen on examination of the fundus.
Atrophy of the optic disc is noticed as the disease
Op – Ophthalmology
OCULAR EXAMINATION
Ron Ofri, DVM, PhD, DECVO
Koret School of Veterinary
Medicine
Hebrew University of Jerusalem
PO Box 12
Rehovot 76100
ISRAEL
ofri@agri.huji.ac.il
An ophthalmic examination should not be a scary
experience! Though admittedly interpretation of
the findings may sometimes be challenging, the
examination itself follows a logical, anatomical
order. Furthermore, it does not require expensive
2006 World Congress WSAVA/FECAVA/CSAVA
equipment. In fact, the most important items
required are non-ophthalmic in nature: a room
that can be darkened, a good source of focal light
and a magnifying loupe. A hand held lens, a direct
ophthalmoscope, a Schiotz tonometer and some
disposable items (stains, solutions, etc.) complete
the list of basic equipment.
As with any other system, the clinician should pay
particular attention to the signalment. Numerous
ocular diseases may be breed- or age-related. Since
many ophthalmic disorders may be manifestations
of systemic diseases, a general history should be
taken and a comprehensive physical examination
should be conducted. Similarly, if neuro-
ophthalmological abnormalities are present
(blindness, strabismus, anisocoria, etc.), the
neurological system should be evaluated, as these
may be signs of a nervous system disease.
590
Back to contents
resolves. Inflammation of more distal parts of the
nerve may present with a normal-looking disc.
C. Treatment
Treatment is based on identifying and treating
the primary cause. Systemic steroids should
be administered if no systemic cause is found.
Prognosis is guarded.
1. Gross Inspection
The patient should be observed as it walks into
the room, since this is an unfamiliar environment
which may highlight visual deficits; these will
be further evaluated later on. Following the
anamnesis and physical examination, the ocular
assessment begins by careful observation of the
patient from a distance, without touching the
patient (as this may cause distortion of palpebral
fissure). While observing, ask yourself:
• Are both eyes open normally? Is there evidence
of pain or photophobia? Is the animal blinking
normally?
• Are the eyes of normal size and position? Is there
evidence of exophthalmous or buphthalmous?
Are the pupils of equal size?
• Is the eyelid conformation normal? Is there
evidence of entropion or ectropion (usually of the
lower lid)? Is the upper lid prolapsed? Is the 3rd
eyelid elevated?
• Is there ocular discharge? What is its nature?
Next, the orbital area is palpated to detect any

fractures, abnormal swellings, etc. Use the
opportunity to press on the globe through the upper
lid. This serves both as a retropulsion test (which
indicates the presence of a retrobulbar mass), and
to proptose the 3rd eyelid, allowing inspection of
its outer surface. It is NOT an effective way of
evaluating intraocular pressure (IOP).
Inspect (grossly) the eyelids. Examine their skin
surface, the mucocutaneous junction, and evert
them slightly to visualize the palpebral conjunctiva
and the two punctas. Use the opportunity to test
the blink reflex in response to touching of the
canthal skin. Continue by examining the bulbar
conjunctiva and the cornea surface.
2. Assessing Vision
a) Menace Response: This involves making a
sudden threatening gesture which is supposed to
elicit a blink response. The afferent arm of the
response consists of the retina, optic nerve axons,
and the optic tract and radiations. The efferent
component of the response includes the primary
motor cortex, cerebellum, and the nucleus and
nerve of cranial nerve VII (facial nerve).
It is important to note that the menace response
involves cerebral cortical integration and
interpretation and therefore is not a reflex. Rather,
it is a cortical response that requires the entire
peripheral and central visual pathways, as well
as the visual cortex and the facial nucleus and
cranial nerve, to be intact. Also, remember that
the menace response is a very crude test of vision,
and in fact requires visual acuity of only 6/600!
The menace response should be evaluated in
one eye, while the other eye is being covered.
Be careful not to touch the eyelashes/hair of
the patient, or to cause wind movement, as this
may lead to a “false positive” response; consider
making the menace gesture behind a glass
partition. Likewise, “false negative” results (lack
of a menace response in a visual animal) are also
possible. One possible reason is facial nerve
paralysis, which is ruled out using the blinking
reflex. The menace response is absent in very
young (<10-12 weeks) animals, and may also be
affected by the patient’s mental state.
b) Additional Visual Tests: Vision can also be
evaluated using an obstacle course. You should
be consistent in the obstacle course that you
construct, and make sure it can be navigated by
normal animals! Test the patient in light and dim
conditions, and consider patching one eye.
Another test is the visual placing response, which
is useful when results of the obstacle course and
menace response are equivocal. It is conducted
by lifting the animal towards the table, allowing it
to see the approaching surface. A normal animal
will extend its leg towards the surface before its
paw touches the table.
Back to contents
Op
3. Examination in the dark
After the light has been dimmed, the dilatation of
the pupils should be evaluated. Use a dim light
(to prevent constriction), and stand at a distance
so you can visualize both pupils simultaneously,
using the tapetal reflection. The tapetal reflection
also serves to highlight (by means of retro-
illumination) any ocular opacities, particularly in
the lens or vitreous.
Next, use a bright light to evaluate the Pupillary
Light Reflex (PLR). Unlike the menace response,
the PLR is a subcortical reflex. Therefore, it does
NOT test vision, and a normal PLR may be found
in a cortically blind animal. Furthermore, the PLR
is usually present (though it may be diminished
or slow) in animals suffering from outer retinal
degeneration (PRA), cataracts, and other causes
of subcortical blindness. Nevertheless, the PLR
is a very important test, which helps localize the
lesion which causes loss of vision.
If one of the pupils does not react to light, or if
it can not be visualized (e.g., in cases of severe
corneal edema or hyphema), the consensual PLR
should be checked. Alternatively, you can check
the dazzle reflex. This is also a subcortical reflex,
which is manifested as a bilateral, partial blink in
response to a bright light.
Magnification is required for the next stages of
the examination. Once again, the lid margins,
conjunctiva and corneal surface are examined.
Use the magnification to check for aberrant
eyelashes (trichaisis, distichia); these can be
best visualized against the white background of
the conjunctiva, by slightly pulling the eyelid.
Following the anatomical order, next inspect
the anterior chamber (looking for opacities in
the aqueous), the iris surface and the anterior
segment of the lens.
4. Ophthalmoscopy
This part of the examination is the one which
clinicians usually dread the most. Part of this
2006 World Congress WSAVA/FECAVA/CSAVA
undoubtedly stems from the large range of normal
variations in the appearance of the canine (and, to
a lesser extent, the feline) fundus. Admittedly, if
you are not in the habit of examining fundii, you
will find it difficult to diagnose abnormalities.
You should therefore make a habit of examining,
however briefly, the fundus of every patient that
you see. Your clients will appreciate the extra
touch, and you will gain the required proficiency.
Due to the high cost of an indirect ophthalmoscope,
only a direct ophthalmoscope is available in most
general practices. This instrument provides a
high magnification (x16 in an average dog). The
unfortunate consequence of the high magnification
is a small viewing field (4o), extending the time
required to examine the entire fundus. A quick
591
Op
overview of the fundus may be obtained using
a bright light source and a handheld lens (20-
30D), providing a means of monocular “indirect
ophthalmoscopy”. The direct ophthalmoscope
comes with several features:
• A grid (graticule) - use it to compare the size of
the lesion to the size of the optic disc
• Red-free filter (emits green light) - helps
evaluation of hemorrhage and blood vessels,
which appear black.
• Apertures of varying diameter-use the largest
one that is appropriate for the patient’s pupil
• Changing lenses permits the examiner to evaluate
the depth/height of a lesion, or to examine more
anterior structures, such as the lens. A raised
lesion will come into focus by adding convex/
converging lenses (+). A depression/coloboma
will come into focus by adding concave/diverging
lenses (-). In dogs, each diopter you add is
equivalent to 0.28 mm.
• Use of a narrow beam allows to evaluate
depressions and elevations of fundus lesions
Ophthalmoscopy should be conducted in a dark
room, following dilatation of the pupil. First
evaluate the tapetal reflection from a distance, to
detect any lenticular or vitreal opacities. As you
approach the patient, focus on successively more
posterior structures- cornea, iris, lens and vitreous-
till you are focused on the fundus. Carefully
inspect the entire fundus, evaluating changes in
the tapetum, non-tapetum, blood vessels and optic
disc. It is best to stay in stationary position and let
the patient’s eye movements bring the structures
to you, instead of trying to “chase” them.
2006 World Congress WSAVA/FECAVA/CSAVA
592
Back to contents
5. Additional tests
• Schirmer tear test is used to evaluate tear
production and diagnose keratoconjunctivitis
sicca. It should be conducted at an early stage of
the examination, as any ocular manipulation may
induce reflex tearing.
• Fluorescein staining is used to diagnose corneal
ulcers. Superficial ulcers may be stained with
Rose Bengal
• Samples for bacteriology, mycology and
cytology may be taken as indicated. The first two
should be taken before any drops are put in the
eye, as ophthalmic solutions frequently contain
preservatives.
• Nasolacrimal patency is evaluated by passage
of fluorescein from the eye to the nose, by
cannulating the nasolacrimal system and by
dacryocystorhinography.
• Ultrasound is frequently used in ophthalmology.
The main indications are imaging of the
retrobulbar area, and imaging of the posterior
segment when it can not be visualized (e.g., due
to hyphema or cataract). CT and MRI techniques
may be used in certain cases.
• Tonometry-measuring IOP to diagnose glaucoma.
• Additional tests, including gonioscopy
(evaluation of the iridocorneal angle as part of the
diagnosis of glaucoma) and electroretinography
(recording electrical responses of the retina to
flashes of light, to determine retinal function) may
be available in referral centers, and are discussed
elsewhere in these proceedings.

Op – Ophthalmology
ELECTRORETINOGRAPHY
Ron Ofri, DVM, PhD, DECVO
Koret School of Veterinary
Medicine
Hebrew University of Jerusalem
PO Box 12
Rehovot 76100
ISRAEL
ofri@agri.huji.ac.il
Electroretinography (ERG) is the recording of
electrophysiological activity in the retina in
response to light stimulation. There are several
indications for conducting ERG recordings in
animal patients:
1. Routine preoperative evaluation of retinal
function before cataract extraction. Unfortunately,
many dogs may be simultaneously affected with
both progressive retinal degeneration (atrophy)
and cataract. Regardless of whether these two
diseases are related or independent, it is obvious
that cataract surgery will not restore vision if
the retina is not functioning. Since the cataract
prevents a thorough ophthalmoscopic evaluation
of the fundus, the retina can not be evaluated
for signs of disease. Therefore, an ERG test is
required to determine the prognosis of the surgery,
and the potential for post-operative vision. It is
important to note that even in the presence of
cataracts (or a corneal opacity), sufficient light
reaches the retina to cause a response, provided
that the retina is functional. This is also the reason
why pupillary light reaction can be elicited in
cataractous patients. If the opposite fundus can
be seen ophthalmoscopically, an ERG test is
unnecessary, as inherited retinal atrophies are
bilateral diseases.
2. Diagnosis of retinal disorders in which no
ophthalmoscopic abnormalities are evident.
These include early stages of progressive retinal
degeneration, hemeralopia in Alaskan malamutes
and sudden acquired retinal degeneration (SARD).
In all of these diseases, ERG abnormalities may
be recorded even though the fundus may seem
normal.
3. Differentiating between retinal and post-retinal
causes of blindness. For example, cases of SARD
and optic neuritis may present similarly with acute
loss of vision, a normal-looking fundus, and fixed,
dilated pupils. An ERG may be used to differentiate
between the two, as it will be extinguished in
SARD (which is a retinal disease) but normal in
optic neuritis, which is a post-retinal disease.
4. Early diagnosis of inherited photoreceptor
Back to contents
Op
atrophies. In some dog breeds, the ERG may
detect changes in retinal function long before
ophthalmoscopic or behavioral signs are
observed. For example, in the standard poodle,
the Portuguese water dog, and the American and
English cocker spaniel, ERG changes can be
recorded years before the appearance of clinical
signs. This early detection is invaluable to
breeders wishing to screen their dogs for inherited
retinal diseases.
Recording the ERG response
Though the ERG is a non-invasive procedure,
the patient is anesthetized to reduce electric noise
and movement artifacts. The stimulating light
is placed close to the eye, and responses to the
light flashes are recorded using 3 electrodes. The
active (recording) electrode is usually mounted
on a contact lens placed on the cornea. Two more
electrodes are placed sub-cutaneously to reduce
electrical noise.
Based on the clinical indication for the ERG, two
recording protocols have evolved for performing
the test in dogs. The first is the rapid, “yes-no”
protocol, used to demonstrate retinal function. It
is conducted to rule out SARD or to determine
if the patient is a suitable cataract surgery
candidate. This is a brief test, which records 2006 World Congress WSAVA/FECAVA/CSAVA
the responses to 2-3 flashes of light. For early
detection and workup of inherited photoreceptor
diseases, a more exhaustive recording protocol
is required. This protocol involves extensive
testing of rod and cone function, based on their
different physiological characteristics. Some of
the photoreceptor properties that are evaluated in
the course of the comprehensive test include:
1.Responses to dim flashes of light (scotopic
vision), which is a feature of rod function, as
opposed to responses to bright flashes (photopic
vision), which indicate cone function.
2.Color stimulation: cones are more responsive to
red light, while rods are more responsive to green
or blue stimulation.
3.Adaptation: Once the room lights are turned off,
593
Op
a process of dark adaptation begins. With time,
the sensitivity of the rods increases, expressed
as increased amplitude of the signal recorded in
response to dim light. Conversely, turning on the
room lights causes light adaptation, as the rods
saturate and do not respond to light.
4. Flicker response: the detection of light
flashes depends on the frequency at which the
stimulus flickers. Rods can detect light flashing
at a frequency < 10Hz, while cones can detect
flickers of up to 30-70 Hz (depending on species).
Beyond these limits, the photoreceptors can not
detect the individual flashes, and their responses
“fuse” (which is why we see a continuous picture
on our TV, even though it is flickering).
These exhaustive tests of retinal function have
been used to detect various types of photoreceptor
diseases in numerous breeds, including cone
degeneration in the Alaskan malamute, prcd in
the poodle, American and English cocker spaniel,
rcd1 in the Irish setter, rcd2 in the collie, and
others. These diseases, and their abnormalities,
are discussed elsewhere in these proceedings.
The recorded ERG signal is analyzed by
evaluating the amplitude and latency (timing)
of two main components: the a wave is the first
negative deflection of the signal, and is indicative
of photoreceptor response. It is followed by
a large, positive peak, the b wave, which is
generated in the mid-retina (bipolar and Müller
cells).
2006 World Congress WSAVA/FECAVA/CSAVA
594
Back to contents
It is important to recall that the ERG has several
limitations. First and foremost, one should
remember that the ERG is a test of retinal
function, not of vision. Therefore, it may be
normal in some cases of blindness. For example,
the ERG is normal in cases of mature cataracts,
even though the patient is functionally blind. It
is also normal in cases of post-retinal blindness,
such as optic neuritis or cortical blindness. Such
cases are best evaluated by recording Visual
Evoked Potential (VEP’s), which represent
cortical responses to flashes of light; these are
recorded by placing the active electrodes on the
scalp over the visual cortex. Another limitation
of the ERG is the fact that it represents a global
retinal response, and therefore can not be used to
diagnose focal areas of dysfunction (scotomas).
Finally, as the ERG records the response of the
photoreceptor cells, it is normal in glaucoma,
which is a disease of the inner retina. These last 2
limitations can be overcome by using specialized
ERG equipment, the focal ERG and the pattern
ERG, respectively. However, this equipment is
not in clinical use in veterinary ophthalmology.
Nevertheless, if these limitations are kept in mind,
and if the recordings are performed according to a
formal protocol, the ERG can be a powerful tool
in the diagnosis of retinal disease.

Op – Ophthalmology
KERATOCONJUNCTIVITIS SICCA – INTRODUCTION AND CASE
REPORTS
Jiri Beranek, DVM
Veterinary Clinic
Husova 1747
530 03 Pardubice
Czech Republic
med.prod@worldonline.cz
Keratoconjunctivitis sicca (KCS) is a chronic
progressive inflammatory and degenerative
disease associated with deficient or absent
production of preocular tear film. In the most
cases it requires a lifelong therapy. It is a serious
disease, particularly when its chronic course
induces conjunctivitis and keratitis.
Exact etiology of this disease remains unknown.
Congenital anomalies, traumatic events, systemic
or local infectious diseases, chronic lacrimal
adenitis, toxic effects of drugs, neurogenic and
idiopathic causes or autoimmune processes with
a breed predilection are considered to be causes
of KCS. The etiology has been categorized by
Slatter as follows:
1. Drug-induced KCS: phenazopyridine, sulfadiazine
and sulfasalazine derivatives cause KCS mainly
in elderly dogs. Appearance of KCS cannot be
excluded even after repeated topical application
of atropine.
2. Surgically induced KCS: can happen as a result
of surgical removal of prolapsed lacrimal gland
of the nictitating membrane.
3. Idiopathic causes of KCS: majority of KCS
cases associated with reduction of cytoplasmic
secretory granules in the glandular cells of both
lacrimal glands (including senile atrophy of
granules) are included in this group.
4. Autoimmune KCS: more than 30% of cases
of destruction of the lacrimal gland and gland
of the nictitating membrane are associated with
the immune system. Dogs with diagnosed KCS
reveal higher affinity to endocrinopathies, such
as hypothyroidism, diabetes mellitus, hyper- or
hypoadrenocorticism, rheumatoid arthritis, lupus
erythematosus, complex pemfingus, and Cushing
syndrome or to conditions, such as polymyositis,
polyarthritis, atopy, pyoderma, seborrhoea,
glomerulonephritis, and ulcerous colitis.
5. Orbital and supraorbital injuries: may influence
function of lacrimal glands either directly or via
damage of their nerves.
Back to contents
Op
6. Febris contagiosa cannum: distemper virus
affects both lacrimal gland and the gland of
the nictitating membrane temporarily or even
permanently.
7. Other causes: all other cases, which do not
fit into the previous categories, are counted into
this group, e.g. KCS following radiotherapy or
vitamin A deficiency.
KCS is a disease with a proven breed
predisposition for breeds, such as shi-tzu,
lhasa-apso, pekinese, english bulldog, West
Highland white terrier, cocker-spaniel, mopse,
yorkshire terrier, miniature poodle, schnauzer,
Chinese crested dog. Congenital KCS occurs
mostly unilaterally in small breeds. The highest
occurrence of the disease was observed at the age
between 4 and 7 years. The likelihood of disease
occurrence increases with age.
A less frequent occurrence of KCS is reported in
cats. One of the possible diagnostic factors may
be lower STT values as compared with dogs.
Clinical signs of the KCS are various and depend
on the severity of disease, acute or chronic stage,
and unilateral or bilateral occurrence.
The typical signs are: 2006 World Congress WSAVA/FECAVA/CSAVA
Blepharospasms: is frequently observed as a
first sign of the disease. It is caused by corneal
irritation as a result of changes in the tear fluid. It
may be associated with photophobia.
Mucoid or mucopurulent discharge: in the absence
of the aqueous layer of the tear film, mucoid layer
of the tear film is insufficiently eliminated from
the eye and can be seen dry around the palpebral
rim. This is together with conjunctivitis one of
the early signs of KCS.
Corneal ulceration: is described mainly in chronic
cases where loss of epithelium occurs in the
central corneal area. This condition may lead to
corneal perforation and endophthalmitis.
Corneal vascularization and pigmentation:
deepness and extent of the corneal changes
correlates with the disease chronicity.
595
Op
Corneal xerosis and conjunctival redness: dry
appearance of the cornea is typical.
Dry ipsilateral nostril
Chronic staphylococcus infection with good
responses to antibiotics
Diagnose of KCS is based on clinical signs, staining
with bengal red, which detects dead cells and epithelial
lesions, as well as staining with fluorescein, which
stains corneal ulcerations. Schirmer tear test (STT) is
a standard approach to assessment of tear production.
Recommended interpretation is as follows: normal
tear production amounts to 15 mm/min. and more
on the test strip; beginning or subclinical KCS
shows 11-14 mm/min., slight to moderate KCS
results in 6-10 mm/min., and severe cases of
KCS are associated with values below 5 mm/
min. In dogs with ulcerative keratitis and dogs
treated with atropine repeated examinations are
recommended. Diagnose of KCS can be postulated
in the presence of a mucopurulent conjunctivitis,
corneal ulceration, and pigment deposition in the
cornea, associated with low STT values.
Due to similarity of clinical signs caused by
bacterial infections or allergic conditions of
the eye, KCS frequently remains undiagnosed.
Results are corneal ulcerations, descemetocele
with corneal perforations and following infections
of deeper eye structures.
Therapy of KCS requires an individual approach
to each patient and drugs used have to address
specific severity grades of the disease. The most
frequently used drugs are combinations of tear
production stimulating drugs, artificial tears,
mucinolytic preparations, and topical application
of antibacterial and anti-inflammatory drugs.
Historically, pilocarpin was topically or orally
used for stimulation of parasympathetic nerves
of the lacrimal gland in order to increase tear
production during KCS. Due to a number of
2006 World Congress WSAVA/FECAVA/CSAVA
adverse side-effects (local irritation, bradycardia,
hypersalivation, vomiting, and diarrhea) and a
failure to prove a significant improvement in tear
production, the clinical usage of pilocarpin was
abandoned.
A significant change in therapy of KCS was
brought by introduction of immunosuppressive
drugs, such as cyklosporin A (Sandimmun,
Sandoz) in the year 1989. Although the
mechanism of action of cyclosporin A in the KCS
is not quite known, its immunomodulatory and
secretion stimulating effects on lacrimal glands
are successfully used. The therapeutic effect can
already be seen during the first treatment days.
Time for stabilization of the clinical condition and
increase of the tear production is usually at least
8-9 weeks. Treatment failures with cyclosporin
596
Back to contents
A are ascribed to atrophy or a total depletion of
secretory tissue of the lacrimal gland. Cyklosporin
also reduces vascularization and pigmentation of
the cornea in chronic corneal processes. It is used
dissolved in corn oil or olive oil at concentrations
of 0.5-2%, applied twice daily or as an ointment
(Optimmune®).
Substitution of tears is achieved by combination
of individual tear components. There is a number
of „artificial tears“ on the Czech market. Their
selection depends on the dog’s clinical condition,
local tolerance, price, and level of collaboration
with the animal owner. Methylcelulose and
hydroxyethylcelulose (AquaSite CIBA Vision) are
the most frequently used corneal lubricants due to
their good local tolerance and easy combinations
with other preparations. Other frequently used
substitutions of tears are polyvinyl alcohol in
1.4% solution (HypoTears, Ciba Vision, Bion
Tears Alcon), furthermore linear polymers such
as dextrane a polyvinylpyrolidone (Tear Plus,
Allergan), or viskose-elastic preparations such as
hyaluronate sodium (Healon, Pharmacia Upjohn),
chondroitine sulfate or high concentrated
methylcelulose or ophthalmologic lubricants such
as lanoline, petrolatum or mineral oils (Lacri-
Lube, Allergan, Lacrisyn Galena).
Broad-spectrum antibiotics are successfully
used as eye drops or ointments in order to
suppress secondary infections. Bacteriological
examinations are rarely necessary. Usually,
combinations of bacitracin - neomycin -
polymyxin B are recommended.
An adequate hygiene of the eyes is inevitable.
A usage of 5-10% solution of acetylcysteine is a
useful complementary therapy of corneal ulcers.
Antiinflammatory drugs used in our country
are in indicated cases topical corticosteroids, in
order to reduce conjunctivitis and clear corneal
opacities in chronic keratitis (fluorescein test
must be negative). Their usage is contraindicated
in chronic conditions and in corneal ulcers. As
KCS is frequently associated with autoimmune
diseases, also systemic corticosteroids can be
used. Topical vitamin A can be added to the
therapy.
Surgical therapy of KCS: In indicated cases,
permanent partial lateral tarsorhaphy, temporary
protection of corneal ulcerations with nictitating
membrane or transposition of parotid duct can be
done.
Surgical approach in the treatment of KCS i.e.
transposition of the parotid duct is always the
last option when all other methods fail. This
method is mostly applied after a treatment
with cyclosporin, when no improvement of
tear production is observed after 8-9 weeks
(STT test).

This method assumes that tears and saliva have similar
characteristics in terms of pH and osmolarity.
There are two approaches to transposition:
occluded (bucal- closed) approach and open
(lateral) approach. In our clinic, we routinely use
the bucal approach, because it is more comfortable
for the animal owner. He does not need to
observe his pet too closely, in order to prevent
auto mutilation. Otherwise both approaches are
equal in the results and their selection depends on
the surgeon’s preference.
Potential complications: Using either method,
it is important to avoid any damage to salivary
papilla or torsion of the salivary duct. Salivary
duct has to be long enough, in order to prevent any
tension during chewing. One of the noteworthy
complications is a closure of the salivary duct at the
entrance into the conjunctival sac – mostly caused
by retraction of the salivary duct. Obstructions of
the salivary duct were also occasionally reported
– either as a result of sialolithiasis or inflammatory
processes (sialoadenitis). A frequent observation
in patients with high concentrations of minerals
in the saliva is their deposition on the corneal
Back to contents
Op
surface and palpebral rims. The precipitates can
be easily removed by using artificial tears or
other lubricants. Another potential complication
that needs to be communicated to the pet owner is
maceration and discoloration of skin in the medial
eye angle, when the fluid is insufficiently drained
through puncta lacrima. We can use ointment
before feeding to protect skin.
In brachycephalic breeds, additional reduction of
the palpebral fissura contributes to spreading of the
tear film across cornea and prevents development
of chronic central keratitis associated with
pigment deposition in the upper corneal layers.
A recommended method is Roberts-Jones pocket
technique.
Summary: KCS is long term disease. We can threat
in 90% topically using long term cyclosporine.
When we don’t have success therapy after 8
weeks, it is time to start surgery. We prefer
bucal approach but it is necessary to explain to
the owner all potential complications and side
effects. Surgery is the best result for busy owners
as well /they don’t have enough time to use drops
or ointment topically/.
2006 World Congress WSAVA/FECAVA/CSAVA
597
Op
Op – Ophthalmology
CLINICAL APPROACH TO THE CAT WITH OCULAR DISEASE
Professor Sheila Crispin
Cold Harbour Farm Underbarrow
Kendal Cumbria
LA8 8HD
UK
s.m.crispin@bris.ac.uk
s.crispin@rcvs.org.uk
In outlining the clinical approach to the cat
with ocular disease it is relevant to remember
that ‘clinical’ is defined as concerned with, or
based on, observation – and the feline eye, in
health and disease, is particularly rewarding to
observe. Knowledge of ocular disease - disease
pertaining to the eye - is based on a thorough
understanding of what is normal and some
variations from normality are so characteristic
that specific diagnosis of the ocular disease is
possible from the history alone. In many cases,
however, clinical diagnosis of ocular disease
requires physical and neurological examination
as well as examination of both eyes and so the
clinical approach adopted in the presentation will
concentrate on the ocular findings, supplemented
by accompanying physical and neurological
findings as appropriate. Additional investigative
procedures, such as laboratory tests, that may
on occasions be needed to confirm the clinical
diagnosis will not be discussed, as they are not an
integral part of the clinical part of the diagnostic
process. Examples of feline ocular disease will be
used to demonstrate the necessity for a meticulous
clinical approach.
It is crucial that the clinical approach to ocular
disease is underpinned by a comprehensive history
2006 World Congress WSAVA/FECAVA/CSAVA
and accurate recording of the clinical findings.
Clinical records for ophthalmic cases should
include illustrations as well as written details and
sequential illustrations are an excellent means of
recording changes over time. Photographs are
a useful adjunct, but they should complement,
rather than replace, simple drawings.
The history should record the age, breed, sex and
vaccination status of the case, information about
the present problem and its duration, as well as
details of any previous health problems. It is
important to ascertain the nature of any treatment,
both for the presenting problem and any previous
problems. Other relevant enquiries include the
management and lifestyle of the cat and, for
example, whether it is kept isolated from other
cats, or is part of a multicat household. Details of
any other animals with which the cat may have
598
Back to contents
come into contact should also be obtained. Some
assessment of the severity of the problem and
the degree of pain should also be made, based
on the client’s own assessment of the cat and the
clinician’s observations.
Physical examination is a logical procedure based
on a standard protocol. Physical examination
should be carried out in a quiet room that can be
darkened completely, to facilitate the subsequent
ophthalmic and neuro-ophthalmological
examination which forms part of the process.
Physical examination involves the whole body
and usually consists of initial observation and
inspection followed by checking the vital signs
including respiratory rate, pulse (rate, regularity
and pressure) and temperature. Inspection
of body systems as part of routine physical
examination includes palpation, auscultation and
percussion. In adult cats it may also be sensible to
measure the blood pressure, particularly if there
are any clinical features that suggest systemic
hypertensive disease. Usually it is the mean
systolic blood pressure that is measured.
Ophthalmic examination is part of the physical
examination and forms the main focus of the
presentation. The cranial nerve tests which
are routinely included as part of ophthalmic
examination are tracking response, vestibulo-
ocular reflex, dazzle reflex, menace response,
palpebral and corneal reflexes and direct and
consensual pupillary light reflex. Ophthalmic
examination is performed in two parts; the first
part in daylight or artificial light and the second
part in the dark.
Initially the cat is observed from a distance in
order to assess the nature and severity of the
ocular problem. If appropriate, obstacles can be
placed on the floor and the cat should be allowed
to move freely about the consulting room, as a
very crude way of assessing vision (the lighting
intensity should be varied). Visual tracking can
also be checked at this stage using cotton wool
balls, or a bright spot of light, but the cat needs
to be interested!
For complete examination of the lens, vitreous

and fundus, instillation of a mydriatic is required,
but this is not regarded as a routine feature of
feline ocular examination. The pupil of normal
cats responds briskly and more completely to
bright light than that of dogs and narrows to a
vertical slit, resulting in a very limited field of
view. Tropicamide 1% is the drug of choice, but
cats resent its bitter taste and it is often more
rewarding to simply keep the light intensity low for
basic examination, especially as many cats resent
illumination with bright light. This sympathetic
approach is also less likely to produce third
eyelid protrusion (there is a voluntary element in
the cat). If a mydriatic is used it must be applied
after other tests such as the Schirmer tear test,
have been performed.
The general appearance of the eyes and adnexa
is observed in daylight or artificial light and
each side compared to ensure that they are
symmetrical. The position of the globe in relation
to the orbit should be assessed from in front of
the patient and from above. The incomplete
bony orbital rim should also be inspected both
visually and manually. The vestibulo-ocular,
dazzle reflex, palpebral and corneal reflexes and
menace response can also be tested at this point.
The direct and consensual pupillary light reflex
can also be checked and should be repeated under
conditions of darkness.
The lacrimal apparatus is not evaluated in any
detail at this stage, although the possibility of
abnormalities of production, distribution and
drainage may be suspected according to the
clinical presentation. Once the basic ophthalmic
examination is completed tear production can
be assessed, usually with a Schirmer I tear test.
The presence and position of the upper and lower
lacrimal puncta should be confirmed and for this
magnification is useful.
The margins, outer and inner surfaces of the upper
and lower eyelids should be examined. There is
close apposition of the upper and lower eyelids to
the globe, so inspection of their inner surface is
not always easy. The position of the third eyelid
should be observed and its outer surface inspected
once the eyelid has been protruded by pressure
on the globe through the upper eyelid. The
inner surface of the third eyelid is not examined
routinely.
The ocular surface (defined as the continuous
epithelium which begins at the lid margin,
extends onto the back of the upper and lower
eyelids, and both surfaces of the third eyelid, into
the fornices and onto the globe) is examined next.
Naked eye examination should indicate whether
the appearance of the ocular surface is normal.
A penlight can be used to ensure that the corneal
reflex is normal (in this situation the corneal
Back to contents
Op
‘reflex’ is the light from the penlight reflected
in miniature on the corneal surface without
disruption). It may also be appropriate to check
corneal sensitivity at this stage, particularly in
those situations in which corneal anaesthesia may
be part of the clinical presentation (e.g. herpetic
keratitis). This can be done in an empirical
fashion by touching the cornea with a fine wisp
of cotton wool, which should elicit a brisk blink
in the normal cat. A more elegant and accurate
method utilises an aesthesiometer. Additional
investigations such as swabs and scrapes for
culture and the application of ophthalmic stains
may be performed once the basic examination
has been completed.
Darkness minimises distracting reflections and
is the next - and essential - part of ophthalmic
examination.
The anterior segment (the internal structures
of the globe up to and including the lens) is
examined with a light source and magnification,
or a slit lamp biomicroscope. The pupillary light
response in darkness can be evaluated using focal
illumination, before the eye itself is examined.
The limbus and cornea are examined first. Most
of the limbus is invisible in the normal cat except,
sometimes, laterally. The limbal zone is usually
clearly defined because of a rim of pigment on
the corneal side.
The anterior chamber should be optically clear.
A slit beam, rather than a diffuse beam, is used
to detect subtle opacities within the aqueous.
The depth of the anterior chamber is most easily
assessed by use of a slit beam, or by shining a
beam of light across the eye from lateral to
medial. The anterior chamber is deep and the
pectinate ligament of the iridocorneal angle can
be observed directly, if somewhat imperfectly,
without a gonioscopy lens.
The iris of most cats is lightly pigmented and the
distinction between the pupillary zone (usually
darker) and ciliary zone (usually lighter) at the
2006 World Congress WSAVA/FECAVA/CSAVA
collarette is not always present, so that the iris is of
uniform colour. Colour variations may be present
between irides and within different sectors of the
same iris. Variations of pigmentation produce a
range of colours. In the least pigmented, almost
albinotic iris, which is very pale in colour, the iris
is often so thin that it can be transilluminated.
The adult pupil is round when dilated and narrows
to a vertical slit on constriction. It is important to
observe the size and shape of the pupil, paying
particular attention to the pupillary margin, as
deviations from normal may indicate posterior
synechiae or neurological abnormalities.
The whole lens can only be examined in detail
when a mydriatic has been used. The light source
is used to demonstrate the anterior and posterior
599
Op
lens surfaces by observing the catoptric images
which are visualised on the anterior lens capsule
(erect) and the posterior lens capsule (inverted).
It is easier to establish these boundaries by noting
the relative movement of the images in relation to
the light source (parallax).
The posterior segment (the internal structures
of the globe beyond the lens) is examined next
using some or all of a light source, slit lamp
biomicroscope, indirect ophthalmoscope and
direct ophthalmoscope.
The anterior vitreous is most easily examined
with a penlight or slit lamp and should be free of
obvious opacities.
Both indirect ophthalmoscopy and direct
ophthalmoscopy are used to examine the ocular
fundus and, to some extent, the posterior vitreous.
Indirect ophthalmoscopy provides low power
examination of a wide area and is particularly
useful when the ocular media lack optical clarity.
Direct ophthalmoscopy provides a magnified
view of a relatively small area.
With either type of ophthalmoscopy the optic
nerve head (optic disc or papilla) which is
situated within the tapetal fundus when a tapetum
is present, is located first and its size, shape and
colour should be noted. In cats the optic nerve
head is usually unmyelinated so that it is round
in shape and slightly recessed, the optic nerve
becoming myelinated posterior to the lamina
2006 World Congress WSAVA/FECAVA/CSAVA
600
Back to contents
cribrosa. The retinal vasculature is examined next,
paying particular attention to the number and
distribution of the retinal vessels, both arterioles
and venules, as they hook over the rim of the
optic nerve head. The terminal choroidal vessels
appear as dark dots where they are viewed end
on. In poorly pigmented eyes, larger choroidal
vessels will also be visible, and they too should
be examined. Finally, all four quadrants (dorso-
medial, dorso-lateral, ventro-lateral, vento-
medial) of the ocular fundus are checked.
It is important to note that because the feline eye
is well adapted to light collection and vision under
dim lighting conditions (large eye, large cornea,
large lens, rod-rich retina, tapetum cellulosum) the
examiner must be prepared to examine the ocular
fundus without the use of excessively bright
light. A non-compliant patient with the ability to
move the third eyelid voluntarily, together with
constriction of the pupil to a narrow vertical slit,
will make the process of ophthalmic examination
both difficult and incomplete. In addition, the
feline tapetum is such an effective mirror that it
is easy to miss subtle lesions if the light intensity
is too high. However, the feline fundus exhibits
fewer normal variants than the canine fundus, so
it is relatively easy to identify pathology provided
that this simple rule is followed.

Op – Ophthalmology
HEREDITARY DISEASES OF THE CANINE EYELID AND CORNEA
Peter Bedford, Professor
Royal Veterinary College
Department of Veterinary Clinical
Sciences
Hawkshead Lane
Hatfield, Hertfordshire AL9 7TA
UK
pbedford@rvc.ac.uk
INTRODUCTION
‘The diseases of the eye constitute a very
important, but most unsatisfactory division of our
work, for the melodies of this organ, although few
in number, are frequent in their appearance. They
are sadly obstinate and often baffle all skill’. W.
C. Spooner, 1852.
Almost 150 years have lapsed since this
judgement on ocular disease in veterinary
medicine was delivered, and most of it remains
true to this day. The exceptions relate to skill and
the paucity of ocular disease. Our treatments of
the ‘melodies of this organ’ have improved as
aetiologies have been explored and research has
produced therapies both medical and surgical.
However, the development of the pedigree dog
in its numerous shapes and sizes has provided
today’s clinician with a wide range of ocular
diseases to treat. These diseases are determined
genetically and have been unwittingly produced
either through the desire to refine a specific
anatomical feature or as a by-product of the close
breeding involved in obtaining a specific feature.
The problems, therefore, have arisen either as
the result of an earnest desire to measure up to
a Breed Standard, or they arose accidentally in
a selection process focussed on improvement.
Thus, microphthalmos may be the result of
producing a small ellipsoidal palpebral fissure,
while progressive retinal atrophy has appeared
within certain breeds because specific lines have
been selected for intensive breeding to perpetuate
their outstanding breed features. It is reasonable
to expect that today’s pedigree dog should be able
to enjoy a normal life free from pain, discomfort
and other incapacity. That would be the measure
of real progress, but in some breeds we have a
situation in which the effects of natural selection
and evolution have literally been reversed.
THE EYELIDS
The two dictating factors in eyelid conformation
are size, and hence the shape, of the palpebral
fissure and the position or size of the globe.
Thus entropion, ectropion, the diamond eye
Back to contents
Op
configuration and anomalies of the membrana
nictitans tend to be dictated primarily by the
requirements of the Breed Standard, while other
defects like distichiasis and aplasia of the lacrimal
puncta occur as the result of intensive breeding
programmes involving affected animals.
Entropion
Several breeds are involved, the incidence varying
from extremely high in the Chow-Chow and
Shar-Pei, to low in breeds like the Labrador and
Golden Retrievers. Entropion is a deformation
of the eyelid in which there is inward rotation
of part of the palpebral margin such that eyelid
hair is brought into contact with the cornea
and/or the bulbar and membrana conjunctival
surfaces. Invariable there is discomfort or pain
and the patient may present in blepharospasm.
Conjunctivitis, superfical keratitis and corneal
erosion are all possible consequences and sight can
be permanently impaired as the result of scar and
pigment formation if the defect is not corrected.
It is normally the lateral part of the lower eyelid
that is involved, but constant blepharospasm can
induce further inward rotation of the palpebral
fissure. Extensive involvement is seen with
regularity in the Chow-Chow and in the Shar-Pei.
Fortunately, corrective surgery is effective and 2006 World Congress WSAVA/FECAVA/CSAVA
skin or skin and orbicularis oculi muscle resection
is well practised. Eyelid tacking, which has been
extensively utilised in the neonatal lamb, can be
used in very young puppies, but a number of these
patients subsequently require the more traditional
approach to achieve correction.
Ectropion
Here the lower eyelid is everted away from the
globe to expose the membrana nictitans and the
ventral conjunctival surfaces. Exposure of this
tissue results in chronic conjunctivitis, and the
lagophthalmos may detract from the efficient
distribution of the precorneal tear film. Exposure
keratitis and even corneal ulceration may ensue
and drainage of the tear film via the nasolacrimal
duct may also be impaired. It is due to the large
601
Op
palpebral fissure which is a required feature of the
Breed Standard for several breeds. Thus, ectropion
is expected in breeds like the St. Bernard, the
Bloodhound, the Mastiff, the Basset Hound and
the Clumber and English Cocker Spaniels and its
incidence will remain high unless considerable
change in the conformation of the head in these
breeds is effected. The Breed Standard of the
Clumber Spaniel, for example, asks for the eyes
that should be enophthalmic with prominence of
the membrana nictitans. The weight of the large
hanging pinnae combined with the heavy jowls
simply pulls the palebral fissures ventrally over
the globes leading to loss of support for the lower
eyelid. Similar commentary applies to the other
breeds, and the recent Breed Standard changes are
not radical enough to effect real improvement.
Surgical correction is possible, but the success of
the techniques used is governed considerably by
the weight of the facial skin. Simply shortening
the palpebral fissure by full thickness wedge
resection does nothing to stablise the lateral
canthus and techniques that shorten the lower
eyelid and provide support by cicatrix formation
at the lateral canthus offer the best chance of
success.
The diamond eye configuration
This severe conformational defect is a
combination of entropion and ectropion, and is
the direct result of a large, unsupported palpebral
fissure. It is simply an exaggeration of the
conditions that produce ectropion and is found
consequently in those breeds in which ectropion
readily occurs. Deficiency of the lateral retractor
muscle allows the lateral canthus to hang loosely
in a position well below the normal line of the
palpebral fissure. This loose tissue distorts easily,
particularly where there is no support from an
enophthalmic and somewhat microphthalmic
eye. Entropion of the lateral parts of the upper and
2006 World Congress WSAVA/FECAVA/CSAVA
lower eyelid is the result, and this is combined
with ectropion of the central part of the lower
eyelid. Conjunctival exposure and inflammation
result in chronic ocular discharge, and corneal
scarring and pigmentation inhibit sight. Often
the eye is not visible and sight is largely a matter
of touch for many affected patients. Surgical
correction is difficult and the extreme examples
simply cannot be helped enough. A combination
of eyelid shortening and lifting procedures
together with rhytidectomy and facelifting
techniques may alleviate the condition, but the
602
Back to contents
real solution lies in the acceptance of the fact
that this condition is a serious defect and that
only radical change in conformation can effect
significant improvement. It requires something
of a U-turn by those currently involved in the
well-being of the affected breeds, but even if
this were to happen overnight it will be many
years before real improvement is seen.
Distichiasis
Unlike the previous eyelid conditions,
distichiasis is not related to conformation. The
corneal irritation, inflammation and ulceration
that can accompany this condition are due to
the presence of accessory or ectopic cilia on the
margo-intermarginalis of the palpebral fissure.
The cilia arise singly or in groups from the
meibomian gland orifices, having found origin
within the distal tarsal plate tissue of the eyelid.
Not all distichiasis is of clinical significance for
in many patients the cilia ‘float’ harmlessly in
the precorneal tear film. However, in others the
hairs cause trigeminal irritation and possible
corneal damage. Distichiasis is commonplace in
several breeds, with the English and American
Cocker Spaniels and the Miniature Long-Haired
Dachshund being signficantly involved. Simple
plucking or cutting of the hairs offers temporary
relief only, and root removal by electrolysis is
not always successful. Cryotherapy, in which the
roots are destroyed by freezing the distal tarsal
plate through the palpebral conjunctiva, can be
successful, but techniques that involve dissection
to remove the roots are governed by the thickness
of the eyelid.
THE CORNEA
The several keratopathies which are considered to
be inherited include chronic superficial keratitis
(pannus or CSK), the epithelial and endothelial
dystrophies, the lipid dystrophies, keratitis
pigmentosa and keratoconjunctivitis sicca whilst
there is a clear breed predisposition associated
with conformation in the aetiology of corneal
ulceration in the brachycephalic types.
CONCLUSION
There is only one conclusion and that is that where
our desire to produce a desired feature in our dogs
has led to discomfort and loss of function, that
feature should be changed or at least modified to
allow man’s best friend to live a healthy pleasant
life.

Op – Ophthalmology
HEREDITARY GLAUCOMA
Ofri Ron, DVM, PhD, DECVO
Koret School of Veterinary
Medicine
Hebrew University of Jerusalem
PO Box 12
Rehovot 76100
ISRAEL
ofri@agri.huji.ac.il
The definition of glaucoma is rapidly changing as
our understanding of the pathogenesis of damage
to the retina & optic nerve improves. However,
the disease can still be generally described as an
elevation in intraocular pressure (IOP) which is
incompatible with normal ocular function. IOP is
the result of a balance between production and
drainage of aqueous humor. In clinical practice,
glaucoma is caused by drainage disturbances, and
cases of increased production are not recognized.
PRODUCTION AND DRAINAGE OF
AQUEOUS HUMOR
Aqueous humor is produced in the ciliary
processes from where it flows into the posterior
chamber, and through the pupil into the anterior
chamber. After circulating in the anterior chamber
and supplying the metabolic requirements of the
lens and cornea, the aqueous exits the eye through
the iridocorneal angle (between the cornea and
iris), which is spanned by pectinate ligaments.
The drainage continues through the uveal and
corneoscleral meshworks, eventually exiting the
eye into systemic venous circulation
Aqueous may also exit the eye through an
unconventional path, in which it diffuses through
the iris and ciliary body (or through the vitreous)
into the suprachoroidal space, and from there it
drains into the venous circulation. The importance
of this route changes between species, accounting
for 15% of the total drainage in dogs and 33% in
horses, but only 3% in humans.
CLASSIFYING GLAUCOMA
Glaucoma may be classified in one of 2 ways.
Based on the cause, it may be classified as primary,
where there is no other ocular disease/abnormality
that affects the drainage (rather, outflow problems
are due to genetic abnormalities in the drainage
pathway) or secondary, where another ocular
disease/abnormality (e.g., lens luxation, uveitis)
decreases outflow. Alternatively, glaucoma may
be classified according to the state of the drainage
angle. The angle may be open (in which case the
Back to contents
Op
obstruction is further downstream), narrow or
closed.
The 2 classifying methods complement each
other, and in dogs it is possible to encounter all 4
possible combinations, e.g., primary open angle
glaucoma, secondary closed angle glaucoma, etc.
This talk is devoted to the inherited (i.e., primary)
glaucomas.
INHERITED GLAUCOMA
Since this disease has a strong genetic component,
diagnosis of primary glaucoma in one eye
mandates prophylactic treatment in the other
eye.
Primary open angle glaucoma
Primary, open angle glaucoma (POAG) is an
inherited disease, which has been investigated
extensively in the Beagle dog (in which it was
shown to be an autosomal recessive disorder),
but has also been documented in the Keeshound,
Norwegian elkhound, poodle and other breeds.
As the name implies, the angle and pectinate
ligaments are normal. It is assumed the outflow
obstruction is in the uveal and corneoscleral
meshworks, and is the result of biochemical
changes in the basement membrane of these
regions. The disease is chronic in nature, with IOP
2006 World Congress WSAVA/FECAVA/CSAVA
increasing slowly over many months or years.
Though the dog may present with buphthalmous,
or even with secondary lens luxation, vision is
frequently retained in advanced stages of the
disease.
Primary narrow- and closed-angle glaucoma/
goniodysgenesis
Primary narrow angle glaucoma is an inherited
disease in the American & English cocker
spaniels, flat coat, labrador & golden retrievers,
Basset hounds, samoyeds, chow-chows, great
Dane, Siberian Husky, and other breeds. A
developmental abnormality results in the
formation of dysplatic pectinate ligaments,
which can be see as sheets of tissue spanning the
603
Op
drainage angle. In the first years of life, aqueous
exits the eye through flow holes in the sheets, but
eventually these fail, resulting in IOP elevation.
Most patients present with an acute attack of
glaucoma, including congestion, edema, fixed,
dilated pupils and loss of sight. Though only one
eye may initially be affected, both eyes should
be carefully evaluated and treated. IOP can be
successfully lowered, but progressive angle
narrowing and closure may develop, and the
long-term prognosis for vision is guarded.
DIAGNOSING GLAUCOMA
1. Measuring IOP - tonometry
In most animal species, normal IOP range is 15-25
mm Hg. Elevation in IOP is defined as glaucoma
(while low IOP is usually a sign of uveitis, due
to increased unconventional outflow). IOP should
be similar in the 2 eyes. Differences > 10 mm
Hg between eyes may also indicate glaucoma.
IOP can not be measured digitally with one’s
fingers. It should be recorded with using a
Schiotz (indentation) or Tono-Pen (applanation)
tonometer.
2. Examining the iridocorneal angle – gonioscopy
It is important to examine the angle to determine
the risk of glaucoma (in case of a breed with
goniodysgenesis or primary glaucoma, or
if the other eye developed the disease). The
state of the angle may also dictate treatment-
there is no point in giving drugs that open the
angle in cases of open angle glaucoma, or in
cases of goniodysgenesis. Drugs that reduce
aqueous production, or increase unconventional
outflow may be more suitable in such cases.
Gonioscopy is performed using a special lens
(goniolens) which is placed on the cornea. The
lens refracts the outgoing light, and allows us
to visualize the entire angle, and to classify its
2006 World Congress WSAVA/FECAVA/CSAVA
state.
3. Based on clinical signs.
Glaucoma is a disease that may affect all ocular
layers and structures.
a. Pain. Glaucoma is a painful disease. The pain
can be expressed as blepharospasm, or as general
depression – many owners report a dramatic
improvement in the animal’s behavior following
enucleation of a glaucomatous eye.
b. Buphthalmous. Glaucoma may cause an
increase in the size of the globe, due to stretching
of the collagen fibers of the cornea and sclera.
Buphthalmous is more frequent in chronic cases,
and in young patients (where the sclera is more
elastic and stretches more easily).
c. Congestion of blood vessels. The eye will
604
Back to contents
appear red due to congestion of vessels (see “red
eye” notes).
d. Corneal pathology. Elevated IOP damages
the corneal endothelium, which is responsible
for maintaining corneal dehydration, resulting
in edema. The stretching of the corneal fibers
in buphthalmous may cause rupture of the
endothelial basement membrane. These ruptures,
seen as straight white lines in the cornea, are
called striate keratopathy and are pathognomonic
for glaucoma.
e. PLR. In the early stages of the disease the pupil
may be slightly dilated, and PLR will be sluggish.
In advanced or acute stages of the disease, the
pupils are dilated and non-responsive.
f. Lens. The lens may luxate (or sub-luxate) due
to stretching and tearing of the zonules.
g. Retina, optic nerve & vision. Glaucoma will
cause atrophy of the ganglion cell layer and
other inner retinal layers. This atrophy is a result
of local ischemia, due to pressure on the retinal
blood vessels (the outer retina is supplied by
the choroid, and is less affected by ischemia).
Additional damage to the ganglion cells occurs
as a result of kinking of their axons as they exit
the eye at the lamina cribrosa region. In this part
of the eye, the effect of elevated IOP may be
seen ophthalmoscopically as cupping of the optic
disc. As a result of the damage to the inner (and,
eventually, outer) retina, the patient will suffer
progressive loss of vision, which may lead to
complete blindness.
h. End stage glaucoma. Due to chronic elevation
of IOP, the ciliary body may atrophy, causing
decreased aqueous production, lowering of
pressure, and atrophy of the eye (phthisis bulbi).
PRINCIPLES OF GLAUCOMA TREATMENT
The aims of glaucoma treatment are to prevent
further loss of vision and decrease the pain caused
by IOP elevation. Currently, it is impossible
to restore vision which has been lost due to
glaucoma. Cases of primary glaucoma require
lifelong treatment. The owner must understand
that the aim of the therapy is to stabilize the IOP,
and that the disease can never be fully cured.
Medical therapy of glaucoma
1. Osmotic diuretics. These drugs are not used
for long-term treatment of glaucoma. Instead,
they serve for emergency lowering of pressure in
cases of acute attacks. The most commonly-used
drug in this category is mannitol (IV, 1-2 g/kg).
The fluid is administered slowly, over 30 min.,
and water is withheld for 3-4 hours.
2. Prostglandin analogues. These drugs act by
increasing the unconventional outflow. They
are most effective in dog, because their effect is

independent of the state of the angle (which is
frequently blocked). The drugs are ineffective
in cats (which lack the receptor), and are contra-
indicated in uveitis. Latanaprost, travaprost
and other drugs in this category are given
1-2 times daily.
3. Carbonic anhydrase inhibitors. Carbonic
anhydrase is a key enzyme in the production of
aqueous humor, and therefore its inhibition will
result in lower production and decreased IOP.
Just like prostaglandin analogues, this effect is
independent of the state of the angle. The topical
form of the drug (dorzolamide, brinzolamide) has
none of the systemic side-effects observed with
systemic drugs. It is given twice daily. Systemic
drugs, such as acetazolamide (10 mg/kg) and
methazolamide (2.5-5 mg/kg) are given BID-TID.
They may cause metabolic acidosis. Monitoring
of side-effects and potassium levels is mandatory.
Also, they are not well-tolerated in cats.
4. Topical miotics. These drugs increase drainage
by opening the irido-corneal angle (through
contraction of the iris and ciliary muscle). The
most commonly-used drug in this category is
pilocarpine (1-4%, BID-TID).
Back to contents
Op
5. ß blockers. These are sympatholytic drugs that
reduce aqueous production by reducing flow of
blood to the ciliary body. They are commonly used
in humans, but their effectiveness in animals is
controversial. Systemic side-effects are common
in small dogs, cats, and animals with pulmonary/
cardiovascular diseases. Drugs in this category
include timolol, levobunolol and betaxolol (use
SID-BID).
Surgical treatment of glaucoma
Referral ophthalmology clinics may perform
surgery to increase aqueous outflow (usually
by implanting drainage tubes in the eye), or to
decrease aqueous production (through partial
destruction of the ciliary body, using laser or cryo).
However, frequently the (surgical or medical)
treatment fails, and the practitioner is faced with
a blind and painful eye. Patient welfare requires
the removal of this eye, through enucleation
or evisceration (implanting a prosthesis in an
empty scleral “shell”, to provide a more cosmetic
appearance).
2006 World Congress WSAVA/FECAVA/CSAVA
605
Op
Op – Ophthalmology
HEREDITARY CATARACTS
Ellen Bjerkås DVM PhD
Dipl ECVO, Professor
Norwegian School of Veterinary
Science
Department of Companion
Animal Clincal Sciences
P.O.Box 8146 Dep
N-0033 Oslo
Norway
ellen.bjerkas@veths.no
The lens is normally transparent and devoid
of blood vessels. Cataract is opacity of the
lens, either due to hereditary factors, incidental
malformation or because of cataractogenous
factors affecting the lens. For full examination
of the lens a mydriatic is needed. Tropicamide is
instilled at least 20 minutes before examination
to allow full pupil dilation. A simple examination
of the lens can be performed with a focal light
source; more sophisticated examination includes
the use of a slit-lamp biomicroscope. In a normal
lens the following findings should be noted. The
suture lines of the lens, shaped as a Y at the anterior
pole and an inverted Y at the posterior pole may
be observed as faint lines. So-called “arrowhead”
opacities may be seen at the peripheral tips of the
suture lines, especially in young dogs. A faint
opacity delineating the nucleus (“nuclear ring”)
is also occasionally seen. A small hyaloid artery
remnant may be seen attached to the posterior
lens capsule and extending into the vitreous.
Occasional pinpoint dots representing remnants
of the tunica vasculosa lentis system may also be
seen on the posterior lens capsule. However, there
should be no concurrent sheath of fibrous tissue.
On the anterior lens capsule small, pigmented
dots representing remnants of the pupillary
2006 World Congress WSAVA/FECAVA/CSAVA
membrane are not infrequently observed. These
small opacities are not connected to the iris with
strings and do not cause secondary cataracts.
In older animals, nuclear sclerosis is the result
of lens growth throughout life, decreased water
content of the lens and subsequent increased
lens density. This increased density, resulting
in a bluish appearing lens, while still allowing
examination of the fundus, must be distinguished
from cataract. Normally, no opacities apart
from what is mentioned here should be seen in
retroillumination.
Hereditary cataracts
Hereditary cataracts may be divided according
to age at presentation in congenital cataract
with or without other ocular malformation and
developmental (“juvenile”) cataract.
606
Back to contents
Hereditary cataracts have been described in
many dog breeds, and the list of affected breeds
continues to grow. The mode of inheritance of
most of the cataracts presumed to be hereditary
has not been adequately documented, however.
When evaluating a dog for cataract, one must
both consider this fact, as well as the fact that
other cause than inheritance may cause cataract
in a dog. AS there will be different breeding
pools in different countries, findings may differ
between countries regarding hereditary cataracts.
Thus, cataract may be a problem in a breed
in one country, while the condition may only
occasionally occur in the same breed in another
country. When the ophthalmologist diagnoses
cataract the main issue is to determine if the
cataract represents an inherited disease or not.
Certain criteria exists, however, that may help in
evaluating the case:
“Classical” criteria for hereditary cataracts
• Cataract has been described in the breed
• Cataract changes should be localized to the
expected area
• Cataract changes should be bilateral (there are
exceptions)
• Cataract changes should progress, but
progression may be slow
Extracts from the American College of
Veterinary Ophthalmologists/Canine Eye
Registry Foundation (ACVO/CERF) criteria for
defining a disease as hereditary
There are published reports in the literature
regarding a condition in a particular breed with
evidence of inheritance
The incidence of affected animals is greater than
or equal to 1% of the examined population with a
minimum of five affected animals per five years
period
A specific request from a breed club that a condition
be included for their breed or overwhelming
opinion by a majority of the committee members
that clinical experience would indicate that a

particular condition should be listed in spite of
the absence of direct evidence of affected animals
on CERF reports
Suspicion is:
• When the frequency is greater than in other
breeds
• When the frequency increases in a given breed
as a whole
• When the frequency is greater in related dogs
within a breed
• When it has a characteristic appearance and
location
• When it has a characteristic age of onset and
of course of progression (predictable stages of
development and time for each stage to develop)
• When it looks identical to an entity which has
been proven to be inherited in another breed
Malformations associated with congenital
cataract include:
Microphthalmia may occur spontaneously in any
breed. Inherited microphthalmia / cataract occurs
among otheris in the miniature schnauzer, cocker
spaniel (English),West Highland white terrier,
old English sheepdog and cavalier King Charles
spaniel
Lenticonus / lentiglobus describes a weakness of
the (most often) posterior lens capsule causing
posterior bulging of the lens and cataract. Known
as a breed-related disease in the cavalier king
Charles spaniel but may occur also in other
breeds.
PHTVL/PHPV (Persistent hyperplastic tunica
vasculosa lentis / persistent hyperplastic primary
vitreous). The fetal vessel system surrounding
the lens are hyperplastic and do not undergo
normal regression. Small changes are present
as pigmented dots on the posterior lens capsule
without concurrent cataract, while more severe
changes may lead to secondary cataract and
blindness. Described in the dobermann and
Staffordshire bull terrier, but occurs also in the giant
schnauzer and the King Charles spaniel.
PPM – persistent pupillary membranes. Breed
predisposition among others in the basenji and
chow chow, although the list can be extended
depending on local variation in the gene pool.
PPM is an incidental finding in many other
breeds. Strands may span from iris to iris, iris to
cornea and/or lens causing secondary cataract, or
the malformation may present as broad sheets of
tissue between iris and cornea.
Developmental (juvenile) cataract
Hereditary cataract not present at birth has been
described in a long list of dog breeds. Cataract
changes most often develop early in life, around
12 months of age, but in some cases the lens
Back to contents
Op
may be normal until the dog is 4-5 years old.
There is therefore no upper age limit on when to
stop re-examining a dog for inherited cataract.
Differential diagnoses of hereditary cataract
include PRA, secondary cataracts (diabetes
mellitus, uveitis, injuries) and non-hereditary
primary cataracts. When hereditary cataract is
suspected in a ”new” breed the breeding advice
should be not to breed affected dog and examine
offspring and close relatives. Developmental
cataracts primarily affect the lens cortex; the
nucleus is rarely involved in the initial stages
of development. Cortical changes are often
restricted to opacities around the posterior pole,
posterior polar cataract. Small posterior polar
cataract changes do not affect the dog’s vision
notably, and may progress only to a limited
extent. However, even posterior polar cataracts
may in some cases progress to affect the whole
lens. In many breeds, posterior polar cataract is
the most common manifestation of hereditary
cataract, but there are breed differences as to
localization of initial cataract changes within
the lens. Thus, initial cataract changes in the flat
coated retriever may be seen in the anterior suture
lines, while cataract in the Afghan hound usually
starts at the equator, in the periphery of the lens.
Late developing cataract in the Boston terrier
presents as discrete linear or wedge-like anterior
subcapsular or outer cortical opacities extending
in a radial fashion from the equator to the centre
of the lens. The fact that some cataract changes
initially appear in the periphery emphasizes
that pupil dilation is necessary for a thorough
examination of the lens.
The list of breeds affected with developmental
(juvenile) cataract is long and includes
Alaskan malamute
American cocker spaniel
Belgian shepherds
Bichon frisé 2006 World Congress WSAVA/FECAVA/CSAVA
Boston terrier (two forms, one developing early
in life, one late)
Cavalier King Charles spaniel
English cocker spaniel
English springer spaniel
Lapland dog (Swedish, Finnish)
German shepherd
Leonberger
Newfoundland dog
Norwegian buhund
Retrievers
Rottweiler
Samoyed
Schnauzers (miniature, standard and giant
schnauzers)
Siberian husky
Standard poodle (and poodle)
607
Op
Welsh springer spaniel
Tibetan terrier
Others (new breeds will be added to the list)
Pulverulent nuclear cataract: A special form
of cataract is seen in certain breeds of dogs,
including the cocker spaniel, flat coated
retriever, leonberger and Norwegian buhund.
Initial presentation is as pinpoint dots along
the suture lines just posterior to the foetal
nucleus. With age, the changes progress to
form a ball of thread-like opacities with a
candyfloss appearance. The cataract changes
never progress to obscure vision significantly.
A dominant mode of inheritance has been
suggested in the Norwegian buhund.
Mode of inheritance of hereditary cataracts
Very few breeds have been investigated
regarding modes of inheritance. An
autosomal recessive model has been shown
2006 World Congress WSAVA/FECAVA/CSAVA
608
Back to contents
for congenital cataract in the miniature
schnauzer and Staffordshire bull terrier
and developmental cataract in the Boston
terrier. For the two latter breeds there is
now a gene test available. Recessive mode
of inheritance has been suggested in the
Afghan hound, American cocker spaniel,
bichon frisé, German shepherd, Siberian
husky and standard poodle. In the golden
retriever cataract has been suggested to be
inherited by a dominant gene with incomplete
penetrance, while others consider a recessive
mode of inheritance more likely. One must
admit that our knowledge regarding modes
of inheritance is restricted. However, with
identification of the dog genome and the
research activity aimed at defining disease
genes in the dog, one must expect more gene
tests to become available in the near future.

Op – Ophthalmology
HEREDITARY RETINAL DISEASES
Peter Bedford, Professor
Royal Veterinary College
Department of Veterinary Clinical
Sciences
Hawkshead Lane
Hatfield, Hertfordshire AL9 7TA
UK
pbedford@rvc.ac.uk
INTRODUCTION
The spectrum of hereditary retinal disease in
the dog is well defined and closely related to
the intensive breeding patterns which are used
in some breeds. Many retinopathies are often
detected as the result of routine screening in
the absence of dramatic clinical features or
noticeable disturbance of sight for, while our
clients may notice the painful or discoloured eye,
few recognise the subtle variation in pupil size
and many do not suspect sight deficiency until
it is well established. The pathognomic features
of retinal disease defined by ophthalmoscopic
examination are changes in tapetal reflectivity
and pigmentation, blood vessel congestion
or attenuation, haemorrhage and retinal non-
attachment. Thus, a combination of reduced
tapetal reflectivity and intraretinal haemorrhage
indicates active inflammation, whereas a zone
of increased tapetal reflectivity or a patch of
reduced pigmentation signifies post-inflammatory
degeneration. Unfortunately, retinal pathology
does not automatically flag its cause and, as
such, dilemma in diagnosis is always possible.
For example, the retinal degeneration which
accompanies retinal dysplasia can be confused
with post-inflammatory retinal degeneration
and, without history, sudden acquired retinal
degeneration (SARD) can look like progressive
retinal atrophy (PRA).
The range of retinopathy in the dog has been
largely defined and new retinopathies are
relatively few and far between. Central PRA
appears to be a misnomer because the condition
is a secondary photoreceptor degeneration due
to abnormal retinal pigment epithelial activity,
which appears to be governed by environmental
or metabolic factors to some extent. Thus, a
classical ocular diagnosis becomes an ocular
feature of a condition of unspecified aetiology, yet
one that demonstrates breed predisposition. Sadly
more canine breeds become involved in the PRA
story of inherited photoreceptor degeneration.
Similarly more breeds are becoming involved
in retinal dysplasia; the multifocal and total
Back to contents
Op
forms of this condition have been joined by a
geographical lesion in the Cavalier King Charles
and Retriever breeds. Collie Eye Anomaly is still
the commonest inherited ocular disease in dogs in
the United Kingdom but its recent appearance in
the Lancashire Heeler suggests that a change in
nomenclature would be appropriate.
THE RETINOPATHIES
Retinal Dysplasia
The term is applied to those inherited neuroretinal
conditions which are seen clinically as either
neuroretinal folds and rosettes or retinal non-
attachment. The simplest manifestation of retinal
dysplasia (R.D.) is a fold in the neuroretina, the
affected dog demonstrating no associated visual
impairment. Complicated folds in which there is
proliferation of photoreceptor and RPE elements
are also referred to as rosettes. This form of
R.D. is inherited in the Cavalier King Charles
Spaniel, the Hungarian Puli and the Rottweiler as
a recessive trait. In the English Springer Spaniel
the neuroretinal folds may be accompanied by
retinal degeneration, these lesions taking on the
appearance of post-inflammatory retinopathy
due to the presence of melanin pigmentation.
Occasionally retinal detachment complicates the 2006 World Congress WSAVA/FECAVA/CSAVA
clinical picture and both intraocular haemorrhage
and cataract formation may be seen.
Collie Eye Anomaly
During organogenesis it is the cells of the posterior
wall of the invaginating optic vesicle which form
the primordial retinal pigment epithelium. Failure
to express growth hormone by these cells affects
the subsequent differentiation of the ocular
tissues. In Collie Eye Anomaly (CEA) the choroid
remains hypoplastic in an area lateral to the optic
disc and there may be failure of the foetal fissure
to close leaving a colobomatous defect involving
either papillary or peripapillary tissue. The
degree of choroidal hypoplasia and the size of the
colobomata vary considerably between affected
individuals and even between the eyes of the
609
Op
same individual. All affected puppies demonstrate
choroidal hypoplasia but by the age of twelve to
sixteen weeks many may have masked the smaller
lesions by melanin pigmentation. The estimates
vary but in the U.K. it is likely that some thirty
per cent of affected puppies demonstrate this
masking procedure: somewhat confusingly this
process is described as “go normal” status. The
phenotype thus appears ophthalmoscopically
normal but genetically these dogs are affected and
must be avoided in disease control programmes.
It is of considerable significance, underlying the
necessity for screening all litters in the affected
breeds
The diagnostic picture is understood well and
painted in the above terms it would appear to be
straightforward. However, like most things in life
the story is not as black and white as it may seem
and we do see problems which, at the very least,
should provide discussion. I believe that there is
a possible ten per cent error in diagnosis due to
several features : the small papillary coloboma in
the six week old puppy, the significance of the
pale pink patch in the six week old fundus, the
reduction of peripapillary pigmentation in the
sable and white or colour dilute dog and the merle
eye. Add to this the “go normal” phenomenon
and the significance of the coloboma which is
unaccompanied by choroidal hypoplasia. Thus
life behind the ophthalmoscope can become
difficult! Fortunately a mutation based DNA test
for choroidal hypoplasia is now available.
A recent publication reported CEA in the
Lancashire Heeler breed of terrier, and this puts
the cat amongst the nomenclature pigeons! The
author suggests that new terminology is required
and suggests that “Congenital Posterior Segment
Anomaly” (CPSA) might fit the bill.
Progressive Retinal Atrophy
Progressive retinal atrophy (PRA) is the umbrella
2006 World Congress WSAVA/FECAVA/CSAVA
term used to describe a number of inherited
neuroretinal degenerations. Generalised PRA,
or simply PRA, describes those degenerations
in which the primary focus of disease is the
photoreceptor unit. Such degenerations are
characterised by a nyctalopia which progresses to
total blindness and involves a high incidence of
secondary cataract formation. All these diseases
bar one are inherited as simple autosomal
recessive traits.
610
Back to contents
The ophthalmoscopic signs are similar for
each type of PRA, but the aetiologies vary
considerably. For example dysplasia of the rod
and cone photoreceptors has been described
in the Irish Setter and Rough Collie breeds. As
such this type of PRA is an early onset disease
with severe impairment of vision being present at
eight months of age and total blindness at twelve
months. The photoreceptor defect is an enzyme
abnormality within the phototransduction cascade.
Specifically the retinal level of the nucleotide
cyclic guanosine monophosphate (cGMP) is
elevated to approximately ten times its normal
value due to reduced cGMP-phosphodiesterase
activity.
A second form of PRA in which the rod
photoreceptor unit is dysplastic and there
is subsequent degeneration of normal cone
photoreceptors has been described in the
Norwegian Elkhound. The initiatory rod defect
remains undermined, as does the cause of a third
form of PRA, a disease seen classically in the
Miniature and Toy Poodle breeds, the English
Cocker Spaniel and the Labrador Retriever.
Here there is normal development of both
photoreceptor units but blindness is caused by
their premature degeneration in middle age.
Fortunately the disease control picture for all
types of PRA is improving in that several DNA
based tests are now available and others are in the
development stages.
Retinal Pigment Epithelial Dystrophy
Originally considered to be a primary
photoreceptor degeneration, this disease is due
to defect of the RPE. One of the many important
functions of RPE cells is the degradation of
utilised photoreceptor outer segment (POS).
Dystrophic RPE cells can neither degrade utilised
POS quickly enough nor effectively participate in
POS production. Their cytoplasm accumulates
phagocytosed POS material and their many
other functions in terms of neuroretinal support
cease. Thus the rod and cone photoreceptors
degenerate and sight is affected. Affected dogs
therefore lose their central field of vision but
maintain peripheral sight. There is undoubtedly
genetic predisposition to this disease as witnessed
by specific breed involvement but many factors
influence the course of degeneration, most
significantly vitamin E.

Op – Ophthalmology
SCHEMES FOR HEREDITARY EYE DISEASES – PART 1
Peter Bedford, Professor
Royal Veterinary College
Department of Veterinary Clinical
Sciences
Hawkshead Lane
Hatfield, Hertfordshire AL9 7TA
UK
pbedford@rvc.ac.uk
The British scheme is run jointly by the British
Veterinary Association (BVA), the Kennel Club
(KC) and the International Sheepdog Society
(ISDS). It was initially established some 30 years
ago to provide help in the control of PRA, but it
has evolved to form the basis for the control of
13 known inherited diseases whilst providing an
early warning system for the emergence of “new
diseases” and old diseases in new breeds.
The author will discuss some of the features of
this scheme but encloses here some introductory
details together with the lists of diseases, the
breeds affected and copies for the certificate and
litter screening forms.
The Scheme
The BVA/KC/ISDS Eye Scheme is primarily
concerned with the examination of the eyes of
dogs for inherited eye disease, but also includes
a general examination of the eye and adnexa
(adnexa = lids, lacrimal apparatus, orbital and
periorbital areas).
Certificates of Eye Examination (Annex A) are
issued tin respect of inherited conditions of the
eye only and not for inherited conditions of the
adnexa.
Dogs may be examined as part of a litter up to
the age of 12 weeks and such examinations are
recorded on the Litter Screening Eye Examination
Form (Annex B). Examination of individual
dogs may be recorded on the Certificate of Eye
Examination at any age.
Eleven different inherited conditions in pedigree
breeds of dog may be certified under the Scheme
(Annex C and Part III). In addition, a number of
Back to contents
Op
other conditions in other pedigree breeds of dog
are listed as “Under Investigation” (Annex D)
and eye examination should also be encouraged
in breeds which are not listed under the Scheme
so that potential inherited problems can be
identified.
Panellists can contribute information on inherited,
or potentially inherited conditions, directly to the
BVA for collation and thence to the Eye Panel
Working Party (EPWP), on eye certificates or
little screening forms.
Group examination of dogs may be arranged
by, for example, an individual, society, or club.
In such cases the panellist should ensure that
the session is advertised correctly and that all
the arrangements (especially the facilities and
finances) have been agreed in advance. The fees
for eye examinations in which litter screening
forms or certificates of eye examination are
issued must be charged at BVA rates. Travelling
expenses may be charged on such occasions and
it is sensible for such charges to be in line with
BVA travelling expenses. If the organisers are
charging an administration fee this must be made
clear.
Gonioscopy is recommended in those breeds in
which goniodysgenesis is listed as an inherited
problem. A separate fee is charged for this 2006 World Congress WSAVA/FECAVA/CSAVA
procedure. Technical information on gonioscopy
is given in Part III, however, it is important to
emphasise that a panellist should not offer this
examination if they lack confidence about the
technicalities of gonioscopy and the diagnosis of
goniodysgenesis.
611
Op
Op – Ophthalmology
SCHEMES FOR HEREDITARY EYE DISEASES – PART 2
HEREDITARY EYE DISEASES AND CURRENT SITUATION IN CZECH
REPUBLIC
Jiri Beranek, DVM
Veterinary Clinic
Husova 1747
530 03 Pardubice
Czech Republic
med.prod@worldonline.cz
The Czech ophthalmology group started its work
in 1999. There are 6 eye examiners so far who
passed an examination under supervision of prof.
Bernard Spiess, Tierspital Zurich, CH.
The examination had two parts – a practical
and a theoretical. Practical part started by eye
examination using own examination equipment,
next was slide show of 15 cases, written part
and presentation of own hereditary case. One
condition was to use own equipment recording
positive and questionable cases to have possibility
to discuss them.
The minimum equipment to be used for
the examination is a binocular indirect
ophthalmoscope and a slit lamp biomicroscope
(at least 10 x magnifications). The use of other
equipment (gonioscopy lens, tonometry, ERG,
etc.) is optional.
It is necessary for all members of the Czech panel
to participate in continue education. Every year
we have working meeting with main speaker -
member of ECVO (for ex. Prof. B. Spiess, prof.
2006 World Congress WSAVA/FECAVA/CSAVA
P. Bedford, prof. E. Bjerkaas). Topic was CEA,
hereditary cataract, condition of cornea.
First year we did 600 dogs examined under the
schema, last year 2800.
Every second year we are organizing meeting with
The Czech union of breeders clubs to inform about
situation of hereditary eye diseases in individual
breeds and to harmonize the various schemes
for the control of hereditary eye disease. Very
important is discussion and our breeding program
recommendation with individual breeders clubs
to find optimal eradication program depending on
breed and hereditary diseases.
612
Back to contents
Current situation of controlled breeds
Dog breeds with the condition to do eye
examination before using in breeding program
and under the Czech eye scheme:
Poodle
Tibetan terrier
Tibetan spaniel
Old English sheepdog
Collie
Sheltie
Border collie
Labrador retriever
Papillon
Cotton de toulear
Australian cattle dog
Dachshund
Miniature schnauzer
American cocker spaniel
Alaskan malamute
Siberian husky
Australian shepherd
Belgian shepherd dog (all varieties)
Cavalier King Charles Spaniel
Briard
Parson Russell Terrier
Chinese crested dog
Details of all lesions and conditions found at the
time of examination should be noted-hereditary
diseases as well as conditions considered not
inherited). Important point is identification of the
dog (readable tattoo or microchip).
One copy of the certificate of the eye examination
is for owner (paper version)
One copy is for eye examiner (paper version)
One copy is for breeders club (paper/electronic
version depends on breeders club)
One copy is for database of panelists (electronic
version). All results are published and free to read
for members of majority of breeders club. Some
clubs use results for information about hereditary
defects situation into the breed.

Op – Ophthalmology
SCHEMES FOR HEREDITARY EYE DISEASES – PART 3
Ellen Bjerkås DVM PhD
Dipl ECVO, Professor
Norwegian School of Veterinary
Science
Department of Companion
Animal Clincal Sciences
P.O.Box 8146 Dep
N-0033 Oslo
Norway
ellen.bjerkas@veths.no
Welfare aspects
The EU Convention for the protection of
pet animals states in Article 5: “Any person
who selects a pet animal for breeding shall
be responsible for having regard to the
anatomical, physiological and behavioural
characteristics which are likely to put at risk
the health and welfare of either the offspring
or the female parent”. This convention has
been ratified by some EU countries, but
not all. Almost the same text is included in
the WSAVA Convention for the protection of
Companion Animals.
What is an inherited eye disease?
This might be a difficult question to answer,
and yet the most important when it comes to
control programs for hereditary eye diseases.
Some diseases do not represent a problem in this
regard, as the gene has been identified and the
mode of inheritance established. For the majority
of diseases, however, the mode of inheritance
has not been established, but there is “substantial
evidence” that the disease in question is inherited.
If a disease has been thoroughly described in the
literature, this may give support to considering a
disease hereditary. It can, however, take a long
time before a disease in a specific breed is written
up in the literature, and some conditions are never
reported other than in annual reports from eye
panels.
The national eye panels
A survey carried out by FECAVA a few years
ago showed that a large number of European
countries had established national eye panels.
Veterinarians issuing certificates with regard to
hereditary eye diseases had received additional
training in ophthalmology, however, the level of
qualifications showed great diversity. In order
to issue certificates that can be accepted all over
Europe, a minimum level of qualifications is
needed. This includes training of veterinarians
Back to contents
Op
(including a qualifying exam), the examination
procedures must be followed, and the animal
examined must be identifiable by microchip or
readable tattoo.
Control programs are common as part of
breeding programs in many countries,
However, the FECAVA survey also showed
great variation in the way the results were
handled and whether they were published
or not. The procedure varies between the
following alternatives:
• All results are published and free to read
• The owner is free to decide if the results should
be made public or not
• Only results from normal (“free”) dogs are
published
• No results are published, the results being the
owner’s property
Examination procedures
Before examination, the owner should be asked to
sign the certificate confirming the dog’s identity.
Examination procedure should be standardized
to give the most reliable examination results and
include at least.
• Examination under darkened conditions 2006 World Congress WSAVA/FECAVA/CSAVA
• A general examination of the eye and adnexa
• The minimum equipment is a binocular indirect
ophthalmoscope and a slit lamp biomicroscope
(at least 10 x magnification). The use of other
equipment (gonioscopy lens, tonometry, ERG,
etc.) is optional.
• A mydriatic should be instilled for maximal
pupil dilatation before examination of deeper
structures.
• Details of all lesions and conditions found at the
time of examination should be noted. This refers
to both presumed hereditary diseases as well as
conditions considered not inherited.
• The dog should be identified either by tattoo or
microchip
613
Op
Education of panelists
As mentioned, there is wide variation within
Europe regarding the level of qualifications of
panel members, and even so throughout the
world. In USA, only Diplomates of the American
College of Veterinary Ophthalmologists are
allowed to issue eye certificates that are to be
nationally registered, while in Europe both
Diplomats and specially trained members of some
national panels are allowed to issue the ECVO
approved certificates. In Japan College members
can issue international certificates, while other
ophthalmologists can only issue certificates for
national use.
In 2004 the ECVO adopted the following rules
for ECVO licenses panelists (see www.ecvo.org):
Panellists licensed by the ECVO to perform the
eye examinations under the Scheme are:
a. practising Diplomates of the ECVO;
b. In countries where this has been decided: Eye
Scheme Examiners (non-Diplomate of the ECVO,
further to be called ESE), being veterinarians,
examined and accepted for a restricted period of
5 years. This contract may be extended ad
infinitum by the ECVO.
Before ESE-candidates can qualify to sit the ESE
examination for the scheme the candidate must
document to have examined at least 500 dogs
under supervision of two different panel members
recognised by the ECVO. At least 50 of the dogs
should be under supervision of a practicing ECVO
Diplomate. Up to 200 dogs can be examined
under supervision of an ACVO Diplomate. A
record should be kept for all animals examined.
The ESE candidate should have examined at least
2006 World Congress WSAVA/FECAVA/CSAVA
614
Back to contents
100 cats of which 10 should be examined under
supervision of a practicing ECVO Diplomate
and 10 under supervision of a panel member. All
cases should be recorded.
The ESE candidate must document to have seen
specific breeds and diseases in a defined number
(a specific list has been worked out).
The ESE candidate should document to have
participated in at least 3 ECVO recognized
continuing education courses in ophthalmology,
of duration of 3 days, including diseases of the
anterior and posterior segments, and basic genetic
principles.
The ESE candidate should be trained in direct and
indirect ophthalmoscopy, slit-lamp examination
and gonioscopy.
Examination procedure for authorisation:
• Slides test
• Written exam
• Practical exam with evaluation of 10 cases,
normal or abnormal. For the practical test a list of
“lethal errors” have been defined, the candidate
failing despite having evaluated the other cases
correctly.
Quality control of the panel - appeals
The owner is free to seek a second opinion from
another panellist
If the diagnoses differ, the animal is examined
either by an ECVO Diplomat or by a group of
panellists at the annual meetings. The decision
taken by either of these two bodies is considered
final
The panellist should examine at least 100 cases a
year to maintain authorization.
 Op
Op – Ophthalmology
OPHTHALMOLOGY CASE PRESENTATION 1
Ellen Bjerkås DVM PhD
Dipl ECVO, Professor
Norwegian School of Veterinary
Science
Department of Companion
Animal Clincal Sciences
P.O.Box 8146 Dep
N-0033 Oslo
Norway
ellen.bjerkas@veths.no

Signalment To be discussed during the session

Neapolitan mastiff, intact female, 5 years old
Clinical history
The dog has formerly been clinically healthy
The left eye was acutely red and painful two
days ago
The dog appears a little depressed
Conscious propriosception is poor in both hind
limbs, normal in both front limbs
The dog has arthrosis in both stifle joints
Make a primary problem list
Define the cause of the red eye
How should this case be approached?
Make an updated problem list
Suggestions for additional tests
Diagnosis and treatment

2006 World Congress WSAVA/FECAVA/CSAVA

615
Back to contents
Op
Op – Ophthalmology
OPHTHALMOLOGY CASE PRESENTATION 2
Peter Bedford, Professor
Royal Veterinary College
Department of Veterinary Clinical
Sciences
Hawkshead Lane
Hatfield, Hertfordshire AL9 7TA
UK
pbedford@rvc.ac.uk

Subject and History
A 4 year old Petit Basset Griffon Vendeen
(PBGV) presented with a history of possible sight
problems over the preceding four week period.
The dog was in good physical health and there
had been no major disease problems in its life. It
was owned by a dog breeder and spent most of
its days in a communal kennel situation together
with some twenty other PBGV’s. The owner had
only noticed the occasional mistake when the dog
had been taken out to dog shows, the mistakes
being knocking into stationary objects, missing
its footing on steps and fear of jumping in and
out of the car. The owner had not noticed any
signs of pain or discomfort and apart from a little
“epiphora” bilaterally there had been no ocular
discharge. To the owner the eyes appeared normal
in all respects.
Clinical Examination
The patient appeared to be clinically sound and
in good coat. There was a hesitancy about its
2006 World Congress WSAVA/FECAVA/CSAVA
walking to the examination room, but it did not
have to be dragged. The performance in both lit
and unlit maze was poor, again the hesitancy was
seen and many mistakes were made. Superficially
the eyes appeared normal : there was no ocular
discharge, no blepharospasm, no photophobia,
they were of normal size and both corneas
were transparent. There was slight episcleral
congestion, but bilateral fixed mydriasis and a
lack of both direct and indirect light reflexes
were obvious. The anterior chambers were deep
and clear, but there was a bilateral subluxation
of the lens. The tapetal reflectivity was judged
to be normal, but there was some attenuation of
the major superficial retinal blood vessels. The
intraocular pressures were recorded as 30mmHg
in the left eye and 32 mmHg in the right eye.
Gonioscopy revealed an open iridocorneal angle
with no pectinate ligament dysplasia.
In the lecture we will discuss the possible
diagnoses and the efficacy of potential treatment.

616
Back to contents
Back to contents
2006 World Congress WSAVA/FECAVA/CSAVA

617
Op
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

Or
O
thopaar
Orthopaedics
e

Back to contents

INVITED LECTURES - FULL PAPERS
Or – Orthopaedics
ARTHROSCOPY OF THE STIFLE. TRADITIONAL &
NONTRADITIONAL PORTAL SITES
Don Hulse DVM, Dip ACVS,
Dip ECVS
Texas A&M University
dhulse@cvm.tamu.edu
Traditional portal sites and technique: The
arthroscope portal is located lateral to the
patella tendon approximately midway between
the the tibial tubercle and the inferior pole of
the patella. The instrument port is placed at
the same proximodistal level but medial to
the patella tendon. The egress port is placed
superior and medial to the patella. Once the
egress port is established, a scope port is made
and the arthroscope inserted. A systematic
examination of the supra-patella compartment
and trochlear ridges is performed. As the joint
is flexed, the arthroscope is positioned lateral to
the intercondylar notch. Further examination of
the joint is limited by the presence of the fat pad.
The latter structure is generally inflamned and
Back to contents
Or
obscures visualization of the cruciate ligaments
and menisci. A viewing window through the fat
pad must be made before thorough examination
of the ligaments and menisci is possible. Use of
a motorized shaver is the best method to remove
inflammed fat pad. The arthroscope is positioned
to view the intercondylar notch and top of the
fat pad. An instrument port is established as
described above and the shaver blade inserted.
The shaver blade is visualized and the shaver
window positioned away from the lens of the
arthroscope. Tissue is removed by the suction and
cutting action of the shaver blade. As a viewing
window is established through removal of fat
pad, the cruciate ligaments (often remnants of
the CCL) are examined. Remnants of a torn CCL
can be removed with the motorized shaver. Both
the lateral and medial menisci are examined for
the presence of fraying or classical bucket handle
tears. The medial meniscus is most commonly
injured (bucket handle tear, radial tears, or 2006 World Congress WSAVA/FECAVA/CSAVA
fraying). Observation of the posteromedial
compartment (medial meniscus) is performed by
placing a Hohmann retractor through a superior
portal. Small hand instruments such as a grasper or
probe are used to hold a torn section of meniscus;
the damaged meniscus is then removed with hand
instruments or a motorized shaver.
Non-traditional portal sites: One alternate
approach is to use a 1.9mm or 2.3mm arthroscope
placed into the joint through a superior portal.
The joint is distended with LRS; a 3mm incision
is made with a number 11 blade through the
skin and soft tissue but does not enter the joint.
The arthroscope enters the joint medial to the
patella tendon just distal to the inferior pole
619
Or
of the patella. The conical blunt obturator and
arthroscope sheath are pushed through the soft
tissue into the joint. The tip of the obturator is
directed toward the intercondylar notch medial
to the fat pad. Egress is established with an 18
gage needle. From this point, the camera and
light post are adjusted to view the medial and
lateral compartments. If needed, a second portal
is made lateral to the patella tendon just distal to
the inferior pole of the patella. A small hohmann
retractor can be placed to distract and open the
medial compartment. An instrument portal can be
established medially at the standard position.
2006 World Congress WSAVA/FECAVA/CSAVA
620
Back to contents
The advantage of the superior portal technique is
that the surgeon is able to explore the medial and
lateral compartments without the need to create
a viewing window. The disadvantages of this
technique are the small field of view available
through the smaller arthroscopes. The close
proximity view with proliferative synovia and
fat pad, can make treatment of meniscal injuries
difficult.
The Posteromedial Arthroscope Portal:
A posteromedial portal can be established
to view the intra-articular structures in the
posterior medial compartment. Joint capsule,
articular surface of the fabella, posterior cruciate
ligament, posterior meniscocapsular ligament,
posterior articular surface of the femoral condyle
are readily examined through this portal. The
arthroscope enters the joint just distal to the
inferior pole of the medial fabella. A 2.3mm or
2.7mm arthroscope is used for this technique. The
inferior pole of the medial fabella is palpated; a
3-4mm skin incision is made and the arthroscope
sheath with blunt conical obturator pushed into the
joint. Egress is established with an 18 gage needle
placed into the anterior medial compartment.
The camera head and light post are positioned to
examine the posterior cruciate ligament, posterior
meniscocapsular ligament, and articular margins
of the femoral condyle and fabella.
 Or
Indications for this arthroscope site include
suspected isolated posterior crucite ligament
injuries, isolated medial meniscal injury, and
other suspected posteriomedial pathology.
Limitations include small working space for
establishing a working instrument portal.

Atypical Lesions: Lateral meniscal tears:

The majority of meniscal injuries involve the
medial meniscus. The medial meniscus is firmly
attachment to the tibial plateau and moves with
the plateau during the abnormal AP translation
associated with a torn CCL. As the medial tibial
plateau and medial meniscus translate cranially
in the CCL deficient stifle, the medial femoral
condyle compresses the body of the medial
meniscus. The result is the classical bucket handle
tear. The lateral meniscus is loosely attached to
the tibial plateau rendering it more mobile; the
lateral meniscus is able to move with the lateral
femoral condyle during abnormal AP translation
rendering it less prone to injury. Nevertheless,
lateral meniscal injury does occur and in some
cases results in serious lateral compartment
degeneration. Lateral meniscal injury occurs in
conjunction with cranial cruciate ligament injury,
following ACL treatment, or as an isolated injury.
Small radial tears arising from the inner free edge
of the lateral meniscus are a common arthroscopic
finding with long standing ACL injury. They
are considered non-clinical and no treatment is
necessary. However, large radial tears and bucket
handle tears of the central or caudal body of the
lateral meniscus are occasionally noted with ACL
tears. These are managed by excision of damaged
meniscus.
Previous studies have shown the incidence
of postliminary meniscal tears following
treatment of CCL injury to range from 5% - 15%
depending upon technique. Slocum indicated
that latent meniscal tears associated with the
Back to contents
TPLO procedure could be as high as 40%. The
overwhelming majority of postliminary meniscal
tears are medial meniscal tears but lateral meniscal
tears do occur. These have generally been bucket
handle tears in the author’s experience and are
managed with excision of damaged meniscus. One
should not do a complete lateral meniscectomy or
a meniscal release of the lateral meniscus. Loss of
a functional lateral meniscus may lead to severe
lateral compartmental OA.
Osteoarthritis (OA) of the stifle joint is a
leading cause of rear limb dysfunction in the
dog. Non-inflammatory OA is often secondary
to an underlying problem; the most frequent
presentation being that of a partial tear of the
cranial cruciate ligament. At times, no palpable
instability is detected and the diagnosis of partial
CCL injury is based on the radiographic presence
of OA. Surgical intervention in these cases
ordinarily confirms the presence of CCL injury.
In a small percentage of cases, open arthrotomy
or arthroscopy cannot confirm injury of the CCL.
In these cases, an isolated lateral meniscal tear
is suspected. Surgical findings are comparable in
all cases: 1. moderate synovitis and osteophyte
formation, intact cranial and caudal cruciate
ligaments, intact medial meniscus, complete
transverse or oblique radial tear of the posterior
horn of the lateral meniscus. Long standing cases
2006 World Congress WSAVA/FECAVA/CSAVA
will develop erosive eburnation of the femoral
condyle and tibial plateau.
621
Or

Articular cartilage lesions of the medial or lateral

femoral condyle associated with TPLO. TPLO
is an accepted method for treatment of the CCL
deficient stifle. Although a very successful
technique complications are reported to be as high
as 28%. The majority of complications are self-
limiting and rarely require surgical intervention.
The author has seen five cases where the osteotomy
has healed but the dog has not returned to normal
function. No abnormal physical or radiographic
findings are apparent in these cases. Second
look arthroscopy has shown erosion of articular
cartilage of the medial femoral condyle in each
case. Assessment was that the femoral condyle
was displaced forward and articulating with
hardened cranial horn of the medial meniscus.
Treatment consisted of motorized shaving of
the soft tissue and microfracture of the abraded
lesion bed.
2006 World Congress WSAVA/FECAVA/CSAVA

622
Back to contents

Or – Orthopaedics
CONTROVERSIES IN ARTHROSCOPIC TREATMENT OF CCL
DISEASE
Brian Beale DVM,
Diplomate ACVS
Gulf Coast Veterinary Specialists
1111 West Loop South #160
Houston
Texas
77027
drbeale@gcvs.com
Introduction
Arthroscopy can be a useful tool when treating
dogs for cranial cruciate ligament rupture.
Arthroscopic-assisted debridement of the
torn ligament and treatment of meniscal tears
prevents the need for arthrotomy and incision of
other periarticular soft tissues. Meniscal release
can also be performed under arthroscopic
guidance. Lower morbidity and enhanced
visualization is achieved with arthroscopy.
Second-look arthroscopic evaluation of patients
undergoing previous stabilization for cruciate
tears is indicated for treatment of meniscal tears,
meniscal release, and evaluation of the cranial
cruciate ligament, caudal cruciate ligament,
previous meniscal procedures, osteoarthritis
and synovitis. Patterns of articular wear can be
assessed in patients having an unsatisfactory
outcome following TPLO. Second-look
arthroscopy is particularly valuable for low
morbidity follow-up evaluations of the joint in
experimental studies.
Arthroscopic Changes
First look arthroscopic evaluation in patients
having cruciate ligament disease often
have substantial synovitis that may obscure
visualization. Synovitis has usually subsided
at the time of second-look arthroscopy.
Villous hypertrophy present at the time of
an acute ligament tear subsides at follow-up
examination in patients having a favorable
outcome following TPLO.
Torn fibers associated with partial tears of the
cranial cruciate ligament can be debrided at
the initial arthroscopic exam. Evaluation of the
ligament during second-look generally reveals
a healthy appearance characterized by reduced
hyperemia, no additional fiber tearing and
grossly normal tensile properties. The improved
appearance of the cranial cruciate ligament at
second-look arthroscopic examination supports
Back to contents
Or
the theory that TPLO reduces strain on the
cranial cruciate ligament.
The caudal cruciate ligament appears normal
in most dogs at the time of second-look
arthroscopy, despite the probable development
of caudal tibial thrust following TPLO. The
caudal cruciate ligament frequently has mild
fraying or tearing of fibers at the time of initial
arthroscopic examination in dogs having cranial
cruciate ligament disease. These fibers can be
debrided carefully with a radiofrequency probe
at the time of TPLO and usually appear normal
at the time of second-look arthroscopy.
Meniscal changes are occasionally found at
second-look arthroscopic exam. Typically
these changes are minor and include mild
fraying of the free edge of the medial or lateral
meniscus. These tears are classified as radial
tears. Small tears can be meticulously debrided
with a radiofrequency probe, being careful to
avoid the articular cartilage. When using the
radiofrequency probe for meniscal debridement,
the probe should be applied in short bursts and
lavaged continuously with ample fluids to reduce
the chance of iatrogenic damage to adjacent 2006 World Congress WSAVA/FECAVA/CSAVA
cartilage. Other meniscal changes that have
been seen at second-look arthroscopy include
bucket-handle tears, meniscal degeneration and
calcification. Menisci typically appear healthy
at second-look arthroscopic exam if previously
treated by partial meniscectomy at the time of
TPLO. Medial meniscal release performed at
the meniscotibial ligament appears to remain
functional and show no evidence of healing at
the time of second-look arthroscopy. Midbody
meniscal release performed caudal to the
medial collateral ligament also appears to
remain functional, but some healing may occur
and is grossly characterized by fibrous tissue
spanning the meniscal gap. In these cases, the
meniscus appears to be elongated with respect
to its original length before meniscal release.
623
Or
Arthroscopic evaluation was recently performed
in 16 dogs (22 stifles) having a partial tear of the
CrCL and TPLO as part of an ongoing clinical
study. A meniscal release incision was performed
in 4 stifles. A second-look arthroscopic evaluation
was performed 3 to 33 months after TPLO (mean
10.4 months). Arthroscopic evaluation of the
cranial and caudal cruciate ligaments, lateral
and medial menisci, femoral and tibial cartilage,
periarticular osteophyte (PAO) formation and
degree of synovitis was performed. Pathologic
changes were identified at initial surgery and
followed over time.
Radiographic evidence of PAOs was unchanged or
minimally increased in 20 stifles and moderately
increased in 2 stifles. Progression of PAOs
was evident arthroscopically in 36% of stifles.
Cartilage wear was unchanged in 12 stifles and
increased in 10 stifles. Cartilage wear was evident
arthroscopically in 7 stifles without radiographic
evidence of increased osteoarthritis. Small radial
tears of the lateral meniscus were seen in 19
stifles at the time of initial surgery. Six of 8 stifles
treated by radiofrequency partial meniscectomy
had increased cartilage wear. Increased cartilage
wear was evident in 2 of 11 stifles with similar
meniscal tears left untreated. The severity of
synovitis was unchanged in 2 and decreased in 20
stifles. The CrCL was intact at follow-up in 19 of
22 stifles. The caudal cruciate ligament (CdCL)
2006 World Congress WSAVA/FECAVA/CSAVA
624
Back to contents
was normal in 18 of 22 stifles at time of TPLO.
Four dogs had obvious fraying of the CdCL at
initial surgery. The CdCL was frayed in 10 of 22
stifles at second-look arthroscopy. The meniscal
release incision was not healed in 2 of 4 stifles
and was spanned with a fibrous tissue in 2 of 4
stifles.
Arthroscopy was a more sensitive indicator
of increased PAO formation following TPLO.
Synovitis was generally decreased at follow-
up. The intact portion of the CrCL had a high
chance of remaining intact following TPLO.
Increased fraying of the CdCL may be due to
the increased load following TPLO. Meniscal
release incisions did not heal or healed with
fibrous tissue. Small radial tears of the lateral
meniscus may not require treatment. TPLO
does not eliminate osteoarthritis in dogs having
partial tears of the CrCL, but does appear to
avoid complete rupture.
Complications
Complications are infrequent following second-
look arthroscopy. The procedure is usually much
shorter in duration, often times completed in less
than 15 minutes. The predominant complication
is subcutaneous fluid extravasation. Infection
is rare if aseptic technique is used. Morbidity
is extremely low- patients rarely have lameness
induced by the procedure.

Or – Orthopaedics
EVIDENCE BASE INFORMATION REGARDING TPLO & TTA
Don Hulse DVM, Dip ACVS,
Dip ECVS
Texas A&M University
dhulse@cvm.tamu.edu
During the past decade, complete or partial
rupture of the cranial cruciate ligament in dogs
has become one of the preeminent topics of
interest in small animal orthopedic surgery.
The high incidence of cranial cruciate ligament
injury and the treatment methods for the CCL
deficient stifle joint have been a focus of interest
for over 50 years. In the past decade, Slocum’s
tibial plateau leveling osteotomy (TPLO) is, by a
broad consensus, a state-of-the-art repair method.
In 2002, Montavon and Tepic described their
technique, called tibial tuberosity advancement
(TTA), which became established for clinical use
in early 2004. Tibial plateau levelng osteotomy
is a surgical technique which converts cranial
tibial thrust in the CCL deficient stifle joint
to a caudal tibial thrust. In doing so the caudal
cruciate ligament then stabilizes the joint against
abnormal cranial caudal translation. Controversy
exists as to whether rotational or varus-valgus
stability returns. The majority of clinical reports
indicate successful improvement in limb function
following TPLO surgery. However, return to
normal function is only achieved in a minority of
cases as determined by owners and gait analysis.
Nevertheless, greatly improved function is
reported by most surgeons in retrospective
studies. For example, Jandi et al reported on
the effect of Tibial Plateau Leveling Osteotomy
on lameness, OA, ROM, postliminary meniscal
injury in dogs with CCLD 2 yr following surgery.
They concluded that TPLO leads to minimal
progression of OA, minimal arthrofibrosis,
minimal post operative meniscal damamge and
resolution of lameness. Sixty-nine per cent of the
cases had normal or near normal gait 6 months
after surgery whereas 94% exhibit near normal or
normal gait 12 months after surgery.
Back to contents
Or
Tibial tuberosity advancement is a surgical
technique designed to neutralize cranial tibial
thrust in the CCL deficient stifle by aligning the
patella tendon perpendicular to the tibial plateau
in the extended weight bearing position. In the
cadaver in vitro experiment, TTA is successful
in neutralizing cranial tibial thrust at a PTA
angle of 90 degrees. However in a separate
experiment, cranial tibial thrust, internal foot
rotation, stifle angle and hock angle only
partially returned with 12mm advancement in
large breed dogs. TTA may not be achieving the
surgical goals of the technique. A prospective
clinical study on 36 dogs indicated that overall
outcome showed TTA to be a practical technique
capable of restoring full function of the CCLD
stifle joint with low morbidity. A separate study
examined the results of TTA surgery performed
in 57 dogs with CCLD. Overall outcome is good
to excellent in 90% of replies (75% excellent).
Activity level greatly improved in 72% and
improved or greatly improved in 90%. Sixty-
seven (67%) showed an increase in radiographic
OA at 8 week follow up. The authors concluded
that TTA appears to be a useful alternative in the
management of CCLD. Another group believes 2006 World Congress WSAVA/FECAVA/CSAVA
that the results of the TTA procedure are at
least as comparable to the TPLO procedure,
with a quicker (subjectively assessed) return to
postoperative weight bearing. The procedure
also is relatively simple to perform with a very
short learning curve, and we have observed
relatively few complications. Vezzoni compared
the results of TPLO and TTA in his practice
and concluded that TPLO may be the preferred
method of treatment in heavy dogs with a tibial
slope of >25°.
625
Or
Or – Orthopaedics
UPDATE IN PATELLAR LUXATION IN DOGS - INDICATIONS FOR
ARTHROSCOPICALLY-ASSISTED SURGERY
Brian Beale DVM,
Diplomate ACVS
Gulf Coast Veterinary Specialists
1111 West Loop South #160
Houston
Texas
77027
drbeale@gcvs.com
Arthroscopy of the stifle has revolutionized
the treatment of knee injury in man. The use
of arthroscopic-assisted surgical techniques
for patellar luxation has benefits compared to
arthrotomy. If arthrotomy can be avoided, lower
patient morbidity is expected. Arthroscopy
allows evaluation of the trochlear groove and
patellar articular surface. Arthrosco py also
allows assessment of the menisci and cruciate
ligaments, both of which may have concomitant
injury in patients with patellar luxation. A release
incision of the medial retinaculum can also be
performed under arthroscopic guidance.
Benefits of arthroscopy
Important advantages of arthroscopy compared to
arthrotomy include decreased pain, earlier return
to function, improved visualization and more
precise and accurate treatment. Other potential
advantages include reduced scarring of the skin,
decreased periarticular fibrosis and improved
long term function.
Postoperative Pain
Pain following surgery of the stifle can be
2006 World Congress WSAVA/FECAVA/CSAVA
substantial. Disruption of tissues leads to pain.
Pain is generated locally by cellular mechanisms
and activation of pain receptors. The perception
of pain is dependent on transmission of impulses
through the peripheral and central neural
pathways. The source of pain may include skin,
subcutaneous tissues, muscle, ligaments, tendons,
synovial membrane, and subchondral bone.
Inflammatory mediators within the synovial fluid
also cause pain. Surgical pain can be decreased
by appropriate preemptive analgesia, adjunctive
NSAID therapy, reducing the number and extent
of tissues invaded, and by meticulous handling
of tissues. Arthroscopic-assisted surgery is
minimally-invasive, sparing soft tissues around
the joint, thereby reducing painful stimuli.
626
Back to contents
Return to Function
Early return to function is desirable to reduce
muscle atrophy and preserve joint motion
following surgery. Limb disuse quickly leads
to muscle atrophy. The loss of muscle mass
results in increased force on the joint, which may
predispose to osteoarthritis and additional injury
to ligamentous structures. Pain, tissue swelling,
activity restriction and bandaging contribute to
postoperative loss of joint range of motion. Early
range of motion exercise is advantageous due to
the tendency for joints to become stiff following
surgery. Arthroscopic-assisted techniques also
help to preserve joint range of motion due to
its effect on decreasing postoperative pain and
swelling.
Visualization of Joint Structures
Arthroscopic evaluation is superior to open
surgical evaluation for 3 reasons:
1. magnification of joint structures
2. greater access to joint structures
3. assessment of joint structures in a fluid medium
Magnification of intraarticular structures allows
for more accurate identification of pathological
change. Early osteoarthritic changes to articular
cartilage not visible to the naked eye, are clearly
seen arthroscopically. Fine and course fibrillation,
superficial erosions and neovascularization of the
cartilage are readily evaluated and documented.
Small radial and axial tears of the menisci
often become evident only after magnification.
Arthroscopic evaluation of the menisci is also
improved due to the ability to position the scope
directly adjacent to meniscus in both the cranial
and caudal joint compartment. The menisci
can be evaluated arthroscopically despite the
presence of an intact cranial and caudal cruciate
ligament. The scope can also be positioned in all
4 compartments of the joint (proximal, medial,
lateral, distal), allowing a thorough evaluation of

the synovium, patella, femoral trochlea, femoral
condyles, tibial plateau, cruciate ligaments and
menisci. These structures can be assessed for
hyperplastic change, inflammation, erosion,
osteophyte production, cartilage defects, tears
and dysfunction.
Assessment of the joint in a fluid medium is
optimal because synovial changes, cartilage
surface morphology, and meniscal pathology
become more evident. The end result of the
enhanced visualization provided by arthroscopy
is an improved ability to identify and document
the presence and severity of pathological change;
which allows for more accurate grading and
classification of lesions.
Arthroscopic-assisted Medial Release Incision
A lateral scope portal and a medial instrument
portal are used. The tip of the scope is positioned
in the medial compartment of the stifle. The
Back to contents
Or
stifle is held in extension. The position of the
patella is noted in relationship to the trochlear
sulcus. The medial joint capsule is identified. The
joint capsule and retinaculum are incised with
a radiofrequency probe or by sharp dissection
using arthroscopic scissors or a meniscal knife.
Bleeding is controlled by increasing fluid flow
and electrocoagulation. The retinaculm is incised
until the medial tension on the patella is released,
allowing the patella to return to a position within
the trochlear groove. The patella should return
to this normal position spontaneously and not
by applying digital pressure. It should be noted
that this technique only addresses one facet of the
pathophysiology of patellar luxation. Alignment
of the quadriceps mechanism should also be
performed as needed. This can be performed
through a minimally-invasive surgical approach
in combination with arthroscopic-assisted medial
release incision.
2006 World Congress WSAVA/FECAVA/CSAVA
627
Or
Or – Orthopaedics
UPDATE IN SURGICAL TREATMENT OF HIP DYSPLASIA
Brian Beale DVM,
Diplomate ACVS
Gulf Coast Veterinary Specialists
1111 West Loop South #160
Houston
Texas
77027
drbeale@gcvs.com
Triple pelvic osteotomy (TPO) is frequently used
in immature dogs for treatment of hip dysplasia.
The acetabular segment is rotated an appropriate
amount after osteotomy of the pubis, ischium
and ilium. The acetabulum is stabilized with a
contoured plate and screws placed over the ilial
osteotomy site. The positional change of the
acetabulum increases the stability and decreases
the chance of subluxation in dogs that meet
the criteria for the procedure. The goal of the
procedure is to decrease the chance of developing
progressive osteoarthritis and to maintain limb
function.
Surgical Technique
A standard approach to the pubis, ischium
and ilium is made as described by Slocum. A
pubic osteotomy is performed adjacent to the
iliopectineal eminence and a small portion of
pubis is removed. The ischial osteotomy is made
at the lateral extent of the obturator foramen and is
stabilized with a 1.0 or 1.25 mm orthopedic wire
2006 World Congress WSAVA/FECAVA/CSAVA
Figure 1 - Lateral scope portal
628
Back to contents
at the surgeon’s discretion. The ilial osteotomy
is made just caudal to the caudal extent of the
sacrum. Care to avoid the sciatic nerve is taken.
The acetabular segment is rotated laterally to the
proper position and stabilized with a bone plate
and screws of the surgeon’s choice.
Arthroscopic Evaluation
Hip arthroscopy can be readily performed with
minimal difficulty. Hip arthroscopy allows
thorough visual assessment of the normal and
pathologic intraarticular anatomy. The prime
indication for hip arthroscopy is assessment of
juvenile canine patients for triple pelvic osteotomy.
There is a significant degree of cartilage, femoral
capital ligament and joint capsule pathology with
no radiographic evidence of osteoarthritis in
some juvenile dogs. A poor correlation between
radiographic and arthroscopic findings, shown by
Holsworth et.al., makes accurate assessment of
suitable surgical candidates by radiography alone
difficult.
Figure 2 - Round ligament as viewed
artroscopically

A recent study by Bevin and Beale documented
and described the intra-articular pathology of
the dysplastic hip joint prior to and at long term
following triple pelvic osteotomy. The goal of
the study was to evaluate the effect of the TPO
on the progression of hip osteoarthritis (OA) and
to identify any variables that may predict the
outcome of the procedure. Pathologic changes
of both the acetabular labrum and articular
cartilage were common arthroscopic findings.
(Figure 1,2) The primary change seen in the
acetabular labrum was tearing at its articular or
free margin. Eleven of the twenty hips (55%)
had labral pathology preoperatively. Seven of
these (35%) hips had an appreciable progression
of labral pathology, and seventeen of the hips
(85%) had some degree of labral tearing at the
final evaluation. Cartilage lesions were graded
using a modified Outerbridge system and their
location was documented. Nine of the nineteen
Figure 3 - Normal labrum
Figure 4 - Labral tear
(arrow)
Radiographic evaluation was not
a reliable indicator of pathologic
changes following TPO
Back to contents
Or
treated hips (47%) had progression of cartilage
pathology. Eight of these dogs had minimal
to mild changes, and one dog had moderate to
severe progression of pathology. Ten hips had no
change in cartilage pathology with nine of these
hips having no pre-operative cartilage changes.
There was a statistically significant correlation
between pre-operative arthroscopic findings and
post-operative radiographic evidence of OA.
This suggests that pre-operative arthroscopic
findings are a better predictor of outcome than
radiographic evidence of OA. These findings are
supported by a previous study presented in 2002
by Holsworth et al., in which there was a poor
correlation between preoperative radiographic
and arthroscopic findings. The results of this
study suggest that the TPO procedure does not
completely stop the progression of OA, however,
clinical use of the affected limbs was good at the
time of follow-up despite presence of OA.
Figure 3 - Normal acetabular Figure 4 - Grade 4 cartiage
cartilage erosion of femoral head
Juvenile Pubis Symphysiodesis (JPS)
JPS is a technique used to influence pubis growth
and acetabular position in puppies having early
hip dysplasia. Experimental studies by Dueland
and Patricelli showed improved hip conformation
and decreased chance of developing osteoarthritis
following this procedure. The procedure must be 2006 World Congress WSAVA/FECAVA/CSAVA
performed between 3 and 5 months of age. Early
diagnosis of hip laxity is best perfomed using
the PennHIP technique. The pubic symphysis
is closed prematurely by application of heat
using an electrosurgical probe. Clinical success
using this technique has been reported, however,
most patients having hip laxity and dysplasia
are diagnosed too late to take advantage of this
procedure.
629
Or
Or – Orthopaedics
ARTHROSCOPIC DIAGNOSIS OF ELBOW DYSPLASIA
Dominique J Griffon, DMV,
MS, PhD, DACVS,
DECVS Associate Professor,
Head, Small Animal Surgery
Director,Laboratory for
Orthopedic Research on
Biomaterials University of Illinois
Small Animal Clinic
1008 W Hazelwood drive
Urbana IL61802, USA
http://www.cvm.uiuc.edu/lorb/
dgriffon@uiuc.edu

What is elbow dysplasia?
“Elbow dysplasia” (ED) is a syndrome that
includes several conditions resulting in an
incongruency of the joint, eventually leading to
degenerative joint disease (DJD). Elbow dysplasia
is a common, inherited condition affecting 17%
of Labrador retrievers, and up to 70% of Bernese
Mountain dogs in the Netherlands. This high
prevalence and the devastating effects of elbow
DJD emphasize the need for early diagnosis,
individualized treatment and preventive measures.
In 1993, the International Elbow Working
Group (IEWG) agreed that “elbow arthrosis
caused by Fragmented Coronoid Process (FCP),
osteochondrosis (OCD), Ununited Anconeal
Process (UAP), articular cartilage anomaly and/or
joint incongruity is the manifestation of inherited
canine elbow dysplasia”.

Conditions included in Elbow Dysplasia:

• Osteochondrosis (trochlea humeri)
• Ununited Anconeal Process (UAP)
• Fragmented Coronoid Process (medial, FCP)
• Incongruity:
1. Radio-ulnar incongruence
a. With or without angular limb deformity
b. Short ulna or short radius
2. Elliptical ulnar notch?
3. Local incongruity (deformed medial coronoid process)?
• Combination of the above

Why consider arthroscopy for the diagnosis of

2006 World Congress WSAVA/FECAVA/CSAVA

elbow dysplasia?
The IEWG developed a radiographic protocol scored according to severity of the arthrosis (DJD)
and scoring system adopted as a screening system and/or presence of a primary lesion (derived from
to diagnose ED. The radiographic findings are Mark Flückiger, IEWG 2003 Estoril meeting):

Elbow Dysplasia Grading Radiographic Findings

0 Normal elbow joint Normal elbow joint, no evidence of incongruency,
sclerosis or arthrosis
I Mild arthrosis Sclerosis of ulnar trochlear notch or, step =/> 2 mm
between radius and ulna or, osteophyte formation less
than 2 mm high
II Moderate arthrosis Osteophyte formation 2 to 5 mm high
III Severe arthrosis or 1° ED Osteophyte formation over 5 mm high and/or primary ED
such as LPA, FMCP or OCD
630
Back to contents

Radiographs of both elbows should be obtained
in all cases diagnosed with elbow dysplasia,
because the condition is often bilateral. UAP and
OCD are typically diagnosed on radiographs, and
do not require advanced imaging.
Radio-ulnar incongruence has traditionally
been diagnosed based on standard radiography.
Degenerative joint disease secondary to elbow
dysplasia is mainly evaluated on hyperflexed
lateral, cranio-caudal and craniolateral /
caudomedial 15°oblique views. An UAP is best
visualized on a lateral hyperflexed radiograph.
The craniolateral / caudomedial 15°oblique view
improves the visualization of the medical coronoid
process compared to the cranio-caudal projection
(Wosar et al. 1999). However the sensitivity of
conventional radiography to image the medial
coronoid process has been estimated to only range
from 10 to 62% (Wosar et al. 1999). The effect
of radiographic positioning on interpretation of
cubital joint congruity has also been studied in
normal dogs. The authors of this study compared
three mediolateral (45°, 90° and 135° of flexion)
and three cranio-caudal views, and concluded that
elbow congruity was best assessed on a 90° flexed
lateral projection with the beam centered over
the joint (Murphy et al. 1998). The superiority
of mediolateral over craniocaudal projections
to evaluate radio-ulnar incongruence was later
confirmed with a surgical model of induced
radio-ulnar incongruence in cadaveric forelimbs
(Mason et al. 2002). However, radiologists were
only able to correctly identify congruent elbows
(specificity) in 86% and incongruent elbows
(sensitivity) in 78% of specimens. The radio-ulnar
step required for each of 4 American College of
Veterinary Radiology board-certified radiologists
to attain 90% sensitivity ranged from 1.5 to
greater than 4 mm. In comparison, the elevation
of the coronoid process in relationship with the
ulna in elbows with FCP has been reported to vary
between 1 and 2 mm (Wind 1986, Trostel et al.
2003) The results of this study did not support
the use of standard radiography for evaluation of
radio-ulnar incongruence.
Computed tomography has previously been used to
help diagnose elbow dysplasia when radiographs
did not provide a definitive diagnosis (Rovesti et
al. 2002). CT eliminated the false positive results
obtained with survey radiographs in the detection
of fragmented coronoid process. Compared to
standard radiographs, it also provided a better
definition of the disease n 46% of elbows examined.
CT scan has been reported to achieve the highest
accuracy (86.7%) and sensitivity (88.3%) when
compared to radiography, xeroradiography, linear
tomography and positive contrast arthrography
for diagnosing fragment medial coronoid process
Back to contents
Or
(Carpenter et al. 1993). CT imaging protocols
have recently been described to measure elbow
incongruity (Holsworth 2004, Gemmill TJ et
al. 2004). Although the accuracy, sensitivity
and specificity of CT to diagnose radioulnar
incongruence has not been studied, this technique
is currently considered as a gold-standard to
diagnose radio-ulnar incongruence, and has been
applied in two clinical studies (Gielen 2004,
Holsworth 2004, Gemmill et al. 2004, Schulz
2004). Both studies compared radio-ulnar
incongruence in normal elbows and in dogs with
FCP (Gemmill et al. 2004, Kramer et al. 2004).
Unfortunately, the results and conclusions of
both studies differed drastically: Gemmill et al.
reported that radio-ulnar incongruity exists at
the apex of the coronoid process but not at its
base, whereas Kramer et al. described exactly the
opposite. Both groups used a similar protocol,
but the discrepancy between their results may
be due to the difference in positioning of the
elbow or in interpretation of images: one group
measured the humeroradial and humeroulnar
joint space (Gemmill et al. 2004), whereas the
other measured the actual step between the radius
and the ulna (Kramer et al. 2004). Although these
studies suggest that the form of incongruency
associated with FCP is more complex than a
simple proximal translation of the articular
surface of the ulna, they also illustrate the need
for further evaluation of CT as a diagnostic tool
for radio-ulnar incongruence. Ultimately, the
ability of computed tomography to diagnose
elbow incongruity will remain limited by the lack
of visualization of the cartilage, leading to an
evaluation of subchondral bone rather alignment
of joint surfaces. From a clinical standpoint,
this diagnostic tool currently requires general
anesthesia of the patient and may not be widely
accessible in private practices.
Arthoscopic evaluation of the elbow also requires
general anesthesia but it allows unparalleled
2006 World Congress WSAVA/FECAVA/CSAVA
visualization of joint surfaces (Schulz 2004). In
addition, arthoscopy is minimally invasive and
can be combined with surgical treatment of the
lesion. One study found no difference in post-
operative gait analysis of normal dogs undergoing
arthroscopic versus open exploration of the
elbow (Bubenik LJ et al, 2002). However, two
other studies documented improved function in
dogs immediately after and over the 21 months
following arthroscopic treatment of FCP,
compared to arthrotomy (Schwarz et al. 1993,
Meyer-Lindeberg A et al. 2003). Arthroscopic
management of FCP therefore appears to minimize
post-operative pain compared to open arthrotomy,
but further studies are needed to long term benefits
on degenerative joint disease.
631
Or
What arthroscopic technique can be used to
diagnose FCP and radio-ulnar incongruence?
The dog is placed in dorsal recumbency with a
sandbag on the lateral aspect of the affected elbow.
An assistant maintains the limb in position over
the sand bag to provide adduction throughout the
study. A 2.7mm arthroscope may be used in large
breeds, although atraumatic insertion of the scope
between the humeral head and the ulna may be
difficult, especially in dogs with radio-ulnar
incongruity. A 1.9mm 30° fore obliqued scope
is therefore preferred. The entire joint is first
explored through a medial portal, including the
anconeal process, the medial and lateral coronoid
processes, the medial and lateral aspects of the
Arthroscopic appearance of fragmented coronoid process (FCP) in dogs:
• Fragment on the medial margin of the medial coronoid process (MCP)
• Erosion of the lateral rim of the MCP
• Incomplete fragmentation (fissure)
• Fragment in situ
• Minimally migrated FCP
• Fully migrated FCP (joint mouse)
• Chondromalacia – Eburnation of the MCP
Elbows with FCP should be carefully evaluated
for degenerative joint disease (especially
cranial to the radial head), cartilage lesions on
the opposing articular surface of the humerus
(“kissing lesions”) and incongruity (Figure 1).
Unfortunately, objective assessment of elbow
incongruity via arthroscopy has not been fully
investigated.
2006 World Congress WSAVA/FECAVA/CSAVA
Figure 1: Arthroscopic evaluation of radio-ulnar
incongruity in two dogs with medial FCP. Both
images show the humeral condyle (triangle), the
ulna commissure and lateral coronoid process
(arrow) and the radial head (block arrow). Left:
congruent radio-ulnar junction. Right: radio-
ulnar incongruence.
We have recently studied the predictive value
of arthroscopy to diagnose experimentally
induced radio-ulnar incongruity (Wagner K
et al. 2006). A surgical model of radio-ulnar
incongruence was used to shorten the radius by
1, 2 and 3 mm increments in cadaveric forelimbs
obtained from adult Labrador Retrievers. Radio-
632
Back to contents
humeral condyle and the entire radial head. A
systematic evaluation of all compartments of
the elbow is crucial to complete the diagnosis of
elbow dysplasia. The egress portal consists of an
18-gauge needle directed in the joint pouch just
proximal to the anconeus. An instrument portal
located in the region of the medial collateral
ligament allows triangulation of a graduated
hook-probe. The probe can be used to mobilize
a fragmented coronoid process, cartilage flap in
OCD and appreciate radio-ulnar incongruence.
The arthroscopic appearance of OCD, UAP and
FCP are well established. In fact arthroscopy
has allowed the identification of variation in
appearance of FCP:
ulnar incongruence was blindly evaluated via
computed tomography (CT) and arthroscopy
before and after each modification. Radio-ulnar
incongruence was measured arthroscopically
with a graduated probe at 3 levels in each study:
the commissure of the medial and lateral portions
of the coronoid process, the apex and the mid-
body of the medial coronoid process. The
distance between the ulnar and radial surfaces in
unmodified elbows was equal to 1.18 ± 0.13 mm
on CT. The overall sensitivity of arthroscopy was
85% and 95%, when the radius was shortened by
1mm versus ≥2mm, respectively. The specificity
was equal to 50%. The ability to detect mild
incongruity (1 mm step) was greater at the
ulnar incisure than at other locations. Although
pronation subjectively appeared to modify the
appearance of the radio-ulnar junction, this factor
was not found to affect the overall predictive
value of arthroscopy. Intra-articular pressure did
not affect the examination. In this study, we found
arthroscopy to be very sensitive for detection of
radio-ulnar incongruence, especially at the ulnar
incisure. The greatest sensitivity obtained at
the ulnar incisure is due to the relative ease of
identifying landmarks compared to the mid body
and apex of the coronoid. The low specificity of
the technique (i.e. our ability to correctly identify
unmodified elbows as congruent) reflects the
physiological degree of radio-ulnar incongruence
previously reported in dogs, and confirmed by
the CT measurements in our study. The clinical
relevance of a mild radio-ulnar incongruence

remains unclear in a normal elbow. However,
a diagnosis of mild incongruity in the presence
of other signs of elbow dysplasia would support
adjunctive osteotomies / ostectomies to modify the
distribution of loads in the diseased joint. Further
studies correlating radiographs, arthroscopy
and computed tomography in clinical cases of
elbow dysplasia are warranted to validate these
findings.
Selected references
Bubenik LJ, Johnson SA, Smith MM, et
al.: Evaluation of lameness associated with
arthroscopy and arthrotomy of the normal canine
cubital joint. Vet Surg 2002; 31: 23-31
Carpenter L, Schwarz P, Lowry J, et al.
Comparison of radiologic imaging techniques for
diagnosis of fragmented medial coronoid process
of the cubital joint in dogs. J Am Vet Med Assoc
1993; 203: 78-83.
Flückiger M: Radiographic diagnosis of elbow
dysplasia (ED) in the dog – Requirements for the
internationally standardized screening procedure
for ED. Proc International Elbow Working Group
May 22 2003, Estoril, Portugal.
Gielen I, Ven Ryssen B, van Bree Henri:
Arthrology – Diagnostic imaging: is CT the
answer. Proc 12th ESVOT Congress, Munich,
Germany, 10-12th September 2004b, pp 140.
Gemmill TJ, Clements DN, Clarke Sp et al.:
Investigation of elbow incongruency in dogs
suffering coronoid disease using reconstructed
computed tomography. Vet Surg, 2004; 33: E6.
Holsworth I: How I manage elbow incongruity,
Proc 12th ESVOT congress, Munich, Germany,
September 10-12, 2004, pp 60.
Kramer A, Filipowicz D, Hosworth IG et al.:
Computerized tomographic evaluation of canine radio-
ulnar incongruence in vivo. Vet Surg 2004; 33: E13.
Back to contents
Or
Mason DR, Schulz KS, Samii VF et al:
Sensitivity of radiographic evaluation of radio-
ulnar incongruence in the dog in vitro. Vet Surg
2002; 31: 125-132.
Meyer-Lindenberg A, Langhann A, Fehr M et al.:
Arthrotomy versus arthroscopy in the treatment
of fragmented coronoid process of the ulna (FCP)
in 421 dogs. VCOT 2003; 16: 204-210.
Murphy ST, Lewis DD, Shiroma JT et al.: Effect
of radiographic positioning on interpretation of
cubital joint congruity in dogs. Am J Vet Res
1998; 59(11): 1351-1357.
Rovesti GL, Biasibetti M, Schumacher A et al:
The use of computed tomography in the diagnostic
protocol of the elbow in the dog: 24 joints. VCOT
2002; 15: 35-43.
Schulz KS: Diagnostic assessment of the elbow
(When in doubt, scope the elbow). Proc ACVS
symposium, Denver, Colorado, October 6-9
2004, pp 329-331.
Schwarz PD, Brevard SM, Baker CG: Arthroscopy
of the shoulder (OCD) and elbow (MFCP)- thirty
consecutive cases each: a comparative study of
the early postoperative period. Vet Surg, Proc 7th
Annual ACVS symposium; 1993: 21-22.
Trostel TC, McLaughlin RM, Pool RR: Canine
lameness caused by developmental orthopedic
diseases: Fragmented medial coronoid process
and united anconeal process. Comp Cont Ed
Pract Vet 2003; 25: 112-120.
Wind AP: Elbow incongruity and developmental
elbow disease in the dog. J Am Anim Hosp Assoc
1986; 22: 711-724.
Wosar M, Lewis D, Neuwirth L, Parker R, et
al. Radiographic evaluation of elbow joints
before and after surgery in dogs with possible
fragmented medial coronoid process. J Vet Med
Assoc 1999; 214: 52-58.
2006 World Congress WSAVA/FECAVA/CSAVA
633
Or
Or – Orthopaedics
CONTROVERSIES IN ARTHROSCOPIC TREATMENT OF FCP
Dominique J Griffon, DMV,
MS, PhD, DACVS,
DECVS Associate Professor,
Head, Small Animal Surgery
Director,Laboratory for
Orthopedic Research on
Biomaterials University of Illinois
Small Animal Clinic
1008 W Hazelwood drive
Urbana IL61802, USA
http://www.cvm.uiuc.edu/lorb/
dgriffon@uiuc.edu
Disease of the medial coronoid process is a
leading cause of osteoarthrosis of the canine
elbow. The ideal candidate for surgical treatment
of a fragmented coronoid process (FCP) is a
dog under 12 months of age with clinical and
radiographic signs of FCP. Surgery is also
indicated in mature dogs, especially if DJD is
absent or minimal. Once severe DJD is present,
conservative management may be as beneficial
as surgery.
This presentation will focus on current
controversies surrounding the treatment of
coronoid disease and associated conditions of the
elbow. Videos of clinical cases will illustrate the
components of arthroscopic management of FCP
in dogs.
Is arthroscopy superior to arthrotomy when
managing FCP?
Excision of FCP has traditionally been performed
via a medial approach to the elbow. Although
several approaches have been described, the
intermuscular approach is technically easier and
associated with less morbidity. The approach is
slightly more complicated that that the caudo-
2006 World Congress WSAVA/FECAVA/CSAVA
lateral compartment of the elbow, but does
not require specialized instruments. Potential
complications include inadvertent transection of
the medial collateral ligament or median nerve.
This approach provides limited exposure to the
joint.
Recent advances in arthroscopy have greatly
improved our ability to explore and treat elbow
disease. In fact, this technique has allowed the
identification of variation in appearance of FCP:
• Fragment on the medial margin of the MCP
• Erosion of the lateral rim of the MCP
• Incomplete fragmentation (fissure)
• Fragment in situ (arrows)
• Minimally migrated FCP
• Fully migrated FCP (joint mouse)
• Chondromalacia – Eburnation of the MCP
634
Back to contents
The disadvantage of this technique consists in
the equipment and technical expertise required
to perform this treatment. A 2.7mm arthroscope
may be used in large breeds, although atraumatic
insertion of the scope between the humeral head
and the ulna may be difficult, especially in dogs
with radio-ulnar incongruity. A 1.9mm 30° fore
obliqued scope is therefore preferred. The entire
joint is first explored through a medial portal,
including the anconeal process, both coronoid
processes, the humeral condyle and radial head.
The main advantage of arthroscopy is that it
provides unparalleled visualization of the joint in
a minimally-invasive manner, thereby decreasing
post-operative morbidity. One study found no
difference in post-operative gait analysis of
normal dogs undergoing arthroscopic versus
open exploration of the elbow (Bubenik LJ et al,
2002). However, two other studies documented
improved function in dogs immediately after
and over the 21 months following arthroscopic
treatment of FCP, compared to arthrotomy
(Schwarz et al. 1993, Meyer-Lindeberg A et
al. 2003). Arthroscopic management of FCP
therefore appears to minimize post-operative pain
compared to open arthrotomy, but further studies
are needed to long term benefits on degenerative
joint disease.
Arthroscopic excision of FCP or arthroscopic
subtotal coronoidectomy?
FCP has traditionally been treated by excision of
the fragmented portion of the medial coronoid
process. This may be achieved arthroscopically,
via insertion of a grasping forceps or
shaver through a triangulated cranio-medial
instrument portal. The sclerotic subchondral
bed is subsequently debrided. A subtotal
coronoidectomy has recently been proposed
for the treatment of dogs with FCP (Fitzpatrick
N, 2005). The technique can be performed via
a limited medial approach or via craniomedial

triangulation of a small osteotome, angled from
the caudomedial border of the medial portion of
the coronoid process to the craniolateral margin
of the radial incisure. Although the author noticed
a progression of DJD on radiographs, only 2%
of 31 dogs followed for 3 years after surgery
had recurrence of lameness. Histopathology of
the coronoid processes removed in this study
confirmed the presence of subchondral fissures
extending beyond the area of visible cartilage
damage. While these findings support the
concept of a subtotal coronoidectomy, one could
argue that these fissures could have healed if
the biomechanical loading of the joint had been
altered. The effectiveness of the procedure was
attributed to the complete removal of diseased
cartilage and subchondral fissures, eliminating
the need for cartilage healing in a contact
environment and unloading the medial aspect of
the humeral condyle. If this procedure decreases
pressure across the medial compartment of
the elbow, it does not fully align the articular
surfaces of the ulna and radius in dogs with
radio-ulnar incongruence. Further studies
are warranted to evaluate the effects of the
procedure on joint stability and biomechanics.
In the meantime, subtotal coronoidectomy
seems especially relevant when the majority of
the medial coronoid process (MCP) is damaged
(Figure 1).
Figure 1: Arthroscopy of the elbow of an 18 month
old German Shepherd with elbow dysplasia.
Note the eburnation of the medial coronoid
process (block arrows) and lesion of the opposing
articular surface of the humeral trochlea (arrow).
This dog was treated via subtotal coronoidectomy
and miscropicking of the “kissing” lesion of the
humerus.
Back to contents
Or
Should an ulnar osteotomy be performed in all
elbows with FCP?
Transient or persistent radio-ulnar incongruence
is now considered as the primary cause for FCP:
the radius is shorter than the ulna, creating a high-
pressure area over the medial coronoid process,
eventually leading to its fragmentation. Ulnar
osteotomy may be combined with removal of a
FCP if radio-ulnar incongruence is present. The
technique actually involves the removal of a
short segment of ulna to allow distal migration of
the proximal ulna. The osteotomy is performed
approximately 25mm distal the elbow and
obliqued in a caudo-cranial, proximo-distal
direction to limit post-operative displacement of
the proximal segment. However, a forward tipping
and mild medial displacement of the proximal
ulna is expected after surgery. This displacement
does not appear clinically significant but can be
prevented by insertion of an intramedullary pin in
the ulna. In a retrospective study of 10 young dogs
(less than 10 months), 5 were normal according
to their owners 17months after excision of FCP
and ulnar osteotomy, while 4 experienced an
occasional stiffness and 1intermittent lameness.
No crepitus and unchanged range of motion were
diagnosed on physical examination in 9 out of
10 dogs (Ness MG 1998). A 93% success rate
was also reported after arthroscopic excision of
the FCP and proximal ulnar osteotomy, in dogs
of all ages (Bardet JF 1997). Further studies are
warranted to document the effects of this technique
and improve our ability to diagnose radio-ulnar
incongruence (see notes on arthroscopic diagnosis
of elbow dysplasia).
In spite of research efforts currently directed
at improving our ability to diagnose all aspects
of elbow dysplasia and optimize the treatment
of this condition, recommendations remain
largely based on clinical impressions and lack
long-term objective evaluation. We currently
perform computed tomography and arthroscopy
2006 World Congress WSAVA/FECAVA/CSAVA
on all elbows suspect of FCP. We recommend
arthroscopic excision of FCP, combined with
proximal ulnar ostectomy, in dogs with radio-
ulnar incongruence. Subtotal excision of the
MCP is limited to elbows where the majority of
the coronoid process appears damaged.
References
Bardet JF, Bureau S: La fragmentation du
processus coronoide chez le chien. Prat Med Chir
Anim Comp 1996; 31: 451-463.
Bardet JF: Arthroscopy of the elbow in dogs.
Part II: The cranial portals in the diagnosis and
treatment of the lesions of the coronoid process.
VCOT 1997; 10: 60-66.
635
Or
Boudrieau RJ, Hohn, Bardet: Osteochondritis
Dissecans of the elbow in the dog. J Am Anim
Hosp Assoc 1983; 19: 627-635.
Boulay JP: Fragmented Medial Coronoid process
of the ulna in the dog. Vet Clin North Am 1998;
28: 51-74.
Bubenik LJ, Johnson SA, Smith MM, et
al.: Evaluation of lameness associated with
arthroscopy and arthrotomy of the normal canine
cubital joint. Vet Surg 2002; 31: 23-31
Morgan JP, Wind A, Davidson A: Hereditary bone
and joint diseases in the dog. Schlütersche, 2000.
Haudiquet PR, Marcellin-Little DJ, Stebbins
ME: Use of the distomedial-proximolateral
oblique radiographic view of the elbow joint for
examination of the medial coronoid process in
dogs. Am J Vet Res 2002; 63: 1000-1005.
Lang J, Busato A, Fluckiger M et al: Comparison
of two classification protocols in the evaluation
of elbow dysplasia in the dog. J Small Anim Pract
1998; 39: 169-174.
Mason DR, Schulz KS, Samii VF et al:
Sensitivity of radiographic evaluation of radio-
ulnar incongruence in the dog in vitro. Vet Surg
2002; 31: 125-132.
2006 World Congress WSAVA/FECAVA/CSAVA
636
Back to contents
Meyer-Lindenberg A, Langhann A, Fehr M et al.:
Arthrotomy versus arthroscopy in the treatment
of fragmented coronoid process of the ulna (FCP)
in 421 dogs. VCOT 2003; 16: 204-210.
Ness MG: Treatment of fragmented coronoid
process in young dogs with proximal ilnar
osteotomy. J Small Anim Pract 1998; 39: 15-18.
Read RA, Armstrong SJ, Black AP et al.:
Relationship between physical signs of elbow
dysplasia and radiographic score in growing
Rottweilers. J Am Vet Med Assoc 1996; 209.
Rovesti GL, Biasibetti M, Schumacher A et al:
The use of computed tomography in the diagnostic
protocol of the elbow in the dog: 24 joints. VCOT
2002; 15: 35-43.
Schwarz PD, Brevard SM, Baker CG: Arthroscopy
of the shoulder (OCD) and elbow (MFCP) - thirty
consecutive cases each: a comparative study of
the early postoperative period. Vet Surg, Proc 7th
Annual ACVS symposium; 1993: 21-22.
Trostel TC, McLaughlin RM, Pool RR: Canine
lameness caused by developmental orthopedic
diseases: Fragmented medial coronoid process
and united anconeal process. Comp Cont Ed
Pract Vet 2003; 25: 112-120.

Or – Orthopaedics
ARTHROSCOPIC TREATMENT OF OCD LESIONS (SHOULDER,
ELBOW, KNEE, HOCK)
Alois Nečas, Prof. MVDr., PhD.
University of Veterinary and
Pharmaceutical Sciences Brno
Department of Surgery and
Orthopedics, Small Animal Clinic
Palackeho 1-3
612 42 Brno
Czech Republic
necas@eurosat.cz
Osteochondrosis (OC) is a multifocal disease of
epiphyseal (growth) cartilage affecting both the
articular-epiphyseal cartilage complex (immature
joint cartilage covering the ends of growing long
bones) and the growth (physeal) plate of bones.
It is a disturbance of endochondral ossification.
Up to the present there are differing views on the
definition and pathogenesis of osteochondrosis
and this disease has several synonyms such as
osteochondritis dissecans (OCD), osteochondrosis
dissecans or dyschondroplasia.
The etiology of osteochondrosis is polyfactorial,
while trauma, ischemia, hereditary factors, rapid
growth and nutrition of the individual are taking
part. Lesions of blood vessels in the cartilage
causing local ischemia play probably the key role.
In small animals, large and giant breeds of dogs
are predisposed to osteochondrosis. Considering
large and giant dogs, such breeds as Dobermann,
Collie and Siberian Husky are relatively of low risk
with regard to the occurrence of osteochondrosis.
The OC of the humeral head was described in the
cat, as well. The first clinical symptoms are seen
in period of rapid growth of animals. Predilection
sites for osteochondrosis are the shoulder, elbow,
stifle and hock joints.
Early intervention, and as possible minimally
invasive method of surgical management,
represent current trends of OCD treatment.
Arthroscopically assisted surgery is the treatment
of choice. Recently, it is routine practice to
manage OCD lesions of the shoulder, elbow, knee
and hock joints arthroscopically.
The principle of managing osteochondritis
dissecans is to remove cartilage flap (free
fragments and/or adherent cartilage) usually with
grasping forceps, and treat the surface of the
lesion with abrasion chondroplasty, subchondral
drilling (forage), or microfracture technigue.
Arthroscopically assisted abrasion
chondroplasty might be performed with a curette,
hand burr, or motorized shaver. The surface is
abraded until the underlying subchondral bone
Back to contents
Or
bleeds. The edges of the defect are debrided with
the same instruments, leaving edges perpendicular
to the bone surface. However, debridement
during arthroscopic surgery should not be too
aggressive, maintaining as much subchondral
bone as possible to keep the bone plate and
overlying cartilage repair tissue contoured to the
normal congruency of the opposing joint surface.
Smoothing of the bed is best accomplished with
the motorized shaver in reverse mode.
Forage or subchondral drilling to stimulate
hemorrhage and fibrocartilage response is usually
done with a small Kirschner wire.
Subchondral bone microfracture technique
(micropicking) has many of the advantages
associated with subchondral drilling, including
focal penetration of the dense subchondral bone
plate to expose cartilage defects to the benefits
of cellular and growth factor influx, as well
as improving anchorage of the new tissue to
the underlying subchondral bone and to some
extent surrounding cartilage. In this technigue,
a microfrature pick and mallet are used to treat
the OC lesion bed. It has been shown that long-
term there is significantly increased filling of full-
thickness articular defects, and that microfracture
has superior results to autologous chondrocyte
2006 World Congress WSAVA/FECAVA/CSAVA
transplantation.
At the end of arthroscopic surgery, the joint is
inspected and flushed thoroughly to remove all
cartilage fragments.
Cartilage repair using osteochondral autografts
transplantation (mosaicplasty) is promissing
treatment of choice in managing large defects,
especially in stifle joint. Mosaic arthroplasty
might be considered as a method of articular
cartilage reconstruction resulting in renewed
cartilage gliding surface.
Joint resurfacing, represented by chondrocyte
transplantation and mesenchymal stem cell
transplantation technigues, remains a challenge
for future scientific research in this field.
637
Or
References
Beale BS, Hulse DA, Schulz KS, Whitney
WO: Small animal arthroscopy. W.B. Saunders
Company, Philadelphia, 2003.
Gal P, Necas A, Adler J, Teyschl O, Fabian P,
Bibrova S: Transplantation of the autogenous
chondrocyte graft to physeal defects: an
experimental study in pigs. Acta Vet Brno 2002,
71: 327-332.
McIlwraith CW: Other methods of cartilage
repair. Proceedings of the 2nd Annual World
Orthopedic Congress, Keystone, Colorado, USA,
25.2.-4.3.2006: 113-114.
Necas A, Beale BS: Traumata kloubů (Joint
injuries). CCB, spol. s r.o., 2005, 88 p.
Necas A, Dvorak M, Zatloukal J: Incidence of
2006 World Congress WSAVA/FECAVA/CSAVA
638
Back to contents
osteochondrosis in dogs and its late diagnosis.
Acta Vet Brno, 1999, 68: 131-139.
Necas A, Gal P, Adler J, Kecova H, Fabian P,
Bibrova S: Transplantation of the autogenous
chondrocyte graft to physeal defects: an
experimental study. Proceedings of the 2nd
Annual World Orthopedic Congress, Keystone,
Colorado, USA, 25.2.-4.3.2006: 236.
Probst CW, Johnston SA: Osteochondrosis. In:
Slatter D: Textbook of small animal surgery. 2nd
ed. W. B. Saunders, Philadelphia, 1993: 1944-
1966.
Whitney WO: Arthroscopic assisted fracture
repair. Proceedings of the 12th ESVOT Congress,
Munich, Germany, September 10-12, 2004: 160.

Or – Orthopaedics
ARTHROSCOPIC MANAGEMENT OF JOINT INJURIES AND
INTRAARTICULAR FRACTURES (HIP, ELBOW, CARPUS, TARSUS)
Alois Nečas, Prof. MVDr., PhD.
University of Veterinary and
Pharmaceutical Sciences Brno
Department of Surgery and
Orthopedics, Small Animal Clinic
Palackeho 1-3
612 42 Brno
Czech Republic
necas@eurosat.cz
Arthroscopically assisted management of joint
injuries and intraarticular fractures is a challenging
procedure. It is technically demanding because a
complexity of the instrumentation and the size
and complexity of the joints in small animals.
The majority of these cases are not routinely
treated under arthroscopic assistance at present.
On the other hand, arthroscopy has been
successfully used to treat e.g. avulsion fractures of
supraglenoid tubercle, lateral condylar fractures
of the humerus, incomplete ossification of the
humeral condyle, and avulsion fractures of cranial
cruciate ligament. The indications for minimally
invasive arthroscopic assisted surgery might be
also some small fragment femoral head fractures,
small fragment carpal and hock fractures. These
cases might be managed by simple arthroscopic
removal of the fragments.
Arthroscopy combined with surgical repair of
injured joint structures using bone anchors is
also becoming more popular. Bone anchors are
used in orthopedic surgeries to anchor the suture
material directly to the bone. Other indications
are anchoring of different soft tissues such as
ligaments, tendons and joint capsule. They are
often clinically used in people to repair injuries of
rotator cuffs, avulsions of distal bicipital tendon
and cruciate ligament ruptures. In man, number
of bone anchors has been successfully used; some
of them can be used also in animals. Their main
disadvantage is their high price. In veterinary
ortopedic surgery, numbers of indications
for use of bone anchors are known. Besides
extracapsular CCL rupture repair, anchors can
be used in following indications: reconstruction
of collateral ligaments in elbow, stifle and tarsal
joints, stabilization of hip luxation, shoulder
instability (rupture of glenohumeral ligaments),
and fixation of avulzion fractures.
Lateral humeral condylar fractures are common
intraarticular fractures in dogs. They are
routinely repaired using open fracture reduction
and fixation, or fluoroscopically guided closed
Back to contents
Or
reduction. Minimally invasive arthroscopy might
be used in closed management of this articula
fractures. Arthroscopy of the elbow can be also
used to diagnose and treat incomplete ossification
of the humeral condyle.
Two types of intraarticular femoral head fractures
are seen associated with coxofemoral dislocation
in mature dogs. Each type presents a challenge
to veterinary surgeon to achieve a satisfactory
outcome. The more common type involves
avulsion of a small portion of the femoral head,
which is normally attached to the round ligament.
The fragment is too small to be adequately
stabilized and its presence may result in failure
of attempts at treatment of the dislocated hip by
closed reduction. Excision of the fragment is
indicated in this case. This procedure can be done
arthroscopically. The second, less common type,
is when dislocation of the hip is associated with a
much larger saggital fracture through the femoral
head. If the fragment is larger than one-quarter of
the femoral head, then the opportunity exists to
reduce and stabilize the fracture with lag screws
or with a combination of a lag screw and a small
pin at the time of open reduction of the hip.
The carpus and tarsus are complex joints and
present diagnostic and therapeutic challenges when 2006 World Congress WSAVA/FECAVA/CSAVA
injured. Instability and/or displaced intraarticular
fractures lead to degenerative joint disease and
chronic lameness with crippling consequences
for the animal. In decision making in carpal
injuries treatment, the surgeon should weigh up
the type of joint instability and character of the
trauma. In such cases, there anatomic reposition
and rigid stabilization of articular fracture and/or
reconstruction of injured ligaments is possible,
the surgeon should attempt to restore the joint
function choosing the reconstructive surgery.
Carpal and tarsal injuries are commonly caused
either falling or jumping from a height. An animal
can sustain these injuries also in a road traffic
accident. Any age or breed and either gender of
dog or cat may be affected. Carpal and tarsal
639
Or
injuries may consist of fractures, ligamentous
injuries, and various combinations. The list of
traumatic conditions of the carpus might be
extended and includes: luxation/subluxation of
the antebrachiocarpal joint, luxation of the radial
carpal bone, fracture of the radial carpal bone,
fracture of the accessory carpal bone, subluxation
of the accessory carpal bone, fracture of the
ulnar and numbered carpal bones, middle carpal
luxation/subluxation, carpal hyperextension and
shearing injury of the carpus. The most often
seen, and therefore in practice the most frequently
treated, carpal injuries are: antebrachiocarpal
subluxation (with medial joint instability due
to the injury of the radial collaterals), carpal
hyperextension and shearing injury of the carpus.
Regarding medial antebrachiocarpal subluxation
the most common affected ligaments in are the
radial collaterals, resulting in medial instability
and valgus deformity of the foot. The medial
carpal instability may be congenital („carpal
dysplasia“) or acquired (injury).
Arthroscopy of the carpal and tarsal joints can
be used as mini-invasive method to diagnose the
extent of intraarticular joint structure damage in
traumatic cases or document possible congenital
anomalies. Recently, the reconstruction of the
medial collateral ligaments is also possible
2006 World Congress WSAVA/FECAVA/CSAVA
640
Back to contents
using a bone suture achor. This method of the
treatment will be presented in the meeting lecture
in the above mentioned case of congenital carpal
instability and tarsal small fragment fracture/
ligament injury in dogs.
Proper case selection is very important regarding
to good prognosis in arthroscopically managed
joint injuries and intraarticular fractures.
References
Beale BS, Hulse DA, Schulz KS, Whitney
WO: Small animal arthroscopy. W.B. Saunders,
Philadelphia, 2003.
Necas A: Carpal injuries and indications for
carpal arthrodesis. Proceedings of the 9th Annual
Orthopedic Surgical Skills Laboratory, Key
Largo, Florida, USA, 18.-21.2.2004: 73-78.
Necas A, Beale BS: Traumata kloubů (Joint
injuries). CCB, spol. s r.o., 2005, 88 p.
Necas A, Dvorak M: Surgical treatment of a
saggital intraarticular femoral head fracture with
coxofemoral dislocation in two mature dogs. Acta
Vet Brno 2003, 72: 261-265.
Whitney WO: Arthroscopic assisted fracture
repair. Proceedings of the 12th ESVOT Congress,
Munich, Germany, September 10-12, 2004: 160.

Or – Orthopaedics
ASSESSMENT OF SHOULDER STABILITY
Don Hulse DVM, Dip ACVS,
Dip ECVS
Texas A&M University
dhulse@cvm.tamu.edu
Being a ball and socket joint, the shoulder joint
is well suited for movement in all directions.
Although capable of movement in all directions,
the shoulder primarily moves in flexion and
extension. Joint stability is provided through a
combination of passive and active mechanisms.
Passive mechanisms include the medial and
lateral glenohumeral ligaments, surrounding
joint capsule, joint conformation, and synovial
fluid cohesion. The medial collateral ligament
(MCL) commonly appears as “y” shaped with
the cranial arm coursing caudally from its origin
at the medial surface of the supraglenoid tubercle.
The caudal arm of the MCL originates from the
medial surface of the scapular neck and joins the
cranial arm to insert onto the humeral neck. The
Dynamic active glenohumeral stability is provided
by contraction of the surrounding cuff muscles.
These include the biceps brachii, subscapularis,
teres minor, supraspinatous, and infraspinatous
muscles. Active contraction of all or selective
cuff muscles induce compression across the
shoulder joint as well as increasing tension in the
joint capsule.
When tested in neutral position, the cranial,
lateral, and medial translation of the humerus
was significantly increased after biceps tendon
transection. In the flexed position, translation of
the humerus in the cranial and lateral directions
was significantly increased after biceps tendon
transection. In the extended position, the medial
translation of the humerus was significantly
Back to contents
Or
MCL and associated joint capsule is a major
factor in providing joint stability; complete
medial luxation occurs following transection
of the MGHL. The lateral collateral ligament
(LCL) originates from the lateral rim of the
glenoid and extends ventrally to insert onto
the humerus at the caudal region of the greater
tubercle. The joint capsule originates from the
periphery of the glenoid cavity. Medially, the
joint capsule forms a synovial recess due to
its attachment several millimeters proximal to
the glenoid rim. The concavity of the glenoid
and the fit of the humeral head into the glenoid
provide joint stability. This is particularly true
when compression across the joint is enhanced
by active muscle contraction.
2006 World Congress WSAVA/FECAVA/CSAVA
increased after biceps tendon transaction.
Examination of the shoulder for stability should
be done in the awake animal as well as under
anesthesia. Flexion, extension, abduction,
adduction, and rotational stability of the shoulder
joint should be assessed. Circumduction of the
shoulder with internal and external rotation of
the humerus is performed to detect signs of
subluxation. The abduction test is completed
to assess medial restraint instability. The dog is
placed in lateral recumbency with the forearm
to be tested extended; the shoulder joint must
be in slight external rotation to prevent a false
positive test. The limb is gradually raised with
a valgus maneuver (bringing the limb upward).
A normal test is approximately 25 degrees
641
Or
of valgus movement. Abnormal movement
exceeds 25 degrees and is often approximately
43 degrees. The importance lies in the
determination of a side to side (right to left
forearm) difference. An abnormal abduction
test does not always signify medial restraint
injury. We have documented cases with long
standing unilateral forelimb lameness will have
an abnormal abduction test in the lame limb.
Our presumption is that the laxity is due to
disuse atrophy and loss of strength of the cuff
muscles and ligaments.

Abnormal abduction test Arthroscopic view of case on left showing torn MCL
2006 World Congress WSAVA/FECAVA/CSAVA

642
Back to contents
 Or
Or – Orthopaedics
LIMB ALIGNMENT IN DOGS WITH CRANIAL CRUCIATE LIGAMENT
INSUFFICIENCY
Dominique J Griffon, DMV,
MS, PhD, DACVS,
DECVS Associate Professor,
Head, Small Animal Surgery
Director,Laboratory for
Orthopedic Research on
Biomaterials University of Illinois
Small Animal Clinic
1008 W Hazelwood drive
Urbana IL61802, USA
http://www.cvm.uiuc.edu/lorb/
dgriffon@uiuc.edu

Cranial cruciate ligament (CCL) rupture is one of
the most common injuries to the stifle of dogs and
is the leading cause of degenerative joint disease
in that joint (Johnson JA et al. 1994, Innes JF et al.
2000, Elkins AD et al. 1991). The annual economic
impact of medical and surgical management of
CCL insufficiency has recently been estimated to
about 1 billion dollars in the United States alone
(Wilke et al. 2005). Whereas traumatic rupture of
CCL predominates in humans, CCL deficiency
in dogs is typically associated with a chronic
history of progressive lameness consistent with
a degenerative process. Misalignment of the joint
surfaces is a well-recognized cause of arthrosis
and gait abnormalities. Techniques altering
overall limb, and specific joint alignment have
recently gained popularity to prevent or correct
surgical diseases of the joints, including CCL
disease.
This presentation will first review the clinical
and radiographic measurements used to evaluate
alignment of the rear leg in the canine patient,
along with potential applications of advanced
imaging techniques. Clinical cases will be
presented to illustrate abnormalities measured
with each technique in dogs with cruciate
ligament disease. The changes in joint and limb
alignment produced by surgical procedures
currently recommended for the treatment of CCL
will be described, along with their limitations
and potential future modifications.
Rupture of the CCL has been associated with
degenerative changes, auto-immune diseases,
hormones (sex predisposition), collagenase
activity and antibodies against type-I and –II
collagen in synovial fluid (Comeford 2003,
Moore KW, Read RA 1996). However, weakening
secondary to repetitive microtrauma is currently
believed to cause the majority of CCL instabilities
diagnosed in dogs, especially in large breeds such
as Labradors (Hayashi K et al. 2003, Duval JM
Back to contents
et al. 1999, Arnoczky SP, Marshall JL 1981). A
great deal of interest has recently focused on the
importance of the “cranial tibial thrust” as an
underlying cause for repetitive microtrauma to
the CCL (Slocum B, Devine T 1983). This force
generated by compression between the tibia and
femur during the stance (weight-bearing) phase,
is partly oriented in a cranial direction, leading
to cranial translation of the tibia. In a stable knee,
this force is actively opposed by the pull of the
stifle flexor muscles (Figure 1).
2006 World Congress WSAVA/FECAVA/CSAVA
Figure 1: Schematic representation of forces
acting at the knee (derived from Slocum B and
Devine TD, 1993). Cranial tibial thrust (CTT) is
generated by weight bearing and contraction of the
gastrocnemius muscle. The extensor mechanism
also contributes to compression between the
femur and the tibia. CTT is counteracted by the
flexor muscles and passive restraints
The magnitude of this force generated by
contraction of the gastrocnemius depends on
the amplitude of the compressive force (70% of
the body weight at trot) but also on the slope of
the tibial plateau with respect to the axis joining
the centers of motion of the stifle and hock. This
theory provides a basis for the Tibial Plateau
643
Or
Leveling Osteotomy (TPLO), a procedure that is
not aimed at restoring the anatomical stability of
the CCL deficient stifle (Slocum B, Devine TD
1993). Instead, it modifies the joint geometry
to neutralize cranial tibial thrust during weight
bearing. Although this procedure has gained
tremendous popularity for treatment of CCL
deficiency in large breed dogs, several studies
have failed to show a correlation between the
steepness of the tibial plateau and the development
of CCL insufficiency (Reif U, Probst CW 2003,
Wilke VL et al. 2002).
This reflects the fact that these stress injuries most
likely result from a combination of, rather than
from a single factor. Indeed, the biomechanical
environment leading to CCL instability can
be described as an imbalance between factors
contributing to the CTT and its active restraints
(illustrated in Figure 1), eventually leading to
fatigue failure of the passive restraints (CCL and
medial meniscus). This model would explain
the association between obesity (increasing
the compressive force applied on the knee)
and CCL deficiency (Duval JM et al. 1999).
The proposed biomechanical model could also
explain the mechanism of action of conformation
abnormalities previously believed to lead to CCL
deficiency, such as genu varum, increase in stifle
angle (straight-legged dogs such as Labrador
Retrievers), tarsal hyperextension, deformation of
the proximal tibia or stenosis of the intercondylar
notch (Fitch RB et al. 1995, Moore KW, Read
RA 1996). Genu varum consists of a varus
deformation of the femur, resulting in a “bow-
legged” stance. This conformation has been
associated with medial patellar luxation (MPL).
MPL tends to cause an internal rotation, which is
prevented in part by the CCL. Misalignment of
the patellar tendon affects the direction of forces
generated by the quadriceps and destabilizes the
anterior compartment of the knee.
2006 World Congress WSAVA/FECAVA/CSAVA
The impact of the thigh muscles on the magnitude
of the CCT remains poorly defined. Yet, an
imbalance between flexor and extensor muscles
of the thigh would contribute to CCL overuse.
This imbalance could result from a difference
in muscle distribution that could potentially be
corrected via physical therapy. Another potential
cause of imbalance between muscle groups could
result from a cranio-caudal misalignment of the
quadriceps, affecting the direction and moment
of forces generated during weight bearing. This
theory would support the mechanism of action of
tibial tuberosity advancement (TTA) as a recently
proposed treatment for CCL deficiency. This
procedure maintains the angle between the patellar
tendon and the tibial plateau to a maximum of
90° in full extension, thereby loading the caudal
644
Back to contents
cruciate ligament throughout the entire range of
motion of the knee (Tepic S, 2004). TTA involves
a pre-determined open wedge osteotomy of the
tibial tuberosity that is fixed with a tension band
plate and grafted.
Proximal tibial shaft deformity was recently
described in 9% of dogs with CCL and steep tibial
plateau slope (Osmond et al. 2006). The deformity
consisted of a caudal tipping (greater than 11°) of
the proximal tibia in relationship with its long
axis, thereby identifying a distinct subpopulation
of dogs with CCL disease. Although these findings
warrant further investigation, they may eventually
affect our therapeutic recommendations. Indeed,
a cranial tibial wedge would re-align the entire
proximal tibia, and may therefore be a better
option than TPLO in these dogs.
The multifactorial origin of CCL deficiency
secondary to repetitive microtrauma most likely
involves the tibial plateau slope along with
other morphometric parameters, whose relative
contributions have yet to be defined. Variations
between breeds, difficulties identifying “normal”
versus “predisposed” dogs, invasiveness
and cost of procedures hinder our ability to
design meaningful studies and improve our
understanding of the pathogenesis of CCL disease.
Studies evaluating the potential contribution of
conformation characteristics to CCL injuries have
largely been based on clinical and radiographic
assessments (Wilke VL et al. 2002, Duval JM et
al. 1999, Aiken SW et al. 1995, Whitehair JG et
al. 1993). The conformation of the entire limb
in dogs predisposed to CCL deficiency has not
been systematically evaluated. Computerized
tomography has been applied to study the
musculature of the thigh and lower extremity in
humans with ACL injuries (Lorentzon R et al.
1989, Gerber C et al. 1985). This non-invasive
imaging technique has also been used to estimate
body segment parameters (such as length, mass and
location of the center of mass) in living subjects.
These morphometric parameters have then been
combined with kinetic and kinematic data to
calculate moment of forces and mechanical power
at a joint, applying inverse dynamic analysis of
gait. This approach to biomechanical gait analysis
has greatly contributed to the understanding of
mechanisms of orthopedic disorders such as
ACL injuries in humans (Decker MJ et al. 2003,
Chappell JD et al. 2002). We are currently applying
this technique to Labradors with and without CCL
insufficiency to try and identify conformation
factors that predispose this breed to the disease.
The long term goal of this research is to allow
the development of preventive measures, such as
physical therapy to correct muscle imbalance and/
or alteration of growth plate(s) to modify skeletal
growth and conformation.

References
Aiken SW, Kass PH, JP Toombs: Intercondylar
notch width in dogs with and without cranial
cruciate ligament injuries. Vet Comp Orthop
Traumatol 1995 8: 128-132.
Arnoczky SP, Marshall JL: Pathomechanics of
cruciate and meniscal injuries. In Bojrab MJ (ed):
Pathophysioloy in Small Animal Surgery. Lea &
Febiger, Philadelphia 1981, p 590.
Chappell JD, Yu B, Kirkendall DT et al.: A
comparison of knee kinetics between male and
female recreational athletes in stop-jump tasks.
American J Sports 2002; 30: 261-267.
Comeford E: Comparison of biochemical and
biomechanical properties of cranial cruciate
ligament in the Greyhounds, Labrador Retriever
and Golden Retriever. PhD thesis, Department
of Clinical Veterinary Science, University of
Bristol, 2003.
Conzemius M, Robinson D, Evans R et al.:
Estimate of the annual economic impact of
rupture of the cranial cruciate ligament in the
dog in the United States. Proc scientific meeting
of the Veterinary Orthopedic Society, Big Sky,
Montana, February 21-28, 2004, pp 44.
Decker MJ, Torry MR, Wyland DJ et al.: Gender
differences in lower extremity kinematics,
kinetics, and energy absorption during landing.
Clinical Biomechanics 2003; 18: 662-669.
Duval JM, Budsberg SC, Flo GL et al.: Breed, sex
and body weight as risk factors for rupture of the
cranial cruciate ligament in young dogs. J Am Vet
Med Assoc 1999; 215: 811-814.
Elkins AD, Pechman R, Kearney MT, et al.:
A retrospective study evaluating the degree of
degenerative joint disease in the stifle of dogs
following surgical repair of anterior cruciate
ligament rupture. J Am Anim Hosp Assoc 1991:
27: 533-540.
Fitch RB, Montgomery RD, Kincaid SA et al.:
The effect of intercondylar notchplasty on the
normal stifle. Vet Surg 1995; 24: 156-164.
Gerber C, Hoppeler H, Claassen H et al.:
The lower-extremity musculature in chronic
symptomatic instability of the anterior cruciate
ligament. J Bone Joint Surg Am 1985; 67: 1034-
1043.
Hayashi K, Frank JD, Dubinsky C et al: Histologic
changes in ruptured canine cranial cruciate
ligament. Vet Surg 2003; 32: 269-277.
Innes JF, Bacon D, Lynch C et al.: Long-term
Back to contents
Or
outcome of surgery for dogs with cranial cruciate
ligament deficiency. Vet Rec 2000; 147: 325-
328.
Johnson JA, Austin C, Breur GJ: Incidence of
canine appendicular musculoskeletal disorders
in 16 veterinary teaching hospitals from 1980 to
1989. Vet Comp Orthop Traumatol 1994; 7: 56-
59.
Lorentzon R, Elmqvist LG, Sjostrom M et al.:
Thigh musculature in relation to chronic anterior
cruciate ligament tear: muscle size, morphology,
and mechanical output before reconstruction. Am
J Sports Med 1989; 17: 423-429.
Moore KW, Read RA: Rupture of the cranial
cruciate ligament in dogs – Part I. Comp Cont Ed
Pract 1996; 18: 223-234.
Osmond CS, Marcellin-Little DJ, Harrysson OL
et al.: Morphometric assessment of the proximal
portion of the tibia in dogs with and without
cranial cruciate ligament rupture. Vet Radiol
Ultrasound, 2006; 47: 136-141.
Reif U, Probst CW: Comparison of tibial plateau
angles in normal and cranial cruciate deficient
stifles of Labrador Retrievers. Vet Surg 2003; 32:
385-389.
Slocum B, Devine TD: Tibial plateau leveling
osteotomy for repair of cruciate ligament rupture
in the canine. Vet Clin North Am Small Anim
Pract 1993; 23: 777-795.
Slocum B, Devine T: Cranial tibial thrust: a
primary force in the canine stifle. J Am Vet Med
Assoc 1983; 183: 456-459.
Tepic S, Montavon PM: Is cranial tibial
advancement relevant in the cruciate deficient
stifle? Proc. 12th ESVOT congress, Munich,
2004: 132-133.
Whitehair JG, Vasseur PB, Willits NH:
Epidemiology of cranial cruciate ligament
rupture in dogs. J Am Vet Med Assoc 1993; 203: 2006 World Congress WSAVA/FECAVA/CSAVA
1016-1019.
Wilke VL, Robinson DA, Evans RB et al.:
Estimate of the annual economic impact of
treatment of cranial cruciate ligament injury in
dogs in the United States. J Am Vet Med Assoc
2005; 227: 1604-1607.
Wilke VL, Conzemius MG, Besancon MF et
al.: Comparison of tibial plateau angle between
clinically normal Greyhounds and Labrador
Retrievers with and without rupture of the cranial
cruciate ligament. J Am Vet Med Assoc 2002;
221: 1426-1429.
645
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

PP Haematology
Cytology,
yto
& Clinical Pathology

Back to contents

INVITED LECTURES - FULL PAPERS
P - Cytology, Haematology & Clinical Pathology
INTERPRETING HEMOGRAMS: WHITE CELL DISORDERS (PART 1 AND 2)
Dr. Alan H. Rebar
Senior Associate Vice President for Research
Executive Director, Discovery Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
Introduction
Hemograms consist of both quantitative data (total
cell counts, differential cell counts, hematocrit,
hemoglobin, red cell indices, etc.) and qualitative
data (blood film evaluation). Proper interpretation
depends upon the integration of the two.
Proper interpretation also depends upon a
systematic approach. For all cell compartments,
interpretation can be guided by asking and
answering a series of key questions.
Key Leukogram Questions
Key Leukogram questions include the following:
1) Is there evidence of inflammation?
2) Is there evidence of stress (high circulating
glucocorticoids)?
3) Is there evidence of tissue necrosis?
4) Is there evidence of systemic hypersensitivity?
5) If there is evidence of inflammation, can the
inflammation be classified as acute, chronic, or
overwhelming?
The following paragraphs will provide guidelines
for answering each of these questions in turns.
Is there evidence of inflammation?
The presence of a neutrophilic left shift (increased
numbers of circulating immature neutrophils,
monocytosis, and persistent eosinophilia, either
alone or in combination, are suggestive of
inflammation. Absolute neutrophilias of greater
than 25,000/μl also suggest inflammation. Total
white cell counts merely reflect the balance
between marrow production and tissue utilization.
In inflammatory disorders, total white cell counts
can be low, normal, or high.
Is there evidence of stress?
Stress (high circulating levels of glucocorticoids)
typically causes mild to moderate lymphopenia
(lymphocyte counts between 750/μl and 1500/
μl). Eosinopenia, mild mature neutrophilia, and
mild monocytosis can also be present but are less
consistent and specific than the lymphopenia.
Back to contents
P
Is there evidence of tissue necrosis?
Monocytosis is an indicator of demand for
phagocytosis and/or tissue necrosis. Monocytosis
ha soften been considered to be an indicator of
chronicity, but it can occur in as little as 8-12
hours.
Is there evidence of systemic hypersensitivity?
Persistent eosinophilia is an indicator of systemic
hypersensitivity. It is important to remember that
systemic hypersensitivity reactions represent a
special form of inflammatory reaction. Causes
include: parasitic diseases with a systemic phase
(flea bite dermatitis, heartworm disease), feline
asthma, allergic tracheobronchitis in dogs,
systemic mastocytosis, allergic gastroenteritis,
and disseminated eosinophilic granuloma
complex in cats. It is important to recognize that
parasitic disease confined to the gastrointestinal
tract (e.g., whipworms) does not cause systemic
persistent eosinophilia.
If there is inflammation, can it be classified as
acute, chronic or overwhelming?
In many cases, inflammatory leukograms cannot 2006 World Congress WSAVA/FECAVA/CSAVA
be further classified. In other instances, the
differential cell count (in absolute numbers)
is typical of acute, chronic or overwhelming
inflammation. Leukogram patterns are determined
by leukocyte kinetics, or the balance between
bone marrow production and release on the one
hand and tissue utilization on the other. Leukocyte
kinetics in turn are regulated through the actions
of chemotactic factors and cytokines.
The typical acute inflammatory leukogram is
characterized by neutrophilia with a left shift,
lymphopenia and variable monocytosis. The
neutrophilia reflects the relatively large bone
marrow storage pool in the dog and cat, and the
movement of more neutrophils from marrow
into blood than from blood into tissue. The left
shift indicates depletion of the marrow storage
pool of mature neutrophils and recruitment of
647
 P
younger cells into circulation. The lymphopenia
is reflective of stress. The presence or absence of
monocytosis depends on the presence or absence
of tissue necrosis.
There are two patterns indicative of chronic
inflammation. The first is characterized by
extremely high white cell counts (150 to 200,000/
μl or more) with marked neutrophilia and a left
shift. Monocytosis and neutrophil toxicity are also
usually present. In this circumstance neutrophil
production in the marrow is greatly expanded,
,and the number of neutrophils entering the
blood is far greater than the number leaving
the blood for the site of inflammation. Because
the inflammation is chronic, the anemia of
inflammatory disease and increased total protein
as a result of hyperglobulinemia are also often
present. This pattern of chronic inflammation is
commonly seen with severe focal suppurative
lesions such as abscesses.
The second form of chronic inflammation is
characterized by a normal to slightly elevated
white cell count characterized by high normal or
slightly elevated mature neutrophils, no left shift,
normal lymphocyte counts, and monocytosis.
The normal to slightly elevated neutrophil count
and absence of a left shift reflect a new balance
between marrow production and tissue demand.
The normal lymphocyte count represents the
counterbalancing effect of stress and antigenic
stimulation on lymphocyte numbers. Monocytosis
reflects demand for phagocytosis and tissue
necrosis. This kind of chronic inflammatory
response is generally seen with chronic low grade
more diffuse inflammatory processes.
Overwhelming inflammation is a circumstance
where tissue demand outstrips marrow production.
Overwhelming inflammatory processes are
therefore characterized by normal or decreased
neutrophil counts with a left shift. Lymphopenia
reflects stress. Monocytosis again indicates
demand for phagocytosis and/or tissue necrosis.
Is there evidence of systemic toxemia?
The presence of toxic neutrophils on the blood
film indicates systemic toxemia. Toxic changes
in neutrophils include foamy basophilia of the
cytoplasm, the presence of Döhle bodies in the
cytoplasm (basophilic precipitates of cytoplasmic
RNA), grantism, and the presence of bizarre
nuclear morphology. These changes occur as
a result of abnormal maturation of neutrophil
precursors in the marrow. Toxicity is the result
either of the direct action of circulating toxins
on neutrophil precursors or shortened maturation
time of neutrophils in response to increased tissue
demand. Systemic toxemia is most commonly
associated with bacterial infections. However,
other causes, such as extensive tissue necrosis,
must also be considered.
General patterns of leukocyte responses in disease
are summarized in Table 1.

Table 1. General Patterns of Leukocyte Responses

WBC Seg Band Lymph Mono Eos

Acute Increased Increased Increased Decreased Variable Variable
Inflammation or no change
Chronic Increased Increased Increased Increased Increased Variable
2006 World Congress WSAVA/FECAVA/CSAVA

Inflammation or no change or no change or no change or no change

Overwhelming Decreased Decreased Increased Decreased Variable Variable
Inflammation or no change or no change or no change
Excitement Increased Increased No change No change No change No change
Leukocytosis in dogs; in dogs;
increased or increased in
no change cats
in cats
Stress Increased Increased No change Decreased Increased Decreased
Leukogram or no or no
change change

Reprinted with permission from Teton New Media; A Guide to Hematology in Dogs and Cats,
A.H. Rebar, P.S. MacWilliams, B.F. Feldman, F.L. Metzger, R.V.H. Pollock, J. Roche;
Jackson WY; 2002

648
Back to contents

P - Cytology, Haematology & Clinical Pathology
INTERPRETING HEMOGRAMS: RED CELL DISORDERS (PART 1 AND 2)
Dr. Alan H. Rebar
Senior Associate Vice President
for Research
Executive Director, Discovery
Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
Introduction
Quantitative red cell data includes red cell count,
hemoglobin, hematocrit, and red cell indices –
mean cell volume (MCV), mean cell hemoglobin
concentration (MCHC), and red cell distribution
width (RDW). Total protein is also included in
red cell data. Red cell count, hemoglobin, and
hematocrit are all measures of red cell mass.
Total protein provides information about state
of hydration. Elevations of total protein most
commonly result from dehydration which can
also falsely elevate indicators of red cell mass.
Qualitative red cell data is red cell morphology
on the blood film. In particular red cell size,
shape, and color are evaluated. Variation in red
cell size is anisocytosis, variation in red cell
shape is poikilocytosis, variation in red cell color
includes polychromasia (increased numbers of
immature red cells) and hypochromasia (reduced
hemoglobin in red cells).
Key red cell questions include the following:
1) Is red cell mass increased (polycythemia),
decreased (anemia), or within reference intervals?
2) If decreased, is anemia regenerative or non-
regenerative?
3) If regenerative, is the mechanism blood loss or
hemolysis?
4) If non-regenerative can the mechanism be
determined without bone marrow evaluation?
5) If red cell mass is increased, is the polycythemia
relative or absolute?
6) If absolute, is the polycythemia primary or
secondary?
Each of these major questions will be answered in
turn in the paragraphs that follow.
Is red cell mass increased, decreased, or within
the reference interval?
This question is answered simply by evaluating
the indicators of red cell mass. These include red
cell count, hemoglobin, and hematocrit.
Back to contents
P
If decreased, is the anemia regenerative or non-
regenerative (Figure 1)?
Evaluation of the blood film is the first step
in differentiating regenerative from non-
regenerative anemias. Increased numbers of
polychromatophilic erythrocytes on the blood film
indicates red cell regeneration. Regeneration is
confirmed by doing absolute reticulocyte counts.
In dogs and cats, absolute reticulocyte counts of
greater than 80,000/μl indicate regeneration.
If regenerative, is the mechanism blood loss or
hemolysis?
History, signs, and physical examination are key
to differentiation. Most causes of blood loss will
be recognized in this way. Hemoglobinemia and/
or hemoglobinuria indicate hemolysis but are
not uniformly present in hemolytic conditions.
Very high reticulocyte counts (>200,000/μl) are
also highly suggestive of hemolysis. Whenever
hemolysis is suspected, red cell morphology
should be scrutinized for abnormal red cells
which are characteristic of certain hemolytic
disorders. These include: spherocytosis associated
with immune-mediated hemolytic anemia, Heinz
bodies and eccentrocytes which are associated
with oxidant induced hemolysis, schistocytes 2006 World Congress WSAVA/FECAVA/CSAVA
associated with microangiopathic hemolysis,
etiologic agents such as Mycoplasma felis, and
ghost cells associated with hemolysis in general.
If non-regenerative, can the mechanism be
determined without bone marrow evaluation?
Several non-regenerative anemias are characteristic
enough that bone marrow evaluation is not
needed to confirm the diagnosis. For example, the
most common anemia of the dog and cat is the
anemia of inflammatory disease. This anemia is a
mild to moderate normocytic normochromic non-
regenerative anemia (hematocrits as low as 30 in
the dog and 25 in the cat). When such an anemia
is present in conjunction with an inflammatory
649
 P
leukogram, additional diagnostic procedures are
not necessary.
Similarly, iron deficiency anemias present
with characteristic peripheral blood finding.
On the blood film, red cells are smaller than
normal and have pronounced areas of central
pallor. Poikilocytosis and red cell fragmentation
are common. Red cell indices often indicate
microcytosis and hypochromasia.
Megaloblastic anemias (nuclear maturation
defect anemias) often have occasional giant red
cells (macrocytes) in circulation. Megaloblasts
(large nucleated red cells with fully or nearly
fully hemoglobinized cytoplasm but immature
reticulated nuclei) may also be seen on blood
films. These findings are highly suggestive of
megaloblastosis but should be confirmed with
bone marrow findings. The most common cause
of megaloblastosis in companion animals is feline
leukemia infection in cats.
Occasionally, dogs and cats with severe non-
regenerative anemias also present with leukopenia
and poikilocytosis characterized by dacryocytosis
(tear-drop shaped erythrocytes) and ovalocytes.
Platelet numbers may be elevated or reduced. These
findings are suggestive of myelofibrosis but require
bone marrow examination for confirmation.
Finally, occasional non-regenerative anemias
characterized by large numbers (>10/100 WBC
counted) of nucleated red cells on blood films in
the absence of polychromasia (an inappropriate
nucleated red cell response) are seen in both
dogs and cats. These peripheral blood findings
are indicative of bone marrow stromal damage.
In dogs this is most suggestive of lead poisoning
while in cats, feline leukemia virus infection is the
most likely cause.
2006 World Congress WSAVA/FECAVA/CSAVA
650
Back to contents
All other non-regenerative anemias have
nonspecific hemogram findings and can only be
further assessed via bone marrow evaluation.
If red cell mass is increased, is polycythemia
relative or absolute?
Relative polycythemia (due to dehydration) is
by far the most common form of polycythemia.
It is characterized by increased red cell mass and
total protein as well as serum chemical indicators
of dehydration (increased sodium, potassium,
chloride, total protein and albumin). When
relative polycythemia is ruled out, the remaining
cases are absolute polycythemias.
If absolute, is polycythemia primary or secondary?
Secondary polycythemia is associated with
a variety of underlying conditions. These
include cardiovascular disease (reduced tissue
oxygenation), pulmonary disease (reduced
oxygen delivery to red cells and therefore tissues),
renal disease (primarily renal neoplasms which
can cause increased erythropoietin levels), and
Cushing’s disease (increased androgen production
results in increased red cell production). When
these potential causes are ruled out, polycythemia
is suspected to be primary.
Primary polycythemia is due to the
myeloproliferative disorder polycythemia vera.
Polycythemia vera is characterized by normal
circulating erythropoietin levels and normal tissue
oxygenation (normal arterial blood gas) with
significant increases in red cell mass (hematocrits
65 or greater). Bone marrow findings may be
normal or indicate red ell hyperplasia.

P - Cytology, Haematology & Clinical Pathology
GENERAL APPROACH TO CYTOLOGIC INTERPRETATION
Rose E. Raskin, DVM, PhD,
Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu
Cytology is a diagnostic tool used to examine
exfoliated cells obtained by aspiration, impression,
scraping, or natural release from any tissue. The
basic indications for diagnostic cytology are to
recognize the presence of inflammation, neoplasia,
or effects of tissue injury, and then determine if
possible an etiologic agent. If a specific disease
condition is not possible to diagnose from
cytologic evaluation, the procedure often rules out
other disorders and may suggest other conditions
to be pursued.
SPECIMEN COLLECTION AND
PREPARATION
Materials used for cytology include solid tissues,
fluid pockets, tissue secretions or discharges,
body cavity effusions, urine, feces, and tissue
washings. The external site is either wiped with
an alcohol soaked gauze pad or, preferably,
scrubbed with warm water and antibacterial soap.
Aspiration may be either with suction or without.
For suction, a 6 or 12 ml syringe is attached to
a 22 gauge needle for soft fluctuant masses. A
20-gauge needle is preferential for amplifying
suction in firm or hard masses composed of
dense connective tissue. The mass is isolated and
immobilized between the thumb and forefinger.
Place the needle into the center of the mass if it is
small (< 2cm). For large masses, the center of the
lesion should be avoided to prevent aspirating only
necrotic material. Suction is applied (3 to 5 ml)
once the needle is within the lesion, advancing the
needle two or three times in different directions.
Following aspiration, gently release the plunger
to avoid splattering the aspirated material into the
syringe barrel.
Aspiration may not even be necessary for obtaining
a diagnostic cytologic specimen from certain
tissues, such as lymph nodes and suspected mast
cell tumors. Based on the principle of capillarity,
a technique referred to as “fine needle capillary
sampling” requires placement of a needle into
the lesion without the syringe attached. One
Back to contents
P
advantage is minimization of blood contamination
and another is reduced risk of cell rupture, both
common with the aspiration technique. The
contents of the needle may not be visible in the
hub of the needle. They are removed by filling a
syringe with air and gently squirting a drop of the
material onto a glass slide. A squash preparation
is made by lightly pressing the material between
two slides while sliding them apart horizontally.
Intact tissue or excised tissue must first be blotted
onto absorbent paper to remove excess blood and
tissue liquids. Gently touch the slide to create a
“dry” imprint. In the case of skin, the surface is
frequently contaminated with debris, bacteria,
and a neutrophilic response, which might obscure
the true pathogenesis.
Make thin smears by gently spreading materials
onto glass slides or coverslips. In a humid
environment, slides may be dried quickly with a
hair dryer. Do not “heat fix” the slides for cytology
as this procedure may rupture cells from the heat.
Following preparation of the aspirate or imprint,
air-dry the glass slides before staining.
Formalin fumes can permeate through plastic
materials. It is necessary to send cytologic and
histologic samples to referral labs in separate
containers and avoid close proximity of cytologic 2006 World Congress WSAVA/FECAVA/CSAVA
samples with formalin fumes in the practice
setting. Glass slides or coverslips should be placed
in sturdy cardboard or plastic containers and then
placed inside a thickly padded envelope or box
for mailing to a referral diagnostic laboratory.
STAINING CONSIDERATIONS
Slides should be stained as soon as possible to
avoid poor stain results due to pH changes. If
staining is to be performed at a later time, slides
should be placed in a closed container to protect
them from insects and light.
Once slides are air-dried, they may be stained
with routine Romanowsky stains. Quick stains
that take less than 5 minutes to perform are the
most commonly used in clinical practices to
651
 P
evaluate cytologic specimens. These may be either
alcohol-based Wright stains such as Hema-Quik
II® or aqueous-based Wright stains, the latter
stains known by a variety of trade names such as
Diff-Quik® or Quik-Dip®. In general, there are
few differences between the stain reactions of the
alcohol-based stains and aqueous-based Wright
stains. Compared with standard alcohol-based
Wright or Wright-Giemsa stains, the aqueous-
based Wright stains give similar cytomorphologic
information but may be more expensive since
they are prediluted. However some differences
exist that the one should know. For example, mast
cell tumors, especially poorly-differentiated ones,
may not stain well relative to their cytoplasmic
granules using an aqueous-based Wright stain
because granule contents are washed away.
Confirmation of a mast cell origin may require an
alcohol-based Giemsa staining technique which
does not affect granule contents.
New methylene blue (NMB) is another common
stain in addition to the Romanowsky-type stains
discussed above that can be used for cytology. It
is used also for urine sediment examination, and
for hematology with reticulocyte or Heinz body
identification. Since it is a water soluble stain, it
does not dissolve lipids and can be easily used to
identify lipomas and cholesterol crystals. Fungi,
bacteria, and mast cell granules are also easily
visible with this stain. In cases of heavy blood
contamination, nucleated cells are best identified
using NMB since red cells do not stain well. A
coverslip must be placed over the stain drop and
the slide should be examined when the stain is
applied as it will evaporate within hours.
Oil-red-O is a helpful stain in cytology to
determine the presence of lipid materials, such
as those found in vacuolated hepatocytes from a
cat with hepatic lipidosis. A drop may be applied
along with one of NMB to an air-dried slide to see
both nuclear and cytoplasmic features.
2006 World Congress WSAVA/FECAVA/CSAVA
MICROSCOPIC EXAMINATION
Artifacts are frequently encountered during
cytologic examination. Fungal hyphae are
often confused with the linear shapes formed
from fractured cells forming nuclear strands or
streaming and from strands of fibrin with entrapped
platelets. Color, shape, and uniform of width are
helpful in making this distinction. Basket cells are
also formed from ruptured cells which resemble
large intact cells. Bacteria, yeast, or rickettsial
organisms are often mistakenly diagnosed as a
result of stain precipitate following inadequate
rinsing or with old stain material that has become
contaminated. Plant spores or fragments may
simulate pathogenic fungi. Poor cellular detail
and staining often results from direct and indirect
652
Back to contents
contact of the cytologic samples with formalin,
for example, by making the cytologic prep in the
same room as an open formalin container, cells
appear blue-green.
Cytologic interpretations are generally classified
into one of five cytodiagnostic groups. An
exception is made for body cavity effusions
which have their own classification categories.
Interpretations of cytologic material may include
more than one category, such as inflammation
along with a response to tissue injury or neoplasia
along with inflammation.
Cytodiagnostic Groups
• Normal/Hyperplastic Tissue
• Cystic Mass
• Response to Tissue Injury
• Inflammation
• Neoplasia
Normal/Hyperplastic Tissue
Normal and hyperplastic tissues are composed
primarily of mature cell types. Look for
uniformity in cell, nuclear, and nucleolar size
and shape. Cytoplasmic volume is usually
high relative to the nucleus. Hyperplasia is a
nonneoplastic enlargement of tissue that can
occur relative to hormonal disturbances or tissue
injury. Hyperplastic tissue has a tendency to
enlarge symmetrically in size in comparison
to neoplasia. Cytologically, hyperplastic cells
have a higher nuclear to cytoplasmic ratio (N:C)
than normal cells. For example, normal salivary
gland epithelium appear as large foamy cells
with condensed nuclei and a low N:C. Prostatic
hyperplasia seen in intact male dogs with a
symmetrically enlarged prostate have cuboidal
epithelium of uniform size and differentiation
commonly with a high N:C.
Cystic Mass
Cystic lesions contain liquid or semisolid
material. The low protein liquid usually contains
a small number of cells. These benign lesions may
result from proliferation of lining cells or tissue
injury. For example, seroma is a light yellow
clear fluid resembling serum which may contain
rare large mononuclear cells having cytoplasmic
granularity. A follicular cyst is a common skin
mass in many species composed entirely of
keratinized anucleated squamous epithelium often
with rectangular cholesterol crystals that are seen
best against a light proteinaceous background or
when NMB stain is used.
Response to Tissue Injury
Common changes include hemorrhage,
proteinaceous debris, cholesterol crystals,
necrosis, or fibrosis. Hemorrhage with the

presence of erythrocytes is pathologic and should
be distinguished from blood contamination
encountered during the cytologic collection.
Blood contamination contains numerous platelets
in addition to unaffected erythrocytes. Acute
hemorrhage is associated with the engulfment of
erythrocytes by macrophages called erythrophages.
Chronic hemorrhage is associated with active
macrophages containing degraded blood pigment
within their cytoplasm, for example, blue-green to
black hemosiderin granules or yellow rhomboid
hematoidin crystals. Hemosiderin represents
an excess aggregation of ferritin molecules.
This form of iron stores stains positive with
the Prussian blue reaction. Hematoidin crystals
may be formed during anaerobic breakdown of
hemoglobin as occurs within tissues or cavities
and do not contain iron. Hematomas often contain
phagocytized erythrocytes if the lesion is acute or
hemosiderin-laden macrophages if the lesion is
chronic.
Proteinaceous debris may appear in the background
of the preparation. This may include mucus that
stains lightly as basophilic to purple amorphous
strands. Lymphoglandular bodies are basophilic
cytoplasmic fragments from fragile cells.
Nuclear streaming is a strand of remnant nuclear
P
material that stains pink to purple. Fibrovascular
stroma appear as clear to light pink strands that
often represent collagen and may be mixed
with spindle cells and endothelium. Amyloid
is an uncommon protein that is amorphous,
eosinophilic, and hyalinized and associated with
chronic inflammation.
Necrosis and fibrosis may occur together in
some cytologic preparations. The death of cells
is represented by fuzzy, indistinct cell outlines
and poor definition of cell type. Accompanying
tissue injury is the reparative response involving
increased fibroblastic activity. It is common to
see very reactive fibrocytes along with severe
inflammation and this appearance often mimics a
neoplastic condition.
Inflammation
Inflammatory conditions are classified
cytologically by the predominance or mixture
of the cell type involved such as neutrophils,
macrophages, and eosinophils.
Neoplasia
Recognition of benign and malignant conditions
may be challenging.

Cytomorphologic Categories of Neoplasia

Category General Features Examples
Epithelial Clustered, tight arrangement of cells Transitional cell carcinoma,
lung tumors
Mesenchymal Individualized, spindle to oval cells Hemangiosarcoma, osteosarcoma
Round/Discrete Cell Individualized, round, discrete cells Lymphoma, transmissible
venereal tumor
Naked Nuclei Loosely adherent cells with free Thyroid tumors, paragangliomas
round nuclei
2006 World Congress WSAVA/FECAVA/CSAVA

SUGGESTED CYTOLOGY REFERENCES Radin MJ, Wellman ML, Interpretation of Canine

Baker R, Lumsden JH, Colour Atlas of Cytology
of the Dog and Cat, Mosby, St. Louis; 2000.
Cowell RL, Tyler RD, Meinkoth JH, Diagnostic
Cytology and Hematology of the Dog and Cat,
Mosby, St. Louis; 2nd Ed. 1999.
and Feline Cytology, Ralston Purina Company
Clinical Handbook Series. The Gloyd Group, Inc,
Wilmington, DE; 2001.
Raskin RE, Meyer DJ (eds), Atlas of Canine and Feline
Cytology, WB Saunders Co, Philadelphia; 2001.

653
Back to contents
 P
P - Cytology, Haematology & Clinical Pathology
CYTOLOGY OF INFLAMMATION
Dr. Alan H. Rebar
Senior Associate Vice President
for Research
Executive Director, Discovery
Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
General Principles of Cytologic Evaluation
It is the primary goal of the cytologist to define a
cytologic response as a normal cell population, a
malignant neoplastic population, an inflammatory
cell population, or a mixed cell population (both
inflammatory and neoplastic) (Figure 1). If the
reaction is inflammatory an attempt is made
to further classify the reaction as to type (for
example, neutrophilic versus macrophagic) and
to identify etiologic agents. The criteria used to
differentiate these various inflammatory cytologic
responses are described below.
Cytology of Inflammation (Table 1)
Inflammatory reactions are cytologic responses
in which inflammatory cells – neutrophils,
eosinophils, lymphocytes, monocytes or
macrophages – are the predominant cells
seen. Inflammatory reactions may be further
classified as neutrophilic, mixed, macrophagic or
granulomatous.
Neutrophilic Inflammation
In neutrophilic inflammation, neutrophils account
for 70% or more of all inflammatory cells. The
2006 World Congress WSAVA/FECAVA/CSAVA
remaining cells usually include varying numbers
of lymphocytes, eosinophils, and macrophages.
Neutrophilic inflammation may have either
non-degenerate or degenerate neutrophils. In
reactions without degeneration, the neutrophils
are unaltered (resemble those in the peripheral
blood) or exhibit only the aging change of nuclear
hypersegmentation. In contrast, in reactions
with degeneration, both neutrophil nuclei and
cytoplasm are abnormal. Nuclear changes are
those of cellular death – pyknosis, karyorrhexis
and karyolysis. Cytoplasmic changes include
basophilia and vacuolation.
Neutrophilic inflammation with degenerate
neutrophils reflects the action of toxins on
infiltrating neutrophils; it is almost invariably
associated with bacterial infections. Consequently,
whenever degenerate neutrophils are seen in
a cytologic specimen, a bacterial etiologic
654
Back to contents
Rose E. Raskin, DVM, PhD,
Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu
agent should also be sought. In contrast, acute
inflammation with non degenerate neutrophils
is usually associated with severe irritation of a
non-infectious nature. It should be emphasized
that this separation of neutrophilic inflammation
into subtypes is a generalization and therefore,
somewhat artificial; for example, nocardiosis is
characterized by neutrophilic inflammation with
degenerate neutrophils in areas immediately
adjacent to bacterial colonies and neutrophilic
response without degenerate neutrophils in areas
where no bacteria are seen.
Separating neutrophilic inflammatory responses
into degenerative and non-degenerative subtypes
may also be of prognostic value. This can be best
illustrated by considering the cytologic responses
encountered in peritoneal fluids associated with
intestinal vascular accidents such as volvulus or
intussusception. In these conditions, the principal
lesion is infarction of the intestinal wall. Early
in the course of the disease process, there is
severe irritation of the intestinal wall and an
acute irritative peritonitis results. Cytologically,
this is reflected as neutrophilic inflammation
with non-degenerate neutrophils. As the process
continues, however, the lesion becomes more
severe and life threatening. Stasis of gut contents
generally occurs in the infracted segment. This
is often accompanied by bacterial proliferation
and toxin production. Additionally, if infarction
of the intestinal wall is complete, necrosis of the
wall occurs and bacterial toxins and bacteria are
leaked into the peritoneal cavity causing acute
septic peritonitis. Cytologically, the response is
one of neutrophilic inflammation with degenerate
neutrophils. In the author’s experience the
prognosis for surgical correction at this point is
considerably more guarded than for the same
disease process at a point in time when only non-
degenerate neutrophils are observed.
Mixed Inflammation
Mixed inflammatory responses are defined
as those responses where 50-70% of the

inflammatory cells are neutrophils and the bulk of
the remaining inflammatory cells are monocytes
and macrophages. Such reactions reflect less
severe irritation than neutrophilic inflammatory
responses. They may represent a stage in the
resolution of a more acute lesion or simply a
tissue response to a less irritating etiologic agent
than pyogenic bacteria. Systemic mycotic agents
such as Histoplasma capsulatum or Blastomyctes
dermatitidis commonly elicit mixed inflammatory
responses. Since mixed inflammatory responses
virtually always reflect less severe irritation
than acute responses, they only rarely contain
degenerate neutrophils. (It is important to
recognize that the degenerate nature of an
inflammatory reaction is evaluated strictly on the
basis of neutrophil morphology – monocytes and
macrophage morphology are not considered.)
Macrophagic Inflammation
Macrophagic (histiocytic) inflammatory responses
are those in which over 50% of the inflammatory
cells are monocytes and macrophages. These
responses imply low-grade irritation and again
are commonly seen with systemic mycotic agents
or non-infectious foreign bodies. They may also
represent the resolution phase of a previously
more active reaction.
Granulomatous inflammation represents a
specific category of macrophagic inflammation
which is occasionally recognized cytologically.
Inflammatory giant cells and epithelioid cells
are the hallmark of granulomatous inflammation.
P
When granulomatous inflammation is observed,
an etiologic agent such as the systemic mycotic
agents or a foreign body can be almost certainly
identified.
Eosinophilic Inflammation
Eosinophilic exudates (inflammatory responses
containing large numbers of eosinophils)
represent special inflammatory responses and
merit specific consideration. Eosinophils are
occasionally seen in large number sin fine needle
aspirates from focal inflammatory skin lesions in
cats including feline rodent ulcers (eosinophilic
granulomas). Aspirates of lick granulomas in
dogs may also contain significant numbers of
eosinophils. Since mast cell neoplasms may also
contain large numbers of eosinophils, care must
be taken to distinguish these two conditions in the
dog. In horses, fine needle aspirates of cutaneous
parasitic lesions (cutaneous habronemiasis or
onchycercosis) often contain significant numbers
of eosinophils. Microfilariae are occasionally
seen in aspirates of onchycercosis.
The author has also seen several eosinophilic
exudates involving the pleural or peritoneal
cavities in horses and dogs. In dogs, these
eosinophilic exudates have been associated
with heartworm disease or disseminated mast
cell neoplasia. In horses exhibiting acute colic
secondary to verminous arteritis, eosinophilic
peritoneal exudates are commonly encountered. In
general, eosinophilic exudates are most prevalent
in parasitic infestations or allergic phenomena.

Table 1. Cytologic Classification of Inflammation

Inflammatory Cell Populations Morphologic Subtypes Possible Etiologies
Classes
Neutrophilic >70% neutrophils Non-degenerative-neutrophils Severe irritant
resemble those of peripheral
blood or feature
hypersegmented nuclei
2006 World Congress WSAVA/FECAVA/CSAVA
degenerate-neutrophils exhibit
karyolysis, pyknosis and
karyorrhexis; cytoplasmic pyogenic bacteria
basophilia and vacuolationeosin
ophilic-large numbers of
eosinophils parasites
Mixed 50-70% neutrophils, resolving acute response
30-50% monocytes
and macrophages irritant of intermediate
severity
Macrophagic >50% macrophages granulomatous-epithelioid cells resolving acute response
(Histiocytic)
cells and/or giant cells low grade irritant:
foreign body systemic
mycosis 655
Back to contents
 P

CYTOLOGIC SPECIMEN

Inflammatory cell populations Uniform non-inflammatory

populations

Complex responses
[Inflammatory cells + “other cell population(s)”]

Neutrophilic Macrophagic Benign reactive Malignant Normal Benign Malignant

hyperplasia neoplasia cells hyperplasia neoplasia
(or benign complicated anatomic or benign
Mixed neoplasia) by site neoplasia
complicated inflammation
by
inflammation

Figure 1. General approach to the interpretation of cytologic specimens.

Modified with permission from Current Veterinary Therapy VII, R.W. Kirk, Ed.,
W.B. Saunders, & Co., Philadelphia, PA 1980.
2006 World Congress WSAVA/FECAVA/CSAVA

656
Back to contents

P - Cytology, Haematology & Clinical Pathology
CYTOLOGY OF NEOPLASIA
Dr. Alan H. Rebar
Senior Associate Vice President
for Research
Executive Director, Discovery Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
Neoplastic processes may be either benign or
malignant. It is virtually impossible to differentiate
between benign neoplasias and hyperplasia
cytologically.
Malignant neoplastic processes are identified
through the recognition of specific malignant
criteria exhibited by the cell population under
consideration. Criteria of malignancy may
be loosely classified into four categories:
(1) General criteria of malignancy; (2) Nuclear
criteria of malignancy; (3) Cytoplasmic criteria
of malignancy; and (4) Structural criteria of
malignancy. These are summarized in Table 1.
General criteria of malignancy refer to the
appearance of the cell population as a whole.
Malignant neoplastic processes are generally
characterized as a uniform population of
pleomorphic cells; that is, cells usually appear
to be of a single cell type (for example, all mast
cells or all spindle-shaped connective tissue cells)
which exhibit variable cell size and variable
nuclear size. These features can generally be
recognized at low magnification and represent the
first suggestion that the cytologic diagnosis is one
of malignant neoplasia. While such pleomorphism
in a uniform population of cells is easy to
recognize in uncomplicated cases, the presence
of large numbers of inflammatory cells may mask
neoplasia. Therefore, whenever an inflammatory
response is associated with a population of non-
inflammatory cells, the non-inflammatory cells
should be carefully scrutinized for evidence of
malignancy. Inflammatory cells are commonly
encountered in large numbers in cytologic
preparations from oral or skin neoplasms with
ulcerated surfaces.
Nuclear criteria of malignancy are the most
important criteria employed in identifying a
malignant neoplasm cytologically. Evaluation
of nuclei of malignancy is best performed under
oil immersion. Features suggesting malignancy
(in Romanowsky stained preparations) include
multiple nucleoli, large irregularly shaped
Back to contents
P
Rose E. Raskin, DVM, PhD,
Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu
nucleoli, coarse chromatin patterns (areas within
the nucleus which stain intensely as well as
other areas which are virtually unstained or only
poorly stained), irregularities and indentations
in the nuclear membrane and variable nuclear/
cytoplasmic ratios among the cells seen. Mitotic
figures per se are not a criterion of malignancy as
they may be seen in hyperplastic cell populations
(e.g., lymph node hyperplasia); however,
abnormal mitoses(e.g., - three or more planes
of division) are a feature of malignancy. Multi-
nucleated tumor cells are occasionally seen,
but giant cells may also occur in inflammatory
reactions (granulomatous inflammation). Since
the nuclear criteria of malignancy are the most
important in establishing the diagnosis of
malignant neoplasia, the author suggests that 3-4
such nuclear alterations be identified before the
diagnosis of malignancy is suggested.
Cytoplasmic criteria of malignancy are
considerably less important in establishing a
diagnosis of malignant neoplasia but do provide
supportive evidence. Cytoplasmic criteria include
cytoplasmic basophilia, cytoplasmic vacuolation
and variation in amounts of cytoplasm.
Cytoplasmic features of malignancy suggest the 2006 World Congress WSAVA/FECAVA/CSAVA
primitive nature of the neoplastic population; for
example, cytoplasmic basophilia results from
a high cytoplasmic content of RNA, a constant
feature of young proliferating cells.
After the nuclear and cytoplasmic criteria of
malignancy have been used to establish the
cytologic diagnosis of malignant neoplasia, the
structural features of the neoplastic cells may
be evaluated in an attempt to further classify the
tumor as a carcinoma, sarcoma, or discrete cell
neoplasm. Carcinomas are neoplasms of epithelial
cell origin. Normal epithelial cells are generally
adherent to one another and this property is
generally reflected in cytologic preparations from
epithelial cell neoplasms. Carcinoma cells are
generally round to oval, and are arranged in sheets
and clusters. Cells from neoplasms of
657
 P
glandular epithelium (adenocarcinomas) are
often arranged in acinar patterns around a central
lumen. Adenocarcinoma cells also often contain
large vacuoles containing secretory product.
Sarcomas are neoplasms of cells of connective
tissue origin. Connective tissue cells generally
are embedded in a matrix which they themselves
secrete. Consequently, aspirates or imprints from
sarcomatous masses are generally less cellular
than cytologic preparations made from epithelial
or discrete cell neoplasms. Structurally, connective
tissue cells are usually spindle-shaped or flame-
shaped (cells with tails) and this morphology is
also typical of sarcomatous cells.
The sarcomas of veterinary significance include
osteosarcoma, fibrosarcoma, liposarcoma,
hemangiosarcoma, melanosarcoma and
chondrosarcoma. Osteosarcoma and
chondrosarcoma cells are more commonly
flame-shaped than spindle-shaped. In addition,
aspirates from these two neoplasms may contain
considerable matrix material – eosinophilic
osteoid in the case of osteosarcoma and
metachromatic (purple) chondroid in the case
of chondrosarcoma. The cytoplasmic margin
of osteosarcoma cells is often irregular and
vacuolated. Melanosarcoma has several
distinguishing cytologic features. Of principal
importance is the presence of brown to black
cytoplasmic granules (melanin) of variable size
and shape. In addition, melanosarcomas are often
comprised of cells of two shapes – spindle-shaped
and round to oval (epithelioid). Fibrosarcoma,
hemangiosarcoma, and liposarcoma may be
indistinguishable cytologically. All are comprised
of basically spindle-shaped cells. Aspirates from
hemangiosarcoma usually contain considerably
more blood than the other sarcomatous masses.
Liposarcoma cells may contain large lipid-filled
vacuoles which may be demonstrated with lipid
stains such as oil red O or the sudan stains.
Illustrations of the various sarcoma cells can be
found elsewhere.
The discrete cell neoplasms constitute a rather
large group of tumors of veterinary importance.
Included among the discrete cell neoplasms
are malignant lymphomas, mast cell tumors
histiocytomas and transmissible veneral tumors.
Structurally, discrete cell neoplasms are seen
cytologically as neoplasms comprised of
individual round or oval cells with no adherence
between cells and no ordered arrangement of cells
(such as cluster formation).

Table 2. Cytologic Criteria of Malignancy

Malignant Criteria Cytologic Features

General Uniform population of pleomorphic cells – can be assessed at low

magnification
Nuclear Abnormal mitoses
Variable nuclear size
Variable nuclear/cytoplasmic ratios
2006 World Congress WSAVA/FECAVA/CSAVA

Multiple nucleoli
Large irregularly shaped nucleoli
Coarse chromatin patterns
Irregular prominence of nuclear margin
Cytoplasmic Basophilia
Vacuolation
Structural Carcinoma – round to oval cells arranged in sheets of acinar patterns
Sarcoma – spindle shaped cells
Discrete cell tumor – individual round or oval cells

658
Back to contents

P - Cytology, Haematology & Clinical Pathology
CYTOLOGY OF EFFUSIONS
Dr. Alan H. Rebar
Senior Associate Vice President
for Research
Executive Director, Discovery Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
Accumulations of excessive fluid in the pleural,
peritoneal, or pericardial space represent edema
of these body cavities. As such, the dynamics of
fluid accumulation are governed by Starling’s law.
In general, pleural, peritoneal, and pericardial
effusions can result from either inflammatory
or non-inflammatory causes. Non-inflammatory
edema results from arterial pressure (a rare
cause in veterinary medicine), venous stasis,
hypoalbuminemia (reduces plasma oncotic
pressure), or lymphatic obstruction. Inflammation
causes fluid accumulation through vascular
damage and leakage.
Evaluation of abnormal fluid accumulation is
based upon integrated assessment of both physical
and cytologic characteristics.
Physical assessment of effusions includes
estimation of total solids (total protein) by
refractometry and determination of total
nucleated cell count with either an automated
particle or manual methods. On the basis of
physical characteristics, effusions are classified
as transudates, modifies transudates, or exudates.
As a general rule (there are exceptions which
will be discussed later), transudates are non-
inflammatory in origin while exudates are
the result of inflammation. Thus, physical
characteristics of effusions allow classification
according to pathophysiologic mechanism of
fluid accumulation but reveal little about specific
disease diagnosis.
Cytologic evaluation of effusions augments
physical evaluation by allowing the
diagnostician to identify specific etiologic
agents, to follow the progression of a disease
process, and to monitor response to therapy. The
decision of whether or not to culture effusion
fluid is based upon cytologic findings. Through
cytologic examination, inflammatory reactions
are classified as to type, hyperplastic responses
of the mesothelial lining can be identified, and
neoplasia is diagnosed.
Back to contents
P
Rose E. Raskin, DVM, PhD,
Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu
Cytologic Evaluation of Effusions
1) Normal Findings
Cells present in normal pleural, pericardial,
and peritoneal fluids include low numbers of
mesothelial cells and occasional inflammatory
cells. Mesothelial cells are present in small
clusters or as individuals. If knocked loose from
the cavity lining during the collection process,
mesothelial cells resemble squamous cells with
a low N/C ratio and abundant faintly basophilic
cytoplasm. Cells with this morphology have
historically been referred to as “pale” mesothelial
cells. Normal mesothelial cells which are present
in the fluid prior to collection have rounded up
and are quite basophilic (“dark” mesothelial
cells). They measure between 25 and 35µ in
diameter. Nuclei are centrally located, round,
and uniformly granular. Cytoplasm is abundant.
The most striking characteristic of these cells is
the presence of an eosinophilic peripheral brush
border or “skirt”.
The inflammatory cells present in normal fluids
have the morphology of normal peripheral
blood leukocytes. The predominant leukocyte
seen varies with the species. In dogs and horses, 2006 World Congress WSAVA/FECAVA/CSAVA
neutrophils are prevalent. In cats and cattle,
lymphocytes predominate.
2) Transudates and Modified Transudates
Cellular morphology in true transudates is similar
to that in normal fluid; as emphasized previously,
the principal alteration in transudation is increased
fluid volume. The principle cellular constituent of
the modified transudate (even the pseudochylous
effusion) is the reactive mesothelial cell.
Because of the ability of mesothelial cells
to respond to irritation by proliferation, the
presence of increased numbers of mesothelial
cell clusters and rafts is a common finding in
reactivity. Mitoses are increased and occasional
multinucleated reactive mesothelial cells are
659
 P
seen. Reactive mesothelial cells in clusters are
capable of imbibing lipid from the effusion fluid
and when they do, they take on the characteristics
of secretory cells. In this form they must be
differentiated from metastatic adenocarcinoma or
primary mesothelioma. This is done by critically
evaluating the cell populations for criteria of
malignancy.
Reactive mesothelial cells also may assume
a variety of other morphologies. Individual
mesothelial cells sloughed into effusions
gradually lose their brush border and may develop
phagocytic capabilities, accumulate intracellular
debris, and become indistinguishable from
macrophages.
As modified transudates mature, the proportion
of inflammatory cells they contain increases.
In most cases the principle inflammatory cell is
the non-degenerate neutrophil, but neutrophils
rarely account for more than 30% of the total cell
population.
3) Exudates
Inflammatory: Inflammatory effusions are
classified according to the standard rules for
inflammation as neutrophilic, mixed, or histiocytic.
In neutrophilic reactions, neutrophils (either non-
degenerate or degenerate) comprise >70% of the
inflammatory cells seen. Mixed reactions are
characterized by a mixture of neutrophils and
macrophages, and in histiocytic inflammation,
macrophages are the prevalent cell seen.
Inflammatory effusions are by their nature
irritative to the lining of involved body cavities.
Consequently, virtually all inflammatory
effusions are characterized by some degree of
reactive mesothelial cell hyperplasia. Because
of the tendency of reactive mesothelial cells
to cytologically merge with the monocyte/
macrophage continuum, they are considered to
be a part of the macrophagic component of any
2006 World Congress WSAVA/FECAVA/CSAVA
inflammatory effusion.
Most inflammatory effusions are cytologically
nonspecific in terms of etiologic diagnosis.
However, as with inflammatory responses
elsewhere, cytologic morphology provides
significant clues as to underlying cause.
Neutrophilic inflammatory effusions indicate
severe irritation. If neutrophils are degenerate,
then an effort should be made to identify bacterial
organisms within phagocytes. This is generally
easiest at the featheredge of the smear. If organisms
are not seen, the fluid should still be cultured.
Mixed inflammatory and macrophagic effusions
reflect less severe irritation and are found with
resolving neutrophilic effusions or in association
with less irritating etiologic agents than bacteria
(e.g., fungal organisms or foreign bodies).
660
Back to contents
Non-Inflammatory:
a) Chylous effusions: Chylous effusions are the
result of leakage of lymph into the body cavity
and may involve either the pleural or peritoneal
space. Most commonly, the thoracic cavity is
involved (chylothorax) as a result of trauma to the
thoracic duct.
Cytologically, chylous effusions are characterized by
the presence of large numbers of morphologically
normal small lymphocytes. Lesser numbers of
reactive lymphocytes are also present. Because
these fluids are mildly irritating, long-standing
chylous effusions also may contain moderate
numbers of reactive mesothelial cells and other
inflammatory cells. We have seen several cases
of chronic chylothorax where significant numbers
of eosinophils were seen. The presence of lipid
in the background of the slide, visualized as
small unsustained droplets at the periphery of the
nucleated cells, is variable.
It is important to note that in the cat, cardiac
disease results in pleural effusions which
are indistinguishable from chylothorax. The
mechanisms behind these effusions have not been
clarified; however, it is well established that heart
failure causes venous and lymphatic stasis with
increases pressure. In the cat it appears that these
circumstances predispose to lymphatic leakage
and result in a secondary chylous effusion.
b) Hemorrhagic effusions: True hemorrhagic
exudates can occur in any of the major body
cavities. Grossly, these effusions are red to
serosanguinous depending upon the age of the
exudate and the extent of the hemorrhage. Physical
evaluation reveals a protein level reflective of but
somewhat less than that of peripheral blood. Both
nucleated cell counts and red blood cell counts are
elevated.
Cytology is needed to differentiate true
hemorrhagic exudates from sample contamination
at the time of collection. Hemorrhagic exudates
contain predominantly red blood cells with lesser
numbers of nucleated cells. The most significant
indicator of true hemorrhage is the presence of
activated macrophages containing phagocytized
red cells (erythrophagocytosis) or hemosiderin.
These cells are best observed at the featheredge
of sediment smears. Erythrophagocytosis is not
seen if hemorrhage is strictly a collection artifact.
A second significant observation is whether or
not platelets are seen. True hemorrhagic exudates
are devoid of platelets but they are commonly
observed in contaminated samples.
c) Neoplastic effusions: Neoplastic processes,
both primary and metastatic, are relatively
common causes of both abdominal and thoracic
effusions in dogs and cats. They are less frequent
but still represent an important cause of effusion
in the horse.

Neoplastic effusions may be accompanied by
significant hemorrhage and/or inflammation but
generally they are non-inflammatory. Grossly,
the fluid may be clear to cloudy and hemorrhagic.
Total protein levels are elevated but nucleated cell
counts are highly variable.
In dogs and cats the common causes of neoplastic
effusions are thymic lymphosarcoma (pleural),
P - Cytology, Haematology & Clinical Pathology
CYTOLOGY OF LUMPS AND BUMPS
Rose E. Raskin, DVM,
PhD, Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu
Follicular Cyst
These cysts are found in a third to a half of the
nonneoplastic noninflammatory tumor-like
lesions removed in dogs and cats, respectively.
The cyst occurs most frequently in middle to
older aged dogs. They may be single or multiple,
firm to fluctuant, with a smooth, round, well
circumscribed appearance. These are often
located on the dorsum and extremities. The cyst
lining arises from well differentiated stratified
squamous epithelium often associated with
adnexal structures. Keratin bars, squames, or
other keratinocytes predominate on cytology.
Degradation of cells within the cyst may lead to the
formation of cholesterol crystals which appear as
negative stained, irregularly notched, rectangular
plates best seen against the amorphous basophilic
cellular debris of the background. The behavior
of these masses is benign, but rupture of the cyst
wall can induce localized pyogranulomatous
cellulitis with evidence of acute and/or chronic
hemorrhage. When this occurs, neutrophils and
macrophages may be frequent.
Mucocele or Sialocele
Duct rupture related to trauma or infection leads to
an accumulation of saliva within the subcutaneous
tissues. The presence of a fluctuant mass
Back to contents
P
and adenocarcinoma or carcinoma (either pleural
or peritoneal). In horses, squamous cell carcinoma
of the stomach (peritoneal) is by far the most
frequent cause, with lymphosarcoma occurring
only occasionally. Mesothelioma can be a rare
cause of effusion in any species.
Dr. Alan H. Rebar
Senior Associate Vice President
for Research
Executive Director, Discovery Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
containing clear to bloody fluid with string-like
features suggests a salivary gland duct rupture. The
cytologic specimen often stains uniformly purple
from the high protein content. The background
may contain scattered, pale basophilic, amorphous
material, consistent with saliva. The fluid is often
bloody with evidence of both acute and chronic
hemorrhage. Erythrophagocytosis is common
and occasional yellow rhomboid crystals may
be seen. These are termed hematoidin crystals
and are associated with chronic hemorrhage. The
nucleated cell population consists predominately 2006 World Congress WSAVA/FECAVA/CSAVA
of highly vacuolated macrophages displaying
active phagocytosis. Distinction between these
cells and secretory glandular tissue may be
difficult, especially when cells are individualized
and nonphagocytic. Nondegenerate neutrophils
are common.
Nodular Panniculitis/Steatitis
This condition may have an infectious or
noninfectious etiology. Causes of noninfectious
panniculitis include trauma, foreign bodies,
vaccination reactions, immune-mediated
conditions, drug reactions, pancreatic conditions,
nutritional deficiencies, and idiopathic. The
condition appears in the cat and dog as solitary or
multiple, firm to fluctuant, raised, well demarcated
661
 P
lesions. These may ooze an oily yellow-brown
fluid. Sites of prevalence involve the dorsal
trunk, neck, and proximal limbs. Cytologically,
nondegenerate neutrophils and macrophages
predominate against a vacuolated background
composed of adipose tissue. Small lymphocytes
and plasma may be numerous, especially in lesions
induced by vaccination reactions. Frequently,
macrophages present with abundant foamy
cytoplasm or as giant multinucleated forms.
When chronic, evidence of fibrosis is indicated by
the presence of plump fusiform cells with nuclear
immaturity. The fibrosis may be so extensive as
to suggest a mesenchymal neoplasm. Multiple
lesions are often associated with systemic disease
in young dogs. Dachshunds and poodles may be
predisposed to this form of the disease.
Dermatophytosis
The lesions vary from alopecia, broken hair
shafts, crusts, scales, and erythema to raised
nodules on the head, feet, and tail of dogs and cats.
Cytologic specimens reveal a pyogranulomatous
inflammation with degenerate neutrophils and
large epithelioid macrophages. Arthrospores and
hyphae are associated with hair shafts that are
best visualized using clearing agents with plucked
hairs. Arthrospores are occasionally present as
oval to round lightly basophilic structures having
a thin clear halo and measuring 2 x 2-3 um. They
may be seen extracellularly or within neutrophils
and macrophages and associated with hair or
keratin.
Squamous Cell Carcinoma
This is a common tumor occurring as solitary
or multiple proliferative or ulcerative masses.
It is most common on the limbs of dogs and
thinly haired areas of the pinnae or face of cats.
Cytologically, purulent inflammation often
accompanies immature or dysplastic squamous
2006 World Congress WSAVA/FECAVA/CSAVA
epithelium. Bacterial sepsis may occur if the
surface has eroded. Characteristic tadpole shape
and keratinized blue-green cytoplasm may be
helpful criteria in determining the cell of origin.
Squames and highly keratinized nucleated
squamous epithelium are frequent in well-
differentiated tumors corresponding to the keratin
pearls seen histologically. Cellular and nuclear
pleomorphism is marked. Perinuclear vacuolation
may be present. The neoplastic epithelium may
appear as individual cells or as adherent sheets of
cells.
Basal Cell Tumor
Found commonly in dogs and cats as typically
a single, firm, elevated, well demarcated round
intradermal mass that may be ulcerated or cystic.
662
Back to contents
Many tumors appear pigmented due to abundant
melanin. Tumors in cats may be cystic. They
are located mostly about the head with frequent
occurrence on the neck and limbs. Cytologically,
basal cells are small cells characterized by high
nuclear to cytoplasmic ratios, monomorphic
nuclei, and deeply basophilic cytoplasm. They
may be arranged as clusters or in row formation.
Perianal Gland Adenoma
The tumor may be single or multiple occurring
generally near the anus, but may also be found
on the tail, perineum, prepuce, thigh, and along
the dorsal or ventral midline. Initially they grossly
appear as smooth, raised round lesions which
become lobulated and ulcerated as they enlarge.
The tumor arises from modified sebaceous gland
epithelium. Cytologically, sheets of mature round
hepatoid cells predominate characterized by
abundant finely granular pinkish-blue cytoplasm.
Nuclei resemble those of normal hepatocytes
appearing round with an often single or multiple,
prominent, nucleolus. A low number of smaller
basophilic reserve cells having a high nuclear to
cytoplasmic ratio may also be present, but these
lack features of cellular pleomorphism.
Fibrosarcoma
In young cats this tumor may be caused by the
feline sarcoma virus and may be multiple. In
older dogs and cats, tumors are solitary with
a predilection for the limbs, trunk, and head.
They are poorly circumscribed and sometimes
ulcerated. Cytologically, fibrosarcoma consists of
abundant numbers of large plump cells occurring
individualized or in aggregates. Multinucleated
giant cells may be present occasionally. Nuclear
pleomorphism may be marked compared with
the benign counterpart. Cells are less uniform
and generally have high nuclear to cytoplasmic
ratios.
Canine Hemangiopericytoma
This is a common tumor generally considered to
affect dogs only. These are often solitary tumors
with a predilection for the joints of the limbs, but
are found commonly on the thorax and abdomen.
They are firm to soft, multilobulated, and often
well circumscribed. Cytologically, preparations
are moderately cellular. Plump spindle cells
may be individualized or arranged in bundles,
sometimes found adherent to the surface of
capillaries. Nuclei are ovoid, with one or more
prominent central nucleoli. Multinucleated cells
are occasionally seen. Associated with cells
may be a pink amorphous collagenous stroma.
The cytoplasm is basophilic and may contain
numerous small discrete vacuoles. Lymphoid

cells have been found in approximately 10% of
cases.
Lipoma
This is the most common connective tissue tumor
in dogs. The tumor may be single or multiple,
occurring mostly on the trunk and proximal limbs.
These are dome-shaped, well circumscribed, soft,
often freely moveable masses within the subcutis
which can grow slowly becoming quite large.
Cytologically, unstained slides appear wet with
glistening droplets that do not dry completely.
Lipid may be best demonstrated with water-
soluble new methylene blue and a fat stain
(oil-red-O). When stained with alcohol-based
Romanowsky stains, lipid is dissolved leaving
slides often void of cells. When present, intact
adipocytes have abundant clear cytoplasm with a
small compressed nucleus to one side of the cell.
Hemangiosarcoma
This is a malignant infiltrative mass of the dermis or
subcutis. Lesions are raised, poorly circumscribed,
ulcerated, and hemorrhagic. Cytologically, slide
preparations are of low cellularity with numerous
blood cells within the background. Evidence of
hemorrhage with hemosiderin-laden macrophages
may be present. Neoplastic cells are pleomorphic
ranging from large spindle to stellate. Cytoplasm
is basophilic, having indistinct cell borders and
occasional punctate vacuolation. Cells have
high nuclear to cytoplasmic ratios, oval nuclei
with coarse chromatin and prominent multiple
nucleoli.
Melanoma
This is a common tumor of dogs and an uncommon
tumor of cats. Older animals are usually affected
as are those with dark skin pigmentation. Gross
features differ for benign and malignant forms.
Benign tumors are mostly dark brown to black,
circumscribed, raised, dome-shaped masses
covered by smooth hairless skin. Malignant tumors
are variably pigmented, infiltrative, frequently
ulcerated and inflamed. Cytologically, cells are
pleomorphic ranging from epithelioid to fusiform,
or occasionally as discrete round cells. In well-
differentiated tumors, nuclei may be masked by
numerous fine black-green cytoplasmic granules.
Poorly differentiated tumors may contain few or no
cytoplasmic granules. Nuclei in benign forms are
small and uniform compared with characteristics
of anisocytosis, anisokaryosis, coarse chromatin,
and prominent nucleoli seen in the malignant
melanomas. Prognosis depends on tumor site
of origin and histologic characteristics. Benign
skin tumors frequently have a good prognosis.
Malignant forms arise more often from the nail
Back to contents
P
bed, lip and other oral mucocutaneous junctions
in dogs. The latter forms carry a guarded or poor
prognosis related to frequent recurrence and
metastasis.
Canine Histiocytoma
This is a very common benign rapidly growing
tumor of mostly young dogs. The tumor appears
as a small solitary, well circumscribed, dome-
shaped, red ulcerated, hairless mass. It occurs
commonly on the head, especially ear pinna,
as well as on the hindlimbs, feet, and trunk.
Cytologically, cells have round to indented nuclei
with fine chromatin and indistinct nucleoli. Cells
exhibit minimal anisocytosis and anisokaryosis.
The cytoplasm is abundant and clear to lightly
basophilic with indistinct cell borders. A variable
number of small well-differentiated lymphocytes
are common in regressing lesions.
Mast Cell Tumor
Tumors in dogs are generally solitary,
nonencapsulated and highly infiltrative into
dermis and subcutis. Mast cell tumors in cats
are usually solitary, well circumscribed, dermal
masses that occur on the head, neck, and limbs.
Multiple masses are common in young Siamese
cats. Mast cell tumors in cats are common also in
visceral organs, spleen, and liver. Cytologically,
tumor cells may vary in the degree of granularity
with some cells having numerous distinct
metachromatic stained granules while others
contain moderate numbers of granules or few to no
cytoplasmic granules. In less differentiated forms,
anisokaryosis, coarse chromatin, and prominent
nucleoli may be present along with a poorly
granulated cytoplasm. Giant binucleated cells are
more commonly found in poorly differentiated
forms. Eosinophils are more numerous in canine
tumors than feline tumors.
Plasmacytoma
2006 World Congress WSAVA/FECAVA/CSAVA
This tumor is infrequent in dogs and rare in
cats. They present as mostly solitary, well
circumscribed masses often on the digits, ears, and
mouth. Cytologically, aspirates are moderately to
markedly cellular. Individual cells have variable
amounts of basophilic cytoplasm in which borders
are discrete. Anisocytosis and anisokaryosis are
prominent features. Nuclei are round to oval with
fine to moderately coarse chromatin and indistinct
nucleoli. The nuclei are often eccentrically placed
and frequently binucleated. Multinucleated cells
may be present. Amorphous eosinophilic material,
representative of amyloid is seen in less than 10%
of plasmacytomas. Prognosis is generally good,
but local recurrences may be common.
663
 P
Cutaneous Lymphoma
The disease may occur primarily in the skin
or rarely as a manifestation of generalized
lymphoma. It is more common in older dogs
and cats. Lesions are solitary to multiple in the
form of nodules, plaques, ulcers, erythroderma,
or exfoliative dermatitis in the form of excessive
scaling. Pruritus may be common. Epitheliotropic
lymphoma is characterized by neoplastic T-
lymphocyte infiltrates of the epidermis and
adnexa. Focal collections of the neoplastic cells,
termed Pautrier microabscesses, are sometimes
formed within the epidermis. B- or T-lymphocytes
are presumed involved in the infiltration of the
dermis and subcutis with nonepitheliotropic
lymphomas. Lymphocytes range in size from
small to large with round, indented, or convoluted
nuclei. Nucleoli may be prominent. Cytoplasm
is scant to moderate and lightly basophilic.
Uniformity of the lymphoid population without
P - Cytology, Haematology & Clinical Pathology
CYTOLOGY OF INTERNAL ORGANS
Rose E. Raskin, DVM,
PhD, Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu
Commonly sampled internal organs include
the liver, spleen, and thyroid gland often by
ultrasound-guided biopsy. Artifacts commonly
encountered involve ultrasound gel that appears
2006 World Congress WSAVA/FECAVA/CSAVA
as particulate eosinophilic material similar to
stain precipitate.
Cytodiagnostic Groups for Liver Cytology
1. Normal epithelial cells
2. Cellular degeneration or injury
3. Hyperplasia or adenoma
4. Pigment abnormalities
5. Inflammation
6. Malignant neoplasia
7. Hematopoietic tissue
Normal Hepatic Tissue
• Hepatocytes consist of clumps or sheets of
large uniform cells. Cells are characterized
by low nuclear to cytoplasmic ratios, lightly
basophilic and granular cytoplasm, centrally
664
Back to contents
significant inflammation or plasma cell infiltration
is suggestive of cutaneous lymphoma. Prognosis
is poor as the disease rapidly progresses
necessitating euthanasia.
Suggested Cytology References
Baker R, Lumsden JH. Colour Atlas of Cytology
of the Dog and Cat: Mosby, St. Louis; 2000
Cowell RL, Tyler RD, Meinkoth JH. Diagnostic
Cytology and Hematology of the Dog and Cat:
Mosby, St. Louis; 2nd Ed. 1999
Radin MJ, Wellman ML. Interpretation of Canine
and Feline Cytology: Ralston Purina Company
Clinical Handbook Series. The Gloyd Group, Inc,
Wilmington, DE; 2001
Raskin RE, Meyer DJ (eds). Atlas of Canine and
Feline Cytology: WB Saunders Co, Philadelphia;
2001
Dr. Alan H. Rebar
Senior Associate Vice President
for Research
Executive Director, Discovery Park
Purdue University
Hovde Hall, Room 332
610 Purdue Mall
West Lafayette, IN 47907-2040
rebar@purdue.edu
placed round nucleus that has stippled chromatin
and a prominent nucleolus. Occasionally cells are
binucleated and nucleoli are multiple.
• Biliary epithelium consists of sheets of small
uniform cells with high nuclear to cytoplasmic
ratios. Large biliary ducts are lined by a simple
columnar epithelium. Nucleoli are often
indistinct.
• Mast cells and macrophages may be occasionally
found in low numbers.
Hepatocellular Degeneration or Injury
• Hydropic change (vacuolar degeneration)
produces a foamy appearance within the
cytoplasm of hepatocytes that is the result of
swelling of endoplasmic reticulum related to
increased intracellular water. This may be seen in
tissue anoxia and toxic hepatopathies.
• Fatty change appears as discrete clear vacuoles
within the hepatocyte cytoplasm that is the result
of accumulation of lipids that can freely coalesce.
This appearance is often diagnostic for lipidosis.

• Glycogen accumulation occurs with altered
glucose metabolism such as seen in steroid
hepatopathy. Cytoplasm appears foamy, similar
to hydropic change. Steroid induced change is
most notable in the dog, but occasionally has been
observed in the cat.
• Necrosis may occur as a result of toxicosis,
infectious disease, or neoplasia. Cells appear
indistinct, with loss of cellular detail.
• Fibrosis is related to increased connective
tissue reaction to damage, such as that seen in
cirrhosis, post-necrosis hepatopathy, or chronic
inflammation.
• Amyloid deposition is an uncommon condition
often related to a chronic inflammatory disease.
Presence of Congo red positive eosinophilic
amorphous material around hepatocytes is
diagnostic.
Hepatic Hyperplasia (Regeneration) or Adenoma
are grouped together since they have a similar
cytologic appearance.
• Frequent binucleation is noted within
hepatocytes.
• Increased nuclear to cytoplasmic ratio indicates
rapid growth.
• Mild to moderate anisocytosis and anisokaryosis
is present.
• Increased cytoplasmic basophilia may be noted
due to rapid growth.
• Increased frequency of intranuclear crystalline
inclusions.
• Conditions to consider include nodular
hyperplasia, toxic hepatopathy, hepatocellular
adenoma, bile duct adenoma, and cirrhosis.
Hepatic Pigment Abnormalities are observed
within hepatocytes appearing as shades of blue
and green with routine stains. The etiology of
these pigments may be differentiated by the
cytochemical reactions.
• Biliary stasis within canniculi appears as green
casts or granular material between hepatocytes.
Conditions associated with bile pigment changes
include cholangitis, liver flukes, lipidosis,
steroid hepatopathy, toxic hepatopathy, nodular
hyperplasia, and cirrhosis.
• Hemosiderosis is an overload condition in
which iron appears as blue or blue-green coarse
granular material that stains positive with
Prussian blue. Chronic hemolysis and excessive
iron supplementation are associated with
hemosiderosis.
• Lipofuscin appears as blue-green granules
on Wright-Giemsa stained preparations which
represent degenerated lipids resulting from
cellular aging.
• Copper accumulation appears blue-green
Back to contents
P
material which stains positive with rubeanic acid.
This may be a primary accumulation or secondary
related to liver disease.
Hepatitis/Cholangitis
• Neutrophilic (suppurative) inflammation is
associated with necrosis, bacterial infection, and
feline suppurative cholangiohepatitis. Degenerate
or nondegenerate neutrophils are increased over
that found in peripheral blood.
• Lymphocytic or plasmacytic (nonsuppurative)
inflammation is common in feline lymphocytic
cholangiohepatitis. Lymphoid cells are small,
well-differentiated forms associated with chronic
disease that may be difficult to distinguish on
cytology from a small cell lymphoma.
• Eosinophilic inflammation may be associated
with liver flukes or mast cell tumor occurring
within the liver.
• Pyogranulomatous inflammation consists of a
mixed population of neutrophils and macrophages.
This is associated with mycobacteriosis,
histoplasmosis, and toxoplasmosis.
Malignant Neoplasms of the Liver
• Primary tumors include: hepatocellular carcinoma,
bile duct carcinoma, and hemangiosarcoma
• Secondary tumors include: myeloid (nonlymphoid)
leukemias, intestinal carcinomas, and pancreatic
islet cell tumor
• Lymphoma and mast cell tumor may be primary
or secondary
Hematopoietic Tissue
• Extramedullary hematopoiesis resembles a
mixed bone marrow cell population including
erythroid, granulocytic, and megakaryocytic
precursors. It is often related to a physiologic
need, such as in bone marrow disease or hypoxic
conditions.
• Myelolipoma is an uncommon tumor resembling
extramedullary hematopoiesis, but also contains
2006 World Congress WSAVA/FECAVA/CSAVA
considerable lipid material. It is benign and often
localized.
SPLEEN
Cytodiagnostic Groups for Spleen Cytology
1. Normal tissue
2. Hyperplasia or reactivity
3. Inflammation
4. Malignant neoplasia
5. Hematopoietic tissue
Normal Splenic Tissue
• Sheets of normal mesothelium from the splenic
capsular surface are encountered with incisional
and excisional biopsies
• Small lymphocytes predominate with occasional
665
 P
medium and large lymphocytes present. A few
macrophages and plasma cells may be seen along
with rare neutrophils and mast cells. Macrophages
may contain small amounts of phagocytized
debris, compatible with hemosiderin.
• Small amounts of reticular tissue with
macrophages and stroma in an aggregated
fashion
Splenic hyperplasia or reactive spleen
• Small lymphocytes still predominate but there is
an increase in medium and large lymphocytes.
• Macrophages and plasma cells are commonly
observed. Associated with the macrophages
may be reticular stroma appearing as basophilic
fibrillar or spindle shaped elements.
• Hemosiderosis may be more noticeable with
large amounts of coarse dark granules.
• Increased numbers of mast cells and neutrophils
may be observed.
• Hyperplasia may result from antigenic reaction to
infectious agents or presence of blood parasites.
Splenitis
• An inflammatory response is likely associated
with splenic hyperplasia.
• Macrophages often increase in number to
systemic fungal infections e.g., histoplasmosis,
protozoal infections e.g., cytauxzoonosis, and
leishmaniasis.
Extramedullary hematopoiesis
• This was the most common cytologic abnormality
in one study accounting for 24% of the patients.
• While precursors from all three cell lines may
be observed, erythroid cells are the most common
with metarubricytes, rubricytes, and prorubricytes
present. Care must be taken as erythroid precursors
and lymphoid precursors appear very similar.
• Conditions associated with extramedullary
hematopoiesis include: chronic hemolytic
2006 World Congress WSAVA/FECAVA/CSAVA
anemias, myeloproliferative disorders, and
lymphoproliferative disorders.
Neoplasia (Primary or Metastatic)
• In myeloproliferative disorders, expect to find
immature hematopoietic cell types. Malignant
histiocytosis presents with bizarre and immature
macrophages, often with evidence of marked
erythrophagocytosis.
• Lymphoid neoplasia includes lymphoma and
plasmacytoma (extramedullary myeloma). A large
granular cell lymphoma arises primarily from the
spleen to infiltrate the blood but not typically the
bone marrow.
•Mast cell tumor may be primary or secondary.
• Hemangiosarcoma is a common primary or
666
Back to contents
metastatic neoplasm. Cells are large, individual,
spindle to stellate with indistinct cytoplasmic
borders. The cytoplasm is often vacuolated and
basophilic.
• Other mesenchymal neoplasms that occur in the
spleen include fibrosarcoma, leiomyosarcoma,
and myelolipoma.
THYROID
Thyroid tumor
Thyroid tumors occur most frequently in the
dog, cat, and horse and often present clinically as
a subcutaneous mass on the neck, lateral to the
trachea or near the thoracic inlet. Ectopic thyroid
tumors are occasionally found at the base of the
heart or base of the tongue. Approximately 90%
of the thyroid tumors identified clinically in the
dog are carcinomas. Aspirates from thyroid
carcinomas often contain a large amount of blood
contamination. The epithelial cell clusters appear
as free nuclei embedded in a background of pale
blue cytoplasm with infrequent appearance of
cytoplasmic membranes or borders. Sometimes
seen within the cytoplasm of epithelial cells is
dark blue to black pigment, which is thought
to represent tyrosine-containing granules.
Amorphous pink material representing colloid
may be associated with some clusters.
The nuclei of most endocrine tumors are round
to oval with minimal anaplastic or malignant
features and generally appear of uniform size.
Cytologically, benign and malignant thyroid
tumors appear similar. As most canine thyroid
tumors are malignant, metastasis is common
to the lungs. However, unlike the dog, the vast
majority of tumors in the cat are benign adenomas
or adenomatous hyperplasia.
Suggested Cytology References
Baker R, Lumsden JH. Colour Atlas of Cytology
of the Dog and Cat: Mosby, St. Louis; 2000
Cowell RL, Tyler RD, Meinkoth JH. Diagnostic
Cytology and Hematology of the Dog and Cat:
Mosby, St. Louis; 2nd Ed. 1999
Radin MJ, Wellman ML. Interpretation of Canine
and Feline Cytology: Ralston Purina Company
Clinical Handbook Series. The Gloyd Group, Inc,
Wilmington, DE; 2001
Raskin RE, Meyer DJ (eds). Atlas of Canine and
Feline Cytology: WB Saunders Co, Philadelphia;
2001
 P
P - Cytology, Haematology & Clinical Pathology
CHRONIC IDIOPATHIC MYELOFIBROSIS – DIAGNOSIS AND
TREATMENT
Rose E. Raskin, DVM,
PhD, Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu

INTRODUCTION an initiative through the American College of

Myeloid neoplasms have undergone a revision
in their classification that has been recently
published by the World Health Organization.1 The
reclassification not only involves morphologic
and cytochemical findings but in addition
includes genetic, immunophenotypic, prognostic,
and clinical features to define specific disorders. A
significant difference in this revised classification
is the number of blast cells used to define acute
myeloid leukemias which has been dropped from
30% to 20% based on prognostic information
in people.2 The nonlymphoid neoplasms occur
less frequently than lymphoid neoplasms but
are important to properly recognize and treat
accordingly. As a result of its clinical importance,
Table 1. Classification of Myeloid Neoplasms as Currently Recognized in Veterinary Medicine
Veterinary Pathologists is underway to evaluate
myeloid neoplasms and their relevance to the
revised human WHO classification.
Four major categories of myeloid neoplasms
are currently recognized in veterinary medicine,
similar to human medicine. (Table 1) The most
recognized category is that of acute myeloid
leukemias. The remaining three categories are:
myelodysplastic syndromes, myelodysplastic/
myeloproliferative diseases, and chronic
myeloproliferative diseases. Within the latter
category are disease entities that are encountered
infrequently and may be problematic to diagnose
since they are chronic with subtle abnormalities
or misdiagnosed as other myeloid neoplasms.

Types and Subtypes Morphologic Characteristics

Acute Myeloid Leukemias (AML) Blast cells >30% of all nucleated bone marrow cells (ANC)

Without maturation:
Acute myeloblastic leukemia Type I myeloblasts >90% ANC
With maturation: 2006 World Congress WSAVA/FECAVA/CSAVA
Types I-II myeloblasts >30% to <90% ANC

Myeloblasts & monoblasts >30% ANC

Acute myelomonocytic leukemia
Acute monocytic leukemia
Without maturation:
Monoblasts & promonocytes >80% nonerythroid cells (NEC)
With maturation:
Promonocytes & monocytes >30% to <80% NEC

Erythroid cells >50% of ANC (M:E < 1);

myeloblasts & monoblasts >30% of NEC
Acute erythroleukemia With erythroid predominance:
Erythroid cells >50% of ANC; rubriblasts, myeloblasts,
and monoblasts >30% of ANC

Megakaryoblasts (>30% of ANC)

Acute megakaryoblastic leukemia
667
Back to contents
 P

Myelodysplastic Syndromes (MDS) Myeloblasts <30% ANC; peripheral cytopenias and

MDS-Er (cats)
MDS-RA (cats/dogs)
MDS-EB (cats/dogs)
Myelodysplastic/Myeloproliferative
Chronic myelomonocytic leukemia
Chronic Myeloproliferative Diseases
dyshematopoiesis are common; may evolve into acute
myeloproliferative disorder
M:E < 1, myeloblasts <5% of ANC
M:E > 1, myeloblasts <5% of ANC
M:E > 1, myeloblasts >5% of ANC
Myeloblasts <30% ANC; hematodysplasia with features
of proliferative disease Diseases
Persistent monocytosis
Myeloblasts <30% ANC; also mild to moderate
hematodysplasia; may evolve into acute myeloproliferative
disorder

Chronic granulocytic leukemia Marked neutrophilia

Eosinophilic leukemia
Basophilic leukemia
Polycythemia vera
Essential thrombocythemia
Chronic idiopathic myelofibrosis
Marked eosinophilia
Marked basophilia
Erythropoietin-independent erythrocytosis
Thrombopoietin-independent thrombocytosis
Anemia with leukoerythroblastosis, extramedullary
hematopoiesis, splenomegaly, and marrow fibrosis

Definition and Synonyms Diagnosis

Chronic idiopathic myelofibrosis is a chronic
myeloproliferative disease that is often
accompanied with an intense fibroblastic reaction
of the bone marrow. It has several synonyms,
such as agnogenic myeloid metaplasia,
osteomyelosclerosis, and chronic megakaryocytic-
granulocytic myelosis. Myeloid metaplasia refers
to those cases in which neoplastic proliferation
occurs from predominately granulocytic and
megakaryocytic precursors, with or without
marrow fibrosis. Some cases were previously
misdiagnosed as acute megakaryoblastic
leukemia.
2006 World Congress WSAVA/FECAVA/CSAVA
Reported clinical signs associated with chronic
idiopathic myelofibrosis include a gradual onset
of lethargy, exercise intolerance, inappetence,
pale mucous membranes, vomiting, diarrhea,
fever, weight loss, and splenomegaly.3-5 A
nonregenerative anemia with poikilocytosis,
particularly dacryocytosis (tear-dropped shaped
erythrocytes) is present in blood smears.
Immature erythroid and granulocyte cells appear
in the peripheral blood permitting the first clue
in the diagnosis, a condition that is termed
leukoerythroblastosis. Dysplastic granulocytes
and platelets have been observed in the blood.
Leukocyte counts may be variable with leukocytosis

Pathogenesis or leucopenia. Basophilia is sometimes found.

This is a true stem cell disease with clonal
involvement of myeloid precursors including
erythroid, granulocytic, monocytic, and
megakaryocytic cells and recently both B and
T lymphoid cells have been demonstrated to be
clonally affected as well. The stromal bone marrow
reaction is considered to be reactive and cytokine
mediated. This is based on demonstration of
polyclonality in bone marrow fibroblasts in human
patients with chronic idiopathic myelofibrosis and
increased cellular and extracellular concentrations
of transforming growth factor-β (TGF-β), basic
fibroblast growth factor, platelet-derived growth
factor, and vascular endothelial growth factor. The
source of the cytokines is likely both monocytes
and megakaryocytes.
668
Back to contents
Both thrombocytosis and thrombocytopenia occur
in veterinary cases. Significant organomegaly of
the spleen and/or liver are commonly observed
related to intense extramedullary hematopoiesis.
Bone marrow histopathology is necessary to
support the diagnosis. Blast cell numbers are
less than 30% and have been reported to be less
than 20%. Intramedullary megakaryocytopoiesis
involving variably sized or polymorphic precursors
is commonly found associated with the fibroblastic
reaction. These dysplastic dwarf megakaryocytes
are usually present in clusters. The bone marrow
has various degrees of reticulin and collagen fiber
deposition as demonstrated by Gomori’s reticulin
(argyrophilic) and Masson’s trichrome stains of
histologic material. Evidence of marrow necrosis

may be noted. As a result of the connective tissue
deposition, aspiration for cytological examination
is frequently difficult, referred to as a dry tap.
Biologic Behavior
The abnormal and increased number of erythroid
and granulocytic precursors found in the blood
and bone marrow arises from intramedullary
and extramedullary hematopoiesis particularly
of the spleen and liver. Primary myelofibrosis in
this disorder involves the replacement of normal
hematopoietic tissue with increased numbers
of fibroblasts depositing fine reticulin and thick
collagen fibers, in response to cytokines released
locally by abnormal megakaryocytes and not
secondary to bone marrow damage. Pancytopenia
may occur as the disease progresses. In humans,
this condition may later evolve into other chronic
myeloproliferative diseases or acute myeloid
leukemia.
Differential Diagnosis
The main differential diagnosis for primary
myelofibrosis is secondary myelofibrosis
associated with bone marrow damage and necrosis
from conditions such as immune-mediated
anemia, marrow neoplasia (lymphoproliferative,
myeloproliferative, or metastatic), tumors outside
the bone marrow, congenital hemolytic anemia,
drug-induced marrow damage, ehrlichiosis, and
irradiation.
Back to contents
P
Treatment
Supportive therapy is often given in the form
of blood transfusions along with corticosteroids
when immune-mediated origin is suspected.
Prednisolone 2-3 mg/kg PO SID for 3-4 weeks,
then every other day with tapering of the dose
as the anemia resolves. Anabolic steroids may
be used e.g., nandrolone decanoate 2 mg/kg IM
weekly for 3 weeks, then once every 3 weeks.
Azathioprine at 2 mg/kg PO every other day is
given if the anemia does not respond to initial
treatments.
REFERENCES
1 Jaffe ES et al. World Health Organization
Classification of Tumours: Pathology and
Genetics of Tumours of Haematopoietic and
Lymphoid Tissues. Lyon, France: IARC Press;
2001, 15-107.
2 Vardiman JW et al. The World Health
Organization (WHO) classification of the myeloid
neoplasms. Blood. 2002; 100: 2292-2302
3 Weiss DJ and Smith SA. A retrospective study
of 19 cases of canine myelofibrosis. J Vet Intern
Med 2002; 16: 174-178.
4 Breuer W et al. Idiopathic myelofibrosis in a cat
and in three dogs. Comp Haematol Int 1999; 9:
17-24.
5 Khan et al. Idiopathic myelofibrosis (agnogenic
myeloid metaplasia) in a marmoset (Callithrix
jacchus): Hematologic and histopathologic
changes. Vet Pathol 1997; 34: 341-345.
2006 World Congress WSAVA/FECAVA/CSAVA
669
 P
P - Cytology, Haematology & Clinical Pathology
SUBCLASSIFICATION OF LYMPHOMAS USING SURFACE
MARKERS
Rose E. Raskin, DVM,
PhD, Diplomate ACVP
Professor of Veterinary Clinical
Pathology
Dept of Veterinary Pathobiology
Purdue University
School of Veterinary Medicine
725 Harrison Street
West Lafayette, IN 47907
rraskin@purdue.edu

Cellular morphology and cytochemistry are the
traditional methods to characterize and classify
hemolymphatic neoplasms. Lymphomas may be
subclassified as B or T cell type or distinguished
from nonlymphoid populations. Cellular
phenotyping in hematopoietic neoplasms has been
found to not only guide therapeutic decisions but
provide prognostic information in both human
and veterinary medicine.
Flow cytometry is a rapid, sensitive, quantitative
method of automated cell analysis. In the veterinary
clinical setting, flow cytometry is used primarily to
determine cellular phenotypes in hemolymphatic
disorders. Cellular phenotypes by flow cytometry
are determined by using monoclonal antibodies
tagged to fluorochromes directed against surface
molecules expressed on leukocytes. Another
technique to evaluate cell phenotype is the use
of immunocytochemistry that can be applied
to affected organ aspirates, impressions and
cytospin preparations. This is a routine protocol
performed at many academic and commercial
laboratories that involves application of a specific,
2006 World Congress WSAVA/FECAVA/CSAVA
monoclonal primary antibody often followed by
application of a biotinylated secondary antibody,
streptavidin-horseradish peroxidase binder and
aminoethylcarbazole or benzidine colorant. The
advantage of immunocytochemistry is the ability
to use routine diagnostic samples and see the
specific cells that are stained. Additionally, not all
antibodies can be applied to histologic specimens
so immunocytochemistry allows more in-depth
identification of cell types than is possible by
immunohistochemistry.
There are several antibodies available to
phenotypically characterize lymphomas or
lymphoid leukemias (Table 1). When applied
as a panel, multiple characteristics become
apparent which relate to the biologic nature of the
lymphocyte. Positive neoplastic cell staining for
any combination of CD21, BLA 36, CD 79alpha,
and immunoglobulins can be interpreted as B-
cell immunophenotype. Positive neoplastic cell
staining for any combination of CD3, CD3epsilon,
CD4, and CD8alpha can be interpreted as T-cell
immunophenotype.1

Table 1. List of antibodies for immunophenotyping in the dog and cat

Antigen Reactivity
CD1 Dendritic cells
CD3/CD3ε Mature T-cells
CD4 T helper cells
CD8α T cytotoxic or suppressor cells
CD18 Granulocytes, mononuclear phagocytes
CD21 Mature B-cells, follicular dendritic cells
CD45RA (dog only) B-cells, some T helper cells
CD79a B-cells
BLA36 B-cells

670
Back to contents

Classification of Lymphoma
Once the determination of immunophenotype is
made the information is correlated with anatomic
disease presentation plus the cytologic and
histologic characteristics of the lymphoid cells to
classify the condition into one of the categories
from the WHO scheme (Table 2)as described
P
in the 2001 WHO publication.2 Placement of
the condition into a disease category provides
prognostic information as well as understanding
about the biologic behavior of the disease. The
relevance of the WHO scheme has been examined
in a number of canine cases (Table 3) and found to
be clinically useful.3

Table 2. Recognized Subtypes for Canine Lymphoid Malignancies Using WHO Classification Scheme
B-Cell T-Cell
Precursor: Lymphoblastic leukemia/lymphoma Precursor: Lymphoblastic leukemia/lymphoma

Mature: Mature:
Lymphocytic lymphoma/CLL T-cell large granular leukemia/lymphoma
Mantle cell lymphoma Prolymphocytic
Marginal cell lymphoma types Adult T-cell leukemia
Follicular lymphoma Hepatosplenic T-cell lymphoma
Lymphoplasmacytic lymphoma Subcutaneous panniculitis-like
Plasmacytic forms: Mycosis fwungoides/Sezary syndrome
myeloma, plasmacytoma Peripheral T-cell lymphoma
Diffuse large cell Enteropathy-type T-cell lymphoma
Mediastinal (thymic) lymphoma Angioimmunoblastic T-cell lymphoma
Primary effusion lymphoma Anaplastic large cell lymphoma
Burkitt lymphoma/leukemia

Table 3. Median Survival Times from 49 Purdue Canine Cases

Classified by WHO Disease Entities with a or b Clinical Substage
Type Disease Entity Days
B Follicular 745
B LP/IgM Macroglobinemia 433
INDOLENT B DLBC a 352
(> 150 days) T Peripheral T a 201
T Prolymphocytic 159
Type Disease Entity Days
T LGL 95
B DLBC b 91 2006 World Congress WSAVA/FECAVA/CSAVA
AGGRESSIVE T Peripheral T b 81
(> 50 < 150 days) T Panniculitis-like 75
B Mediastinal 65
HIGHLY Type Disease Entity Days
AGGRESSIVE B B-LB 32
(< 50 days)

References Genetics of Tumours of Haematopoietic and

1. Wilkerson M J. Lineage differentiation of Lymphoid Tissues. Lyon, France: IARC Press,
canine hematopoietic disorders: Lessons from 2001;109-271
the human side, in Proceedings. 22nd Annu Meet 3. Raskin RE, Fox LE. Clinical relevance of
ACVIM Forum 2004; 625-627. the World Health Organization classification of
2. Jaffe ES et al. World Health Organization lymphoid neoplasms in dogs. Vet Pathol 2003;
Classification of Tumours: Pathology and 40: 5
671
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

R
R –R
Rep
Reproduction

Back to contents

INVITED LECTURES - FULL PAPERS
R – Reproduction
RECENT ADVANCES IN CANINE FEMALE REPRODUCTION
Prof. Stefano Romagnoli, DVM,
MS, PhD
Diplomate European College of
Animal Reproduction
Department of Veterinary Clinical
Sciences
University of Padova Agripolis
Legnaro 35020 (PD)
Italy
stefano.romagnoli@unipd.it
The reproductive cycle
Most bitches ovulate on day 12 of their season,
therefore there is a widespread tendency of owners
to assume that day 12 is the ideal breeding day
for all bitches. As a matter of fact, some bitches
ovulate early (such as on day 8, or 6 or even 4
from the onset of proestrus) while others may
ovulate as late as day 17, 19 or 22-24. One should
never assume that a given bitch will ovulate
on day 12 unless proven. Managing a canine
breeding requires the client taking the bitch to
the veterinary clinic as soon as the first signs of
proestrus are displayed (vulvar discharge, male
attractiveness) for a first check, and then coming
back every 2-3 days to monitor how quickly
the female is progressing towards ovulation
through vaginal smears and serum progesterone
assays. Vaginoscopy and ovarian ultrasound can
be very helpful clinical tools in identifying and
monitoring the ovulation process. When the first
day of ovulation is identified, there are still a few
days to achieve a breeding, thanks to longevity of
canine oocytes (4-6 days following ovulation).
Timing ovulation: Canine proestrus and oestrus
last on average 9 days each with ovulation taking
place 3 days after onset of oestrus (or day 12
after onset of proestrus). However ovulation
can occur as early as 5 days or as late as 27 after
onset of proestrus. Therefore, it is very important
to check the female’s behavior, perform vaginal
smears every 2-3 days starting on the first day of
proestrus in order to catch early ovulators, and
draw blood samples to measure progesterone
once behavior and/or vaginal smear indicate
oestrus. Oestrus is indicated by acceptance of the
male or by a degree of vaginal cornification of
>70%. Serum progesterone has a concentration
of (values are approximate) 2.0-3.0 ng/ml on
the day of the peak of luteinizing ormone (LH),
4.0-10.0 ng/ml on the day of ovulation, 10-25
ng/ml during the 2 days following ovulation,
Back to contents
R
which is when oocytes are reaching maturity in
the ampulae of the oviducts and fertilizations
are taking place. Ovarian structures can be
visualized with ultrasound using 5.0 to 7.5
sectorial MHz probes; follicular growth can be
followed and ovulation can be estimated based
on disappearance of the hypoechogenic areas
representing follicles (which become luteinized)
and on appereance of an hypoechogenic area at
the periphery of the ovary representing follicular
fluid accumulation within the ovarian bursa.
Performing vaginal citology as well as checking
the bitch´s behavior to look for onset of male
receptivity are the 2 most practical ways of
determining the best time for breeding. Owners
should be instructed to bring their bitch to a
male dog to check her behavior regularly as
soon as possible after proestrus onset as well
as to have a vaginal smear taken from the
veterinarian every 2-3 days. Breeding should
be performed as soon as the bitch stands and/or
as soon as her smear is fully cornified, in order
not to miss early ovulators. However, behavior
does not always correlate with vaginal citology: 2006 World Congress WSAVA/FECAVA/CSAVA
some bitches will not stand to be mounted even
though their smear is fully cornified. Provided
that vaginal abnormalities (strictures, bands of
tissue, hymen) are ruled out, serum P4 as well
as using different male dogs (to rule out male
preference) are helpful in such cases, although
some bitches become receptive to mating only in
mid to late oestrus. Ovulation should always be
timed using serum P4 assay every 2-3 days and
the bitch should be bred when a high P4 value is
observed (>5.0 ng/ml). Vaginal cytology should
also be used to confirm serum P4 data (serum P4
kits which use a semi-quantitative colorimetric
system are only 80% accurate) during and (most
importantly) after breeding until the first day of
cytological dioestrus (D1) is identified, which
occurs 6-8 days after ovulation.
673
 R
The Canine Pregnancy
Gestation length in the dog varies considerably
depending on whether it is calculated from a single
breeding (57-72 days), from an LH surge (64-66
days), from ovulation (62-64 days) or from the
onset of cytological dioestrus (D1 – 56-58 days).
The relative timing of the most important events
in the canine pregnancy is shown in Table n° 1.

Reproductive event Days from the LH peak Days from ovulation Days from D1
Onset of proestrus -25 to -3 variable variable
Vaginal cornification1 -1 to +7 -4 to +4 -10 to -2
Onset of oestrus -4 to +5 -7 to +2 -13 to -4
LH peak 0 -2 to –3 -8 to -9
Maximum fertility -1 to +6 -3 to +4 -3 to -10
Ovulation2 +2 to +3 0 -5 to -7
Fertilization +4 to +6 +2 to +4 -2 to -5
D1 +8 to +9 +5 to +7 0
Behavioral dioestrus +10 to +14 +7 to +11 +1 to +5
Zygotes enter uterus +11 to +12 +8 to +9 +2 to +3
Attachment +16 to +18 +13 to +15 +7 to +9
Ultrasound diagnosis possible +19 to +22 +16 to +19 +10 to +13
Abdominal palpation possible +20 to +25 +17 to +22 +11 to +16
Foetal heartbeats +22 to +25 +17 to +22 +11 to +16
Pregnancy anemia +25 to +30 +22 to +27 +16 to +21
Radiopaque foetal skeleton +44 to +46 +41 to +43 +35 to +37
Luteolysis and hypothermia +63 to +65 +60 to +62 +55 to +57
Parturition +64 to +66 +62 to +64 +56 to +58
Table n° 1 – Some of the most relevant reproductive event of the canine pregnancy timed as relative to the
LH peak, ovulation and onset of Cytological Dioestrus (D1). Adapted from Concannon and Lein (1989)

Events relative to the most important hormones
have been studies mostly in Beagles. Data on
other breeds are lacking and extrapolating results
from breed to breed may not necessarily be correct
at all times.
Implantation: Canine embryos enter the uterus
as zygotes or morulae around day 8-9 after
ovulation. For the first 1-2 days they move
2006 World Congress WSAVA/FECAVA/CSAVA
fibrinogen increase as soon as placentation starts,
due to the inflammatory reaction that takes place
at the endometrial level when the trophoblast
starts eroding it. Fibrinogen is produced by the
liver and is found at values of 100-150 mg/dl
in normal dogs, and rises to values of 250-300
mg/dl around day 25-28 post-ovulation. A value
of 300 mg/dl at 28 days is considered 100%

actively up and down the uterine horn in which
they arrived, and then for the remaining 2 days
they migrate to and from the opposite horn
mixing with the other embryos. Implantation
starts around day 13-15 after ovulation. The
canine placenta is endotheliochorial and zonary,
with blood accumulation and extravasation in the
marginal areas; blood components are observed
as green and brown borders of the placenta and
are thought to be important for foetal nutrition.
Because of the type of placentation, only 5-10%
of the total immunoglobulin provided by the
bitch is transferred through the endotheliochorial
placenta to the pup. Therefore, the majority of
passive immunity is derived through colostrum.
Acute phase proteins such as C-reactive proteins,
haptoglobin, acid glycoprotein, ceruloplasmin and
1
674 This is intended as “Maximum” vaginal cornification, or ≥ 50% of cheratinized cells on a vaginal
smear 2Primary oocytes Back to contents
accurate in diagnosing pregnancy in the bitch.
Haptoglobin and ceruloplasmin are bound to
iron and haemoglobin, respectively. Haptoglobin
is normally found at values of 35-50 mg/dl, and
in pregnant animals increases to values of 75-
100 mg/dl around day 18-20 after ovulation.
In healthy females, an increase in acute phase
proteins is considered a good indirect indicator of
implantation, and can be used in practice as an aid
in pregnancy diagnosis (or to rule out pregnancy).
Obviously, a pre-breeding sample must be drawn
to make the test accurate; also, a rise in acute phase
proteins could be due to a variety of other factors
associated to inflammatory reaction anywhere in
the organism, including endometrial inflammation
due to a pyometra.

Hormones of pregnancy
Maintenance of pregnancy in the bitch depends
on ovarian secretion of progesterone for the entire
length of gestation. The ovaries are the only
source of progesterone, as demonstrated by the
fact that abortion inevitably follows ovariectomy
at any stage of gestation. The canine feto-
placental unit has the possibility to metabolize
small amounts of exogenous progesterone, but
no progesterone-synthesizing activity has been
demonstrated. Corpora lutea secrete progesterone
based on stimuli provided for by the pituitary,
initially with Luteinising Hormone (LH), then
with LH and prolactin. Administration of anti-LH
compounds during the first half of pregnancy or
prolactin-lowering drugs during the second half
of pregnancy causes luteolysis and abortion.
The luteotrophic action of LH is present at all
stages of the canine gestation, even towards
the end of pregnancy when serum progesterone
concentrations start to decline. Such a decline is
probably due to luteolytic factors which override
the luteotrophic action of LH itself.
Prolactin increases during the second half
of dioestrus, after day 25 post-LH peak, and
reaches concentrations which are much higher
in pregnant than in non pregnant bitches.
Prolactin-lowering drugs such as cabergoline,
bromocriptine and metergoline cause a dose-
dependant decrease in serum prolactin as well
as progesterone concentrations. Serum LH does
not always decrease following treatment with
an antiprolactinic drug, therefore its mechanism
of action in supporting progesterone secretion
form the corpora lutea remains not totally clear.
Prolactin concentrations are low (<2.0 ng/ml)
during the second half of dioestrus in non-pregnant
bitches, perhaps increasing in those bitches
demonstrating clinical signs of pseudopregnancy.
Prolactin values tend to increase during the last
week of pregnancy to about 40 ng/ml, to reach
values of approximately 100 ng/ml during the
last 1-2 days prior to whelping, peaking at values
slightly above 100 ng/ml during the 1-2 days after
parturition. Prolactin increases in response to
suckling by pups.
In the bitch there is no regulatory effect of the
endometrium on luteal function as is known in
other species. Hysterectomized bitches cycle
normally and have normal luteal phases. In both
species prostaglandin F2a is secreted by the
endometrium, and its absence in hysterectomized
bitches does not have any effect on duration of
dioestrus. Prostaglandin F2a administered in
luteolythic doses will cause a decrease in serum
progesterone such as what happens prior to
parturition. Progesterone concentrations are
similar in pregnant and non-pregnant diestrous
Back to contents
R
bitches. Therefore, assaying progesterone
cannot be used as test for diagnosing pregnancy.
Differences in serum progesterone concentrations
between pregnant and non-pregnant beagle dogs
have been observed, although these are not
significant and therefore of no practical use. A
peak in serum progesterone concentration in the
bitch occurs around the 3rd week of pregnancy
to levels of 15-80 ng/ml, after which P4 levels
fluctuate between 10 and 20 ng/ml until the end
of pregnancy or until day 50-80 in non-pregnant
bitches. The relative amount of progesterone
secreted by pregnant bitches with a large litter has
never been compared to the amount secreted by
bitches with a small litter, although a difference is
likely to occur depending on the number of active
corpora lutea present. The number of corpora
lutea should be equal to the number of foetuses
except if foetal loss or embryo splitting (resulting
in birth of twins) occur. The lack of clinical data
on serum progesterone concentrations in pregnant
bitches of breeds other than the Beagles as well
as in middle age to older bitches makes it difficult
to manage cases of infertility, especially cases of
hypoluteoidism when exogenous progesterone
supplementation is necessary.
Relaxin is a key hormone of pregnancy both in the
bitch and queen, as it rises between the third and
fourth week of gestation, peaks at 4-6 ng/ml in the
bitch (6-8 ng/ml in the queen) 2-3 weeks prior to
parturition and remains at high levels throughout
the early puerperium. Relaxin is non-detectable
in males, in non pregnant females and during
stages other than pregnancy or the puerperium. It
remains high in pregnant bitches ovariectomized
and treated with progesterone, and is produced by
the uterus as it becomes rapidly undetectable after
hysterectomy. Relaxin concentrations may vary in
bitches of different breeds, as Labrador retrievers
were observed to have higher levels than Beagles.
Commercial kits for rapid determination of canine
relaxin as a pregnancy test have developed over
2006 World Congress WSAVA/FECAVA/CSAVA
the last decade, but have not been very successful
as the time at which pregnancy could be diagnosed
was not early enough to give an advantage over
the use of ultrasound. Still, if available a relaxin
kit can be of help to establish if foetal death and
resorption have occurred in a risk pregnancy.
Care of the pregnant female
Good pregnancy management starts before the
beginning of proestrus, at a time when vaccination
or immunization protocols should be checked
and updated. In proestrus health status should
be assessed with a clinical exam which should
include palpation of the mammary glands as
well as of the abdominal organs. In bitches with
a history of infertility a blood sample should be
675
 R
drawn to perform a complete blood count and
serum biochemistry in order to assess baseline
values of blood cells and serum proteins/enzymes.
Pregnancy status should be assessed during the
5th week in normal, healthy females, while it
should be anticipated to the 4th week in females
with a history of infertility, as progesterone
supplementation may be needed already at
implantation time. Also, if not pregnant a bitch
with a history of cystic endometrial hyperplasia
might be treated with prostaglandins or with a
progesterone antagonist to spare her uterus from
an excessive progestational stimulation. Pregnant
females should not be exposed to foreign animal
as they can be potential source of infection with
viruses against which the female may not be
immunized. A pregnant female displaying signs
of disease should be seen by a veterinarian as
soon as possible. If possible, anything that can
be performed at the animal’s premises such as
clinical exam, sample collection (feces, urine,
blood etc.) or remote miometrial monitoring
should be done there rather than bringing the
female to the veterinary clinic.
Pregnant bitches should do a moderate physical
exercise to maintain a good body condition and
muscle tone, which will help having a normal
parturition process. Vaccinations should be
avoided unless it is specifically requested by
the vaccination protocol that the injection be
done during pregnancy, such as with the Canine
Herpes Virus (CHV) vaccine, which should be
administered at the beginning of proestrus and
then again during the second month of pregnancy.
A good maintenance diet should be fed from week
1 through 5. The commonest mistake made by
owners at this time, whether they prepare home
made food or not, is overfeeding because they think
that increased food intake is necessary already
at an early stage of pregnancy. However, food
intake should not be increased during the initial
2006 World Congress WSAVA/FECAVA/CSAVA
stages of pregnancy only less than 1/3 of foetal
growth occurs during the first 2/3 of gestation.
Foetal size increases rapidly during the last 1/3
of pregnancy. Therefore, during the 6th week the
amount of food should be increased of about
30%. During the last 1-2 weeks of gestation the
female should be gradually switched to a growth/
lactation type diet, which should be maintained
also during lactation. Whenever litter size is large
(and especially in small size bitches), the enlarged
uterus will compress the stomach thus making
ingestion of large quantities of food difficult.
Therefore, a very concentrated food (>3.6 kcal/kg
food dry matter) should be used in small amounts
to be fed several times daily to compensate for
reduced stomach capacity. In pregnant bitches,
transient periods of reduced appetite may be
676
Back to contents
observed especially during or just before labor
stage 1 as well as during the expulsion phase.
Periods of anorexia earlier in pregnancy should be
looked at with caution especially if the pregnant
female stops eating completely for more than half
a day, as severe ketoacidosis leading to pregnancy
toxaemia can be induced experimentally in the
bitch by fasting. Periods of reduced food intake
are described in pregnant bitches around the 3rd
week of pregnancy, a time when implantation is
taking place.
In the bitch, calcium requirements increase in late
gestation and during lactation. However, such
increased requirements do not justify providing
extra amounts of calcium and vitamin D in the
diet, as this has been associated in other species
with a higher risk of developing hypocalcemia and
eclampsia during early lactation. Similar studies
have not been conducted in the bitch. Considering
the scarcity of data and the fact that bitches of
different breeds might have different requirements
in terms of mineral supplementation, there is no
need to add calcium or vitamin D especially if a
properly balanced diet is used. Also, in the bovine
a low blood pH has been associated with a reduced
ability of parathyroid hormone to stimulate bone
calcium release, and the use of blood acidifiers
such as dietary anions reduces the incidence of
milk fever. The relationship between blood pH
and bone metabolism has not been studied in the
bitch.
From day 54-55 on owners should be instructed
to measure rectal temperature on their bitches at
least 3 times daily and plot the temperature data
on graph paper. A clinical exam during the last
week of pregnancy, including an X-ray of the
abdomen, is advisable in bitches with a history of
dystocia, or if the owner is particularly anxious to
know about litter size in case it is her/his first time
in assisting parturition of a bitch or a queen.
Using drugs in pregnancy
The most delicate period of the canine pregnancy
is the first month during which organogenesis takes
place. Prior to day 20-22 following ovulation (when
implantantion occurs and placental development
starts) canine embryos are surrounded by “uterine
milk”, a protein endometrial secretion which
is in homeostatic equilibrium with the blood
compartment, i.e. any substance that arrives in the
bloodstream reaches the endometrium. Therefore,
use of any substance during this time carries the
potential risk of harming foetal development
even though there is no risk associated for the
mother. After placental development foetuses
become more resistant to toxic insults. Although
no real “placental barrier” exist, most substance
cannot reach the placental circulation unless they

are present in high concentration and for a long
time in the bloodstream. However, any drug that
reaches the foetal circulation must be metabolised
by the foetal kidney (in carnivores the foetal liver
is not metabolically active) which in itself might
threaten foetal survival. Aspirin, dexamethasone,
bromocriptine, carbaryl, estradiol benzoate and
cypionate, prostaglandin F2a a nd antiestrogen
R
drugs are widely described as capable of causing
embryonic/foetal death in the dog. The effect of
various drugs on the canine pregnancy is reported
in details by Papich (1989). Table n° 2 shows a
brief summary of drugs which have been either
tested in pregnant dogs and proven safe or used in
pregnant laboratory animals and pregnant women
without any side effect.

CATEGORY OF DRUGS ACTIVE PRINCIPLES SAFE FOR USE IN PREGNANT BITCHES

Antibiotics Ampicillin, amoxicillin, carbenicillin, cephalosporins, clindamycin,
cloxa- and dicloxacillin, hetacillin, lincomycin, neomycin, oxacillin,
penicillin G, ticarcillin
Antimicotics Miconazole (for topical use only)
Antiparasitics Diethylcarbamazine, fenbendazole, mebendazole, ivermectin,
piperazine, praziquantel, bunamidine, pyrantel, thenium
Anticancer drugs None
Anesthetics Lidocaine, naloxone
Gastrointestinal drugs Antacids, sucralfate
Cardiovascular drugs Digitalis
Anticonvulsivant drugs None
Muscle relaxants None
Endocrine drugs None
Table n° 2 – Drugs which have been either tested in pregnant dogs and cats and proven safe or used in
pregnant laboratory animals and pregnant women without any side effect.

Suggested Readings Concannon PW, Gimpel T, Newton L et

Abitbol MM – A simplified technique to produce al. – Postimplantation increase in plasma
toxaemia in the pregnant dog. Am J Obst Gynec fibrinogen concentration with increase in relaxin
139: 526-534, 1981 concentrations in pregnant dogs. Am J Vet Res
Bebiak DM, Lawler DF, Reutzel LF – Nutrition 57: 1382-1385, 1996
and management of the dog. Vet Clin North Am, Eckersall PD, Harvey MJA, Ferguson JM et al.
Small An Pract 17: 505-533, 1987 – Acute phase proteins in canine pregnancy. J
Chakraborty PK - Reproductive hormone Reprod Fert Suppl 47, 159-164, 1993
concentration during oestrus, pregnancy and England GCW, Allen WE – Studies on canine
pseudopregnancy in the Labrador bitch. pregnancy using B-mode ultrasound: diagnosis of 2006 World Congress WSAVA/FECAVA/CSAVA
Theriogenology 27: 827-840, 1987 early pregnancy and the number of conceptuses. J
Concannon PW, Hansel W, Visek WJ – The Small An Pract 31: 321-323, 1990
ovarian cycle of the bitch: plasma estrogen, LH Freak MJ - Practitioners’-breeders approach to
and progesterone. Biol Reprod 13: 112-121, 1975 canine parturition. Vet Rec 96: 303-308, 1975
Concannon PW, Powers ME, Holder W, Hansel Olson PN, Bowen RA, Behrendt MD et al.
W - Pregnancy and parturition in the bitch. Biol – Concentrations of progesterone and LH in
Reprod 16: 517-526, 1977 the serum of diestrous bitches before and after
Concannon PW, Butler WR, Hansel W, Knight hysterectomy. Am J Vet Res 45: 149-153,
PJ, Hamilton JM - Parturition and lactation in the 1984a
bitch: serum progesterone, cortisol and prolactin. Papich M - Effects of drugs on pregnancy. In:
Biol Reprod 19: 1113-1118, 1978 Current Veterinary Therapy X. Small Animal
Concannon PW, Lein DH – Hormonal and Practice. Edit RW Kirk, WB Saunders 1989, p
clinical correlates of ovarian cycles, ovulation, 1291
pseudopregnancy and pregnancy in dogs. Current Romagnoli S, Ometto T, Mollo A, Gelli D
Vet Therapy Small Anim Pract 10: 1269-1282, – Haptoglobin and ceruloplasmin as early
1989 indicators of implantation in the canine pregnancy. 677
Back to contents
 R
Proceedings Annual Congress British Small
Animal Veterinary Association, Birmingham,
April 2005
Shimizu T, Tsutsui T, Murao I et al. – Incidence
for transuterine migration of embryos in the dog.
Jpn J Vet Sci 52: 1273-1275, 1990
Sokolowsky J – The effects of ovariectomy on
pregnancy maintenance in the bitch. Lab Anim
Sci 21: 696-699, 1974
2006 World Congress WSAVA/FECAVA/CSAVA
Steinetz BG, Goldsmith LT, Lust G – Plasma
relaxin levels in pregnant and lactating dogs. Biol
Reprod 37: 719-725, 1987
Tsutsui T, Stewart DR – Determination of the
source of relaxin immunoreactivity during
pregnancy in the dog. J Vet Med Sci 53: 1025-
1029, 1991

678
Back to contents
 R
R – Reproduction
INFERTILITY IN THE BITCH
Alain Fontbonne DVM, MSc,
Dipl. ECAR,
Maître de Conférences
Reproduction Animale - Ecole
Nationale Vétérinaire d’Alfort
(Paris)
7 avenue du Général de Gaulle
94704 Maisons - Alfort Cedex
France
e-mail: afontbonne@vet-alfort.fr

In comparison to the last 10 or 20 years, Nowadays, numerous available techniques

veterinarians are now frequently requested to may be utilized to investigate the “optimal time
solve fertility problems in the dog, mainly due to for breeding”: vaginal cytology, endoscopic
the increased popularity of purebred dogs as well appearance of vaginal folds and progesterone
as for sentimental or financial reasons. In fact, assays are the most commonly used methods.
breeders may be concerned about different kinds Ovarian ultrasonography is especially indicated
of problems which include but are not limited to in infertile bitches, as it represents the most
true infertility (their bitches produce no pups after
mating or Artificial Insemination), anoestrus or a
low prolificity rate.
Many different problems can lead to infertility
including hormonal problems, infectious diseases,
congenital or acquired defects of the genital tract.
We recommend that veterinarians follow a very
strict progression, commencing with the most
frequent cause to the most uncommon cause. In
the bitch, things become even more difficult when
we realize that apparent infertility can be due to
very different situations which prove difficult to
distinguish, such as lack of fertilization (no union
between eggs and sperm) and early embryonic
death.

1. MISTIMED BREEDING
According to the vast majority of scientific
publications, mistimed breeding represents by far 2006 World Congress WSAVA/FECAVA/CSAVA
the most common cause of infertility in the bitch.
The incidence may vary between 40% to 80% of
infertile bitches.
Although the following belief has been clearly
proved erroneous in approximately 30% of
bitches, many breeders are still convinced that a
bitch will conceive when mated around the 12th
day of the heat period. Actually, it has been clearly
demonstrated that a bitch may ovulate as early as
the 3rd or 4th day after the onset of pro-oestrus and
as late as the 30th day of the heat period.
Clinical factors such as the increased swelling
of the vulva and the decreasing bleeding of the
genital tract at the time of the ovulation period
may help veterinarians determine if bitches are
obviously mated at a wrong time. But, these
criteria are in no way precise enough.
679
Back to contents
 accurate way to determine the precise date of
ovulation (see ultrasound ovarian scanning
below). This method also helps quantify the
number of growing follicules as well as follicules
undergoing ovulation and as such, it helps to
evaluate the fertility potential of the bitch.
2. MALE INFERTILITY
After mistimed breeding, male infertility is
the most common cause of conception failure
in bitches presented with infertility. This is
developed in the second lecture.
3. OTHER CAUSES OF INFERTILITY
As it is often ascertained in large animals, we
suggest that veterinarians should first consider
if infertile bitches show regular inter-oestrus
intervals or irregular ovarian cycles.
3.1. INFERTILITY WITH PROLONGED
INTERESTROUS INTERVALS
The apparent prolongation of interestrous
intervals occurs in dogs with a silent heat, defined
as ovarian activity in the absence of overt physical
and behavioral changes characteristic of canine
estrus.
Among the hormonal causes of anoestrus we
find hypothyroidism, hyperadrenocorticism,
hyperprolactinemia, or bitches treated with
hormonal compounds such as progestagens,
androgens (racing dogs) or anabolic steroid
compounds.
Ovarian cysts that secrete progesterone may cause
prolonged interestrous intervals. The surgical
removal of the cyst is often the best solution.
Hormonal attempts using prostaglandins are not
well documented in bitches.
Bitches housed in very bad environmental
conditions (including a high concentration of
animals, low luminosity, low quality foood) may
undergo prolonged interestrous intervals.
2006 World Congress WSAVA/FECAVA/CSAVA
3.2. INFERTILITY WITH SHORTENED
INTERESTROUS INTERVALS
This type of infertility may be divided into two
major causes: bitches suffering from ovarian
hyperstimulation (mainly follicular cysts or
Granulosa cells tumor), and/or bitches showing
a premature decline in progesterone during
diestrus.
3.2.1. Ovarian cysts or tumors
It is important to diagnose and remove these
hormonally active cysts or tumors as quickly
as possible for at least two reasons. First, it
is necessary to cure them and try to restore
fertility. Second, the secretion of high quantity
of estrogens may act on the uterus as a potential
680
Back to contents
factor towards the cystic endometrial hyperplasia
– pyometra complex, but also on the bone
marrow in creating progressive non regenerative
anemia.
Follicular cysts may be single or multiple;
if multiple cysts are present in one ovary, the
cysts do not communicate. The ovarian cysts
in the bitch may be present in only one or both
ovaries.
Estradiol assays during the pro-estrus period
may be useful for practitioners who do not
perform ultrasonography. The patterns of
estrogen secretion are often modified.
Still, when possible, it is much more valuable
to perform ovarian ultrasonography. Follicular
cysts appear as focal hypoechoic to anechoic
structures. Many authors consider that anechoic
structures greater than 1cm are supposed to be
cystic structures.
The treatment of choice of ovarian follicular
cysts is ovariectomy or ovario-hysterectomy
when the uterus is damaged. Some authors
recommend induction of luteinization of the
cystic follicles, using GnRH or hCG. We
personally do not recommend such protocols, as
they increase the progesterone plasma level after
a prolonged period of estrogen secretion. Based
upon our clinical experience, this treatment very
often leads to the occurrence of pyometra in the
following weeks.
Surgical removal of a cyst, or aspiration of a
cyst with a fine sterile needle under laparotomy
or ultrasonography may be new alternatives in
therapy.
Granulosa cells produce estrogens; and therefore,
it is not surprising that GCTumours often lead
to infertility with prolonged heat periods.
(Note: Exogenous estrogens administered to
elderly ladies receiving treatment after the end
of genital activity with estrogens containing
gels can penetrate through the skin of miniature
breeds when they are frequently handled on the
forearm and cause prolonged estrus signs).
Premature decline in progesterone
Split heats are defined as successive short
proestrus signs, at intervals of 2 weeks to
2 months, associated with short interestrus
intervals. This pattern is more often observed in
young bitches and leads to no real infertility in
the rest of the genital life of the bitch.
Anovulatory cycles are not frequent in bitches.
In such anovulatory cycles, serum progesterone
level never increases above 3.5 to 6 ng/ml. This
explains why the following heat period will
often occur earlier than usual.
Bitches may also suffer from hypoluteoidism,
which is the lack of progesterone secretion
during pregnancy which makes the pregnancy
impossible to maintain. Some breeds are
well known to express hypoluteoidism,
like Rottweilers and German Shepherds.
Progesterone supply can be given parentally
(progesterone in oil: 2 mg/kg every 3 days; ally-
trenbolone…). In France, veterinarians often use
oral micronised progesterone which is currently
given to women.
A “short anoestrus syndrom” has also
been described in Rottweilers and German
Shepherds.
Early embryonic or fetal death remains most
of the time impossible to detect, as no vulvar
swelling occurs in general. Possible causes
include endometritis, cystic endometrial
hyperplasia, embryonic defects and possibly
inbreeding. Our clinical data seem to show
that it is often associated with a decline in blood
progesterone concentration.
3.3. INFERTILITY WITH NORMAL
INTERESTROUS INTERVALS
3.3.1. HORMONAL PROBLEMS
Hormonal defects may be suspected also in
bitches with regular interestrous intervals, and
veterinarians should control the hormonal status
of the bitch during the heat period and also during
pregnancy.
3.3.2. INFECTIOUS DISEASES
Many infectious agents have been suspected to
induce infertility in bitches. However, a paucity
of studies has been conducted in this field.
Several viruses have been shown to play a
potential role in canine infertility. Canine
Herpes Virus (CHV) is well known to have
a pathogenic action on neonate pups. Several
elements suggest however that CHV may well
act on infertility in the bitch.
Tranplacental infection by Canine Distemper
Virus has been shown in experimental
conditions. Recently, some papers have pointed
out the potential incidence of a parvovirus
Minute Virus of Canines (CPV1) on resorption
during the first half of pregnancy.
The incidence of bacterial infections on
canine infertility is better documented. Canine
Brucellosis, which is well known as an
abortive agent during late pregnancy, could also
generate early embryonic or fetal death through
endometritis.
Other specific bacterial diseases have been
suspected to act on canine infertility. However,
usual genital bacteria may play a real role
on infertility. Canine Mycoplasms and
Ureaplasms are commonly isolated in the
Back to contents
genital tract of fertile and infertile bitches. But it
has been shown that there is a higher incidence
of these agents in the vagina of infertile bitches.
Many bacteria are commonly isolated from the
uterus and the vagina of normal fertile bitches.
Several studies barely demonstrate any
difference in the composition of the vaginal
flora between fertile and infertile bitches. But
it has been shown that in case of vaginitis,
there are significant qualitative and quantitative
variations. Strong evidence exists that bacteria
causing vaginitis may lead to infertility. It may
well have been underestimated due to lack of
specific clinical signs and due to the difficulty
of the clinical examination of the vagina of the
bitch.
The role of parasitic infections on infertility
is better documented. Recent experimental data
suggest that Neospora caninum could cause
early fetal death in the bitch.
3.3.3. DRUGS INDUCED INFERTILITY
In practice, many breeding bitches may be treated
with drugs that may contribute to the decline
of fertility. Steroid hormones and anti-fungic
compounds may create hormonal defects in pre-
puberal or adult bitches. Abortive drugs such as
prostaglandins, antiprogestins and antiprolactinic
substances have to be avoided during pregnancy.
3.3.4. ANATOMICAL ABNORMALITY OF
THE VULVA, VESTIBULE OR VAGINA
Some bitches do not manage to mate because of
congenital abnormalities of the posterior genital
tract (vulva, vestibule or vagina).
Acquired diseases or abnormalities of the
posterior genital tact (scars after a bad parturition,
episiotomy, violent mating…) may also lead to
the lack of copulation.
3.3.5. UTERINE PATHOLOGY
Endometritis is a common cause of infertility
2006 World Congress WSAVA/FECAVA/CSAVA
in mares. In bitches, however, it is hard to
diagnose. Endometrial smears, eventually
performed after endoscopic canulation of the
cervix, may be valuable.
Bitches with cystic endometrial hyperplasia
(CEH) are often infertile due to implantation
failure after conception. Somehow,
ultrasonography usually permits the
visualization of the glandular endometrium.
One succesful therapy has been described
with mibolerone oral administration, 30
microgrammes per 25 lb body weight daily
during 6 months.
CEH often leads to pyometra, which may be
treated in many cases by a mixed treatment
using prostaglandins and antiprogestins
681
 R
(aglepristone). A healing of the endometrium
seems to occur, as many bitches may have
successful pregnancies at their next heat
period.
3.3.6. ABNORMAL SEXUAL BEHAVIOR
Many psychological factors may influence sexual
receptivity in bitches. Some authors think that
psychology may influence factors like ovulation
or early embryonic death in the bitch.
3.3.7. MISCELLANEOUS CAUSES
Bitches with systemic diseases like diabetes
mellitus, hyperadrenocorticism or renal
insufficiency may likely be infertile.
Finally, breeders stress nutrition when their
breeding kennel suffers from decreased
reproductive results. Little is known in this
regard.
FURTHER READING
BJURSTROM L Aerobic bacteria occuring in
the vagina of bitches with reproductive disorders
Acta. Vet Scand. 1993, 34 (1), 29-34.
ENGLAND GCW and RUSSO M.
Ultrasonographic characteristics of ealy pregnancy
failure in bitches. 5th International Symposium
on Canine and Feline Reproduction. 4th to 6th
August 2004. Sao Paulo. Brazil.
FAYER-HOSKEN R, CAUDLE A. et al.:
2006 World Congress WSAVA/FECAVA/CSAVA
682
Back to contents
Evaluating the infertile breeding bitch, Veterinary
Medicine 1994, 1026-1038.
GUNZEL-APEL,AR, ZABEL S, BUNCK CF,
DIELEMAN SJ, EINSPANIER A and HOPPEN
HO: An investigation on the luteal phase and
pregnancy in normal and short cycling german
shepherd dogs. 5th International Symposium
on Canine and Feline Reproduction. 4th to 6th
August 2004. Sao Paulo. Brazil.
JOHNSTON S.D.: “Clinical approach to Infertility
in bitches with primary anestrus” Vet. Cl. North
Am. Small. An. Pract. 1991, 21(3), 421 – 425
JOHNSTON S.D., ROOT-KUSTRITZ M.V.
and OLSON P.N.S.: Canine and Feline
Theriogenology, WB Saunders Ed. Philadelphia
2001, 592 p.
LINDE-FORSBERG C and BOLSKE G: Canine
genital mycoplasms and ureaplasms. In Bonagura
and Kirk: Kirk’s Current Veterinary Therapy XII,
Small An. Pract., WB Saunders, Philadelphia
1995, 1090-1094.
WATTS JR, WHRIGHT PJ and WHITBEAR KC:
Uterine, cervical and vaginal microflora of the
normal bitch throughout the reproductive cycle J.
Small An. Pract., 1996, 37, 54-60.
WRIGHT P and WATTS JR “The infertile female”
in England and Harvey, BSAVA Manual of Small
Animal Reproduction and Neonatalogy, BSAVA
Ed. 1998

R – Reproduction
RECENT ADVANCES IN CANINE MALE REPRODUCTION
Alain Fontbonne DVM, MSc,
Dipl. ECAR,
Maître de Conférences
Reproduction Animale - Ecole
Nationale Vétérinaire d’Alfort
(Paris)
7 avenue du Général de Gaulle
94704 Maisons - Alfort Cedex
France
e-mail: afontbonne@vet-alfort.fr
Advances regarding different aspects of canine
male reproduction have been made in the past
5 to 10 years. This lecture will try to review the
most practical ones, in various fields of veterinary
andrology.
1. RECENT ADVANCES IN CONTROL OF
REPRODUCTION
1.1. Surgical control of reproduction
Early spaying has been studied in male dogs, and
also its effect on future health. However, in Europe,
veterinarians are often reluctant to perform such
early surgeries, although they bear no detrimental
effect.The normal and side-effects of vasectomy
in the dog have also been recently documented
(Ferreira de Souza 2006, Perez-Marin et al. 2006).
In the States, intratesticular or intra-epididymal
injections of zinc arginate have been proposed to
control male reproduction and avoid castration. Zinc
gluconate was also successfully studied recently in
the same purpose (Tepsumethanon et al. 2005).
1.2. Medical control of reproduction
The use of GnRH agonists has been studied by several
authors, as these molecules are commercialized
in some countries (Australia, New-Zealand,
USA…) and may well be soon put on the market
in Europe. GnRH agonists act by down-regulating
GnRH receptors in the pituitary, and they therefore
exert a suppressive action, leading to a reversible
“medical castration”, without any side effects.
Potential clinical application may be postponement
of puberty, reduction of aggressiveness, control of
fertility and control of prostatic diseases. It may also
be valuable in working dogs (like guide dogs for
blind or handicapped people) which could be used
without being castrated and therefore may be able
to mate bitches at the end of their working carrier.
Deslorelin has been the most studied GnRH agonist
drug in the male dog (see lecture from Pr. Stefano
Romagnoli).
A review of the non-surgical methods of
contraception and sterilization has just been
published by Kützler and Wood (2006).
Back to contents
R
2. RECENT ADVANCES IN PATHOLOGY OF
MALE REPRODUCTIVE ORGANS
2.1. New descriptions
Recently, a Granulosa cell tumour of the testis
was described in a spitz dog (Bontempo et al.
2005). The first case of a primary osteosarcoma
of the penis bone in a 13 years old mixed breed
dog was also reported (Bleier et al. 2003). A case
of an atresia of the preputial orifice in a 2 month-
old puppy, with subsequent fistulous tracts, was
described (Meilan 2066). In 2005, Niebauer et
al. suggested that relaxin of prostatic origin may
be a local factor involved in connective tissue
weakening and subsequently in perineal hernia
formation in old male dogs.
2.2. New ways of diagnosing male organic
pathology
Many studies have been published about the use of
ultrasound to diagnose prostatic problems. Atalan
et al (1999) have studied the accuracy of this
technique to estimate the volume and the weight
of the canine prostate. They showed that the best
ultrasound predictors were the prostate width and
length. Powe et al. (2004) found a strong accordance
between cytologic and histopathologic diagnoses
for prostatic conditions. Levy et al. (2006) recently 2006 World Congress WSAVA/FECAVA/CSAVA
showed that a prostate with a normal ultrasound
examination may be considered as not infected.
These authors also showed that, in case of a dog
suffering from a “prostatic syndrome”, a negative
urinalysis offers a good exclusion test of prostatic
infection. In case of a positive urinalysis, it is
recommended to further perform a bacteriological
identification after an ultrasound-guided biopsy
in order to confirm the infection. Root Kustritz
(2006) reviewed the indications, techniques,
possible side-effects and interpretation of tissue
and culture samples from the canine reproductive
tract, including prostatic tissue samples. Madrigal
et al (2006) also studied specific changes in the
proteinogram from dog semen prostatic fractions,
which may proved useful in a near future in the
683
 R
diagnosis of highly advanced prostate processes.
Some new approaches have also been made in the
diagnosis/treatment of prostatic diseases, like the
use of trans-urethral ultrasound (TUUS), which
could find potential applications in prostate cancer
diagnosis and staging, accurate measurement
of the prostate, image guided biopsy or even in
surgery of the prostate. Ultrasound also bears some
perspectives in the treatment of prostatic abcesses,
performing an ultrasound-guided drainage (+/-
a local or general antibiotic therapy) instead of
applying a heavier surgery like omentalisation.
Some authors have also studied the use of Doppler
system in male genital pathology. Günzel-Apel
et al. (2001) found significant changes in case
of begign prostatic hyperplasia or testicular
neoplasia. Agut (2004) found an increased blood
flow when using colour doppler in case of orchitis
and a reduced blood flow in case of testicular
torsion.The interests of computer tomography
has also lead to preliminary studies, for example
in diagnosing neoplasms and/or metastasis in case
of retained intra-abdominal testis. This technique
may also help to differentiate prostatic abcesses
(ring-effect after IV administration of contrast
medium) from cysts (no ring-effect). In case of
prostatic abcedation, it may also help to evaluate
extracapsular spreading of pus.
Masserdotti et al (2005) studied the cytologic
features of testicular tumours after fine needle
biopsies performed in 92 dogs. Cytology provided
a sensitivity of 95% for seminomas, 88% for
sertolinomas and 96% for Leydig cells tumours.
The specificity was 100% for all the tumours
types, thus showing that cytology is a very reliable
technique.
2.3. New treatments
When trying to reduce the volume of the
prostate, some trials using anti-estrogenic drugs,
such as clomifene and tamoxifene citrate, have
been attempted. However, they may also induce
2006 World Congress WSAVA/FECAVA/CSAVA
an estrogenic response, due to their partially
agonist effect. Potential applications in treatment
of prostatic diseases in dogs are currently
being studied by researchers. But they remain
experimental at the moment.
Lévy et al. (2006) have studied the aerobic
bacteria in the prostate of 45 dogs suffering from
infectious prostatitis and found that most bacteria
found showed a relatively low sensitivity to usual
anti-infectious agents often used in veterinary
medicine. In this study, overall bacterial sensitivity
was best towards marbofloxacin, cefquinom and
enrofloxacin.
New surgical treatments involving male genital
tract have been described. In France, a debate
about the use of orchidopexy in case of inguinally
located retained testis has occurred. New surgical
684
Back to contents
treatments of urethral prolapse in the dog has also
been published.
3. RECENT ADVANCES IN MALE INFERTILITY
Veterinarians are more and more often asked to
diagnose and solve fertility problems in male pure-
bred dogs. Still, in 2006, very little is known about
male infertility in the dog.
3.1. New discovery concerning the causes of
infertility
3.1.1. Prostatic problems
The prostate is the only accessory gland present in
the dog, as no seminal vesicles exist. A prostatic
problem often plays a direct role in decreasing
fertility. Chronic prostatitis has been shown to be
a rather common cause of infertility in dog. It is
often suspected when a dog brought for semen
collection for Artificial Insemination or freezing of
the semen suffers from haematospermia, especially
in the 3rd fraction of the ejaculate. In case of
haematospermia, when suspecting an infectious
prostatitis, Lévy et al.(2006) showed that bacterial
examination after an ultrasound-guided biopsy
seems the only reliable diagnosis technique, much
more than semen culture.
When treating prostatic problems in the dog,
the use of common anti-androgenic compounds
may definitively alter the quality of semen and
subsequent fertility. That is why many reports have
been made about the use of 5 α reductase inhibitors
(finasteride). Finasteride is a 4-azasteroid synthetic
drug that inhibits 5α-dihydroreductase, an
enzyme that is responsible for the metabolism of
testosterone to dihydrotestosterone in the prostate,
liver and skin.
Different regimes have been proposed :
- 1 mg/kg daily PO for 21 weeks. Treated dogs had
a marked decrease in prostate size 5–15 weeks after
treatment began. The prostate size was significantly
reduced (30% of the initial value) and fertility was
fully restored after a20-22 weeks recovery (Iguer-
Ouada 1997)
- reduced doses of 0.1 mg/kg or 0.5 mg/kg daily
PO for 16 weeks have proved to be effective (43%
reduction of the prostatic volume). Finasteride
treatment reduced the volume of the ejaculates
without affecting sperm number, sperm defects,
libido or fertility after Artificial Insemination
(Sirinarumitr et al. 2002).
Recently, some new anti-androgenic drugs
(osaterone acetate) seemed to decrease the
size of the canine prostate without altering
spermatogenesis and may be potentially used in
breeding dogs (Mimouni et al. 2006).
3.1.2. Retrograde ejaculation
Retrograde ejaculation consists of a retrograde
backflow of semen into the bladder when
ejaculation occurs. This leads to either aspermia

or oligospermia. In dogs, retrograde ejaculation
is not well documented. This problem does not
seem to be permanent. Treatment of retrograde
ejaculation has been better documented recently
(Romagnoli 2004, Beaufays et al 2004). Treatment
may be attempted by collecting semen when
the bladder is full (which makes the sphincter
close more firmly). Sympathomimetic drugs like
phenylpropanolamine (3 to 4 mg/kg per os twice
daily) or pseudoephedrine (4 to 5 mg/kg per os
three times daily or 1 to 3 hours before semen
collection or attempted breeding) may be tried.
3.1.3. Hormonal dysfunctions
Central hormonal causes are not well documented.
Testicular tumors which are responsible for
excessive hormonal secretion (Sertoli cells tumors,
Leydig cells tumors) may cause a decrease of
spermatogenesis, even when these tumors are
located only in one testicle and still quite small
in size. Hypothyroidism is often stated as a
potential cause of infertility. The link between
hypothyroidism and low quality semen is still
unclear and probably very much overestimated.
3.1.4. Infectious diseases
Infectious diseases probably represent a major
cause of infertility in male dogs living in breeding
kennels. Germs can cause prostatitis, which may
alter the biochemical composition of prostatic
fluids and may induce a permanent or temporary
blockage of the ducts as they enter the prostate. But
infections often lead to an orchitis/epididymitis,
with a subsequent alteration of the quality of the
semen. Canine Brucellosis infection in males have
been well described and any male dog suffering
from infertility with a bad spermogram should
be serologically tested for this disease. Recently
also, the interest of leukocytes quantification in the
ejaculate has been further studied (Martin 2005).
3.2. New diagnosis tools
Veterinarians should be aware that in many cases
of true azoospermia the size of testes remain
unchanged.
In case of azoospermia, it is recommended to
assay the alkaline phosphatase concentration in
seminal fluid. This concentration is much higher
in the epididymis than in the testes or prostate. A
normal intact dog with an incomplete ejaculation
usually shows a concentration of this enzyme in
seminal fluid at less than 5000 units/L, because
little epididymal fluid has been ejaculated. Male
dogs with true azoospermia, due to causes other
than bilateral blockage of the outflow tract usually
have concentrations over this level. In males with
bilateral obstructive azoospermia, the concentration
may be very low (sometimes as less than 10 units/L).
In the case of true azoospermia, ultrasonography
of testes may show tumors, or heterogeneous
Back to contents
R
testicular tissue, which makes the veterinarian often
believe that spermatogenesis is reduced and that the
seminiferous tubes are empty. Ponzio et al (2002)
have studied the interest of testicular ultrasound in
evaluating fertility in the dog. In wild canids, it was
shown that males with proven fertility had larger
testis, a greater diameter of mediastinum testis or a
parenchyma of higher echogenicity.
Testicular biopsy should be considered as among
the last attempts to know the exact state of decline
of the spermatogenesis. If some sperm cells (for
example, spermatids) remain present inside the
seminiferous tubes, the prognosis may not be
desperate. In some cases, karyotype could also be
evaluated.
3.3. New treatments
Aromatase inhibitors, such as formestane, exert an
anti-androgenic effect by inhibiting the conversion
of testosterone into estradiol 17 β. in peripheral
tissues. Recently some of these compounds (4-
androsten-4-ol-3,17-dione) have been successfully
used experimentally to improve spermatogenic
function in oligozoospermic and azoospermic dogs
(Kawakami 2003).
Intra-cytoplasmic sperm injection (ICSI) has been
poorly studied yet in the dog (Fulton et al. 1998).
4. RECENT ADVANCES IN SEMEN
PROCESSING
In the past few years, many papers have reviewed
the new techniques for a precise assessment
of canine semen quality and male fertility.
Rijsselaere et al (2004) showed that, in case of
haematospermia, the presence of up to 10% blood
is not detrimental for chilling canine semen at
+4°C, but is not recommended in case of semen
freezing.The recovery and freezing of epididymal
sperm has been successfully tried, which may be
performed in recently dead dogs (post-mortem
recovery). Hermansson & Linde-Forsberg (2002)
and Verstegen et al. (2002) have showed that
preliminary chilled semen at +4°C could further
2006 World Congress WSAVA/FECAVA/CSAVA
be succesfully frozen, thus making it possible for
veterinary practitioners to collect the semen and
send it to specialised semen banks, by overnight
express services, to have it frozen afterwards. The
same successful study was done by Ponglowhapan
et al. (2004) using epididymal sperm. Finally,
the improvement of fertility after A.I. by adding
prostatic fluid to respectively collected or
epididymal dog semen was studied by some
authors (Nöthling et al. 2005, Hori et al. 2005).
REFERENCES
An exhaustive list of related publications will be
given on demand.
685
 R
R – Reproduction
TWO COMMON CAUSES OF INFERTILITY IN THE MALE DOG
Prof. Stefano Romagnoli,DVM,
MS, PhD
Diplomate European College of
Animal Reproduction
Department of Veterinary Clinical
Sciences
University of Padova Agripolis
Legnaro 35020 (PD)
Italy
stefano.romagnoli@unipd.it
1. BENIGN PROSTATIC HYPERTROPHY
Benign prostatic hyperplasia (BPH) is the
most common canine prostatic disorder,
with almost 100% of intact dogs developing
histologic evidence of BPH with aging. BPH
is characterized by an increase in epithelial cell
numbers (hyperplasia) as well as an increase in
epithelial cell size (hypertrophy), but the increase
in cell number is more marked. It begins as
glandular hyperplasia in dogs as young as 2.5
years of age. Intraparenchymal fluid cysts may
develop in association with hyperplasia. Such
cysts are variable in size and contour, contain a
thin, clear to amber fluid and, if intraprenchymal,
may communicate with the urethra thus leading
to intermittent haemorrhagic or clear, light yellow
urethral discharge.
Etiology: Hyperplasia is probably due to an
altered androgen: estrogen ratio, and requires
the presence of the testes to start and continue
to develop. Dihydrotestosterone (DHT) within
the prostate gland probably serves as the
main hormonal mediator for hyperplasia. The
hyperplastic prostate is highly vascularized and
therefore the gland bleeds easily, which explains
the common clinical sign of blood from the tip of
2006 World Congress WSAVA/FECAVA/CSAVA
the penis or blood in the urine. Blood loss in the
prostatic urethra can be so intense that the ejaculate
may appear completely red. Although presence of
blood in the semen is typically considered to be a
cause for infertility, dogs with some blood in their
ejaculates may sometimes be fertile. The reason
for BPH being a common cause of infertility in
the dog is probably due to the alteration of the
biochemistry of the prostatic fluid whose important
action of nutrition of spermatozoa is decreased.
Prostatitis or abscessation are likely consequences
of presence of blood in the prostate.
Diagnosis: An enlarged, hypertrophic prostate
may cause blood dripping from the tip of penis, or
it may grow and expand in the rectal canal, causing
tenesmus and sometimes difficult defecation.
Other than the above signs, affected dogs are
686
Back to contents
usually normal and the prostate on palpation is non-
painful, symmetrically enlarged and with variable
consistency. Urine may contain blood (gross or
microscopic). If hyperplasia is accompanied by
urethral discharge, this is typically haemorrhagic
or clear but not purulent. Prostatic enlargement
may be visualized on abdominal radiography
as causing dorsal displacement of the colon and
cranial displacement of the bladder. On retrograde
urethrocystography the prostatic urethra may be
normal or narrowed and undulant with mucosal
irregularity, and the urethroprostatic reflux may
be normal or greater than normal. On ultrasound,
the prostate may appear diffusely hyperechoic
with parenchymal cavities (which means that
intraprenchymal cysts have developed). The
canine prostate is best evaluated in the sagittal and
transverse planes using 5.0 or preferably 7.5 MHz
scanners. An enema should be administered prior to
scanning to eliminate colonic contents which may
mimic peripheral prostatic disease. Conditions
such as cysts or abscesses are visualized easily.
Other less distinct but echogenically complex
areas may indicate neoplasia or areas of infection
within the gland. Although technically a definitive
diagnosis of BPH is only possible by biopsy, such
an invasive approach is not necessary to institute
a therapy if clinical signs are present, and from
a practical standpoint ultrasound assessment
of prostatic size and presence of cysts is often
the only thing that is necessary to identify the
problem and start dealing with it. No alteration
of haematological or biochemical parameters are
commonly observed in dogs with BPH.
Treatment: If the dog is asymptomatic owners
should be advised to watch for the development
of clinical signs in order to start treatment as
soon as possible. The most effective treatment
is castration, following which prostatic size may
decrease as much as 50% in 3 weeks and 70% over
9 weeks. As post-castration involution begins
within days of surgery, clinicians should palpate
the dog’s prostate 3 weeks post-operatively

to make sure the involution rate is normal thus
ruling out a more serious prostatic disease such
as neoplasia or abscessation. When castration
cannot be considered, drugs such as estrogens,
steroidal or non-steroidal antiandrogens or GnRH
agonists can be used. Estrogens act indirectly
by reducing androgen concentrations through
an inhibition of gonadotropin secretion/release
by the pituitary. Prostatic size is thus decreased
through a reduction of cellular mass. Size and
number of intraparenchymal cysts may not be
affected. Because of the potential risk of serious
bone marrow side effects (anemia, leukopenia,
thrombocytopenia, pancitopenia) as well as
because of the risk of growth of the fibromuscular
stroma of the prostate, metaplasia of the prostatic
glandular epithelium and secretory stasis resulting
in prostatic enlargement and predisposition to cyst
formation, bacterial infection and abscessation,
the clinical use of estrogens to treat prostatic
hyperplasia is currently not advised.
Steroidal Antiandrogens: Steroidal antiandrogens
compete with androgen receptors and perhaps
also with DHT receptors at the cellular level in
target organs. Compounds such as megestrol
acetate, medroxyprogesterone acetate,
delmadinone acetate, chlormadinone acetate
and ciproterone acetate are successfully used in
the dog, although for the majority of them there
is only a limited amount of experimental data
on their effectiveness in the dog. Their action
causes a sort of pharmacologic castration and is
rather precociously observed during treatment,
as improvement can be observed already after
7-15 days. Megestrol acetate can be used at the
dose of 2.2 mg/kg per os MID for a maximum
of 2 weeks, or at the dose of 0.55 mg/kg/day PO
for 4 weeks. Medroxyprogesterone acetate can be
used at the dose of 3-4 mg/kg SC every 10 weeks.
Chlormadinone acetate can be used at the dose of
1-2 mg/kg orally for 1 month, or as a subcutaneous
implant of 5.0 mg/kg which lasts for 12 months.
Recent studies done at the University of Pisa,
Italy, show a good clinical effect on cases of dogs
suffering from prostatic disease when treated with
ciproterone acetate at the daily dose of 0.5 mg/kg
per os. All steroidal antiandrogens should not be
used in breeding animals as their prolonged use
will remarkably decrease libido and fertility.
Non-Steroidal Antiandrogens – Non-steroidal
antiandrogens include finasteride and flutamide.
Finasteride inhibits 5-a-reductase (the enzyme
responsible for the final transformation of
testosterone into di-hydro-testosterone or DHT)
thereby lowering the concentration of DHT which
is the active metabolite at the level of target tissues,
without altering serum testosterone concentrations.
This leaves spermatozoa production undisturbed,
Back to contents
R
which makes finateride a good choice for breeders
(although a chronic use may be associated with a
decrease in ejaculate volume as well as decrase
in semen quality). Finasteride is only approved
for use in men, but it is well known to produce
a dose-dependent decrease in prostatic size also
in dogs. It can be used at the daily dose of 1.5
mg (approximately 1/3 of a 5.0 mg pill) for dogs
<15 kg body weight, 2.5 mg (approximately half
pill) for dogs of 15-30 kg body weight, and 5.0
mg for dogs of >30 kg body weight. Finasteride
is well tolerated and can be administered for
long periods of time. However, as soon as it is
discontinued the prostate will start growing
again. Flutamide is a human antiandrogen which
can cause a significant decrease in prostatic size
as detected by ultrasonography within 10 days.
When administered to research dogs at 5 mg/kg/
day PO for 1 year, it did not alter libido or sperm
production. In most countries flutamide is not
approved for use in veterinary medicine, although
it appears safe, effective and well tolerated in
dogs.
GnRH Agonists: A recent development in the field
of control of prostatic disease in dogs is the use of
agonists of GnRH disolved in a lipid base. GnRH
agonists act by down-regulating GnRH receptors
at the gonadotropes in the pituitary, thereby
suppressing the function of the hypothalamic-
pituitary-gonadal (HPG) axis. Their suppressing
action, generally devoid of side effects, is the
result of a continuous release provided by the
delivery system. Suppression of the HPG axis
leads to suppression of release of LH and FSH
with consequent lack of secretion of estrogens,
progesterone and testosterone as well as their by-
products. Such blockade of steroidogenesis can be
used in small animals for a variety of indications
including the reduction of prostatic size thereby
helping in the control of BPH. In experiments
performed in the dog, prostatic size decreases in
parallel with the decrease of testosterone following
2006 World Congress WSAVA/FECAVA/CSAVA
administration of a GnRH agonist. When adult
dogs are implanted with deslorelin at a dose of
0.5-1.0 mg/kg body weight, their prostatic volume
decreases more than 50% and serum testosterone
concentrations decreases 90% already from the
6th week of treatment when compared to controls.
Once treatment is discontinued, prostate returns to
approximate pre-implantation volume by week 48.
Therefore, use of GnRH agonists can effectively
help in the treatment of prostatic disease such as
benign prostatic hyperplasia.
2. AZOOSPERMIA
Azoospermia means ejaculation of seminal fluid
devoid of spermatozoa. Its incidence in the dog
is estimated to be around 35%. Dogs may fail
687
 R
to ejaculate the second, sperm-rich fraction if
they feel uneasy or apprehensive at the time of
semen collection and/or if there is no bitch in heat
present. In such cases only the pre-sperm fraction
is ejaculated, which is prostatic fluid. Some dogs
need to be trained to give semen through manual
stimulation, and this may require repeating the
procedure a few times in the presence of a bitch
in full heat. Before a diagnosis of azoospermia is
confirmed, semen collection should be repeated
(in a trained dog) at least 3-4 times over several
days. Whenever an azoospermic sample is
collected, carnitine or alkaline phosphatase (AP)
should be measured on seminal plasma. Both
compounds are secreted in the epididymis and
their concentration is high in normal semen. While
carnitine assay is not often easy to achieve, AP
can be measured using normal clinical chemistry
laboratory equipment. Normal dogs with semen
coming from the testicles have AP values >
5.000, while when an incomplete sample is
collected AP is < 5000 U/L but often even < 2000
U/L. Therefore, assaying AP is a good way to
distinguish on the source of the collected sample.
Seminal plasma AP is measured by laboratory
equipment routinely used to measure the enzyme
in serum. Seminal plasma samples must diluted
properly as AP concentrations is normally very
high (> 5.000 U/L, but often > 20.000 U/L)
and therefore gets out of the normal range for a
reference serum AP assay. Laboratory technicians
should be advised to centrifuge the semen sample
(some sophisticated equipments may be damaged
by spermatozoa) and also to dilute the centrifuged
sample as seminal plasma AP concentrations may
be as high as 40.000 IU/L, and the result of the
undiluted sample could be so high that might
be not readable. An azoospermic semen sample
with high AP comes from the testicles, while an
azoospermic sample with low AP may come from
the prostate (indicating incomplete ejaculation) or
2006 World Congress WSAVA/FECAVA/CSAVA
its source is however posterior to the epididymis
(indicating bilateral duct outflow blockage. When
AP concentrations are equivocal, two ejaculates
may be collected 1 hour apart and AP can be
assayed on the second one, which gives a higher
accuracy.
Azoospermia is more commonly diagnosed in
purebred adult (3-7 years of age) dogs, although it
may also occur in crossbreds. Azoospermic dogs
may have sired one or more litters previously.
In the few reports in the literature about this
condition in the dog, the Labrador breed seem to
be at a somewhat higher risk than other breeds.
Heritability is suspected as azoospermic related
Scottish terriers and Labrador retrievers have been
reported, with 2 male offsprings of an azoospermic
Labrador retriever becoming infertile between 2
688
Back to contents
and 7 years of age (while another male offspring
was fertile until the age of 12).
Etiology: Azoospermia may be due to pre-
testicular, testicular or post-testicular factors. Pre-
testicular factors include endocrine conditions
such as hypopituitarism, hypothyroidism, steroid
excess (Cushing syndrome or exogenous steroid
administration), or treatment with antineoplastic
drugs, inguinal or scrotal hernia. Prolonged fever
may also cause spermatogenic dysfunction,
although in humans fever is responsible for a
decline in semen quality but not for azoospermia.
Testicular causes of azoospermia include intersex,
germinal cell aplasia, bilateral cryptorchidism,
testicular injury due to trauma, irradiation,
thermal insult, orchitis, autoimmune testicular
disorders (such as spermatogenic arrest) and
testicular cancer.
The following intersex condition may cause
azoospermia: female pseudohermaphroditism
refers to individuals with male external genitalia
and female gonads, is rather uncommon and
is due to masculinization of female fetuses in
utero due to exogenous hormonal treatment of
the dam in pregnancy; 79,XXY characterized by
hypoplastic testicles, lack of spermatogenesis and
underdeveloped external genitalia; presence of
spermatozoa in the ejaculate of affected dogs is
poorly reported, but is thought to be rare as only
6% of humans with this conditions can be fertile;
XX sex reversal characterized by presence of
male external genitalia and testicular and/or
ovarian gonadal tissue in a dog with a 78,XX
karyotype, has been reported in Kerry blue
terriers, pugs, English cocker spaniels, Beagles,
Weimaraners and German shorthaired pointers;
affected dogs are sterile.
Germinal cell aplasia occurs in about 10%
of azoospermic dog and is characterized by
presence of only Sertoli cells. From the histologic
point of view germinal cell aplasia may be not
distinguishable from testicular atrophy unless
fibrotic changes are also present. Bilateral
cryptorchidism causes degeneration of the
germinal cell line without altering Sertoli and
Leydig cell function, which means that endocrine
function is normal in these dogs. Orchitis and/or
epididymitis may determine fibrotic changes of
the duct system causing stenosis which results
in oligozoospermia and frequently evolves
in azoospermia despite antibiotic treatment.
Autoimmune orchitis has also been associated
with azoospermia. Autoimmune orchitis in the
Beagle is reported to occur concomitantly with
autoimmune thyroiditis, as evidenced by a rise in
the concentration of serum thyroid autoantibodies
in these azoospermic individuals. Sertoli cell
tumor may cause azoospermia either by direct

destruction of testicular tissue, inflammation,
rise in intratesticular temperature and/or altered
estrogen:androgen ratio exerting a negative
feedback on the hypothalamic-pituitary axis.
Post-testicular diseases responsible for
azoospermia are those which cause outflow
obstruction such as spermatocele, sperm
granuloma or segmental aplasia of the epididymis.
Incidence of post-testicular causes of azoospermia
in humans is <1% while it is unknown in dogs.
Diagnosis: No specific clinical signs has been
associated with azoospermia in dogs: although
often smaller and softer than usual, testicles
of affected dogs may be normal in size and
consistency. Testicular degeneration and
softening of both testicles is reported in dogs after
bilateral vasectomy or bilateral ligation of the
cauda epididymis, which seems to suggest that an
altered consistency of testicular tissue may occur
in dogs with an outflow obstruction (obstructive
azoospermia). Libido is usually normal to
excellent in affected dogs.
Diagnosis of azoospermia needs to be confirmed
by repeating semen collection, and characterized
by localization and type of defect present.
Measurement of AP is of utmost importance in
confirming and characterizing the diagnosis, its
concentration being low in male dogs with bilateral
outflow obstruction. Epididymal abnormalities
may or may not be palpable or even visible
ultrasonographically. Fine needle aspiration of
the cauda epididymis may help rule out absence
of spermatogenesis but does not differentiate
between outflow obstruction and incomplete
ejaculation; since extravasation of spermatozoa
may lead to development of sperm granulomas,
less invasive techniques should be considered in
the initial diagnostic process. If an azoospermic
semen sample has high AP concentration, pre-
testicular and testicular causes should be carefully
investigated. The clinical approach includes a
complete physical examination, endocrine testing
(thyroid hormone testing ACTH measurement and
ACTH stimulation or dexamethasone suppression
test, as well as measurement of FSH and LH),
karyotype, culture of ejaculated seminal fluid for
aerobic and anaerobic bacteria and mycoplasma
cytology of the sediment of the seminal fluid
following centrifugation, testicular/epididymal
ultrasonography, and Brucella canis serology.
Serum LH and FSH are normal to slightly elevated
in dogs with gonadal failure. FSH concentrations
increase in dogs with testicular disease and
its rise correlates with degree of severity of
spermatogenetic alteration. As spermatogenesis
progressively decreases, testicles produce less
and less inhibin which results in higher and higher
concentration of FSH being released from the
Back to contents
R
pituitary. Both FSH and LH are released in pulses
from the pituitary, therefore their assay requires
frequent blood samplings (3 samples at 20-minute
intervals) or a GnRH stimulation test using 50-
100 mcg of GnRH IV and collection of a basal
(pre-GnRH) sample followed by a second sample
collected after one hour. Normal LH, FSH and
testosterone concentration in the adult dog post
GnRH stimulation are approximately 30 ng/ml,
60-300 ng/ml and 1-4 ng/ml, respectively.
Karyotype (normal male dogs have 78,XY)
should be performed in all dogs with a congenital
problem, e.g. those dogs who have never sired a
litter and/or with abnormal or immature external
genitalia. Definitive diagnosis of azoospermia
requires assessment of testicular function by
aspiration or biopsy of a tsticular specimen. Fine
needle aspirate is a good technique for confirming
presence of an outflow obstruction and ruling out
germinal cell aplasia, but in case of soft testes it
generally does not deliver enough cells to make
a diagnosis. Although more invasive techniques
will yield more adequate samples, cost, risk for
the animal (including anesthesia) and value of
the data obtained for treatment generally do not
justify using a core or incisional biopsy for an
azoospermic dog, especially if testicular volume
and consistency are greatly decreased. Testicular
histology in azoospermic dogs is highly variable,
with many dogs showing some evidence of normal
spermatogenesis (>50% of normal seminiferous
tubules). The fact that a certain percentage of
testicular parenchima appears to be normal is not
necessarily of good prognostic value. When a
bilateral outflow obstruction is diagnosed, often
this is a result of a chronic inflammatory disease
causing stenosis of the duct system at various
levels. In humans, bilateral outflow obstruction
is treated with 5-15 mg prednisone/day orally
(based on body weight) for one month, after which
semen collection is attempted; such treatment is
often successful although ductal patency is not
2006 World Congress WSAVA/FECAVA/CSAVA
permanently restored and outflow obstruction
frequently recurs after some time.
SUGGESTED READINGS
Barsanti JA et al – Effect of induced prostatic
infection on semen quality in the dog. Am J Vet
Res 47: 709-712, 1986
Barsanti JA, Finco DR - Medical management
of canine prostatic hyperplasia. In Bonagura
JD, Kirk W eds, Current Vet Therapy XII, WB
Saunders, 1995, pp 1033-1034
Freshman JL, Amann RP et al – Clinical evaluation
of infertility in dogs. Comp Cont Ed Pract Vet 10:
443-461, 1988
Iguer-Ouada M, Verstegen J – Effect of finasteride
689
 R
(Proscar MSD) on seminal composition, prostate
function and fertility in male dogs. J Reprod Fert
Suppl 51: 139-149, 1997
Johnston SD., Kamolpatana K., Root-Kustritz
MV., Johnston GR. Prostatic disorders in the dog.
Animal Reproduction Science, 60-61: 405-415,
2000.
Olson PN, Mulnix JA, Nett TM – Concentrations
of LH and FSH in the serum of sexually intact and
neutered dogs. Am J Vet Res 53: 762-766, 1992
Olson PN – Clinical approach for evaluatin dogs
with azoospermia or aspermia. Vet Clin North Am
21:591-608, 1991
Olson PN, Behrendt MD, Amann RP et al. –
Concentrations of carnitine in the seminal fluid of
normospermic, vasectomized and castrated dogs.
Am J Vet Res 48: 1211-1215, 1987
Frenette G, Dubé JY, Tremblay RR – Origin of
alkaline phosphatase of canine seminal plasma.
Arch Androl 16: 235-241, 1986
Ponglowhapan et al. – Prostatic volume during
deslorelin treatment in the dog. Atti EVSSAR
Congress, Milan 2001, p. 150
Romagnoli S, Concannon P W - Clinical Use of
Progestins in bitches and queens: a review. In:
Concannon P W; England G ; Verstegen J, Linde-
Forsberg C. (Eds). Recent Advances in Small
Animal Reproduction. International Veterinary
Information Service, Ithaca NY (www.ivis.org)
(Document number A1206.0903) 2003
Romagnoli S, Nassuato C, Stelletta C, Mollo
A, Gelli D, Lorenzon A – Serum Testosterone
concentrations and scrotal diameter in male dogs
treated with deslorelin implants. Congress of the
2006 World Congress WSAVA/FECAVA/CSAVA
690
Back to contents
European Veterinary Society of Small Animal
Reproduction, Amsterdam, April 2005, pp 27-28
Romagnoli S - Deslorelin in small animal
andrology. Proceedings Annual Congress
European Veterinary Society for Small Animal
Reproduction. Budapest, Hungary, 7-9 april 2006
(vol. 7) pp. 213-217).
Sirinarumitr K., Johnston SD., Root-Kustritz
MV., Johnston GR., Sarkar DK., Memon MA.
Effects of finasteride on size of the prostate gland
and semen quality in dogs with benign prostatic
hypertrophy. JAVMA, 218(8): 1275-1279, 2001.
Ticer JW – Canine infertility associated with
Pseudomona aeruginosa infection. JAVMA
146:720-722, 1965
Trigg TE, Doyle AG, Walsh J, Theeerawat S
– Advances in the use of the GnRH agonist
deslorelin in control of reproduction. 5th
International Symposium on Canine and Feline
reproduction. S. Paolo, Brazil 4-6 August 2004,
pp 49-51
Trigg TE, Wright PJ, Armour AF, Williamson PE,
Junaidi A, Martin GB, Doyle AG, Walsh J – Use
of a GnRH analogue implant to produce reversible
long-term suppression of reproductive function in
male and female domestic dogs. J Repro Fertil
Suppl 57, 255-261, 2001
Vare AM, Bansal PC – Changes in the canine
testis after bilateral vasectomy – experimental
study. Fert Steril 24: 793-797, 1973
Vare AM, Bansal PC – The effect of ligation of
the caudal epididymis on the dog testis. Fert Steril
25: 256-260, 1974

R – Reproduction
CANINE PYOMETRA: NEW APPROACHES TO AN OLD DISEASE
Susi Arnold, Prof. Dr. med. vet.,
DECAR
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
sarnold@vetclinics.unizh.ch
Madeleine Hubler, Dr. med. vet.,
DECAR
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
Definition
Canine pyometra is the accumulation of purulent
secretions in the uterine lumen of sexually intact
bitches, with an open (open pyometra) or closed
cervix (closed pyometra).
Incidence
Pyometra is a common disease. Nulliparous
bitches and bitches of more than 4 years of
age seem to be predisposed (1). In a colony of
Beagles, 15.2% of the bitches more than 4 years
of age were affected, whereas the mean age was
9.4 + 0.4 years at the time of clinical signs(2). A
Swedish study, based on Animal insurance data,
showed that 23.24% of all bitches developed
pyometra before the age of 10 years(3). Bernese
Mountain dog, Rottweiler, rough-haired Collie,
Cavalier King Charles Spaniel and Golden
Retriever are listed as predisposed breeds (3).
Aetiology
The exact aetiology of the pyometra is still
unknown. In the initial phase of the disease process
the stimulation of the uterus by endogenous or
exogenous gestagens over an extended period
seems to play an important role. A canine uterus
under the influence of progesterone is susceptible
to bacterial infections, as progesterone stimulates
the growth of the endometrial glands and their
secretory activity, along with cervical closure and
the suppression of myometrial contractions (4).
In addition, gestagens have an inhibitory effect
on the leucocytes in the uterus, adding support
to a bacterial infection(5). As progesterone is
already the dominant hormone during the oestrus
Back to contents
R
Iris Reichler, Dr. med. vet.
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
phase when the cervix is still open, there is at this
time an increased risk for an ascending bacterial
infection.
To now it has not being possible to induce a
pyometra by the application of oestrogen alone.
However, the subsequent effect of gestagen is
obviously enhanced by oestrogens. This explains
why mismated bitches treated with oestrogens,
for pregnancy prevention, have a significant
increased risk for pyometra.
Escherichia coli is the bacteria which is most often
isolated, in up to 90% of cases. Certain serotypes
are more often isolated and this is presumably
correlated with the presence of certain virulence
factors. One possible virulence factor is CNF
(cytotoxic necrotizing factor), as the production
of CNF is associated with extensive endothelial
damage and enhanced inflammatory reactions. 2006 World Congress WSAVA/FECAVA/CSAVA
Bacteriological genotype examinations indicate
that pyometra is most likely caused by E. coli
originating from the normal flora of the affected
bitch. That means, that a healthy bitch cannot be
infected by transmission of E. coli clones of an
affected bitch(3).
Diagnosis
Most bitches affected with pyometra are presented
during the luteal phase of the cycle. Predominant
clinical signs are purulent vaginal discharge in
case of open pyometra and polyuria / polydipsia.
Bitches suffering from a closed pyometra are often
presented at a later stage of the disease, when
endotoxins absorbed from the uterine lumen have
already resulted in a generalised illness. Affected
animals usually have en elevated WBC-count, in
691
 R
many cases they also have a prerenal acotemia,
hyperproteinemia and hyperglobulinemia.
The preferred methods in establishing the diagnosis
are ultrasonography and radiology. Caution: A
pregnancy of less than 40 days duration can be
misinterpreted as pyometra on a radiograph, but
not if an ultrasound examination is performed
Ovariohysterectomy
Elderly bitches
Non-breeding bitch
Presence of systemic disease
Closed cervix
Bitch is not predisposed to side effects
after spaying
Endometrial glandular cysts are demonstrated
ultrasonography
Conservative Therapy
For the medical treatment of pyometra varying
prostaglandins are mainly used. Over the last
few years an anti-progesterone is also available.
These can be used as a single treatment or in
combination. Additionally, a broad-spectrum
antibiotic treatment is recommended. In the
literature there are many different treatment
protocols. In the following section the proven
treatment applied at our clinic will be presented.
Conservative therapy during Anoestrus
If the last heat occurred more than 2.5 months
ago, the bitches are treated with Prostaglandin
F2α (PG F2α) at 20-30 µg/kg BW (Dinolytic®,
Upjohn) tid i.m. PG F2α promotes the opening of
the cervix and contractions of the myometrium.
Within the recommended dose rate side effects
are rarely observed and the duration of treatment,
2006 World Congress WSAVA/FECAVA/CSAVA
until the complete emptying of the uterus, is 5
– 8 days(6). At the same time a broad spectrum
antibiotic or chemotherapeutic is given per os for
3 weeks.
A week after beginning the therapy an ultrasound
examination of the uterus is recommended.
Conservative therapy during Metoestrus
If the bitch is presented within 2.5 months
after the last heat a combination therapy of the
progesterone antagonist,
Aglépristone and Prostaglandin F2α (PG
F2α),is recommended. Aglépristone blocks
the progesterone receptors and thus impedes
the adhesion of bacteria on the surface of the
endometrium. At the same time Aglépristone
causes the opening of the cervix. Aglépristone
(Alizine®, Virbac) is injected in a dosage of
692
Back to contents
Treatment
In principal, pyometra can be treated by surgical or
medical therapy. However, the decision depends
on several factors (see table).
Medical treatment
Younger bitch, intended for breeding
Bitch is in a good general condition
Open cervix
Bitch is predisposed for side effects after spaying
Absence of endometrial glandular cysts by
by ultrasonography
10 mg/kg KG s.c. 2 x 24 hours apart. One day
after the second injection Prostaglandin (PG
F2α) treatment is initiated at a dosage of 20-30
µg/kg BW PG F2α (Dinolytic®, Upjohn) tid.
i.m.. Additionally, a broad spectrum antibiotic
or chemotherapeutic is given per os for 3 weeks.
One week after the beginning of treatment a re-
examination of the uterus by ultrasonography
should be performed.
Prognosis
The risk of reoccurrence is relatively high. This
can be reduced by mating the bitch in the next
oestrus cycle.
References
1. Chastain CB, Panciera D, Waters C:
Associations between age, parity, hormonal
therapy and breed, and pyometra in Finnish dogs.
Small Anim Endocrinol 1999; 9: 8.
2. Fakuda S: Incidence of pyometra in colony-
raised beagle dogs. Exp Anim 2001; 50: 325-328.
3. Hagman R: New aspects of canine pyometra.
Doctoral thesis, Swedish University of
Agricultural Sciences, Uppsala, 2004.
4. Cox JE: Progestagens in bitches: a review. J
Small Anim Pract 1970; 11: 759-778.
5. Sugiura K, Nishikawa M, Ishiguro K et al.:
Effect of ovarian hormones on periodical changes
in immune resistance associated with estrous
cycle in the beagle bitch. Immunology 2004; 209:
619-627.
6. Arnold S, Hubler M, Casal, M et al.: Use of
low dose prostaglandin for the treatment of canine
pyometra. J Small Anim Pract 1988; 29: 303-308.

R – Reproduction
INFERTILITY AND INBREEDING: HOW VETERINARIANS SHOULD
TELL WHAT BREEDERS DO NOT WANT TO HEAR
Dr. Irene Sommerfeld-Stur
Department of Animal Breeding
and Reproduction
Institute of Animal Breeding and
Genetics
University of Veterinary
Medicine in Vinna
Veterinärplatz 1
1210 Vienna
Irene.Sommerfeld-Stur@vu-
wien.ac.at
Inbreeding seems to be something like a myth in
dog breeding. Whilst some of the breeders use
inbreeding or line breeding in a do-or-die-way to
improve the quality of their dogs as fast as possible
others avoid inbreeding as a matter of principle
believing that all genetic problems will be solved
by decreasing the inbreeding level alone.
Despite those somewhat emotional approaches
inbreeding – from the population geneticists
point of view – is nothing else than a breeding
system with advantages and disadvantages that
have to be considered. To have the chance to
efficiently deal with it, it seems necessary to be
informed about those genetic mechanisms that
cause the advantages of inbreeding as well as the
disadvantages.
When dealing with the association between
inbreeding and reproductive traits in dogs
therefore we have to answer some questions.
1. What does inbreeding mean: Inbreeding is
defined as mating of two individuals that are
closer related as two randomly chosen individuals
of the respective population. The degree of genetic
relation between two individuals depends on the
number and the position of common ancestors in
their pedigree and can be measured by calculating
the “coefficient of inbreeding” (COI) which was
established by Sewall Wright in 1922. The COI is
based on the calculation of combined probabilities
and expresses the expected percentage of identical
genes an individual inherits from one or more
common ancestors of its parents (FALCONER,
1984).
It has to be kept in mind that the COI only
represents a probability value that varies with
the number of generations considered when
calculating it. Moreover the COI is the same for
full sibs although they can strongly differ in their
individual degree of homozygosity.
Back to contents
R
2. What are the consequences of inbreeding: The
basic consequence is the increase of the percentage
of homozygote genloci. The practical consequences
depend on the quality and the function of those
genes that become homozygote. If these are genes
that are associated with desirable traits inbreeding
leads to improvement respectively fixation of
those traits in the population. If these are defect
genes that cause hereditary diseases inbreeding
leads to increased prevalence respectively
increased severity of those diseases. Furthermore
the increase of homozygosity has some unspecific
consequences. As the increase of homozygosity
is always associated with an increase in the gene
frequencies of those genes that become homozygote
more often, simultaneously the gene frequencies
of the allelic genes decrease and sometimes those
allelic genes disappear from the population. This
change in gene frequencies results in a loss of
genetic diversity on the population level as well
as on the individual’s level. It usually is associated
with an unspecific decrease of fitness also known
as “Inbreeding depression”. Fitness in the context
of population genetics is defined as the proportion 2006 World Congress WSAVA/FECAVA/CSAVA
the offspring of a single animal contributes to the
following generation. Fitness therefore includes
attributes of disease resistance and vitality as well
as attributes of reproductive performance. The
symptoms of inbreeding depression mainly are
caused by an impaired adaptability against harmful
environmental influences. Especially attributes
with low heritability and therefore high reactivity
against environment are prone to be influenced by
homozygosity.
There exist an almost innumerable number
of papers that deal with associations between
inbreeding and fitness in different species.
Although the actual influence of a defined
inbreeding level differs from population to
population due to the individual genetic burden of
the population, the individual selection pressure
693
 R
and the individual quality of the environment the
overall accepted position is that an increasing
level of homozygosity leads to decrease in fitness
(KRISTENSEN and SORENSEN, 2005).
3. What is an increase of the inbreeding level caused
by: There are four main factors that unavoidably
lead to an increase in the level of inbreeding and
therefore to an increase in homozygositiy:
• Genetic drift in small and genetically isolated
populations.
• Intentional inbreeding strategies by breeders that
focus on fast improvement of desirable traits.
• Intensive selection in favour of desirable traits
or against undesirable traits.
• Overuse of special sires (popular sires).
4. What has inbreeding depression to do with
insufficient reproduction: Failure in reproduction
principally can be due to problems in three
different biologic units: The father, the mother
and the offspring.
Regarding the above-cited effects of inbreeding
there can be different reasons of reproductive
problems when looking at those three biologic
units.
• Looking at the father: Reduced vitality and
motility of the sperms and reduced resistance of
the male against infections of the reproductive
tract can be effects of unspecific inbreeding
depression. Homozygosity of defect genes can
cause defects of sexual organs.
• Looking at the mother: Also in females
reduced resistance against infections can cause
reproductive failure. But also hormonal imbalances
due to unspecific inbreeding depression or defects
in genitals may have an impact on fertility.
• Looking at the offspring: Increased mortality
in all phases of the early life from fertilisation to
weaning can be due to homozygosity of defect
2006 World Congress WSAVA/FECAVA/CSAVA
genes as well as due to reduced resistance against
environmental influences.
5. What about inbreeding and fertility in dogs:
Although a lot of scientific evidence exists
concerning the association between inbreeding
and fertility in different species there is only little
scientific evidence available on that subject in
dogs.
• In 1982 WILDT et al. compared an inbred group
of Foxhounds with a not inbred group and found
lower conception rate, smaller litter size as well
as smaller number of sperms in the inbred group.
Motility of sperms and ejaculate volume as well
as volume of the testes also was different between
the two groups although failing the significance
limit.
694
Back to contents
• In 1987 SCHMIDT et al. investigated in the
association between COI and litter size in four
dog breeds. Only in one of those breeds, the Short
Haired Dachshund, the COI of the mother was
associated with the number of raised puppies. In
the other investigated breeds no such association
could be proved. But it seems remarkable that the
COI of the latter breeds was significantly lower
than that of the Short Haired Dachshund.
• DAHLBOM et al. (1997) investigated in fertility
parameters in male Irish Wolfhounds. Although
the Irish Wolfs frequently exhibited low libido,
small and soft testicles and poor semen quality
compared with control dogs of other breeds, no
association of that traits with the COI could be
established. Remarkably the overall COI of the
Irish Wolfhounds investigated was quite low.
• In a study in Boxers (BEEK et al., 1999) the
authors found an influence of inbreeding level
of the litter on puppy mortality especially due to
infections.
• A study in a recently created new breed, the
“Elo” (KAUFHOLD et al., 2005) proved an
influence of the COI of the mother and the COI of
the puppies on the mortality of the puppies up to
the time of weaning.
• In a study in Dachshunds (GRESKY et al., 2005)
the litter size and percentage of stillborn puppies
was influenced by the COI of the mother, of the
father and of the litter.
Despite that small amount of dog specific scientific
evidence on the association between fertility
and inbreeding the findings are quite consistent
at all. And due to the fact that the principal
effects of homozygositiy are not species specific
(KRISTENSEN and SORENSEN, 2005) one
can suppose that a high inbreeding level means
harm concerning fertility in dogs. Therefore an
important measure to prevent fertility problems in
dogs is the control of the inbreeding level.
6. How to control the inbreeding level of a population
The suitable methods of limiting the homozygositiy
level in practice are strongly associated with the
causative factors mentioned above.
• Increasing the effective population size:
From the population genetics point of view
most dog breeds seem to be strongly endangered
populations. Although it was claimed that a
minimum size of effective population of 50 is
enough to avoid inbreeding depression in the
short term (KRISTENSEN and SORENSEN,
2005) even this postulation seems unrealistic in
many of the dog breeds. Especially when looking
at European breeding populations that have
experienced a strong genetic bottleneck during
the first half of the 19th century the actual genetic
variance depends on the number of animals that
have passed that bottleneck rather than on the
actual number of breeding animals.

Increase of population size can be managed in
different ways:
• As the size of the effective breeding population
not only depends on the total number of dogs but
on the relative number of males and females as is
indicated in Table 1 the simplest way to increase
the size of the effective breeding population is to
use a greater number of males and to avoid the
overuse of single males. A further advantage of
that strategy is that the wide distribution of defect
genes a single sire could be burdened with can be
avoided.
• Immigration of breeding animals, usually of
sires from other populations of the same breed or
even from other breeds. Although in dog breeding
the use of dogs of other breeds usually is out of
question in some cases it may be the last hope for
the survival of a population.
Anyway one has to consider that each form
of immigration bares the risk of immigrating
undesirable genes as well.
• Considering genetic diversity of a breeding
population also when planning selection
strategies. This can be done by weighting selection
criteria due to their impact on the breeding goal
respectively on the health status. The classic
Table 1: effective population size(Ne) depending on the actual number of males(m) and females(f)
calculated by Ne=4*m*f/(m+f)(FALCONER,1984)
males/fem ales 5 10
1 3 4 4
5 10 13
10 13 20
50 18 33
100 19 36
References:
Beek, S. van den, Nielen A.L.J., Schukken,
Y.H., Brascamp, E.W. (1999): Evaluation of
genetic,common-litter and within-litter effects of
preweaning mortality in a birth cohort of puppies.
AJVR 60(9), 1106-1110.
Dahlbohm, M., Andersson, M., Juga, J., Alanko,
M. (1997): Fertility parameters in male Irish
wolfhounds: a two-year follow-up study. Journal
of Small Animal Practice 38, 547-550
Falconer, D.S. (1984): Einführung in die
quantitative Genetik. Eugen Ulmer, Stuttgart.
Gresky, C., Hamann, H., Distl, O. (2005): Einfluss
von Inzucht auf die Wurfgröße und den Anteil tot
geborener Welpen beim Dackel. Berl. Münch.
Tierärztl. Wschr. 118, 3/4, 134-139
Kaufhold, J., Hamann, H., Distl, O. (2005):
Back to contents
R
method of calculating a selection index is the best
suitable way.
• Considering the genetic relation between mating
partners
• Calculating the COI of the prospective offspring
when planning a special mating. This can be done
manually or by using one of the available software.
When using software one have to keep in mind
that the actual value of the COI depends on the
number of generations included and therefore
can show quite different sizes in the same animal
when calculated in different ways.
Although some geneticists claim defined limits of
COI that should not be exceeded in my opinion
this makes little sense at all as the consequences
of inbreeding rather depend on the actual genetic
situation of the respective population as on the
value of the COI. The strategy therefore should
focus on the choice of that matings that result in
a preferably low COI but also regarding other
desirable and undesirable aspects of the planned
mating.
• Actual research in molecular genetics possibly
will result in methods to plan matings by
heterozygosity of molecular markers.
20 50 100
4 4
16 18 19
27 33 36
57 100 133
67 133 200
Populationsgenetische Aspekte der neu 2006 World Congress WSAVA/FECAVA/CSAVA
gezüchteten Hunderasse Elo. Berl. Münch.
Tierärztl. Wschr. 118, 1/2, 67-75
Kristensen,T.K., Sorensen, A.C. (2005):
Inbreeding – lessons from animal breeding,
evolutionary biology and conservation genetics.
Animal Science 80, 121-133
Schmidt, A., Müller, S., Stur, I.(1987):
Untersuchung über den Zusammenhang zwischen
Inzuchtgrad und Wurfgröße bei verschiedenen
Hunderassen. Zeitschrift für wissenschaftliche
Kynologie 26
Wildt, D.E., Baas, P.K., Chakraborty, P.K., Wolfle,
T.L., Stewart, A.P. (1982): Influence of inbreeding
on reproductive performance, ejaculate quality
and testicular volume in the dog. Theriogenology
17(4), 445-452
695
 R
R – Reproduction
RECENT ADVANCES IN FELINE REPRODUCTION
Prof. Stefano Romagnoli,DVM,
MS, PhD
Diplomate European College of Animal Reproduction
Department of Veterinary Clinical Sciences
University of Padova Agripolis
Legnaro 35020 (PD)
Italy
stefano.romagnoli@unipd.it
The Reproductive cycle
The cat is a seasonally polyestrous species and a
long photoperiod breeder. Anoestrus is induced
by decreasing hours of daylight. Artificial light
may influence seasonality and in fact cats who
live permanently indoor often do not show any
seasonal cyclicity. A minimum of 10 hours of light
is required for queens to cycle, and using a short
photoperiod (8 hrs of light) can be used to suppress
oestrus in queens. The feline reproductive cycle
is divided into proestrus, oestrus, postoestrus,
dioestrus and anoestrus. Proestrus is indicated
by continuous rubbing of the head and neck
against any object, some vocalizing but refusal
of mating, and it is reported to be very short and
often not observed. It lasts an average of 1.2+0.8
days. Oestrus behaviour in the queen, as in other
mammals, is indicative of receptivity to mating,
and is characterized by signs which are similar to
those of proestrus but more intense, more frequent
vocalizing, crouching with the forequarters
pressed to the ground and hyperextension of the
back which causes lordosis, so that the vulva is
presented for mating. Unlike canine oestrus
which begins with decreasing serum estradiol
concentrations, oestrus in the queen occurs at peak
2006 World Congress WSAVA/FECAVA/CSAVA
follicular activity. Vaginal epithelial cornification
occurs in the queen as in the bitch, although in
felines the sudden decrease in superficial cells
at the end of oestrus is not observed. Although
useful, vaginal cytology does not have as many
clinical applications in the queen as in the bitch.
The term Postoestrus has been used to indicate the
stage which follows one oestrus and precede the
next in queens which did not ovulate. The term
metoestrus is sometime used, but may be a source
of confusion as it generally refers to a phase of
corpus luteum development which does not occur
in non-ovulating queens. Queens that ovulate
show evidence of corpus luteum development,
therefore going through a normal Dioestrus
whose length varies depending on occurrence
of conception. Dioestrus lasts approximately 40
696
Back to contents
days in non-pregnant queens. An interoestrus
interval of 35-45 days in the queen is generally
indicative of occurrence of ovulation, suggesting
development of corpora lutea and progesterone
secretion whether or not breeding occurred.
Following luteolysis, cyclicity resumes with a 7-
10 days delay both in pregnant and non-pregnant
females, although lactation and suckling may
inhibit resumption of cyclicity for 2-3 weeks post-
weaning. Queens exposed to natural photoperiod
undergo Anoestrus, a phase of reproductive
quiescence, during late Fall and early Winter
(October-December).
Breeding management: Feline ovulation is
induced by LH released from the pituitary in
response to a neural reflex originating from the
vagina stimulated by the Tom’s penis. Ovulation
may occur spontaneously in approximately 30-
35% of queens, even if the female never comes
in contact with anybody else (human, animal).
This has been demonstrated in studies performed
in laboratory queens who live their lives in cages,
as well as in household queens in which (thanks
to faecal progesterone assay) ovulation has been
demonstrated as soon as a tomcat was placed in a
room nearby where queens could see him but not
interact with him. Occurrence of ovulation does
not shorten duration of oestrus which averages
8.5+4.2 days (range 2-19 days) in bred queens
(regardless of whether or not follicle/s ovulated).
Instead, absence of coitus is associated with a
shorter duration of oestrual behaviour (6.2+2.9
days). The number of follicles ovulating has been
related to the number of matings, with one mating/
oestrus not being sufficient to cause ovulation in
up to 50% of bred females, and 4 matings/oestrus
being associated with high numbers of follicles
ovulating.
Oestrus behaviour may fail to be displayed
when a queen is intimidated or taken to a new
environment which makes her nervous and
anxious. Experienced tomcats can often overcome
such situations, and the owner can sometime help

by carefully holding the queen (although the male
may then refuse to mount her). Trying a different
male can sometime solve the problem, but
occasionally a frightened queen will refuse every
male and therefore artificial insemination may be
the only choice. Feline follicular maturation is not
characterized by a serum progesterone rise, which
makes choosing the right day sometimes difficult.
Vaginal cytology can help differentiate between
heat and non-heat, but will not indicate whether
the queen is at the beginning or at the end of heat.
Ultrasonography can be very useful to follow
follicular maturation in the queen, with follicles
progressively growing from 2.0 to 4.2 mm in
diameter prior to ovulation.
In the majority of queens, ovulation occurs
following a copulation-induced pituitary LH peak
whose magnitude is directly proportional to the
number of breedings; ovulation occurs in only 50%
of queens bred just once, and in 100% of queens
bred >4 times. More than one day of exposure
to increasing estrogen stimulation is necessary
before the feline pituitary can release an ovulatory
surge of LH in response to a coital stimulus.
The threshold of estradiol-17β concentrations
indicating active hormonal secretion by growing
follicles is generally considered to be 20 pg/ml,
with >20 pg/ml indicating oestrus and <20 pg/ml
indicating anoestrus or interoestrus. However,
significantly higher concentrations of estradiol-
17β (approximately 50 pg/ml) are reported on the
day of the ovulatory LH surge than on the previous
day (approximately 35 pg/ml). Therefore, breeding
too early (such as on the 1st day of heat) may not
induce ovulation as the pituitary may not be ready
to release LH or the follicles may not be mature
enough to rupture in the presence of an LH surge.
An LH response may not be elicited when queens
are bred 2-3 times during the first day only or even
the first and second day of oestrus. Therefore, it is
PROTOCOL DOSAGE
PMSG 100-1000 IU, 5-7 d
PMSG+hCG 100-150 IU on day 1 + 50-100 IU
on day 5-7
FSH+hCG 2 mg/day 4-5 days + 50-250 IU
FSHp+hCG 2 mg on day 1, 0.5-1.0 mg days 2-5
+ 50-250 IU
huFSH + hCG 7.5 or 15 IU days 1-4 + 100 IU on day 4.5
hMG + hCG 15 IU days 1-5, + 100 IU on day 6.5
FSHp (ultra pure) 2.5-10 mg total dose, in 5 days
Antiprolactin drugs Cabergoline 5 mg/kg, max 15 days
Table n° 1 – Oestrus induction protocols in the queen.
Back to contents
R
always best to wait untile the third day of oestrus
to take the queen to the tom.
Artificial insemination: Semen collection in the
cat is not as easy as in dogs; it requires the use
of a purpose-made artificial vagina (AV) or of
electroejaculation. While the latter is a rather
complicated and expensive technique which
requires anesthesia, the use of an AV is relatively
easy and inexpensive, with the only disadvantage
being the fact that the tomcat needs to be trained,
and training may require up to 2 weeks of
attempts using a teaser queen in heat. The AV can
be assembled using a 2 ml rubber bulb (from a
Pasteur pipette) and a small (2-3 ml) test tube; the
device is placed in a polyethylene bottle filled with
52°C water. Semen deposition can be achieved in
the cranial vagina or posterior cervix using a 9 cm,
20 G needle with a bulb at the tip. Vaginal dilation
is performed with a 1.5 mm nylon probe or a 2.0
mm stainless steel probe. The queen is under
general anesthesia or well sedated and placed
in dorsal recumbency with the hind quarters
elevated and maintained in this position for 15-20
to prevent backflow of semen. Ovulation must be
induced with GnRH (50 mcg/queen, IM) or hCG
(50-100 UI/queen, IM). Vaginal stimulation with
a cotton fioc or a glass rod may occasionally cause
ovulation, although this is not a very reliable
way and should not be used when performing an
artificial insemination.
Oestrus induction: Oestrus induction in the queen
is commonly achieved using PMSG. A variety
of different treatments have been used as shown
in Table n° 1, but PMSG at the dose of 100-150
IU a single time followed by 50-100 IU of hCG
5-7 days later is the protocol that consistently has
given the best results. Although prolactin does not
seem to play a role in determining feline anoestrus,
some efficacy of antiprolactinics (cabergoline) has
been anecdotally reported.
2006 World Congress WSAVA/FECAVA/CSAVA
REFERENCE
Cline et al., Lab An Sci 1003, 1980
Cline et al., Lab An Sci 1003, 1980;
Donoghue et al., Biol Reprod 46:972, 1992;
Swanson et al., Biol Reprod 57:295, 1997
Dresser et al., Therio 28:915, 1987
Tsutsui et al., Jap J Vet Sci 51:677, 1989
Orosz et al., Therio 37:993,1992
Orosz et al., Therio 37:993,1992
Verstegen et al., J Reprod Fert Suppl 47:209, 1993
Verstegen, unpublished; Zambelli, unpublished
697
 R
The Feline Pregnancy
Coital stimulation is considered necessary in the
queen for LH peak to occur, which is then followed
by ovulation 24-27 hours later. Although queens
housed in single cages without any physical
contact with other cats may ovulate spontaneously
without cervical stimulation, ovulation can
certainly be timed based on occurrence of mating,
and pregnancy length can therefore be accurately
calculated. Fertilized ova reach the uterine
horn 3-4 days post-ovulation, and implantation
occurs around 12-13 days after ovulation. In a
large study performed recently in the UK mean
length of feline gestation was 65 days with 90%
of values occurring between 63 and 67 days and
97% of values occurring between 61 and 69 days.
The normal range of feline gestation is 54-74
days timed from the first or last breeding and does
not appear to be influenced by age of the queen,
parity, number of kittens per litter, mean weight
of kittens born, weight gain during pregnancy or
genetic background.
Hormones of pregnancy: Plasma progesterone
(P4) concentrations increase above the 2.0 ng/ml
threshold level about 4 days after mating, peak
at values > 15 ng/ml between day 11 and 30 of
pregnancy, and remain above threshold until
day 62. Parturition occurs approximately 24-48
hours after luteolysis. Early work from the USA
reporting that ovariectomy could be done after
day 45 of gestation without causing abortion
(because of placental production of P4) was
challenged from experiments done in Belgium
where queens were showed to abort 7-10 days
following ovariectomy performed at day 45 of
gestation. As in dogs, prolactin is considered a
major luteotrophic factor in the feline pregnancy,
and anti-prolactin compounds such as cabergoline
have been shown to lyse the feline corpus luteum
causing abortion as early as day 30 of gestation,
whereas the luteolytic action of prostaglandin F2a
2006 World Congress WSAVA/FECAVA/CSAVA
in the queen is evident only after day 30 to 40.
Pregnancy diagnosis: Pregnancy can be
diagnosed by abdominal palpation of 2.5 up to
3.5 cm diameter foetal vesicles 21 to 35 days
following breeding, respectively. Radiography
and ultrasound can be used for pregnancy
diagnosis as early as day 17 after breeding, while
calcification of the foetal mandible, cranium,
scapula, humerus, femur, vertebral bodies and ribs
can be observed as early as day 38 after breeding.
Radiographic identification and measurement
of crown-rump length has been used to estimate
foetal age: feline foetuses measure approximately
10.5 cm at 50 days, 12 cm at 55 days and 14.5 cm
at parturition.
Cat breeders generally do not have pregnancy
diagnosed on their queens on a regular basis.
698
Back to contents
Occasionally queens with a history of infertility
may be brought in to the veterinarian for a uterine
ultrasound around 20-25 days post-breeding,
a time when manual palpation of the abdomen
easily allows to detect foetal vesicles of 2.5 cm
diameter. Radiography and ultrasound can be
used for pregnancy diagnosis as early as day 17
after breeding, while calcification of the foetal
mandible, cranium, scapula, humerus, femur,
vertebral bodies and ribs can be observed as
early as day 38 after breeding. Radiographic
identification and measurement of crown-rump
length has been used to estimate foetal age:
feline foetuses measure approximately 10.5 cm
at 50 days, 12 cm at 55 days and 14.5 cm at
parturition.
Care of the pregnant female: Doing a moderate
physical exercise during gestation will help
pregnant queens to maintain a good body condition
and muscle tone, which will allow for a better and
quicker parturition process. Vaccinations should
be avoided unless it is specifically requested by
the vaccination protocol that the injection be
done during pregnancy. Modified live virus feline
panleukopenia vaccines are teratogenic in the
queen and their use should be avoided. The use
of griseofulvin during pregnancy in the queen
causes congenital malformations in kittens such
cleft palate, exencephaly, hydrocephalus, spina
bifida, cyclopia and anophtalmia, atresia ani and
atresia coli, and abnormalities of the heart.
Feline Parturition: During parturition, the queen
alternates pacing with purring behaviour, and
when abdominal contractions begin she assumes
a semi-squatting position with her calcaneous
bones pointed almost straight up and wide apart.
In between contractions, she lays on her side and
continues purring. Fluids are generally expelled
from the vulva before the birth of the 1st kitten.
Each kitten is expelled partially through the
vulva generally head first, and then the mother
seems to pause for a few minutes while keeping
contracting her abdomen, while the kitten remains
half outside the vulva. Once born, the kitten is
licked vigorously to remove the allantois and the
amnios, whose remnants are frequently found on
newborn kittens. Posterior presentation is common
and does not predispose to dystocia. The queen
usually ingests most if not all the placentas. Mean
duration of stage-1 labour (the preparatory phase)
is 0.5-1.0 hr, with >80 of queens taking less than 2
hrs. The duration of stage-2 labour (the expulsion
phase) is <6 hrs in the majority of queens, but in a
small minority of cases it can be more than 24 hrs,
and occasionally intervals of up to 48 hrs have
been reported. Parturition of normal, live kittens
several days apart is anecdotally reported in the
queen (although it has never been documented).

First nursing occur within the first hour of life,
with the majority of kittens suckling already by
30 to 40 minutes from birth. Litter size varies
from 1 to 10, with a modal litter of 4 kittens.
Mortality is higher in one-kitten litters and in
low-birth-weight kittens, and lower in adult queen
that are not overweight and who deliver litters of
5 kittens.
Using drugs in pregnancy
The most delicate period of the feline pregnancy is
the first month during which organogenesis takes
place. Prior to day 20-22 following ovulation
(when implantantion occurs and placental
development starts) feline embryos are surrounded
by “uterine milk”, a protein endometrial secretion
which is in homeostatic equilibrium with the blood
compartment, i.e. any substance that arrives in the
bloodstream reaches the endometrium. Therefore,
use of any substance during this time carries the
potential risk of harming foetal development
even though there is no risk associated for the
mother. After placental development foetuses
R
become more resistant to toxic insults. Although
no real “placental barrier” exist, most substance
cannot reach the placental circulation unless they
are present in high concentration and for a long
time in the bloodstream. However, any drug that
reaches the foetal circulation must be metabolised
by the foetal kidney (in carnivores the foetal liver
is not metabolically active) which in itself might
threaten foetal survival. Bromocriptine, estradiol
benzoate and cypionate and prostaglandin F2a 
drugs are cause embryonic/foetal death in the cat.
Aspirin, dexamethasone, carbaryl and antiestrogen
are described as capable of causing embryonic/
foetal death in the bitch, and therefore should
be suspected to have the same effect also in the
queen. The effect of various drugs on pregnancy
in small animals is reported in details by Papich
(1989). Table n° 2 shows a brief summary of
drugs which have been either tested in pregnant
dogs and cats and proven safe or used in pregnant
laboratory animals and pregnant women without
any side effect.

CATEGORY OF DRUGS ACTIVE PRINCIPLES SAFE FOR USE IN PREGNANT BITCHES

Antibiotics Ampicillin, amoxicillin, carbenicillin, cephalosporins, clindamycin,
cloxa- and dicloxacillin, hetacillin, lincomycin, neomycin, oxacillin,
penicillin G, ticarcillin
Antimicotics Miconazole (for topical use only)
Antiparasitics Diethylcarbamazine, fenbendazole, mebendazole, ivermectin, piperazine,
praziquantel, bunamidine, pyrantel, thenium
Anticancer drugs None
Anesthetics Lidocaine, naloxone
Gastrointestinal drugs Antacids, sucralfate
Cardiovascular drugs Digitalis
Anticonvulsivant drugs None
Muscle relaxants None 2006 World Congress WSAVA/FECAVA/CSAVA
Endocrine drugs None
Table n° 2 – Drugs which have been either tested in pregnant dogs and cats and proven safe or used in
pregnant laboratory animals and pregnant women without any side effect.

SUGGESTED READINGS J Small An Pract 12: 501-506, 1971

Baldwin C – Pregnancy termination in the domestic
cat using natural prostaglandins. Proceedings
Annual Meeting Society for Theriogenology, S.
Antonio, Texas, USA, Sept 13-15, 1995, pp 169-175
Banks DR, Stabenfeldt G - Luteinizing
hormone release in the cat in response to coitus
on consecutive days of oestrus. Biology of
Reproduction 26, 603-611, 1982
Boyd JS: The radiographic identification of the
various stages of pregnancy in the domestic cat.
Back to contents
Concannon PW, Hodgson B, Lein DH - Reflex
LH release in estrous cats following single and
multiple copulations. Biology of Reproduction
23, 111-117, 1980
Gudermuth DF, Newton L, Daels P, Concannon PW
- Incidence of spontaneous ovulation in young, group
housed cats based on serum and faecal concentrations
of progesterone. Journal of Reproduction and Fertility,
Suppl 51: 177-184, 1997
Feldman EC and Nelson RW – Feline reproduction.
699
 R
In: Canine and Feline Endocrinology and
Reproduction. EC Feldman and RW Nelson
editors, WB Saunders, 3rd edition, 2004, pp
1016
Johnston SD, Root-Kustritz MV, Olson PNS – The
feline oestrus cyclen. In: SD Johnston, MV Root-
Kustritz and Olson PNS (eds), Canine and Feline
Theriogenology. Philadelphia: WB Saunders, pp
396-405, 2001
Lawler DF, Johnston SD, Hegstad RL, Keltner
DG, Owens SF: Ovulation without cervical
stimulation in domestic cats. J Reprod Fert -
Suppl 47: 57-61, 1993
Lofstedt RM - The estrous cycle of the domestic
cat. Compendium Continuing Education for the
Practicing Veterinarian 4: 52-58, 1982
Munday HS and Davidson HPB: Normal gestation
lengths in the domestic shorthair cat. J Reprod
Fert Suppl 47: 559, 1993
Papich M - Effects of drugs on pregnancy. In:
Current Veterinary Therapy X. Small Animal
Practice. Editore RW Kirk, WB Saunders 1989,
p 1291
Romagnoli S - Clinical Approach to infertility
in the queen. Journal of Feline Medicine and
Surgery. vol. 5, pp. 143-146, 2003
Romagnoli S – Failure to conceive in the queen.
Journal of Feline Medicine and Surgery. 7 (1): 59-
64, 2005
Scott FW, De Lahunta A, Schultz RD et al. –
Teratogenesis in cats associated with griseofulvin
therapy. Teratology 11: 79-86, 1975
2006 World Congress WSAVA/FECAVA/CSAVA
700
Back to contents
Smith RN – Appearance of ossification centers in
the kitten. J Small Anim Pract 9:497-511, 1968
Shille VM, Lundstrom KE, Stabenfeldt GM
(1979) Follicular function in the domestic cat
as determined by estradiol-17b concentration
in plasma: relation to estrous behavior and
cornification of exfoliated vaginal epithelium.
Biology of Reproduction 6, 953-963,
Sparkes AH, Rogers K, Henley WE, Gunn-Moore
DA, May JM, Gruffydd-Jones T, Bessant C – A
questionnaire-based study of gestation, parturition
and neonatal portality in pedigree breeding cats in
the UK. J Fel Med Surg 8: 145-157, 2006
Verstegen J, Onclin K, Silva LDM, et al.
– Regulation of progesterone during pregnancy
in the cat: studies on the roles of corpora lutea,
placenta and prolactin secretion. J Reprod Fertil,
Suppl 47: 165-173, 1993
Verstegen J, Onclin K, Silva LDM, Donnay I –
Abortion induction in the cat using prostaglandin
f2alpha and a new antiprolactinic agent,
cabergoline. J Reprod Fertil, Suppl 47: 411-417,
1993
Wildt DE, Seager SWJ, Chakraborty PK (1980)
Effect of copulatory stimuli on incidence of
ovulation and on serum luteinizing hormone in
the cat. Endocrinology 107, 1212-1217
Zambelli D, Cunto M – Artificial insemination
in the cat. Proceedings 5th EVSSAR Congress,
Budapest, Hungary, 7-9 April 2006, pp 225-231

R – Reproduction
CONTROL OF REPRODUCTION IN DOGS AND CATS: USE AND
MISUSE OF HORMONES
Prof. Stefano Romagnoli,DVM,
MS, PhD
Diplomate European College of
Animal Reproduction
Department of Veterinary Clinical
Sciences
University of Padova Agripolis
Legnaro 35020 (PD)
Italy
stefano.romagnoli@unipd.it
PROGESTOGENS
Synthetic analogues of progesterone, also
termed progestins or progestogens (PG), are
pharmaceutical compounds commonly used
to control the reproductive cycle of domestic
animals. The following PGs are commonly used in
dogs and cats for temporary (starting the treatment
shortly before proestrus onset) or prolonged
(starting in anestrus) postponement of estrus, or for
suppression of estrus (starting the treatment after
proestrus onset) : medroxyprogesterone acetate
(MPA), megestrol acetate (MA), proligestone
(PR), chlormadinone acetate (CMA), delmadinone
acetate (DMA), norethisterone acetate (NTA) and
melengestrol acetate (MGA). From the clinical
point of view all these product act in the same way
through a block of the production and/or release
of GnRH from the hypothalamus. If used at
suprapharmacologic doses or for excessively long
periods, these compounds show a variety of action
on the reproductive and endocrine system (such
as hyperplasia of the endometrium, hyperplasia of
the mammary parechima, decreased production
of adrenocorticosteroids, increased secretion of
prolactin and growth hormone, insuline resistance)
as well as some local skin reactions at the injection
site and behavioral modification (increased
appetite and weight, polydipsia, slight depression,
decreased libido in males). In pregnant bitches and
queens use of PGs may cause masculinization of
female fetuses if administered early in pregnancy
(during organogenesis) or delayed parturition if
administered in the last decade of pregnancy.
Clinical considerations for a safe use of
progestogens: All the above cited effects may
occur also after normal dosing but are generally
subclinical, fully reversible and do not cause
problems in healthy young to adult animals. In
general, a treatment period of 6-12 months is
considered safe in healthy individuals, although
longer treatments can also be as safe provided
Back to contents
R
that the female is given a rest of 1-2 months
every year or so. While most bitches and queens
may tolerate treatment periods of more than 12
months, animals with a pre-existing disease such
as subclinical diabetes, microscopic mammary
lesion/tumor or cystic endometrial hyperplasia
may see their condition worsen rapidly as a result
of the PG treatment. The following is a series of
considerations on patient selection and type of
presenting complaint for which a PG treatment
should or should not be used.
• Do not use long acting compounds (such as
MPA or PR or any other compound marketed for
long term use) prior to puberty in felines, as this
may cause the queen to develop a long-lasting
mammary hypertrophy which could become a
life-threatening situation. In prepuberal animals
it is best to use initially a short acting compund
(such as MA) per os for 1-2 weeks and then
change to a long acting PG once potential side
effects have been ruled out.
• Do not treat pregnant females, as this may cause
fetal developmental defects as well as delayed
parturition, thereby causing fetal death in utero 2006 World Congress WSAVA/FECAVA/CSAVA
due to placental ageing and detachment.
• Do not treat pseudopregnant bitches. During a
PG treatment clinical signs of pseudopregnancy
will disappear but will recur once treatment is
discountinued, and the problem may worsen.
• Do not treat a female during diestrus. The
stage of the reproductive cycle should always be
identified using vaginal cytology and/or serum
progesterone assay, and the bitch or queen should
best be treated during anestrus. Diestrus should
be ruled out in felines too, as approximately 30%
of queens ovulate spontaneously, maintaining
thereafter a 30-45 day-long diestrus.
• Do not treat females with uterine haemorrhage.
Prolonged sanguineous vulvar discharge following
parturition in the bitch can be a critical problem
which should either be treated with a uterine
701
 R
contractant (i.e. as ergonovine) or sent to surgery.
Milder bloody vulvar discharge can be caused by
uterine neoplasia, cystic endometrial hyperplasia
with superimposed endometrial inflammation,
pyometra, metritis. None of these conditions will
benefit from administration of a progestogen.
• Do not treat diabetic patients. Although not
always necessary, it would be wise to measure
blood glucose before and/or after a prolonged
treatment to confirm health status with regard to
glucose metabolism.
• Do not use PGs in females with prolonged heat.
A prolonged heat may be due to ovarian cyst(s),
a granulosa cell tumor, or may be due to a split
heat (in the bitch) or to a misinterpretation of
normal estrous signs by the owner. For none
of these categories is a progestogen treatment
indicated (although in some cases an ovarian cyst
may benefit from aministration of a progestogen).
Therefore, bitches or queens with a prolonged
heat should not be treated with a progestogen,
unless a diagnosis of cystic ovarian disease
has been carefully confirmed and surgery or
administration of GnRH or hCG are not a valid
therapeutic option.
Choosing the right candidate: The ideal candidate
is an adult postpuberal female in anestrus.
Prepuberal females should not be treated with
long acting compounds because of the risk of
precipitating a subclinical uterine, endocrine or
mammary condition (such as diabetes, cystic
endometrial hyperplasia-pyometra in the bitch or
mammary hyperplasia in the queen) which are rare
but have been reported in young animals. If one of
the above conditions is present the administration
of a long acting progestogen prior to diagnosis
may pose a serious health threat on the female.
A minimum database of clinical information to
be gathered prior to administering a long-acting
compound should include:
• collecting a thorough reproductive history to
rule out occurrence of estrus within the last 1-2
months (which would mean that the female is in
diestrus)
• performing a complete clinical exam which
includes thorough palpation of the mammary
gland to rule out presence of mammary nodules
• collecting a vaginal smear to rule out presence
of oestrus
Table n° 1 shows the suggested dosages of
the most commonly used progestogen-based
compounds in the bitch and queen.

Suggested Dosage Dog Cat

Medroxy- 2.5-3.0 mg/kg IM every 5 months
progesterone
Acetate
Megestrol <2.0 mg/kg administered for <2 weeks
in proestrus, or <2.0 mg/kg
administered for a longer duration
of time in anestrus. A typical
dosage for estrus suppression
2006 World Congress WSAVA/FECAVA/CSAVA
2.0 mg/kg IM every 5 months
for the feline
in anestrus: 5 mg/cat every 2 weeks or
2.5 mg/cat/week (better if divided into
2 administrations every 3.5 days)in
proestrus: 5 mg/cat/day for 4 days, then
5 mg every 2 weeks.

is 2.0 mg/kg/day for 8 consecutive

days, while a typical dosage
for temporary postponement
is 0.5 mg/kg/day in late anestrus
Proligestone 10-33 mg/kg SC every 3,4,5,5 months 10 mg/kg SC every 3,4,5,5, months
Table n° 1 – Suggested dosages of the 3 most commonly used progestogen compounds in bitches and
queen for the control of estrous.

PROSTAGLANDINS the progesterone supporting pregnancy is entirely

The abortifacient efficacy of prostaglandins (PGF) from the corpora lutea throughout gestation. PGF
involves induction of luteolysis, stimulation of will induce luteolysis and depress progesterone
uterine contraction and cervical dilation. Of these, concentrations to nearly non-detectable levels
the luteolytic effect is the most important in the very easily after day 25 or 30, although also
bitch, while the cervical dilating action has never earlier in pregnancy. The later in the cycle PGF
quite been demonstrated in this species. In dogs, is administered, the easier and more rapid the
702
Back to contents

induction of luteolysis. Use of PGF requires
subcutaneous administration 2 or 3 times a day,
for 6 days or longer. Treatment should initially be
administered under the supervision of a clinician,
after which bitches can be sent home once side
effects have been carefully after the 1st PGF
administration, and the treatment continued at
home by the owner. No PGF products are marketed
with an indication for use in dogs or cats.
Natural prostaglandins: A course of natural PGF
therapy is successful if injections are given at least
twice a day, using a maximum dosage of 80-100
mcg/kg twice daily, starting with half the dose
for the first day (or the first 2 administrations).
Side effects (which include emesis, salivation,
defecation, urination and slight tachipnea) are dose
dependent (displayed in 75% of bitches using doses
of 250 mcg/kg and only in 25% of bitches using
doses of 50 mcg/kg) and self-limiting, decreasing
in intensity with repeated dosing. Treatment must
be continued until verification of efficacy by
ultrasound or palpation. Partial abortion of litters
can occur if treatment is discontinued prematurely.
With most dosages, 9 or more days may be
required to terminate some pregnancies, although
5 to 7 days is usually sufficient. Although the use of
premedication with atropine sulphate or prifinium
bromide is reported prior to administration of
natural PGF compounds, we have never used it
and feel that its use is almost always unnecessary.
Synthetic prostaglandins: Highly potent,
synthetic analogs of PGF, such as cloprostenol
or alphaprostol have been effectively used for
pregnancy termination in dogs, with cloprostenol
being used at doses of 1-2.5 mcg/kg, administered
three times, at 48 hour intervals, while alphaprostol
must be administered twice daily for several days
like natural PGF, at the doses of 20 mcg/kg. Side
effects have been reduced by administration of
various drugs, including anticholinergic drugs
like atropine. A study of 67 pregnant bitches
demonstrated a 100% efficacy in termination
of pregnancy using cloprostenol at the dose of
2.5 ug/kg subcutaneously, administered three
times, at 48 h intervals, starting at day 30 of
pregnancy. Pre-medication given at 15 minutes
before prostaglandin injection included atropine
sulfate, prifinium bromide, and metopimazine, it
eliminated side effects in 58% of the bitches, and
presumably reduced them in others. Cloprostenol
at even lower doses has been used in combination
with the dopamine agonist cabergoline to terminate
pregnancy in dogs shortly after implantation.
Prostaglandins in cats: PGF treatments have
been successful in terminating pregnancy in cats
when injected after day 40 in some studies but
not in all. Recently it has been shown that natural
PGF alone, at a dose of 2 mg/cat IM once a day,
Back to contents
R
beginning at day 33 of pregnancy, can induce
luteolysis and terminate pregnancy by expulsion
of fetuses in pregnant cats. Side effects included
prostration, vomiting and diarrhea. The PGF
analogue cloprostenol has been successfully used
in combination with cabergoline in cats, at the dose
of 5 mcg/kg administered once daily from day 33
post-mating onwards.
DOPAMINE AGONISTS
Prolactin secretion by the lactotroph cells of the
anterior pituitary gland is regulated by multiple
neuro-transmitters and hormones, with the
major control mechanism being the activation of
prolactin-inhibiting dopaminergic neurons in the
hypothalamus. Prolactin is a major luteotrophic
hormone and appears to be an absolute requirement
for canine and feline progesterone secretion by
day 30 after ovulation. Dopamine agonists like
bromocriptine or cabergoline are ergot alkaloids,
with strong dopamine D2-receptor agonist activity,
and thus can reduce prolactin secretion and thereby
suppressing progesterone levels. The seretonin
antagonist metergoline stimulates endogenous
dopamine secretion and thus can inhibit prolactin
secretion as well.
Cabergoline has a slow clearance, which allows
for a single oral daily administration. Furthermore,
its action is longer than 48 hours due to its
particularly long (minimum 48 hours) half-life
at the hypophyseal level. Because of its more
specific D2-type action, cabergoline presents only
few side effects when used at clinical dosages.
Bromocryptine mesylate inhibits PRL secretion
during relatively short periods of time (half-life: ±
4-6 hours) and in a dose-dependent mode. In order
to effectively inhibit PRL tone in a continuous
fashion for therapeutic purposes, bromocryptine
should be administered at least twice a day,
administered orally at doses 10-50 mcg/kg. Its
lack of specificity leads to side effects on the
cardiorespiratory system, causing hypotension
2006 World Congress WSAVA/FECAVA/CSAVA
due to vasodilatation (adrenergic type effect), or
emesis due to stimulation of the Chemioreceptive
Trigger Zone (CTZ).
Metergoline is essentially a serotoninergic
antagonist with dopaminergic agonist properties
when used orally at doses >0.3 mg/kg. Its shorter
half-life requires at least administrations twice a
day. Its antiserotoninergic properties can induce
marked central effects such as depression,
nervousness, increased excitability, changes
in appetite (anorexia or bulimia), psychotic
effects (escaping from home, aggressiveness).
Gastrointestinal side effects due to stimulation
of the CTZ are evaluated by the emetic dosage
in 50% of the bitches or DE50. The DE50 of
cabergoline and bromocryptine are identical.
703
 R
However, when considering dosages commonly
used in a clinical setting, the emetic effect of
bromocryptine is almost always present while
it is negligeable with cabergoline. The DE50 of
metergoline is much higher, but it is very close to
the therapeutic dosage. Therefore, emetic effects
are sometimes observed when using metergoline,
especially when overdosing it.
Antiprolactinic drugs can be used in the bitch and
the queen with three indications: pseudopregnancy,
induction of abortion and induction of estrus.
Pseudopregnancy: The anti-lactogenic action
of both metergoline and cabergoline is well
known. Their administration for 4-5 days at
pharmacological doses is effective in treating
pseudopregnancy signs and reducing milk
production. Occasional failures can be dealt with by
repeating the treatment protocol and extending it to
8 to 10 days, and also by administering at the same
time metergoline (at the usual antigalactogenic
dosage of 500 mcg/kg BID) or bromocriptine
(10-20 mcg/kg BID) (see table n° 2).

Antiprolactinic Daily dosage in the bitch/queen N° treatments/day

Cabergoline 5 μg/kg 1
Bromocriptine 10-30 μg/kg (*) 2
Metergoline 500 μg/kg (*) 2
Table n° 2 – Dosages of the 3 antiprolactinic most commonly used in small animals: cabergoline
(Galastop™, CEVA-VETEM, a veterinary compound) and bromocriptine (Parlodel™, Sandoz, a human
compound) are dopamine agonists (they increase the concentration of dopamine, a PRL-inhibiting
factor) while metergoline (Contralac™, Virbac, a veterinary compound) is a serotonine antagonist (it
lowers the concentration of serotonine, a PRL-stimulating factor). (*) There is no scientific information
available for the queen.

Antiprolactinics are currently considered the
treatment of choice for pseudopregnancy. Until
the last part of last century, when antiprolactinics
became commercially available, progestogens
were thought to be an appropriate treatment for
false pregnancy due to their lowering action on
PRL concentrations at the end of the luteal phase;
infact, progestogen administration is clinically
demonstrated to be effective in preventing the
occurrence of lactation and of pseudopregnancy
as well as in eliminating related clinical signs.
However, a rebound effect is frequently observed
following treatment withdrawal, similarly to what
occurs at the end of a normal luteal phase, when
2006 World Congress WSAVA/FECAVA/CSAVA
antiprolactinic drugs was initially thought to be
due to the lowering of prolactin concentrations,
but studies done at Utrecht have demonstrated
that shortening of anestrus occurs irrespective of
prolactin concentrations. All the 3 antiprolactinic
products (cabergoline bromocriptine and
metergoline) have been used for oestrus induction
in the bitch. Cabergoline and bromocriptine
have consistently given positive results, while
metergoline’s results have been more variable
depending on dosage. Using low dose (0.1 mg/kg
BID) of the commercial oral preparation of
metergoline administered from 100 days after
ovulation until the following proestrus, the

the progesterone decline triggers a PRL peak.
Therefore, progestogens should not be used as a
treatment for false pregnancy.
Induction of abortion: The abortion induction
properties of antiprolactinic drugs have been
well studied for cabergoline, while not as much is
known for metergoline. Cabergoline is effective in
terminating pregnancy in dogs when administered at
mid-gestation or later. When administered after day
40 at doses of 5 mcg/kg, PO, for 5 days cabergoline
is approximately >50% effective in causing abortion
in treated bitches. If cabergoline administration is
started earlier in pregnancy, at day 25, treatments that
are effective later in pregnancy fail in most bitches
and the pregnancy continues until terminated by
retreatment at day 40. Cabergoline produces little
if any side affects at pharmacological doses.
Estrus induction: The estrus inducing action of
704
Back to contents
interoestrous interval can be significantly shortened.
The administration of bromocriptine in anoestrus
will induce oestrus within 28-50 days. We have
used bromocriptine at the dose of 10-25 mg/kg
in 5 bitches with prolonged anoestrus: 4/5 came
in oestrus within 13-28 days, and all 4 conceived
and whelped. Using cabergoline (5 μg/kg, once
daily for up to 28 days) or natural PGF2alpha (100
μg/kg SC, BID for 5 days starting on cytological
dioestrus day 10) we achieved an interoestrous
interval of 6 months in 6 treated bitches as opposed
to an interval of 9 months in 9 control bitches.
We have also used cabergoline (5 μg/kg, once
daily for up to 28 days) in 9 bitches for a total of
11 cycles: fertile oestrus was induced in 10/11
cycles in 24+11 days with a reduction of the
interoestrous interval of 1.8+0.2 months. In our
experience, the clinical use of antiprolactinics to

induce oestrus has proven to be safe and highly
effective. Side effects are minimal (particularly
with cabergoline), being mostly related to the
gastrointestinal tract (nausea, rare vomiting) with
no other reproductive effect (unlike estrogens or
PMSG which can both cause estrogen toxicity).
Dopamine agonists in cats. The use of dopamine
agonists alone appears not to have been studied
extensively in cats. Production of litters by feral
cats was prevented by addition of cabergoline to the
diet of pregnant individuals at a dose of 5-15 ug/kg/
day for 4-12 days. In a controlled laboratory study,
cabergoline at doses of 1.7 ug/kg given i.m. daily
for 5 days, starting at day 30 of pregnancy, induced
luteolysis and terminated pregnancy in 4 of 5 cats,
with negligible side effects. In another study, the
oral cabergoline formulation administered per os
at a dose of 15 mcg/kg for 4 to 7 days terminated
pregnancy in 8 cats when started between day 30
and 42, but failed in 2 cats when started at day
45. This failure of abortifacient efficacy in late
pregnancy is perhaps not surprising, since the
feline placenta is thought to produce progesterone
during the last 3 weeks of pregnancy. Emesis was
a side effect in some animals. Cabergoline has
been used to induce estrus in the queen with some
efficacy.
PROGESTERONE ANTAGONISTS
Antiprogestins (progesterone antagonists) are
synthetic steroids that bind to the progesterone
receptor, but fail to initiate activities normally
initiated by progesterone, and by occupying the
receptors they prevent the actions of endogenous
progesterone. Progesterone is required for the
maintenance of pregnancy, as it provides the
hormonal stimulus for endometrial development
and placental attachment, and also acts to maintain
uterine quiescence by reducing the contractility
of uterine musculature. Anti-progestins disrupt
reproduction and terminate pregnancy in all
species studied to date. All anti-progestins to date
also have anti-glucocorticoid activity, but are more
potent as antiprogestins than as anti-corticoids.
Induction of abortion: The anti-progestin
mifepristone (RU486) is a drug developed for
human application, is available in a few countries
and is not marketed for veterinary use. An
injectable formulation of an analog of RU486, i.e.
RU 534 or aglepristone, has been made available
for veterinary use in France and Sweden since the
mid 90’s and in many other european countries
over the last 2-5 years. Aglepristone is currently
marketed with an indication for pregnancy
termination in dogs (Alizineä or Alizinä, Virbac).
The aglepristone preparation is an oily-alcohol
solution containing 30 mg of aglepristone per ml,
to be used at a dosage of 10 mg/kg, administered
Back to contents
R
two times 24 hrs apart; it causes no untoward side
effects. The early administration of aglepristone at
0 to 25 days after mating always is approximately
98% effective in prevention of pregnancy. The
later administration of aglepristone, at Day 26
to 45 after mating induces resorption or abortion
within seven days in approximately 95% of cases
studied.
Treatment of pyometra: Antiprogestins can be
used also for the treatment of pyometra. In our
experience, administration of the usual dosage of
10 mg/kg on days 1, 2, 8 and then also 15 and 28
depending on the clinical situation has resulted
in positive results in a preliminary trial in bitches
with both open cervix and closed-cervix pyometra.
The use of aglepristone can be associated with
PGF provided that cervical opening has occurred.
In bitches with closed cervixy pyometra,
administration of algepristone is often followed by
cervical opening within 24-48 hrs.
Antiprogestins in cats: Aglepristone can induce
abortion in cats. The suggested dosage is higher
than in the dog, being 15 mg/kg twice 24 hrs apart.
There is no information on the effect of aglepristone
on pyometra in the queen, but efficacy for this
indication is thought to be the same as in dogs.
ESTROGENS
Estrogens have always been considered as
potentially dangerous drugs because of their
role in inducing mammary neoplasia and bone
marrow aplasia in women as well as in bitches.
However, only long-acting synthetic compounds
such as diethylstilbestrol, estradiol, estrone and
other esther compounds are characterized by
such dangerous action because of their prolonged
nuclear occupance time in estrogen receptors of
target tissues. Short-acting estrogenic compounds
such as estriol, characterized by short nuclear
occupance time and minimal metabolism following
absorption (estriol does not bind to sex-hormone
binding globulin) prevent development of full (late)
2006 World Congress WSAVA/FECAVA/CSAVA
estrogenic effects such as endometrial hyperplasia,
pyometra and bone marrow suppression.
Unwanted pregnancy: Several estrogenic
compounds have been used for this purpose,
but for most of them the risk of side effects has
discouraged their clinical application. Only
estradiol benzoate, when given at low doses has
proven to be fairly efficacious and relatively safe.
A compound with estradiol benzoate is marketed
for veterinary use in mismated bitches in several
European countries (Mesalinâ, Intervet), which is
to be administered at the dose of 10 mcg/kg SC on
day 3, 5 and 7 post breeding. No side effects have
been reported following this protocol, although the
only clinical data available for bitches are those
produced by the company that is marketing it.
705
 R
LOTRIFEN
Lotrifen is an isochinolinic product marketed in
some European countries for veterinary use in
mismated bitches (Privaprolâ, Fatro). At the dose
of 2.5 mg/kg, administered only once no later than
15 days post-mismating it will cause abortion
by inhibiting embryonic and placental growth.
Although no immediate side effects have been
reported (e.g. immediately after administration),
anorexia, abdominal pain, gastrointestinal
problems and uterine inflammatory diseases
have been reported anecdotally. A study done in
Spain reported also parturition of live foetuses,
parturition of live and dead foetuses, pyometras,
prolonged gestation and foetal maceration.
Because of potential serious consequence for
the health of the bitch, this drug is currently
considered unsafe and therefore should not be
used in the dog.
SUGGESTED READINGS
Concannon PW, Meyers-Wallen VN. Current
and proposed methods for contraception and
termination of pregnancy in dogs and cats. J Amer
Vet Med Assoc 1991; 198: 1214-1225.
Curtis EM, Grant RP – Masculinization of female
pups by progestogens. JAVMA 144: 395-398,
1964
Eigenmann JE, Eigenmann RY, Rijnberk A, Van
der Gaag I, Zapf J, Foesch ER – Progesterone-
controlled growth hormone overproduction
and naturally occurring canine diabetes and
acromegaly Acta Endocrinologica 104: 167-176,
1983
Eilts BE, Paccamonti DL, Hosgood G et al. – The
use of Ally-trenbolone as a progestational agent
to maintain pregnancy in ovariectomized bitches.
Theriogenology 4: 1237-1245, 1994
Evans JM, Sutton DJ – The use of hormones,
2006 World Congress WSAVA/FECAVA/CSAVA
especially progestagens, to control oestrus in
bitches. J Reprod Fert Suppl 39: 163-173, 1989
Fieni F, Martal J, Marnet PG, Siliart B, Bernard
F, Riou M, Bruyas JF, Tainturier D – Hormonal
variation in bitches after early or mid-pregnancy
termination with aglepristone. J Reprod Fert
Suppl 57: 243-248
Freshman JL, Olson PN, Amann RP, et al. The
effects of methyltestosterone on reproductive
function in male Greyhounds. Theriogenology
1990; 33: 1057-1073.
Mansfield PD, Kemppainen RJ, Sartin JL – The
effects of megestrol acetate treatment on plasma
glucose concentration and insulin response to
glucose administration in cats. JAAHA 22: 515-
518, 1986
706
Back to contents
Mayenco-Aguirre M, Daza-Gonzalez MA,
Sanchez-Muela M, Garcia-Fernandez P, Gonzales-
Bulnes A – Efectos observados en nueve perras
remitidas a la facultad de veterinaria de Madrid,
entre los cursos 1995-1997, tras la dministracion
de un abortivo precoz no hormonal. Proceedings
1st EVVSAR Congress, Barcelona (Spain) 1-3
May 1998, pp 337-338
Onclin & Verstegen - Practical use of a
combination of a dopamine agonist and a
synthetic prostaglandin analogue to terminate
unwanted pregnancy in dogs. J Small An Pract
37: 211, 1996
Onclin K, Verstegen J – Termination of pregnancy
in cats using a combination of cabergoline, a
new dopamine agonist, and a synthetic PGF2a,
cloprostenol. Journal of Reproduction and
Fertility Suppl 51: 259-263, 1997
Olson PN, Nett TM, Bowen RA, et al. A need for
sterilization, contraceptives, and abortifacients:
Abandoned and unwanted pets. Part II.
Contraceptives. Comp Cont Ed 1986; 8: 173-
177.
Romagnoli SE, Cela M, Camillo F - Use of
prostaglandin F2a for early pregnancy termination
in the mismated bitch. Veterinary Clinics of North
America: Small Animal Practice 21: 487-499
(1991)
Romagnoli SE, Camillo F, Cela M, Johnston SD,
Grassi F, Fedeghini M, Aria G - Clinical use of
prostaglandin F2a to induce early abortion in
bitches: serum progesterone, treatment outcome
and interval to subsequent oestrus. J Reprod Fert,
Suppl 47: 425-431 (1993)
Romagnoli SE, Camillo F, Novellini S, Johnston
SD, Cela M - Luteolytic effects of prostaglandin
F2alpha on day 8 to 19 corpora lutea in the bitch.
Theriogenology 45 (2): 397-403, 1996
Romagnoli S, Concannon P W - Clinical Use of
Progestins in bitches and queens: a review. In:
Concannon P W; England G ; Verstegen J, Linde-
Forsberg C. (Eds). Recent Advances in Small
Animal Reproduction. International Veterinary
Information Service, Ithaca NY (www.ivis.org)
(Document number A1206.0903) 2003
Sutton DJ, Geary MR, Bergman GHE – Prevention
of pregnancy in bitches following unwanted
mating: a clinical trial using low dose oestradiol
benzoate. J Reprod Fert Suppl 51: 239-243, 1997
Van den Broek AHM, O’Farrel VO – Suppression
of adrenocortical function in dogs receiving
therapeutic doses of megestrol acetate. J Small
Anim Pract 35: 285-288, 1994.

R – Reproduction
TECHNIQUES FOR NEONATAL RESUSCITATION AND CRITICAL
CARE
Dr. Danielle Gunn-Moore
University of Edinburgh
Danielle.Gunn-Moore@ed.ac.uk
For discussion of the normal physiology of
neonates, and what may causes them to ‘fade’
see lecture: Small Animal Neonatology: They
look normal when they are born and then die.
However, the most common health problems in
young kittens are hypothermia, hypoglycaemia,
dehydration, diarrhoea, and constipation.
Diagnosis
Recognition of illness: It is important to realise
that while an individual kitten may be presented
for investigation, trying to find a specific cause
can be difficult as most cases are multifactorial. It
is often only be taking a complete history of the
kitten, the rest of its litter, their birth, their mothers
health, and the overall health and management of
the other cats in the cattery that the true nature of
the problem can be determined. In the long term,
a number of factors may need to be addressed to
reduce overall mortality within a cattery:
Causes of ‘fading’ or sick kittens:
• Birth-related factors (anoxia, trauma,
hypothermia)
• Congenital abnormalities
• Low birth weights
• Inappropriate environment (temperature,
humidity, hygiene, overcrowding, over-handling)
• Inappropriate nutrition
• Neonatal isoerythrolysis (NI)
• Infection (viral, bacterial, parasitic)
If sick kittens are not to die, they must be
detected and treated early as their health status
can deteriorate rapidly. All neonates need to be
closely observed and, without over-handling,
checked for congenital defects, and monitored
for weight gain. Failure to gain weight over 24h
requires attention.
Normal kittens eat or sleep 90% of the time for
their first 2 weeks. Unfortunately, neonates tend
to show limited responses to disease, so their
presenting signs are rarely indicative of a particular
condition. Regardless of whether they are hungry
Back to contents
R
or ill they typically cry excessively, and/or fail
to suckle. Common signs of illness include
weakness, hypothermia, lethargy, restlessness,
and/or regurgitation of milk. Sick kittens respond
poorly to their environment, and typically have
either very thin abdomens from lack of food or
very swollen abdomens from swallowing air.
They often lay separated from the other kittens
and are ignored by the queen. Sick kittens need to
be treated immediately as they cope very poorly
with anorexia or hypothermia. They, and their
mother, should be examined.
Physical examination: Examination of a conscious
kitten can be difficult as they often wriggle, and
can be aggressive if poorly socialised. They
should be assed for:
• Weight and body condition, and signs of
trauma, congenital defects, or disease. (While
some congenital defects, such as cleft palate or
atresia ani should be readily evident, others,
like congenital heart defects, are only evident
on a careful post mortem examination [PME] or
following further investigation). It is important to
be aware of normal age-related changes and not
over-interpret normal findings e.g. neonatal joint
instability or cardiac murmurs. The coat should
be checked for quality, cleanness and parasites. 2006 World Congress WSAVA/FECAVA/CSAVA
The thorax and head should be checked for
normal shape and feel; HR ~200-220 beats per
minute; respiration ~15-35 breaths per minute.
The abdomen should feel gently full, not swollen,
tight or empty. The intestines and bladder should
feel soft, mobile and non-painful. The extremities
should be pale pink (extremity erythaemia is often
associated with sepsis).
• Eyes and nose – Kittens eyes should open
between days 5-14; a mild cloudiness is normal
and should resolve quickly. While a small amount
of sticky discharge is not of major concern, closed
eyelids that are swollen or matted with pus is.
• Gums - Until about a week old healthy neonates
have dark pink or red gums. However, sick
neonates often have pale, grey or bluish gums.
• Umbilical cord – This should be dry and free
707
 R
of discharges, and normally falls off between 3-
7 days of age. It is of concern if it is still moist,
painful, inflamed or discharging.
• Defaecation and urination – Since stimulation
of the perineal area in kittens of <3 weeks of age
results in defaecation and urination this technique
can be used to look for the presence of diarrhoea
or constipation (present in ~60% of sick kittens),
and to check urine colour (see below).
Blood sampling: The small size of kittens makes
collection difficult. It is usually only possible to
take very small volumes of blood (max 1.5ml
because total blood volume = ~75ml/kg, so at
1 week a kitten of 200g only has ~15ml total).
Blood should be collected from the jugular
vein. Care should be taken not to induce a large
haematoma. This can result in significant loss of
circulating volume, and can, if severe, obstruct
the airway. Collect samples into 0.5ml EDTA and
heparin tubes, run glucose on a single drop using
a glucometer, and run packed cell volume (PCV)
and total protein (TP) on a micro-haematocrit
tube. It is often only possible to assess PCV, TP,
urea, glucose, and blood smear cytology.
In order to correctly interpret the results it is
important to know what is normal for kittens of
that age (Chandler 1992; Hotston Moore and
Sturgess 1998). For example, normal neonatal
kittens have mild normochromic normocytic
anaemia, and blood urea and creatinine levels in
kittens are considerably lower than adults.
Few biochemical and haematological results
are specific for a particular disease. Severe
anaemia may be seen with NI, or a heavy flea or
hookworm infestation. Panleukopenia may be
seen with FPV, FeLV, or sepsis. Hypoglycaemia
is common, regardless of the cause of illness.
Hyperbilirubinaemia may be seen in NI or
liver disease. Hyperammonaemia may occur
with hepatic encephalopathy and a congenital
2006 World Congress WSAVA/FECAVA/CSAVA
portosystemic shunt.
Urine collection: Stimulating the kitten’s perineum
with a warm moist cotton ball is a useful method
for collecting a urine sample. Urinalysis can be
helpful in the diagnosis of NI, where brown-
staining urine results from haemoglobinuria.
Pyuria is suggestive of a urinary tract infection,
while a specific gravity of >1.017 indicates
dehydration. Glucosuria is not abnormal in
neonates.
Further investigations: More specific tests include
serology (e.g. FeLV, FIV), slide agglutination or
Coombs’ test for NI, pharyngeal swabs for the cat
flu viruses, or ocular swabs for chlamydophila
felis. If a bacterial infection is suspected swabs,
blood or urine can be taken for culture and
sensitivity. In cases of septicaemia, it is difficult to
obtain sufficient blood to perform blood culture. It
708
Back to contents
is usually more rewarding to sacrifice a moribund
kitten, and then send fresh samples of heart blood,
heart tissue, liver, lungs, etc. for culture. Survey
radiography or ultrasound examination may be
considered, but there is little radiographic contrast
in kittens (so reduce the kV by half of that used
in an adult of the same body thickness), and
ultrasound examination may require a ‘stand-off’
for the probe.
Faecal cultures can be examined for the presence of
pathogenic bacteria, Giardia spp., Tritrichomonas
foetus, coccidia, and intestinal parasites.
PME: Despite best attempts sick neonates often
die, so it is important to gain as much information
as possible. Gross changes can be helpful in
determining the cause of some illness: Kittens with
an empty or gas filled stomach, a full gallbladder,
and a full urinary bladder may indicate maternal
neglect or lack of nursing. A stomach filled with
milk may indicate sudden death (peracute infection
or trauma), or gastrointestinal dysfunction. Kittens
with NI show various changes depending on the
duration and severity of disease. The bladder may
be full of dark brown urine, the body may be pale
and/or jaundiced, the liver and spleen may be
enlarged (due to extramedullary haematopoiesis
and erythrophagocytosis), and acute tubular
necrosis may be present in the kidneys. Septic
kittens may show petechiation of internal organs.
Atelectatic lungs (dark red lungs that do not float
in water) indicate stillbirth.
When collecting samples, be it by mouth or eye
swab, blood, faeces or urine collection, coat
brushing, skin scrapping, or at PME, it is essential
to discuss the procedure with the laboratory that
will be undertaking the analysis. Incorrect sample
handling can result in erroneous results.
Treatment of individual kittens
1. Peri-natal kitten revival: Hypoxia related to
dystocia is probably the single most significant
factor in neonatal mortality. Since the healthy
mother cat will generally make a good job of
nursing her kittens, it is important not to interfere
unless necessary. However, intervention is
recommended when a kitten is not breathing,
or on the few occasions when maternal instinct
appears to be lacking. The aim is to imitate the
cat’s own methods; she ensures that the kitten’s
nose and mouth are clear, then, with a nipping/
licking action, she chews through the umbilical
cord. This, and more vigorous licking of this area,
provides stimulation of respiration. The cat then
gives the kitten a more general drying lick, then
concentrates on the perineal area in order initiate
bowel and bladder functions. Human intervention
should follow this plan, with additions in cases of
emergency.

• Tear the membranes from the nose, wipe the
nose and open the mouth, tilt the kitten’s head
down and clear away any fluid.
• If the umbilical cord has not broken on
delivery, separate it using 2 haemostats >1 inch
from the kitten. Complicated cutting and tying
are not usually necessary. Dip the stump in
chlorhexidine.
• Clearing the airways: If the kitten is not
breathing, or if it has come tail first and possibly
inhaled fluid, it is necessary to clear debris and
fluid from the airway. If suction equipment is
available this can be done by sucking the debris
out of the airway. This can also be achieved
using a Jackson cat urinary catheter attached to a
5-10ml syringe as a gentle suction apparatus. The
catheter can also be used to induce the kitten to
sneeze and cough by stimulating its nose/throat.
One of the traditionally used methods involves
swinging the kitten. To do this, place the kitten in
the palm of your hand, its back towards your palm
and neck between your forefinger and third finger,
its head protruding between your fingers. Enclose
the kitten in your fingers and, turning your hand
palm downwards with your arm extended, give a
gentle swing several times; make quite sure first
that you are not too near any protruding edges
or disaster will follow. The swing will have the
effect of forcing fluids out of the kitten’s airway
and a further wipe of its nose and mouth will
clear any debris away. The swing will also serve
to stimulate respiration. Take care; if performed
too vigorously this method can result in brain
haemorrhage.
• Stimulation of respiration: If the kitten is still not
breathing, some form of artificial respiration may
be necessary. Mouth-to-mouth respiration can
be useful, but only if very carefully performed.
There are several points to remember. It is no use
blowing fluids and debris further down the airway;
these must be cleared away first (see above).
Secondly, the capacity of kitten lungs compared
to humans is minute. Blow very gently and allow
a pause for expiration. Repeat this cycle every
3-5 seconds. Breathing into the kitten’s airway
through a small endotracheal tube or drinking
straw may help to reduce the risk of over-inflating
the kitten’s lungs, and be more hygienic than
direct mouth-to-mouth. Various methods have
been used to make the new-born animal gasp,
including the administration of brandy or other
spirits to the kitten’s tongue, flicking its chest
sharply but gently with a fingertip, alternate warm
and cold water applications, or the insertion of
a 25-g needle into the nasal philtrum. However,
it is more reliable to apply a drop of doxopram
hydrochloride (20mg/ml) sublingually. A strong
regular heart beat should be easily palpable, if
Back to contents
R
not; external cardiac massage can be attempted.
It is important to note that unlike adults neonatal
heart rates fall in a protective response to hypoxia,
and this should not be misinterpreted. If the dam
was given opioids prior to delivery naloxone
hydrochloride (0.4mg/ml) can be administered
to the offspring (1 drop sublingually) to reverse
respiratory depression.
If in doubt persist with stimulating the kitten;
some can still be revived after >30 minutes from
birth. That said, the longer the duration before
breathing the higher the risk of hypoxia causing
brain damage or blindness. Hypoxic bradycardic
puppies may respond to the administration of
atropine into the umbilical vein. While the author
has not used this method in kittens, it may be
worth considering. Since premature kittens
often have very poor pulmonary development
the administration of dexamethasone (0.1mg)
may help to stimulate surfactant production.
Supplementary oxygen should be given until
the kitten is breathing regularly and is obviously
vigorous. This can be done using a small face mask,
an oxygen box, or using a fine urinary catheter to
administer intranasal oxygen (the adapter to a 3
French endotracheal tube can be used to connect
the oxygen supply to the catheter). The kittens
tongue is a reliable indicator of respiration. If the
kitten is receiving sufficient oxygen its tongue
will be pink, if not it will have a bluish tint.
• Provide warmth: The kitten should then be
rubbed all over with a clean towel. This further
stimulates respiration and dries the kitten. It
should then be kept warm. If the mother is ill or
uncooperative, place the kittens in contact with a
warm, well-covered hot water bottle and conserve
the heat by covering the bed with a blanket. Great
care must be taken not to inflict contact burns on
the kittens by having the bottle too hot.
2. Treatment of neonatal kittens
Sick kittens need to be treated immediately.
2006 World Congress WSAVA/FECAVA/CSAVA
Supportive therapy is aimed at re-warming,
maintaining blood glucose levels, correcting
dehydration and, when required, supplying
additional oxygen.
1. Drug metabolism: Care should be taken when
medicating kittens as the pharmacokinetics of drug
metabolism can be quite different from those of
adults. Neonates often have increased absorption,
decreased protein binding (due to lower serum
albumin concentrations), and altered drug re-
distribution (due to a higher percentage body
water and decrease fat). They are also more likely
to show toxic side effects as they have increased
permeability of the blood-brain barrier, and a
reduced ability to detoxify drugs by metabolism
or excretion. Few drugs have been evaluated in
709
 R
neonates so great care should always be taken
when considering administering medications to
this age group. As a general guide give 30-50% of
the adult dose e.g. with opioids; however, many
drugs are strongly disadvised, including many
antibiotics (see later), and NSAIDS (if <6weeks
of age; because to renotoxicity).
2. Hypothermia: Neonatal kittens cannot thermo-
regulate, they lack insulating fat and thermogenic
brown, and they cannot react to cold by shivering.
They loose heat rapidly, especially if left wet.
Body temperature generally falls from ~36oC at
birth, to 30oC within a few hours, then increases
to 38oC over the first week. It is important that
these temperatures are maintained as hypothermia
can initiate a number of other problems:
e.g. A week-old kitten should have a temperature
of 35-37oC and a HR of 200-250bpm, but if its
temperature falls to 30oC, its HR will fall to
40-50 bpm. While this is a protective mechanism,
if persistent, it can results in a decrease in
respiratory rate that may in turn leads to
cardiopulmonary failure. Also, a hypothermic
kitten will not suckle effectively; it may develop
gastrointestinal ileus, and will have an increased
susceptibility to infection. It is important to check
the temperature of any potentially weak or ill
kittens, however, if their temperature is <34oC
they are likely to die.
When attempting to re-warm hypothermic kittens
it is important to do so gradually, ideally over 1-
4h, depending on the severity of chilling. Rapid
re-warming can lead to cardiovascular collapse
and death. Importantly, overheating can also be
detrimental, and can quickly lead to dehydration
and death. Because hypothermia can markedly
reduce the absorptive ability of the intestines
concurrent hypoglycaemia and dehydration cannot
be corrected using oral solutions; parenteral fluids
are needed.
3. Hypoglycaemia: This results from inadequate
2006 World Congress WSAVA/FECAVA/CSAVA
or infrequent feeding. It can cause severe
depression, muscle twitching and occasionally
lead to convulsions and death. If a kitten refuses
to feed, prompt action is required. Kittens have
no energy reserves and will deteriorate rapidly. If
a kitten is showing signs of hypoglycaemia, a few
drops of glucose syrup placed on its gums can be
life saving. However, if the kitten is cold, glucose
solution should not be given by mouth as it will not
be adsorbed from hypothermic intestines. More
severe cases can be corrected by the parenteral
administration of isotonic glucose solutions. It is
important to correct any hypothermia at the same
time. When giving supplemental glucose it is
important to monitor glucose blood concentrations
as kittens can easily become hyperglycaemic.
Once recovering the kitten can be fed a small
710
Back to contents
amount of glucose solution, and either the amount
and/or frequency of routine feeding should be
increased. Note: the nutritional requirements of
a septic kitten are increased (~1.5x maintenance)
so in these cases it may be necessary to provide
nutrition al support by tube feeding (see later).
This is not the lecture for a detailed discussion
of the nutritional requirements of kittens,
the pro and cons of different types of milk
replacement formulation, or the various methods
of supplemental feeding. Sufficient to say that
is generally best to feed commercially available
kitten formula, and to make it up and feed it as per
the manufacture’s recommendations as for either
supplemental or full replacement feeding.
Tube feeding: If kittens are too weak to suckle
for themselves, then tube feeding is perhaps the
cleanest and most efficient method by which to
deliver nutrition. However, it requires proper
equipment and good technical skills. Also, as the
kittens have no control over how much they are
fed, they can easily be given too much (or too
little). Stomach tubes must be soft, flexible, blunt-
ended and generally not more than 2-3 mm wide.
A premature human infant feeding tube is ideal
(6-10 French feeding tube for neonates and 8-10
French for kittens over 300g), or a soft rubber
canine urethral catheter may also be used. The
tube must be measured to the correct length (from
the kitten’s nose to the last rib), and an indelible
mark should be made on the tube at this point. The
tube should be lubricated with K-Y jelly before it
is used. To place the tube the kitten’s mouth must
be opened by pressing gently at the corners, and,
keeping the head flexed downwards, the tube is
then slid along the roof of the mouth and down
the back of the kitten’s throat into the oesophagus.
The tube is passed down the oesophagus until the
mark on the tube is level with the kitten’s nose. The
other end of the tube will then be in its stomach.
A syringe containing pre-warmed milk can then
be attached, and the milk can be delivered slowly,
directly into the stomach. If the kitten’s head is
kept flexed forward, it is quite difficult to miss the
oesophagus and so pass the tube into the airway
by mistake. Many kittens mew loudly throughout
the whole procedure, and it is useful to note that
they cannot do this if the tube is in the airway. If
the tube does not pass easily or if coughing occurs
withdraw the tube from the kitten’s mouth and try
again.
Frequency of feeding:
0-2 weeks: 6-10 feeds/24h at 2-4h intervals.
2-4 weeks: 4-8 feeds/24h at 3-6h intervals.
4-5 weeks: 3-5 feeds/24h at 5-8h intervals.

4. Diarrhoea and dehydration: Diarrhoea is
common in kittens, particularly those fed milk
replacement formula. It may also be caused by over
feeding; giving too concentrated a solution of milk
replacement formula; or as a result of infection
(usually caused by poor hygiene). Treatment must
be prompt as dehydration can develop rapidly,
followed by collapse, hypothermia, and death.
Looking for skin tenting is an unreliable method
of assessing dehydration in neonates. Instead,
dehydration should be assessed by weight loss,
dryness of mucus membranes, and urine specific
gravity (>1.017).
• Mild cases respond well to dilution of the milk
replacement formula 50:50 with boiled water,
which can then be given until the diarrhoea stops.
Treatment with SQ fluids may be required (see
below, but starting with ~1ml/30g is reasonable).
• Severe cases should be given no milk at all.
Instead they can be given oral support with 5-
10% glucose solution, glucose-saline, or isotonic
electrolyte solution (e.g. “Lectade”) until the
diarrhoea stops. While oral supplementation
may help, it is generally better to give parenteral
fluids. If the neonate is cold, do not give any oral
medication/fluid.
• Intravenous (IV) or intraosseous (IO) routes
are used most frequently for parenteral access.
IV access can often be gained using a 23-25-g
catheter placed in the cephalic or jugular vein.
However, kittens’ short legs can make catheter
placement difficult and flow hard to maintain. IO
access can be easily gained using the proximal
femur (see separate notes). Subcutaneous (SQ),
intramuscular and intraperitoneal (IP) routes are
less advisable as the absorption is slower and less
reliable than in adults, especially if dehydration
or shock is present. In addition, the IP route
requires strict asepsis, and carries a small risk of
puncturing viscera. If the IP route is to be used the
daily fluid requirement is calculated (see below)
then the volume is divided, and given 2-3x daily.
• Fluid requirements per kg are higher in neonates
than adults but total volumes required are low.
Immature kidneys lack the ability to concentrate
urine so fluid losses cannot be controlled,
especially if there is concurrent vomiting and/or
diarrhoea. Maintenance fluid rates in kittens <2
weeks of age are 130-220ml/kg/24h (ave. 180ml/
kg/24h), by weaning ~120ml/kg/24h, and adult
levels of ~50-65ml/kg/24h from 6 months.
e.g. 1 week old kitten, 200g, needs 36ml fluid/24h
maintenance; 1.5ml/h (~1 drop/40 seconds using
a paediatric giving set).
If 7% dehydrated; deficit = 14ml.
Fluid rate ~2.5ml/h over 6h (1 drop/20sec), then
reduce to ~2ml/h (1 drop/30sec); but always
monitor for over-hydration.
Back to contents
R
• Use fluid pumps, syringe pumps, or a burette with
a paediatric giving set (60 drops/ml) to reduce the
risk of over-hydration to which all neonates are
particularly susceptible (in part because of their
immature kidneys).
• While sick neonates are often acidotic their
reduced hepatic ability to metabolise lactate to
bicarbonate means that lactated Ringers should
not be given. Saline or Ringer’s are better choices
in kittens <7 weeks of age. In severe acidosis
bicarbonate can be given as per known acid-
base status, or ~2mmol/kg can be given over 10-
15mins. Hypoglycaemic kittens should be given
5% dextrose solution mixed 50:50 with saline, or
1-2ml of 10-25% glucose in very severe cases.
All fluids should be carefully warmed prior to
administration and kittens should be closely
observed for signs of over-hydration.
• Once the kitten has been warmed up and given
fluid therapy it must be allowed to recover quietly.
Feeding can only begin once the kitten is warm
and able to suck. Stomach tubing is not helpful
here, since when a kitten is cold and collapsed its
intestines stop functioning, so stomach contents
can be easily regurgitated and then aspirated. As
soon as the kitten is able to suck, it should be
given isotonic glucose or Lectade solution (~1ml/
100g body weight) given every 15 minutes until
it is rehydrated and can urinate when massaged.
If all goes well, diluted milk replacement formula
can then be introduced after 24 hours, and full
strength milk 24 hours after that.
• The administration of antibiotics is not
recommended, particularly for the treatment of
diarrhoea. Antibiotics severely disrupt the process
of normal colonisation of the gut by harmless
bacteria, and can therefore make the situation
worse. Antibiotics cannot be used as a substitute
for colostrums and good hygiene.
5. Constipation: This is a very common problem,
particularly in hand reared kittens, probably
due to the difficulty in stimulating defecation
2006 World Congress WSAVA/FECAVA/CSAVA
sufficiently frequently. Normal kitten faeces have
the consistency of toothpaste. If the faeces become
very hard, making the kitten strain excessively,
or if a kitten does not pass any motions for 2-3
days, small doses of liquid paraffin or “Katalax”
should be given, (about 0.5 ml per feed for 2-3
days should have the desired effect). Severe cases
may require de-impaction.
6. Treatment for NI: For the cause of NI see notes
on Neonatology. Kittens showing signs of NI, if
<24h old, should be immediately removed from
their mother to prevent further absorption of anti-
A antibodies. In kittens, most colostral antibodies
are absorbed by 12-24h of age. Once removed, the
kittens can either be fostered to a type-A queen, or
fed milk replacer for 24 hours. After this time it
711
 R
is generally safe for them to be returned to their
dam.
If the anaemia is severe or progressing a blood
transfusion should be performed. While kittens
can survive with very low PCV (6-8%) they are
very unstable, and should be pre-oxygenated
prior to intervention. New born kittens lack anti-
erythrocyte antibody, so at this time the only
circulating antibody is that which was gained
from the queen (anti-A antibody). Therefore, if the
kitten is transfused with A-type blood, these cells
will also be destroyed by the queen’s antibodies,
exacerbating the clinical signs. In the first 3 days
of life it is therefore most appropriate to give a
transfusion of the queen’s erythrocytes as these
will not be destroyed by her antibodies. It is
advisable to wash the queen’s erythrocytes prior
e.g. 200g kitten with a PCV of 8%. If the PCV of the donor is 30% and target PCV for the kitten is 20%,
then the volume of blood needed is:
target PCV-actual PCV x 100 x body weight (kg) = 0.2-0.08 x 100 x 0.2 = 8ml
donor PCV
Blood should be given at 7-15ml/kg/h.
7. Infections:
• Treatment of bacterial infections:
Ideally, antibiotics would be selected according
to culture and sensitivity testing. However, it is
often not possible to wait for laboratory results as
illness in neonates can progress rapidly. In many
situations antibiotics must be selected empirically.
The penicillins are generally less toxic than most
other antibiotics, and are often used as a first
choice. However, oral ampicillin must be given
with caution as it can alter the gastrointestinal flora
and cause diarrhoea. Generally, the parenteral
administration of antibiotics is preferred, because
2006 World Congress WSAVA/FECAVA/CSAVA
oral medications may not be absorbed efficiently.
Cephalosporins are often used as a second choice,
with perhaps azithromycin as a third (although
extensive studies have not been performed with
this drug).
Other antibiotics may be considered depending
of the nature of the infection. In all cases consult
the data sheets. Trimethoprim-sulphonamide
combinations may be used at reduced dosages,
but should be avoided in kittens with anaemia
or leukopenia. Macrolides (erythromycin,
clindamycin and lincomycin) and metronidazole
(MZL) should be used with caution in kittens
with impaired hepatic function (and in the case
of MZL should be give at much reduced doses
~5mg/kg/12h).
Antimicrobials that should be avoided in
712
Back to contents
to transfusion. To do this it is necessary to collect
2-5ml of the queen’s blood (anti-coagulated with
EDTA or heparin), centrifuge it at 1000 rpm for
1 minute, discard the supernatant, restore it to its
original volume with normal saline, centrifuge as
before, discard the supernatant, then re-suspend
again in saline. The cells can then be transfused,
via a 22-g needle via IO access (see separate
notes). The kitten will start making its own anti-
B antibodies soon after birth. After the first day
the level of maternally derived anti-A antibody
will fall. If the kitten needs a transfusion after 3
days of age it is usually safer to use washed type-
A erythrocytes. Despite removing the kittens as
soon as clinical signs are noted, most kittens that
develop NI die within their first week of life.
0.3
neonates include aminoglycosides (renal damage
and ototoxicity), tetracyclines (binding to bone
causing dental damage), chloramphenicol (bone
marrow suppression) and, perhaps, quinolones
(damage to growing cartilage – risk probably
overstated in kittens, but should be avoided in
pregnant animals).
Sepsis is common in neonates, and very difficult
to treat. In addition to parenteral fluids and broad-
spectrum antibiotic cover, plus good nursing
care, the increased energy requirements in these
cases (x1.5 neonatal maintenance requirements),
means that supplemental feeding is essential
in patients that typically have vomiting and/or
diarrhoea, necessitating the use of anti-emetics
(which are not licensed and not without risks in
neonates) or the use of parenteral nutrition (which
is incredibly difficult to do). If failure of passive
transfer is suspected, consider giving adult serum
IV (volume as per fluids).
• Treatment of viral infections:
Treatment of viral disease is often very difficult,
which is probably why in a large study of causes of
kitten death 75% of cases occurred post-weaning,
and most of these resulted from viral infection
(FCV, FHV-1, FPV and FIP). Neonatally FeLV,
FIP, or FPV-infected kittens rarely survive. In all
cases supportive therapy is essential; including
fluids, nutrition, and covering antibiotics.
• Treatment of parasitic infections:

Toxocara may be treated with pyrantel or
fenbendazole. Giardia may be treated with
fenbendazole or metronidazole. T. foetus may be
treated with ronidazole (not licensed). Coccidal
infections may be treated with trimethoprim/
sulphonamide and improved sanitation.
Toxoplasma infections may be treated with
clindamycin. Neonates from 2 days of age may be
treated with fipronil for fleas and lice. Ivermectin
is not recommended for the treatment of ear mites
as idiosyncratic reactions can occur. For more
information on the use of therapeutics in neonatal
infections see Hotston Moore and Sturgess
(1998).
Useful references and information:
Cave TA, Thompson H, Reid SWJ, Hodgson DR
and Addie D (2002) Kitten mortality in the UK:
Back to contents
R
histopathological examinations (1986-2000). VR
151: 497-501
Chandler LM (1992) Pediatric normal blood
values. Kirk’s Current Veterinary Therapy XI,
eds. RW Kirk and JD Bonagura, WB. Saunders,
Philadelphia. pp. 981-984
Hoskins JD (1995) Fluid therapy in the puppy and
kitten. Kirk’s Current Veterinary Therapy XII,
eds. RW Kirk and JD Bonagura, WB. Saunders,
Philadelphia. pp. 34-37
Hotston Moore P and Sturgess CP (1998) Care of
Neonates and Young Animals. BSAVA Manual
of Small Animal Reproduction & Periparturient
Care, p 153-169
Sturgess CP (2006) Feline paediatric medicine.
EJCAP 16(1): 83-94
2006 World Congress WSAVA/FECAVA/CSAVA
713
 R
R – Reproduction
SMALL ANIMAL NEONATOLOGY: THEY LOOK NORMAL WHEN
THEY ARE BORN AND THEN THEY DIE
Dr. Danielle Gunn-Moore
University of Edinburgh
Danielle.Gunn-Moore@ed.ac.u
Kitten deaths
Sadly, it is inevitable that some kittens will die,
and a low level of loss is to be expected, even
in the best run breeding cattery. It is generally
found that pedigree cats have higher levels
of neonatal mortality than non-pedigree. In
one study, pedigree cats had an average kitten
mortality of 34.5% from birth to one year of age
(range of 8-40%), compared to 10-17% in non-
pedigree cats. These higher levels of mortality
may reflect inbreeding within pedigree cats.
However, there may also be bias in the non-
pedigree data as it is difficult to get accurate
figures for pet cats.
Kitten deaths can be divided into those occurring
in the pre-weaning period (stillbirths and deaths
in the first 4 weeks of life), and those occurring
in the post-weaning period (deaths occurring
from weaning to ~6 months of age). Overall,
pre-weaning mortality is commonly 15-30%,
and stillbirths typically account for <10% of all
kittens born; although, the prevalence can vary
considerably; from 6-22% in pedigree cats.
Kitten mortality is highest in the first week of
life (typically >90% of all kitten mortality),
2006 World Congress WSAVA/FECAVA/CSAVA
after which it declines, only to rises again just
after weaning. Pre-weaning losses usually result
from non-infectious causes while infectious
causes are more prevalent post-weaning. This
is because prior to weaning the kittens are
relatively protected from infectious disease by
maternally derived antibody (MDA) (see section
on infectious disease for more information on
MDA). Kittens dying between birth and weaning
are frequently called ‘fading kittens’.
Neonatal kittens may die suddenly, or present
as ‘poor doers’ and ‘fade’ within a few days.
Unfortunately, the clinical signs of many
neonatal diseases are very similar and vague.
While normal kittens tend to cuddle together and
sleep contentedly between feeds, sick kittens
tend to lie separately, are generally more restless,
714
Back to contents
are not keen to suckle, and cry frequently (if still
strong enough to do so).
Neonates are vulnerable because their
thermoregulatory mechanisms are poorly
developed, they are at increased risk of
dehydration and hypoglycaemia, and they
are immunologically immature. Therefore,
regardless of the initiating cause, neonates
rapidly become hypothermic, hypoglycaemic,
dehydrated, hypoxic, and die. They are
predisposed to hypothermia because they
cannot thermoregulate, lack insulating fat and
thermogenic brown, cannot induce peripheral
vasoconstriction, cannot react to cold by
shivering, and have a large surface area to volume
ratio over which to loose body heat. Hypothermia
then triggers ileus and reduced intestinal
absorption, increases susceptibility to infection,
and eventually leads to cardiopulmonary failure.
Neonates are predisposed to hypoglycaemia
because they have high energy requirements (2-
3x the metabolic rate of adults/kg body weight),
but have no energy reserves and their immature
livers are inefficient at generating energy. This
can then be exacerbated by hypothermia-induced
reduction of intestinal absorption. The neonatal
risk of dehydration is because they have a higher
percentage of body water (82%) than adults,
while incurring greater loses through their
immature kidneys, lungs and skin.
Causes of ‘fading’ or sick kittens:
• Birth / queen-related factors (kitten hypoxia,
trauma, hypothermia)
• Congenital abnormalities
• Low birth weight
• Inappropriate environment (temperature,
humidity, hygiene, overcrowding, over-handling)
• Inappropriate nutrition
• Neonatal isoerythrolysis (NI)
vInfection (viral, bacterial, parasitic)

1. Birth / queen-related factors
Kittens that suffer dystocia have a significantly
increased risk of death within the first few weeks
of life. In fact, prolonged labour or dystocia are
probably the most significant causes of neonatal
death. This results from the effects of hypoxia and/
or trauma. Dystocia occurs in ~6% of pregnancies
(range 0-18%). Studies have shown that cats with
extremes of conformation, such as the Siamese
and Persians, experience much higher levels of
dystocia (7-10%; see FAB Manual) than cats with
normal conformation (generally <5%). Hypoxia
during birth can result in stillbirth, or the birth
of weak, slow, kittens that fail to suckle. These
kittens usually die within the first week of life or,
due to failing to ingest sufficient colostrum, have
an increased risk of infectious disease.
Kitten mortality is usually highest in the first litter
born to a particular queen and after her fifth litter.
The high death rates in kittens from first-time
queens probably relates to inexperience, trauma
and cannibalism. Older queens tend to have
smaller litters and tend to produce more kittens
with congenital defects. The negative effect of
extremes of litter size is seen as reduced survival
of single kittens, and of kittens from litters of
7 or more. Kitten mortality also increases with
increasing maternal obesity, and with other queen-
related causes, including a lack of milk, mastitis,
or maternal neglect.
2. Congenital abnormalities
Obvious physical defects may be seen in 10-20%
of stillborn kittens. However, the prevalence
varies considerably; from 1-10% of kittens born to
research cats, to 1-31% of kittens born to pedigree
cats. Congenital disorders are present from birth,
and can affect any body system. They may result
from genetic disorders (see refs.) or teratogenic
factors. Because inbreeding increases the risk
of genetic disease, congenital disorders are seen
more frequently in pedigree cats. In addition,
certain defects are seen more frequently in some
breeds than others (see FAB Manual and refs.).
Congenital defects resulting from exposure to
teratogenic substances may be seen in cats of
any breed. For example, cleft palates may result
from treatment with griseofulvin, corticosteroids,
or excessive amounts of vitamin A; skeletal
deformities may result from the administration
of organophosphate anti-flea products. It has
also been suggested that overheating, in some
pregnant cats, may result in an increased risk of
skeletal deformity in their kittens. Severe defects
usually result in stillbirth or early neonatal death.
Milder disorders may result in fading kittens, or
only become apparent later in life.
Back to contents
R
3. Low birth weight
Underweight kittens have a significantly
increased risk of neonatal death. They are
physiologically immature compared to normal-
weight kittens, and they may be too weak to nurse
adequately. In addition, they lack insulating fat
and thermogenic brown fat, and they have weak
thoracic muscles and immature lung development.
They are particularly susceptible to hypothermia,
dehydration, respiratory failure, and sepsis.
Kittens may be born underweight because of
maternal malnutrition or ill-health; congenital
disease; in utero infections; or any condition that
results in poor placental blood supply. The average
birth weight for most breeds of cat is 100g ± 10g.
However, it is normal for some breeds to have
significantly smaller kittens (Oriental; ave. 80g);
while others (Maine Coon) have significantly
larger kittens (ave.120g) (see FAB Manual).
It is therefore very important to know what the
average weight for kittens of a particular breed is
when trying to decide whether or not a particular
kitten is underweight. As a general guideline
newborn kittens <75g are likely to have very high
death rates.
4. Inappropriate environment
Environmental factors, such as extremes of
temperature and humidity, poor hygiene,
overcrowding, or over-handling, all result in
increased kitten mortality. Ideally, the kittening
room should be well ventilated, draft free,
and maintained at a fairly constant 18-24oC,
55-60% humidity. This will allow the dam to be
comfortable, and she can supply any additional
heat required by the offspring. Where kittens
have to be hand-reared it is necessary to supply
additional heating. Ideally the temperature in
the box should be maintained at 29-32oC, but
the box should be large enough for the kittens to
move away from the heat if they become too hot.
The temperature is gradually reduced to 27oC by
2006 World Congress WSAVA/FECAVA/CSAVA
7-10 days and 22oC by the end of the first month.
Overcrowding will lead to increased infectious
disease and disease resulting from competition at
the mother’s nipples (which can in turn result in
inadequate nutrition [see below]). Over-handling
will not only limit the kitten’s feeding time, but
with nervous queens, may result in cannibalism
of her kittens.
Providing kittens with a suitable environmental
temperature is essential. A kitten that has ceased
to suckle regularly will quickly become cold and
hypoglycaemic. Since neonates cannot shiver and
are unable to control their own body temperature
hypothermia will result, and this will lead to a
further reduction in activity and suckling. The
rectal temperature of new-born kittens ranges
715
 R
from 35-37oC in the first week, to 36-38oC in the
second and third weeks, and reaches normal adult
levels of 38-39oC by the fourth week.
Hypothermia is particularly harmful as it can
initiate a number of other problems. For example:
a week-old kitten should have a temperature
of 35-37oC and a heart rate of 200-250 bpm.
However, if its temperature falls to 30oC, its
heart rate will fall to 40-50 bpm. While this is
initially a protective response, if sustained, it can
lead to a decrease in respiratory rate, which may
in turn lead to cardiopulmonary failure. Also, a
hypothermic kitten will not suckle effectively, its
gastrointestinal motility will become depressed,
and it will have an increased susceptibility to
infection. It is therefore important to check the
temperature of any potentially weak or ill kittens.
However, if their rectal temperature is <34oC the
kitten is likely to die.
5. Inappropriate nutrition
Care should be taken to feed the queen an
appropriate diet. Incorrect nutrition of the
queen can affect the quality of the milk she
produces. Generally, when the queen is healthy
and producing adequate milk the kittens should
have no problems with inappropriate nutrition.
Inadequate milk production may be associated
with an inexperienced or overly nervous queen,
old queens, sick or malnourished queens,
dystocia, certain familial traits, systemic
illness or mastitis. Inadequate milk uptake by
the kitten can also result from anything causing
kitten ill-heath or weakness, from competition
and bullying by siblings, or any environmental
factor that distracts or upsets the queen-kitten
bond.
Normal kittens should suckle within 2 hours of
birth as they can only adsorb colostrum in the first
16-24 hours of life. Since any kitten not gaining
2006 World Congress WSAVA/FECAVA/CSAVA
sufficient weight has an increased risk of neonatal
death it is important to weigh kittens regularly (at
birth, daily for the first week, then at least twice
weekly until after weaning). A loss of <10%
may be expected in the first 24h, but after that
there should be daily weight gain (~10-15g/day;
5-10%); they should double their birth weight
by 1-2 weeks of age and weight gain should be
steady and progressive. Any weight loss (or lack
of weight gain) should be investigated, and any
kittens losing more than 10% body weight are
unlikely to survive.
It is essential that kittens gain adequate nutrition
as they have a greater risk of developing
hypoglycaemia than adults. This is because they
are metabolically less able to generate glucose than
adults, while having a much larger requirement
716
Back to contents
for it. Any kitten that is ill or stressed may develop
hypoglycaemia. This may be seen as weakness,
hypothermia, crying, difficult breathing, seizures,
coma and, eventually, death.
Neonatal kittens are also very susceptible to
dehydration. This may result from inadequate
consumption of milk, or excessive fluid losses
(usually associated with overheating, excessively
low humidity, or diarrhoea). Kittens contain
relatively more body water than adults and
their water turnover rate is twice that of adults.
Neonatal kitten maintenance fluid requirements
are ~130-220ml/kg/24h, compared to 50-65ml/
kg/24h for a mature cat. This is because kittens
have greater fluid losses through their skin, lungs
and kidneys, which are all immature.
Since the kittens derive all of their food and
water in the form of milk, when the supply is
inadequate, supplemental feeding is needed.
Where the kittens have been orphaned or the
queen is unable to feed them they will need
total replacement feeding (see FAB Manual).
Weaning should begin at 3-4 weeks of age.
It is important to ensure that all of the kittens
gain sufficient food at this time. In large litters
competition at the food bowl can lead to weaker
kittens being bullied and so eat less.
6. Neonatal isoerythrolysis (NI)
In certain cat breeds NI is a relatively common
cause of fading kittens. It results from the immune-
mediated destruction of a kitten’s erythrocytes by
its mother’s antibodies. The maternal antibodies
enter the kittens via the colostrum when the
kittens first suckle. The kittens are born healthy.
However, after suckling, affected kittens may die
suddenly or stop feeding, become weak, and show
haemoglobinuria (brown stained urine). These
kittens may then develop jaundice, anaemia,
tachypnoea, and tachycardia. In severe cases this
leads to collapse and then death. Surviving kittens
may develop necrosis of the tail-tip and other
extremities, which may then slough between 3
days and 2 weeks of age.
Cats have 3 blood groups; Type A, B, and AB.
Type A is genetically dominant to Type B.
Genetically, a Type A cat may therefore be A/
A or A/b. The rare blood type AB is inherited
slightly differently, and is recessive to Type
A but dominant to Type B. AB cats are only
found in breeds in which the Type B has been
identified, usually increasing in frequency as
the percentage of Type B cats increases. The
frequency of Type A, B and AB blood types
varies between breeds (Table below), and also,
to some extent, between countries. Generally,
most domestic short and longhaired cats (DSH/
DLH) are Type A (75-100% Type A; 0-25%

Type B; 0-10% Type AB). Interestingly, the
Bengal breed appears to have a particularly high
Table: Breed prevalence of feline blood types
100% Type A ~80% Type A 75-100% Type A
Siamese Somali DSH/DLH
Burmese Abyssinian Persian
Tonkinese Birman
Oriental Maine Coon
Norwegian Forest Cat
Cat
All Type B cats have high levels of naturally
occurring antibody directed against Type A
erythrocytes, while only a third of Type A cats
have naturally occurring antibody directed
against Type B erythrocytes (and the amounts of
antibody are usually rather low). NI occurs when
a Type B queen gives birth to a Type A kitten.
When the kitten suckles colostrum the maternal
anti-A antibodies enter the kitten’s circulation
and attack its erythrocytes, causing anaemia and
jaundice. Since these antibodies occur naturally,
the queen does not need to be sensitised by
previous pregnancies or blood transfusions. Since
the highest proportion of Type B cats are seen in
BSH cats, NI is seen most frequently in this breed
of cat.
Where NI is seen, all sexually active cats should
be blood-typed to prevent further inappropriate
mating. In addition, it is recommended that
all BSH cats should be blood-typed prior to
breeding. This can be done using a simple in-
house test card (Rapid Vet-H, dms laboratories).
It is important to ensure that Type B queens do
not mate with Type A toms. Where an unknown
mating has occurred, placental blood can be used
to determine a kitten’s blood type. If the queen’s
blood-type is known to be Type B, and a kitten is
found to be a Type A, it can be prevented from
suckling the queen, at least until it is >24h old.
While this procedure will prevent the occurrence
of NI, the lack of colostrum will leave the kitten
at risk of infectious disease.
Kittens showing signs of NI, if <24h old, should
be immediately removed from their mother to
prevent further absorption of anti-A antibodies.
In kittens, most colostral antibodies are absorbed
by 12-24h of age. Once removed, the kittens can
either be fostered to a Type-A queen, or fed milk
replaced formula for 24 hours. After this time it
is generally safe for them to be returned to their
Back to contents
R
number of AB cats, although actual prevalence
data are not yet available.
60% Type A 40% Type A
Devon Rex British Short
Hair (BSH)
dam. If the anaemia is severe a blood transfusion
will need to be performed (see separate notes).
However, despite removing the kittens as soon as
clinical signs are noted, most affected kittens that
die within their first week of life.
7. Infection
In general, infections are involved in relatively
few early neonatal deaths. However, they can
result in significant mortality from 3-4 weeks
of age onwards. Since neonatal kittens have
immature immune systems, and gain <5% of
their MDA transplacentally, they need to gain
protection from infectious disease via transfer of
MDA in the colostrum. The passive protection of
the intestines by MDA continues for the entire
duration of suckling as IgA antibodies resist gastric
degradation and can bind potential pathogens in
the gut lumen, preventing them from attaching to
or penetrating the intestinal mucosa. The ability
of neonates to absorb MDA begins to decline 6h
after birth, and is no longer possible after ~48h.
The majority of neonatal infections are caused
by agents to which vaccines are not available; 2006 World Congress WSAVA/FECAVA/CSAVA
it is therefore important that neonates are born
into the same environment as their dam has been
living since she will then have raised antibodies
against its resident infectious organisms. The
protective effect of systemically absorbed MDA
usually begins to wane from 3-4 weeks of age.
The kittens’ natural immunity is still developing
at this time, and since most vaccine regimens do
not start until ~8 weeks of age, this can leave a
period of time when the kittens are particularly at
risk from these infectious diseases.
A healthy kitten should be able to cope with
a low level of infectious organisms within its
environment. It will generally experience no more
than occasional mild and brief clinical signs.
However, if the kitten’s immune system becomes
717
 R
suppressed serious disease or fatal infections
may occur. Factors which may contribute to an
inadequate immune response include inadequate
colostrum intake, inadequate nutrition, low birth
weight, peri-natal hypoxia, congenital disorders
(especially of the immune system), previous trauma
or infection, a low environmental temperature, or
an unhygienic environment leading to a build up
of contamination with infectious agents.
Respiratory and gastrointestinal infections are
seen most frequently. (See FAB Manual, refs
and separate lecture for the treatment of sick
neonates).
Viruses
• The cat flu viruses (feline calicivirus [FCV] and
feline herpes virus [FHV-1]) are perhaps the most
commonly seen viral infections of kittens. While
in healthy kittens infection may be mild and brief,
weak kittens may develop more severe clinical
signs or secondary bacterial infections. FHV-1
infection may also be associated with abortion.
• Feline coronavirus infection (FCoV), like
the cat flu viruses, is hard to eliminate from
breeding catteries. When present infection may
be associated with an increased incidence of
reproduction failure, abortions and stillbirths.
Affected kittens may show signs of diarrhoea,
malaise, or ‘fading’, and occasional cases of more
classical effusive feline infectious peritonitis
(FIP).
• Feline panleukopenia virus (FPV) is usually
seen in catteries that fail to vaccinate properly.
It is occasionally seen in kittens from vaccinated
queens, possibly resulting from severe
environmental contamination. Infection may
result in abortions, stillbirths, fading kittens,
diarrhoea, panleukopenia, septicaemia, cerebellar
ataxia, and/or death.
• Feline leukaemia virus (FeLV) has been
almost eliminated from the pedigree breeding
2006 World Congress WSAVA/FECAVA/CSAVA
population in many countries. Neonatal disease
caused by this infection is therefore seen mainly
in rescue catteries. In this situation it may result
in reproductive failure, abortions, stillbirths,
fading kittens, a panleukopenia-like syndrome,
septicaemia or death.
• (In puppies canine herpes virus is a common
cause of puppy loss, and can result in abortion,
or neonatal death associated with abdominal
distension and pain at <3weeks of age. Other
common viral infections of puppies include
canine distemper virus, canine parvovirus, canine
coronavirus [which appears to be changing
in significance], canine adenovirus-2, and
parainfluenza).
Where infectious disease is suspected it is
important to ensure that the queens’ vaccination
718
Back to contents
programme is up to date. Since kittens gain some
protection from infectious disease in the form of
MDA passed in the colostrum, it may help to give
booster vaccines prior to mating. In some cases
it may be appropriate to instigate an isolation
breeding and early weaning programme (see FAB
Manual).
Bacteria
In kittens, bacterial infections are often seen
secondary to viral infection (cat flu, FeLV, FIV,
FPV, FIP). However, bacterial infections can
also be seen without prior viral infection. In most
cases the bacteria originate from the queen’s birth
canal (beta haemolytic Streptococcus sp. [Strep.
G infection]), gastrointestinal tract (E. coli,
Salmonella sp., Campylobacter sp., many normal
enteric bacteria), or respiratory tract (Bordetella
sp., Pasturella sp., Mycoplasma sp.). Clinical
signs depend on the site, nature, and severity of the
infection. They may include diarrhoea, coughing,
dyspnoea, polyarthritis, omphalophlebitis, or
dermatitis, as well as the less specific signs more
typical of fading kittens.
Ultimately, many of these infections may result
in septicaemia and death. The increased risk of
sepsis in neonates results from the factors listed
above, especially failure of passive transfer of
MDA. In addition, neonatal propensity to develop
hypoglycaemia and intestinal ileus (especially
when cold), significantly increases the risk of
translocation of enteric bacteria into the blood
stream. This is exacerbated by sepsis further
predisposing to hypothermia and hypoglycaemia
(possibly resulting from impaired liver function,
depletion of glycogen, and peripheral utilisation
of glucose by bacteria and leucocytes). Disease
may be very sudden or may run a more protracted
course. While the clinical signs are varied, they
frequently result in bradycardia, dyspnoea,
dehydration, weakness, crying, seizures, coma
and death. Sepsis often occurs as the final stage
of other conditions, and is particularly associated
with systemic viral infections. The most common
cause of sepsis are gram-negative bacteria, but can
include; Streptococcus, E. coli, Staphylococcus,
Klebsiella, Enterobacter, Enterococcus,
Pseudomonas, Clostridium, Bacteroides,
Fusobacterium, Pasteurella and Salmonella.
Parasites
In well-run catteries parasite infestation should
not be a problem. Where queens are not wormed,
heavy kitten infestations can result in a poor body
condition, soft or bloody stools, lack of appetite,
a pot-bellied appearance, weight loss, and
occasionally death. A severe flea, tick or hookworm
infestation can result in significant anaemia. Gut

parasites, such as Giardia, Tritrichomonas foetus,
Isospora or Cryptosporidia may cause diarrhoea
and a failure to thrive. Toxoplasma infection may
result in abortion, stillbirths and fading kittens.
In general
Where specific infections keep recurring it may
be necessary to try to detect carrier animals.
However, since a number of infections can cross
R
between species, affecting both cats and dogs,
and even humans, it may be necessary to look for
carriers amongst pet dogs, or even the owners.
This is true for many of the bacterial and protozoal
gut infections (e.g. Salmonella, Campylobacter,
Giardia and Cryptosporidia), and can also occur
with Bordetella bronchiseptica (which is one of
the causes of ‘Kennel Cough’).

Table: Infectious agents which may cause disease in kittens

Respiratory tract Feline herpes virus (FHV) (Also called feline rhinotracheitis virus)
Feline calicivirus (FCV)
Chlamydophila felis (formerly Chlamydia psittaci)
Mycoplasma sp.
Bordetella bronchiseptica
Feline coronavirus (FCoV)
Gastrointestinal tract Feline panleukopenia virus (FPV)
FCoV
Salmonella sp.
Campylobacter sp.
Giardia sp.
Tritrichomonas foetus
Isospora sp.
Cryptosporidia sp.
Toxocara cati
Ancylostoma tubaeforme
Cutaneous Fleas
Lice
Otodectes sp.
Microsporum canis
Systemic Bacterial sepsis (Streptococcus sp., E. coli, Salmonella sp. etc.)
Feline leukaemia virus (FeLV)
Feline immunodeficiency virus (FIV)
FCoV
FPV
Toxoplasma gondii
Misc. Staphylococcus and Streptococcus sp (bacterial omphalitis, polyarthritis)

2006 World Congress WSAVA/FECAVA/CSAVA

General approach to unravelling causes of kitten
mortality
Trying to find out what may be causing kittens
to ‘fade’ can be very difficult. Firstly, it is hard
to decide exactly when there is a significant level
of neonatal mortality. Secondly, most cases are
multifactorial, so a number of factors may need to
be addressed in order to reduce mortality. Thirdly,
clinical signs are generally non-specific and the
small size of kittens makes collection of samples
difficult. Generally, concern should be raised
when pre-weaning losses exceed 20%, post-
weaning losses exceed 10%, the number of losses
suddenly increases, or a particular cause of death
is seen more frequently than previously.
It is strongly advised that cattery owner’s should
keep detailed records of all animals within their
Back to contents
premises; including details of matings, litter
sizes and birth weights. All incidents of disease
should be noted. It is by noting changes in the
morbidity and mortality patterns that problems
can be recognised early. Using this data it may be
possible to track the spread of infectious disease
or determine the breed-line of a genetic disorder.
Since there are usually no particular clinical
signs that suggest a specific disease, investigation
usually involves looking at the entire cattery.
In most cases some aspect of the environment
is not ideal, or aspects of the management and/
or nutrition are unsound. A full investigation is
often needed before any recommendations can be
made. The investigator will need a background
history of the cattery and want to examine
all sick animals; looking for obvious signs of
719
 R
trauma, congenital defects or disease. Because it
is difficult to collect blood samples from young
kittens the most useful samples are often collected
after a kitten has died. For this reason it can be
very useful to have post mortem examinations
performed on any kittens that die. The breeding
queens, particularly the mothers of any fading
kittens, should also be examined. Ideally, they
should be observed interacting with the rest of
the litter, then examined for signs of general ill
health, metritis, mastitis, or aggression towards
the kittens.
In order to determine if environmental factors are
involved, the investigator may need to visit the
cattery. They may want to look at the design and
construction of the premises, consider the source
of new stock, the genetic relationships between the
cats, the total number of cats (and other animals)
within the household, the size of any subgroups,
and the day-to-day cleaning protocols. They may
also want to discuss any recent changes in the
management of the cats (feeding, vaccination,
worming, flea treatment, use of isolation facilities,
etc).
It is useful to remember that a single design
defect or a particular bad practice rarely causes
an outbreak of disease. More typically, disease
outbreaks result from an ‘event cascade’, where
a number of different confounding factors come
into play.
(See separate lecture for specific treatment options
for sick neonates).
2006 World Congress WSAVA/FECAVA/CSAVA
720
Back to contents
Useful references and information:
Blunden AS (1998) The Neonate: Congenital
Defects and Fading Puppies. BSAVA Manual
of Small Animal Reproduction & Periparturient
Care, p 143-152
Feline Advisory Bureau Manual of Cat Breeding
(2006), FAB Publications, Tisbury.
Feldman DC and Nelson RW (1987) Feline
reproduction. In: Canine and Feline Endocrinology
and Reproduction. Ed. Feldman DC and Nelson
RW, WB. Saunders, Philadelphia. pp. 525-548 (or
the 2004 edition).
Hoskins JD (1995) Fading puppy and kitten
syndrome. Kirk’s Current Veterinary Therapy XII,
eds. RW Kirk and JD Bonagura, WB. Saunders,
Philadelphia. pp. 30-33
Hotston Moore P and Sturgess CP (1998) Care of
Neonates and Young Animals. BSAVA Manual
of Small Animal Reproduction & Periparturient
Care, p 153-169
Little S (2004). Breed Specific Reproduction
Projects; Heritable Aspects of Cat Breeding;
Feline Reproduction: A Manual for Cat Breeders
and Veterinarians (CD ROM); www.catvet.
homestead.com , SusanLittleDVM@compuserve.
com
Sturgess CP (2006) Feline paediatric medicine.
EJCAP 16(1): 83-94
 R
R – Reproduction
HOW TO PERFORM TRANSCERVICAL CATHETERIZATION
IN THE BITCH
Alain Fontbonne DVM, MSc,
Dipl. ECAR,
Maître de Conférences
Reproduction Animale - Ecole
Nationale Vétérinaire d’Alfort
(Paris)
7 avenue du Général de Gaulle
94704 Maisons - Alfort Cedex
France
e-mail: afontbonne@vet-alfort.fr

It has been proven that intra-uterine artificial The catheters have to be ordered in Norway
inseminations (AIs) in the bitch is likely to give (Dr Jan Fougner: fougner@norpels.no). The
better results, especially when using chilled or price for each of the three ordinary catheters is
frozen semen (Linde Forsberg et al. 1995, 1999). approximately in NOK (Norwegian crowns). 350.
The number of veterinarians practicing these two All catheters is included the plastic/nylon incerting
techniques is increasing nowadays, and we can tube. (Extra plastic speculums cost NOK 50,-, but
expect that, in the coming 10 years, the exchanges can only be delivered as emergency if the original
is damaged).
of dog semen between countries will increase a
lot. In some countries, however, surgical intra-
uterine AIs are forbidden for ethical reasons.
And when they are not, many bitch owners are
reluctant to see their animal anaesthesied only to
be inseminated.
To practice intra-uterine AIs, two major techniques
are available.

1. INTRA-UTERINE INSEMINATION USING

THE SCANDINAVIAN INSEMINATING
DEVICES Fig.1: the three sizes of the scandinavian catheters
This technique has been developped in Norway by (© Linde-Forsberg)
Kjell Andersen. It is close to what is done in cattle
for example. Palpating the uterine cervix through To understand the technique, veterinarians have to
the abdominal wall, the inseminating veterinarian remember that, in the bitch, the cervix is located at
will try to pass a thin metallic catheter inside the end of a dorsal median fold, and its opening is
the opening of the cervix. This technique needs dorsal to a big ventral dead-end (fornix) in the far
a rather long training to be confident with it, but vagina. Therefore, to pass the metallic catheter, 2006 World Congress WSAVA/FECAVA/CSAVA
once veterinarians are skilled in practicing it, it the inseminating veterinarian must first push as
becomes a fast and reliable way of performing far as possible in the vagina, and then retract it
intra-uterine AIs. Only fat and giant bitches are one to three centimetres behind with the right
end, while the left hand grabs the cervix and turns
difficult to inseminate in this way.
it (pivots it) cranially so that the opening of the
The inseminating devices are made of two parts: cervix becomes horizontal.
one plastic white cylindric speculum is inserted
into the vagina and helps finding the cervix and
guiding a metallic inseminating catheter up to
the far vagina. The catheters comes in 3 different
sizes: small; 20 cm. long with thinner tip for the
miniature dogs, medium; 30 cm., fits most sizes,
long; 40cm., for the larger dogs, (there is also an
oversized which is 45 cm. long for the extreme
dogs, but both the long and x-long sometimes
need a stainless steel tube outside as support,
otherways they tend to bend and it is then difficult Fig. 2: position of the two hands of the inseminating
to reach the cervix for fixation). veterinarian (© Fontbonne)
721
Back to contents
 R
requirements, having a 29 cm working length and
22 fr diameter. The endoscope consists of a rigid
telescope with a 30 degree viewing angle together
with a sheath and bridge; a cold light source and
cable complete the essential equipment.

Fig. 3: virtual representation of the inseminating

technique (Andersen 1975)

Fig. 4 and 5: anatomy of the far vagina, explaining

the intra-uterine technique (© Fontbonne)
Fig. 6: position of the inseminating veterinarian
When the tip of the catheter is very close to (© Fontbonne)
the opening of the cervix, most of the time the
operator gets a cartilaginous sensation.
Sedation is most of the time not necessary.
Sometimes, when a bitch is too nervous or has a
firm abdominal wall, it may be useful to sedate the
animal: xylazin (Rompun®): 0.1 to 0.4 mL IV.

2. INTRA-UTERINE INSEMINATION USING

A RIGID ENDOSCOPE
This technique has been developed in New-
Zealand by Marion Wilson. It consists of
guiding an inseminating catheter (most of the
time a urinary catheter - an 8 Fr is suitable but
occasionally a 6 Fr may be necessary), through Fig. 7: visualization and catheterization of the
the cervix opening which is visualised by an cervix through the endoscope (© Fontbonne)
endoscope often linked to a camera and to video-
or computerized monitoring. FURTHER READINGS
This technique needs an expensive equipment Andersen K. Insemination with frozen dog
semen based on a new insemination technique.
2006 World Congress WSAVA/FECAVA/CSAVA

but is nearly always successful – however in

some bitches it may take more than 30 minutes to
manage to pass the cervix. Only miniature breeds
are sometimes difficult to catheterize, as in these
breeds the far vagina is often too narrow to pass
the endoscope.
Endoscopic inseminations bear the great
advantage of allowing the bitch owner to see
what the veterinarian is doing. In this respect they
may be more “commercially” valuable than the
Scandinavian technique.
The requirements result from the significantly
reduced space in the far vagina caused by the
dorsal median fold and the particularly long
vagina, which can be up to 30 cm.
Marion Wilson recommends an extended
length cystourethroscope which best meets the
Zuchthygiene, 1975 Mar, 10(1), 1-4.
Linde-Forsberg C. et al. Comparison of fertility
data from vaginal vs intrauterine insemination of
frozen-thawed dog semen: a retrospective study.
Theriogenology. 1999 Jul 1; 52(1): 11-23.
Linde-Forsberg C. Intra-uterine Insemination in
the Dog using the Scandinavian trans-cervical
catheter and a comparison with other methods. In
“Recent advances in small animal reproduction”
www.ivis.org, 2 feb 2001. 6 pages.
Wilson M.S. Endoscopic transcervical
insemination in the bitch. In “Recent advances in
small animal reproduction” www.ivis.org, 12 dec
2003. 8 pages.

722
Back to contents

R – Reproduction
HOW TO PERFORM INTRAOSSEOUS FLUID ADMINISTRATION IN
NEONATES
Dr. Danielle Gunn-Moore
University of Edinburgh
Danielle.Gunn-Moore@ed.ac.u
Indications
• Intraosseous (IO) infusion is a recommended
route for securing intravascular access in small
cats and dogs, and neonates. It is particularly
useful when peripheral vessels are very small or
collapsed (e.g. with circulatory collapse [shock],
and/or cardiac arrest). Because the vessels in the
bone are supported by a rigid matrix the IO route
remains useful even when all other vessels are
collapsed.
• The IO route can be used for the administration
of resuscitation drugs (any drug that can be given
intravenously), and for volume replacement
with crystalloid, colloids, whole blood, or blood
products.
• Potential access sites vary depending on the age,
size and species of the animal (and include any site
that is routinely used for bone marrow aspiration).
In cats (and small dogs) the most frequently used
route is via the proximal femur. Whichever site is
used it is important that the bone selected for IO
access is intact (i.e. not fractured), and that the
skin over the insertion site is not damaged.
Equipment
• Clippers + skin prep solution
• Sterile gauze + gloves
• Gaseous anaesthesia + face mask, or local
anaesthetic in a 1-2ml syringe + 23-25-gauge
needle.
• 15-18-gauge bone marrow aspiration needle
(but these are too large for small neonates) or 18-
22-gauge 1.5-3.0-inch spinal needle, or narrow-
gauge IO infusion needle. In patients large enough
to use standard bone marrow needles (e.g. Illinois
or Jamshidi needles) these are usually easier to
place than the specifically designed IO infusion
needles (e.g. as supplied by Cook). In very small
neonates 5/8-1.5-inch 18-23-gauge intravenous
needles can often be used.
• Heparinised saline flush solution.
• T-port, intravenous fluids + tubing, suture.
Back to contents
R
Method
• Aseptically prepare the skin over the greater
trochanter (hip). The point of insertion into the
bone is the trochanteric fossa.
• Depending on the stability of the patient, either
‘gas down’ to a light plain of anaesthesia or, if
patient is to remain conscious, administer local
anaesthetic to the insertion site. In the case of the
latter, 1% lignocaine is injected into the subcutis
over the point of insertion, then extended down to
the periosteum of the trochanteric fossa. In order
to avoid the sciatic nerve (which runs caudal to
the femur and can be injured if the needle slips
caudally from the femur) the needle should be
introduced down the medial side of the greater
trochanter, and moved slowly down the bone
into the fossa, injecting small amounts of local
anaesthetic as the needle is advanced.
• Hold the stifle in 1 hand with your thumb laying
along the long axis of the femur and the ball of
the thumb over the greater trochanter. Puncture
the skin with a scalpel point then direct the IO
needle (whichever type has been selected) into
the bone in a similar fashion to the application of
the local anaesthetic (i.e. down the medial side of
the greater trochanter into the trochanteric fossa) 2006 World Congress WSAVA/FECAVA/CSAVA
(Figures 1). Keep the needle parallel to your
thumb at all times. Advance the needle with a
downward “to-and-fro” rotary motion. However,
very little force is needed with neonates as the
bone is usually so soft that it allows the needle
to pass through easily. When the needle passes
through the bone into the marrow cavity, the
feeling of resistance should decrease.
723
 R

Figure 1. Placement of the IO needle in the bone marrow. A) The wing of the ileum can be useful in
dogs, while the proximal femur is preferred in the cat. Picture: Slatter D, Textbook of Small Animal
Surgery, third Edition, 2000, WB Saunders, Philidelphia. B) Detail of the placement of the IO needle
within the bone marrow of the proximal femur. Picture: http://courses.vetmed.wsu.edu/samdx/bm.asp.

• Once in place, the needle should be checked for
proper positioning by manipulation of the femur.
If an IO needle with a stylet has been used, the
stylet should then be removed. In either case,
the needle should be flushed with heparinised
saline. If correctly positioned, saline should
infuse easily into the medulla of the bone. The
needle is then sutured in place, and a T-port and
fluid line attached, before being covered with a
protective bandage.
• Since it is not normally possible to secure the
needle in place using bandage alone, it is best
to suture it to the skin of the outer thigh. The
2006 World Congress WSAVA/FECAVA/CSAVA
giving fluids to small and neonatal cats and
cats with potential cardiac compromise. This is
because fluid overload is a very significant risk,
so it is advisable to use significantly less fluid in
these patients. In addition, their hydration status
should be regularly assessed to ensure that over-
hydration does not occur.
• Gravity flow through a single catheter can be
used in animals of <7.3kg (16lb) body weight.
• Pressurised flow through a single catheter or
gravity flow through multiple catheters can be
used in animals of 7.3-16.4kg (16 to 36lb).
• Pressurised flow through multiple catheters can

leg may be restrained in place, if needed, and
the infusion site should be kept clean while the
needle is in place.
• IO needles can be left in place for up to 72
hours, although their use is often limited by
clotting within the needle. To try to reduce this
risk, the needle should be flushed regularly with
heparinised saline, usually every 6 hours.
• IO fluid administration rates are limited to
~11ml/min with gravity flow and ~24ml/min
with 300mmHg pressure. Care should be taken
if positive pressure infusion is to be used.
• The following recommendations for delivering
shock doses (cats 45-60ml/kg/hr; dogs up to
90ml/kg/h) come from Greg Martin (U of
Queensland, Australia, see Arnold’s website,
below). However, care should be taken when
be used in animals of >16.4kg (36lb). However,
a separate bone must be used for each catheter.
• Rapid IO fluid replacement can be used to
restore sufficient vascular pressure to enable
routine intravenous catheter placement and
continued fluid therapy.
• Once removed, further cannulation of the same
bone cannot be performed as infused fluids
will leak out from the original hole into the
surrounding tissue.
Possible complications
• Before attempting this procedure for the first
time it is advisable to read one of the references
listed below and, ideally, to practise IO needle
placement on a cadaver.
• Occasional animals feel pain during

724
Back to contents

administration of the fluids (especially if the
fluids are cold or irritant, or are run in too fast).
• Infection is the most common complication
of IO fluid administration. It can lead to either
osteomyelitis and/or subcutaneous abscess
formation.
• Extravasation of fluids into subcutaneous
tissue may increase the risk of sterile or infected
cellulitis.
• Poor IO needle placement can lead to traumatic
damage to the sciatic nerve.
• Epiphyseal injury can lead to altered bone
growth.
• Fracture of the femur is an exceedingly rare
complication of this procedure.
• Interestingly, local haemorrhage is almost
unheard of, even in cases of pre-existing
thrombocytopenia and delayed clotting
capability.
Useful references and websites
Hoskins JD (1995) Fluid therapy in the puppy
and kitten. Current Veterinary Therapy XII,
eds. RW Kirk and JD Bonagura, WB. Saunders,
Philadelphia. pp. 34-37
Back to contents
R
Otto C and DT Crowe (1992), Intraosseous
resuscitation techniques and applications, in
Current Veterinary Therapy XI, eds. RW Kirk
and JD Bonagura, Philadelphia: L&B Saunders,
pp.107-109.
Otto, C.M., G.M. Kaufman and D.T. Crowe
(1989), Intraosseous infusion of fluids and
therapeutics, Compend Contin Educ Pract Vet 11
(4): 421-30
Greg Martin, Practical tips on intraosseous fluid
administration: Arnolds Veterinary Products:
www.arnolds.co.uk/intraosseousfluidtherapytips.
asp
Washington State University, College of
Veterinary Medicine, Small Animal Diagnostic
& Therapeutic Techniques: Bone Marrow
Aspiration:
• http://courses.vetmed.wsu.edu/samdx/bm.asp
2006 World Congress WSAVA/FECAVA/CSAVA
725
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

S
S -S
Sof
Soft Tissue Surgery

Back to contents

INVITED LECTURES - FULL PAPERS
S - Soft Tissue Surgery
EMERGENCY WOUND MANAGEMENT
Richard A. Read, BVSc(Hons),
PhD, FACVSc
Professor, Small Animal Surgery
Murdoch University
South St Mudroch
Western Australia
6150
Australia
r.read@murdoch.edu.au
INTRODUCTION
Clinical experience tells us that the potential for
wounds to heal well is enormous. Our knowledge
of wound healing should help us to appreciate
the various roles of the four processes involved
in wound healing:
• Inflammation
• Fibroplasia
• Epithelialisation
• Wound contraction
The relative importance of epithelialisation and
wound contraction varies with each particular
wound, and in particular with the type of wound
closure technique that we choose for a particular
case. Emergency management of wounds is not
fundamentally different from general wound
management – it is the timing of decision making
and the decisions about ordering the steps of the
treatment that are important in the management
of emergency wounds.
In emergency medicine, patients will present with
very different types of wounds. For example:
• acute fresh wounds due to laceration injuries in
which hamorrhage may be the major issue
• acute fresh degloving injuries due to motor
vehicle trauma where open joints, dessication of
deeper structures and pain are the major issues
• dog bite injuries where deep necrosis and sepsis
are the major issues
• grossly infected wounds in animals that have
been injured and have gone missing for days,
where the main issues are often sepsis and its
systemic effects.
The first steps in wound management will
vary with each of these situations. There are
some situations where the wound itself is life-
threatening (eg wounds that penetrate the thorax
or trachea), but in most situations the wound
can be temporarily managed while other life-
threatening issues are addressed.
Back to contents
S
DECISIONS IN MANAGING EMERGENCY
WOUNDS
1. What are the life-threatening issues for this
patient?
2. Will this wound be managed initially by
temporary measures followed by definitive
treatment, or is immediate definitive treatment
indicated?
3. What major impediments to wound healing are
present in this wound?
4. Is there likely to be sufficient local skin
available for closure?
Life threatening issues
• Haemodynamic stability - is there serious
haemorrhage that needs immediate attention,
either by pressure bandage or immediate
sedation/anaesthesia and surgery?
• Is respiratory function compromised (eg
thoracic/neck wounds)?
• Neurological status of the patient (spinal or
head trauma)?
• SIRS/MODS/Sepsis issues present? 2006 World Congress WSAVA/FECAVA/CSAVA
Initial temporary treatment vs definitive
treatment?
• How exposed are underlying tissues (dessication,
hypothermia, contamination issues)?
• Life threatening issues take precedence over
wound needs (head trauma, respiratory
compromise, cardiovascular instability, SIRS/
MODS issues)?
• Physical location of the wound - how easy is it
to temporarily cover this wound?
Impediments to wound healing?
• Presence of necrotic tissue or foreign material?
• Dessicated deeper tissues needing rehydration?
• Presence of sepsis?
• Lack of blood/nerve supply to wounded region?
727
 S
Sufficient local skin for closure?
• Can the edges of the wound be roughly
approximated?
• Is all the local skin viable?
• Anatomical location and availability of skin for
local flaps?
Once these questions have been addressed, the
answers need to be communicated with the
animal owner and the importance of each of
these factors explained in full. Following this, a
treatment plan can be established, laying out the
priorities and the steps in managing the patient in
the order that they will be addressed.
PROBLEMS IN WOUND MANAGEMENT
The most common reasons for failure of a wound
to heal are:
• foreign body/material in the wound
• necrotic tissue present in the wound
• dead space
• infection
• denervation
• failure to create the right local wound
environment (choice of dressing material)
• host factors/disease
• lack of available skin/tension on wound edges.
It is important for the emergency clinician to
have this list in mind when making decisions
about the emergency treatment of wounds.
However, regardless of whether we are dealing
with an emergency wound, or a problem wound,
the principles of wound treatment/ management
remain the same.
TREATMENT PRINCIPLES
1. Remove any barrier to healing.
2. Create an environment that supports and
encourages wound healing.
3. Repair any underlying deficiency (nutrition,
vascular or nerve supply).
2006 World Congress WSAVA/FECAVA/CSAVA
STEPS IN MANAGING EMERGENCY
WOUNDS – DEBRIDEMENT, CLEANING,
COVERING
Debridement is the removal from the wound of
gross contaminating material and tissue which is
either necrotic or of questionable viability. More
specifically, the aims of debridement are:
• thorough wound exploration - may require
substantial but gentle dissection to expose deep
lacerations
• remove dead, damaged and contaminated tissue
• remove foreign bodies
• arrest haemorrhage
• restore structural normality where possible
• provide drainage of dead space.
728
Back to contents
In some emergency situations, wounds will
be very fresh and require minimal if any
debridement.
Surgical debridement involving surgical
excision of unwanted material and tissue is the
most commonly used method. In cases where
there is abundant loose skin available, this may
involve “en bloc” resection including the wound
margins and an area around them to create
a surgically clean wound. However in many
cases, particularly involving the head and limbs,
conservation of viable tissue is paramount. Deeper
structures need to be conserved where possible
– eg tendons and nerves. Surgical debridement
in many wounds will be achieved in a number of
stages, particularly where the viability of certain
important structures is questionable.
Bandage/dressing debridement: certain types
of wound dressings (eg wet-to-dry saline gauze
dressings) which adhere to the wound surface
can be used to remove necrotic tissue because
the adhesion results in the necrotic tissue being
removed with the bandage when it is changed.
Alternatively, hydrocolloid and hydrogel
dressings assist debridement by mixing with
wound exudate which can then be washed from
the wound.
Cleaning the wound involves decisions on the
nature of the cleaning solution and how it is to be
delivered to the wound. Antiseptic solutions must
be carefully diluted so that the concentration
used is not toxic to the remaining tissue
fibroblasts that will help initiate healing. There
is a strong tendency towards the use of more
gentle wound cleaning solutions such as normal
saline or Lactated Ringers solution to minimize
any damage to remaining host cells. The volume
of fluid used is far more important than the type
of fluid – in some heavily contaminated wounds,
the use of moderate pressure warm tap water is
warranted simply due to the large volumes that
can be rapidly delivered.
The use of sugar and honey as a topical
treatment in the management of wounds has
a long history and a resurgence in interest has
recently been evident in the veterinary literature.
Unpasteurised honey is best as it contains a
number of chemically active constituents that
can assist wound healing. Both sugar and honey
act through a number of mechanisms, including
acting as a source of nutrition for local cells, as
a medium for cleaning wounds and through local
antibacterial effects. Regular sugar is certainly a
cheap wound cleaning material and is useful in
the emergency treatment of certain wounds.
Covering relates to the type of bandage that will
be used to protect the wound during healing. The

functions of wound dressings/bandages are:
• Maintain wound hydration
• Maintain wound temperature
• Minimise self-trauma
• Reduce contamination
• Immobilisation/patient comfort
There are now many different types of wound
dressing materials marketed in most countries.
These various types of dressings all can
contribute in many different ways to creating a
wound environment that is conducive to normal
wound healing. The cost of these dressings
Back to contents
S
varies considerably, and it is not always true that
the most expensive dressing is the best dressing
for a particular wound. However, if a wound is
not healing normally, even in the emergency
situation and the ensuing 5 days, it is important
that the reason for this poor healing is identified
and changes made to the dressing/bandaging
regime if indicated.
REFERENCES
Mathews K & Binnington A. Comp Contin Educ
24: 41-52 and 53-60.
2006 World Congress WSAVA/FECAVA/CSAVA
729
 S
S - Soft Tissue Surgery
EMERGENCIES OF THE UROGENITAL SYSTEM
Richard A. Read, BVSc(Hons),
PhD, FACVSc
Professor, Small Animal Surgery
Murdoch University
South St Mudroch
Western Australia
6150
Australia
r.read@murdoch.edu.au

INTRODUCTION • Prostatic disease

This lecture deals with urogenital emergencies
that fall into the categories of urinary obstruction/
leakage and sepsis (prostate in males, pyometra
in females).
URINARY OBSTRUCTION/URINE
LEAKAGE IN DOGS
Obstruction to the flow of urine, especially if
complete, causes serious metabolic disturbances
and has serious consequences for both health and
life. Urinary obstruction rapidly leads to urinary
retention, and failure to excrete various waste
products of cellular metabolism. These waste
products are toxic to many cellular processes so
illness and death will inevitably follow.
The causes of urine retention include
• Luminal obstruction(uroliths)
• Trauma/rupture
• Functional obstruction (eg with neurological
disease)
• Intramural obstruction (eg tumours, stricture
formation)
• Prostatic disease
• Hernia entrapment (perineal)
2006 World Congress WSAVA/FECAVA/CSAVA
• Penile neoplasia
• Perineal hernia
• Neurological disease (UMN)
Working up the problem – if the patient is
straining without success, ask yourself:
1. Is the bladder full or empty?
2. Does the patient continue to strain after voiding
successfully?
3. Does the patient exhibit pain while attempting
to urinate?
4. Is their any urine flow or is a complete
obstruction present?
5. Is the urine discoloured (blood/pus)?
6. Any history of trauma?
7. Any history of previous urinary tract disease
or other disease?
If the bladder is full
• Where is the bladder – normal location?
• Perform a cystocentesis to relieve obstruction
• Attempt to identify the location of the
obstruction:
- Pass a urethral catheter to assess level of
any obstruction

- Perform a retrograde contrast

The consequences of urine retention are cystourethrogram (CCU)
• Post-renal azotaemia/uraemia
• Hyperkalaemia (bradycardia, arrhythmias, The usual points of obstruction are bladder neck,
death) prostate, perineal urethra, penile urethra and os
• Metabolic acidosis penis.
• Ascending infection
• Severe soft tissue injury if urine leaks into Differential diagnosis associated with various
subcutaneous tissues locations of urinary obstruction
• Hydronephrosis 1. Bladder full and bladder neck obstruction:
• Bladder atony • Perineal hernia – check bladder position
• Bladder mass – check urine, ultrasound, CCU
The differential diagnosis of urinary obstruction • Male – prostate – FNAB, prostatic wash, CCU
would include • Female – granulomatous urethritis – CCU
• Urolithiasis - catheter biopsy
• Bladder wall neoplasia 2. Bladder full and pelvic urethra obstruction:
• Granulomatous urethritis • Trauma/pelvic Fracture – history, plain
• Trauma/rupture radiography
730
Back to contents

• Urethral neoplasia- check urine, ultrasound,
CCU
• Male – prostate – FNAB, prostatic wash,
CCU
• Female – granulomatous urethritis – CCU,
catheter biopsy
3. Bladder full and penile urethra obstruction:
• Trauma/os penis fracture – history,
radiographs, catheter
• Urethral calculus – urinalysis, catheter,
radiographs (plain +/- contrast)
4. Bladder empty/straining unproductively due
to irritation:
• Urolithiasis –urinalysis, plain/contrast
radiography, ultrasound
• Cystitis/urethritis – urinalysis, plain/
contrast radiography, ultrasound
• Bladder/urethral neoplasia - check urine,
ultrasound, contrast cystourethrogram
• Granulomatous urethritis – contrast
cystourethrogram, catheter biopsy
• Vaginitis – history, vaginal discharge,
speculum examination
• Bladder rupture – catheter to confirm
no urine flow, ultrasound, contrast
cystourethrogram, abdominocentesis, fluid
urea/creatinine
Functional obstruction – the neurological bladder
If the bladder is full, the patient is not voluntarily
voiding urine and there is no physical obstruction
to urine flow (check with catheter), the most
likely causes are an upper motor neuron
neurological disorder (eg I/V disc), pain, or
reflex dyssynergia.
Management of these cases can be difficult
– a dog with multiple pelvic fractures may be
unwilling to urinate not only due to pain, but
because he/she cannot posture to urinate due to
weakness as well as pain.
Upper motor neuron neurological disease results
in increased urethral tone to the point where
dangerously high pressures can be generated
within the bladder as urine continues to
accumulate. The bladder attempts to reduce the
pressure by stretching but this rapidly leads to
poor detrusor tone. Eventually, the bladder lumen
pressure rises above that of the urethra and urine
will begin to leak out, resulting in wet cage and
the appearance of the animal voluntarily voiding
urine. This assumption cannot be made unless
the bladder is empty and the cage/bedding is wet
with urine.
Emergency workup of the dysuric patient
When you are presented with a very distressed
patient that is constantly straining to urinate
with a full bladder, the first step is to relieve
Back to contents
S
the pressure in the bladder, either by passing a
urethral catheter, or if this is not possible, by
cystocentesis. Catheterisation provides useful
diagnostic information about urethral patency
and the site of any obstruction.
The owner should be carefully questioned about
the recent history of pattern of urination:
• Has the urine flow appeared normal?
• Any straining to urinate?
• Any change in frequency?
• Any urethral discharge?
• Any intermittent urination problems?
A thorough examination of the urinary tract
should then follow. Because of their close
association both anatomically and functionally,
the examination will inevitably involve the
reproductive tract as well.
PRINCIPLES OF URETHRAL SURGERY
• Urethral mucosa is tough and holds sutures well
• Handle the mucosa gently and ensure epithelial
surfaces are apposed
• Monofilament absorbable sutures are preferred
• Haemorrhage can be minimised by avoiding the
cavernous tissue when suturing
• Postoperative catheterisation???
Many absorbable suture materials lose strength
rapidly in the presence of urine, particularly if the
urine is alkaline. This is especially true of chromic
catgut, which should never be used in the urinary
tract for this reason. In the presence of bacterial
infection in urine, sutures such as polyglactin 910
(Ethicon – Vicryl) and polyglycolic acid (Davis
& Geck – Dexon) can lose their strength within
24 hours. Polydioxanone (Ethicon = PDS II)
and poliglecaprone (Ethicon – Monocryl) suture
materials being monofilament and absorbable
appear to be the best suited for urethral surgery.
The benefits/disadvantages of placing a catheter
in the urethra to support and protect the site of
urethral repair have been a hotly debated point 2006 World Congress WSAVA/FECAVA/CSAVA
among urologic surgeons for decades. Catheters
have been accused of promoting ascending
infection and causing fibrosis and stricture,
particularly if large sizes are used. Using a
catheter to divert urine from the surgical site can
probably be better achieved using a cystostomy
tube.
Urethral obstruction associated with prostatic
disease
Although dysuria and urine dribbling can be
associated with most forms of prostatic disease,
urethral obstruction is more commonly associated
with prostatic neoplasia than with the other types
of prostatic disease.
The most important diagnostic test for detecting
731
 S
prostatic disease is a thorough rectal examination.
Ancillary diagnostic tests are then helpful
to differentiate between the various types of
prostatic disease.
Ancillary diagnostic tests include cytology of
FNAB (+/- ultrasound guided, ultrasonography,
histopathology of needle biopsy samples
(+/- ultrasound guided), radiography –plain
and contrast, urinalysis and culture, CBC,
biochemistry, electrolytes and exploratory
laparotomy.
Prostatic adenocarcinomas usually start as
firm nodules within the gland but many are not
diagnosed until they have reached a substantial
size. Neoplastic prostates tend to adhere to the
surrounding tissue, but this characteristic is
also a feature of inflammatory prostatic disease.
Metastasis occurs early, usually to the iliac,
lumbar and pelvic lymph nodes, periprostatic
tissue, lung and bladder. Bone metastasis is
2006 World Congress WSAVA/FECAVA/CSAVA
732
Back to contents
not common, in contrast to the disease in man
in which bony metastases may become evident
before the primary tumour has caused any
clinical signs.
Summary
The primary goal in any case of dysuria is to
locate the level of the obstruction. In dogs with
complete obstruction to urine flow, relieving the
pressure in the system is of paramount importance,
followed by attention to the consequences of
failure to void urine (uraemia, electrolyte and
acid-base disturbances; bladder injury through
stretching leading to atony).
Surgery of the urinary tract is demanding in that
precise suturing and respect for the tissues are
requirements for restoring a patent urethra with a
functional diameter.
After care may require urinary diversion, either
via a temporary or permanent procedure.

S - Soft Tissue Surgery
MANAGING HERNIAS THAT PRESENT AS EMERGENCIES
Richard A. Read, BVSc(Hons),
PhD, FACVSc
Professor, Small Animal Surgery
Murdoch University
South St Mudroch
Western Australia
6150
Australia
r.read@murdoch.edu.au
Introduction
A hernia can be defined as the protrusion of an
organ or part through a defect in the wall of
the anatomical cavity in which it lies. Changes
in function of both the body cavity and the
herniated contents can be important in herniation.
These changes may be insignificant but in some
cases may result in serious pathophysiological
consequences that can lead to acute severe
illness and in some cases to the death of the
animal. This usually occurs when an organ that
is herniating through the defect in the abdominal
wall becomes trapped (incarcerated hernia)
and/or its blood supply becomes compromised
(strangulated hernia).
Incarceration of hernial contents involves the
development of adhesions between the contents
and the hernial sac or ring. These adhesions may
not cause any functional disturbance per se but
if they result in occlusion of the lumen of the
bowel, a rapid build-up of fluid and gas can occur
with important effects on fluid and electrolyte
balance. Bladder obstruction in perineal hernias
can also result in post-renal uraemia and fluid
retention.
Strangulation involves interruption to or
obstruction of the vascular supply to the
contents of the hernia. Vascular obstruction
of hernial contents can occur in two ways.
Firstly if incarceration leads to serious luminal
obstruction, the distension of the obstructed
organ with fluid and gas may eventually result
in sufficient intramural pressure to obstruct the
vascular supply. Necrosis of the wall (eg of the
bowel or bladder) will then follow. Secondly,
incarceration may directly compromise the
vascular supply to the herniated organ resulting
in necrosis and rupture. This may then lead on to
blood or body fluid loss, toxaemia or septicaemia
depending on the organ involved.
Principles of Herniorrhaphy
Four main aims of hernia repair can be identified:
Back to contents
S
1. Return of viable contents to their normal
anatomical location (within the abdomen).
2. Secure closure of the neck of the hernia, thus
preventing recurrence.
3. Obliteration of any redundant tissue in the sac.
4. Use of the patient’s own tissues wherever possible.
Because the hernial contents are often
friable, adequate exposure is essential in all
herniorrhaphies. Both the contents and the ring
must be exposed sufficiently to allow accurate
visual inspection so that the extent of adhesions
and their relationship to the vascular supply of
the hernia can be properly evaluated. This also
allows careful assessment of the viability of
the herniated tissue and facilitates its resection
if required. The hernial ring may need to be
enlarged to allow adequate exposure - this is
often required in inguinal hernia repair.
Once all adhesions have been broken down
and the viable hernial contents replaced in their
normal position, closure by direct apposition of
local tissues is the preferred technique. Some
local dissection may be required to decrease
the tension on the closure. Good examples of
this technique are the internal obturator and
superficial gluteal muscle flaps used in perineal 2006 World Congress WSAVA/FECAVA/CSAVA
hernia repair.
HERNIAS THAT PRESENT AS
EMERGENCIES
1. INGUINAL HERNIA
Inguinal hernias may be direct (direct outpouching
of peritoneum and abdominal contents adjacent
to the inguinal canal) or indirect (outpouching
of peritoneum (vaginal process) and abdominal
contents through the inguinal canal.
Indirect inguinal hernia in dogs occurs
predominantly in young males and mature
females. This type of hernia is also referred
to as a scrotal hernia. Emergency situations
usually occur in the young male group because
the inguinal canal is longer and more narrow in
733
 S
males than it is in females. As a result of this
anatomical difference, herniated contents are
more likely to become strangulated in males
than in females. In addition, the circulation to the
testis may become compromised by compression
of the spermatic artery and vein.
Signs of scrotal herniation are closely related
to the pathophysiology of incarceration and
strangulation, so these include local pain,
swelling and inflammation. Specific presenting
signs depend on the specific abdominal structure
that has herniated and become compromised.
If small intestine is involved, gastrointestinal
signs may predominate. If omental fat alone is
involved, pain, swelling and discolouration of
the overlying skin may be the primary signs.
Testicular swelling and pain are usually present.
Diagnosis is centred on identifying the abnormal
local signs and then using palpation and
ultrasound to identify the hernial contents. If
needle aspiration is considered important then it
should be performed under ultrasound guidance.
Supportive therapy will vary with individual
cases – if small intestine has become strangulated
and has ruptured, signs of local sepsis, peritonitis
and in some cases Systemic inflammatory
response syndrome (SIRS/septic shock) may
be present and aggressive fluid therapy with
crystalloids, colloids and antibiotics will be
indicated, with surgery performed as soon as the
patient is sufficiently stable. Surgical treatment
may involve dealing with local and peritoneal
contamination with bowel contents. In other
cases, surgery will be more routine.
Owners of dogs with scrotal herniation should be
counselled to have the dog neutered at the time
of hernia correction. The incidence of recurrence
of the hernia or persistent swelling of he testis is
significant as it is difficult to judge how much to
narrow down the inguinal canal when the local
tissues are inflamed and swollen.
2006 World Congress WSAVA/FECAVA/CSAVA
2. TRAUMATIC ABDOMINAL HERNIA
Most traumatic hernias are caused by blunt
trauma and involve the ventrolateral caudal
abdominal (inguinal or prepubic areas) and
paracostal regions. In the latter case, rupture of
the diaphragm may also occur. The direction of
the traumatic force and resultant changes in intra-
abdominal pressure influence the location of the
hernia. If the abdominal muscles are contracted at
the time of trauma and the glottis remains open,
the increase in intra-abdominal pressure will
be minimal and avulsion injuries to minimally-
elastic structures (e.g. pre-pubic tendon). In
contrast, a sudden increase in intra-abdominal
pressure may result in abdominal wall rupture.
Direct local trauma at the site of the injury may
734
Back to contents
tear the abdominal musculature. Patients with
pelvic/pubic fractures may also have herniation
through the prepubic or inguinal regions.
Crushing, rupture or avulsion of intra-abdominal
organs may occur with blunt trauma, but sharp
trauma (such as bite wounds, or gunshot wounds)
carries a higher risk of perforation and laceration
of intra-abdominal structures.
The masking of the signs of traumatic herniation
by the swelling and contusions caused by the
trauma itself can pose a very real problem in
diagnosing traumatic herniation. Extent of
organ herniation is very variable - gravity may
help to maintain the abdominal viscera in their
normal location, so that external swelling is
minimal. Alternatively, the contents may migrate
significant distances in the subcutaneous space,
so that the site of the swelling may be very
misleading as to the location of the hernia.
Other clinical signs reflect the extent of damage
to abdominal organs - hypovolaemia due to blood
loss (liver, spleen damage) or fluid sequestration
into obstructed or strangulated bowel. Concurrent
pelvic fractures are common and the clinical
signs associated with these injuries may be the
most obvious.
Radiography is an important diagnostic tool, due
to the limitations in thorough abdominal palpation
in the painful, traumatised patient. Subcutaneous
emphysema may be present. Definitive signs of
herniation are absence of abdominal organ from
its normal position, an obvious discontinuity
in the abdominal wall, and displacement of
abdominal organs into the subcutaneous space.
Ultrasonography may be helpful to differentiate
fluid-filled hernias from other soft tissue masses.
Diagnostic peritoneal lavage should be used in
any traumatic hernia case where serious injury to
internal organs is suspected.
The choice of surgical approach and the precise
location and extent of the surgical incision are
very important in facilitating the definitive repair.
For the emergency patient, a midline approach
should be used so that access is afforded to all
possible sites of herniation and all abdominal
viscera are accessible for examination and repair
of injured structures as required.
3. PERINEAL HERNIA
Perineal hernia is usually a chronic condition
but a small subset of patients will present as
emergency cases due to prolapse of the bladder
and/or prostate into the hernia, resulting in urinary
obstruction. The dogs will usually present with a
history of straining to urinate and as the pressure
of the bladder increases the perineal swelling
becomes very hard.
Diagnosis is assisted by the above history and

confirmed by either needle drainage of urine via
the perineum or relieving the urine via urethral
catheter if possible. Once the pressure is relieved,
rectal examination should confirm the presence
of the hernia.
Treatment options include standard herniorrhaphy
techniques but in some cases an abdominal
approach to perform cystopexy and colonopexy
Back to contents
S
can be sufficient to eliminate the clinical signs of
straining to defaecate and stranguria.
References
Brissot H N, Dupré G P, Bouvy B M. Vet Surg,
33: 412-421, 2004.
Waters, Ray and Stone Vet Surg 22: 44-49, 1993
2006 World Congress WSAVA/FECAVA/CSAVA
735
 S
S - Soft Tissue Surgery
PERITONITIS – REDUCING MORTALITY AND MORBIDITY
Richard A. Read, BVSc(Hons),
PhD, FACVSc
Professor, Small Animal Surgery
Murdoch University
South St Mudroch
Western Australia
6150
Australia
r.read@murdoch.edu.au
INTRODUCTION
Peritonitis in dogs and cats can be classified
in a number of ways: primary vs secondary,
septic vs aseptic, acute vs chronic or diffuse vs
localised. Most cases of peritonitis are secondary
to gastrointestinal leakage and are septic.
Other sources of sepsis in septic peritonitis
include the urogenital tract (ruptured pyometra,
ruptured prostatic abscess, ruptured bladder or
renal abscess), hepatobiliary tract (necrotizing
cholecystitis, liver lobe torsion or liver abscess),
or from penetrating wounds, pancreatic or
splenic abscesses. Reviews cases of generalised
peritonitis in dogs showed an overall mortality
rate of between 30 and 68%.
CLINICAL SIGNS AND PATHOPHYSIOLOGY
Clinical signs of septic peritonitis vary significantly
between patients depending on the duration and
extent of the peritoneal contamination and the
type and number of bacteria present. However,
it can be assumed that all these patients are
somewhere on a spectrum the end point of which
is septic shock and multiple organ dysfunction.
The peritoneum has enormous absorptive capacity
but consequently has equally enormous capacity
2006 World Congress WSAVA/FECAVA/CSAVA
to deliver fluid into the abdominal cavity when
the normal balance is disturbed. The following
sequence can rapidly develop:
• Sepsis results in vasodilation and increased
capillary permeability, which delivers fluid and
plasma proteins into the abdominal cavity.
• Further fluid and protein losses may occur due
to anorexia, vomiting and diarrhoea.
• The resulting hypovolaemia results in decreased
cardiac output, poor perfusion, hypoxia and cell
death.
• Ischaemia and inflammation of intestinal mucosa
compromises its integrity and translocation of
bacteria occurs.
• Influx of neutrophils and macrophages
which release cytokines and other active
substances, along with bacterial toxins, further
736
Back to contents
exacerbate peripheral vasodilation and capillary
permeability
• Cardiac function is compromised, the
coagulation cascade is activated and the systemic
inflammatory response syndrome (SIRS) is fully
activated.
Blood samples reveal leucocytosis with left shift,
hypoproteinaemia and hypoglycaemia, along
with other specific signs related to the organ
systems involved.
DIAGNOSIS
There is usually a high suspicion of septic
peritonitis based on clinical signs and history,
and once an abdominal effusion is suspected,
obtaining a sample of this fluid for cytology,
culture and chemical analysis is essential.
Abdominocentesis should be performed first and
if initially unsuccessful, ultrasound guidance and
repeated sampling in different areas may improve
yield rates. If still negative, diagnostic peritoneal
lavage can be performed: 15-20 ml/kg of warmed
0.9% NaCl is infused into the abdominal cavity
and the patient is rolled from side to side. Fluid
is then collected by gravity and submitted for
culture, cytology and chemistry. The presence of
degenerate neutrophils along with intracellular
bacteria is grounds for exploratory surgery.
Various chemical analyses of abdominal effusion
fluid have been evaluated in dogs to try to find
the definitive diagnostic test for septic peritonitis.
The most accurate measure appears to be the
differential between blood glucose and abdominal
fluid glucose – 100% of dogs with abdominal
fluid glucose more than 20mg/dl lower than the
blood glucose had septic peritonitis.
EMERGENCY TREATMENT
Aggressive fluid therapy with crystalloids
and colloids is indicated in most patients,
with vasopressors and inotropes used where
hypotension persists. Blood or plasma
transfusions may be indicated, especially if
coagulation abnormalities are present.

SURGICAL MANAGEMENT
There is a small window of opportunity for
timing surgical intervention in many patients
with septic peritonitis. Some patients will
respond dramatically to resuscitatory therapy
but if the diagnosis has been made, surgery
should proceed as soon as possible to find the
source of contamination. As stated earlier, the
source of contamination in most cases is the
gastrointestinal tract, so this should be the first
focus of attention, starting at the large bowel and
working proximally.
Once the site of leakage has been definitively
dealt with, large volume lavage with isotonic
warmed fluid is essential to dilute the bacteria
and remove particulate contaminating matter.
How much lavage is a matter of judgement – the
aim is to clear all particulate matter but there is
a down side to peritoneal lavage – mesothelial
lining cells are damaged, the ability of the
peritoneal defense mechanisms to clear bacteria
may be further reduced, and in some cases the
infection can be further spread in cases where
the peritonitis was being somewhat contained in
one area of the abdomen. What is clear is that
as much of the lavage fluid as possible should
be removed as possible to minimise these issues.
The addition of antibiotics or antiseptics to the
lavage fluid has not been shown to be beneficial.
TO DRAIN OR NOT TO DRAIN?
The need to provide ongoing drainage of the
abdominal cavity in cases of septic peritonitis
is a very controversial topic. Following the
trend in human medicine in the 1980’s, open
peritoneal drainage became the preferred method
for some surgeons wishing to provide ongoing
postoperative drainage of septic peritonitis in
dogs and cats. This was partly fuelled by studies
in normal dogs showing that drainage of the
peritoneal cavity with sump penrose drains was
rapidly compromised by adhesion formation
around the drains. However, there is some
evidence to suggest that these adhesions may not
obstruct the drainage of fluid. In an experimental
study in normal dogs, sump-penrose drainage and
open peritoneal drainage were established in two
separate groups via laparotomy. Fluid was then
infused into the abdomen over 72 hours and the
volume of drainage was estimated by weighing
the bandage covering the ventral abdomen. It
was shown that despite developing significant
adhesions around them, the sump-penrose drains
were just as efficient at allowing drainage as the
open peritoneal technique.
In open drainage, the ventral abdominal incision
is left partly open at the end of exploratory
surgery and covered with sterile dressings to
Back to contents
S
allow continued drainage by gravity. Regular
bandage changes are required which may require
sedation or anaesthesia, but these changes also
provide the opportunity to either infuse fluid into
the abdomen for ongoing lavage, or introduce
a sterile gloved finger through the incision to
break down any adhesions. The duration of
open drainage can vary between 2-14 days.
Complications can include further contamination
of the abdominal cavity and serious loss of
protein and electrolytes; disadvantages of the
technique focus around the need for intensive
monitoring and the cost.
Early studies of open peritoneal drainage showed
promising results, but the ensuing published
studies varied both in duration of drainage and
technique used. Overall, the mortality rate for
cases treated by open drainage does not appear
to be any different from that of cases in which
the abdomen is closed at the end of surgery. A
recent study evaluated postoperative suction
drainage using Jackson Pratt drains placed
between the liver and the diaphragm and in this
group of 40 patients the mortality rate was 30%.
Those advocating closed drainage or no drainage
suggest that since the outcome is possibly no
different, the complications of open peritoneal
drainage are sufficient reason not to use it.
The decision about whether to leave an abdomen
open at the end of surgery for septic peritonitis
still rests with the surgeon and will be
governed by:
• The severity of the peritonitis
• The surgeon’s personal experience and preference
• The finances of the owner
• The availability of postoperative intensive
monitoring
• The serum albumen of the patient
• The temperament of the patient.
OTHER SUPPORTIVE TREATMENT 2006 World Congress WSAVA/FECAVA/CSAVA
Providing adequate nutritional support for patients
with septic peritonitis is essential. Consideration
should be given to the placement of enteral
feeding tubes at the time of definitive surgery.
These should be placed so as to maximise the
use of whatever normal gastrointestinal tract is
available. Alternatively, total parenteral nutrition
may be preferred in some patients.
Antimicrobial therapy will be based on results
of culture and sensitivity but in most cases
combination therapy will be indicated initially
to provide cover against both gram positive and
gram negative aerobes and against anaerobic
bacteria.
737
 S
PROGNOSIS
As stated earlier, the published mortality rates
for septic peritonitis in dogs and cats ranges
from 30-68%, with no clear evidence for any
particular post-operative management system
offering superior results. The cause/source of
the contamination does not appear to have a
significant impact on prognosis, although there is
some evidence that septic bile peritonitis carries
a poor prognosis – in one study of 26 dogs and
cats with bile peritonitis, only 27% of patients
with septic bile peritonitis survived whereas
100% of patients from which no bacteria could
be detected in the abdominal fluid survived. It has
been postulated that the presence of bacteria and
bile salts impairs peritoneal phagocytic activity
and increases lipopolysaccharide levels.
There are no studies that have identified any other
clinical or diagnostic parameters that offer a clear
2006 World Congress WSAVA/FECAVA/CSAVA
738
Back to contents
guide to prognosis in cases of septic peritonitis.
The development of a standardized diagnostic
and therapeutic protocol in a prospectively
designed study is possibly necessary to identify
any potential prognostic indicators.
REFERENCES
Hosgood and Salisbury. JAVMA 193: 1448-1450,
1988.
Hosgood, Salisbury & Denicola JAAHA 27: 115-
121, 1991.
Lanz, Ellison, Bellah et al. JAAHA 37:87-92, 2001.
Ludwig, McLoughlin, Graves & Crisp. Vet Surg
26:90-98, 1997.
Mueller, Ludwig & Barton. JAVMA 219: 789-
794, 2001.
Staatz, Monet & Seim. Vet Surg 31:174-180, 2002.
 S
S - Soft Tissue Surgery
GASTRIC DILATATION VOLVULUS: WHAT’S NEW?
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery
Texas A&M University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu

Classically, GDV syndrome is an acute condition
with a mortality rate of 20% to 45% in treated
animals. The gastric enlargement is thought to
be associated with a functional or mechanical
gastric outflow obstruction. The initiating cause
of the outflow obstruction is unknown; however,
once the stomach dilates, normal physiologic
means of removing air (i.e., eructation, vomiting,
and pyloric emptying) are hindered because the
esophageal and pyloric portals are obstructed.
The cause of GDV is unknown, but exercise
after ingestion of large meals of highly processed
food or water has been suggested to contribute
to it. Epidemiologic studies have not supported a
causal relationship between feeding soy-based or
cereal-based dry dog food and GDV. However,
Irish setters fed a single feed type appear to
have an increased risk of GDV compared to
those fed a mixture of feed types. Likewise,
adding table food or canned food to the diet of
large and giant breed dogs is associated with a
decreased incidence of GDV. Feeding dry dog
foods in which one of the first four ingredients
are oils or fats may also increase the risk of
GDV. Other contributing causes include an
anatomic predisposition, ileus, trauma, primary
gastric motility disorders, vomiting, and stress.
Recommendations for clients of animals at high
risk are provided in Table 1.

Table 1 Recommendations for Clients

• Feed several small meals a day rather than one large meal.
• Avoid stress during feeding (if necessary, separate dogs in multiple-dog households
during feeding).
• Restrict exercise before and after meals (of questionable benefit).
• Do not use an elevated feed bowl.
• Do not breed dogs with a first-degree relative that has a history of gastric dilatation-volvulus.
• For high-risk dogs, consider prophylactic gastropexy.
• Seek veterinary care as soon as signs of bloat are noted. 2006 World Congress WSAVA/FECAVA/CSAVA

Generally, with GDV the stomach rotates in
a clockwise direction when viewed from the
surgeon’s perspective (with the dog on its back
and the clinician standing at the dog’s side,
facing cranially). The rotation may be 90 to
360 degrees but usually is 220 to 270 degrees.
The duodenum and pylorus move ventrally and
to the left of the midline and become displaced
between the esophagus and stomach. The spleen
usually is displaced to the right ventral side of
the abdomen.
Caudal vena cava and portal vein compression
by the distended stomach reduces venous
return and cardiac output, causing myocardial
ischemia. Obstructive shock and inadequate
tissue perfusion affect multiple organs, including
the kidneys, heart, pancreas, stomach, and small
intestine. Cardiac arrhythmias occur in many
dogs with GDV, particularly those with gastric
necrosis.
Partial or chronic GDV may occur in dogs and
usually is a progressive but non-life-threatening
syndrome that may be associated with vomiting,
anorexia, and/or weight loss. These dogs may have
chronic, intermittent signs and appear normal
between episodes. Gastric malpositioning may
be intermittent or chronic but without dilatation.
Plain or contrast radiographs are diagnostic,

739
Back to contents
 S
but repeat radiographs may be necessary if the
stomach is intermittently malpositioned.
DIAGNOSIS
Clinical Presentation
Signalment. GDV primarily occurs in large, deep-
chested breeds (i.e., Great Dane, Weimaraner,
Saint Bernard, German shepherd, Irish and
Gordon setters, Doberman pinscher) but has
been reported in cats and small-breed dogs. Shar
peis may have an increased incidence compared
with other medium-sized breeds. Basset hounds
may have a higher risk of GDV, despite their
relatively small size. GDV may occur in a dog of
any age but is most common in middle-aged or
older animals. The thoracic depth to width ratio
appears to be highly correlated with the risk of
bloat.
History. A dog with GDV may have a history
of a progressively distending and tympanic
abdomen, or the owner may simply find the
animal recumbent and depressed with a distended
abdomen. The dog may appear to be in pain
and may have an arched back. Nonproductive
retching, hypersalivation, and restlessness are
common.
Physical Examination Findings
Abdominal palpation often reveals various
degrees of abdominal tympany or enlargement;
however, it may be difficult to feel gastric
distention in heavily muscled large-breed or
very obese dogs. Splenomegaly occasionally is
palpated. Clinical signs associated with shock
may be present, including weak peripheral
pulses, tachycardia, prolonged capillary refill
time, pale mucous membranes, and/or dyspnea.
Diagnostic Imaging
Radiographs are necessary to differentiate
2006 World Congress WSAVA/FECAVA/CSAVA
simple dilatation from dilatation plus volvulus.
Affected animals should be decompressed
before radiographs are taken. Right lateral and
dorsoventral radiographic views are preferred in
order to facilitate filling the abnormally displaced
pylorus with air so that it can be easily identified.
The pylorus is normally located ventral to the
fundus on the lateral view and on the right
side of the abdomen on the dorsoventral view.
On a right lateral view of a dog with GDV, the
pylorus lies cranial to the body of the stomach
and is separated from the rest of the stomach by
soft tissue (reverse C sign or double bubble). On
the dorsoventral view, the pylorus appears as a
gas-filled structure to the left of midline. Free
abdominal air suggests gastric rupture and air
within the wall of the stomach indicates necrosis,
both of which warrant immediate surgery.
740
Back to contents
MEDICAL MANAGEMENT
Stabilizing the patient’s condition is the initial
objective. Either isotonic fluids (90 ml/kg/
hour), hypertonic 7% saline (4 to 5 ml/kg over
5 to 15 minutes), hetastarch (5 to 10 ml/kg
over 10 to 15 minutes) or a mixture of 7.5%
saline and hetastarch (dilute 23.4% saline with
6% hetastarch until you have a 7.5% solution;
administer at 4 ml/kg over 5 minutes) is
administered. Blood should be drawn for blood
gas analyses, a CBC, and a biochemical panel.
Broad-spectrum antibiotics (e.g., cefazolin,
ampicillin plus enrofloxacin) should be
administered. If the animal is dyspneic, oxygen
therapy may be given by nasal insufflation
or mask.Gastric decompression should be
performed while shock therapy is initiated.
SURGICAL TREATMENT
Surgery should be performed as soon as the
animal’s condition has been stabilized, even if
the stomach has been decompressed. Rotation of
an undistended stomach interferes with gastric
blood flow and may potentiate gastric necrosis.
The goals of surgical treatment are threefold:
(1) to inspect the stomach and spleen so as
to identify and remove damaged or necrotic
tissues; (2) to decompress the stomach and
correct any malpositioning; and (3) to adhere the
stomach to the body wall to prevent subsequent
malpositioning. Upon entering the abdominal
cavity of a dog with GDV, the first structure
noted is the greater omentum, which usually
covers the dilated stomach.
Intraoperative manipulation of the cardia usually
allows the tube to be passed into the stomach
without difficulty. If adequate decompression is
still not achieved or an assistant is not available,
a small gastrotomy incision can be performed
to remove the gastric contents, although this
should be avoided if possible.
Gastropexy
Gastropexy techniques are designed to
permanently adhere the stomach to the body
wall. The most common indications are GDV
(pyloric antrum to right body wall) and hiatal
herniation (fundus to left body wall). Numerous
gastropexy techniques have been described.
Although the strength and extent of adhesions
created by these techniques differ, all of them
(when properly performed) prevent movement
of the stomach
Muscular flap (incisional) gastropexy. Muscular
flap (incisional) gastropexy is easier than
circumcostal gastropexy and avoids the possible
complications associated with tube gastropexy.
Make an incision in the seromuscular layer of

the gastric antrum. Then make an incision in the
right ventrolateral abdominal wall by incising
the peritoneum and internal fascia of the rectus
abdominis or transverse abdominis muscles.
Suture the edges of the incisions in a simple
continuous pattern using 2-0 absorbable or
nonabsorbable suture. Make sure the muscularis
S
layer of the stomach is in contact with the
abdominal wall muscle. Suture the cranial
margin first, then the caudal margin. As an
alternative, you may raise flaps in the stomach
and body wall to increase the extent of muscle
contact between these tissues.

Figure 1
From: Fossum, TW: Small Animal Surgery, Mosby Publishing Co., St. Louis, Mo, 2002

2006 World Congress WSAVA/FECAVA/CSAVA

741
Back to contents
 S
S - Soft Tissue Surgery
DIAPHRAGMATIC HERNIAS: DIAGNOSIS AND EMERGENCY
TREATMENT
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery
Texas A&M University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu
Diaphragmatic hernias are commonly recognized
by small animal clinicians and may be congenital
or occur secondary to trauma. Congenital
pleuroperitoneal hernias are seldom diagnosed in
small animals because many affected animals die
at birth or shortly thereafter. Most diaphragmatic
hernias in dogs and cats are caused by trauma,
particularly motor vehicle accidents. The abrupt
increase in intraabdominal pressure accompanying
forceful blows to the abdominal wall causes the
lungs to rapidly deflate (if the glottis is open),
producing a large pleuroperitoneal pressure
gradient. Alternately, the pressure gradient that
occurs between the thorax and the abdomen may
cause the diaphragm to tear. The tears occur at
the weakest points of the diaphragm, generally
the muscular portions. Traumatic diaphragmatic
hernias are often associated with significant
respiratory embarrassment; however, chronic
diaphragmatic hernias in asymptomatic animals
are not uncommon.
Clinical Presentation
Signalment. There is no breed predisposition
2006 World Congress WSAVA/FECAVA/CSAVA
for traumatic diaphragmatic hernias. Young
males have historically thought to be more
commonly affected; however, a recent study of
traumatic diaphragmatic hernias identified no
sex predilection.
History. The duration of a diaphragmatic hernia
may range from a few hours to years. Many (15%
to 25%) are diagnosed weeks after the injury. The
animals may be presented in shock acutely after
the trauma, or the hernia may be an incidental
finding. Animals sustaining trauma often suffer
from associated injuries (e.g., fractures). With a
chronic diaphragmatic hernia, the clinical signs
most often are referable to either the respiratory
(i.e., dyspnea, exercise intolerance) or the
gastrointestinal systems (i.e., anorexia, vomiting,
diarrhea, weight loss, pain after ingestion of food)
742
Back to contents
or they may be nonspecific (e.g., depression).
Many animals with chronic hernias are not
dyspneic at the time of diagnosis.
Physical Examination Findings
Animals with recent traumatic diaphragmatic
hernias frequently are in shock when presented
for treatment; therefore, clinical signs may
include pale or cyanotic mucous membranes,
tachypnea, tachycardia, and/or oliguria. Cardiac
arrhythmias are common and associated with
significant morbidity. Other clinical signs
depend on which organs have herniated and may
be attributed to the gastrointestinal, respiratory,
or cardiovascular system. The liver is the most
commonly herniated organ, a condition that
often is associated with hydrothorax caused by
entrapment and venous occlusion.
Diagnostic Imaging
Definitive diagnosis of pleuroperitoneal
diaphragmatic hernia usually is made by
radiography or ultrasonography. It may be
difficult to diagnose diaphragmatic hernias
radiographically if only a small portion of the
liver is herniated. In a recent study, thoracic
radiographs revealed evidence of diaphragmatic
hernia in only 66% of affected animals.
Ultrasound examination of the diaphragmatic
silhouette may help when herniation is not
obvious radiographically (i.e., hepatic herniation,
pleural effusion).
Positive contrast celiography occasionally may
be helpful. Prewarmed water-soluble iodinated
contrast agent is injected into the peritoneal cavity
at a dosage of 1.1 ml/kg (the dose is doubled if
ascites is present), the patient is gently rolled
from side to side or the pelvis is elevated, and
films are taken immediately after the injection
and manipulation. Criteria used in evaluating
these imags should include the presence of

contrast medium in the pleural cavity, absence
of a normal liver lobe outline in the abdomen,
and incomplete visualization of the abdominal
surface of the diaphragm. Positive-contrast
celiograms should be interpreted cautiously,
because omental and fibrous adhesions may seal
the defect, resulting in false negative studies.
MEDICAL MANAGEMENT
If the animal is dyspneic, oxygen should be
provided by face mask, nasal insufflation, or an
oxygen cage. Positioning the animal in sternal
recumbency with the forelimbs elevated may
help ventilation. If moderate or severe pleural
effusion is present, thoracentesis should be
performed. Fluid therapy and antibiotics should
be given if the animal is in shock.
SURGICAL TREATMENT
Chronic diaphragmatic hernias may have a
higher mortality than acute diaphragmatic
hernias; however, the prognosis with both
groups is good to excellent with surgery. If
pulmonary contusions are severe, surgical repair
of diaphragmatic hernias should be delayed
until the patient’s condition has been stabilized;
however, herniorrhaphy should not be delayed
unnecessarily. Animals with gastric herniation
should be evaluated carefully for gastric
distention and should be operated on as soon as
they can safely be anesthetized, because acute
gastric distention within the thorax may cause
rapid, fatal respiratory impairment.
Preoperative Management
Prophylactic antibiotics should be given before
induction of anesthesia in animals with hepatic
herniation. Massive release of toxins into the
circulation may occur with hepatic strangulation
or vascular compromise. Premedicating such
patients with steroids may be beneficial. An
ECG should be performed on all trauma patients
before surgery.
SURGICAL TECHNIQUE
Make a ventral midline abdominal incision; if
greater exposure is needed, extend the incision
cranially through the sternum. Replace the
abdominal organs in the abdominal cavity (if
necessary, enlarge the diaphragmatic defect).
If adhesions are present, dissect the tissues
gently from the thoracic structures to prevent
pneumothorax or bleeding. With chronic hernias,
debride the edge of the defect before closure. Close
the diaphragmatic defect in a simple continuous
suture pattern. If the diaphragm is avulsed from
the ribs, incorporate a rib in the continuous
suture for added strength (Figure 1). Remove air
Back to contents
S
from the pleural cavity after closing the defect.
If continued pneumothorax or effusion is likely,
place a chest tube. Explore the entire abdominal
cavity for associated injury (i.e., compromise of
the vasculature to the intestine or splenic, renal,
or bladder trauma) and repair any defects.
Figure 1
From: Fossum, TW: Small Animal Surgery,
Mosby Publishing Co., St. Louis, Mo, 2002
PERITONEOPERICARDIAL
DIAPHRAGMATIC HERNIA
Peritoneopericardial diaphragmatic hernias are
less commonly recognized by small animal
clinicians than traumatic diaphragmatic hernias.
Although PPDH often are associated with
respiratory embarrassment, asymptomatic PPDH
is common. PPDH may occur as a result of trauma
in human beings (in whom the diaphragm forms
one wall of the pericardial sac); however, these
2006 World Congress WSAVA/FECAVA/CSAVA
hernias are always congenital in dogs and cats, in
which no direct communication exists between
the pericardial and peritoneal cavities after birth.
The most widely accepted theory regarding the
embryogenesis of this defect is that the hernia
occurs because of faulty development or prenatal
injury of the septum transversum. This could be
a result of a teratogen, genetic defect, or prenatal
injury.
DIAGNOSIS
Clinical Presentation
Signalment. Although PPDH is congenital, it
is not uncommon for the diagnosis to be made
when the animal is middle-aged or older because
743
 S
clinical signs vary and may be intermittent.
Weimaraners and cocker spaniels may be at
increased risk. Domestic longhair and Himalayan
cats may be predisposed.
History. The clinical signs may be referable
to the gastrointestinal, cardiac, or respiratory
systems and include anorexia, depression,
vomiting, diarrhea, weight loss, wheezing,
dyspnea, exercise intolerance, and/or pain after
eating. Neurologic signs may occur as a result of
hepatoencephalopathy.
SURGICAL TECHNIQUE
Make a ventral midline abdominal incision. If
greater exposure is needed, extend the incision
cranially through the sternum. Enlarge the
diaphragmatic defect if necessary and replace
the abdominal organs in the abdominal cavity.
If adhesions are present, gently dissect the
2006 World Congress WSAVA/FECAVA/CSAVA
744
Back to contents
tissues from the thoracic structures, resecting or
debriding necrotic tissue as necessary. Debride
the edges of the defect and close in a simple
continuous suture pattern. Do not close the
pericardial sac. Remove air from the pericardial
sac or pleural cavity or both after closing the
defect. If continued pneumothorax or effusion
is likely, place a chest tube. Repair concomitant
sternal or abdominal wall defects.
PROGNOSIS
If the animal survives the early postoperative
period (i.e., 12 to 24 hours), the prognosis is
excellent, and recurrence is uncommon with
proper technique. A postoperative mortality
rate of 14% was recently reported in cats. The
prognosis is worse in patients with PPDH that
have concurrent cardiac abnormalities.

S - Soft Tissue Surgery
PNEUMOTHORAX AND LUNG LOBE TORSION: EMERGENCY
MANAGEMENT TO REDUCE MORTALITY
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery
Texas A&M University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu
PNEUMOTHORAX
Traumatic pneumothorax is the most common
type of pneumothorax in dogs. It most often
occurs as a result of blunt trauma (i.e.,
vehicular accidents, being kicked) which causes
parenchymal pulmonary damage to the lung and a
closed pneumothorax. Pneumomediastinum may
be associated with pneumothorax or tracheal,
bronchial, or esophageal defects, or it may be
due to subcutaneous air migration along fascial
planes at the thoracic inlet.
Tracheal rupture may occur due to trauma; it is
especially associated with overinflation of the
endotracheal tube cuff in cats. Tracheoscopy may
be the method of choice for documenting tracheal
rupture. The primary signs of tracheal rupture
are pneumomediastinum and subcutaneous
emphysema; pneumothorax is rare. It is
important to distinguish tracheal rupture without
pneumothorax from that causing pneumothorax.
Spontaneous pneumothorax occurs in previously
healthy animals without antecedent trauma and
may be primary (without underlying pulmonary
disease) or secondary (with underlying disease
such as pneumonia, pulmonary abscess,
neoplasia, chronic granulomatous infection,
or pulmonary parasitic infection, such as with
Paragonimus spp.).
Clinical Presentation
Signalment. Traumatic pneumothorax is most
common in young dogs because they are more
likely to be hit by cars or to suffer other trauma
resulting in pulmonary damage. For similar
reasons, males may be more commonly affected
than females. Spontaneous pneumothorax
usually occurs in large and deep-chested breeds;
however, it may occur in small dogs. Purebred
dogs, particularly Siberian Huskies, may be more
commonly affected than mixed breed dogs.
History. Pneumothorax due to trauma usually
Back to contents
S
causes acute dyspnea. Trauma is often not
reported, making differentiation between
traumatic and spontaneous pneumothorax
difficult. Although the history of dogs with
spontaneous pneumothorax varies depending
on underlying etiology, most animals have acute
onset of dyspnea. Occasionally a chronic cough
or fever may be noted. Recurrence of dyspnea in
an animal previously treated for pneumothorax
suggests spontaneous rather than traumatic
pneumothorax.
Physical Examination Findings
Most animals with pneumothorax have bilateral
disease and are presented for treatment with an
acute onset of severe dyspnea. Other evidence
of trauma (i.e., rib fractures, limb fractures,
traumatic myocarditis, pulmonary contusions)
may be evident in animals with trauma-induced
pneumothorax. Most animals with pneumothorax
show a restrictive respiratory pattern (i.e., rapid,
shallow respirations).
Diagnostic Imaging 2006 World Congress WSAVA/FECAVA/CSAVA
On a recumbent lateral thoracic radiograph, the
lungs collapse and retract from the chest wall,
and the heart usually appears to be elevated from
the sternum. Radiographs should be carefully
evaluated for underlying pulmonary disease
(e.g., abscess, neoplasia) or associated trauma
(e.g., rib fractures, pulmonary contusion).
Pulmonary blebs found in some animals with
spontaneous pneumothorax are seldom visible
radiographically, although CT is more sensitive
for finding these lesions. If imaging does not
identify the lesion, surgical or thoracoscopic
identification of bullae is indicated.
MEDICAL MANAGEMENT
Medical management of pneumothorax consists
of initially relieving dyspnea by thoracentesis. If
745
 S
the pleural air accumulates quickly or cannot be
managed effectively with needle thoracentesis, a
chest tube should be placed. Thoracentesis should
be performed as necessary to prevent dyspnea
while the pulmonary lesion heals, usually within 3
to 5 days. Recurrence is uncommon. Conversely,
animals with spontaneous pneumothorax
commonly have recurrent pneumothorax if
surgery is not performed.
SURGICAL TREATMENT
Surgical therapy of animals with traumatic
pneumothorax is seldom necessary. However,
nonsurgical management of spontaneous
pneumothorax usually results in an unsatisfactory
outcome. Thoracoscopic treatment of bullous
emphysema has been reported in dogs.
Mechanical pleurodesis of the lungs may reduce
the recurrence of pneumothorax in animals that
undergo surgery for spontaneous pneumothorax.
Mechanical pleurodesis damages the pleura,
causing it to thicken.
If an underlying pulmonary lesion is readily
identified (i.e., pulmonary abscess or neoplasia)
and can be localized to one hemithorax, an
intercostal thoracotomy allows lobectomy to
be performed more readily than from a median
sternotomy approach. However, dogs with
spontaneous pneumothorax usually have diffuse,
bilateral pulmonary disease with multiple bullae.
A median sternotomy allows visualization of all
lung lobes and partial resection of any diseased
lobes. Mechanical pleurodesis might be of
benefit in dogs with spontaneous pneumothorax
to reduce recurrence.
LUNG LOBE TORSION
Any mechanism that increases mobility of a
lung lobe seems to favor torsion (Table 1).
Partial collapse of the lung (i.e., with pulmonary
disease or trauma) frees it from its normal
2006 World Congress WSAVA/FECAVA/CSAVA
spatial relationships with the thoracic wall,
mediastinum, and adjacent lung lobes. This
may enhance mobility. Pleural effusion or
pneumothorax, along with subsequent atelectasis
of lung lobes, can allow increased movement of
a lobe, predisposing to torsion. Although LLT
has been reported to cause chylothorax in dogs,
it may be chylothorax that caused LLT. LLT has
been reported secondary to previous thoracic
surgery in which lung lobes are manipulated and
remain partly collapsed after thoracic closure.
LLT has typically been reported most commonly
in the right middle lung lobe; however, in a recent
study right middle lobe torsion was predominant
in large dogs while left cranial lobe torsion was
more common in small dogs (D’Anjou et al,
2005). Underlying thoracic disease was found in
746
Back to contents
only 5 of 15 dogs in the aforementioned study.
Midlobar torsion of the right caudal lung lobe has
been reported in a dog (Hofeling et al, 2004).
Clinical Presentation
Signalment. Deep-chested, large-breed dogs,
especially Afghan hounds, are more commonly
affected; however five of 22 dogs with LLT in a
recent study were toy breeds (Neath et al, 2000).
Young, male pugs appear to be predisposed to
LLT (Rooney et al, 2001; Murphy et al, 2005).
Lung lobe torsion in Afghan hounds may be
associated with chylothorax. In large breed dogs
and pugs, LLT frequently occurs spontaneously
without previous history of disease or trauma.
LLT in other small breeds is often secondary
to primary pleural effusion, thoracic surgery, or
trauma. LLT is rare in cats. Middle-aged dogs are
more commonly affected, but LLT may occur in
animals of any age.
History. In a recent study of 22 dogs with
LLT, dyspnea was the most common reason for
examination (Neath et al, 2000). Coughing and
hemoptysis can also occur and may be chronic
in nature. Some animals may be anorectic and
depressed. There may be a previous history of
pneumothorax, pneumonia, or trauma or all
three.
Physical Examination Findings
Pleural effusion is consistently present in animals
with LLT, therefore findings often include
muffled heart and lung sounds. Other findings
may include depression, anorexia, coughing,
fever, dyspnea, hemoptysis, hematemesis, and/or
vomiting.
Diagnostic Imaging
Thoracic radiographic changes vary depending
on the volume of pleural fluid, the presence or
absence of preexisting disease, and the duration
of the torsion. The most consistent finding is
pleural effusion accompanied by an opacified
lung lobe. Initially, air bronchograms are present
in the torsed lobe and may be seen running
in an abnormal direction. Air bronchograms
eventually disappear as fluid and blood fill the
bronchial lumen. The presence of a noninflated,
radiopaque lung lobe that persists after removal
of pleural fluid should increase suspicion for LLT.
Bronchoscopy typically reveals a bronchus that is
occluded and appears to be “twisted”. Sometimes
the tissue at the site seems edematous. There may
or may not be blood in the bronchi.
SURGICAL TREATMENT
Spontaneous correction of a torsed lung lobe is
uncommon because of swelling of the lobe and

rapid formation of adhesions. The treatment
of choice for LLT is lobectomy of the affected
lobe. Unless LLT is diagnosed very quickly (i.e.,
immediately after a surgical procedure), damage
to the pulmonary parenchyma generally is severe
enough that attempts to salvage the lobe are not
warranted. Recurrence has been reported after
surgical correction where lobectomy was not
performed.
Before attempting to derotate the affected
pedicle, clamp it with a noncrushing forceps to
prevent release of toxins into the bloodstream
or fluids into the dependent lobes. Untwisting
the lobe before its removal may help facilitate
Back to contents
S
identification of the vascular structures and
bronchus for ligation; however, in many cases
the lobe cannot be easily returned to its normal
position because of extensive adhesions. A
transfixation suture or Miller’s knot can often
be used in such cases to ligate the vessels and
bronchus. Check the remaining lobes for position
and normal expansion. Culture the pulmonary
parenchyma after removal of the lobe. Submit
excised tissue for histologic examination to help
determine underlying causes (i.e., pneumonia,
neoplasia). Place a chest tube before closing the
thoracic cavity.
2006 World Congress WSAVA/FECAVA/CSAVA
747
 S
S - Soft Tissue Surgery
ONCOLOGIC GE EMERGENCIES
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
Pathophysiology
Acute gastrointestinal emergencies are caused
by gastrointestinal perforation, obstruction,
or intraluminal hemorrhage. Perforation
occurs as a sequelae to ulceration of gastric or
intestinal tumors, poor wound healing after
enterotomy, chemotherapy for lymphoma and
mast cell tumors, or mast cell tumor-induced
ulceration. Gastrointestinal perforation quickly
induces fulminant peritonitis resulting in
fluid, electrolyte and protein losses, acid-base
imbalances, hypoglycemia, diffuse intravascular
coagulopathy, circulatory collapse, and septic
shock. Gastrointestinal obstruction is caused
by tumor encroachment or by adhesions from
intraabdominal masses. Obstruction causes
fluid and gas accumulation proximal to the site
of obstruction and an increase in intraluminal
pressure. Continued distension results in venous
congestion, mural edema, decreased absorption,
and increased secretion. Fluid and electrolytes
are lost and significant vascular compromise
may result in devitalization of the intestinal wall.
At this point, the mucosal barrier is impaired
and bacterial translocation results in progressive
2006 World Congress WSAVA/FECAVA/CSAVA
septic and hemodynamic shock. Intraluminal
hemorrhage is commonly seen after ulceration
of such tumors as mast cell tumors, gastrinomas,
gastric and intestinal carcinomas, lymphoma,
and metastatic tumors. Gastric and intestinal
tumors are relatively uncommon in dogs and
cats and include adenocarcinoma, leiomyoma,
leiomyosarcoma, malignant lymphoma, mast cell
tumor, polyps, and fibrosarcoma. Mainly older
animals are affected and adenocarcinoma seems
to be most common in dogs and lymphoma in cats.
Relatively more nonlymphoid gastrointestinal
tumors are reported in Siamese cats, Boxers,
Collies, Staffordshire Bull terriers, and German
shepherds compared to other breeds. Over two-
thirds of gastrointestinal tumors are malignant
and early metastasis to regional lymphnodes,
748
Back to contents
liver, and lung in combination with ulceration
are observed frequently.
Clinical presentation and diagnosis
Clinical signs associated with gastrointestinal
tumors are nonspecific and include vomiting,
diarrhea or constipation, anorexia, abdominal
pain, ascites, and distension. Partial or total
obstruction of the gastrointestinal tract is
relatively common and the most common
signs are protracted vomiting, abdominal pain,
and abdominal distension. With perforation,
signs quickly progress to severe depression,
dehydration, and signs of cardiovascular and
septic shock. Intestinal bleeding is associated
with signs of anemia, weight loss, hematemesis,
hematochezia, diarrhea, and melena. Ascites,
dilated intestines, solitary masses, and excessive
borborygmi can be detected during physical
examination. Radiography and ultrasonography
allow further examination and localization of
abdominal masses, ileus, or free air. Diagnosis
can be obtained using ultrasound-guided
fine needle or cutting biopsy of the tumor.
Barium or iodine (if perforation is suspected)
contrast studies may locate the tumor if plain
radiography does not. Endoscopy is useful in
locating and obtaining biopsy specimens from
gastric, duodenal, colonic, and rectal tumors,
but is seldom used in an emergency situation.
Gastrointestinal perforation is accurately
diagnosed by paracentesis or peritoneal lavage
and immediate exploratory surgery is necessary
if intra and extracellular bacteria, or foreign
material are found on cytological examination.
Rarely, diagnostic peritoneal lavage may fail to
demonstrate bacteria if the spillage caused by
the perforation is localized. Repeat peritoneal
lavage, radiography with water soluble contrast
material, or exploratory surgery is indicated in
these cases.

Surgical therapy and aftercare
Severe active bleeding into the digestive tract,
partial or complete obstruction, or gastrointestinal
perforation necessitate emergency explorative
laparotomy. Preoperative supportive care is
directed to correcting fluid, electrolyte, and
acid-base imbalances; and treating septicemia
and endotoxic shock. Supportive therapy
may consist of blood transfusion, intravenous
fluid or colloid, and antibiotic administration
covering gram-negative and anaerobic bacteria
(e.g. cephalosporins or aminoglycosides in
combination with metronidazole). After routine
celiotomy, the abdomen is explored and the
extent of gastrointestinal involvement is assessed.
Regional lymph nodes and liver are inspected
for possible metastasis. At this point, biopsy
specimens of tumor and regional lymph nodes
can be obtained and submitted for cytological and
histological examination. Histologic examination
of frozen sections allows immediate diagnosis in
most cases.
For gastric tumors, complete resection is
the therapy of choice. Because of frequent
involvement of anthrum and pylorus (50% of
cases), partial gastrectomy as a Billroth I or II
procedure is often necessary to obtain wide
surgical margins. Enlarged local lymph nodes are
biopsied, or excised en-bloc. Partial gastrectomy
is contraindicated in dogs with gastrointestinal
lymphoma because of the diffuse nature of the
disease, effective chemotherapy options, and
associated complications with wound healing.
Solitary lymphomatous lesions seem to respond
better to surgery and adjunctive chemotherapy
than to either surgery or chemotherapy alone.
Intestinal neoplasms are usually treated by wide
surgical resection and anastomosis. A simple end-
to-end anastomosis often is sufficient but more
complex intestinal reconstruction techniques
are sometimes necessary. Tumors that already
have metastasized may be effectively excised for
palliation. Resection of regional lymph nodes and
other sites of metastasis may decrease the total
tumor burden enhancing the effect of adjuvant
therapy. The use of serosal or omental patching
at the surgery site is indicated for extensive
resections or in patients with suspected impaired
wound healing. The need for esophageal, gastric
or intestinal feeding tubes should be assessed
before closure. Placement of an esophagostomy,
gastrostomy or jejunostomy tube is relatively
easy. The benefits of improved nutritional status
in cachectic cancer patients far outweigh the
management disadvantages of surgically placed
feeding tubes. General peritonitis after intestinal
perforation is treated aggressively. Intraoperative
cultures are obtained and the abdominal cavity
Back to contents
S
is lavaged with copious amounts of a warm
isotonic solution. Open abdominal drainage
is used in severe cases of peritonitis. For open
abdominal drainage, the linea alba is closed with
a loose simple continuous polypropylene suture
pattern and the subcutis and skin are left open.
A sterile bandage is placed over the wound and
changed as often as required. Periodic surgical
lavage under strict aseptic conditions may be of
benefit. The use of sterilized commercial diapers
decreases the need of frequent bandage changes
caused by fluid penetrating the outer bandage.
Postoperative care includes continuing fluid and
electrolyte therapy. Initially small quantities
of water are offered, and if vomiting does
not occur, small quantities of soft food can be
fed. Anorectic animals may be force fed by
nasogastric, esophageal, endoscopically or
surgically placed gastrostomy, or jejunostomy
tubes. After intestinal anastomosis, breakdown
of the suture line most commonly occurs during
the second and fourth day postoperatively
and signs of physical deterioration during that
time should be aggressively investigated. Non-
perforating ulceration of the gastrointestinal tract
directly or indirectly caused by tumors can be
treated medically using antacids (e.g., aluminum
hydroxide), histamine2-antagonists (e.g.,
cimetidine), coating agents (e.g., sucralfate),
and proton pump inhibitors (e.g., omeprazole).
Malignant tumors of the gastrointestinal tract
may benefit from adjunct chemotherapy because
of their aggressive metastatic behavior. The
effect of chemotherapy for canine gastric
adenocarcinoma and canine and feline intestinal
adenocarcinoma have been discouraging,
however. Gastrointestinal malignant lymphoma
appears less responsive to chemotherapy than the
multicentric type. Also, complications associated
with intestinal perforation after chemotherapy
should be taken into consideration. Due to
their aggressive metastatic behavior (up to 75%),
2006 World Congress WSAVA/FECAVA/CSAVA
the overall prognosis for gastrointestinal
malignancies is guarded. The prognosis is poor if
the tumor is extensive, if metastases are present,
or when the tumor erodes through the serosal
surface. The mean survival time of 12 dogs with
malignant nonlymphoid gastrointestinal tumors,
that survived the first two weeks after surgery,
was 114 days without adjunctive chemotherapy.
The mean survival of cats with resected
adenocarcinoma was 15 months.
Conclusion
Surgical abdominal emergencies are relatively
common in small animal cancer patients and
pose a clinical and ethical challenge for the
oncologist. The most common abdominal
749
 S
emergencies include abdominal hemorrhage,
and urogenital, or gastrointestinal obstruction
or perforation. After emergency stabilization,
the question of whether surgical intervention
is proper and necessary needs to be answered.
Immediate surgery is only indicated in life-
threatening situations where the risk versus
S - Soft Tissue Surgery
ONCOLOGIC UROGENITAL EMERGENCIES
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
Pathophysiology
Urogenital oncologic emergencies are often
related to obstruction of the ureter, bladder neck,
or urethra, or to hemorrhage from the tumor.
Obstructive lesions can be located extramural
(intraabdominal, retroperitoneal, or intrapelvic),
intramural (renal, ureteral, bladder, or urethral
wall), or intraluminal. Extramural obstruction is
caused by tumors in various anatomical locations
including prostate (adenocarcinoma), rectum or
colon (adenocarcinoma), vagina (leiomyoma
2006 World Congress WSAVA/FECAVA/CSAVA
or fibroma), regional lymph node (lymphoma
or metastasis). Intramural and intraluminal
obstructions are most often caused by transitional
cell carcinoma, renal tumors, and benign
proliferations. Serious and life-threatening
abdominal hemorrhage and hematuria is often
caused by renal tumors from direct extension
of the tumor into the peritoneal or renal pelvic
space. Renal tumors are usually malignant in the
dog and cat, metastasize in up to 50% of cases,
and most commonly affect older animals. Primary
renal tumors include tubular cell carcinoma,
transitional cell carcinoma, fibrosarcoma,
hemangiosarcoma, and nephroblastoma in the
dog; and lymphoma, renal carcinoma, sarcoma,
and nephroblastoma in the cat. Ureteral tumors
are rare but can cause hydronephrosis.
Bladder and urethral tumors are more common
750
Back to contents
benefit of surgery has been weighed, and should
be accompanied by adequate preoperative and
postoperative supportive care.
Reference
Kirpensteijn J, et al. Vet Clinics of North America
[Small Animal] 1995; 25: 207-223
than renal or ureteral tumors and are most
prevalent in female dogs and male cats. Except
for rhabdomyosarcoma, bladder tumors affect
older animals, and the most common tumor type
in dogs and cats is transitional cell carcinoma.
Transitional cell carcinomas are highly invasive
tumors which grow slowly often in the trigone
area and bladder neck. Emergencies associated
with bladder and urethral tumors are usually
caused by obstruction of the urethra or ureter.
These tumors eventually metastasize in 80% of
dogs. Common sites include the lung, lumbar
lymph nodes, kidney, prostate, and liver.
Benign diseases must also be considered in the
differential diagnosis. Chronic and acute renal
failure, urinary tract infections, urolithiasis,
ureteral strictures, cyclophosphamide-induced
cystitis, and neurologic abnormalities could
cause similar signs.
Clinical presentation and diagnosis
Clinical signs depend on the location and size
of the tumor. Renal and ureteral tumors are
associated with hematuria, renal enlargement,
abdominal pain, anorexia, depression, and
weight loss. Physical examination may reveal a
large, painful abdominal mass and the diagnosis
is confirmed by abdominal radiography,
ultrasonography, contrast studies (intravenous

pyelogram), renal scintigraphy, CT, or MRI scans.
Routine serum chemistry and urinalysis allows
evaluation of kidney function. Ultrasonographic
guided fine needle aspiration of the tumor
facilitates early diagnosis. Dysuria, hematuria,
polyuria, pollakiuria, or anuria are observed
with lower urinary tract tumors. Neoplasms
associated with the bladder and urethra may be
palpated by abdominal and rectal examination.
Other useful diagnostic procedures include
abdominal radiography, ultrasonography, and
contrast studies (intravenous pyelogram, double
contrast cystogram, retrograde urethrogram).
Malignant cells are seldom found in the urine
sediment but may be obtained by catheter biopsy
or percutaneous fine needle aspiration of prostate
and urethra. Direct cystoscopic visualization
of the tumor in the bladder or urethra is often
possible in female dogs and the diagnosis is
confirmed by cystoscopic biopsy.
Surgical therapy and aftercare
Surgical therapy depends on the site of obstruction.
Unilateral nephrectomy and ureterectomy are
indicated for renal tumors if the opposite kidney
is functional, and if metastases are not present.
Mean survival time after nephrectomy for dogs
with renal tubular cell carcinoma was 7 months
and for dogs with transitional cell carcinoma it
was 11 months.
Surgical excision is the therapy of choice for
cystic and urethral transitional cell carcinoma but
is often impossible because of tumor location.
Partial cystectomy may be successful in tumors
not affecting the trigone. The tumor must be
excised with a wide margin of normal tissue and
the remainder of the bladder wall is inspected.
Even after excision of more than 75% of the
urinary bladder, function can eventually return to
normal or near normal. A modified “cup-patch”
cystoplasty can be performed in resections of
more than 80% of the bladder. When the trigone
is involved, reimplantation of the ureters in
the remaining bladder may be necessary. Total
cystectomy has been combined with urinary
diversion, but postoperative complications have
Back to contents
S
made these salvage procedures less beneficial.
Ureterocolonic anastomosis seems to be most
successful of the urinary diversion techniques. In
general, survival times after surgical excision of
bladder and urethral transitional cell carcinoma
are limited because of recurrence or metastasis.
Temporary relief can also be obtained using
an indwelling urinary or prepubic, cystostomy
catheter. The placement of cystostomy catheter
is relatively simple and is associated with few
complications and easy home management.
This technique can be used in combination with
adjuvant therapies or as palliation. A permanent
cystostomy catheter eliminates the need for
immediate euthanasia in dogs with advanced
bladder and urethral cancer.
Adjuvant radiation or chemotherapy may be
indicated, but has been associated with high rate
of complications and tumor recurrence. Results
of systemic or intravesicular administration of
chemotherapy for transitional cell carcinoma
have been variable. Partial response or stable
disease was seen after intravenous cisplatin
therapy in 9 out of 12 dogs. Also, the use of the
nonsteroidal antiinflammatory drug piroxicam
has been beneficial in obstructive canine
transitional cell carcinoma, at least for palliation.
Complications after oncologic bladder or urethral
surgery include incontinence, postoperative
diuresis, pollakiuria (“small bladder syndrome”),
and infection. Incontinence is treated with
parasympathomimetic drugs (e.g., bethanechol
chloride) for partially denervated bladders,
adrenergic agonists (e.g., ephedrine) for low
pressure incontinence, anticholinergics (e.g.,
probanthine) for reflex neurogenic bladders, and
sympatholytic drugs (e.g., phenoxybenzamine)
for urethral spasm. Postobstructive diuresis
should be appropriately compensated with
intravenous fluid administration. Infection should
be treated with antibiotics based on culture and
sensitivity results.
2006 World Congress WSAVA/FECAVA/CSAVA
Reference
Kirpensteijn J, et al. Vet Clinics of North America
[Small Animal] 1995; 25: 207-223
751
 S
S - Soft Tissue Surgery
ONCOLOGIC HEMORRHAGIC AND ENDOCRINE EMERGENCIES
Prof. dr. Jolle Kirpensteijn
Diplomate ECVS & ACVS
Head Soft Tissue Surgery
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
Utrecht University
PO Box 80.154
3508 TD Utrecht
j.kirpensteijn@vet.uu.nl
INTRODUCTION
Emergencies often occur because of an underlying
oncologic problem and pose a challenge for
the medical and surgical oncologist. Many
tumor related emergencies require immediate
surgical intervention but are complicated by
the debilitated state of the patient or ethical
concerns for the patient’s ultimate prognosis.
The acute nature of the problem, the physical
status of the animal, and the availability of
alternative treatment determine the necessity of
immediate surgery. A decision has to be made
in which the progression of the disease, general
health status of the animal, and experience of
the clinician are of extreme importance. All
these factors influence surgical morbidity and
mortality, the extent of surgery, postoperative
management, and overall prognosis. Thus
every oncologic emergency requires a thorough
evaluation and individual therapeutic approach.
The surgeon often has a central role in the
diagnosis, treatment, and aftercare of the cancer
patient in an emergency situation. The first step
in managing the emergency is to evaluate the
patient’s pathophysiologic status and eliminate
immediate threats to the patient’s life. The
2006 World Congress WSAVA/FECAVA/CSAVA
anamnesis should include previous oncologic
diagnoses, procedures, and therapies. At the
same time, a cursory physical examination will
point out signs of life-threatening complications
that should be dealt with immediately to
stabilize the patient’s physical functions. After
stabilization, a thorough physical examination
is performed and a diagnostic and therapeutic
plan is formulated. Further diagnostic steps
include general tests (complete blood count,
biochemistry and clotting profiles, and
urinalysis) and cancer specific tests (fine needle
aspiration, radiography, ultrasonography, CT-
, and MRI scans). The timing, selection, and
purpose of surgical therapy vary with the type
of cancer and the site of involvement. Timing
depends on whether the emergency involves 1) a
patient with stable vital functions and a problem
752
Back to contents
requiring surgical correction, 2) a patient with
compromised vital functions and a delayed threat
to life, or 3) a patient with an immediate threat
to life requiring surgical correction. Immediate
surgery is only necessary in life-threatening
situations and should be accompanied by
adequate supportive care. The goal of surgery
may be complete excision of the tumor and
cure, palliation, cytoreduction, or histologic
confirmation of the tumor type. Regardless
of resection type, surgery should resolve the
emergency situation. Complete excision of the
tumor is the hopeful goal of surgery. Palliative
surgery must improve the patient’s quality of life,
and perhaps prolong it. The aim of cytoreduction
is to decrease tumor bulk to improve the efficacy
of adjunctive treatment. Cytoreduction without
adjunctive therapy is of no benefit to the patient.
Biopsy specimens always should be examined
to aid in evaluating the prognosis and further
therapy. Postoperative management includes
monitoring the return of normal physiologic
functions, evaluation of wound healing, the use
of adjunctive therapy, and periodic assessment
of tumor recurrence and metastasis. Intensive
supportive therapy is often necessary after
emergency surgery and may include intravenous
administration of fluids, blood, or plasma,
antibiotic therapy, and nutritional support.
The benefits of surgical intervention in cancer
patients must be weighed against the risks of
surgery. Operative morbidity and mortality
depend on the basic disease process, the
surgical procedure, anesthesia, and the patient’s
general status and ability to withstand operative
trauma. In oncologic patients, the basic disease
process and debilitated state of the patient are
major determinants of operative morbidity and
mortality. Surgery may alleviate clinical signs
in an emergency situation but mortality rates can
be high. Every emergency cancer patient should
be evaluated individually and carefully, and the
risks and benefits of therapy should be explained
to the client.

Exploratory laparotomy
The ventral midline approach is the standard
access route for almost all of the abdominal
contents and should be referred to as celiotomy.
A laparotomy strictly refers to flank incisions.
The aim is to incise through the linea alba and to
avoid cutting into the rectus abdominal muscles.
This is caudally more difficult than cranially,
because the width of the linea decreases caudally.
The falciform ligament is the first ‘organ’ that
is encountered. To improve the exposure of the
abdomen this ligament is normally dissected and
ligated cranially. Insufficient ligation may lead
to abdominal hemorrhage. The abdomen should
always be explored in a standard manner to avoid
skipping certain abdominal structures. The author
prefers a cranio-caudal method starting with the
diaphragm and liver and ending with the caudal
GI tract. Closure of the abdomen is performed
by a continuous closure pattern of absorbable
monofilament suture material.
Hemorrhagic abdominal emergencies
Pathophysiology
Hemorrhagic abdominal emergencies develop
secondary to direct extension and ulceration of
various malignant tumor types into the peritoneal
cavity, or to rupture of an organ enlarged from
tumor invasion. Abdominal hemorrhage is
most frequently associated with splenic and
hepatic tumors but can also be caused by
tumors of other organs such as the adrenal
gland. The most common canine splenic tumor
is hemangiosarcoma. It usually affects older
animals and metastasizes in more than 50% of
cases to other organs including lungs, heart,
liver, kidney, omentum, and peritoneum. Mast
cell tumor and malignant lymphoma occur most
frequently in the spleen of cats. Any enlarged
spleen may rupture, resulting in internal blood
loss and hypovolemic shock.
Primary hepatic tumors occur in older dogs and
cats but are rare. Hepatocellular carcinoma is
most common and it frequently metastasizes to
regional lymph nodes, lung, and peritoneum.
Metastatic liver tumors are more common
than primary tumors and include malignant
lymphoma, pancreatic adenocarcinoma, and
hemangiosarcoma. Massive hemorrhage can
occur from any hepatic tumor and may require
emergency laparotomy.
Adrenal tumors consist of adenomas, carcinomas
and pheochromocytomas and these tumors can
be functional and non functional. Most clinical
signs are caused by the local growth of the tumor
or by signs caused by the hypersecretion of
hormones but in some cases adrenal tumors will
rupture and cause significant hemorrhage
Back to contents
S
Clinical presentation and diagnosis
Abdominal hemorrhage results in abdominal
enlargement, pale mucous membranes, lethargy,
abdominal pain, tachycardia, tachypnea, and
vomiting. Clinical signs vary with the severity
of bleeding. In patients with exsanguinating
hemorrhage, clinical signs of hypovolemic
shock will predominate. Once a diagnosis of
abdominal effusion is made, little additional
information is obtained by radiographic
examination. The presence of fluid decreases
the value of radiography but enhances the use
of ultrasonography. Radiography after removal
of fluid by abdominal paracentesis may improve
visualization of intra-abdominal structures and
assist in diagnosis. Fluid obtained should be
examined cytologically. Neoplastic cells may be
identified in aspirated fluid but neoplastic disease
should not be excluded on basis of negative
findings. To differentiate hemorrhage from
serosanguinous exudate, the packed cell volume
(PCV) and white blood cell counts are compared
to those of peripheral blood. The packed cell
volume of serosanguinous exudates rarely
exceeds 5%. An increase in PCV in sequential
samples may indicate continuing intraabdominal
bleeding.
Alternatively, intraabdominal masses can be
diagnosed by ultrasonography in comination
with a guided fine needle aspiration biopsy. Non-
diagnostic samples are relatively common because
of sampling errors and because little material
is obtained from some tumor types. Definite
diagnosis often requires histologic examination
of a surgical biopsy specimen. In patients with
abdominal hemorrhage, clotting ability should
be investigated before surgery since disturbances
can be caused by the tumor. In up to 50% of dogs
with splenic hemangiosarcoma there are signs of
diffuse intravascular coagulation.
Adrenal tumors are easily identified using
ultrasonographic, CT or MRI imaging techniques.
2006 World Congress WSAVA/FECAVA/CSAVA
Surgical therapy and aftercare
The clinical status of the patient dictates the
type of treatment. An initial period of medical
stabilization prior to surgical intervention may
improve prognosis. Supportive therapy consists
of intravenous fluids, hypertonic saline, or colloid
therapy, blood transfusions, and pressure wraps.
Blood transfusions are often necessary in dogs
with exsanguinating abdominal hemorrhage.
Autotransfusion, rather than heterologous
blood transfusion, is contraindicated in tumor-
induced abdominal hemorrhage, because it can
spread tumor cells. In emergency situations it
may prevent the animal from dying, however.
Increased intraabdominal pressure by application
753
 S
of an abdominal pressure wrap may help control
hemorrhage. Compressive abdominal and pelvic
bandages are the practical alternative for seldom
available antishock garments. Emergency
laparotomy is indicated if, despite fluid and
blood replacement, the animal deteriorates.
The abdomen should be thoroughly explored to
locate the source of bleeding and search for signs
of metastases. Total splenectomy often is life-
saving in hemorrhaging splenic malignancies,
but a cure is rarely obtained if it is caused by a
hemangiosarcoma. The prognosis for dogs with
a splenic hemangiosarcoma after splenectomy
is still poor, because of the tumor’s aggressive
metastatic behavior. An average survival time of
2 months without and 6 months with adjuvant
chemotherapy has been reported. In contrast to
malignant tumors, benign splenic tumors have
an excellent prognosis after surgical removal.
The use of ligating-dividing or other staplers
will allow expedient and safe surgical removal
of hemorrhaging splenic neoplasms.
Surgical excision by partial or total hepatic
2006 World Congress WSAVA/FECAVA/CSAVA
754
Back to contents
lobectomy is the treatment of choice for
bleeding hepatic tumors located in a single
lobe. The prognosis for benign hepatic tumors
is excellent if they can be removed completely.
Survival times greater than two years have
been reported. Malignant hepatic tumors carry
a poorer prognosis, although lobectomy in dogs
with hepatocellular adenocarcinoma resulted in a
mean survival of 377 days.
The bleeding adrenal tumor should be removed
in toto. This is often possible except when there
is extensive ingrowth into the vena Cava. The
paralumbar laparotomy is the preferred approach
for most adrenal tumors; however large tumors
sometimes can be better removed through a
median celiotomy. The overall survival of dogs
with adrenal tumors has increased significantly
because of refinement of the surgical technique.
Reference
Kirpensteijn J, et al. Vet Clinics of North America
Small Animal Pract 1995; 25: 207-223

S - Soft Tissue Surgery
CHYLOTHORAX: SURGERY IS EFFECTIVE!
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan
Read Chair in Veterinary Surgery
Director, Clinical Programs and
Biomedical Devices,
Michael E. DeBakey Institute
Professor of Surgery
Texas A&M University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu
In most animals, abnormal flow or pressures
in the thoracic duct (TD) are thought to lead
to exudation of chyle from intact but dilated
thoracic lymphatic vessels (a condition known
as thoracic lymphangiectasia. These dilated
lymphatic vessels may form in response to
increased lymphatic flow (caused by increased
hepatic lymph formation), decreased lymphatic
drainage into the venous system as a result of
high venous pressures, or both factors acting
simultaneously to increase lymph flow and reduce
drainage. Any disease or process that increases
systemic venous pressures (i.e., right heart
failure, mediastinal neoplasia, cranial vena cava
thrombi, or granulomas) may cause chylothorax.
Trauma is an uncommonly recognized cause of
chylothorax in dogs and cats because the thoracic
duct heals rapidly after injury, and the effusion
resolves within 1 to 2 weeks without treatment.
Clinical Presentation
Signalment. Any breed of dog or cat may be
affected; however, a breed predisposition has
been suspected in the Afghan hound for a
number of years. Recently, it has been suggested
that the Shiba Inu breed may also be predisposed
to this disease. Among cats, Oriental breeds
(i.e., Siamese and Himalayan) appear to have an
increased prevalence. Chylothorax may affect
animals of any age; however older cats may be
more likely than young cats to develop it. This
finding was believed to indicate an association
between chylothorax and neoplasia. Afghan
hounds appear to develop this disease in middle
age, but affected Shiba Inus have been less than
1 year old. A gender predisposition has not been
identified.
History. Coughing often is the first (and
occasionally the only) abnormality until the
animal becomes dyspneic. Many owners report
that coughing began months before presenting
the animal for care; therefore, animals that
cough and do not respond to standard treatment
Back to contents
S
of nonspecific respiratory problems should be
evaluated for chylothorax. Coughing may be
due to irritation caused by the effusion or may
be related to the underlying disease process (i.e.,
cardiomyopathy, thoracic neoplasia).
Physical Examination Findings
Most animals with chylothorax have a normal
body temperature unless they are extremely
excited or severely depressed. Additional findings
may include muffled heart sounds, depression,
anorexia, weight loss, pale mucous membranes,
arrhythmias, murmurs, and pericardial effusion.
Diagnostic Imaging
The radiographic signs of pleural effusion are
provided on. Animals that have collapsed lung
lobes that do not appear to reexpand after removal
of chyle or other pleural fluid should be suspected
of having underlying pulmonary parenchymal
or pleural disease, such as fibrosing pleuritis.
Although the etiology of the fibrosis is unknown,
it apparently can occur subsequent to any
prolonged exudative or blood-stained effusion.
Diagnosis of fibrosing pleuritis is difficult. The
atelectatic lobes may be confused with metastatic
or primary pulmonary neoplasia, lung lobe
torsion, or hilar lymphadenopathy. Radiographic 2006 World Congress WSAVA/FECAVA/CSAVA
evidence of pulmonary parenchyma that fails to
reexpand after removal of pleural fluid should be
considered possible evidence of atelectasis with
associated fibrosis. Fibrosing pleuritis should
also be considered in animals with persistent
dyspnea in the face of minimal pleural fluid.
CT lymphangiography may be able to quantify
branches of the thoracic duct more accurately
than standard radiographic lymphangiography.
In a recent study, CT lymphangiography was
performed by percutaneously injecting 1 to 2 ml
of nonionic contrast material into the mesenteric
lymph nodes of 4 dogs with chylothorax using
ultrasound guidance (Johnson et al, 2005).
Helical thoracic CT images were acquired before
and after injection of the contrast media. The
755
 S
technique documented the location and character
of the TD and its tributary lymphatics and may
prove useful for surgical planning in animals
with chylothorax.
Laboratory Findings
Fluid recovered by thoracentesis should be placed
in an EDTA tube for cytologic examination.
Placing the fluid in an EDTA tube rather than a clot
tube allows cell counts to be performed. Although
chylous effusions routinely are classified as
exudates, the physical characteristics of the fluid
may be consistent with a modified transudate. The
color varies depending on the dietary fat content
and the presence of concurrent hemorrhage. The
protein content is variable and often inaccurate
because of interference with the refractive index
by the high lipid content of the fluid. The total
nucleated cell count usually is below 10,000/ul
and consists primarily of small lymphocytes or
neutrophils with lesser numbers of lipid-laden
macrophages. Chronic chylous effusions may
contain low numbers of small lymphocytes
due to the body’s inability to compensate for
continued lymphocyte loss. Nondegenerative
neutrophils may predominate with prolonged
loss of lymphocytes or if multiple therapeutic
thoracenteses have induced inflammation. The
most diagnostic test is comparison of serum
and fluid triglyceride levels. Chylous effusions
have a higher triglyceride concentration than
simultaneously collected serum.
MEDICAL MANAGEMENT
If an underlying disease is diagnosed, it should
be treated and the chylous effusion managed
by intermittent thoracentesis. If the underlying
disease is effectively treated, the effusion often
resolves; however, complete resolution may take
several months. Surgical intervention should
be considered only in animals with idiopathic
2006 World Congress WSAVA/FECAVA/CSAVA
chylothorax or those that do not respond to
medical management. Chest tubes should be
placed only in animals suspected of having
traumatic chylothorax (very rare) with rapid
fluid accumulation, or occasionally after surgery.
Electrolytes should be monitored; hyponatremia
and hyperkalemia can occur in dogs with
chylothorax undergoing multiple thoracentesis.
A low-fat diet may reduce the amount of fat in
the effusion, which may improve the animal’s
ability to resorb fluid from the thoracic cavity.
Benzopyrone drugs have been used for the
treatment of lymphedema in human beings for
years. Whether these drugs might be effective
in reducing pleural effusion in animals with
chylothorax is unknown; however, preliminary
findings suggest that some animals treated with
756
Back to contents
rutin (50-100 mg/kg, PO. TID) have complete
resolution of effusion 2 months after initiation
of therapy. Whether the effusion resolves
spontaneously in these animals or is associated
with the drug therapy is unknown.
Somatostatin is a naturally occurring substance
that has an extremely short half-live. It inhibits
gastric, pancreatic, and biliary secretions (i.e.,
glucagon, insulin, gastric acid, amylase, lipase,
and trypsin) and prolongs gastrointestinal transit
time, decreases jejunal secretion, and stimulates
gastrointestinal water absorption. In recent years
analogues of somatostatin have been used to
successfully treat chylothorax in humans with
traumatic or postoperative chylothorax. In these
patients, reduced gastrointestinal secretions may
aid healing of the TD by decreasing TD lymphatic
flows. It has also been reported to result in early
decreased drainage and early fistula closure in
dogs with experimental transection of the TD. The
mechanism by which non-traumatic chylothorax
may benefit from this treatment is unclear;
however, resolution of pleural fluid (chyle and
postoperative serosanguineous effusion) in both
dogs and cats has occurred after administration
of octreotide. Octreotide (sandostatin; 10 mcg/kg
subcutaneously three times a day for 2 to 3 weeks)
is a synthetic analogue of somatostatin that has
a prolonged half-life and minimal side effects.
Soft stools that resolve after withdrawal of the
drug may occur. Prolonged treatment should be
discouraged because people treated for longer
than 4 weeks are at risk for gallstones.
SURGICAL TREATMENT
Surgical intervention is warranted in animals
that do not have underlying disease and in which
medical management has become impractical or
is ineffective. Properly performed, TD ligation
results in over 80% of dogs and cats resolving
their effusion (Fossum et al, 2004). Formation
of a nonchylous effusion (from pulmonary
lymphatics) may occur in some animals after
surgery. Mesenteric lymphangiography may be
particularly difficult to perform in cats. While
mesenteric lymphangiography is not essential,
catheterization of a mesenteric lymphatic and
injection of methylene blue makes identification
of the TD and its branches much easier.
Thoracic duct ligation has been performed using
thoracoscopy (Radlinsky et al, 2002).
Many animals with chylothorax have either a
thickened pericardium or tissue overlying the
pericardium is thick. When the pericardium or
overlying tissues are thickened or abnormal in
animals with derangements in lymphatic flow
(be it chylothorax or continued serosanguineous
flow after TD ligation), pericardiectomy may act

to lower right-sided venous pressures. Therefore,
pericardiectomy is recommended in conjunction
with TD ligation.
SURGICAL TECHNIQUES
Thoracic Duct Ligation
Perform an intercostal thoracotomy (right side
for dogs, left side for cats) at the eighth, ninth,
or tenth intercostal space or make an incision in
the diaphragm. Locate the thoracic duct and use
hemostatic clips and/or silk suture (2-0 or 3-0) to
ligate it. Visualization of the thoracic duct is greatly
aided by injecting methylene blue into the lymphatic
catheter. Perform a subtotal pericardectomy by
Back to contents
S
reaching forward under the rib cage.
NOTE: Wear magnification and use a headlight
to help visualize the TD and its small branches!
References
Fossum TW, Mertens MM, Miller MW, et al:
Thoracic duct ligation and pericardectomy for
treatment of idiopathic chylothorax, J Vet Intern
Med 18: 307, 2004.
Radlinsky MG, Mason DE, Biller DS, Olsen D:
Thoracoscopic visualization and ligation of the
thoracic duct in dogs, Vet Surg 31, 138, 2002.
2006 World Congress WSAVA/FECAVA/CSAVA
757
 S
S - Soft Tissue Surgery
INTRAHEPATIC SHUNTS: TO CUT OR TO COIL?
Theresa W. Fossum, DVM, PhD
Diplomate ACVS, Tom and Joan Read Chair in Veterinary Surgery
Director, Clinical Programs and Biomedical Devices,
Michael E. DeBakey Institute Professor of Surgery
Texas A&M University
College of Veterinary Medicine
College Station, Texas 77843-4474
tfossum@cvm.tamu.edu
When portal blood bypasses the liver, many
substances that are normally metabolized or
excreted in the liver enter the systemic circulation.
Also, important hepatotrophic substances from
the pancreas (e.g., insulin) and intestines do
not reach the liver, resulting in hepatic atrophy
or failure of the liver to attain normal size.
Hepatic insufficiency or hepatic encephalopathy
frequently occur. Hepatic encephalopathy is
a clinical syndrome of altered CNS function
resulting from hepatic insufficiency. A variety
of substances (i.e., ammonia, methionine/
mercaptans, short-chain fatty acids, alterations
in the ratio between circulating levels of
branched-chain and aromatic amino acids, and γ-
aminobutyric acid) have been incriminated in the
resulting elaboration of false neurotransmitters.
Portosystemic shunts (PSS) may be broadly
categorized as intrahepatic or extrahepatic.
Congenital extrahepatic shunts usually are
single anomalous vessels that allow abnormal
blood flow from the portal vein to the systemic
circulation. Intrahepatic shunts usually are
congenital, singular shunts that occur because
the ductus venosus fails to close after birth,
or they may arise when other portal to hepatic
vein or caudal vena cava anastomoses exist.
2006 World Congress WSAVA/FECAVA/CSAVA
Congenital intrahepatic portosystemic shunts
(IHPSS) constitute about 35% of single shunts in
dogs and approximately 10% in cats.
DIAGNOSIS
Clinical Presentation
Signalment. Purebred dogs are at increased
risk for PSS. Domestic shorthair cats are most
commonly affected, although these aberrations
also occur in purebred cats (i.e., Himalayan).
Single PSS usually are congenital and are most
commonly diagnosed in animals under 1 year
of age although dogs as old as 13 years have
been diagnosed. Intrahepatic PSS are more
commonly diagnosed in large-breed dogs (e.g.,
German shepherds, golden retrievers, Doberman
pinschers, Labrador retrievers, Irish setters,
758
Back to contents
Samoyeds, and Irish wolfhounds). Small breed
dogs most likely to have IHPSS are toy and
miniature poodles. There may be a hereditary
basis for IHPSS in Irish wolfhounds. Congenital
extrahepatic and IHPSS have been reported in
cats. There is no convincing gender predisposition
for these anomalies in either species.
NOTE: In general, small-breed dogs are more
likely to have extrahepatic shunts, and large-
breed dogs are more likely to have IHPSS.
History. The presenting history for animals
with PSS varies considerably. Affected animals
usually are evaluated because of failure to grow,
small body stature, or weight loss. Other common
abnormalities include intermittent anorexia,
depression, vomiting, polydipsia or polyuria,
ptyalism (especially in cats), pica, amaurosis,
and behavioral changes. Some animals are
presented for evaluation of urinary dysfunction
(i.e., hematuria, dysuria, pollakiuria, stranguria,
urethral obstruction) associated with urate
urolithiasis. Signs of hepatic encephalopathy can
vary tremendously from those that are extremely
mild and hard to identify as a significant
abnormality (e.g., lethargy, being “tired”, being
“slow”) to severe changes (e.g., ataxia, weakness,
stupor, head pressing, circling, amaurosis,
pacing, seizures, or coma). These signs may be
constant or intermittent and sometimes, but not
invariably, worsen after eating (especially a
high-protein diet composed of animal protein).
Hepatic encephalopathy may also worsen after
gastrointestinal hemorrhage (e.g., caused by
parasites or ulceration). In a recent study, 82%
of dogs had CNS signs, 76% had gastrointestinal
signs, and 39% had urinary signs. In addition to
ptyalism, affected cats typically show episodic
central blindness.
Physical Examination Findings
Most animals with PSS have microhepatica,
and the kidneys may feel prominent or plump.
A golden or copper color to the iris has been

observed in many cats with PSS. Neurologic
abnormalities may be noted (see above).
Ptyalism is a common finding in cats but rare
in dogs. Animals with hepatic A-V fistulae may
have a palpably enlarged liver (rare) or ascites.
An audible bruit sometimes can be auscultated in
the cranial abdomen of affected animals.
Diagnostic Imaging
Survey abdominal radiographs are an important
part of screening for congenital PSS. It is
extremely rare to find a dog with PSS that
does not have some degree of microhepatica.
Plain abdominal radiographs are more sensitive
in finding microhepatica than abdominal
ultrasound.
Definitive diagnosis of PSS is made by surgical
identification of the shunt, intraoperative positive
contrast portography, ultrasound identification
of the shunt, or nuclear hepatic scintigraphy.
Jejunal vein portography is the simplest and most
effective portographic technique. Ultrasound
guided splenoportography can also be performed
in large breed dogs. The most consistent finding on
survey abdominal radiographs is microhepatica.
Ultrasound has become the diagnostic tool
of choice for imaging PSS. Both intrahepatic
and extrahepatic shunts have been identified
with this technique; however, an inconclusive
ultrasound examination does not rule out PSS.
Occasionally a dilated intrahepatic vessel or the
communication of an intrahepatic shunt with the
caudal vena cava is noted. Nuclear scintigraphy
is a rapid, noninvasive method of documenting
abnormal hepatic blood flow. Sodium
pertechnetate technetium 99m (99mTc) is typically
used in scintigraphic studies to detect PSS. A
new scintigraphic technique has recently been
reported —trans-splenic portal scintigraphy. This
technique is unique in that it utilizes ultrasound
guidance to inject a small amount of 99mTc into
the parenchyma of the spleen.
Laboratory Findings
Hematologic, serum biochemical, and urine
analysis of animals with PSS may disclose
various abnormalities, but dogs can have a
congenital PSS without any abnormalities on
CBC or serum biochemistry panel. Low serum
albumin is a common finding in dogs; however,
some dogs (and most cats) with PSS have normal
albumin levels. Low BUN results from reduced
conversion of ammonia to urea in the hepatic urea
cycle, but the polyuria-polydipsia seen in many
patients may contribute. Other abnormalities
occasionally include mild to marked increases
in serum alanine aminotransferase, aspartate
aminotransferase, and alkaline phosphatase
Back to contents
S
Hepatic function tests are important in screening
for congenital PSS. Serum bile acids have been
the standard hepatic function test in dogs and
cats for years, but it is now recognized that they
have some major limitations. First, it is critical to
measure both pre- and post-prandial serum bile
acid concentrations; approximately 20% of dogs
have a higher pre-prandial value. Second, some
dogs with very high serum bile acid concentrations
(> 150 umol/L) do not have clinically significant
hepatic disease while some dogs with congenital
PSS have serum bile acid concentrations that are
only moderately increased (e.g., 50-60 umol/
L, normal < 30 umol/L). Third, unlike what is
expected for most biochemical determinations,
there can be substantial variation in bile acid
concentrations from day to day (as much as or
greater than 100%). Currently, urinary bile acids
appear to be about as useful as serum bile acids
but may have the advantage of being easier to
collect, especially in cats.
Ligation or Attenuation of Intrahepatic Shunts
Both intravascular and extravascular methods
have been described for ligation of IHPSS.
Ligation of IHPSS can be extremely challenging
because the vessel often is difficult to locate.
Occasionally the shunt can be identified as a
palpable depression or soft spot in a liver lobe,
or it may be seen entering the caudal vena cava
if it is not completely encircled by hepatic
parenchymal tissue. Intraoperative ultrasound
scans have been used to help identify the shunt
in hepatic tissue, but this technique is not always
successful. Intrahepatic shunts are classified
as left, central, or right sided. Left and central
divisional shunts account for a majority of shunts
(see Fig. 20-14). Left sided IHPSS (patent ductus
venosus) are typically located in the left lateral or
medial hepatic lobes. Ligation or attenuation of
the left hepatic vein may be performed in these
animals. Central shunts are generally found in the 2006 World Congress WSAVA/FECAVA/CSAVA
right medial lobe, while right shunts are typically
located in the right lateral or caudate lobes. An
intravascular technique involving temporary
hepatic vascular occlusion in conjunction
with caudal caval venotomy was described
by Breznock for intrahepatic shunt occlusion;
however, because this procedure is technically
difficult and surgery time is prolonged, many
surgeons prefer extravascular techniques.
Isolation and obstruction of the specific branch
of the portal vein supplying the IHPSS have been
described. Indirect passage of suture for ligation
of right-sided intrahepatic PSS was recently
reported (Tobias et al, 2004). The ligature should
encircle the right portal branch approximately 4
mm lateral to it bifurcation from the parent vein
(see below).
759
 S
NOTE Warn owners that ligation of IHPSS is
difficult because the shunts are often hard to
identify at surgery.
Isolation and ligation of IHPSS involving the left
medial or lateral liver lobes. Many shunts can be
found cranial to the liver.
Extend the abdominal incision proximally into
the caudal sternebrae. Incise the diaphragm if
necessary. Incise the left triangular ligament and
free the left lateral liver lobe so that it can be
retracted to the right. Use a combination of sharp
and blunt dissection to isolate the anomalous
vessel at its junction with the hepatic vein. Place a
single silk ligature around the vessel and attenuate
flow while measuring portal pressures. Alternately,
ligate or attenuate the left hepatic artery as it
2006 World Congress WSAVA/FECAVA/CSAVA
760
Back to contents
enters the liver while measuring portal pressures.
Isolation and ligation of right sided IHPSS.
If necessary, ligate the right hepatic duct. Pass
a Carmalt forceps from the dog’s right to left
over the dorsal surface of the main portal vein,
just caudal to its bifurcation, but cranial to the
termination of the gastroduodenal vein. Grasp
one end of a 2-0 silk suture and pull it back
across the dorsal aspect of the portal vein. Then,
pass the forceps from the dog’s right to left,
dorsal to the left portal vein and within 5 mm of
its bifurcation from the main portal vein. Grasp
the opposite end of the suture and pull it back
over the vein.
Back to contents
S

2006 World Congress WSAVA/FECAVA/CSAVA

761
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

T
T –T
No
Nose-Ear-Throat

Back to contents

INVITED LECTURES - FULL PAPERS
T – Nose-Ear-Throat
DERMATOLOGIC DISEASES OF THE AURICLE
Craig Griffin DVM,
Diplomate ACVD
Animal Dermatology Clinic
5610 Kearny Mesa Rd
San Diego, California
USA 92111
itchypet@aol.com
The pinnae may be affected by the majority of
dermatologic diseases described in dogs and
cats. For some diseases the pinna is a preferred
or commonly affected site. For a small number
of diseases the pinnae are often the only affected
site and some of these will be discussed in this
session.
Relapsing polychondritis is a rare disease
of dogs, cats and humans characterized by
inflammation and destruction involving
both articular and non articular cartilaginous
structures. (Scott, Miller et al. 2001) It has been
classified among the immune-mediated diseases
because of similarities to rheumatoid arthritis
and lupus erythematosus as well as its favorable
response to immunomodulatory therapy. In
humans, antibodies against type II collagen may
be demonstrated in some cases. In dogs and
cats it has not been reported to be relapsing and
virtually all cases have been limited or apparently
limited to involvement of auricular cartilage.
(Boord and Griffin 1998) It would appear that
aural chondritis is a more appropriate term for
this disease syndrome. In one dog and three cats
I have no definitive cause was determined though
chronic otitis preceded the development of the
auricular chondritis. FIV and FeLV are reported
in cats though my cases have routinely been
negative for these viruses.
Affected cats and dogs presented with a history of
swollen, erythematous, painful ears. Examination
will show deformed, sometimes curled, swollen
usually firm pinnae that are erythematous to
violaceous. Cats may be otherwise healthy
or may show signs of pyrexia, lethargy, and
anorexia. One dog had a history of non erosive
polyarthritis and laxity of digital and carpal
joints as well as otitis prior to the development
of auricular chondritis. One case was seen in a
Back to contents
T
puppy with multiple papules on both pinna that
were non painful and of normal skin color.
Biopsies usually reveal lymphoplasmacytic
inflammation, loss of cartilage basophilia, and
cartilage necrosis. One cat has an eosinophilic
mixed infiltrate, and the pathologist suggested
and insect bite as an underlying cause.
Cats that are in no pain and show no systemic signs
may do fine without therapy. In one cat, systemic
glucocorticoids were ineffective, but dapsone
(1 mg/kg q24h) induced a remission within
2 weeks. (Scott, Miller et al. 2001) Permanent
deformity of the pinnae is to be expected,
whether or not the cat is treated. In one dog
surgical excision was effective in eliminating the
discomfort and gross lesions.
Canine ear margin dermatosis is a scaly, greasy
condition of the margin of the pinnae. It is
described mainly in dachshunds but other breeds
may be affected, most of which have pendulous
ears. I have seen this in erect eared dogs and
dogs with ear crops as well. Follicular casts and
partial alopecia are common. In severe cases 2006 World Congress WSAVA/FECAVA/CSAVA
secondary infections may occur. Severe cases
may develop necrosis or fissures. The concern
for a vascular component is then warranted.
Usually these cases are asymptomatic unless
infected, fissured or necrotic. Moisturizing agents
and topical sulfur salicylic acid shampoos and
topical hydrocortisone creams are most helpful
in managing uncomplicated cases. Severe cases
with a vascular necrosis respond best to partial
pinnectomy though pentoxifylline may be
beneficial and should be tried prior to surgery.
Cutaneous vascular perfusion disorders are
uncommon disorder in dogs and cats but when
occur often affect the auricle and in many
cases may be limited to the apex of the pinnae.
One disease, proliferative thrombovascular
763
 T
necrosis, has only been seen involving the pinna.
(Scott, Miller et al. 2001) These diseases are
characterized by abnormalities in blood flow do
to vascular damage which may occur secondary
to vessel inflammation (vasculitis), trauma,
thrombosis or degenerative changes.
Cutaneous vasculitis often is idiopathic or
secondary to vaccines, drug reactions and
infections. (Scott, Miller et al. 2001) However
causes are quite variable and it may be associated
food allergy, insect bites, malignancies, connective
tissue disorders such as lupus erythematosus
and other immune mediated diseases. Breed
predispositions have been described with some
forms of idiopathic or vaccine related vasculitis.
Pinnal lesions of vascular perfusion diseases are
often distinct and characteristic but not associated
with specific causes. Pinna lesions are often
more prevalent on the apex and concave surface.
Early lesions are scale, alopecia, acrocyanosis or
hyperpigmentation. Eventually erosions, crust.
There is often a surrounding area of discoloration
and vessels may appear more prominent as they
approach the lesions. Most often lesions are
elongated wedge shaped with the wide base and
more severe changes seen towards the ear margin
at towards the apex. After necrosis occurs there is
permanent deformed pinna. Permanent scarring
may occur in the central and more severely
affected areas adjacent to areas of necrosis.
Histopathology varies depending on the cause
and stage the lesions are sampled. In the cases
where active vasculitis is occurring then
varying degrees of neutrophilic, eosinophilic
or lymphocytic vasculitis, may be present, but
usually without fibrinoid necrosis. In some
biopsies the diagnosis of vasculitis vasculopathy
is suspected on the basis of a cellτpoor hydropic
interface dermatitis and the loss of definition
and staining intensity of hair follicles (“fading
follicles”). Proliferative thrombovascular
2006 World Congress WSAVA/FECAVA/CSAVA
necrosis of the pinnae is characterized by
arteriolar proliferation, sclerosis, hyaline
degeneration, and eventually thrombosis.7 No
inflammatory vasculitis is present.
When vaccine induced or related to ischemic
dermatopathy then the offending drug or vaccine
often was given 2-4 months prior to the initial
lesions being noted by the owners. Once the
diagnosis of cutaneous vasculitis has been
established, it is imperative that underlying
etiologic factors be sought and eliminated.
If present in your areas then the presence of
antibodies for the tick borne and blood borne
infectious diseases should be determined.
Treatment of vasculitis consists of correction
of the underling cause and immunomodulatory
drug treatment. In suspect cases a trial with
764
Back to contents
doxycycline is often prescribed while awaiting
biopsy results and prior to initiating immune
suppressive therapies as it is effective for many of
the blood borne infectious causes of vasculitis. In
less severe cases and for all cases of proliferative
thrombovascular necrosis initial therapy with
pentoxifylline is indicated due to its relative lack
of side effects and moderate efficacy. In more
severe cases, systemic prednisone or prednisolone
(2 to 4 mg/kg orally q24h) is initially utilized
with pentoxifylline. For other cases that are
refractory to glucocorticoids then cyclosporine
and azathioprine may be added to the treatment
regimen. Other rarely used treatment options
include sulfones, dapsone (1 mg/kg orally q8h, not
cats) or sulfasalazine (20 to 40 mg/kg orally q8h.
For proliferative thrombovascular necrosis that
is unresponsive to pentoxifylline the treatment of
choice is partial surgical removal of the pinna.
Relapses have occurred only when attempts were
made to save as much tissue as possible. Focal
cutaneous vasculitis and alopecia subsequent to
injections may also respond to pentoxifylline or
may be treated by complete surgical excision.
Aural hematomas develop as a result of
hemorrhage intrachondrally or parachondrally
and are usually brought on by self-trauma.
Though is was suggested this may be immune
mediated another study refuted this observation
and correlated most cases with dermatologic
diseases. (Joyce and Day 1997) Some hematomas
can be small and present as a soft fluctuate
nodular swelling most commonly on the concave
surface of the pinna. They may also spread
to involve the majority of the scaphae of the
auricular cartilage.
Diagnosis is based on the classic clinical lesions.
It is important to examine the ear canal and look
for causes of aural or head pruritus. It there is
a positive pinnal pedal reflex trial selamectin is
indicated to rule out sarcoptic mange. Treatment
is required to minimize discomfort and
secondary scarring and deformity as untreated
lesions heals with scars, nodules and folds of the
auricular cartilage. Most treatments incorporate
drainage of the hematoma, possible flushing of
the hematoma space and suturing of the pinna to
close the space and prevent repetitive filling with
more blood. A non suture less technique just used
a Penrose drain with systemic prednisone while
another technique was described using carbon
dioxide laser. (Joyce 1994; Dye, Teague et al.
2002)
Boord, M. J. and C. E. Griffin (1998). “Aural
chondritis or polychondritis dessicans in a dog.”
Proc Acad Vet Dermatol Am Coll Vet Dermatol
14: 65.

Dye, T. L., H. D. Teague, et al. (2002). “Evaluation
of a technique using the carbon dioxide laser for
the treatment of aural hematomas.” J Am Anim
Hosp Assoc 38(4): 385-90.
Joyce, J. (1994). “Treatment of canine aural
haematoma using an indwelling drain and
corticosteroids.” J Small Anim Pract 35(7): 341-344.
Back to contents
T
Joyce, J. and M. Day (1997). “Immunopathogenesis
of canine aural haematoma.” J Small Anim Pract
38(4): 152-158.
Scott, D. W., W. H. Miller, Jr,, et al. (2001).
Muller and Kirk’s Small Animal Dermatology.
Philadelphia, W.B. Saunders.
2006 World Congress WSAVA/FECAVA/CSAVA
765
 T
T – Nose-Ear-Throat
DISEASES OF THE EXTERNAL EAR CANAL, MIDDLE AND INNER
EAR; MANAGEMENT AND SURGERY
Gert Ter Haar, DVM, DECVS
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
PO Box 80 154
3508 TD Utrecht
The Netherlands
G.terHaar@vet.uu.nl
Clinical signs of ear diseases
Clinical signs associated with outer ear diseases
are head shaking, scratching, otic pain (otalgia)
and otic discharge (otorrhea). In some cases,
aural hematomas (othaematoma) can be seen.
Clinical signs associated with middle ear disease
are often subclinical or very subtle, especially
in cats or reflects concurrent otitis externa,
especially in dogs. Otalgia (otic pain), lethargy,
inappetence and pain on opening of the mouth
are more suggestive of middle ear involvement.
Neurologic signs like facial nerve paresis or
paralysis or Horner’s syndrome may be present.
Peripheral vestibular ataxia (head tilt, horizontal
or rotary nystagmus, circling or falling toward
the side of the lesion) is usually the most obvious
sign of inner ear disease. Hearing loss usually
goes unnoticed until complete deafness is
recognized.
Clinical examination of the ears
When confronted with animals with clinical signs
of ear disease, clinical examination should include
a general physical, dermatologic, neurologic
(cranial nerves) and otoscopic examination. For
2006 World Congress WSAVA/FECAVA/CSAVA
complete visualization of the tympanic membrane
and prior to therapy, ear flushing is necessary. In
some cases material should be obtained from
the horizontal part of the ear canal for cytologic
examination, culture and susceptibility testing.
After flushing, masses can easily be identified
and samples can be taken for histopathology.
Increased opacity and hyperemia of the tympanic
membrane may be present with otitis media. A
paracentesis can be performed in dogs with an
intact tympanic membrane to obtain samples for
culture and susceptibility testing and cytologic
examination. Radiographs of the bullae may be
useful although not very sensitive; ventrodorsal,
lateral oblique and open-mouth views are most
helpful. Advanced imaging with CT and MRI
is necessary in most cases for proper evaluation
766
Back to contents
of the middle ear (and inner ear to some extent)
however. When objective information on hearing
capacity is needed, brainstem-evoked response
audiometry can be performed.
Otitis externa
Otitis externa is common in dogs and cats and
has numerous causes, usually classified as
primary, predisposing or perpetuating factors.
Primary factors directly cause otitis externa and
include parasites, foreign bodies, inflammatory
polyps, tumors, hypersensitivities, endocrine
abnormalities and keratinization disorders.
Predisposing causes of otitis externa make the
ear canal more susceptible to inflammation and
secondary infection, while perpetuating factors
exacerbate and maintain the disease even after
the primary factors are eliminated and include
secondary bacterial and/or yeast infection and
otitis media.
In chronic cases, elimination of underlying factors
however, usually doesn’t end the inflammatory
process. Management should then be aimed at
thoroughly cleaning and drying the ear canal
and administering appropriate topical therapy
for a longer period of time, sometimes even a
life-long treatment is necessary. Ointments with
broad-spectrum antibiotics and corticosteroids
should be used with careful attention to complete
filling of the entire ear canal and tapering off the
frequency of treatment based on clinical effect
and control otoscopy. Total ear canal ablation is
reserved for unresponsive or proliferative chronic
otitis externa.
Ear mite
Otodectes cynotis is the most common parasite
affecting the ear canal of especially young dogs,
cats and ferrets. This highly infectious disease
is transmitted by direct contact. Pruritis can
be significant, accumulation of dark brown to
black cerumen is usually noted. The diagnosis is

made by observation of the mites on otoscopy
or on microscopic identification (mineral oil
cytology). Various commercially prepared topical
medications are available for the treatment of
otocariasis of which selamectin has recently
been proven save and effective. Considering
the lifecycle of the parasite, treatment should be
repeated after 3 weeks.
Foreign body
Acute inflammation, scratching at the ear and
head shaking are usually noted in acute cases of
foreign body associated otitis externa. Common
causes are grass awns, foxtails, dirt, sand or toys.
In chronic cases, suppurative inflammation is seen
and even otitis media as a result of migration can
occur. The diagnosis can be made on otoscopy
after flushing the ear canal. With special forceps
the foreign body usually can be removed with
aid of otoscopy. Severe edema of the epithelial
lining of the ear canal can prevent visualization
of foreign bodies. Treatment with ointments with
antibiotics and corticosteroids can be necessary
to reduce the edema before a foreign body can
be detected and removed or after removal to treat
secondary infection and inflammation.
Inflammatory polyp
Polyps in cats, originating from the mucosal
lining of the middle ear, auditory tube and
nasopharynx, have been associated with rhinitis
and otitis resulting from various bacterial
and viral agents. A congenital origin has been
suggested as well. Polyps in the external or
middle ear mimic signs of otitis externa, otitis
media or otitis interna. Otoscopy after flushing
may reveal a visible pink or gray smooth, spheric
mass occluding the canal. Cytologic or histologic
examination of biopsies will reveal the nature of
the tissue when diagnosis is not straightforward.
Recurrence is uncommon with simple traction-
avulsion after an incision in the vertical ear canal.
Ventral bulla osteotomy is reserved for patients
with recurrence of polyps after this procedure.
Removal of middle ear polyp by traction-avulsion
After aseptic preparation of the surgical site, an
incision is made in the skin in a dorsoventral
direction over the palpable vertical part of the
ear canal. The subcutaneous tissue and parotid
gland are dissected with small scissors to free the
cartilage of the vertical ear canal to the level of
the junction between the auricular and annular
cartilages. A vertical stab incision is made in the
auricular cartilage and stay sutures are placed
on both sides of the incision in the ear canal to
increase visualisation and avoiding damage to
the cartilage. A small closed haemostatic forceps
Back to contents
T
is then introduced into the ear canal and advanced
deeper over the polyp until it can be grasped as
close as possible to the osseous meatus. When a
firm grip has been achieved, the forceps is gently
rotated and traction is applied until the polyp is
removed. The middle ear cavity is flushed with
warm saline and with a small curette the osseous
meatus and most lateral aspect of the tympanic
cavity is “palpated” to check for additional
inflammatory tissue which is removed with this
curette when encountered. The stay sutures are
removed and the cartilage of the ear canal is
closed with 4-0 monofilament suture material
in an interrupted pattern. The subcutis is closed
in a continuous pattern with 4-0 absorbable
monofilament material and the skin is closed
in a subdermal suture pattern using the same
material.
Tumor
Ear tumors occur in older cats and dogs. The most
frequently observed clinical signs are those of a
mass, otic discharge, odor, pruritis, and local pain.
Neurologic signs are uncommon. Approximately
25% of malignant forms will have evidence of
bulla involvement, and skull radiographs and/or
computed tomography are recommended as part
of the diagnostic work-up. Benign tumors like
papillomas and basal cell tumors can sometimes
be removed otoscopically. Malignant tumors
are usually epithelial in origin and can usually
be treated successfully by complete surgical
resection; total ear canal ablation.
Total ear canal ablation
Indications for TECA are chronic unresponsive
or proliferative otitis externa or neoplasia of the
ear canal. A V-shaped incision is made in the
skin from the intertragic incisure to the ventral
limit of the vertical ear canal and from the
tragohelicine incisure to the same ventral point.
The skin flap is retracted dorsally and the lateral
2006 World Congress WSAVA/FECAVA/CSAVA
aspect of the vertical ear canal is exposed. The
cartilage and the skin of the medial wall of the
ear canal are separated from the cartilage and the
skin on the inner side of the base of the pinna by
use of strong scissors. The vertical ear canal is
now dissected to the level of the horizontal ear
canal. Appropriate care should be taken to avoid
the facial nerve in this area. The dissection is
continued with freeing the horizontal part of the
ear canal from the surrounding tissues to the level
of the external acoustic meatus. The cartilaginous
part is separated from the osseous part with
scissors and removal of all of the skin lining the
osseous external ear canal is accomplished with
a small curette. The pinna is then remodeled
and sutured with absorbable suture material. A
767
 T
penrose drain is placed and subcutaneous tissue
and skin under the pinna are closed in a routine
matter. Complications are facial nerve paralysis,
wound infection and dehiscence and chronic
fistulation.
Otitis media and interna
Otitis media generally develops as an extension
of otitis externa through a perforated tympanum
in dogs. Cats may develop otitis media as a
sequela to upper respiratory tract disease with
infection ascending through the Eustachian tube
into the middle ear cavity. Organisms cultured
most frequently from affected middle ears
include Pseudomonas species, Stpahylococcus
intermedius, beta-hemolytic streptococcus,
Malassezia, Corynebacterium species,
Enterococcus species, Proteus species, E. Coli
and anaerobes. Bacteria can directly infect the
middle and inner ear, or the bacteria can produce
toxins that inflame the labyrinth.
Other causes of otitis media include fungal
infections (Aspergillus, Candida), neoplasia,
inflammatory polyps, trauma and primary
tumors.
The therapy of otitis media and/or interna consists
of systemically delivered broad-spectrum
antibiotics. Amoxicillin potentiated with
clavulonic acid or enrofloxacine are first choice
antibiotics. No ototoxic topical medications
2006 World Congress WSAVA/FECAVA/CSAVA
768
Back to contents
should be used when the tympanic membrane is
not intact to avoid ototoxicity.
Chronic unresponsive or recurrent otitis media
warrants surgical intervention. Total ear canal
ablation with lateral bulla osteotomy should
be considered in cases with severe secondary
changes of the external ear canal and concurrent
otitis media or para-aural abscessation. If the
external ear canal is not affected, a ventral bulla
osteotomy may be performed to remove gross
exsudate and establish drainage from the middle
ear.
Ventral bulla osteotomy
An incision is made parallel with the midline,
centered 2-3 cm toward the affected side from
halfway the mandible to the level of the atlas.
The platysma muscle is incised and linguofacial
vein is retracted. The incision is deepened by
blunt dissection between digastricus muscle and
hypoglossal and styloglossal muscles until the
bulla can be palpated. A Steinmann pin can be
used to make a hole on the ventral aspect, the
opening can be enlarged with a small rongeur.
In cats both compartments should be opened.
Material is collected for culture, sensitivity
testing, cytology and histopathology. The cavity
is flushed and drained with a penrose drain.
Closure is routine.

T – Nose-Ear-Throat
DISEASES OF THE THROAT (PHARYNX AND LARYNX)
Anjop J. Venker-van Haagen,
DVM, PhD, Dipl. ECVS.
University Utrecht,
Companion Animal Sciences,
Stationsstraat 142,
Utrecht, 3511 EJ,
The Netherlands
aj.venkervanhaagen@wanadoo.nl
THE PHARYNX
History
The medical history in diseases of the pharynx
usually reveals specific problems caused either
by dysfunction of the airway through the
oropharynx or nasopharynx or by difficulty
in swallowing (dysphagia). In some cases
the appearance of the pharyngeal mucosa may
suggest a systemic disorder, but in all cases
additional questions are asked about any changes
in the animal’s general condition, appetite,
eating, drinking, physical activity, and habits.
The answers to these questions together with a
general physical examination will provide an
impression of the patient’s condition.
Clinical signs
Dyspnea in pharyngeal disease. Signs of dyspnea
in pharyngeal disease are caused by obstruction of
the nasopharynx or the oropharynx. Obstruction
of the laryngopharynx primarily hinders the
passage of air through the nasopharynx and
hence it also results in signs of nasopharyngeal
obstruction. Severe obstruction of the oropharynx
or laryngopharynx hinders the passage of food as
well as air and thus causes dysphagia as well as
dyspnea. Large masses in the nasopharynx can
also obstruct the oropharynx and thus also result
in dysphagia.
When dyspnea is caused by pharyngeal obstruction
the signs are those of more forceful inspiration,
which usually produces a snoring stridor. In cats
the sounds may be soft and sometimes difficult
to distinguish from the wheezing stridor caused
by nasal obstruction. Dysphagia in pharyngeal
disease. The signs of dysphagia involving the
pharyngeal phase are gagging, choking, and
repeated swallowing of one bolus. The food may
be regurgitated and will be seen to be covered
with thick mucus, and the dog may eat it again.
When there is severe dysphagia and part of
Back to contents
T
the food or liquid passes into the larynx and
trachea, there is immediate coughing and, after
successful ejection of the misdirected particles of
food into the pharynx and after signs of choking,
swallowing is repeated. If the food or liquid
is ejected into the nasopharynx, snoring and
sneezing may follow. When given solid food, a
dog with severe dysphagia may stop eating and
walk away from the pan. When this dog drinks it
drools much of the water and mucoid saliva into
and around the water pan. Knowledge of these
signs can be helpful in composing meaningful
questions for the history and in recognizing
dysphagia.
Special diagnostic techniques
Pharyngoscopy. Direct inspection of the
pharynx with a laryngoscope is the most
important diagnostic procedure in disorders
of the oropharynx and laryngopharynx. Under
anesthesia it is possible to inspect the soft palate,
the base of the tongue, the palatine tonsils, and
the hypopharynx including the laryngopharynx,
with a minimum of instruments. The animal
is intubated and placed in lateral recumbency
with the mouth open and fixed in that position. 2006 World Congress WSAVA/FECAVA/CSAVA
The soft palate can be retracted with a forceps
to facilitate inspection of the nasopharynx, in
which any large masses can be recognized and
biopsies can be taken. Complete inspection,
including the rostral part of the nasopharynx,
the caudal part of the choanae, and the openings
of the auditory tubes, can be performed with a
flexible endoscope capable of 180˚ retroflexion
and having a working channel for the passage of
biopsy forceps.
Radiographic examination. Plain radiographs
of the pharyngeal area are especially useful for
recognition of structures obstructing the airway
and the passage of food; for locating radiopaque
foreign bodies such as stones, needles, and bones;
and for inspection of the hyoid bone for fracture
769
 T
and for arthritis of its joints, either of which
can cause dysphagia. Laterolateral radiographs
usually provide sufficient information.
Computed tomography and MRI are indispensable
in determining the location and extent of
neoplasms in the pharyngeal area.
Contrast videofluorography is almost
indispensable for imaging the dynamics of the
swallowing process in dogs. Recordings are
made while the animal eats food (ground meat)
mixed with barium. The procedure needs the
cooperation of the patient and is extremely time
consuming, even in a routine set-up.
Electromyography (EMG) of the pharyngeal
muscles is useful in dogs with signs of
dysphagia when no abnormalities are found by
pharyngoscopy. Further information may be
found in the abstract “Electromyography for
diagnosing pharyngeal and laryngeal diseases”.
Nasopharyngeal polyps. The most common
polyp in the nasopharynx of the cat originates in
the middle ear and descends to the nasopharynx
via the auditory tube. These polyps develop on a
stalk and reach the nasopharynx, where they may
grow substantially—a diameter of 3 cm is not
uncommon—and thus form a nasopharyngeal
polyp.
The clinical signs of a nasopharyngeal polyp are
due to obstruction of the nasopharynx, inspiratory
dyspnea being the principal effect. Food intake is
interrupted because of blockage of the passage
of air through the nose, but there is no nasal
discharge initially.
Treatment consists of removal of the polyp under
anesthesia. The soft palate is retracted rostrally
or incised so that a curved mosquito forceps
can be inserted between the dorsal wall of the
nasopharynx and the polyp in order to clamp the
polyp stalk. After rotating the forceps and polyp,
to be certain that no nasopharyngeal mucosa
is included, the polyp is removed by a sharp
2006 World Congress WSAVA/FECAVA/CSAVA
tug. Bleeding is controlled by pressing a gauze
sponge into the nasopharynx at the location of
the openings of the auditory tubes.
A foreign body in the nasopharynx is accompanied
by secondary bacterial infection. The usual route
of entry is via the intrapharyngeal isthmus. When
a cat chews on grass, a ball of grass and mucus
may become lodged in the hypopharynx and a
blade of grass may enter the nasopharynx during
attempts to swallow the grass ball. The blade may
remain behind when the grass ball finally passes
the upper esophageal sphincter. Sometimes the
blade of grass enters one of the nasal cavities and
causes unilateral rhinitis, and sometimes snoring
and repeated swallowing indicate that the blade
of grass is also located in the nasopharynx and
sometimes the laryngopharynx.
770
Back to contents
Hyperplasia of the soft palate is associated with
brachycephaly and a relatively narrow pharynx.
It is thought that the genetic defect responsible
for shortening the nose does not affect the soft
tissue, the result being too much tongue and
soft palate in a narrow pharynx. The clinical
signs of an overlong soft palate are snoring,
regurgitation, and dyspnea, usually increasing
in severity during the second and third years of
the dog’s life. The pharyngeal disproportions are
not the same in all brachycephalic dogs. In some
the pharyngeal mucosa and soft palate are very
thick and the musculature is insufficient, which
results in snoring during closed-mouth breathing.
Little can be done for these dogs when dyspnea
eventually develops. This is in contrast to those
with an overlong soft palate, which can be
reduced in length so that it no longer covers the
laryngeal inlet. The surgical technique to shorten
an overlong soft palate is simple but the patient’s
recovery following surgery may be complicated
by obstruction of the airway due to swelling of
the mucosa of the remainder of the soft palate.
THE LARYNX
History
The medical history in laryngeal disease often
includes clear statements of specific problems
caused by laryngeal dysfunction. The most
specific of these are a dry cough and dyspnea
with remarkable respiratory sounds. Additional
questions are then asked about the animal’s
general condition, appetite, drinking, physical
activity, and endurance, and about changes in
its habits. The answers to these questions and
a general physical examination may lead to
an overall impression of the condition of the
patient.
Clinical signs
Coughing in laryngeal disease. When coughing
is the prominent sign, the time and specific
circumstances of onset, the frequency, the sound,
the productivity, and changes in severity since
the cough began will provide information about
the nature of the disease. An acute onset may
indicate a foreign body in the trachea or bronchi.
The onset of coughing shortly after a stay in a
kennel or cattery may indicate infectious disease,
while the frequency of coughing indicates the
severity and persistence of the stimulus. The
cough may be sharp and short and be followed
by gagging, as in laryngitis, or deep and soft, as
in chronic bronchitis.
Dyspnea in laryngeal disease. When dyspnea
is the leading sign in the medical history, it is
usually described as labored breathing in cats

and as diminished endurance in dogs. When the
dyspnea is caused by laryngeal dysfunction, a
laryngeal stridor is to be expected as an additional
sign. Especially in dyspneic dogs with laryngeal
obstruction or hypoplasia of the larynx or
laryngeal paralysis, the forced panting respiration
may cause hyperthermia. Body temperature may
rise above 40 ºC, even within a matter of minutes,
at which point, while the mucosa is still red,
cooling is more important than oxygen. Spraying
or sponging cool water over the entire surface
of the dog will lower the body temperature to
normal in about 20 minutes.
Laryngoscopy
When laryngoscopy is performed for diagnosis
of laryngeal disease, the dog or cat is usually
in a certain state of dyspnea. The laryngoscope
is fitted with a blade suitable for the size of the
animal and lubricated endotracheal tubes of
several sizes are prepared. The anesthetic is then
administered to effect, preferably by intravenous
injection. Propofol is satisfactory and may be
used after premedication with medetomidine.
Medetomidine premedication is given to cats
intramuscularly and to dogs intravenously. When
the laryngeal movements are absent and the
depth of anesthesia may be the cause, the short
half-life of propofol is advantageous because
after a short pause there is sufficient recovery for
the inspection to proceed.
Diagnostic imaging
Radiographs, CT, and MRI. Radiographs of
laryngeal structures are not easy to interpret.
In the lateral projection the overlapping of
structures and the presence of “air pockets” are
unpredictable, particularly in the dyspneic patient.
The extension of neoplastic or cystic masses and
the presence of calcification of the laryngeal
cartilages can be recognized. When surgery
is being considered for removal of a laryngeal
tumor, CT or MRI will be found indispensable
for estimating the involvement of laryngeal and
surrounding structures by the tumor. CT is less
expensive than MRI and almost always answers
the question. MRI is added in only a few cases.
In human patients these techniques do not always
require anesthesia and endotracheal tubes are
avoided. In dogs and cats the use of anesthesia
and endotracheal intubation cannot be avoided
and this will influence the aspect of processes in
the lumen of the larynx.
Electromyography
Laryngeal dysfunction is often an indication
for electromyography (EMG) of the intrinsic
laryngeal muscles. EMG can be performed
Back to contents
T
routinely in the dog but the cat is not a good
candidate because it has a small larynx and is too
prone to develop laryngeal edema after the larynx
is touched. . Further information may be found in
the abstract “Electromyography for diagnosing
pharyngeal and laryngeal diseases”.
Laryngeal paralysis and functional disorders of
the larynx
Paralysis is the loss or impairment of motor
function in a part due to lesion of the neural
or muscular mechanism; also, by analogy,
impairment of sensory function (sensory
paralysis). Fine-tuned vocalization is of minor
social importance in dogs and cats and partly
because dogs can produce a bark without very
highly specialized vibrations of the vocal folds.
Dogs use the loudness of the voice more than
its tone. Some cats use their voice to produce
a variety of tones in communication and thus
loss of the voice is recognized by the owner and
is part of the clinical history. In dogs and cats
respiratory dysfunction is the primary cause
of signs and symptoms of laryngeal paralysis.
In most cases it is insufficient abduction of the
glottis that causes the clinical signs of laryngeal
stridor and sometimes dyspnea.
Tumor in the larynx
Primary laryngeal tumors occur occasionally
in dogs and cats. In a review of 36 reported
primary laryngeal tumors in dogs, 8 were
oncocytomas, 6 were rhabdomyomas, and 4 were
rhabdomyosarcomas.
Ventral midline approach to the larynx. The
procedure is essentially for the dog, in which it is
safe, while all approaches to the larynx of the cat
can be complicated by laryngeal edema. The aim
of approaching through the ventral midline of the
thyroid cartilage is to obtain satisfactory visibility
of the glottis and supraglottic area. In this way
biopsy material can be taken or proliferations
2006 World Congress WSAVA/FECAVA/CSAVA
can be removed. The laryngeal lumen should not
be obstructed by an endotracheal tube passing
through the larynx and hence the procedure
begins with a tracheostomy for insertion of a
tube into the trachea caudal to the larynx.
References
Venker-van Haagen AJ. The Pharynx. In: Ear,
Nose, Throat, and Tracheobronchial Diseases
in Dogs and Cats. Hannover: Schlütersche
Verlagsgesellschaft, 2005: 83-116.
Venker-van Haagen AJ. The Larynx. In: Ear,
Nose, Throat, and Tracheobronchial Diseases
in Dogs and Cats. Hannover: Schlütersche
Verlagsgesellschaft, 2005: 121-161.
771
 T
T – Nose-Ear-Throat
DISEASES OF THE TRACHEA AND BRONCHI
Anjop J. Venker-van Haagen,
DVM, PhD, Dipl. ECVS.
University Utrecht,
Companion Animal Sciences,
Stationsstraat 142,
Utrecht, 3511 EJ,
The Netherlands
aj.venkervanhaagen@wanadoo.nl
History
Diseases of the trachea and bronchi are usually
manifested by specific problems such as
coughing, dyspnea, or stridorous breathing.
Since all three of these signs may originate from
parts of the airway other than the trachea and
bronchi, as well as from the circulatory system,
additional questions are asked about the animal’s
general condition, appetite, drinking, activity,
and endurance, and about changes in its habits.
The answers to these questions together with the
results of a general physical examination will
point the way to the diagnosis.
Clinical signs
Coughing. Coughing is a reflex for protection of
the respiratory mucosa. The reflex is activated
by stimulation of the “cough receptors” or is
evoked voluntarily. Cough receptors are sensory
receptors located in the mucosa of the larynx,
trachea, carina, and bronchi. They respond
to airway pressure, vocal fold motion, tactile
stimuli, and chemical stimuli. The threshold for
each of these stimuli is variable, according to the
variable condition of the mucosa. For example,
in laryngitis coughing is evoked by barking. The
2006 World Congress WSAVA/FECAVA/CSAVA
afferents of the receptors run with the cranial
laryngeal and vagus nerves to the solitary tract
and nucleus. The interneuronal network of the
reticular formation activates the respiratory center
and the motor nucleus of the vagus nerve and the
nucleus ambiguus, inducing the cough reflex.
The cough reflex begins with a deep inspiration
with the glottis wide open. This is followed by
closure of the glottis and strong contraction of the
expiratory muscles, which builds up air pressure
against the closed glottis. Then sudden opening
of the glottis allows the air and any material that
is present to be expelled forcefully. This basic
pattern can have many variations. It may be
repeated to produce a paroxysm of coughing. It
may be fragmented by the repeated opening and
closing of the glottis during a single expiratory
772
Back to contents
effort. The relative contributions of inspiration
and expiration may vary.
Dyspnea. Dyspnea can be caused by obstruction of
the trachea, as occurs in tracheal collapse in small
breeds of dogs or tracheal neoplasia in both dogs
and cats. In bronchitis and bronchopneumonia,
mucopurulent exudate may obstruct the airway
during both inspiration and expiration. In
asthma-like diseases in cats, constriction of the
smaller bronchi and bronchioles may obstruct
communication with the alveoli. These diseases
must be distinguished from diseases of the lung
parenchyma, but in both diseases of the trachea
and bronchi and those of the lung parenchyma,
the dyspnea is predominantly expiratory.
Stridorous breathing. Partial obstruction of the
trachea may result in a particular extra sound
during the respiratory cycle. It occurs during
expiration and differs from coughing in being a
softer, wheezing sound. It must be distinguished
from the various stridors caused by upper airway
disease and from the soft vocalization that
is sometimes heard when there is pain in the
thorax.
Special diagnostic techniques
Special techniques are indispensable for diagnosis
of most diseases of the tracheobronchial tree.
Although kennel cough can be diagnosed by the
association of the history and the clinical signs,
chronic coughing and dyspnea require further
investigation. Radiographs of the cervical trachea
and the thorax can reveal changes in the cartilages
of the tracheobronchial tree or the mucosa when
the lumen of the trachea and bronchi is altered by
the disease process. Radiographs always precede
inspection of the lumen of the tracheobronchial
tree by bronchoscopy. Bronchoscopy provides
visual confirmation of the changes in the
tracheobronchial tree, such as anomalies in the
shape of the tracheal or bronchial cartilaginous
rings or obstruction of the lumen by foreign
bodies or masses. When the mucosal lining

is reddened by hypervascularization or when
mucopurulent material is found covering
the mucosa, bronchial and bronchoalveolar
lavage with subsequent culture and cytological
examination of the material obtained will often
lead to the diagnosis or at least an indication of
the underlying disease.
Diagnostic imaging
Radiography is a very important technique
for the diagnosis of tracheal and bronchial
diseases. Radiographic imaging of the changes
in the pulmonary parenchyma is of additional
importance because bronchial diseases may be
associated with bronchopneumonia. Radiographic
sensitivity can be improved by the use of high-
quality equipment—including screens, grids,
etc.—and correct positioning, effective restraint,
appropriate exposure, and good development
procedures.
The lateral view is the most important in
radiographic examination of the cervical trachea.
The dorsoventral view is wanted occasionally,
especially to evaluate dislocation of this part of
the trachea. The lateral radiographic examination
must be performed with careful positioning
of the head and neck in relation to the thorax.
Excessive flexion of the occipitoatlantal joint or
the neck may cause an undesirable change in the
lumen of the trachea, which could be mistakenly
interpreted as an abnormality. The thoracic part
of the trachea should be examined on radiographs
of the thorax. The tracheal images should be
surveyed for abnormalities in the diameter of the
luminal air column, the continuity of the mucosa,
and the contrast of the tracheal rings. In order
to detect possible external changes affecting
the trachea, the position of the trachea relative
to the cervical and thoracic surroundings should
be examined. The normal diameter of the trachea
is difficult to define, for the diameter decreases
slightly from cranial to caudal, but as a rule of
thumb the diameter of the trachea at the level the
third rib should be approximately three times the
width of the rib at the level of the trachea.
On radiographs of the normal lungs the bronchial
tree is mainly visible in the central area. When
the lung parenchyma is adequately inflated only
a slight density indicates the lung contours. The
bronchi are more apparent in older dogs due
to calcification of the bronchial walls. Visible
thickening of bronchi, which suggests pathologic
changes, gives them the appearance of ring-like
structures like doughnuts and parallel lines like
tram lines. The presence of air bronchograms
indicates that there is consolidation of the lung
tissue adjacent to the bronchi.
Back to contents
T
Bronchoscopy
The usefulness of bronchoscopy in the diagnosis
of diseases of the tracheobronchial tree in
the dog and the cat is well recognized. The
equipment has been described and bronchoscopic
findings in the dog and cat have been illustrated.
Although the cost of good-quality equipment
is substantial, it is a worthwhile investment for
the more specialized small animal practitioner.
Videoendoscopy is ideal for teaching, since a
group of students can follow the bronchoscopic
examination in real time. Bronchoscopic
technique differs according to whether a flexible
or rigid bronchoscope is used. Rigid systems are
less expensive and much more durable. Several
sizes of high-quality rigid bronchoscopes can be
purchased for the price of just one size of a good-
quality flexible bronchoscope. The advantage of
the flexible bronchoscope in human medicine
is that it makes bronchoscopy possible without
anesthesia, but this is in any case never possible
in dogs and cats. On the other hand, the thorax
is narrower laterally in dogs and cats than in
humans, facilitating access to all bronchial
divisions using rigid bronchoscopes.
Videofluoroscopic examination of the trachea
is practically indispensable for the functional
evaluation of the collapsing trachea or a partially
stenosed trachea. The animal should be conscious
and in lateral recumbency while the entire
trachea is visualized on the monitor. Playback
of the observations in slow motion can reveal
functional features missed during the initial
examination. When recording equipment is not
available, comparing an end inspiratory and end
expiratory radiograph will give some indication
of the functional consequences of the anomaly.
Infectious tracheal bronchial disease
Viral tracheobronchitis in dogs. The most
important viruses causing tracheobronchitis in
dogs are canine adenovirus type 2 and canine
2006 World Congress WSAVA/FECAVA/CSAVA
parainfluenza virus. These viruses may damage
the respiratory epithelium to such an extent that
bacteria and mycoplasmas are able to cause
secondary disease. Other viral infections are
caused by canine adenovirus types 1, 2, and 3,
and canine herpesvirus. Canine adenovirus type
2 and canine parainfluenza virus are transmitted
by aerosol droplets. Canine adenovirus type 2 is
moderately resistant and can survive for months
in the environment, while canine parainfluenza
virus is relatively labile, but quaternary
ammonium disinfectants are effective against
both.
The history and clinical signs of viral tracheitis
without bronchitis differ from those of
tracheobronchitis. Viral tracheitis is characterized
773
 T
by a history of contact with coughing dogs or a
stay in a kennel or visit to another place where
dogs are brought together and where viruses
may survive. The harsh, dry cough develops 3
to 5 days after initial exposure. In most cases
the infection is self-limiting in about 3 weeks.
Palpation of the larynx and trachea elicits a cough
or paroxysmal coughing. In mild infections there
is no fever and the dog is otherwise healthy. The
coughing may continue during the night and may
also be stimulated by barking and by drinking.
It may even cause the dog to avoid barking and
drinking.
In viral tracheobronchitis a productive cough is
to be expected, for the production of mucus is
more abundant in the bronchial tree than in the
trachea. The history is usually suggestive of viral
tracheitis at the onset of the clinical signs, but it
is the change from a dry cough to a productive
cough that is the alarming sign. The dog can still
appear to be otherwise healthy, but the presence of
a productive cough should direct attention to the
possible development of bronchopneumonia, for
Bordetella bronchiseptica infection is commonly
associated with tracheobronchitis.
This condition is also self-limiting, but its natural
course may require 3 months. The diagnosis
can rest on the history and clinical signs alone,
unless they include evidence of complications,
such as malaise and fever. Then further clinical
examination, laboratory tests, and radiographs
of the thorax are needed to estimate the
seriousness of the disease. If no complications
develop but the disease is not resolved after 3
months of care as described below, radiographic
examination and bronchoscopy with bronchial
lavage should be performed. An underlying
disease such as tracheal hypoplasia or allergic
tracheobronchitis may be revealed as the reason
for the delay in spontaneous resolution of the
tracheobronchitis.
2006 World Congress WSAVA/FECAVA/CSAVA
Treatment of viral tracheitis in its usual mild form
of laryngotracheitis without fever is symptomatic.
House or kennel rest with only short walks and
avoidance of excitement is important so long as
774
Back to contents
the dog is coughing. Daily monitoring of body
temperature is helpful in following the progress
of the disease. The coughing will diminish if the
dog is kept calm. Leading the dog on a leash
will provoke coughing and should be avoided.
When drinking provokes coughing, dogs tend to
avoid the water pan. However, a drink of water
activates the glands that moisten the laryngeal
mucosa, which diminishes the irritation, and
thus water should be given orally (20 cc for a
dog of 15 kg) several times daily according the
frequency of the cough. Excessive coughing may
be treated by sedatives, especially during the
night. Phenobarbital is satisfactory in a dose of
2 mg/kg once or twice daily, depending on the
effect. Most dogs recover from kennel cough
without complications, but when it becomes a
serious problem in a kennel, intranasal vaccines
are recommended for puppies as young as 2 to
4 weeks of age. Intranasal vaccines may contain
attenuated canine parainfluenza virus together
with attenuated Bordetella bronchiseptica.
Attenuated canine adenovirus 2 vaccines are also
available).
Treatment of tracheobronchitis without fever can
be similar to that of uncomplicated viral tracheitis.
Antibiotic treatment with broad-spectrum
antibiotics is indicated when fever, malaise,
or systemic disease complicate the infection.
Further therapy should be guided by the results
of special diagnostic procedures. Antitussives
should not be used if the cough is predominately
productive, since coughing removes obstructive
mucus from the bronchial tree. Water should be
given orally (20 cc for a dog of 15 kg) several
times daily, to prevent desiccation of bronchial
mucus or mucopurulent material.
Reference
Venker-van Haagen AJ. The Trachea and Bronchi.
In: Ear Nose, Throat, and Tracheobronchial
Diseases in Dogs and Cats. Hannover:
Schlütersche Verlagsgesellschaft, 2005: 167-
205.

T – Nose-Ear-Throat
DISEASES OF THE NOSE; NASAL PLANE, NASAL CAVITY AND
FRONTAL SINUS
Gert Ter Haar, DVM, DECVS
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
PO Box 80 154
3508 TD Utrecht
The Netherlands
G.terHaar@vet.uu.nl
Clinical signs of diseases of the nasal plane and
nasal cavities
The same is true for all respiratory patients in that
the history provides very important information.
For instance abnormalities of the nasal plane;
depigmentation, inflammation, crustformation,
dehydration and hyperkeratosis are usually noted
by the owner. Especially unilateral discharge,
purulent material coming from one side of the
nose, is the most clear indicator of intranasal
disease. Sneezing and reverse sneezing are
other indicators of nasal and nasopharyngeal
disease. Nature and type of the discharge (serous,
mucopurulent, haemorrhagic) are important in
determining the diagnostic approach.
Clinical examination of the nose
After the history has been taken, a thorough
clinical examination of the respiratory tract
has to follow. The following items give the
most diagnostic information however on nasal
diseases and should always be checked. Nasal
plane depigmentation can be associated with
inflammation of the nasal plane or can be the
result of a severe or very chronic rhinitis and is
often seen for instance in patients with fungal
disease. Because of the destruction of conchae
with fungal disease, the air passage usually
is normal. Air passage is usually abnormal,
diminished, in patients with tumors or large
foreign bodies. Pain on palpation of the nose is
highly indicative of fungal disease as well and is
almost never encountered in patients with nasal
tumours. Checking the oral mucosa and teeth
by simply lifting the upper lip, can show dental
problems as a likely cause of nasal discharge.
Especially in bilateral nasal discharge, a check up
for systemic abnormalities should be performed.
Additional examination of the nose and nasal
cavities primarily consists of diagnostic imaging
(radiography, CT-scan, MRI) and endoscopy.
Culture, cytology and histology are only used in
conjunction with nasal endoscopy.
Back to contents
T
Finally, when a diagnosis cannot be made with
the diagnostic procedures discussed above, or in
case of foreign bodies that cannot be removed
via endoscopy, a surgical exploration of the nasal
sinuses or nasopharynx can be necessary.
Diagnostic imaging of the nose
Radiography is the number one additional
diagnostic procedure to perform for patients
with nasal disease. The standard lateral view is
especially helpful for detecting abnormalities
of the frontal sinuses, the nasopharynx and in
combination with oblique views in detecting
dental problems. The standard dorsoventral
view does not provide any information on the
rostral aspect of the nose, since upper and lower
jaw overproject each other here. The intra-oral
dorsoventral view is the most informative and
helpful view for assessment of the nasal cavity.
CT-scan imaging is a more expensive technique,
and requires general anesthesia as well, but
produces images that represent thin, cross-
sectional slices of the skull without problems of
superimposition inherent to survey radiography.
Endoscopy of the nasal cavities 2006 World Congress WSAVA/FECAVA/CSAVA
The simplest method of rhinoscopy is the one
using an otoscope. Depending on the size of
the animal and the cones used, a fair part of
the rostral nasal cavity can be visualized. For
a complete rhinoscopy, a variety of rigid and
flexible instruments can be used, but a rigid scope
is preferable and provides adequate visualisation
of the nasal sinuses. Wolf and Storz endoscopes
are the most used types, a 2.7 mm rigid scope can
be used for cats, a 3.5 mm scope for big cats and
small dogs and the 4.5 mm scope can be used in
very large dogs. Different types of grasping and
biopsy forceps can be brought into the nose, next
to the scope itself (rigid forceps), or through the
working canal of the scope (flexible forceps).
775
 T
Diseases of the nasal plane
Congenital malformation of the nasal plane in the
form of stenotic nares is part of the brachycephalic
obstructive syndrome (BOS) and is a common
finding in brachycephalic dogs, but also occurs
in Persian cats. Other congenital malformations
are clefts of the primary or secondary palate.
Most abnormalities can be corrected surgically.
Primary inflammation of the nasal plane is
associated with loss of the parasympathetic
nerve supply and can occur for instance with
chronic otitis media. Secondary inflammation
can be due to any chronic rhinitis or epistaxis
or is associated with general skin disorders like
thallium intoxication, leishmaniasis, pemfigus,
DLE, SLE, mycosis, contact dermatitis and
vasculitis.
Depigmentation of the nasal plane can be diffuse,
idiopathic and acquired in the Labrador retrievers
and Siberian Husky or focal (vitiligo) as seen in
Rottweiler dogs and Collie dogs. Depigmentation
can also be the result of auto-immune disease
processes like DLE and SLE or develop in the
course of for instance fungal disease of the nasal
cavities, but is then accompanied by inflammation
of the nasal plane and/or chronic rhinitis.
In dogs squamous cell carcinoma is the most
common tumour type of the nasal plane. Other
tumours in this site are lymphoma, fibrosarcoma,
hemangioma, melanoma, mast cell tumour and
fibroma. SCC’s are usually seen in adult or
aged animals and are locally invasive but late
to metastasise. They are however erosive and
deeply infiltrative. Diseases of the nasal plane
in cats are uncommon with the exception of
tumours. The most common tumor of the nasal
plane in cats is squamous cell carcinoma (SCC).
This tumor manifests itself as a progressive
ulcerative and erosive inflammation of the nasal
plane. Excessive sunlight exposure and lack of
skin pigmentation are two major risk factors
2006 World Congress WSAVA/FECAVA/CSAVA
associated with development of SCC. Various
methods have been described to successfully
treat cats with squamous cell carcinoma of
the nasal planum including radiation therapy,
hyperthermia, intratumoural administration of
carboplatin, cryosurgery, conservative surgery
and photodynamic therapy. The most cost-
effective, reliable treatment for selected patients
with invasive SCC is nasal plane resection
however. This is also the recommended treatment
for other tumors of the nasal plane in dogs and
cats.
Diseases of the nasal cavities
Bilateral rhinitis is very common in both dogs
and cats and is usually the result of a primary
viral infection with secondary bacterial
776
Back to contents
infection. Although definite criteria are lacking,
loud and frequent sneezing with large amounts
of bilateral watery discharge fit with allergic
rhinitis. An exact etiology is unknown, but these
signs are commonly seen in dachshunds in the
Netherlands, but other breeds, for instance terrier
breeds, are affected as well. In most cases,
histopathologic examination of inflamed mucosa
shows an eosinophilic inflammation. Chronic
lymphoplasmacytic rhinitis in dogs and chronic
non-specific rhinitis in cats are diagnosed when
all other causes of chronic rhinitis have been
excluded. This chronic form of rhinitis in cats
is most probably the result of a chronic viral
upper respiratory tract infection. In case of
bilateral nasal discharge and systemic illness,
bronchopneumonia should be suspected.
Nasal foreign body
Frequent sneezing is the primary clinical sign
of nasal foreign body, with rubbing of the front
paws at the nose. In subacute to chronic cases,
unilateral mucopurulent discharge will be the
most obvious clinical sign. During rhinoscopy
under general anesthesia the foreign body
usually can be seen and be removed with special
forceps. Flushing and suction of nasal discharge
are necessary when foreign bodies are covered in
discharge and cannot be visualised immediately.
Foreign bodies that cannot be removed under
endoscopic guidance, will have to be removed
surgically.
Nasal aspergillosis
Mycotic rhinitis is a common disease in dogs
and usually caused by Aspergillus species. This
disease is rare in very young and brachycephalic
dogs, but is often seen in Golden Retriever and
Rottweiler dogs in the Netherlands, male and
female dogs are equally affected. Erosion of
the nasal planum with depigmentation and an
abundant unilateral or bilateral sanguinopurulent,
mucopurulent or hemorrhagic nasal discharge
are usually noted.
The diagnosis can be made on clinical signs
and radiographs of the nasal cavity and frontal
sinus with evidence of turbinate destruction
and irregular areas of increased and decreased
radiolucency. On rhinoscopy cavernous areas
caused by marked destruction of turbinates
and conchal atrophy can be seen, as well as
obvious mats of fungal hyphae. When there is no
macroscopical evidence of fungal hyphae in the
nasal sinus, trepanation of the frontal sinus should
be done. Samples for culture and cytologic and
histopathologic examination should always be
collected.
Oral administration of azole antifungal agents

is effective in only 43% to 70% of cases,
requires months of therapy and is costly. Topical
therapy is therefore indicated and advised by
most specialists. Natamycine, amphotericine B,
itraconazole and clotrimazole can be infused
into the nasal passages and frontal sinuses of
dogs either as a single or with repeated infusion.
A success rate of 70% has been reported with
single infusions of clotrimazole. Success rates up
to 90% have been described after surgical tube
placement and treatment with enilconazole; after
trepanation of both the nasal and frontal sinus on
the affected sides, tubes are sutured in place for
topical instillation of an enilconazole solution
(2dd 10 mg/kg, dilute 1:10) for 14 days.
Nasal tumor
Intranasal tumours are more common in dogs
than in cats. Most tumours are malignant and
occur in middle-aged and old animals (median
age between 8 and 10 years). No sex or breed
disposition has been found. Eighty percent of
canine intranasal tumours are malignant and
approximately two thirds of them are of epithelial
origin (adenocarcinoma, SCC and undifferentiated
carcinoma). Their malignant nature is reflected
more by their progressive local invasiveness than
by distant metastasis to lymphnodes and lungs.
Micrometastases have been reported however
and remained subclinically for 12-36 months.
Clinical signs include nasal discharge, sneezing,
epistaxis, facial and/or oral deformity, epiphora
due to obstruction of the nasolacrimal duct,
stridor, exophthalmos due to a retrobulbar mass
effect and central neurologic signs usually due to
expansion of the tumour through the cribiform
plate. Air passage through the nose is usually
obstructed.
The diagnosis is made on clinical signs,
radiographic signs showing destruction of normal
turbinate pattern and diffuse increased soft tissue
density, CT-scan or MRI and histopathologic
examination of rhinoscopy assisted biopsy.
Radiotherapy appears to be the most effective
treatment for nasal tumours. Most studies have
investigated orthovoltage irradiation (125-400 keV)
but megavoltage irradiation has been reported
as well. The optimum dosage and method of
delivery have not been determined. Median
survival times of 13 months for dogs and
11.5 months for cats with non-lymphoid nasal
tumours treated with megavoltage have been
reported. Whether radiation therapy should be
combined with surgical debulking is controversial.
Surgery as the sole treatment of dogs with
nasal tumours has not prolonged survival time.
However, surgery may palliate clinical signs
Back to contents
T
in some dogs by alleviating obstruction and
epistaxis. Chemotherapy, immunotherapy and
cryosurgery do not improve survival. Malignant
lymphoma can be treated rather successfully
however with combination chemotherapy.
Oronasal fistulae and palatal defects
Acquired oronasal fistulae are abnormal
communications between the nasal and oral
cavities caused by trauma or disease. They are
most often caused by dental disease. An oronasal
fistula results when a deep maxillary periodontal
pocket progresses to the apex of the tooth, lysing
bone between the apex of the alveolus and the
nasal cavity or maxillary sinus. They are usually
seen in middle-aged and older small breed dogs
with a history of dental disease. Common clinical
signs are sneezing and chronic unilateral serous
or mucopurulent nasal discharge. Periodontal
pockets and oronasal fistulae are treated with
dental extraction and closure of the defect with
mucoperiostal or mucosal flaps and antibiotics.
Congenital oronasal fistulas are abnormal
communications between the oral and nasal
cavities involving the soft palate, hard palate,
premaxilla and/or lip. Congenital palatal defects
result when the two palatine shelves fail to fuse
during fetal development as a result of inherited,
nutritional, hormonal, mechanical and toxic
factors. Particularly brachycephalic breeds are
affected purebred dogs have a higher incidence
than mixed breeds. Females are more commonly
affected than males. The cleft is present at
birth, although it is not always recognized
immediately.
Clinical signs are difficulty nursing, nasal
regurgitation (drainage of milk from the
nares), nasal discharge, coughing (aspiration
pneumonia), gagging and failure to thrive are
common problems.
The diagnosis is based on clinical signs and
visual examination of the lip, hard and soft
2006 World Congress WSAVA/FECAVA/CSAVA
palate. Radiographic examination of the skull is
not necessary, but thoracic radiographs are useful
in evaluating for aspiration pneumonia.
Most animals with defects of the palate are
euthanised or die. Surgical treatment generally
is delayed until the patient is at least 8 weeks
of age. At that time they are better anesthetic
candidates and tissues are less friable and hold
sutures better. The primary goal of repairing cleft
palate is to reconstruct the nasal floor. Several
procedures may be necessary before the entire
cleft is permanently reconstructed. The prognosis
for hard palate defects is good, but dogs with
large defects of the soft palate and muscular
hypoplasia have a poor prognosis.
777
 T
T – Nose-Ear-Throat
ELECTROMYOGRAPHY IN DIAGNOSIS OF PHARYNGEAL AND
LARYNGEAL DISEASES
Anjop J. Venker-van Haagen,
DVM, PhD, Dipl. ECVS.
University Utrecht,
Companion Animal Sciences,
Stationsstraat 142,
Utrecht, 3511 EJ,
The Netherlands
aj.venkervanhaagen@wanadoo.nl
Electromyography (EMG) is used for diagnosis
in dysphagia, when no abnormalities are
found by pharyngoscopy. The motor supply
to the pharyngeal muscles is distributed by the
pharyngeal plexus. The glossopharyngeal nerve
and the pharyngeal branch of the vagus nerve
contribute to this plexus. EMG examination of
the pharyngeal muscles is performed in dogs
with spontaneous pharyngeal dysfunction, to
detect possible muscular diseases. EMG is also
used in research to study the swallowing action
in dogs.
Electromyography of the pharyngeal muscles
The animal must be anesthetized for
electromyography. The instruments needed are
a laryngoscope fitted with a blade suitable for
the size of the animal, a long tissue forceps, a
Senn retractor with blunt prongs, and several
sizes of endotracheal tubes. After premedication
with medetomidine, anesthesia is induced
by intravenous administration of propofol to
effect. For inspection of the oropharynx and
the hypopharynx, the dog is placed in a sphinx
2006 World Congress WSAVA/FECAVA/CSAVA
posture with its head supported by an assistant
standing at its side. The assistant opens the
dog’s mouth and extends its neck, using one
hand to raise the upper jaw and the other to
depress the lower jaw and flatten the tongue.
The laryngoscope is introduced over the tongue
and then the mouth, oropharynx, palatine
tonsils, soft palate, and base of the tongue are
inspected. Then the hypopharynx is inspected by
using long forceps or a Senn retractor to extend
visibility caudal to and above the soft palate.
It is advantageous to perform pharyngoscopy
without an endotracheal tube in place, but if
the animal is dyspneic endotracheal intubation
precedes pharyngeal inspection.
The appropriate level of anesthesia is that at
which there is just a low degree of normal
electromyographic activity in the pharyngeal
778
Back to contents
muscles, synchronous with respiration. The
bipolar needle electrode (Danica, 9013L0601)
is inserted into the muscles of both halves
of the tongue and soft palate and into the
bilateral thyropharyngeal, hyopharyngeal,
and cricopharyngeal muscles, to record
the spontaneous muscle action potentials.
Fibrillation potentials were found to predominate
in denervated pharyngeal muscles. In dogs with
histological evidence of muscular dystrophy in
the pharyngeal muscles, there were fibrillation
potentials, positive sharp waves, and, most
characteristic, abundant complex repetitive
discharges. Following electromyography of the
pharyngeal muscles, recordings can be made
from the cervical part of the esophagus with
the aid of a long holder for the bipolar needle
electrode.
EMG studies demonstrating the swallowing
action in dogs
Continuous EMG recordings were made from
paired wire electrodes implanted in the left
and right hyopharyngeal, thyropharyngeal, and
cricopharyngeal muscles of 5 normal beagles
to determine the sequence of activity in each
muscle and the combined muscle activity, both
at rest and during swallowing of food. The
data were digitized during 30-second periods
and stored on diskette for further analysis.
In all 5 dogs the pattern of muscle activity
during swallowing was distinct, in a constant
sequence (hyopharyngeal, thyropharyngeal,
cricopharyngeal), and bilaterally synchronous.
During eating, there were 5 to 12 short periods
of synchronous activity in each muscle between
swallowing actions, tentatively interpreted as
bolus formation. During the resting period,
there were longer periods of activity that were
synchronous with respiration. These EMG
recordings were made to improve understanding
of the swallowing mechanism in dogs.

Electromyography of the intrinsic laryngeal
muscles
The larynx acts as a sphincter at the cranial end
of the tracheobronchial tree. In order of priority,
its functions are to protect the lower airways, to
regulate the respiratory airflow, and to vocalize.
The cartilages of the larynx—the cricoid, thyroid,
and arytenoid cartilages and the epiglottis—
interact under the control of the neuromuscular
system of the larynx to perform these functions.
The cartilages of the larynx simultaneously
support and respond to the activity of the
extrinsic and intrinsic laryngeal muscles. These
muscles move the larynx in swallowing and they
open and close the vocal folds in order to protect
the larynx and lower airways, and to facilitate
respiration and vocalization. Knowledge of
the neurophysiology of laryngeal innervation
is necessary for understanding of laryngeal
dysfunction. The motor innervation of the
intrinsic laryngeal muscles is provided by the
bilateral recurrent laryngeal nerves.
Laryngeal dysfunction is often an indication
for EMG examination of the intrinsic laryngeal
muscles. EMG can be performed routinely in the
dog but the cat is not a good candidate because
it has a small larynx and is to prone to develop
laryngeal edema after the larynx is touched.
When a dog has signs of laryngeal dysfunction
and laryngoscopic examination does not produce
a diagnosis, EMG of the intrinsic laryngeal
muscles can be helpful, for it can distinguish
among normal activity, neurogenic paralysis,
ankylotic paralysis, and muscular disease.
When laryngoscopy is performed for diagnosis
of laryngeal disease, the dog or cat is usually
in a certain state of dyspnea. The laryngoscope
is fitted with a blade suitable for the size of the
animal and lubricated endotracheal tubes of
several sizes are prepared. The anesthetic is then
administered to effect, preferably by intravenous
injection. Propofol is satisfactory and may be
used after premedication with medetomidine.
Medetomidine premedication is given to cats
intramuscularly and to dogs intravenously.
If laryngeal function is to be investigated the
anesthesia should be superficial, for if it is
too deep the activity of the intrinsic laryngeal
muscles, abduction and adduction, is absent.
When the laryngeal movements are absent and
the depth of anesthesia may be the cause, the short
half-life of propofol is advantageous because
after a short pause there is sufficient recovery
for the inspection to proceed. For diagnostic
laryngoscopy the animal is placed in a sphinx
posture with its head supported by an assistant
standing at its side. The mouth is then opened
and the neck extended by the assistant, using
Back to contents
T
one hand to hold the upper jaw and the other to
hold the lower jaw and flatten the tongue. The
laryngoscope is introduced over the tongue and
the mouth, oral pharynx, and ventral side of the
epiglottis are inspected before the epiglottis is
depressed for inspection of the glottis. The size
of the laryngeal opening (rima glottidis) is the
first concern, for spontaneous breathing requires
an adequate laryngeal opening and if the opening
is obstructed, endotracheal intubation must be
performed immediately. Artificial ventilation
via the tube will then be needed, at least for a
short while. If intubation is not required, the
glottis (the paired arytenoid cartilages dorsally
and the paired vocal folds ventrally) is inspected,
the movement of the glottis and the color of
the laryngeal mucosa are evaluated, and the
cartilages are inspected for deformities.
EMG procedure
The epiglottis is depressed with the blade of the
laryngoscope, giving access to several of the
intrinsic laryngeal muscles. Recordings are made
via a bipolar needle electrode (Danica, 9013L0601)
which is fixed in a long, rigid holder that enables
the tip of the electrode to be inserted through the
mucosa into separate laryngeal muscles under
visual guidance. The thyroarytenoid, ventricular,
and dorsal cricoarytenoid muscles are accessible
beneath the mucosa in this way). In the paired
abductors (dorsal cricoarytenoid muscles) of
normal dogs action potentials are observed
predominantly during inspiration. In the paired
thyroarytenoid and vocal muscles, visible as the
paired vocal folds, action potentials are observed
mainly but not exclusively during expiration. In
the paired ventricular muscles action potentials
are synchronous with expiration. No action
potentials are observed if the level of anesthesia
is too deep, but abnormal potentials such as
fibrillation potentials and complex repetitive
discharges (CRDs) will be observed irrespective
2006 World Congress WSAVA/FECAVA/CSAVA
of the level of anesthesia. Fibrillation potentials
are the result of denervation, which can be due to
recurrent laryngeal nerve trauma or progressive
neurogenic laryngeal paralysis. CRDs are also a
common finding in the latter and they are also
abundant in muscular disease.
References
Venker-van Haagen AJ. The Pharynx. In: Ear,
Nose, Throat, and Tracheobronchial Diseases
in Dogs and Cats. Hannover: Schlütersche
Verlagsgesellschaft, 2005: 83-116.
Venker-van Haagen AJ. The Larynx. In: Ear,
Nose, Throat, and Tracheobronchial Diseases
in Dogs and Cats. Hannover: Schlütersche
Verlagsgesellschaft, 2005: 121-161.
779
 T
T – Nose-Ear-Throat
BRAINSTEM EVOKED RESPONSE AUDIOMETRY FOR HEARING
ASSESSMENT IN DOGS
Gert Ter Haar, DVM, DECVS
Department of Clinical Sciences
of Companion Animals
Faculty of Veterinary Medicine
PO Box 80 154
3508 TD Utrecht
The Netherlands
G.terHaar@vet.uu.nl
Anatomy & Physiology
The inner ear is located within the osseous
labyrinth of the petrous part of the temporal
bone. The membraneous labyrinth consists
of three parts: the cochlea, vestibule and the
semicircular canals. The sensory transduction
for hearing occurs in the organ of Corti, which
is situated in the scala media en separated from
the scala vestibuli and the scala tympani by
reissner’s membrane and the basilar membrane
respectively. It is here where the hair cells interact
with supporting elements to convert fluid waves
into the bending of hair bundles and resultant ion
influxes.
The release of neurotransmitter from the basal
portions of stimulated hair cells leads to neural
impulses, action potentials. Once the nerve impulse
is generated in the cochlea, the signal travels along
the acoustic nerve to the cochlear nuclei. From
here, many projections lead to the olivary nuclei
at the same level. The axons of the olivary neurons
project via the lateral lemniscus to the inferior
colliculi, where they synapse on neurons that
project to the primary auditory cortex.
2006 World Congress WSAVA/FECAVA/CSAVA
Sounds
Like all wave phenomena, sound waves have
four major features: waveform, phase, amplitude
and frequency. These four determine our
perception of sound, especially the frequency
and amplitude of the waves. The frequency of a
sound, expressed in cycles per second or Hertz
roughly corresponds to the pitch of a sound,
whereas the amplitude, usually expressed in
decibels, determines the loudness of a sound.
The receptors, the hair cells, act like miniature
amplifiers and provide a maximal electrical
response when vibrated at a particular frequency
by the fluid waves of the inner ear.
Along the cochlea, all small groups of hair cells
have their own specific frequency by which they
are stimulated maximally; those with high-pass
780
Back to contents
frequencies occupy the base and those with low-
pass frequencies occupy the apex. Therefore,
a sound with a high frequency will cause
maximal displacement of a portion of the basilar
membrane at the base of the cochlea. The greater
the displacement of the basilar membrane, the
more sensory receptor and neurons that are
stimulated, leading to increased sound intensity.
A sound wave with a higher amplitude leads to a
greater basilar membrane displacement. A sound
with a low frequency causes displacement of a
more apical situated portion of the cochlea.
Hearing assessment
Several methods have been employed to test
hearing ability in dogs, ranging from behavioural
studies to measurement of electrical responses
after auditory stimulation, using impedance
audiometry (tympanometry, acoustic reflex
testing), evoked response audiometry (brainstem
(BAER) and middle latency (MLAER) auditory
evoked responses), and cochlear microphony.
The brain responds to auditory stimuli by
consistent changes in electrical activity and these
changes can be recorded from scalp electrodes.
It is generally agreed that the recorded brainstem
evoked potentials represent the passage of
auditory input from the inner ear through the
various structures of the brainstem towards the
auditory cortex. The last two decades, brainstem
auditory evoked responses have been used
increasingly to test hearing ability in veterinary
medicine. The acoustic signal usually consisted
of a click stimulus, which stimulates a large part
of the cochlea.
Brainstem evoked response audiometry using
clicks will suffice for differentiating neurologic
from conduction deafness and is of use in
assessing some brainstem pathologic changes.
Frequency-specific information, however, is
needed in assessing the extent of neurologic
deafness, e.g. noise-induced deafness, deafness

caused by ototoxicity and presbycusis, which can
all be partial and frequency-specific.
Results of hearing assessment using brainstem-
evoked response audiometry
In our laboratory a method was developed to
deliver tone bursts ranging in frequency from
1 - 32 kHz for frequency-specific assessment of
the canine cochlea.
Brainstem auditory evoked responses (early
latency responses, 0 - 10 ms) to a click (CS) and
to 1, 2, 4, 8, 12, 16, 24, and 32 kHz tone burst
stimulations (TS) were compared at 80 dB sound
pressure level stimulus intensity in 10 clinically-
healthy dogs, 3.5 to 7.0 years of age (mean, 5.7 years)
weighing 12.5 to 21.3 kg (mean, 17.8 kg). The
responses were obtained with the animals under
a light plane of anaesthesia.
All stimulations yielded a 5-7 positive wave pattern,
with the exception of the 1 kHz TS, which evoked
a frequency-following response. Thresholds were
lowest for CS, 12, and 16 kHz TS.
We concluded that specific tone burst
stimulation of the canine cochlea using low to
high frequencies yields reproducible results
and that results are in agreement with results of
behavioral studies on frequency thresholds and
hearing sensitivity in dogs. To reliably determine
the extent of neurological damage due to ototoxic
drugs, presbycusis, or noise, frequency-specific
assessment should be done. Our report provides
a normative database for parameters necessary to
evaluate these frequency-specific hearing losses
in dogs.
Back to contents
T
Age Related Hearing Loss
Deafness is classified as inherited or acquired,
conductive or sensorineural and congenital or late
onset. Conductive deafness results from a lack
of presentation of sound to the inner ear, usually
secondary to otitis externa or media and therefore
amenable to therapy. Sensorineural deafness
occurs with abnormalities of the cochlear system,
cranial nerve VIII or auditory pathways and
higher brain centers. The most common forms of
sensorineural deafness are the congenital forms
of deafness, deafness as a result of ototoxicity
and presbycusis or age-related hearing loss. To
evaluate hearing in old dogs, animals older than
12 years of age were examined with brainstem-
evoked response audiometry using the same
method as in the previously mentioned group.
The results showed that their hearing range did
not differ much from the first group, but their
thresholds were significantly higher, especially
in the high-frequency area. The histology of the
cochlear changes was studied and preliminary
results show profound hair cell loss and neuronal
loss, most prominent in the basal coils of the
cochlea, comparable to presbycusis in humans.
There is no cure for sensorineural hearing loss,
but ungoing research in human and veterinary
medicine regarding middle ear implants, cochlear
implants, neurotrophic factors and stem cell
research is yielding promising results.
2006 World Congress WSAVA/FECAVA/CSAVA
781
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

U
U -U
Nep
Nephrology & Urology

Back to contents

INVITED LECTURES - FULL PAPERS
U - Nephrology & Urology
MEDICAL MANAGEMENT OF URINARY INCONTINENCE
Susi Arnold , Prof. Dr. med. vet.,
DECAR
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
sarnold@vetclinics.unizh.ch
Madeleine Hubler, Dr. med. vet.,
DECAR
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
The underlying pathophysiological mechanism
of urinary incontinence after spaying is a reduced
closure pressure of the urethra, known as “urethral
sphincter mechanism incompetence” (USMI).
Within one year after spaying the urethral closure
pressure is significantly reduced. Because many
bitches only become incontinent years after surgery
it took a long time until spaying was considered
to be the cause. In one study, 83 (=20%) of 412
bitches, incontinence occurred 3 to 10 years after
surgery (1).
The medical treatment of USMI is the method
of choice and should always precede a surgical
therapy. The action of the used substances implies
an increase of the urethral closure pressure. In the
first line alpha-adrenergic agonists are used. The
effect of these sympathomimetic drugs is explained
by the fact, that 50% of the urethral closure pressure
is generated by the sympathetic nervous system.
Alpha-adrenergic agonists improve the urethral
closure pressure by stimulation of the alpha-
receptors of the smooth urethral musculature (2-7).
The treatment with alpha-adrenergic agonists results
in continence in 75% of incontinent bitches.
An alternative is the treatment with estrogens,
which is successful in 65% (1,8,9). But with
estrogens unwanted side effects can occur such as
swelling of the vulva and attractiveness for male
dogs (8). Nowadays only short-acting estrogens
(Estriol, Incurin®, Intervet, Netherlands)are used
(10). The depot preparations used in the past are
Back to contents
U
Iris Reichler, Dr. med. vet.
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
obsolete, in part because they can potentially cause
a bone narrow depression (11). Estrogens indirectly
increase the urethral closure pressure; they sensitise
the alpha-receptors for endogenous and exogenous
catecholamines (12). If therapy with alpha-
adrenergic agonists is unsatisfactory, a combination
with estrogens may potentiate the effect.
The alpha-receptors are divided in alpha1- and
alpha2-subtypes. These receptor subtypes are
distributed differently in each single effector.
Alpha-1 receptors are found in many target organs
of the sympathetic nervous system. With a few
exceptions, alpha-2 receptors are not present in
target organs of the sympathetic nervous system, 2006 World Congress WSAVA/FECAVA/CSAVA
but in neuronal synapses. It is now known, that the
alpha-receptors at the bladder neck and proximal
urethra of the bitch, which are responsible for
continence, belong to the subtype 1 (13).
The side effects of alpha-adrenergic agonists is
explained by the fact that alpha-1 receptors are
not just found at the bladder neck, but also in other
organs, especially in the wall of blood vessels.
Phenylpropanolamine (PPA) acts selectively on
alpha-1 receptors.
The older substance Ephedrine is less selective
than PPA. It also stimulates beta-receptors and
therefore has the tendency to have more side
effects (2,3). In contrast to PPA a habituation to
Ephedrine occurs. Because of these reasons PPA
is the therapy of first choice.
In humans treatment with PPA sometimes
783
 U
causes side effects, such as an increase in blood
pressure and headache. It may occasionally
trigger a stroke or a heart attack and is therefore
no longer used. With PPA used in dogs, at the
recommended dose of 1.5 mg/Kg BW bid
or tid, an increase in blood pressure was not
observed (5, 14). The side effects observed in dogs
were never life threatening and usually were self-
limiting; diarrhoea, vomiting, anorexia, apathy,
nervousness and aggressiveness (1,7,15).
For refractory cases different surgical therapies
are available, of which colposuspension (16),
urethropexie (17) and the endoscopic injection
of collagen (18) are mainly used, with a success
rate of 50 – 75%. With all three techniques a
deterioration in the response rate was seen over
time. At our clinic, we prefer the endoscopic
injection of collagen as this method is least
invasive, with a minimal rate of complications
and the results are as good as the more invasive
techniques.
References:
1. Arnold S, Arnold P, Hubler M, Casal M, Rüsch
P. Incontinentia urinae bei der kastrierten Hündin:
Häufigkeit und Rassedisposition. Schweiz Arch
Tierheilkd 1989; 131: 259-263.
2. Awad SA, Downie JW, Kirulata HG. Alpha-
adrenergic agents in urinary disoders of the
proximal urethra. Part I Sphincteric incontinence.
Br J Urol 1978; 50: 332-335.
3. Awad SA, Downie JW. The effect of alpha-
adrenergic drugs and hypogastric nerve
stimulation on the canine urethra. A radiologic
and urethral pressure study. Invest Urol 1976;
13: 298-301.
4. Gillberg PG, Fredrickson MG, Öhman BM,
Alberts P. The effect of Phenylpropanolamine
on the urethral pressure and heart rate is retained
after repeated short-term administration in the
2006 World Congress WSAVA/FECAVA/CSAVA
unanaesthetized, conscious Dog. Scand J Urol
Nephrol 1997; 32: 171-176.
5. Hensel P, Binder H, Arnold S. Einfluss
von Phenylpropanolamin und Ephedrin auf
den urethralen Verschlussdruck und den
arteriellen Blutdruck bei kastrierten Hündinnen.
Kleintierpraxis 2000; 45: 569-656.
6. Richter KR, Ling GV. Clinical response
and urethral pressure profile changes after
Phenyolpropanolamine in dogs with primary
sphincter incompetence. JAVMA 1985; 187:
605-610.
7. White RAS, Pomeroy CJ. Phenylpropanolamine:
an α-adrenergic agent for the management of
urinary incontinence in the bitch associated with
urethral sphincter mechanism incompetence. Vet
Rec 1989; 125: 478-480.
784
Back to contents
8. Mandingers RJ, Nell T. Treatment of bitches
with acquired urinary incontinence with Oestriol.
Vet Rec 2001; 149:764-767.
9. Nendick PA, Clark WT. Medical therapy
of urinary incontinence in ovariectomised
bitches: a comparison of the effectiveness of
Diethylstilboestrol and Pseudoephedrin. Aust
Vet J 1987; 64(4): 117-118.
10. Janszen BPM, van Laar PH, Bergman JGHE.
Treatment of urinary incontinence in the bitch:
A pilot field study with Incurin®. Vet Q 1997;
19: 42.
11. Teske E. Estrogen-induced bone marrow
toxicity. In: R.W. Kirk (Ed.). Current Veterinary
Therapy IX, Philadelphia, W.B. Saunders Co.,
1984; pp.495-498.
12. Schreiter F, Fuchs P, Stockamp K. Estrogenic
sensitivity of alpha-receptors in the urethra
musculature. Urol int 1976; 31: 13-19.
13. Shapiro E, Lepor H. Alpha1-adrenergic
receptors in canine lower genitourinary tissues:
Insight into development and function. Urology
1987; 138:979-983.
14. Scott L, Leddy M, Berney F, Davot JL.
Evaluation of Phenypropanolamine in the
treatment of urethral sphincter mechanism
incompetence in the bitch. J Small Anim Pract
2002; 43: 493-496.
15. Blendinger C, Blendinger K, Bonstedt H.
Die Harninkontinenz nach Kastration bei der
Hündin. 2. Mitteilung: Therapie. Tierarztl Prax
1995; 23: 402-6.
16. Holt, PE. Urinary incontinence in the bitch
due to sphincter mechanism incompetence:
surgical treatment. J Small Anim Pract 1985, 26:
237-246.
17. White RN. Urethropexy for the management
of urethral sphincter mechanism incompetence
in the bitch. J Small Anim Pract 2001, 42: 481-
486.
18. Arnold S, Hubler M, Lott-Stolz GH, Rüsch
P. Treatment of urinary incontinence in bitches
by endoscopic injection of glutaraldehyde cross-
linked collagen. J Small Anim Pract 1996, 37:
163-168.
19. Barth A, Reichler IM, Hubler M, Haessig
M, Arnold S. Evaluation of long-term effects of
endoscopic injection of collagen into the urethral
submucosa for treatment of urethral sphincter
incompetence in female dogs: 40 cases (1993-
2000). JAVMA 2005, 226: 73-76.

U - Nephrology & Urology
SURGICAL MANAGEMENT OF URINARY INCONTINENCE
Professor Peter Holt
University of Bristol
Department of Clinical
Vetrerinary Science
Langford house
Langford
Bristol BS40 5DU
UK
Peter.holt@bristol.ac.uk
There are a large number of causes of urinary
incontinence. It is not possible to cover all of
these in this lecture. The common causes of
incontinence are ureteral ectopia (in juveniles)
and urethral sphincter mechanism incompetence
(in juveniles and adults) and these conditions
will be covered in this lecture.
Ureteral ectopia
This is mainly a problem of dogs (but is also
reported in cats, horses and cattle). The cause
is unknown but hereditary factors and vitamin
imbalance in the dam may play a role. Incontinence
may be continuous or intermittent and even in
bilateral cases, normal micturition usually occurs.
Diagnosis is by contrast radiography, cystoscopy
and/or ultrasonography. Most ectopic ureters
terminate in the urethra or, sometimes, the vagina.
Ectopic ureter is commoner in female than male
animals. There is a breed predisposition in the UK
in Labradors, Golden Retrievers and Skye terriers.
Secondary ureteral or renal problems (hydro-ureter,
hydronephrosis and pyelonephritis) can develop
and may influence the choice of treatment.
Treatment involves transplanting the ureter
into the bladder or excision of the ureter and
associated kidney if severe secondary disease
is present. Approximately 50% of animals are
completely cured and in most of the remainder,
the incontinence is markedly reduced. These
cases are best referred.
A few animals show no improvement after
surgery, possibly due to undiagnosed bilateral
ectopia, concomitant sphincter mechanism
incompetence, bladder hypoplasia or anomalous
ureteric branches.
Urethral sphincter mechanism incompetence
The surgical treatment of cases of sphincter
mechanism incompetence may be difficult since
this condition is multifactorial and most therapies
correct only one of the factors. It is unlikely,
therefore, that any one form of treatment alone
will cure 100% of cases in the long-term.
Back to contents
U
The main options for surgical treatment are to
attempt to:
• increase urethral resistance - e.g. peri-urethral
surgical slings (Muir et al 1994; Nickel et al
1998) or artificial sphincters (Dean et al 1989);
intra-urethral injection of bulking agents (Arnold
et al 1989, 1996; Barth et al 2005);
• increase urethral length, using bladder neck
reconstruction techniques (Holt 1993);
• re-locate the bladder neck to an intra-abdominal
position by means of colposuspension (Holt
1985, 1990), urethropexy (White 2001), vas
deferentopexy (Weber et al 1997; Salomon et al
2002) or prostatopexy (Holt et al 2005).
The problem with techniques intended to increase
urethral resistance is that they may increase the
morbidity by making an incontinent animal
dysuric. Similarly, increasing urethral length
carries potentially serious surgical risks and, in
the author’s view, should be reserved for animals
with severe congenital urethral hypoplasia (these
are mainly cats). The author’s preferred technique
is colposuspension. The greater experiences
of medical urologists treating incontinent
women suggests that colposuspension provides
firmer anchorage of the lower urogenital tract
than urethropexy and avoids urethral trauma,. 2006 World Congress WSAVA/FECAVA/CSAVA
However, a recent review of urethropexy as
a treatment for urethral sphincter mechanism
incompetence in 100 bitches (White, 2001)
revealed similar results to colposuspension
although the prevalence and severity of urethral
complications was higher.
Colposuspension is intended to move the
intrapelvic bladder neck of bitches with urethral
sphincter mechanism incompetence to an intra-
abdominal position so that increases in intra-
abdominal pressure can act simultaneously on
the bladder and urethra. Thus, any increase
in intravesical pressure is counteracted by an
increase in urethral resistance. During the
procedure (which is described in detail in a
separate lecture), the vagina is stretched cranially
and anchored on either side of the urethra to
785
 U
the prepubic tendon. This cranial movement
of the vagina results in similar displacement of
the urethra and bladder. Care is taken to avoid
compression of the urethra during the technique.
A long-term evaluation of cases treated by
the reviewer indicates that a cure-rate of
approximately 50% can be expected with most of
the remaining bitches improved. Ten percent of
bitches fail to respond at all to colposuspension
and the complication rate is low.
Urethral sphincter mechanism incompetence
in male dogs is uncommon. Conservative
management is frequently disappointing. In
comparison with the bitch, the condition is
less likely to respond to medical therapy. The
pathophysiology of male urethral sphincter
mechanism incompetence is poorly understood,
making rational treatment difficult. Surgical
attempts have been made to relocate the
intrapelvic bladder neck to an intra-abdominal
position. These have mainly involved pexy of
the deferent ducts to the abdominal wall (Weber
et al 1997; Salomon et al 2002) although the
author has used prostatopexy (in castrated males)
to the prepubic tendon (Holt et al 2005). As with
medical treatment, the impression in a limited
number of cases is that surgical treatment alone
of urethral sphincter mechanism incompetence is
less successful in males than in bitches.
Before we become too despondent about our
results, despite over 200 operations being
described for human stress incontinence, an
eminent urologist ended his editorial “It leaves
me asking, when it comes to my own patients,
what to do?” (Blavais 2005).
References and Further Reading
ARNOLD, S., JAGER, P., DIBARTOLA, S.P.,
LOTT-STOLZ, G., HAUSER, B., HUBLER,
M., FAIRBURN, A. & RUSCH, P. (1989)
Treatment of urinary incontinence in dogs by
2006 World Congress WSAVA/FECAVA/CSAVA
endoscopic injection of Teflon. Journal of the
American Veterinary Medical Association, 195,
1369-1374.
ARNOLD, S., HUBLER, M., LOTT-STOLZ, G.
& RUSCH, P. (1996) Treatment of
urinary incontinence in bitches by endoscopic
injection of glutaraldehyde cross-linked collagen.
Journal of Small Animal Practice 37, 163-168.
BARTH, A., REICHLER, I.M., HUBLER, M.,
HASSIG, M. & ARNOLD, S. (2005) Evaluation
of long-term effects of endoscopic injection
of collagen into the urethral submucosa for
treatment of urethral sphincter incompetence in
female dogs: 40 cases (1993-2000). Journal of
the American Veterinary Medical Association
226, 73-76.
786
Back to contents
BLAVAIS, J.G. (2005) What to do? Neurourology
and Urodynamics 24, 201.
CANNIZZO, K.L., McLOUGHLIN, M.A.,
MATTOON, J.S., SAMII, V.F., CHEW, D.J.
& DIBARTOLA, S.P. (2003) Evaluation of
transurethral cystoscopy and excretory urography
for diagnosis of ectopic ureters in female dogs:
25 cases (1992-2000). Journal of the American
Veterinary Medical Association 223, 475-481.
DEAN, P.W., NOVOTNY, M.J. & O’BRIEN,
D.P. (1989) Prosthetic sphincter for urinary
incontinence: results in three cases. Journal of
the American Animal Hospital Association, 25,
447-454.
HOLT, P.E. (1985) Urinary incontinence in the
bitch due to sphincter mechanism incompetence:
surgical treatment. Journal of Small Animal
Practice, 26, 237-246.
HOLT, P.E. (1990) Long-term evaluation of
colposuspension in the treatment of urinary
incontinence due to incompetence of the urethral
sphincter mechanism in the bitch. Veterinary
Record, 127, 537-542.
HOLT, P.E. & GREGORY, S.P. (1991) Can
urethral pressure profilometry predict the response
to colposuspension in bitches? Veterinary Record
128, 281-282.
HOLT, P.E. & GIBBS, C. (1992) Congenital
urinary incontinence in cats: a review of 19
cases. Veterinary Record 130, 437-442.
HOLT, P.E. (1993) Surgical management
of congenital urethral sphincter mechanism
incompetence in eight female cats and a bitch.
Veterinary Surgery, 22, 98-104.
HOLT, P.E. & HOTSTON MOORE, A. (1995)
Canine ureteral ectopia – analysis of 175 cases
and comparison of surgical treatment. Veterinary
Record 136, 345-349.
HOLT, P.E., THRUSFIELD, M.V. & HOTSTON
MOORE A. (2000) Breed predisposition to
ureteral ectopia in bitches in the UK. Veterinary
Record 146, 561.
HOLT, P.E., COE, R.J. & HOTSTON MOORE,
A. (2005) Prostatopexy as a treatment for urethral
sphincter mechanism incompetence in male dogs.
Journal of Small Animal Practice 46, 567-570.
MASSAT, B.J., GREGORY, C.R., LING, G.V.
CARDINET, G.H. & LEWIS, E.L. (1993)
Cystourethropexy to correct refractory urinary
incontinence due to urethral sphincter mechanism
incompetence. Preliminary results in ten bitches.
Veterinary Surgery 22, 260-268.
McLOUGHLIN, M.A. & CHEW, D.J. (2000)
Diagnosis and surgical management of ectopic
ureters.

Clinical Techniques in Small Animal Practice 15,
17-24.
MUIR, P., GOLDSMID, S.E. & BELLENGER,
C.R. (1994) Management of urinary incontinence
in five bitches with incompetence of the urethral
sphincter mechanism by colposuspension and a
modified sling urethroplasty. Veterinary Record
134, 38-41.
NICKEL, R.F., WIEGAND, U. & VAN DEN
BROM, W.E. (1998) Evaluation of a transpelvic
sling procedure with and without colposuspension
for treatment of femlae dogs with refractory
urethral sphincter mechanism incompetence.
Veterinary Surgery 27, 94-104.
RAWLINGS, C.A., MAHAFFEY, M.B.,
CHERNOSKY, A.C. & HUZELLA, L.(2000)
Immediate urodynamic and anatomic response
to colposuspension in female Beagles. American
Journal of Veterinary Research 61, 1353-1357.
RAWLINGS, C.A., BARSANTI, J.A.,
MAHAFFEY, M.B. & BEMENT, S. (2001)
Evaluation of colposuspension for treatment of
incontinence in spayed female dogs. J o u r n a l
of the American Veterinary Medical Association
219, 770-775.
Back to contents
U
SALOMON, J.F., COTARD, J.P. & VIGUIER,
E. (2002) Management of urethral sphincter
mechanism incompetence in a male dog with
laparoscopic-guided deferentopexy. Journal
of Small Animal Practice 43, 501-505.
SUTHERLAND-SMITH, J., JERRAM,
R.M., WALKER, A.M. & WARMAN, C.G.A.
(2004) Ectopic ureters and ureteroceles in
dogs: presentation, cause, and diagnosis.
Compendium on Continuing Education for the
Practicing Veterinarian 26, 303-310.
WEBER, U. T., ARNOLD, S., HUBLER, M. &
KUPPER, J.R. (1997) Surgical treatment
of male dogs with urinary incontinence due to
urethral sphincter mechanism incompetence.
Veterinary Surgery 26, 51-56.
WHITE, R.N. (2001) Urethropexy for the
management of urethral sphincter mechanism
incompetence in the bitch. Journal of Small
Animal Practice 42, 481-486.
2006 World Congress WSAVA/FECAVA/CSAVA
787
 U
U - Nephrology & Urology
URINARY TRACT INFECTION
David Senior
Professor and Head, Veterinary
Clinical Sciences, Louisiana State
University.
Department of Veterinary Clinical
Sciences
School of Veterinary Medicine
Louisiana State University
Baton Rouge, LA 70803
USA

ETIOLOGY against the flow of urine. Further ascending

Urinary tract infection (UTI) encompasses
a wide variety of clinical entities caused by
microbial invasion of any part of the urinary
system. Infection induces inflammation of the
urethra (urethritis), prostate gland (prostatitis),
bladder (cystitis), ureters (ureteritis), and kidneys
(pyelonephritis).
Hematogenous renal infection such as septic
infarcts from bacterial endocarditis can induce
acute renal failure. However, the hematogenous
route is not a common mechanism for
establishment of UTI in dogs and cats. Most
UTI is caused by bacteria emanating from the
gastrointestinal tract crossing the perineum
and colonizing the external genitalia prior to
retrograde invasion of the urethra and bladder
colonization of the ureters and kidneys can occur
but this is relatively uncommon. Development
of UTI depends upon the balance between
infectious agents and host resistance, and the
status of host defense mechanisms appears to be
important in the pathogenesis of UTI. Although
UTI can occur when a very virulent organism
invades a normal urinary tract, many times
UTI develops when there is a disturbance of
anatomical or functional factors that normally
prevent microbial invasion.
The recognized etiological agents involved in
UTI are mainly bacteria (Table 1). However,
fungi can colonize the urinary tract in special
circumstances. The role of viruses in UTI is
currently not known.

Table 1: Bacterial isolates in canine UTI

Per cent of total isolates
a) (b) (c)
E. coli 37.8 67 20.1
Staphylococcus spp. 14.5 21 9.6
2006 World Congress WSAVA/FECAVA/CSAVA

Proteus mirabilis 12.4 3 15.4

Streptococcus spp. 10.7 6 10.6
Klebsiella pneumoniae 8.1 0 3.4
Pseudomonas aeruginosa 3.4 0 6.9
Enterobacter spp. 2.6 3 3.3

Number of isolates: 1,400 40 187

(a) Ling, G.V. et al. Vet. Clin. North Amer. 1979; 9: 617-630
(b) Kivisto, A.K. et al. J. Sm. Anim. Pract. 1997; 18: 707-712
(c) Wooley RE et al. Mod Vet Pract. 1976; 57: 535-538.

Whether or not UTI develops depends on a Host defense mechanisms

balance between virulent bacteria that tend to Many host defense mechanisms have been
ascend the urinary tract and natural host defenses identified or hypothesized to be important in
that tend to keep them out. protection against UTI (Table 2).
788
Back to contents

Table 2: Local host defenses of the urinary tract
• Normal Micturition
- Adequate urine flow
- Frequent voiding
- Complete voiding
• Anatomic Structures
- Urethral high pressure zone
- Surface characteristics of urethral
urothelium
- Urethral peristalsis
- Prostatic antibacterial fraction
- Length of urethra
- Ureterovesical flap valves and ureteral
peristalsis
• Mucosal Defense Barriers
- Antibody production
- Surface glycosaminoglycan layer
- Intrinsic mucosal antimicrobial properties
- Bacterial interference
- Exfoliation of cells
• Antimicrobial Properties of Urine
- Extremes (high or low) of urine pH
- Hyperosmolality
- High concentration of urea
- Organic acids
• Renal Defenses
- Glomerular mesangial cells?
- Extensive blood supply and large blood flow
Bacterial virulence
Of all the bacterial species resident in the
gastrointestinal tract only a few are capable
of causing UTI. In order to be successful
uropathogens, bacteria must possess special
properties that enable them to invade and persist
in the urinary tract. The intrinsic motility of some
bacteria may aid in their retrograde migration
through the excretory pathway against the flow
of urine. The ability to adhere to the surface of
uroepithelial cells is very important because it
prevents urine flow from washing bacteria out
and it allows more efficient delivery of bacterial
toxins to the mucosal wall.
The consequences of UTI are variable. In many
cases, infection will be transient, signs will be
minimal, and the condition responds readily to
treatment. However, UTI is often subclinical
and goes undetected for long periods. Many
infections can persist for a prolonged period
in a commensal-like relationship with the host
animal causing few if any detrimental effects.
However, serious consequences of persistent
UTI include formation of struvite uroliths,
chronic prostatitis, prostatic abscess formation,
discospondylitis and ascending renal infection
with scarring, progressive loss of renal function
and chronic renal failure. Whether an infection
will be benign or injurious cannot be predicted,
so all UTI should be treated vigorously.
Back to contents
U
DIAGNOSIS
In animals that exhibit overt clinical signs of
lower urinary tract inflammation, the major
diagnostic possibilities include UTI, urolithiasis
and lower urinary tract neoplasia. Bladder and
urethral neoplasia is rare in dogs under 7 years
of age. Clinicians should always remember that
UTI could coexist with both urolithiasis and
neoplasia.
The diagnosis of UTI is often made on clinical
history and physical examination alone. However,
a more definitive approach with urinalysis, urine
culture, and antimicrobial sensitivity testing is
recommended, particularly if previous treatment
has been unsuccessful. The interpretation of
urinalysis and bacterial culture results depends
upon the method of collection. Urine collected
by mid-stream voiding, catheterization and
cystocentesis can all be useful but cystocentesis
urine is best for culture.
Urine should be set up for bacterial culture as
soon as possible after collection and certainly no
longer than 4 hours.
Antimicrobial sensitivity tests
Antimicrobial sensitivity tests on uropathogens
are best performed using the minimum inhibitory
concentration (MIC) method. The mean urinary
concentration (MUC) achieved with standard
dose regimens has been determined for most of
the antimicrobial agents used to treat UTI. If an
antimicrobial reaches an MUC of at least 4 times
the in vitro MIC, treatment with that drug has a
high chance of therapeutic success.
The MUC in dogs of commonly used
antimicrobials when given at usual recommended
doses can be obtained by contacting the author.
Localization of infection
Clinically it is difficult to determine if UTI
is confined to the lower urinary tract or has
extended to involve the kidneys. Animals with
2006 World Congress WSAVA/FECAVA/CSAVA
pyelonephritis can have WBC casts in the
urine sediment, dilute urine, and peripheral
leukocytosis. About 90 % of intact male dogs
with UTI have colonization of the prostate.
TREATMENT
Several bacteria commonly isolated from UTI
in dogs and cats have predictable antimicrobial
sensitivity and their presence can be deduced
from a urinalysis. If cocci are observed in the
urine sediment (Staphylococcus intermedius,
Streptococcus spp., and Enterococcus spp.) or the
urine is very alkaline and small rods in pairs are
evident in the urine sediment (Proteus mirabilis),
over 90 % will be sensitive to ampicillin or
amoxicillin. Combination with the β–lactamase
789
 U
inhibitor clavulanic acid may be preferable.
Other bacteria causing UTI must be identified
by culture. Fluoroquinolones are very effective
in the treatment of Pseudomonas aeruginosa and
for lower urinary tract infections in female dogs,
tetracyline may be quite effective as well. The
antimicrobial sensitivities of E. coli, Klebsiella
spp. and Enterobacter spp. are not predictable and
sensitivity tests must be performed to determine
appropriate treatment.
Duration of treatment
The accepted duration of treatment for UTI of
the lower urinary tract is 14 days. Treatment
duration of up to 30 days is usually recommended
for patients where the infection is suspected to
involve prostatic or renal tissue.
A urine culture should be performed 8-10
days after beginning treatment to ensure that
the chosen antimicrobial is effective. Another
urine culture should be performed 10 days after
cessation of treatment to ensure that treatment
has been successful and persistent or recurrent
UTI is not present.
Special considerations
For intact male dogs with UTI, antimicrobial
agents must be weak bases or at least lipid
soluble and they must achieve a plasma
concentration of 4 times MIC. Fluoroquinolones
(broad spectrum weak bases), trimethoprim
(a weak base), and chloramphenicol (lipid
soluble) are all suitable for male dogs with
prostatic involvement.
Occasionally fungal and yeast overgrowth
will colonize the urinary tract, particularly in
patients with diabetes mellitus. Elimination
of the underlying cause usually is sufficient
to clear the infection. Amphotericin B used
as a local irrigant into the bladder has been
suggested for persistent infections. Fluconazole
2006 World Congress WSAVA/FECAVA/CSAVA
and ketoconazole have been used successfully to
treat fungal cystitis in humans but information is
lacking in veterinary medicine. Mild alkalinization
of the urine is also thought to be helpful.
790
Back to contents
Treatment failure
Failure of an antimicrobial agent to sterilize the
urine should alert the clinician to one or more of
the following possibilities:
1. Inappropriate drug, dose, or duration of therapy.
2. Failure of the antimicrobial agent to reach
sufficient concentrations in urine.
3. The presence of a nidus of infection
4. The presence of anatomical or functional
abnormalities.
When UTI recurs after apparently effective
treatment has been given for a reasonable
period of time, in male dogs a routine work
up for prostatic disease should be performed
including ultrasonic examination of the
prostate and cytology and culture of a prostatic
aspirate. Plain and contrast radiographic studies
including IVP, double contrast cystography and
retrograde and voiding urethrography should be
sufficient to diagnose or rule out the presence
of identifiable anatomical defects. Urolithiasis
is a frequent cause of recurrent lower urinary
tract inflammation in animals of all ages, while
neoplasia of the bladder, urethra or prostate can
be the underlying problem in older dogs.
PREVENTION
When an animal suffers frequent recurrences
of UTI despite adequate treatment and in the
absence of detectable or correctable anatomic and
functional disturbances, long term management
with antimicrobial agents may be necessary to
prevent additional recurrences. Patients must first
be given a standard treatment of antimicrobial
based on sensitivity results for 14 or 30 days, as
required. Then, the protocol calls for continued
administration of an antimicrobial at 30-50 % of
the usual total daily dose given as a single dose
at night before bedtime immediately after the
animal is allowed to void. Treatment should be
given for 6 months.
REFERENCES
Available on request

U - Nephrology & Urology
DIAGNOSIS AND MANAGEMENT OF CANINE PROSTATIC
DISORDERS
Professor Peter Holt
University of Bristol
Department of Clinical
Vetrerinary Science
Langford house
Langford
Bristol BS40 5DU
UK
Peter.holt@bristol.ac.uk
Problems affecting the canine prostate include
benign enlargement (hyperplasia/metaplasia),
prostatitis (acute or chronic), abscessation,
prostatic cysts, neoplasia, idiopathic haemorrhage
and displacement into ruptures or hernias.
The clinical signs in dogs with prostate
disease include haematuria, dysuria, urinary
incontinence, dyschezia, pain and weight loss.
These signs are not pathognomonic and so must
be differentiated from similar signs due to non-
prostatic disorders.
Once it is determined that the signs are
associated with a prostatic condition, the
nature of that condition should be determined.
Useful differential features are that only acute
prostatitis (+ abscessation) and neoplasia are
painful conditions; prostatic abscesses, cysts
and tumours result in asymmetrical prostatic
enlargement; in some dogs with prostatic tumours
a small, irregular, painful prostate is present.
Prostate cancer is also one of the few prostate
conditions to affect castrated dogs. Indeed, some
authors believe prostate cancer to have a higher
prevalence in castrated versus entire animals.
Apart from clinical examinations, useful
investigative techniques include contrast
radiography (especially retrograde positive
contrast urethrocystography), ultrasonography,
fine needle aspirates and biopsies, cytology and
histology.
Prostatic hyperplasia responds to oestrogen (or
anti-androgen) therapy and more permanently, to
castration. Prolonged oestrogen therapy is contra-
indicated since squamous metaplastic prostatic
enlargement may result. Most prostatic tumours
are malignant and the prognosis is hopeless;
prostatectomy is not to be recommended in the
author’s view although some palliation may be
obtained in some animals using tube cystostomies,
transurethral debulking and urethral stenting and/
or non-steroidal anti-inflammatory drugs such as
piroxicam or metacam. Prostatitis may respond
to antibiotics and castration but abscesses and
Back to contents
U
cysts require surgical drainage. The prognosis
associated with prostatic cysts and abscesses
is guarded and no one form of treatment
(marsupialisation, drainage procedures, partial
or complete prostatectomy) is 100% successful.
Mild cases may respond to castration and repeated
needle drainage. Omentalisation of prostatic
abscesses has been used with good results. This
may be combined with partial resection of the
prostate. A biopsy should always be taken during
surgery since a proportion of prostatic cysts and
abscesses have a carcinoma of the lining.
Further Reading
ATALAN, G., HOLT, P.E. & BARR, F.J. (1999)
Ultrasonographic estimation of prostate size in
normal dogs and relationship to bodyweight and
age. J. small Anim. Pract. 40, 119-122.
ATALAN, G., BARR, F.J. & HOLT, P.E. (1999)
Comparison of ultrasonographic and radiographic
measurements of canine prostate dimensions.
Vet. Radiol. Ultrasound 40, 408-412.
BOLAND, L.E., HARDIE, R.J., GREGORY,
S.P. & LAMB, C.R. (2003) Ultrasound-guided
percutaneous drainage as the primary treatment 2006 World Congress WSAVA/FECAVA/CSAVA
for prostatic abscesses and cysts in dogs.
J. Am. Anim. Hosp. Ass. 39, 151-159.
BRAY, J.P., WHITE, R.A.S. & WILLIAMS,
J.M. (1997) Partial resection and omentalisation:
a new technique for management of prostatic
retention cysts in dogs. Vet. Surg. 26, 202-209.
CANEY, S.M.A., HOLT, P.E., DAY, M.J.,
RUDORF, H. & GRUFFYDD-JONES, T.J.
(1998) Prostatic carcinoma in two cats. J. small
Anim. Pract. 39, 140-143.
GOBELLO, C. & CORRADA, Y. (2002)
Noninfectious prostatic diseases in dogs. Comp.
Contin. Ed. Pract. Vet. 24, 99-107.
HAYASHI, K. & HARDIE, R.J. (2003) Use
of cystostomy tubes in small animals. Comp.
Contin. Ed. Pract. Vet. 25, 928-934.
791
 U
HOLT, P.E. (1994) A Color Atlas and Text of
Small Animal Urology. Mosby-Wolfe, London.
HOLT, P.E. & WHITE, R.A.S. (2000) Prostatic
cysts and abscesses in the dog: treatment options
Veterinary International 12, 11-18.
LIPTAK, J.M., BRUTSCHER, S.P., MONNET, E.,
DERNELL, W.S., TWEDT, D.C., KAZMIERSKI,
K.J., WALTER, C.U., MULLINS, M.N., LARUE,
S.M. & WITHROW, S.J. (2004) Transurethral
resection in the management of urethral and
prostatic neoplasia in 6 dogs. Vet. Surg. 33, 505-
516.
MULLEN, H.S. et al (1990) Results of surgery
and postoperative complications in 92 dogs
treated for prostate abscessation by a multiple
2006 World Congress WSAVA/FECAVA/CSAVA
Penrose drain technique. J. Am. Anim. Hosp.
Ass. 26, 369-379.
WEAVER, A.D. (1977) Transperineal punch
biopsy of the canine prostate gland. J. small
Anim. Pract. 18, 573-577.
WHITE, R.A.S. & WILLIAMS, J.M. (1995)
Intracapsular prostatic omentalisation: a new
technique for management of prostatic abscesses
in dogs. Vet. Surg. 24, 390-395.
WILLIAMS, J. & NILES, J. (1999) Prostatic
disease in the dog In Pract. 21, 558-575.

792
Back to contents

U - Nephrology & Urologyt
CLINICAL EVALUATION OF THE KIDNEYS
Scott Brown, VMD, PhD,
DACVIM
Associate Dean for Academic
Affairs
Josiah Meigs Distinguished
Professor and Head
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
sbrown@vet.uga.edu
Katie Surdyk, DVM
Internal Medicine Resident
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
ksurdyk@vet.uga.edu
The clinical assessment of the urinary tract
generally focuses separately upon (i) identifying
the presence of a disease and (ii) evaluating
the effects of a disease process upon function
of the tract. Thus, renal structure and function
must be evaluated separately as they are often
not clearly related. Tests performed to detect
the presence of structural change affecting the
kidneys include urinalysis, imaging studies, and
renal biopsy. The impact of a disease process
on renal function, however, is generally assessed
by tests that evaluate glomerular filtration rate
(e.g., measurement of serum concentrations of
creatinine and blood urea nitrogen or specialized
tests to estimate glomerular filtration rate and renal
blood flow), glomerular permselectivity (e.g.,
measures of proteinuria), and by consideration of
renal solute handling and urinary concentrating
ability.
Evaluating glomerular function: Glomerular
filtration rate (GFR)
Massive amounts of glomerular filtrate are
formed continuously, necessitating energy
expenditure and complex carrier processes as
most filtered solutes and water are reabsorbed in
a futile cycle. The GFR amounts to approximately
115 liters/day in a 20 kg dog, nearly 20 times the
dog’s extracellular fluid volume. Still, the central
measure of renal function is an evaluation of
GFR, largely because formation of glomerular
filtrate is the primary event that drives urine
formation and nitrogenous waste excretion.
Back to contents
U
Cathy Brown, VDN, PhD,
DACVP
Profesor
Department of Pathology
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
cabrown@vet.uga.edu
Although measurement methods will alter exact
values, normal ranges for GFR are generally
3.5 – 4.5 ml/min/kg body weight in dogs and
2.5 – 3.5 ml/min/kg body weight in cats.
Assessing GFR: Measurement of urinary
clearance
The ideal measure of renal function is the
determination of GFR via a urinary clearance
procedure in which a timed, total collection of
urine is used for the standard clearance formula:
C = (Uv X Uc)/Pc
Where C = clearance (ml/minute), Uv is urine
flow rate (ml/minute), Uc is concentration of
the solute in urine, and Pc is concentration
of solute in plasma. As intraspecies GFR is 2006 World Congress WSAVA/FECAVA/CSAVA
positively related to body mass and surface area,
the clearance is usually expressed per kg body
weight as noted above.
Inulin, a fructose polymer that is freely filtered,
not metabolized, and is neither reabsorbed nor
secreted, is often used in the research laboratory
for measurement of GFR (urinary inulin
clearance). Urinary inulin clearance determined
by the above formula from timed collection of
urine following parenteral administration of
inulin is the gold standard for measurement of
GFR in dogs, cats, people, and other species. An
alternative endogenous marker of GFR is urinary
clearance of creatinine. However, all urinary
clearance measurements require an indwelling
urethral catheter and considerable technical time
and expertise. While any clinic can utilize these
793
 U
procedures, these limitations generally restrict the
clinical application of urinary clearance testing.
Assessing GFR: Measurement of plasma
clearance
Clearance from plasma of a variety of
substances, such as iohexol, determined from
serial determinations of plasma concentration of
the indicator substance is technically easier than
urinary clearance determination and may be used
to estimate GFR. For these procedures, a known
amount of an indicator substance is injected
intravenously and the blood concentration of
the substance is then determined at various
intervals thereafter. Pharmacokinetic models
are then employed to estimate GFR from
calculated plasma clearance of the test substance.
Plasma clearance procedures do not require the
collection of urine, substantially reducing the
technical difficulties of measurement of GFR by
urinary clearance procedures. Such techniques
may provide a more reliable measure of GFR
than determination of plasma concentration of
creatinine and BUN, but they are clearly less
reliable than urinary clearance procedures.
Assessing GFR: Serum creatinine and blood urea
nitrogen
Despite the increased utility of urinary and
plasma clearance determinations to estimate
GFR, clinical assessment of adequacy of renal
function generally focuses upon measurement
of plasma concentrations of creatinine and BUN.
These compounds provide an index of the level of
GFR and thus are markers to detect deterioration
of renal function.
Urea is the product of the hepatic urea cycle, being
involved in amino acid metabolism and nitrogen
excretion. Urea is passively filtered through
the renal glomeruli. Because some segments
of the tubular epithelium are permeable to urea,
2006 World Congress WSAVA/FECAVA/CSAVA
urea may exit or enter tubular fluid, passively
recycling during the urine concentrating process.
Thus, the BUN reflects not only GFR but also
urea production by the liver and renal tubular
fluid flow rate. Therefore, ingestion of a high
protein meal, gastrointestinal hemorrhage, the
presence of a catabolic state, and dehydration
all will tend to raise BUN even with no change
in GFR. In contrast, hepatic insufficiency, low
protein diets, anabolic states, and polyuria will
tend to lower BUN independent of changes
in GFR. These important extrarenal factors
complicate the interpretation of BUN values.
Muscle cells take up creatine produced by
the liver, which then undergoes irreversible
decomposition to creatinine. Creatinine is
excreted by the kidneys through filtration in
794
Back to contents
dogs and cats and also by a small amount of
proximal tubular secretion in dogs. Creatinine
production will be affected by lean muscle
mass, and thus there are trends among gender,
age, and breed that alter plasma concentration
of creatinine. However, this is rarely taken into
account in veterinary medicine. Nomograms
for determining normal ranges for plasma
creatinine concentration in people consider these
and other factors. Furthermore, the presence
of noncreatinine chromogens in the plasma of
normal dogs and cats complicates interpretation of
plasma concentrations of creatinine, particularly
with mild increases.
The pattern of change in the reciprocal of serum
creatinine (1/[creatinine]) over time has been used
to identify a temporal pattern of renal function
in animals with chronic renal failure.1 The
limitations of measurement of serum creatinine
remain, and although some affected animals have
a linear decline in this value (i.e., 1/[creatinine])
over time, others do not. Utility of this ratio has
been questioned because of increasing extrarenal
creatinine catabolism in end-stage kidney disease
and poor correlation between rate of change of
GFR and this reciprocal.
Evaluating glomerular function: Permselectivity
The glomerular filtration barrier is composed of
glomerular capillary endothelial cells, a negatively
charged basement membrane, and podocyte slit
membranes. This barrier serves to allow water
and electrolytes to freely traverse into the urinary
space, while preventing macromolecules from
leaving the plasma. Loss of normal selectivity
of the glomerular filtration barrier (loss of
permselectivity) can be identified by the presence
of proteinuria, using urine dipstick evaluation or
by quantitative assessment of proteinuria. In
veterinary medicine, determination of the urine
protein-to-creatinine ratio is frequently a useful
adjunctive measurement. The urine protein-
to-creatinine ratio is calculated as the urine
concentration of protein divided by the urine
concentration of creatinine, with both expressed
as mg/100 mL of urine, providing a useful
method for semi-quantitative assessment of urine
protein excretion. It should be remembered that
any leakage of plasma protein into the urine
(e.g., hematuria, traumatic cystocentesis, and
urinary tract inflammation of any kind) often
dramatically increase the ratio. Values for the
urine protein-to-creatinine ratio, which vary
somewhat depending upon analytical methods
employed, are generally < 0.5 in normal dogs
and cats. Disruption of the glomerular filtration
barrier, such as that observed with glomerular
amyloidosis or glomerulonephritis, may cause

the ratio to rise several-fold, and the ratio will
occasionally exceed 15.
Assessing renal tubular function: Electrolyte and
mineral imbalances
Tubular functions may have a dramatic impact on
surgical patients through consequent electrolyte
disturbances. Kidney disease is associated with
a variety of disorders of mineral and electrolyte
balance. These are most readily assessed with
routine plasma biochemical determinations. As
an adjunct specifically for evaluating difficult
cases of hypokalemia, the fractional excretion
(fractional clearance) of potassium can be
determined from a single urine sample as:
FE K+ = 100% X (UK X Pcr)/Ucr X PK
Where FE K+ is fractional excretion (or clearance)
of potassium, UK and PK are the concentrations of
potassium in the urine and plasma respectively,
Ucr and Pcr are the concentrations of creatinine
in the urine and plasma respectively. This
determination can have utility when the excretion
rate is high (>20-25%) for potassium in the face
of hypokalemia (if evaluated prior to potassium
supplementation). Fractional clearances can be
calculated for any solute but interpretation is often
problematic. Except in specific circumstances,
the measurement of urinary electrolyte clearances
(fractional excretion rates) or urine solute
concentrations adds little to the information
provided by serial biochemical determinations
and other routine clinical observations.
Assessing renal tubular function: Urinary
concentrating ability
A urinary concentrating defect is a frequent
consequence of diseases of the kidneys, and it may
be the only clinically identifiable consequence of
renal disease in some patients. Urine specific
gravity will vary considerably in animals with
normal renal function, particularly when fluid
therapy and/or water intake vary. Thus, any value
for urine specific gravity between 1.001 and
1.070 may be “normal” and should be interpreted
Back to contents
U
in the context of therapy, hydration status, and
other clinical information. In this regard, a
urinary concentrating defect in dogs and cats is
generally assumed to be present whenever urine
specific gravity is inappropriately below 1.035
(i.e., in the presence of clinical dehydration).
References
1. Allen TA, et al: A technique for estimating
progression of chronic renal failure in the dog. J
Am Vet Med Assoc 190: 866, 1987.
2. Brown S: Evaluation of chronic renal disease:
A staged approach. Compendium Contin Educ
21: 752, 1999.
3. Brown SA: Evaluation of a single injection
method for estimating glomerular filtration rate
in dogs with reduced renal function. Am J Vet
Res 55: 1470, 1994.
4. Brown SA, et al: Evaluation of a single
injection method, using iohexol, for estimating
glomerular filtration rate in cats and dogs. Am J
Vet Res 57: 105, 1996.
5. Center S, et al: Clinicopathologic, renal
immunofluorescent, and light microscopic
features of glomerolonephritis in the dog: 41
cases (1975-1985). J Am Vet Med Assoc 190:
81, 1987.
6. DiBartola S, et al: Clinicopathologic findings
associated with chronic renal disease in cats: 74
cases (1973-1984). J Am Vet Med Assoc 190:
1196, 1987.
7. DiBartola S: Clinical approach and laboratory
evaluation of renal disease. In: Ettinger S and
Feldman E (eds) Textbook of Veterinary Internal
Medicine. WB Saunders, Philadelphia, 2000, p
1600.
8. Finco DR, et al: Simple, accurate method for
clinical estimation of glomerular filtration rate in
the dog. Am J Vet Res 42: 1874, 1981.
2006 World Congress WSAVA/FECAVA/CSAVA
9. Heinne R, Moe L: Pharmacokinetic aspects of
measuremetn of glomerular filtration in the dog:
A review. J Vet Int Med 12: 401, 1998.
795
 U
U - Nephrology & Urology
MEDICAL MANAGEMENT OF CHRONIC KIDNEY DISEASE
Scott Brown, VMD, PhD,
DACVIM
Associate Dean for Academic
Affairs
Josiah Meigs Distinguished
Professor and Head
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
sbrown@vet.uga.edu
Katie Surdyk, DVM
Internal Medicine Resident
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
ksurdyk@vet.uga.edu
Chronic kidney disease (CKD)
CKD in dogs and cats generally progresses
along a continuum from an initial nonazotemic
stage to end-stage uremia. As veterinarians, we
are obligated to address the specific problems
and patient needs that characterize the animal’s
disease, and this varies from stage to stage.
The International Renal Interest Society has
proposed a classification system for CKD which
facilitates this staged approach to CKD in dogs
(Table 1) and cats (Table 2). This classification
scheme is based on the use of serum creatinine
concentration to estimate degree of decline of
GFR caused by the kidney disease. The IRIS
proposal recognizes that the degree of azotemia
2006 World Congress WSAVA/FECAVA/CSAVA
in cats is not synonymous with that in dogs. This
classification system employs 4 stages as Stage 1:
Nonazotemic CKD disease, Stage 2: Mild renal
azotemia, Stage 3: Moderate renal azotemia, and
Stage 4: Severe renal azotemia.
Stage I: Nonazotemic CKD
In the initial stage of CKD, the animal is not
azotemic and generally has no observable clinical
signs!
Stage II: Mild renal azotemia
This stage of CKD occurs when there is sufficient
loss of renal tissue such that azotemia is now
present, usually without clinical signs. During
this stage, slowing progression of the disease is
an important factor. The rate of progression is
often slow in cats (months to years) but erratic
796
Back to contents
Cathy Brown, VDN, PhD,
DACVP
Profesor
Department of Pathology
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
cabrown@vet.uga.edu
and more rapid in dogs (weeks to months).
Therapies to delay.
Stage III: Moderate renal azotemia
This stage reflects the effects of further declines
in GFR and increased likelihood of clinical signs
of advancing CKD. Both progression and uremia
are concerns in this stage.
Stage IV: Severe renal azotemia
Patients in stage generally have clinical signs,
referred to as the uremic syndrome. Prospectively
identifying and alleviating these complications is
critical in this stage.
Staged Diagnostic Approach to CKD
In early CKD (Stages I and II), it is important
to try to establish a diagnosis of the disease
that is affecting the kidney, herein referred
to as the “renal evaluation”. This generally
includes serum biochemistry panel, hematology,
urinalysis, specific assessment of proteinuria,
renal imaging studies, and ideally also includes
specialized renal function tests and a renal
biopsy. The goal in these early stages is to
identify the renal disease that is present and to
characterize its severity.
There is believed to be a final common pathway
of progression of renal disease that begins during
stage II or III in many animals. As the disease
progresses on the pathway, the structural and
functional changes observed tend to be similar
across specific renal diseases.

A second important diagnostic goal is to
determine the rate of progression of the disease
(“Characterization of Progression “). This will
vary with the disease process, species, and
individual patient. This is an important task
for the attending veterinarian as efforts to slow
the progression of the disease depend upon an
understanding of the rate of progression in the
animal. Some diseases progresses very rapidly,
other slowly, still others will be stable for very
prolonged periods of time. Understanding the
rate of progression in an individual patient will
allow the judicious use of intervention.
In latter stage II and stage IV, the clinical
manifestations of the uremic syndrome (i.e.,
biochemical and clinical abnormalities due to
severe renal dysfunction) are important. It is
critical that a diagnostic plan be formulated
to identify these problems in their incipient
phases (“Patient Evaluation”). These problems
include, for example, disorders of potassium,
phosphorous, calcium and acid-base homeostasis,
anemia, systemic hypertension, weight loss, and
gastrointestinal abnormalities.
Staged Therapeutic Approach to CKD
In the early stages of CKD, institution of
treatment for any identified renal disease is a
goal (“Specific Therapy”). If the identity of
U
the disease is known (e.g., pyelonephritis), this
therapy may be the critical (e.g., appropriate
antibiotic therapy).
Further therapeutic concerns include therapy
designed to slow the progression of renal disease
(“Renoprotective Therapy”), such as dietary
modification (e.g., dietary omega-3 PUFA
supplementation) or the use of antihypertensive
agents with specific intrarenal effects (e.g., ACE
inhibitors).
In the latter stages, some of these complicating
factors, such as electrolyte disorders and anemia
are readily identified by laboratory assessment
of the patient and should be treated on an
individualized basis (“Symptomatic Therapy”).
References
1. Brown SA, Barsanti J, Finco DR.
Pathophysiology and management of progressive
renal disease in dogs. Brit Vet J 1996; 152: 1-24.
2. Brown SA: Evaluation of chronic renal
disease: A staged approach. Compend on Contin
Educ 1999; 21: 752-763.
3. Finco DR, Brown SA, Brown C, Crowell W,
Copper T, Barsanti J. Progression of chronic
renal disease in the dog. J Vet Int Med 1999; 13:
516-528.

Table 1: IRIS* Classification of Canine Chronic Kidney Disease (CKD)

Stage I ii iii iv
Non-azotemic Mild renal Moderate renal Severe renal
CKD azotemic azotemia azotemia
Creatinine:
(mmol/L) < 125 125 to 180 181 to 440 >440
(mg/dl) <1.4 1.4 – 2.0 2.1 to 5.0 >5.0
*IRIS: International Renal Interest Society
2006 World Congress WSAVA/FECAVA/CSAVA

Table 2: IRIS* Classification of Feline Chronic Kidney Disease (CKD)

Stage I ii iii iv
Non-azotemic Mild renal Moderate renal Severe renal
CKD azotemic azotemia azotemia
Creatinine:
(mmol/L) < 140 140 to 250 251 to 440 >440
(mg/dl) <1.6 1.6 – 2.8 2.9 to 5.0 >5.0
*IRIS: International Renal Interest Society

797
Back to contents
 U

Figure 1: Diagnostic focus in different stages of chronic kidney disease (CKD)

2006 World Congress WSAVA/FECAVA/CSAVA

Figure 2: Therapeutic focus in different stages of chronic kidney disease (CKD)

798
Back to contents

U - Nephrology & Urology
DIAGNOSIS AND TREATMENT OF SYSTEMIC HYPERTENSION
Scott Brown, VMD, PhD,
DACVIM
Associate Dean for Academic
Affairs
Josiah Meigs Distinguished
Professor and Head
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
sbrown@vet.uga.edu
Katie Surdyk, DVM
Internal Medicine Resident
Department of Small Animal
Medicine and Surgery
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
ksurdyk@vet.uga.edu
Overview
The principal function of the cardiovascular
system is to generate the appropriate amount
of intravascular pressure in order to assure
adequate tissue perfusion. In clinical practice,
we can measure pressure within systemic arteries
(commonly referred to as blood pressure or BP)
or pressure within central systemic veins (central
venous pressure). While the latter parameter is
most well correlated with body fluid volume
status, it is the arterial pressure that served as
the driving force for tissue blood flow. As with
most physiological parameters, control systems
normally regulate BP within an appropriate
range and this range is referred to as normal BP.
If BP falls too low (i.e., systemic hypotension)
organ perfusion may be inadequate; if it rises too
high (i.e., systemic hypertension) organs may be
overperfused or suffer barotrauma.
Systemic hypertension (i.e., high pressure within
systemic arteries) is often observed in dogs
or cats with kidney disease, hyperthyroidism,
as well as other metabolic conditions. To
properly manage these metabolic conditions,
it has becoming increasingly important for
veterinarians to measure BP. Further, a diagnosis
of systemic hypertension should always be based
upon determination of systemic arterial blood
pressure. Indiscriminate use of antihypertensive
agents without reliable measurements of BP
should be avoided.
Back to contents
U
Cathy Brown, VDN, PhD,
DACVP
Profesor
Department of Pathology
College of Veterinary Medicine
University of Georgia
Athens, GA 30602 USA
cabrown@vet.uga.edu
Patient Selection
While it is possible to measure BP in all clinical
patients, currently there is not sufficient rationale
to do so in veterinary medicine. Hypotension
may be present in anesthetized animals as well as
those with suspected or confirmed cardiovascular
diseases, such as heart failure, arrhythmias,
shock, or excessive hemorrhage. Hypertension is
often suspected in dogs and cats that present with
clinical diseases associated with hypertension or
with clinical findings compatible with end-organ
injury from high BP (Table 1). Because of the
high prevalence of certain occult diseases in
elderly patients, such as chronic kidney disease,
the routine screening of geriatric dogs and cats is
an appropriate consideration. We will focus upon 2006 World Congress WSAVA/FECAVA/CSAVA
the measurement of BP in conscious animals
as would be done in screening for the presence
of systemic hypertension. The same general
principles apply to the diagnosis of hypotension
in anesthetized or critical care patients as well.
Methods of measurement
Blood pressure may be measured by either
direct or indirect methods. While direct blood
pressure measurement is the “gold standard”,
it is technically difficult in unsedated dogs
and cats, may be painful, and complications,
such as hematoma formation, are more likely
to develop. The indirect techniques are more
readily applicable to a clinical setting, as they
require less restraint and are technically easier to
perform.
799
 U
Indirect methods of blood pressure measurement
include auscultatory, ultrasonic Doppler,
oscillometric, and plethysmographic devices
(Table 2).
Blood pressure measurement technique
You should provide an environment that is quiet,
away from other animals and (generally) have
the owner present. You should allow for a quiet
equilibration time for the animal in this room of
5-15 minutes. The same individual (preferably a
technician with calm demeanor) should perform
all BP measurements following a standard,
written protocol. Measurements should be
obtained only in a patient that is calm, minimally
restrained, and motionless. Regarding choice of
equipment, it is perhaps most critical to utilize
an indirect device in which the operator has
experience and confidence (often developed
by practice on normal animals presented for
vaccination).
Select a cuff with a width that is approximately
30-40% of the carefully measured circumference
of the chosen site for cuff placement. Choice of site
depends on preference of the operator and patient
comfort. Generally, the median artery is used for a
Doppler device and the brachial (cat) or coccygeal
(dog) artery for the oscillometric devices.
The operator should obtain at least 5 - 7 consistent
measurements (<20% variation in systolic
readings) from the first cuff placement. The
cuff should be removed and replaced with
5 - 7 consistent measurements being from this
second cuff placement. This cuff repositioning
should be repeated, as often as necessary, until
results from cuff sites agree.
The first value from each cuff positioning
should be discarded and then an average of all
other values calculated. An alternate approach
is to average all values obtained after the
first, highest and lowest pressure readings are
2006 World Congress WSAVA/FECAVA/CSAVA
discarded. The overall average is then taken as
the final value. If in doubt, repeat measurement
session on another day or later the same day. A
diagnosis of systemic hypertension should never
be based solely on a single BP measurement
session. Measuring BP is complex interaction
among technician(s), animal, owner, and device
and will require at least 15 minutes in the best of
circumstances (45 minutes or more in difficult
cases).
What is normal BP?
This is actually a very difficult question. The
Veterinary Blood Pressure Society has suggested
BP values should be interpreted in light of
clinical and laboratory findings. The species,
gender, and age may also be considered in
800
Back to contents
evaluating a patient’s BP. The Society suggests
that elevation of BP in a patient produces a risk
which is directly related to the severity of the
hypertension (Table 3). Thus systolic/diastolic BP
(mmHg) that exceeds 150/95 pose some risk for
hypertensive end-organ injury and intervention
should be considered; values above 180/120 pose
a high risk and intervention (e.g., administration
of a pharmacological antihypertensive agent)
is clearly indicated. Similarly systolic/diastolic
BP (mmHg) below 100/60 poses some risk for
reduced organ perfusion; values below 70/40
pose a high risk that mandates intervention (e.g.,
IV fluid therapy and/or reduction of dosage of
anesthetic agent).
ANTIHYPERTENSIVE THERAPY: GENERAL
Treatment is generally by sequential trials.
Generally, dosage adjustments or changes
in treatment should be instituted no more
frequently than every 2 weeks, unless extreme
hypertension necessitating emergency treatment
is present. When using pharmacological agents,
a wide range of dosages should be considered
with initial dosages at the low end of the
range. If an agent or combination of agents
is incompletely effective, the dosage(s) may
increased or additional agents added. Often,
especially in dogs, multiple agents will be used
concurrently.
The diagnosis of hypertension associated
with chronic renal disease necessitates life-
long antihypertensive treatment with periodic
dosage adjustments based upon blood pressure
measurements. Hypertension associated with
hyperthyroidism and hyperadrencotorticism
can be expected to resolve within 1-3 months
following effective treatment of the underlying
condition, unless chronic renal failure is also
present. Occasionally, dogs with well controlled
hyperadrenocorticism remain hypertensive. In
other patients, the duration of treatment cannot
be predicted, though it may be required life-
long. Periodic dosage adjustments based upon
blood pressure measurements are indicated.
It is usually not possible to restore blood pressure
to normal values when treating a hypertensive
animal. It should be the veterinarian’s
goal to lower the blood pressure to within
25-50 mmHg of the normal ranges for blood
pressure, thus lowering pressure (systolic/
diastolic) to < 170mmHg/100mmHg. If an
oscillometric unit is employed, the systolic, mean,
or diastolic blood pressure can be used to judge
effectiveness of therapy. If a doppler ultrasonic
device is used, the systolic blood pressure should
be used to monitor effectiveness of treatment.
In general, the doppler ultrasonic device will

be most reliable in cats and either unit will
provide equivalently reliable results in dogs.
DIETARY THERAPY
Though poorly studied, the usual recommendation
is to initially institute a low sodium diet which
provides <0.25% sodium on a dry weight
basis. Frequently, dietary sodium restriction is
employed as a first step in order to enhance the
efficacy of pharmacological agents. In animals
with chronic renal disease and hypertension, it
may more important to maintain adequate caloric
rather than to insist that a low sodium diet be
fed.
Obesity can elevate systemic arterial pressure
in human beings and dogs and, perhaps, in cats.
Consequently, weight loss is desirable in obese,
hypertensive animals.
PHARMACOLOGICAL AGENTS
Medical treatment of hypertension in dogs
and cats has, until recently, been extrapolated
from human protocols. Recommendations for
medical therapy have included vasodilators,
beta-blockers, and diuretics; these agents are
generally given in concert with dietary sodium
restriction. In human beings with systemic
hypertension and renal disease, vasodilator
therapy is the preferred initial choice because
of the renoprotective effects of certain classes
of these agents (angiotensin converting enzyme
inhibitors and calcium channel).
An inhibitor of angiotensin converting enzyme
U
(e.g., 0.5 mg enalapril/kg orally every 12 hours or
0.25-0.5 mg benazepril/kg every 12-24 hours) will
lower blood pressure inmany hypertensive dogs.
In cats, the role of the renin-angiotensin system
in the maintenance of systemic hypertension has
been questioned and though less effective in cats,
a higher dosage (1-2 mg enalapril/kg orally evey
24 hours) may prove efficacious in hypertensive
cats.
Some drugs classified as calcium channel
antagonists reduce total peripheral resistance,
leading to a decrease in blood pressure.Amlodipine
besylate, a long-acting dihydropyridine calcium
antagonist, has been used successfully as a single
agent in hypertensive cats at a dosage of 0.625
mg/cat orally every 24 hours.14 Larger cats (>4
kg) often require 1.125 mg orally every 24 hours.
Blood pressure decreases significantly during
amlodipine treatment, and significant adverse
effects (i.e., azotemia, hypokalemia, weight loss)
are not frequently identified. Because amlodipine
has a slow onset of action, adverse effects such
as hypotension and loss of appetite are usually
avoided. In dogs with chronic renal disease, a
dosage of 0.05 mg/kg given orally once daily
lowered blood pressure in initial pharmacokinetic
trials. In many hypertensive dogs, though,
amlodipine appears to be less effective, even at
dosages as high as 1 mg/kg twice daily. However,
dosages utilized in hypertensive dogs should
generally be in the range of 0.05 - 0.25 mg/kg
once daily.

Table 1: Indications for screening dogs or cats for systemic hypertension

Acute or chronic kidney disease
Hyperthyroidism (especially cats)
2006 World Congress WSAVA/FECAVA/CSAVA
Hyperadrenocorticism
Diabetes mellitus (especially dogs)
Hyperaldosteronism
Pheochromocytoma
Marked obesity
Geriatric patients (dogs and cats > 10 years of age)
Clinical findings compatible with hypertensive end-organ injury such as:
• blindness, retinal vascular tortuosity or hemorrhage, retinal detachment, hyphema
• seizures, ataxia, sudden collapse
• dyspnea, unexplained left ventricular hypertrophy or gallop rhythm
• proteinuria or low urine specific gravity

801
Back to contents
 U
Table 2: Examples of indirect blood pressure measurement devices in use in dogs and cats
Device
Cardell Model 9401,2,3
Dinamap Model 8300
Jorgensen Model J5373
Memoprint, Memodiagnostic
Parks Model 811-B
Vet-Dop
VetSpecs Model BP2,3
Manufacturer Device Type
Sharn Veterinary Inc. Oscillometry
(800) 325-3671
http://www.sharnvet.com
No longer available Oscillometry
Jorgensen Labs Doppler ultrasonography
(800) 525-5614
http://www.jorvet.com
S & B medVET Oscillometry
http://www.submedvet.de
Parks Medical Electronics Doppler ultrasonography
(800) 547-6427
http://www.parksmed.com
Vmed Technology Doppler ultrasonography
Inc (800)926-9622
http://www.vmedtech.com
VetSpecs Medical Systems Pressure plethysmography
(800) 599-2566
http://www.vetspecs.com

Table 3. ACVIM Hypertension Panel: Classification of blood pressure levels (mmHg) in dogs and
cats based on risk for future target-organ damage (TOD)1,2
Systolic Diastolic Risk of Future TOD
<150 <95 Minimal
150-159 95-99 Mild
160-179 100-119 Moderate
≥180 ≥120 Severe
1
BP measurements should always be interpreted in light of the condition of the animal. Factors to
consider include those that may alter cardiovascular control mechanisms (e.g., excitement, anxiety,
2006 World Congress WSAVA/FECAVA/CSAVA

and/or pharmacological agents) as well as those that may affect cardiovascular function directly (e.g.,
dehydration and/or pharmacological agents).
2
There are breed, gender and age variations that should be considered in evaluating BP measurement.
Known effects are generally small, except for the increased BP commonly observed in Sight hounds
(approximately 15 mmHg).

References Bodey AR, Michell AR: Epidemiological study

Egner B, Carr A, Brown S: Essential facts of of blood pressure in domestic dogs. J Small Anim
blood pressure in dogs and cats, Vet Verlag, Pract 1996; 37: 116-25.
Babenhausen, Germany, 2003.
Littman MP: Spontaneous systemic hypertension
Brown SA, Henik RA: Diagnosis and treatment in 24 cats. J Vet Intern Med 1994; 8: 79-86.
of systemic hypertension. Vet Clin North Am
Small Anim Pract 1998; 28: 1481-94. Sansom J, Rogers K, Wood JL: Blood pressure
Jacob F, Polzin DJ, Osborne CA, et al: Association assessment in healthy cats and cats with
between initial systolic blood pressure and risk hypertensive retinopathy. Am J Vet Res 2004; 65:
of developing a uremic crisis or of dying in dogs 245-52.
with chronic renal failure. J Am Vet Med Assoc
2003; 222: 322-9.
802
Back to contents
 U
U - Nephrology & Urology
FELINE LOWER URINARY TRACT DISEASE
David Senior
Professor and Head, Veterinary
Clinical Sciences, Louisiana State
University.
Department of Veterinary Clinical
Sciences
School of Veterinary Medicine
Louisiana State University
Baton Rouge, LA 70803
USA

ETIOLOGY pollakiuria, stranguria, hematuria and urination

Feline lower urinary tract disease (FLUTD) in inappropriate places. FLUTD is one of most
includes inflammatory diseases of the lower common reasons for cats to be presented to
urinary tract and non-inflammatory conditions veterinary hospitals. In various surveys, the
that cause urination in inappropriate places. Both incidence of the syndrome has usually been
male and female cats are affected but mostly about 0.6% in the cat population and 3-13 % of
only male cats develop urethral obstruction. cats presented for veterinary care.
Typical signs in non-obstructed cats include
Table 1: Diagnoses in cats with FLUTD
1981-19851 1993-19952
(Number of cases) (47) (43) (47) (62)
Male Female Male Female
No urethral obstruction % % % %

Idiopathic 79 58 64 65
Urolith 17 40 9 19
Anatomical defect - - 11 10
Behavioral problem - - 13 6.5
Urolith and UTI 0 2 0 0
UTI 0.04 0 0.02 0
Neoplasia 0 0 4 0
Data from:
1. Osborne CA et al. Feline lower urinary tract disorders. Definition of terms and concepts. Vet Clin
North Am Small Anim Pract. 1996 Mar; 26(2): 169-79. 2006 World Congress WSAVA/FECAVA/CSAVA
2. Buffington CA et al. Clinical evaluation of cats with nonobstructive urinary tract diseases. J Am Vet
Med Assoc. 1997 Jan 1; 210(1): 46-50.

The etiology of FLUTD was investigated prospectively in two studies a decade apart (Table 1). These
data suggest that non-obstructive FLUTD is phosphorus content and urine acidification caused
most likely to be idiopathic. Identifiable causes by these diets may predispose to formation of
of non-obstructive FLUTD included urolithiasis, calcium oxalate uroliths.
anatomical defects and behavioral problems. Cats with FLUTD tend to urinate in inappropriate
Urinary tract infection and neoplasia were rare. places. However, this sign could be an indication
Urolithiasis is one of the major identifiable causes of a behavioral abnormality. Marking or spraying
of FLUTD. The composition of bladder uroliths is a normal territorial behavior response in cats,
submitted for analysis has recently changed from so urination outside the litter box can be confused
predominantly struvite to mostly calcium oxalate. with FLUTD.
The reason for this change appears to be related Vesicourachal diverticula visible on contrast
to reformulation of commercial diets to prevent cystography have been reported in 25 % of cats
struvite crystalluria. Reduced magnesium and with signs of hematuria, dysuria and urethral
803
Back to contents
 U
obstruction. Clinical evidence suggests that
diseases that induce increased intravesicular
pressure can cause potential diverticula to open
up. Once the underlying condition causing
increased pressure is resolved, the diverticula
disappear. As such, vesicourachal diverticula
appear to be a consequence rather than a cause
of FLUTD.
In most surveys of cats with FLUTD, the incidence
of urinary tract infection is very low, around 3-
4 %. This low incidence may be related to very
effective host defense mechanisms and the high
concentration of urea in cat urine may be a major
contributing factor to resistance. The incidence
of urinary tract infection increases with age
above 10 years. This may be due to loss of urine
concentrating capacity but other factors may be
involved. Also, cats with a perineal urethrostomy
are prone to urinary tract infection.
Bladder cancer is relatively rare in the cat.
Almost all affected animals are older than 5 years,
about 80% are malignant and about 30% are
transitional cell carcinomas.
Many possible etiologies have been proposed
for idiopathic FLUTD including viral infection,
Mycoplasma spp. infection, food allergy, the
presence of toxic metabolites in urine, and a
defect in the protective glycosaminoglycan
(GAG) layer which covers the uroepithelium of
the bladder, mast cell abnormalities, and visceral
pain syndrome.
The discovery of viral particles in the mucus of
urethral plugs is intriguing but the significance is
not yet clear. Several attempts have been made
to implicate mycoplasmas in FLUTD but the
evidence is strongly against their involvement as
a causative agent.
Food allergy has been proposed as a cause
of FLUTD on the basis that elimination diets
appeared to reduce signs in some clinical
situations. Unfortunately, no controlled studies
2006 World Congress WSAVA/FECAVA/CSAVA
have been performed to support or deny this
possibility.
There has been no work performed to confirm
or deny the contention that a toxic metabolite
in urine causes uroepithelial irritation and
inflammation.
Idiopathic FLUTD bears some similarity to the
syndrome in humans called interstitial cystitis.
Both humans and cats demonstrate chronic
ongoing sterile inflammation of the lower
urinary tract, submucosal hemorrhages visible on
cystoscopy after mild bladder distention, reduced
excretion of glycosaminoglycans, increased
bladder mucosal permeability, and infiltration of
mast cells.
Unfortunately the causes of interstitial cystitis
in humans are not known and there is suspicion
804
Back to contents
that the abnormalities observed in both species
may be non-specific stereotypic responses of
the lower urinary tract to a variety of insults.
Proposed causes of interstitial cystitis in humans
have been as fanciful as proposed causes of
FLUTD. Suggestions have included viruses,
fastidious bacteria, deficient protective GAG
layer and psychosomatic. Some veterinarians
have associated episodes of idiopathic FLUTD
with stress. Interesting comparative research
continues on this line of investigation.
CLINICAL SIGNS
Cats with nonobstructive FLUTD have periodic
episodes of urgency, dysuria, urination outside the
litter box, pollakiuria and hematuria. Urination
may be sufficiently painful for cats to vocalize
during urination. The episodes can last for one to
ten days separated by days to weeks of apparent
normalcy.
On physical examination the bladder may be
thickened and sensitive to direct palpation.
Uroliths can be difficult to detect in the bladder
of cats particularly if they are solitary because
crepitus will not be present.
DIAGNOSIS
The history should be carefully assessed
to determine the possibility of behavioral
abnormalities. Careful bladder palpation should
be performed to detect the presence of crepitus
and masses, which may indicate stones or
tumors. The thickness of the bladder wall can
also be assessed.
A problem specific database includes urinalysis,
urine culture, radiographs, ultrasound, cystoscopy,
biopsy, and urolith and crystal analysis.
Urinalysis and culture and sensitivity should be
performed on urine obtained by cystocentesis.
Urine can be collected by caging the cat without
a litter for 2-3 hours, then sedation with ketamine
given at 1-3 mg intravenously. Once the cat is
sedated, an assistant can grasp the urethra
while a cystocentesis is performed. Attempts at
cystocentesis in the fully conscious cat usually
result in reflex micturition as soon as the bladder
is manipulated and collection by cystocentesis
becomes impossible.
Radiographs including double contrast
cystography should be performed to investigate
the possibility of uroliths, tumors and diverticula.
Ultrasound examination can be used instead.
Although not available in many practice
settings, cystoscopy can allow visualization
of submucosal hemorrhages, uroliths, tumors
and diverticula. Biopsy can also be performed
through the cystoscope. Histologic examination
of bladder biopsies can reveal inflammation and
mast cell infiltration.

Mineral analysis of crystals and uroliths should
be performed as appropriate.
MANAGEMENT
The management of urolithiasis and urinary tract
infection is discussed in other sections. Little
is known about treatment of bladder tumors in
cats because they are so rare. Management of
behavioral abnormalities is beyond the scope of
his chapter.
The development of effective management
strategies for idiopathic FLUTD has been
confounded by not knowing the etiology (or
etiologies) and a paucity of controlled studies.
Unfortunately, the waxing and waning nature of
clinical signs leads investigators to conclude that
certain treatments are successful when, in fact, a
placebo would have been just as effective.
Feeding canned food instead of dry food seems
to reduce recurrence of idiopathic FLUTD.
Investigators postulated that this effect could
be due increased urine volume associated with
a canned food diet that would dilute toxic
metabolites in urine.
Anticholinergic agents have been suggested
to reduce bladder spasticity and increase the
time between urination in cats with FLUTD.
Propantheline given at 0.2-0.4 mg/kg po sid or
bid has been suggested but controlled studies to
determine efficacy are lacking.
Antiinflammatory agents such as corticosteroids
U
have been proposed to reduce inflammation
associated with idiopathic FLUTD. A short-term
study indicated that predisolone given at 1 mg/
kg po bid failed to reduce the magnitude and
duration of clinical signs faster than in control
cats. However, long-term studies have not been
performed to see if glucocorticoids have a
preventive effect.
Intravesicular dimethyl sulfoxide (DMSO) is
established as a treatment of interstitial cystitis
in humans. Although intravesicular instillation
of 10-20 mL of 10 % DMSO has been reported
to reduce clinical signs in cats with FLUTD, no
controlled studies have been performed.
In humans with interstitial cystitis, GAGs have
been reported to alleviate clinical signs. The
proposed mechanism of action is to set up a
barrier between potentially irritating urine and the
uroepithelium. There is evidence that the normal
GAG layer is deficient in humans with interstitial
cystitis and similar evidence exists in cats.
Pentosan polysulfate is used in humans. Safety
and efficacy need to be established in cats.
The tricyclic antidepressant, amitriptyline, acts
as an anticholinergic, anxiolytic and analgesic. In
a study of cats severely affected with idiopathic
FLUTD, amitriptyline seemed to reduce clinical
signs for up to a year when given at 5-10 mg po
sid at night. The drug is in popular use at present
and further studies are needed.

2006 World Congress WSAVA/FECAVA/CSAVA

Distension of the bladder associated with PREVENTION

cystoscopy is thought to give humans affected Feeding canned food rather than dry food may
with interstitial cystitis a prolonged symptom- prevent recurrence in some forms of idiopathic
free period. The proposed mechanisms of action FLUTD. Reduction of stress is thought by many
include dissipation of inflammatory mediators to reduce clinical signs in many affected cats.
from nerve fibers in the submucosa of the bladder
and die back of sensory nerves. Whether this REFERENCES
procedure has a beneficial effect in FLUTD has Available on request.
not been established. 805
Back to contents
 U
U - Nephrology & Urology
SUBMUCOSAL COLLAGEN INJECTION OF THE URETHRA FOR
INCONTINENCE
Susi Arnold , Prof. Dr. med. vet.,
DECAR
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
sarnold@vetclinics.unizh.ch
Madeleine Hubler, Dr. med. vet.,
DECAR
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
Urinary incontinence is a common adverse effect
of spaying and is reported in 20% of spayed dogs
(1). The cause is acquired incompetence of the
urethral closure caused by spaying, called urethral
sphincter mechanism incompetence USMI (2). The
pathophysiologic mechanism leading to reduced
urethral closure after spaying is still unknown.
According to the pathophysiology the medical
and surgical treatments aim at improving the
urethral closure. Alpha-adrenergic agonists
such as phenylpropanolamine or ephedrine
hydrochloride are treatments of choice for USMI.
If medical treatment is unsatisfactory, or the effect
diminishes over time, surgical procedures such as
colposuspension (3), urethropexy (4) or endoscopic
2006 World Congress WSAVA/FECAVA/CSAVA
injection of collagen into the submucosa of the
proximal portion of the urethra (5) may be used.
The endoscopic injection of collagen has been
described (5). Via general anesthesia, the dogs
are positioned in dorsal recumbency with the hind
limbs extended cranially. A human cystoscope
(Karl Storz GmbH & Co. KG, 78532 Tuttlingen,
Germany; KARL STORZ Veterinary Endoscopy,
Goleta, CA 93117) is passed into the urethra via
the external orifice. Approximately 1.5 cm caudal
to the neck of the bladder, 3 injections of collagen
(Zyplast, Inamed, Santa Barbara, 93111 California,
USA) are made into the urethral submucosa at 2:00,
6:00, and 10:00 o`clock positions. The deposits
bulge into the urethral lumen and improve urethral
closure at the site of the injections. The procedure
is considered complete when, on viewing through
the cystoscope, the urethral lumen is closed by the
collagen deposits.
806
Back to contents
Iris Reichler, Dr. med. vet.
Clinic for Reproductive Medicine
Vetsuisse-Faculty, University of
Zurich
Winterthurerstr. 260
8057 Zurich
Switzerland
A retrospective study was recently performed
to evaluate the long-term success of endoscopic
injection of collagen as a treatment for USMI
in 40 female dogs (6). Endoscopy was used
for diagnosis and treatment with 3 urethral
submucosal injections of collagen in the proximal
portion of the urethra. In 5 dogs, it was not
possible to pass the cystoscope into the urethra
via the external orifice. Therefore, a laparotomy
and cystotomy were performed for placement of
the collagen. Dogs that had recurrence of urinary
incontinence after surgery were either treated
with phenylpropanolamine (1.5 mg/kg , q 8 h,
Incontex, Dr. Gräub AG, 3018 Bern, Switzerland;
Proin, PRN Pharmacal, Pensacola, FL 32514)
or ephedrine hydrochloride (1.0 mg/kg, q 12 h,
Caniphedrin, G. Streuli & Co. AG, 8730 Uznach,
Switzerland) orally at the recommended dose or
underwent a second collagen injection procedure.
With a follow-up period of 9 to 78 months (mean,
33 months), 27 (68%) dogs were continent for
1 to 64 months (mean, 17 months) after treatment.
In 10 dogs, incontinence improved, and in 6 dogs,
continence was achieved for 9 to 47 months
(mean, 23 months) with additional treatment with
alpha-adrenergic drugs. In 3 dogs, incontinence
was unchanged.
As long as 12 months after treatment, there
was a progressive deterioration in the results in
16 dogs, after which their condition stabilized
(see table). Flattening of the deposits, rather than
resorption, was likely the cause of reoccurrence of
incontinence. Mild and transient adverse effects

developed in 6 (15%) dogs. Long-term success
was satisfactory. In most dogs, the final result was
evident within the first 12 months after treatment.
The success rate in dogs was similar to that
of polytef paste (7), but in contrast to polytef
no foreign body reactions were observed after
collagen injections. In dogs in which there is
only a partial response to the collagen injection,
continence may be achieved by additional use of
phenylpropanolamine, ephedrine hydrochloride,
or both, although these were ineffective before the
injection. It appears that even in treatment-resistant
cases, sympathomimetic substances have an effect
on smooth muscle fibers of the urethra, which is
not clinically apparent without the presence of
collagen deposits.
The incidence of complications was 15%, which is
comparable to that of women (8). However, in dogs
the complications were mild and of short duration.
Urinary retention is a dreaded complication and
Success rate of collagen injection in 40 bitches
success rate at 6 months
after injection
Total number of continent dogs (1 + 2) 33 (83%)
1 continent only because of collagen 27 (68 %)
injection
2. continent with additional medication 6 (15%)
3. incontinence improved with 4 (10%)
additional medication
4. incontinence persistent 3 (7%)**
* at the time of death or end of the study
** were euthanized 3 months after injection
References:
1. Arnold S, Arnold P, Hubler M, et al.
Incontinentia urinae bei der kastrierten Hündin:
Häufigkeit und Rassedisposition. Schweiz Arch
Tierheilkd. 1989; 131: 259–263.
2. Rosin AE, Barsanti JA. Diagnosis of urinary
incontinence in dogs: Role of the urethral
pressure profile. J Am Vet Med Assoc. 1981; 178:
814–822.
3. Holt PE. Urinary incontinence in the bitch due
to sphincter mechanism incompetence: surgical
treatment. J Small Anim Pract. 1985; 26: 237-246.
4. White RN. Urethropexy for the management of
urethral sphincter mechanism incompetence in the
bitch. J Small Anim Pract. 2001; 42: 481-486.
5. Arnold S, Hubler M, Lott – Stolz G, et al.
Treatment of urinary incontinence in bitches by
endoscopic injection of glutaraldehyde cross–linked
collagen. J Small Anim Pract. 1996; 37: 163–168.
6. Barth A, Reichler IM, Hubler M, Haessig M,
Back to contents
U
develops in from 1.9% to 18% of treated women
(8, 9). In the present study this complication was
not observed.
Collagen injection compares well to established
surgical methods for treatment of canine
USMI. After urethropexy, 56% of affected dogs
were continent and 27% had improvement of
incontinence (4). A similar success rate was
observed after colposuspension, with 53% of
the female dogs continent and 38% with marked
improvement (10).
Collagen injection into the submucosa of the
proximal portion of the urethra is a suitable method
for treatment of urethral sphincter incompetence
in female dogs because of the good success rate,
minimally invasive nature of the procedure, and
the risk of adverse effects. However, the initial
result may deteriorate up to 12 months after the
procedure and administration of alpha-adrenergic
substances or re-treatment may be necessary.
final success rate*
26 (65%)
11 (28%)
15 (37%)
7 (17.5%)
7 (17.5%)
Arnold S. Evaluation of long-term effects of
endoscopic injection of collagen into the urethral
submucosa for treatment of urethral sphincter
incompetence in female dogs: 40 cases (1993-
2000). JAVMA. 2005; 226: 73-76. 2006 World Congress WSAVA/FECAVA/CSAVA
7. Arnold S, Jäger P, Di Bartola SP, et al.
Treatment of urinary incontinence in dogs by
endoscopic injection of Teflon. J Am Vet Med
Assoc. 1989; 195: 1369–1374.
8. Stothers L, Goldenberg SL, Leone LF.
Complications of periurethral collagen injection
for stress urinary incontinence. J Urol. 1998;
159: 806–807.
9. Gorton E, Stanton S, Monga A, et al.
Periurethral collagen injection: a long-term
follow-up study. BJU Int. 1999; 84: 966-971.
10. Holt PE. Long-term evaluation of
colposuspension in the treatment of urinary
incontinence due to incompetence of the urethral
sphincter mechanism in the bitch. Vet Rec. 1990;
127: 537–542.
807
 U
U - Nephrology & Urology
COLPOSUSPENSION SURGICAL TECHNIQUE
Professor Peter Holt
University of Bristol
Department of Clinical
Vetrerinary Science
Langford house
Langford
Bristol BS40 5DU
UK
Peter.holt@bristol.ac.uk
Colposuspension is indicated for the treatment
of urinary incontinence due to urethral sphincter
mechanism incompetence in bitches. Urethral
sphincter mechanism incompetence is mainly a
problem of large breeds of dog. Urine leakage
occurs predominantly during recumbency,
probably since intravesical pressure rises when
a bitch’s position changes from standing to
recumbency. A number of factors contribute to
urine leakage in bitches with urethral sphincter
mechanism incompetence. As well as body size
and breed, these include poor urethral tone,
ovariohysterectomy/ovariectomy, a shorter
urethral length than normal (both physical
and functional, allowing for body size) and a
bladder neck located more caudally than normal.
Colposuspension is intended to correct the
position of the bladder neck (although it may also
have a beneficial effect on urethral urodynamic
parameters). If urethral tone is adequate, the
position of the bladder neck does not matter but
in animals with urethral sphincter mechanism
incompetence, a caudally-positioned bladder
neck may be sufficient to tip the balance in
favour of urine leakage, since increased external
pressures on the bladder are not counteracted by
similar pressures on the urethra.
2006 World Congress WSAVA/FECAVA/CSAVA
Accurate diagnosis is essential. It is insufficient
to assume that a spayed, incontinent bitch is
suffering from urethral sphincter mechanism
incompetence without performing adequate
diagnostic investigations to eliminate other
possible diagnoses. These should include
contrast radiography, laboratory examinations
and, if available, urodynamics.
Surgery on juvenile bitches with congenital
urethral sphincter mechanism incompetence
should be deferred until after the bitch’s first or
second oestrus period. The oestrus periods may
result in improvement in urinary continence
control and more than half of affected juvenile
bitches will become continent after their first
oestrus.
In adult bitches, the pros and cons of surgery
versus management with drugs (alpha-
808
Back to contents
adrenergics, oestrogens) should be discussed
with the owners first. Oestrogens should not be
used for long-term control in entire (especially
juvenile) bitches because of possible adverse
feed-back effects on the pituitary gland. In some
juveniles, these effects may be sufficient to
prevent the bitch ever having a normal oestrus
period. In our clinic, colposuspension cures 53%
of cases and improves most of the remainder but
does nothing for 10%. The author’s approach
is to treat younger (less than 8 years of age)
adult bitches surgically in the first instance in
the hope that prolonged use of drugs such as
oestrogens and alpha-adrenergics can be avoided.
Colposuspension is performed on older bitches in
which drug therapy has failed to control urinary
incontinence.
The technique involves loosening the attachments
of the lower urogenital tract to the pelvis (through
a caudal mid-line laparotomy) by breaking down
the pubovesical peritoneal fold and blunt finger
dissection. The vagina is then stretched cranially
and attached, usually using two 0 monofilament
polyamide sutures (each side), to the prepubic
tendon on each side of the urethra. This cranial
stretching of the vagina results in cranial
movement of the urethra and bladder, relocating
the bladder neck to an intra-abdominal position.
Post-surgical complications are few. Since the
surgery involves vaginal stimulation and some
trauma to intrapelvic fascia, some animals are
stimulated to strain, usually immediately after
recovery from the general anaesthetic. This can
be controlled by the administration of appropriate
analgesics pre-, peri- and post-operatively.
Rarely, some bitches find the first defaecation
after surgery to be uncomfortable if the faeces
are firm and bulky. This can be controlled with
stool softeners.
Dysuria may occur immediately post-
operatively. This is rare (less than 3% of cases
in the author’s experiences). It may be due to
vaginal stimulation by the surgery leading to
suppression of the micturition reflex and/or
reflex dyssynergia. Clinical observations and

the response to diazepam suggest that reflex
voluntary dyssynergia is the most likely cause
of dysuria after colposuspension. It appears to be
exacerbated by recent oestrogen therapy and so
any oestrogen therapy should cease at least one
month pre-operatively. Voluntary dyssynergia
usually responds within a few days to diazepam
at a dose of 0.2 mk/kg by mouth two or three
times daily. An indwelling urinary catheter
can be used for a few days if necessary in the
minority of animals which are unable to urinate
at all. A further potential cause of dysuria is
compression of the urethra against the pubis by
the vagina. Care should be taken during surgery
to avoid placement of vaginal sutures too close
to the urethra.
Bitches which are allowed to be very active after
colposuspension may tear the sutures from the
vagina. This is more likely to happen if they
are allowed to run and jump and owners should
be advised of the necessity for restricting the
exercise of their animals to walks on the lead
only for one month after surgery.
Hymen formation and accumulation of vaginal
secretions causing dysuria and/or dyschezia is
an extremely rare, longer-term complication of
colposuspension. It is due to breakdown of a
pre-existing vestibulovaginal stricture during the
operation and subsequent healing of apposing
raw areas of vagina to form a barrier across the
vaginal lumen.
Further Reading
ATALAN, G. HOLT, P.E. & BARR, F.J. (1998)
Ultrasonographic assessment of bladder neck
mobility in continent bitches and bitches with
urinary incontinence attributable to urethral
sphincter mechanism incompetence. American
Journal of Veterinary Research, 59, 67
GREGORY, S.P. & HOLT, P.E. (1992) Effect
of body position on intravesical pressure in the
anaesthetised bitch. Veterinary Record 130, 288-
290.
GREGORY, S.P. & HOLT, P.E. (1993)
Comparison of stressed simultaneous urethral
pressure profiles between anesthetized continent
Back to contents
U
and incontinent bitches with urethral sphincter
mechanism incompetence. American Journal of
Veterinary Research 54, 216-222.
GREGORY, S.P. & HOLT, P.E. (1994) The
immediate effect of colposuspension on resting
and stressed urethral pressure profiles in
anaesthetized incontinent bitches.
Veterinary Surgery 23, 330-340.
HOLT, P.E. (1985) Importance of urethral length,
bladder neck position and vestibulovaginal
stenosis in sphincter mechanism incompetence
in the incontinent bitch. Research in Veterinary
Science, 39, 364-372.
HOLT, P.E. (1985) Urinary incontinence in the
bitch due to sphincter mechanism incompetence:
surgical treatment. Journal of Small Animal
Practice, 26, 237-246.
HOLT, P.E. (1990) Long-term evaluation of
colposuspension in the treatment of urinary
incontinence due to incompetence of the urethral
sphincter mechanism in the bitch. Veterinary
Record, 127, 537-542.
HOLT, P.E. & STONE, E.A. (1998)
Colposuspension for Urinary Incontinence. In
Current Techniques in Small Animal Surgery,
Fourth Edition (Ed. M.J. Bojrab). Williams &
Wilkins, Baltimore. pp. 455-459.
HOLT, P.E. & JONES, A. (2000) In vitro study
of the significance of bladder neck position in
incontinent bitches. Veterinary Record 146, 437-
439.
RAWLINGS, C.A., MAHAFFEY, M.B.,
CHERNOSKY, A.C. & HUZELLA, L. (2000)
Immediate urodynamic and anatomic response
to colposuspension in female Beagles. American
Journal of Veterinary Research 61, 1353-1357.
RAWLINGS, C.A., BARSANTI, J.A.,
MAHAFFEY, M.B. & BEMENT, S. (2001)
Evaluation of colposuspension for treatment of 2006 World Congress WSAVA/FECAVA/CSAVA
incontinence in spayed female dogs. Journal of
the American Veterinary Medical Association
219, 770-775.
809
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

W
WW
– Ani
Animal Welfare

Back to contents

INVITED LECTURES - FULL PAPERS
W – Animal Welfare
OVERVIEW OF CANINE AGGRESSION
Karen L. Overall, MA,VMD,
PhD
Diplomate ACVB
ABS Certified Applied Animal
Behaviorist
Center for Neurobiology and
Behavior
Psychiatry Department - Penn
Med Translation Research
Laboratory
125 S. 30th St.
Philadelphia, PA 19104
overallk@mail.med.upenn.edu
http://psych.ucsf.edu/
K9Behavioral/Genetics/
OVERVIEW OF CANINE AGGRESSION
– PART 1: BREED, GENETICS, AND
BEHAVIORS IN SELECTING A DOG
The breed selection paradigm: Hundreds of
years of artificial selection has developed a
degree of canine size and shape variability
that exceeds thousands of years of natural
selection on wolves (1-3). Much of the physical
variation in dog breeds is a consequence of overt
selection for specific behavioral suites (e.g,
herding v. retrieving behaviors). Accordingly,
the manner in which dogs communicate to each
other and people is likely to be influenced by
these selected traits, and when dogs develop
behavioral problems for which a diagnosis can
be made, some of the traits for which humans
selected are likely to manifest themselves in the
way in which these problems are expressed.
All breeds share characteristics with humans
that have rendered dogs so compatible for
joint working and social relationships: they
have extended and extensive parental care,
other family members contribute to the care
and social development of offspring, they are
socially mature after they are sexually mature,
social systems are based in deference, and rules
governing it so that signaling is often redundant,
and most signaling or affirmation of signaling
is non-vocal rather than vocal. Unfortunately,
these similarities may lead people to under-
rate subtleties of canine behavior and to
anthropomorphize or anthropocentrize. For
example, a dog who wags his tail may or may
not be happy; a wagging tail is indicative of a
willingness to interact and stiff tail whose tip
is wagging is common in confident, aggressive
Back to contents
W
dogs. If the dog has a problem aggression,
staring at or reaching for the dog may be
sufficient to trigger further agonistic behavior
and frank aggression.
In the case of most aggressions and anxieties
related to social maturity, the condition manifest
by the dog has actually been changing because
of changes in the interactive social environment.
Most aggressive dogs are clinically behaviorally
abnormal; the abnormality is usually progressive
and is influenced by the social environment,
so the signs noted by the client and clinician
have been changing. We can easily understand
such progressive changes in infectious and
non-infectious disease, and so should be able
to understand them as conditions that manifest
as behavioral illness, yet regular screening for
behavioral propensities is not a common part of
routine veterinary examinations.
Role of selection for breed-associated traits:
2006 World Congress WSAVA/FECAVA/CSAVA
Before breed-based legislation gains credibility,
we need to ask if such an impetus is warranted
and substantiated by biological and scientific
knowledge. To do this we need understand the role
that we have played, both actively and passively,
in selecting for inappropriate or aggressive
behavior. The data previously discussed suggest
that demographics of breeds involved in dog
bites may co-vary with popularity of the breed,
and that these changes may have relevance for
the one group of children (males between 5-9
years) who are over-represented in dog bite data.
Behaviors of breeds do not remain static as the
breed become popular - these behaviors change
in ways well known to population geneticists.
Examples of these types of changes follow.
811
 W
If a breed was bred and selected to display a
relatively narrow suite of behaviors that were
considered acceptable and individuals outside
the bounds of acceptability were either culled
or not bred. Twenty generations later when
the breed got popular, two things happened:
(a) first, selection was relaxed, and because there
was still underlying additive genetic variance,
the less favorable traits were expressed, and
(b) the individuals expressing these traits and
behaviors were not selected against; rather,
they were highly desired because the dogs were
“hot”, or “tough”, or “sexy” or “sharp”. In this
case the owners are tolerating, selecting for,
and enhancing inappropriate out-of-context
behaviors (see Table 1 for some idea of how
popularity influences frequency of reported
bites, and variable popularity of different breeds
is over time and space).
If the breed was bred and selected to look a certain
way or to do a suite of behaviors (e.g., guarding,
or herding) and the breeders deliberately
wanted to move the mean of the population to
a slightly more “perfect” dog - forgetting that,
in the absence of selection against undesirable
traits, the entire normal distribution shifts, and
the proportion of dogs with undesirable traits or
behaving inappropriately also increases.
Other than these broad population level
associations, we do not understand much about
canine behavioral genetics even when normal
behavior is involved (4). Studies designed to
elucidate heritable components of breed specific
performance traits have not produced definitive
results. Tracking and scenting ability in German
wire-haired pointers appears moderately
heritable (having high additive genetic variance)
and so should respond rapidly to selection. For
a more complex behavioral suite, such as sheep
herding, the mode of inheritance and the extent
to which any of the behaviors comprising the
2006 World Congress WSAVA/FECAVA/CSAVA
style of approach and instinct are heritable
is arguable and complex. Investigations of
unpredictable aggression have produced no
firm results regarding heritability although for
many breeds in which dominance aggression is
a relatively common diagnosis, each generation
may contain affected individuals suggesting that
simple dominant inheritance may be operating
and should be further explored. Shyness or lack
of exploratory behavior has been investigated
in pointers; while these behaviors appear to
run in lines, environmental factors can not
be eliminated. Some evidence exists to link
812
Back to contents
temperament and the probability of developing
hip dysplasia in German shepherds; however, this
assessment involved a scored system for rating
temperament that may have obscured individual
behaviors. The genetics of normal and abnormal
behaviors requires intensive work.
Applicability for choosing pets: Every study
that has looked at “temperament” - a still
poorly defined concept - has found, regardless
of breed and purpose for which dog was bred
and was being raised - that between individual
variability is greater than that for litters,
families, and breeds. This finding should give
us pause. It means that unless some fabulous or
hideous trait has been deliberately selected, the
behaviors of any dog are largely a manifestation
of that individual dog’s ‘individuality’. Breed
will shape the form any “normal” - and some
“abnormal” behaviors will take. Accordingly,
if clients need a silent dog, beagles are a poor
choice. If clients live on a lake and don’t want
to deal with wet dogs, Labrador retrievers,
Newfoundlands, et cetera are poor choices. If
clients do not want to stimulate their dogs and
redirect herding behaviors, border collies and
Australian shepherds - particularly those from
working lines - are seriously poor choices.
The point is simply this: we have selected dogs
to be good at jobs. Until breed fancy valued
looks over performance and when we were more
mercenary in our relationships with animals who
co-habited with us, we also indirectly selected
for dogs that were “good family dogs”. That
selection criterion has largely been ignored for
the past 50 years, and there was never a time
when a breed was developed especially to “be
good with children”. If clients need a risk-free
dog, the best bet is a stuffed one. If clients want
the closest we can currently come to a dog who
was bred to be “good with children”, they need
to go the town square in any small town in an
impoverished country and buy any of the dogs
who so gratefully and quietly hang around
hoping for any cast-off love or food. Those
dogs survive because they excell at reading
human behavior and have posed no overt risks
to humans. However, once that dog is removed
from that environment, the dog is removed from
a rule structure. American lifestyles impose a
very different rule structure. Only if the new rule
structure is clear, humane, and cognizant of the
fact that their new dog is a cognitive, soverign
individual, will the dog retain the behaviors
which the clients originally so valued.
 W
Table 1: Dog bite data from various studies that specify breed data for at least 3 breeds; top 3 breeds in each
study listed (references can be found in (5))

Study 3 top breeds (+ / - level of significance)

1993 breed distribution of bite quarantine
dogs in a WI, USA humane shelter
compared with total dogs of the listed
breeds received at the shelter
for other reasons
Chow chow (13 / 170; 7.6%) P < 0.05; Gadj = 9.49 †
Cocker spaniel (23 / 316; 7.3%) P < 0.05; Gadj = 15.543 †
Lhasa apso (14 / 203; 6.9%) P < 0.05; Gadj = 8.261 †

†log-likelihood 2, our statistics

Incidence rates of dog bites by breed Bites /100 Relative risk

at 2 USAF bases animals/ year compared to mixed breed (all P < 0.01)
January 1976 - December 1977 Collie (20/100) 2.9
G. Shepherd (17.4/100) 2.6
Cocker spaniel (13.7/100) 2.0

Predominant breed in case Biting Non-biting

controlled study of 178 non-biting Chow chow 31 9
and 178 biting dogs 17.4% 5.1%
P < 0.001; Yates corrected 2 test
G. shepherd 34 13
19.1% 7.3%
P < 0.001; Yates corrected 2 test
Collie 8 1
4.5% 0.6%
P = 0.04; Fisher’s exact test, 2 tailed

Breed in prospective study of dog bite G. shepherd 35 (20.8%)

related injuries seen at CHOP, 1989; Pit bull *** 33 (19.6%)
156 dogs of identifiable breeds plus Rottweiler 8 (5.4%)
those identified as mixed breeds *** of these biting dogs, pit bulls were over-represented
in unprovoked bites and those inflicted by roaming
dogs; p < 0.01 or better, 2 test

Bites seen in 1975 at UCLA Mixed 41/135 (31%)

emergency department G. shepherd 28/135 (37%)
referred for surgery Terrier 5/135 (7%)
(unspecified)
2006 World Congress WSAVA/FECAVA/CSAVA
Survey of 455 families in a Denver Bites
Owned by family
pediatric practice comparing N (%)
breeds that had bitten and those G. shepherd + shepherd mixes 34 (17.5) 21(11.0)*
owned by families in practice Mixed breed > 30 lbs 24 (12.4) 27 (14.2)
Poodle 20 (10.3) 27 (14.2)
2
*p < 0.05; test; based on distribution of breeds when known

Retrospective study of breeds Mixed 350 (41.5%)

involved in 835 dog bites reported G. shepherd 211 (25%)
in Norfolk VA USA Poodle 37 ( 4.4%)
1 January-30 June 1971 no statistical analysis possible

813
Back to contents
 W
Retrospective study of
16 severe / fatal dog bites in
5 SC USA counties,
1 July 1979-30 June 1982
Retrospective study of 250 dog
bites recorded by Guelph
Health Unit, 1986-1987
2
† Gadj is the log-likelihood ratio test statistic. 108
References:
1. Wayne RK. Molecular evolution of the dog
family. Trends Genetics 1993; 9: 216-224.
2. Wayne RK, Vilà C. Phylogeny and origin of the
domestic. In: The Genetics of the Dog, edited by
A. Ruvinsky and J. Sampson, CABI International,
New York, 2001: 1-14.
3. Wayne RK. Consequences of domestication:
morphological diversity of the dog. In: The Genetics
of the Dog, edited by A. Ruvinsky and J. Sampson,
CABI International, New York, 2001: 43-60.
4. Houpt KA, Willis MB. Genetics of behaviour. In:
The Genetics of the Dog, edited by A. Ruvinsky and
J. Sampson, CABI International, New York, 2001:
371-400.
5. Overall KL, Love M. Dog bites to humans:
demography, epidemiology, and risk. J Am Vet Med
2006 World Congress WSAVA/FECAVA/CSAVA
Assoc 2001; 218: 1-12.
OVERVIEW OF CANINE AGGRESSION
– PART 2: FEAR, AGGRESSION, AND
FIGHTING WITH OTHER DOGS
There are at least 2 separate populations of clients
whose dogs are aggressive to other dogs: those who
think that this is “normal” behavior and that the
dogs will “sort it out” and those who are genuinely
scared and concerned.
Those in the former group are sometimes right,
but often wrong. If they are correct, the activities
involved in the aggression should cease in a short
period of time. If they are wrong, the activities
will intensify and may even become more subtle.
If the client believes that all dog-dog aggression is
normal they will miss this. If their worries come up
814
Am Staff ** 5
St. Bernard 3
Cocker spaniel 2
** possibly - “pit bulls”
no statistical analysis possible
Relative risk* %population
Am staff
39.81 0.6%
Duck tolling retriever
39.81 0.6%
St. Bernard
26.72 1.3%
* relative risk = biting rate of breed (# licensed biting
in breed / total # licensed x 1000) / biting
rate of all other breeds
* indicates P < 0.05.
against their instilled belief, they will may excuses.
Either way, veterinarians are unlikely to know about
these clients because the clients will not volunteer
the information. It is absolutely essential that every
single time a veterinarian sees a client that they
screen for behavioral concerns just as they would
medical ones. If the veterinarian is not doing this
they are missing serious problems (1).
Clients in the latter group often bring dogs to
either their personal veterinarian or a specialist in
behavioral medicine because their dog has “growled
or snarled” at or “fought with” another dog. They
are often concerned for reasons of image, liability,
and the well-being of their pet. Although these
clients seek help, they may be just as disadvantaged
as the clients in the first group because what they
are labeling aggression may not be aggression. The
first step in any work up involving any fighting or
aggression between dogs is to learn what the dog did.
Just because clients tell you that the dog “growled”
does not mean (a) that they really growled or (b) that
the behavior was abnormal or a concern. Canine
vocalizations are poorly understood although some
progress is finally being made (2,3). Many clients
mistake normal vocalization that is part of play
- especially if the play is exuberant or the breed is
deep chested and heavily muscled - as an aggressive
“growl”. Many clients are concerned about any
rough play, tussling, or vocalization that may erupt
from their dogs, and if they have had a problem with
serious interdog aggression in the past, the clients’
concern moves to terror quickly. The first step is to
ascertain whether the dog growled. Clients should
provide videotapes of interactions about which they
Back to contents

are concerned. Second, if the dog actually growled,
was the context appropriate. For a species without
verbal speech and opposable thumbs, there must
be a mechanism for telling another individual the
‘it’s enough’; hence, growls, barks, grumbles, and
a series of other sounds that we humans, no doubt,
ignore to our own detriment.
At the outset, whether the dogs are exhibiting rough
play, pushy behavior, or true pathological aggression
we must always ask the question, “Are both of these
dogs behaving appropriately, given the context?”.
If the answer is no, then some intervention is
necessary.
There are many pushy dogs who must go through
doors before other dogs, must be able to take toys or
rawhides from other dogs, and who are always able
to blackmail some other poor canine house-mate
from his or her morning biscuit. These same dogs
control all dog play and all access to people. The
conventional wisdom views such dogs as normal.
In fact, these dogs are often hailed as the “alpha”,
“top”, “boss”, “head”, or “leader”dog and clients
who express concern are instructed to encourage
the other dogs to take this dog’s lead, and then they
are encouraged to reinforce the lower “ranks” of the
other dogs by a reward and reinforcement schedule.
This is truly appalling logic, and with genuinely
pathological dogs can be profoundly dangerous
advice.
Unfortunately, we know so little about dog behavior
that we have no idea how many “pushy” dogs go
on to develop truly pathological behavior. If they
stay “pushy” without truly threatening the lives of
their down-trodden house-mates, they’re socially
obnoxious, but survivable. In fact, most “normal”
dogs will learn to avoid the circumstances that cause
the “pushy” dog to exert his or her forcefulness,
which has the effect of lowering the overall level
of reactivity, and socially ostracizing the bratty dog.
The bratty dog likely barely notices this because his
or her attention from humans comes when he or she
is alone. The close, supportive, playful relationships
that the other dogs will share is not truly enjoyed by
this dog, but we have no idea if they know this.
If the dog goes on to be truly pathological, it is
not sufficient that the other dogs get out of the
aggressor’s way and allow him or her first access to
everything. Even if these dogs defer to everything
the “boss” dog wants, it is not sufficient. The
aggressor targets a dog that they wish to banish from
the social hierarchy, and they continually attack that
dog, looking for an opportunity to kill.
The key to understanding this difference in these
2 types of dogs - the truly dangerous, aggressive
dog and the socially undesirable “pushy” dog -
lies in understanding why social systems evolved,
in the first place. Social systems, which are rule
structures designed to minimize counterproductive
Back to contents
W
error, evolved because, by distribution of effort and
clear, redundant signaling, everyone in the group
does better than they would alone. Is the behavior
exhibited by the “pushy” dog above consistent
with a social network where tasks are shared,
responsibilities are distributed, and play is likely to
be about learning to make mistakes successfully?
Absolutely not. No one should have to control
everything. The thing that makes most social
interactions work is the pattern of deference that’s
found in every true social system: individuals defer
to those who may make more appropriate decisions,
given the context. If clients are allowed to watch
their dogs without pre-imposed labels, they usually
cannot identify an “alpha” dog.....instead they note
that one dog is more outgoing with new people,
another with new dogs, and perhaps, yet another in
situations when the dogs aren’t on their own turf.
Status is always conferred by a group - it cannot
be taken and maintained - and when it is conferred
it’s given to the individual who makes the most
contextually appropriate decisions. All members of
groups are not all good at the same things.
In such social systems, people often fail to recognize
the elegant dance that maintains order because by
using terms like “alpha” we have convinced clients
that dogs fight for status. Nothing could be further
from the truth. Unless a dog is defending itself
against an attack, fights are the exception and a
signal that there is social breakdown. Normal dogs
can accommodate pushy compatriots. They have
trouble accommodating truly pathological bullies
because - by definition - that’s not on the agenda
of the aggressor. With a video or a few observant
minutes clients can tell the different. If behaviors
involving deference (eg, looking away, turning the
neck, disengaging by rolling on the back, trying to
leave, et cetera) are offered to the aggressor and
the aggressor continues to block access, intensify
the threat, or bite, there is a pathological problem
here. Dogs who are working out relationships grab
around the ears, sides of the neck, and shoulders,
2006 World Congress WSAVA/FECAVA/CSAVA
and although the noise is terrible, there is almost
never any damage. True aggressors go for the front
legs, the throat, the belly, and the eyes. The recipient
of such aggression may grab the aggressor by the
ear and hold on, because the aggressor then cannot
get hold of the recipient’s throat.
If there is true pathological aggression (4, 5) clients
must realize that one of their dogs can be killed,
and it will likely be the sweetest one. This situation
cannot be ignored. Clients have 2 initial choices:
(1) treat the dogs; (2) place one dog. If placement
is the option the aggressor can only go to a single
dog home where the new clients have a complete
grasp of the situation and can and will comply with
the degree of protection necessary. If the aggression
involves only a 2 dog household, the victim may be
815
 W
very easy to place. If the clients decline placement
and refuse treatment - they MUST either live with
the dogs separately. The people - as the guardian
of the dogs - must put their needs aside and
address those of the dogs. Clients and dogs can
live safely and happily with the dogs separated,
but it is a lot of work.
The biggest determent to fixing or controlling
the problem is the client who wants to have the
peaceable kingdom. These clients believe that
they can love and reason with the dogs enough
and the behavior will stop. This client behavior is
generally followed by the most serious attack yet.
Clients who are committed to keeping their dogs
and keeping them safe, can live well and happily
with baby-gates, doors, and rotating car, play,
training, and access schedules. The dogs can live
happily, as well, with these rules.
These rules are almost impossible to enforce if
you have young children or a deliberately non-
cooperative housemate (dogs and cats are often
victims of hidden agendas), and the smaller the
house, the harder it is to succeed. However, before
time-share co-habitation can happen, people have to
realize in their gut - not intellectually - but at the gut
level - that they can be responsible for the needless
death of one of their dogs. People don’t generally get
this at once. But when they do, they often comment
on what a “nice” dog the aggressor has become,
and how calm the rest of the dogs are. Of course
they are calm. They now have a rule structure that
guarantees them safety, whereas before they had a
totally unpredictable, mobile explosive device.
Belling the aggressor (Bear Bells, Silverfoot,
Squamish BC, Cananda; silverft@mountain-inter.
net) also helps: the other dogs always know exactly
where he or she is. It should be noted that in such
households some dogs may be able to spend
time with the victim and aggressor and never be
attacked. When this is true, that dog can go back
and forth and all lives will be enriched.
2006 World Congress WSAVA/FECAVA/CSAVA
Behavior modification involves 2 passive first
steps: (1) teaching each dog to sit and be calm
before they can have any human attention (eg,
walks, tick removal, play, food, head collar
placement, et cetera) [The Protocol for Deference]
(6) , and (2) the clients must reward the dog who is
behaving most appropriately. That determination
is made as discussed above. The reward structure
means that the most appropriate dog is fed, played
with, let out, et cetera first, and the least appropriate
dog, last. Size, age, and health, believe it or not, are
second order concerns unless the differences are
extreme.
If the clients start this early enough in the ontogeny
of the conflict, the conflict will stop. If serious fights
have occurred, this, alone, will not be sufficient.
Medication (generally a selective serotonin re-
816
Back to contents
uptake inhibitor [fluoxetine, paroxetine, sertraline]
or a trycyclic antidepressant [e.g., amitriptyline,
clomipramine]) and active behavior mod to
desensitize and counter-condition the dogs to
each other, first on lead, and then off lead must be
combined. It’s important to remember that most is
aggression is the result of an underlying anxiety
disorder (7): the aggressive reaction, itself, when
exhibited by the aggressor, is a non-specific sign
of underlying anxiety. Aggression is the outcome
of a rule system gone wrong, not a normal, first
line response in social interactions. It’s equally
important to remember that although the victims
may have started out ‘normal’, they are likely not
after a few months of unrecognized torture from
one of their housemates. Most often, the victim
becomes fearfully aggressive, and if they have any
confidence at all they become adroit at pre-emptive
strikes. Hence, both the victim and aggressor are
likely to benefit from medication, albeit possibly
not the same one.
Finally, the behavior mod must be intensive
and consistent. Clients with serious fights more
often opt for some behavior mod, +/- medication
to decrease anxiety, and separation of the dogs.
These clients know, to their sadness, that the
victim often now needs medication, too.
Regardless, if the clients are at all worried about the
dogs, or if the veterinarian is worried about the dogs,
the dogs should be separated behind locked doors
when no one supervises them. Threats can be as
debilitating as a blow, and when a dog cannot escape
a threat (and they cannot in most kennel situations)
they become profoundly debilitated. By putting
on “hold” the artificial concept of the peaceable
kingdoms, clients can have a different kind of
harmony, and develop a deeper understanding of,
and relationship with, their dogs.
1. Overall KL. Early intervention and prevention
of behavior problems: Step 2 - Routine screening
for behavioral problems, Veterinary Forum
August 2001: 42-46.
2. McConnell PB. Acoustic structure and receiver
response in domestic dogs, Canis familiaris. Anim
Behav 1990; 39: 897-904.
3. Ohl F. Ontogeny of vocalizations in domestic
dogs, breed standard-poodle (Canis lupus f.
familiaris). Zool Beitr 1996; 37: 199-215.
4. Overall KL. Animal Behavior Case of the
Month: Use of fluoxetine (Prozac) to treat
complicated interdog aggression. J Am Vet Med
Assoc 1995; 206: 629-632.
5. Overall KL. Animal Behavior Case of the
Month: Intrasexual interdog aggression in two
pugs. J Am Vet Med Assoc 1995; 207: 305-307.
6. Overall KL. Clinical behavioral medicine for
small animals. Mosby, St. Louis, 1997.

7. Overall KL: Neurobiology and neurochemistry
of fear and aggression (1 hour CE). Proceedings
- NAVC 1997; 11: 33-39.
OVERVIEW OF CANINE AGGRESSION
– PART 3: THE TRUTH ABOUT DOG BITES
Incidence of dog bites: As of 2000 there were are
approximately 52.9-58.2 million pet dogs in the
United States in about 35% of all households.
Reports estimating the incidence of dog bites vary
widely in their findings, with estimates ranging
from 0.5 -1 million bites per year in the late 1950s
through the early 1970s to 3.5-4.7 million bites
per year from the late 1970s through the 1990s.
Data for other countries, when available, are
similar.
The proportion of dog bites that are reported to
medical or legal authorities appears to be low:
published estimates range from 10 to 50%. To
the limited extent that the frequency of medically
treated bites can be used to estimate the frequency
with which bites are reported, only about 17%
of dog bites are reported. Estimates indicate
that approximately 17-18% of all bites receive
medical attention and that approximately 1-2% of
all bites require hospitalization. Dog bite related
injuries comprise approximately 0.4-1.5% of all
emergency department visits, 1.2% of all surgical
cases seen in emergency departments, and 0.3-1%
of all pediatric emergency room visits. Dog bite
related injuries comprise approximately 3.6% of
emergency department visits by male children
between ages 5-9 years.
Information about factors that affect dog bites
may be biased because of the heavy reliance on
data from bites that receive medical attention. The
nature and magnitude of these biases is unknown
and will remain so until more systematic studies
are conducted. Unfortunately, the most complete
data are from cases that receive medical and, or
surgical treatment. The focus for these cases is on
age of victim, type of dog, ownership status of
dog, and type of human injury sustained, rather
than on the behavioral circumstances of the bite.
Few data on canine and human behaviors or bites
are collected in a manner that allows critical
comparison. Such deficiencies in the available
data should be addressed in future veterinary
studies (1).
Demographics of dog bites
Effect of victim’s age: The type of human injury
incurred in the context of a dog bite depends on
physical attributes of both the human and the dog.
With few notable exceptions, available studies
generally do not define what constitutes a “bite”,
and do not distinguish between minor injuries
like bruises, and more severe injuries, like
Back to contents
W
punctures and lacerations. Data from reported
bites requiring medical attention indicate that the
majority of dog bites are to children under the age
of 15 years. Once a child becomes 1 year old bite
incidence increases through 5-9 years. Children
are bitten 2-3 times more frequently than would
be indicated by their population representation,
were all bites distributed equally over victim
class. Estimates suggest that by the age of 11
the majority of children have been bitten by a
dog, generally one known to them. Children
are at least 3 times more likely to experience a
medically attended bite than are adults, and 48%
of dog-bite related emergency room visits at one
center were from children under 10 years.
Effect of victim’s sex: There are 3 types of
studies available that examine the association
of sex of the victim and propensity to be
bitten: those that present actual data that allow
relative risk to be calculated, those that report
only calculated relative risk or odds ratios, and
those that report the incidence of bites without
population level data that permit the calculation
of relative risk. Studies that present actual data
are the most valuable and represent the type of
data future veterinary studies should endeavor to
collect. Detailed data that allow a comparison
of the relative risk of dog bites for males and
females are available from 4 studies: males are
bitten significantly more frequently for than are
females for all age groups examined in each of
these studies.
Dog bites to human males are reported 1.4 - 3
times4 more frequently than are bites to females.
The proportion of males bitten compared
with females ranges from 1.5:1 to 1.7:1 in a
population where males outnumber females
1.2:1. Proportions of bites to male children
compared with female children varies with age
of victim: boys outnumber girls 1.6:1 in the less
than 4 year age group and 2.3:1 in the 4-16 year
age group. When compared with bites to females
2006 World Congress WSAVA/FECAVA/CSAVA
19 years or older (relative risk = 1.0), males 19
years or older have a relative risk of 1.9, females
0-18 years have a relative risk of 4.2, and males
0-18 years have a relative risk of 5.4. This pattern
suggests an interaction between age and sex that
is also apparent in other geographic and cultural
locales.
Finally, males comprise a significantly larger
proportion of victims involving dog bite-related
fatalities than do females.
Relationship of dog to victim: The vast majority
of bites in the United States are inflicted by
owned, pet animals, not by strays. The family
dog is involved in 25% to 33% of the bites. Free-
ranging, owned dogs may be more aggressive
than strays when approached, and may be more
817
 W
aggressive when closer to home. One excellent
study reported that, only for dogs identified as
“pit bulls” (P <0.001), were the majority of bites
attributable to freely roaming animals that did not
belong to the person bitten.
In 96 dog bites for which data on domain in
which the bite occurred and relationship of the
victim to the dog were available 54% (52) of bites
involved victims less than 15 years, 85% (82) of
bites occurred in the dog’s own home, and 62%
(28/44) of adult victims were bitten by their own
dog, where as 75% (39/52) of child victims were
bitten by dogs belonging to neighbors or friends.
Such data strongly suggest that human behaviors
may be implicated in dog bites.
Bites inflicted by strays (50.3%) are more likely
to be examined by a physician than are bites from
family pets (29.1%). It is important to realize that
not all stray dogs are unowned. Many “strays” are
owned dogs that are allowed to run free.
Victims’ behaviors and dog bites: Human
behaviors factor into the circumstances initiating a
bite and contribute to the amount of damage done.
Children aged 5 or younger are significantly more
likely to provoke animals prior to injury than are
older children (P <0.001).
Most dog bites, particularly to children, occur in
the summer, most bites occur on weekends, and the
diurnal peak in bite activity is in the late afternoon
and early evening. Most children hospitalized for
dog bites are bitten on weekends. The temporal
environment matters because children are more
likely to come into contact with dogs at certain
times. The physical environment also contributes
to the circumstances of the bite. More children and
dogs are outdoors and active during the periods
listed. The greater the number of both children and
dogs, the greater the potential reactivity of each
group. Again, there are no objective measures of
this, but empirical evidence from pack situations
for both dogs and people (mobs at soccer games,
et cetera) indicates that the more excited any
participant, the less stable and predictable the
2006 World Congress WSAVA/FECAVA/CSAVA
situation. Such circumstances are ideal for unilateral
or joint misinterpretation by the participants of any
signaling behavior. Proximity facilitates violence,
rather than retreat, as a response in such conflicts.
In the case of canine aggression towards children,
there are two participants with enough overlap
in patterns of sociality that it is possible to
misunderstand the extent to which the same signal
has two different messages and meanings. Just as
humans can misinterpret a wagging tail, dogs can
misinterpret a screaming child. Children may be
uncoordinated and may appear unpredictable to
dogs because of their sudden shifts in postures and
vocal range when excited. Some behaviors and
some intensities of behaviors in young children
can frighten dogs. Other behaviors, like shrill
squealing, could be misinterpreted by the dog
as sounds and signals given by prey. Excitable
818
Back to contents
states facilitate misunderstanding by making all
participants less aware of changes in signaling and
interactive behaviors. The potential for bilateral
misunderstanding and inappropriate reaction
with concomitant disastrous circumstances is
particularly great for children who may not have
the sophistication or maturity to correctly interpret
and react in rapidly changing interactions.
Conclusions: Issues of fact and dangerous myth
An extensive literature review (2) of the literature
about dog bites revealed that the only robust data
are those supporting the following conclusions:
(1) There is a substantially greater injury and
fatality rate for children when compared with
adults.
(2) Male children are injured and killed more
frequently than female children, suggesting that
human behavior may be a significant issue.
(3) There is a preponderance of owned, family
dogs in those involved in bites and fatalities.
Robust conclusions regarding breed cannot be
drawn. The breeds most frequently involved in
dog bites at present are mixed breeds, German
shepherds, German shepherd crosses, pit bull
terriers, and pit bull crosses; the latter four groups
are most frequently implicated in fatality.
A careful reading of the literature supports
3 conclusions regarding breed.
(1) The breeds most represented in the dog bite
data change rank with time. This may indicate
changes in breed preference by owners, rather
than changes in breed specific aggressive
tendencies per se.
(2) The breeds most frequently represented
in the published data are popular ones and
no one breed may be represented in the bite
data in disproportion to its occurrence in the
population. Good data on population size of each
breed and mixed breeds for the human victim
populations studied are unavailable, but essential
if any legitimate statements about breed over-
representation are to be supported.
(3) The term “pit bull” is widely applied, often
without biological basis, to a range of dog types,
regardless of the underlying genetic stock. This
latter problem is probably magnified in areas that
have already experienced one publicized “pit
bull” related attack.
So, are dog bites a problem? Yes, but even with
this extensive review of the data, we know little
about the actual behaviors of dogs involved in
bites, regardless of breed. If we wish to understand
why dogs bite and to minimize morbidity and
mortality associated with bites, the following goals
must be met.

(1) The prevalence of dog breeds, and ages, sex, and
reproductive status within those breeds, needs to be
established within the demographic population for
which bites are to be investigated. Any discussion
of breed specific aggressive propensities must
be critically viewed. Caution is urged regarding
any generalizations about inappropriate breed
based behaviors. It is best to view selection for
specific behaviors as a risk assessment analysis:
breeds that have been selected for one or a few
particular and specific behaviors may be more at
risk for developing undesirable variation for those
behaviors. This does not mean that dogs selected
for protective behaviors are more aggressive than
dogs for which this selective pressure was absent.
It does mean that that breed may be more at
risk for developing a disproportionate number of
dogs who exhibit inappropriate, out of context
protective aggression given the selection/breeding
conditions outlined above. Inherent in this
concept is that any dog, regardless of breed, can
also exhibit the inappropriate behavior. A further
corollary is that dogs who are selected for tenacity
and jaw strength in their in-context work (bull
terriers, rottweilers, Rhodesian ridgebacks), will,
when they respond inappropriately or out-of-
context in another behavioral setting, exhibit this
same tenacity. Coupled with the physical traits
attendant with such selection (large jaws, heavy
musculature), they can and will do large amounts
of damage on a first strike. These factors, rather
than increased breed-specific aggression, are the
cause of the severity of wounds, when inflicted.
More research about all of these factors is needed.
(2) Canine and human behaviors that limit or
exaggerate relative exposure need to be defined
and quantified. Any dog breeder or owner who
accepts the occurrence of inappropriate aggression
or who feels that such aggression is “normal” for
their breed, or not dangerous because the dog is
small, is contributing to the problem.
(3) We need to know which dogs bite and whom
do they bite. We must develop specific behavioral
profiles of dogs that do and do not bite, and of their
owners’ behaviors, within the specific population
in question. Such studies will indicate whether
dog bites are associated with and attributable to
a behavioral diagnosis involving aggression, and
the extent to which certain human behaviors foster
aggression.
(4) The situation in which the bite occurred needs
to be thoroughly, rigorously, and consistently
reviewed and documented by health care personnel
in a repeated manner using validated assessment
tools, so that the appropriateness of the situation,
the extent to which provocation may have been
involved, the nature of the provocation (1), and
the behavioral propensities of the dog (including
whether the dog has a behavioral diagnosis) can
be evaluated. This aspect is particularly important,
given the association between dog abuse and child
Back to contents
W
abuse, and the extent to which violent behaviors
are learned and practiced.
Achieving these goals will require a tremendous
amount of work, and anyone who is serious about
dogs - especially the AKC - should have a vested
interest in seeing projects that address these issues
get funded, accomplished, and published. In the
absence of actual numerical demographic data,
conclusions and discriminatory legislation based
on breed are being drawn from, at best, incomplete,
and at worst, skewed data and are premature. These
data suggest that initiatives like those mounted
by the AVMA, HSUS, State Farm Insurance
Company, and many other groupsto teach children
how to interact appropriately in specific situations
involving dogs, particularly unfamiliar dogs, may
be addressing only the exceptional situation. If this
is true, such initiatives will be of extremely limited
benefit in reducing the overall numbers of dog bite-
related injuries and fatalities. Regardless, widely
disseminate application of knowledge about age-
associated child and dog behaviors can only help,
and veterinarians must take an acktive role in this
aspect of public health care and education (3).
The dog bite issue is so heavily burdened with
emotion and rhetoric that we must take extra care
to employ scientific reasoning and methodology
in the debate. A review of the data to date indicates
that popular and numerically dominant breeds are
most frequently involved in bites, bites to children
are relatively common, most bites to children are
to male children, and most fatal dog bites involve
male children. No matter how incomplete the
data, we still have better data on the children than
on the dogs or the behaviors surrounding the bite.
To outlaw some breeds, especially in the absence
of the needed information discussed, would not
make us safer, and the illusion that it would is
a dangerous one. To refuse to collect these data
is to abdicate our responsibility as scientific
professionals. Accurate data can help us to be
better guardians of our pets and patients, to raise
our children to be responsible and humane with 2006 World Congress WSAVA/FECAVA/CSAVA
pets, and to become better, kinder, and more
humane, ourselves.
References:
1. Bollan J, Caudron D, De Keuster T, et al.
Les Enfants victimes de morsures de chien. Ms.
2002.
2. Overall KL, Love M. Dog bites to humans:
demography, epidemiology, and risk. J Am Vet
Med Assoc 2001; 218: 1-12.
3. Love M, Overall KL. Dogs and children: how
anticipating relationships can help avoid disasters.
J Am Vet Med Assoc 2001; 219: 446-453.
* Most of these notes were adapted and updated
from reference 2.
819
 W
W – Animal Welfare
DANGEROUS DOGS LEGISLATION – THE WRONG SOLUTION?
Ray Butcher MA Vet MB
MRCVS
The Wylie Veterinary Centre
UK (On behalf of the Blue Dog
Trust)
ray.butcher31@tiscali.co.uk
Introduction
Injuries to people resulting from dog bites are a
real problem throughout the world. In the 1990’s
it became fashionable to blame only certain
“dangerous” breeds, and much “Media-hype”
pressurised governments to introduce breed
specific legislation to address this. The logic and
efficacy of such legislation has been the subject
of a previous FECAVA symposium in 2001, the
proceedings of which were printed in EJCAP
2002.
Breed specific legislation
The Dangerous Dogs Act (1991) has been
described as one of the most ill conceived pieces of
legislation introduced into the UK. The resulting
welfare problems and difficulties of enforcement
will be discussed. These relate mainly to the fact
that the legislation was:
• Breed specific despite the difficulty of identifying
these particular breeds
• Strict provisions
• Automatic destruction order
• Court given no discretionary powers
• Reversal of the “burden of proof”
Sadly such a model is being copied in other
2006 World Congress WSAVA/FECAVA/CSAVA
European countries.
Whilst “dangerous breeds” may be a problem in
some circumstances, consideration will be given
as to whether legislation is really effective in
reducing the incidence of dog bites.
The Facts
This presentation summarises the facts presented
by Tiny De Keuster at the FECAVA Blue
Dog Symposium in Amsterdam 2005 (and
subsequently published in the Autumn 2005
edition of EJCAP).
In a survey in Belgium (Gisle et al 2001) 1% of the
population was found to be a victim of a dog bite
incident that required medical attention. Further
studies (Kahn et al 2004) showed that children
under 16 years of age were twice as much at risk
820
Back to contents
than adults. Further, most dog bite accidents in
young children (median age 5 years) occur during
everyday activities in the home environment with
dog that is familiar to them. Eighty-six percent of
the dog bites occurring at home were found to be
triggered by an interaction initiated by the child.
In many cases there was no parental supervision
at the time.
There was no evidence of breed differences, nor
evidence that any breed is safer with children
The need for a novel education approach
In the past, extensive information regarding
interactions between dogs and children has been
published in the veterinary and medical literature.
However, most programmes are aimed at the
age group of 7 years and older (ie not the main
group at risk). Also these programmes focus
mainly on public safety rules, such as how to
behave when encountering an unfamiliar dog.
In Europe, programmes intended to prevent bite
accidents at home are very rare. In addition, most
of the recommendations in dog bite prevention
programmes are not based on research and this is
a serious deficiency.
According to data from dog bite surveys,
particular situations are more likely to lead to
dog bite accidents than others. Most dog bites
in children happened while there was no adult
supervision. Therefore, a first step in this project
was solving the question how to translate these
data into a tailored prevention tool for children
and parents. The idea of the blue dog was born.
Improving the behaviour of dogs
Tiny De Keuster will speak more about the Blue
Dog in her presentation. It is clearly also important
to make every effort to correctly socialise
puppies that are destined to enter a family home.
Breeders and veterinarians have an important
role here. Dogs may also enter family homes via
rescue shelters, and so it is important that their
management within the shelter facilitates this
transition.

Wider perspectives
The Blue dog project was initially aimed at
“Western style” developed countries. However
bites are a real issue in so-called developing
countries, especially where endemic dog rabies is
present. Although the actual scenarios leading to
dog bites may be different, and the methods of
Back to contents
W
education may need to be adapted, the lessons of
the Blue Dog in educating children and parents
how best to behave around dogs may have
great relevance to many cultures. The author’s
experiences in Sri Lanka, India and Africa will
be discussed.
2006 World Congress WSAVA/FECAVA/CSAVA
821
 W
W – Animal Welfare
TEST YOURSELF – A FIRST ASSESSMENT OF THE DOG BITE
PREVENTION PROJECT “BLUE DOG”:
PART I: EDUCATION - THE “BLUE DOG” IS BORN
PART II: THE “BLUE DOG” - DO CHILDREN REALLY GET THE
MESSAGE?
Kerstin Meints M.A., PhD
University of Lincoln
Department of Psychology
Brayford Pool
Lincoln LN6 7TS
UK
kmeints@lincoln.ac.uk
Introduction
The majority of dog bite accidents happen at
home and involve younger children. In the
majority of accidents (86%), a child’s interaction
with a familiar dog appears to trigger the biting
(Kahn et al. 2003). The prevalence of dog bites
in children is 2,2 % which is double as in the
general population (Kahn et al. 2004 ) and often,
children suffer from dog bites resulting in facial
injuries (Bernardo et al. 2002, Kahn et al. 2003,
Schalomon et al. 2006). 55% children suffer post-
traumatic stress disorder following a substantial
bite (Peters et al. 2004). Dog bite prevention
programmes exist mainly for children aged 7
years and older (Chapman et al. 2000) and mainly
focus on public safety rules, like how to behave
when encountering an unfamiliar dog. Only very
2006 World Congress WSAVA/FECAVA/CSAVA
few programmes are aimed at children under 7
and intend to prevent bite accidents at home
(British Kennel Club 2004, Jung et al. 2001;
ONE 2003, Pillonel, 2003).
However, as children who are bitten are five years
on average, the authors attempted to remedy the
lack of early prevention programmes - our aim was
to empirically assess if children can learn from a
CD; we used a specially selected and adapted subset
of the Blue Dog interactive prevention scenes. The
Blue Dog project targets children under the age of
7 and uses an interactive CD to tell children about
an abstract “Blue Dog” and to teach them via the
character of the Blue Dog about safe and unsafe
interactions with a dog. The CD also includes a
“Test Yourself” module, which is the part that has
been used for assessment of the CD’s effect on
822
Back to contents
Tiny De Keuster, DVM,
Dipl ECVBM- Ca
Oostveldkouter 222,
9920 Lovendegem
Belgium
tiny.dekeuster@telenet.be
children’s learning. This module has been shown
to teach children successfully about safe and unsafe
behaviour with dogs in a home context.
Method
Participants: Children were tested at 3, 4, 5 and
6 years of age. Testing of children’s progress in
learning was carried out in schools in Lincolnshire,
UK, with 3-year-olds being tested using the
interactive CD in nursery schools. 3-year-olds were
also tested using Intermodal Preferential Looking
(IPL; method used as in improved adaptation, see
Meints et al. 1999) – a method that is frequently
used in developmental psychology, for example
in word learning and which does not require
the children to interact with the experimenter,
the laptop keys etc., but relies solely on infants’
looking preferences.
IPL was used in the purpose-built Infant Lab at
the University of Lincoln, UK, as 3-year-olds’
ability to use a laptop successfully was more
limited. About 26 children per age group per
setting were tested.
Materials
The interactive learn and test CD module was
created from the existing Blue Dog CD (De
Keuster et al. 2005) that is usable for children
from as early as 3 years of age.
The clips were condensed to 8 different 10-
second clips with varying, in real-life frequently
occurring situations (e.g. dog eating, dog
sleeping, etc.) which children need to learn to
react to appropriately.

Procedure
All children were shown three different
experimental phases (each containing the 8 clips).
They were first exposed to the stimulus videos,
(exposure phase), then trained how to distinguish
safe from unsafe situations (training phase) and
finally tested on what they have learned (testing
phases 1 and 2).
More specifically, in the 8 exposure trials,
children saw see a child and dog interacting
up until a point in time when the child has to
choose an outcome. The child is free to choose
any outcome. Then, the training phase began in
which children were shown a possible negative
(dangerous) and positive (safe) outcome of each
child-dog-interaction. Half the children received
additional, pre-recorded verbal feedback.
Finally, in the first test phase, children saw the
initial 8 scenes again straight after the training
phase, but with different dogs and children.
They were asked to choose the interaction that
leads to a safe outcome. The second test phase
Figure 1. Mean scores of total correct answers as a function of phase and age.
There was also a significant main effect of
parental input (F(1,94)=13.29; p< .0004) that
demonstrated that children who received parental
input performed better than those who did not
receive parental feedback. More specifically,
those children who received parental input seem
Back to contents
W
took place in the same way, but with a two week
delay. In the meantime, half of the children had
received parental feedback, (half of these had
received verbal input as well). Learning with
parental reinforcement included looking at the
story again at home with parents explaining /
giving feedback. For IPL, eye-gaze direction
was recorded on video and measured afterwards
offline. For assessment via laptop children’s
button press choices were recorded.
Results
Results show a main effect of learning
(F(2,184)=85.03; p< .0001) between the first
exposure phase and the test phases. Results
further show a main effect of age with older
children exhibiting more correct responses than
younger children (F(3,92)=6.23; p< .0007).
Figure 1 demonstrates the increase in correct
responses with age over the different testing
phases.
2006 World Congress WSAVA/FECAVA/CSAVA
to retain their acquired knowledge better than
those without parental feedback as there is a
significant difference in the first and second test
phase with children supported by their parents
performing significantly better than the control
group (p< .0001). Figure 2 illustrates this result.
823
 W
Figure 2. Mean scores of total correct answers as a function of phase and parental input.
While older children did not exhibit improvement
via verbal, pre-recorded feedback, 3-year-olds,
however, show a marked improvement in retaining
their knowledge if they have received additional
verbal feedback while watching the CD.
Discussion
The results of this first assessment indicate that
children do indeed learn from the specifically
adapted “Test yourself” module on the Blue Dog
CD. Future research will have to show whether
this learning is transferred not only to other
dogs and children seen on a CD, but also to real
child-dog-interactions. It will further have to be
2006 World Congress WSAVA/FECAVA/CSAVA
assessed whether the overall Blue Dog story can
act as a learning facilitator by itself. In addition, as
the role of parental feedback plays a role, further
research will need to show the nature of this
feedback and the best conditions and learning/
teaching/feedback mechanisms for improving
children’s safety. As not all parents have access to
computers, other forms of feedback should also
be investigated and tested in a systematic way.
The effectiveness and long-term impact of the
learning should be tested as well (e.g. duration of
retaining knowledge).
Conclusion
Overall, this first assessment of the effects of a
CD aimed at improving children’s understanding
of safe and unsafe behaviour with dogs learning
824
Back to contents
has successfully shown that children from 3 to 6
years are able to apply the acquired knowledge,
even after a delay of two weeks.
References
Bernardo L, Gardner M, Rosenfield R, Cohen
B, Pitetti R (2002) A comparision of dog bite
injuries in younger and older children treated in
a pediatric emergency department. Pediatr Emerg
care 2002 Jun; 18(3): 247-249.
British Kennel Club - Safe and Sound http://
www2.the-kennel club.org.uk/web_portal/
Chapman S , Cornwall J, Righetti J, Sung
L: Preventing Dog Bites in Children (2000):
Randomised Controlled Trial of an Educational
Intervention. BMJ 2000, 320: 1512-1513.
De Keuster T, Moons C, De Cock I (2005) Dog
bite prevention - How a Blue dog can help.
EJCAP Vol 15; 2: 137-139
Jung H., Falbesaner U and Döring-Schätzl
D. (2001) Grundwissen Gefahrenvermeidung
im Umgang mit Hunden , Ed. Bayrische
Landestierärztekammer und Institut für
Tierschutz, Verhaltenskunde und Tierhygiëne ,
Universität München, ISBN 3-934302-05-x.
Kahn A, Bauche P, Lamoureux J and the Members
of the Dog Bites Research Team (2003): Child
victims of dog bites treated in emergency
departments. European J Pediatr 2003; 162:
254-258.

Kahn A, Robert E, Piette D, De Keuster T,
Lamoureux J, LevêqueA (2004) Prevalence
of dog bites in children. A telephone survey.
European J Pediatr 2004; 163: 424.
Meints K, Plunkett K, Harris PL (1999) When does
an ostrich become a bird? The role of typicality
in early word comprehension. Developmental
psychology, 1999 Jul ; 35(4): 1072-8.
ONE (Office de la Naissance et de l’Enfance)
http://www.one.be/home.htm
Peters V, Sottiaux M, Appelboom J, Kahn A
(2004) Posttraumatic stress disorder after dog
W – Animal Welfare
THE BLUE DOG – HOW DOES THE PROGRAMME WORK IN
PRACTICE?
Tiny De Keuster, DVM,
Dipl ECVBM- Ca
Oostveldkouter 222,
9920 Lovendegem
Belgium
tiny.dekeuster@telenet.be
This topic is covered in two pars (I & II).
The Blue Dog package will be launched at the
WSAVA/FECAVA Prague Congress in 2006. It
takes the form of an interactive CD-ROM and a
printed Parent/Teacher guide. The welfare session
of the previous day will outline the background and
development of the project.
Back to contents
W
bites in children. J Pediatr 2004 Jan; 144 (1):
17-22.
Pilonell C., BVET: “Milou viens” http://www.
bvet.admin.ch/index.html?lang=fr
Schalomon J, Ainoedhofer H, Singer G, Petnehazy
T, Mayr J, Kiss K, Hollwarth M (2006): Analysis
of dog bites in children who are younger than 17
years. J Pediatr 2006 Mar; 117 (3) pp 374-379.
Key words
Child, Dog bite, Prevention programme, testing
Ray Butcher MA Vet
MB MRCVS
The Wylie Veterinary Centre
UK (On behalf of the Blue Dog
Trust)
ray.butcher31@tiscali.co.uk
2006 World Congress WSAVA/FECAVA/CSAVA
This session will take the form of a workshop.
Various scenes of the CD will be shown. The
presenters will then relate these scenes to aspects of
the relevant sections of the parent/teacher guide.
In this way it is hoped that the delegates will get a
working knowledge of the programme and will be
encouraged to use it further.
825
 2006 World Congress WSAVA/FECAVA/CSAVA

826
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

POST POSTERS -
-ABSTRACTS
ABSTRACT
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

POSTE POSTERS -
-ABSTRACTS
ABSTRACT

POSTERS - ABSTRACTS
PREPUCIAL URETHROSTOMY PERFORMED USING THE COATING TECHNIQUE
S.E. Acar1, M. Saroglu1, D.J. Sadalak2
1
I.Ü. Veterınary Faculty, Avcılar, Istanbul, Turkey; 2Practitioner Veterinary Medicine Dr., Bath, Bristol, U.K.
Penile urethral obstruction in cats is a commonly
seen clinical presentation. In cases where there is no
response to catheterisation or medical intervention,
surgery is needed to enable urination and correct
uremia and hyperkalemia. Several surgical
techniques have been described. Great care must
be taken to minimize leakage in the anastomosis
site and promote healing when performing the
pelvic urethra and prepucial mucosa anastomosis.
To achieve this, the line of anastomosis has been
reinforced by covering the anastomosis with the
bilateral bulbourethral tissue, m. ischiourethralis
and m. ischiocavernosus using simple mattress
sutures. This modification, which varies from the
technique performed by Yeh and Saroglu, has been
termed the coating technique. Advantages of this
POSTERS
new technique over standard perineal urethrostomy
have been discussed. This technique was used
in the treatment of 49 cats with penile urethra
obstruction presented to our clinic. 47 cats showed
uncomplicated recovery. Stenosis developed after
1 month in 2 cases in which normal urination
was resumed by performing the standard perineal
urethrostomy technique. Following anastomosis, a
male dog urethral catheter with an outer diameter
of 2.6 mm was placed in each patient. The
reasons for using a catheter in this technique were
explained. In order to avoid infection, the catheter
was changed at 7-day intervals, remaining in situ
for 2 weeks and was removed after 14 days. All
cats with obstruction returned to good health.

THORACOSCOPIC BIOPSY OF LUNG TUMOURS WITH ROEDER LOOP IN

DOGS
Z. Adamiak1, K. Kalinowska2
1
Department of Surgery, Faculty of Veterinary Medicine, ul. Oczapowskiego 14, 10-957 Olsztyn, Poland; 2Private
veterinary Clinic, ul. Wesola 18, 15-232 Bialystok, Poland

ERS
Thoracoscopy is a minimal invasive technique for
diagnostic and operative procedures on thoracic
organs and cavity. The aim of the study was to
estimate Roeder loop for biopsy of lung tumour
specimens for histopathological evaluation in
dogs.
Materials and Methods: Five dogs with lungs
at the right 5th intercostals space, endoforceps
and scissore were placed at right 6th intercostals
space, Roeder loop was introduced at the right 8th
intercostals space. After visualisation of tumour
changes biopsy specimens were obtained using
Roeder loop. Tumour tissue was grasped, pulled
into Roeder loop. The loop was tightened at the

TS
neoplasm changes were used in examinations.
All dogs before thoracoscopy were clinically
and radiologically examined. X-ray examination
reviled diffuse neoplasm in four cases, and solitary
lung tumour in one case. After general anaesthesia
dogs were underwent thoracoscopic procedure
to obtain lung tumour biopsy specimens. An
endoscope was inserted into the pleural space
base biopsy specimen, and neoplasm tissue was
transacted free. Tumour biopsy specimens were
hand down for histopathological examination. 2006 World Congress WSAVA/FECAVA/CSAVA
Results and Discussion: Our data demonstrate that
Roeder loop allows for acquire adequate biopsy
specimens for histopathological evaluation. In all
five dogs no Roeder loop failed during transection
of the biopsy specimen.

TETRALOGY OF FALLOT IN A DOG

C.F. Agudelo Ramírez1, P. Scheer2
1
Department of Internal Medicine, Clinic of Dog and Cat Diseases, Faculty of Veterinary Medicine, Veterinary and
Pharmaceutical Sciences University Brno, Czech Republic; 2Veterinary Clinic MaScHEER, Malešovice, Czech
Republic

Objective: Tetralogy of Fallot (TF) is a congenital the aorta with septal override. The purpose of this
malformation that consists of (1) ventricular septal paper was to evaluate and describe the findings
defect (VSD), (2) obstruction to right ventricular from the history, cardiovascular examination and
outflow tract (pulmonary stenosis) (PS), (3) right diagnostic tests in one dog diagnosed with TF.
ventricular hypertrophy, and (4) dextroposition of Case presentation: A 17-month-old 9 kg, non
829
Back to contents
POSTERS

– spayed female Border terrier with history of
intermitent exercise intolerance and mild cyanosis
during strong activity. The dog was taking at
that time enalapril (0.25 mg/kg SID PO). The
main findings on the clinical examination were
subcyanotic membran mucous and the auscultation
revealed a pansystolic murmur degree 3/6,
localized at the right side of the thorax over the
tricuspid valve area. The X-rays (LL and DV views)
revealed enlargement of the right ventricle (VHS:
11.2) with no evidence of pulmonary edema. The
ECG showed jagged QRS complexes (leads III,
aVL, aVF and V10), enlargement of the left atrium‚
(PII: 0.26 mV, 44 ms) and the right ventricle (SI,
SII, SIII pattern, S wave in lead CV6LL and CV6UL
greater than 0.8 mV). Echocardiographically
(21.10.2005) presented VSD, dextroposition of
the aorta (no more than 50%), infundibular PS
with minimal flow, hypertrophy and flattening (D-
shape) of the interventricular septum (IVS) and
right ventricular hypertrophy (right ventricular
wall thickness was same as thickness of IVS). Next
control (27.1.2006) showed reduction of diastolic
(1.5 vs. 1.02 mm) and systolic (1.63 vs. 1.37 mm)
thickness of the IVS and extension of left ventricle
posterior wall (diastolic 1.05 vs. 1.28 mm, systolic
1.2 vs. 1.77).
Conclusion: Due to financial reasons owners
declined surgical correction and the patient was
medicated with atenolol 0.5 mg/kg SID PO.
During the following months (12 months), clinical
condition of the patient has been stable but the
echocardiographical values improved and patient’s
quality of life is satisfactory up to now.

CANINE HERPES VIRUS INFECTION: A SERO-EPIDEMIOLOGICAL SURVEY IN

TUNISIA AND ESTIMATION OF VACCINE EFFICIENCY
C. Ahmed1, F. van Gool2, M. Rmili3, F. Kallel1, F. Landolsi1, S. Haddad3
1
Veterinary School, Sidi Thabet, Tunis, Tunisia; 2Merial Laboratory, Lyon, France; 3Centre Canin, Bizerte, Tunisia

We carried out, in the first part, a canine herpes
virus infection sero-epidemiological survey by
ELISA test on 49 reproductive bitches aged 2.9
± 1.7 years and coming from Bizerte and Tunis
regions. This survey has revealed a seropositive
rate of 37%. No significant differences were
found according to the sanitary status or the age
of the dogs in the breeding units. In the second
part, we carried out a medical prophylaxis against
canine herpes virus infection in a canine centre.
For that, we have used EURICAN® herpes virus
vaccine produced by MERIAL Laboratories,
Lyon, France. This study allows us to estimate
vaccine efficiency by observing its impact on
neonatal mortality. Twenty three reproductive
females housed at a canine center were included
in this study. These bitches were divided into
2006 World Congress WSAVA/FECAVA/CSAVA
made up of 6 bitches that did not receive any
herpes virus vaccine but instead, they received
a vaccine against other diseases (Distemper,
hepatitis, leptospirosis, parvovirosis and rabies).
The second group: contains 10 females that have
received a single injection of herpes virus vaccine
at the end of pregnancy period according to the
protocol proposed by Lanting (2004). The third
group: comprises 7 bitches that have received
vaccination according to the following protocol
(Poulet et al. 2001):
•First injection 10 days after mating
•Second injection 10 days before delivery date.
The result of vaccinations has shown a decrease in
neonatal mortality rate. In fact, in the control group
(Group1) a neonatal mortality rate was of 43.33%,
while in the vaccinated groups it was of 23.4% and

3 groups: The First group (control group) was 7% respectively in the second and the third group.

INVESTIGATION OF PERIPHERAL AND INTEGRAL PROTEINS IN TYPE II

DIABETIC CATS
A. Akdogan Kaymaz1, I. Albeniz2, Ş. Tamer3
1
Faculty of Veterinary Medicine, Dept of Internal Medicine, Istanbul University, University Street, İstanbul, Turkey;
2
Istanbul Medical Faculty, Dept of Biophysics, Istanbul University, Sehremini, İstanbul, Turkey; 3İstanbul Medical
Faculty, Dept of Physiology, İstanbul University, Sehremini, İstanbul, Turkey

Endothelial and vascular disorders with the
coagulation disorders, altered blood flow and
increased permeability, vasoconstriction in
diabetic patients and animals were seen. The
membrane structures of blood components were
affected by the disorders of blood flow and
increased blood viscosity. For that reason, the
830 investigation of diabetic effects on changing
of peripheral and integral protein structures’ in
erythrocyte membrane in diabetic cats were aimed
in this study. Totally 20 cats which of 10 were
diabetic and their ages varied between 1.5 and
10 years old brought to Department of Internal
Medicine, Faculty of Veterinary Medicine, İstanbul
University were used. Haematologic parameters
were determined by Sysmex KX 21 haematology

Back to contents

analyser. Erythrocyte membrane proteins were
determined by SDS-PAGE electrophoresis
using a 10% gel and a discontinuous buffer
system. When compared to controls, SDS-PAGE
revealed that the band 5 corresponding to actin
was weaker while band 4.5 corresponding to
integral membrane proteins (glycophorin A, B and
POSTERS
C) had disappeared in diabetic cats. It was also
seen that band 4.9, which is composed of dematin
(a protein with actin-bundling capacity), was lost.
The findings were thought that diabetes mellitus
degenerate the structural proteins of the cell and
affect the blood flow.

TARTRATE-RESISTANT ACID PHOSPHATASE IN SYNOVIAL FLUID OF NORMAL

AND OSTEOARTHRITIS STIFLE SECONDARY
M.R. Alam1, H.B. Lee3, S.Y. Park3, S.Y. Heo1, K.M. So1, Y.H. Lee2, I.S. Kim1, H.S. Kang3, N.S. Kim1
1
College of Veterinary Medicine, Chonbuk National University, Jeonju, South Korea; 2School of Dentistry, Chonbuk
National University, Jeonju, South Korea; 3Center for the Development of Healthcare Technology, Chonbuk National
University, Jeonju, South Korea

This study investigated the concentration of
tartrate resistance acid phosphatase (TRAP)
in the stifle synovial fluid of normal and
osteoarthritis secondary to experimental medial
patellar luxation (MPL). MPL was surgically
produced in the left stifle (index) of 20 mixed
small breed dogs (age 1 to 10 years, weight 2.8
to 10 kg) by placing purse string sutures around
the parapatellar fibrocartilage and anchoring the
patella with the fabellar ligament, and by medial
imbrication and lateral release. The animals were
randomly allocated in 2 groups; sham group
(n=10), the right stifle was sham operated and
control group (n=10). Radiographs were taken
and synovial fluid was aspired from both stifles
preoperatively and postoperatively at every
1.5 month intervals. One dog was euthanatized
at every 1.5 month and tissue samples from both
stifles were collected for histopathology. TRAP
assay was performed using a biochemical assay
in 96-well plates with p-nitrophenylphosphate
(pNPP) as substrate. The clinical signs of
osteosrthritis were obvious in the experimental
dogs by 12 weeks of the surgical induction of
MPL which was also evidenced in histopathology
of the tissue samples. The concentration of TRAP
in the index stifles significantly increased after 3
months as compared with that of the sham and
control stifles. The surgically made MPL can be
a tool for experimental induction of osteoarthritis.
The TRAP assay can play an important role for the
diagnosis and therapy of osteoarthritis in the dog.

TREATMENT OF BENIGN PROSTATE HYPERPLASIA WITH OSATERONE ACETATE

TABLETS
M. Albouy, A. Sanquer
VIRBAC, 13e rue LID, Carros, France

Benign Prostatic Hyperplasia (BPH) is a common
disease of non-castrated dogs, with a high
prevalence (>80%) in dogs over 5 years. The
use of anti-androgens represents an interesting
alternative to surgery. A multicentric, controlled
and randomised clinical field trial was conducted
in 4 European countries to evaluate the efficacy
of Osaterone acetate (OSA) tablets on dogs
presenting with clinical signs of BPH. OSA tablets
administered at a dose of 0.25 mg/kg bw once daily
for 7 days were compared to delmadinone acetate
(Tardak®, Pfizer) administered once IM or SC at
a dose of 3 mg/kg bw. Over a 6-month follow-up
period, the dogs were examined on 5 different time
points: D0, D14, D60, D120 and D180. At each visit,
a clinical examination was performed and the size
of the prostate was determined by ultrasonography.
Efficacy of the products was assessed by the percent
reduction of the prostate size and the clinical
recovery rate (complete resolution of clinical
Back to contents
signs) on D14. Product persistence of activity was
estimated from the average time to requirement of a 2006 World Congress WSAVA/FECAVA/CSAVA
second course of treatment. One-hundred forty-two
dogs of various breeds were included in the study:
73 were treated with OSA and 69 with Tardak. On
D14, the prostate volume was reduced by 38% with
OSA and 27.6% with Tardak (p=0.002). Clinical
recovery was reported in 36 dogs (49.3%) in the
OSA group and 33 (47.8%) in the Tardak group
(p=0.8592). Over the whole 6-month period, a
clinical score of 0 was achieved in 92% of dogs
treated with OSA. OSA persistence of activity was
at least 161 days, an intermediate estimation to be
re-evaluated after additional long term follow-up
of the dogs. Tolerance to OSA was good, a slight
increase in appetite was sometimes recorded and
managed with appropriate food intake monitoring.
A short 7-day course of Osaterone acetate tablets
proved an efficient, long-lasting and safe therapeutic
regimen for Benign Prostatic Hyperplasia in dogs.
831
POSTERS

COMPARATIVE STUDY ON IRON DEFICIENCY ANEMIA IN PUPPIES FED WITH

MATERNAL AND NON MATERNAL MILK
S.J. Aldavood1, P. Keyhani2, A.R. Karegar3, A. Moghadami4, H. Salari Seddigh5
1
Azad University, Science and research center Campus, Sarv Sq., Tehran, Iran; 2Shahre kord Azad University,
Veterinary faculty, Daghighi st., Isfehan, Iran; 3Shahre kord Azad University, Veterinary faculty, Daghighi
st., Isfehan, Iran;4Veterinary Organization, N osrat St., Tehran, Iran; 5Veterinary faculty of Kerman University,
University, Kerman, Iran

Anemia and particularly iron deficiency anemia
is one of the most important factors in growing
problems in puppies. It can make a lot of negative
effects in growing process. Iron deficiency
anemia is produced by depletion of iron reserves.
Due to this depletion, no iron is available for
haemoglubin (Hb) synthesis. Iron reserves
depletion happens when the iron consumption or
iron loss be considerably, more than synthesis. In
this study two groups of puppies (25 puppies in
each group) with 3 months old in average, were
selected randomly. The first group was considered
as the control group and the puppies of this group
were fed with maternal milk. The second group
was the test group and the puppies of this group
were separated from their mother maximum at
2006 World Congress WSAVA/FECAVA/CSAVA
Haemoglubin concentration (Hb), Hematocrit
(PCV) and cellular indexes of MCHC, MCH and
MCV were measured. The result showed that
there is significant difference in “mean red blood
cells count” between control and test groups.
(P≤0.05) Differences of “MCHC” between these
two groups were also significant (P≤0.05). More
ever all of these parameters were compared
statistically with their corresponding standard
values and all differences were significant except
for “MCHC” and “MCV” between control group
and relevant standard values. It means that
the RBCC in puppies fed with maternal milk
are normocytic-microchromic and somehow
iron deficiency in this group of puppies can be
neglected. In other hand, “MCV” in test group

two weeks old. These puppies were fed manually had significant difference with normal values,
with the cow‫׳‬s milk. One ml of blood was so in this group the RBCC are microcytic-
collected from each puppy and haematological normochromic and this issue can be early stage
factors such as red blood cells count (RBCC), of iron deficiency anemia.

ABDOMINAL DEEP PYODERMA DUE TO PSEUDOMONAS AERUGINOSA IN

A DOG
S.J. Aldavood, S. Mokaram, M. Saberi, M. Abdi
Veterinary faculty of University of Tehran, Azadi St., Tehran, Iran

A male spayed 4 years old terrier dog weighting abdominal erythema with yellowish to green
4900 gr was presented to the small animal skin discharge, pustules, abdominal skin slough,
hospital of Tehran university with the history superficial skin necrosis, tachypnea, tachycardia,
of abdominal skin pruritis, anorexia treated for pyrexia (39.8 centigrade degree) was revealed.
ectoparasites one week before referring to the Hemogram result was: PCV: 36%, WBC: 3500,
hospital. In primary physical examination severe neutrophil: 60%, band: 2%, lymphocyte: 31%,
832
Back to contents

eosinophil: 5%, monocyte: 2%, total protein:
7gr/dl. In biochemistry profile, hepatic and renal
factors were in normal range. The dog suffers from
leucopenia and regenerative anemia. Numerous
white blood cells, RBC and cocci shape bacteria
were seen in microscopic evaluation of the stump
skin sample. Fungal culture was negative and
pseudomonas aeruginosa detected as the dominant
infective agent in the bacterial culture. Medical
therapy with parentral and topical gentamicin,
POSTERS
diluted white vinegar (10%), and levamisole by
the immunostimulatory dosage (2.2 mg/kg po q
48 h for 3 weeks) was prescribed. There were
significant improvement after one week and the
leukogram was normal after 2 weeks.
1- Muller, Kirk. Skin pyoderma in: Small animal
dermatology. Saunders, 2002; 891-95.
2- Slatter D. Skin and adnexa In: Textbook of
Small Animal Surgery, Philadelphia, Saunders
2003; 259-274.

A CASE REPORT OF GLUMERONEPHRITIS AND RENAL INFARCTION IN A CAT

S.J. Aldavood, M. Saberi, S. Hesaraki, S. Mokaram
Veterinary faculty of University of Tehran, Azadi St., Tehran, Iran

A 4 years old domestic short hair cat was presented
in the small animal hospital of the University of
Tehran with signs of vomiting, lethargy, anorexia,
diarrhea, stomatitis, lingual erosions, oliguria and
haematuria. Physical examination revealed pale
mucus membrane, 8% dehydration and normal
respiratory sounds. In abdominal palpation
unilateral renomegaly was detected. CBC
results included: total WBC: 14000, segmented
neutrophils 70%, Lymphocytes 18%, Monocytes
1%, Eosinophils 2%, PCV 41%, NRBC 2%,
Polychromasia and anisocytosis. Hypoglycemia
(60 mg/dl), BUN 90 mg/dl, Creatinine
175 µmol/l, Urea 192 mg/dl were detected
in serologic examination. Urinalysis findings
included: Specific gravity 1025, pH 5, protein
4+, RBC 3+, WBC 4+, Epithelial cell 1, Bacteria
positive and Amorphus uric acid crystals.
Ultrasonographic findings were increased
echogenisity of renal cortex, poor definition
between cortex and medulla and spot like
echogenicities in urinary bladder. The case was
suspected to glumeronephritis and supportive
therapy was performed for 2 weeks. The cat died
after 2 weeks and in necropsy glumeronephritis and
renal infarction in both kidneys were confirmed.

PRIMARY CUTANEOUS EXTRAGENITAL CANINE TVT IN A DOG

S.J. Aldavood, M. Saberi, S. Hesaraki, S. Mokaram
Veterinary faculty of University of Tehran, Azadi St., Tehran, Iran

The clinical signs and histopathological features
of a primary extragenital canine transmissible
venereal tumour (TVT) are described in a 5
months old spayed male spitz dog. subcutaneous
4×2.7 cm oval shape alopecic nodule was located
on the caudoventral region of the right flank.
The prefemoral and inguinal lymph nodes were
not involved (FNA procedure). Cytologically,
tumour cells were intermediate in size with a
moderate amount of cytoplasm, and the nuclei
were immature with finely reticular chromatin.
The nucleus to cytoplasmic ratio was large. The
cytoplasm was lightly to heavily basophilic and
contained distinct small vacuoles at the periphery.
On the basis of these characteristics, a diagnosis
of TVT was made and confirmed by histological
investigations. The skin bump was surgically
excised and in his annual check up there were no
skin bump or other forms of TVT.
1- Muller, Kirk. Skin pyoderma in: Small animal 2006 World Congress WSAVA/FECAVA/CSAVA
dermatology. Saunders, 2002; 891-95.
2- Vermooten MI. Canine transmissible venereal
tumor (TVT): a review. J S Afr Vet Assoc 1987;
58(3):147-150.
3- Brown NO, MacEwen EG. Calvert CA.
Transmissible venereal tumor in the dog.
California Vet 1981; 3:6-10.

STEROID-RESPONSIVE MENINGITIS IN A MALE SPITZ DOG

S.J. Aldavood, M. Saberi, D. Shirani, N. Khorami, S. Mokaram
Veterinary faculty of University of Tehran, Azadi St., Tehran, Iran

Steroid-responsive meningitis-arthritis is an cerebrospinal fluid. A 5-year old male spitz dog

immunopathological disease in dogs. Typically presented because of neck pain and cervical
are characterized by neutrophilic pleocytosis rigidity. There was no significant clinical
and an elevated protein concentration of the response when referring veterinary surgeon
833
Back to contents
POSTERS
prescribed systemic antibiotic therapy and
aspirin as a first clinical approach. CSF Analysis
showed increased protein concentration and
neutrophilic pleocytosis. Cultures of the CSF
remained sterile. These findings, in combination
with declining markers of CSF infection, are
OSTEOSARCOMA IN FRONTAL BONE IN A DOG IN IRAN
S.J. Aldavood1, A. Veshkini1, M.H. Karimi-Nejad2, E. Gorgin1
1
Veterinary faculty of University of Tehran, Azadi St., Tehran, Iran; 2Pathologist, Shahrake gharb, Tehran,Iran
Seventy five per cent of the osteosarcomas
originate in the long bones. The skull bones are
rarely involved and in our present knowledge
there was no report of osteosarcoma arising from
frontal bones in Iran. A 11 years’ old male German
shepherd dog was referred to the Small Animal
Hospital, faculty of Veterinary medicine, because
of a mass on the head of two months duration.
The lesion was a hard nodule on the left Frontal
bone, measuring 10 cm in diameter. There was
mild tenderness on palpation and no warmer than
body temperature. The owner gave no history of
head trauma or fractures. A CBC, biochemistry
work-up, and urinalysis showed no abnormalities.
Melena was positive in the stool because of
passage of blood through the nasal cavity and
pharynx. The neurological examinations were
normal, excluding brain invasion. Lat. oblique
view of the skull showed cortical destruction of
PHARMACOKINETICS OF OSATERONE ACETATE AFTER REPEATED ORAL
ADMINISTRATION AT 0.25 MG/KG/DAY FOR 7 DAYS
V. Allix1, M. Sillon1, T. Mezzasalma2, L. Maynard1
1
VIRBAC, 13e rue LID, Carros, France; 2AVOGADRO, Parc de Genibrat, Fontenilles, France
A GLP study was performed on 6 non-fasted
Beagle dogs to evaluate the pharmacokinetics of
2006 World Congress WSAVA/FECAVA/CSAVA
osaterone acetate (OSA) (YPOZANE, Virbac)
after a 7-day oral repeated administration at the
therapeutic dosage of 0.25 mg/kg/day. Blood
samplings were collected at 0.5, 1, 1.5, 2, 3, 4, 6, 8,
12 and 24 hours after the 1st treatment, at 1, 2, 4, 6,
8, 12 and 24 hours after the 4th treatment, and at 0.5,
1, 1.5, 2, 3, 4, 6, 8, 12, 24 hours and 2, 3, 5, 8, 12,
15 days after the 7th treatment. OSA in plasma was
quantified by validated Liquid Chromatography
with Mass/Mass detection with a LOQ of 2.0ng/ml.
According to a model for repeated administration,
Tau (Interval between 2 administrations), Cmaxss
(Maximal observed concentration at steady state
during Tau), Tmaxss (Time for Cmaxss), Cmin
(Minimal observed concentration at steady state
during Tau), AUCss (Area Under the Curve at
steady state during Tau), Cav (Mean concentration
between 2 administrations: AUCss/Tau), Cmax1
834
Back to contents
consistent with sterile meningitis. Corticosteroid
therapy improved clinical signs but Recurrence
developed with steroid stopping. Longer term
corticosteroid therapy for duration of 4 months
resulted complete improvement without any
relapse.
the left frontal bone with amorphous extra cortical
new bone formation extending into the soft tissue
neoplastic mass. The lesion seems to be more
osteoclastic. Right frontal bone is intact. Lat.
oblique radiography revealed more aggressive
changes in left frontal bone which shows rapid rate
of changes of this malignant lesion. Microscopic
examinations revealed highly cellular neoplastic
tumor, compose of fairly uniform stellate
vacuolar or slightly eosinophilic cytoplasm. The
nuclei are irregular in shape and vesicular with
one or two prominent nucleoli. The Tumor cells
tend to produce osteoid tissue. Numbers of giant
osteoclastic cells around osteoid formation are
evident. Occasionally spicules of bone formation
also present. After radiographic and pathologic
confirmation of osteosarcoma and because of
owner request dog was euthanasied.
(Cmax after the 1st administration) were calculated
with Kinetica software (InnaPhase). Accumulation
ratio (R1) was calculated as the ratio of Cmaxss to
Cmax1. According to a non-compartmental analysis
for extra-vascular administration, for single day
of administration (1st, 4th and 7th administration),
Cmax, Tmax, AUC0-t (AUC between t0 and time of
the last quantifiable concentration), Lz (Constant of
elimination rate, slope of the log-linear regression
(ln concentration versus time) calculated for the
last points to maximise the r coefficient), AUC0-24h
(AUC from 0 to 24h after each administration) were
calculated with Kinetica. Accumulation ratio (R2)
was calculated as the ratio of AUC0-24h between
7th and 1st administration. The plasma concentration
and the AUC of OSA were higher after the 7th dose
than after the 1st dose (see table and figure). After 7-
day oral administration, a bioaccumulation of OSA
was demonstrated (R1 = 3.1 ± 1.0 and R2 = 4.2 ±
1.0) in correlation with a long elimination half-life.
 POSTERS
ENROFLOXACIN EFFICIENCY IN URINARY INFECTION CONTROL OF THE
DOGS WITH TRANSITIONAL CELL CARCINOMA
A.L. Andrade1, M.C.R. Luvizotto1, M.G. Laranjeira1, F.R. Eugênio1, M.A.R. Fernandes2, H.F. Ferrari1
1
Curso de Medicina Veterinária, Rua Clóvis Pestana, 793, Araçatuba, Brazil; 2Centro de Ensino e Tecnologia de
Araçatuba, Rua Humaitá, 231, Araçatuba, Brazil

The transitional cell carcinoma (TCC) is the
most common form of canine urinary bladder
cancer and its most often trigonal in location
and can result in partial or complete urinary
tract obstruction. The etiology of canine bladder
cancer is most likely multifactoral. Bacterial and
virus infections and you capsize as being one the
involved causes in vesical carcinogenesis. The
enrofloxacin efficiency in controlling the urinary
infections associates the vesical neoplasias was
studied. Eleven dogs, male and female, with
papillary infiltrative transitional cell carcinoma
associated with urinary infection caused by
Eschechiria coli and Proteus Mirabilis, had
been treated by means of tumoral resection in
association with 90-Strontium betatherapy
(3.000 cGy) with bladder preservation. The
respective infections had been treated during
15 days with enrofloxacin after surgery and
betatherapy. The animals were observed during
one year and they did not have the disease returns,
which was confirmed by clinical and uroculture
laboratory analysis. Finally, in this study the
enrofloxacin demonstrated to be efficient in
controlling the urinary infection in these cases. 2006 World Congress WSAVA/FECAVA/CSAVA

BRAIN GLIOMA IN A DOG - CASE REPORT

N. Andric1, M. Matic2, S. Spasojevic2, M. Curcic2
1
Faculty of veterinary medicine, Bulevar oslobodjenja 18, Belgrade, Serbia; 2Private veterinary clinic “SPINA”,
Bulevar Arsenija Carnojevica 17a, Belgrade, Serbia

Clinical History: The Irish setter, female, 15
years old, was brought to the Small animals clinic
at Faculty of veterinary medicine in Belgrade,
with the history of seizures. Within five days the
dog had four tonic - clonic seizures, that lasted
for ten to fifteen minutes each. Other than that,
the owners have recently noticed behavioral
change which manifested in anxiety, and, a day
before coming to the Clinic, the dog was unable
to stand.
Back to contents
Physical and Neurological Examination:
Depressed/obtunded, heads tremor, depressed
cranial reflexes of the right side of the head and
hemiparesis of the right side of the body.
Diagnostic testing: cbc and serum chemistry - no
abnormalities; urin analysis: no abnormalities;
radiograph examination of calvarum: no
abnormalities; CT scan without contrast and with
contrast: omnipaq (350mg/ml) in the doses of 1ml/kg
of body weight IV was used as the contrast. CT
835
POSTERS

scan without contrast points out to the existence of
expansive formation in the area of the left parietal
lobus, completely compressing the left lateral
ventricle, while the right lateral ventricle dilated.
After IV contrast aplication, contrast enhancement
in the compressed area is noticed, whereas changed
formation was not clearly defined.
Diagnosis: Neoplasia was suspected.
Therapy: After consultations, colleagues from
private veterinary clinic «SPINA» decided to
operate the dog, in order to remove the most of
the tumor. During the operation, the sample
of tumorous mass was taken for histologic
examination. Tissue samples were colored by
haematoxylin – eosin (HE) and examined through
microscope. Histological examination confirmed
changes that point out to the glioma. The euthanasia
was carried out.

MALIGNANT PERIPHERAL NERVES SHEATH TUMOUR (MPNST) IN A DOG

– CASE REPORT
N. Andric1, M. Knezevic1, V. Kukolj1, D. Djurdjevic2
1
Faculty of veterinary medicine, Bulevar oslobodjenja 18, Belgrade, Serbia; 2Military academy of medicine,
Crnotravska 17, Belgrade, Serbia
Clinical History: The Siberian husky, male, 13
years old, was brought to the Small animals clinic
at Faculty of veterinary medicine in Belgrade,
with incapability of standing on the thoracic left
limb. The dog started limping on left thoracic
limb one year ago, and lameness increased during
time. A month ago, the dog stopped leaning on
that limb (in case of leaning on that limb, it would
show signs of pain). The dog started to drag the
limb ten days ago, and the pain was increasing,
and manifested with whining and biting its limb
in the area of m. brachialis.
Physical and Neurologic Examination: sensorimotor
monoplegia with apparent muscles atrophy of
the thoracic left limb with no other neurological
abnormalities.
Diagnostic Testing: cbc and serum chemistry: no
abnormalities; vertebral radiographs C6 – T2: no
abnormalites; MRI without contrast: above the
top of the left lobe of a lung parathrahealy, oval,
clearly limitied, expansive formation is noticable,
with the dimensions 43x57mm, which holds back
the trachea contralateraly and pushes down the top
of lungs. The tumor had moderate unhomogenous
hypersignal in T1W, and distinctive hypersignal
in T2W. The suspected diagnosis was neoplasia
of brachial plexus peripheral nerves. Following
euthanasia, histological examination confirmed
infiltrative and poorly circumscribed tumorous
mass, composed of a dense population of spindle-
shaped cells arranged in fascicles, whorls or
sheats. There were two to five mitotic figures
per high-power field. Immunohistochemically,
most spindle cells were positive for vimentin and
negative for S-100, keratin and GFAP. Based on
the morphological and immunohistochemical
features, the tumour was classified as a malignant
peripheral nerve sheath tumour (MPNST) with
dominant mesenchymal component.

PERIODONTAL REGENERATION WITH LOW LEVEL LASER THERAPY (SOFT

LASER) - EXPERIMENTAL STUDY IN BEAGLE DOGS
2006 World Congress WSAVA/FECAVA/CSAVA

C.A. Antunes Viegas1, U. Thams2, J. Rodrigues1, G. Watzek3, M.I.R. Dias1, P. Llorens2, F. San Román2
1
Veterinary Science Department – University of Trás-os-Montes e Alto Douro, Portugal; 2 Animal Medicine and
Surgery Department –University Complutense of Madrid, Spain; 3 Medical School – University of Vienna, Austria

The purpose of this study was to prove the effect
of the soft laser (low level laser therapy) in
the reconstruction and healing of hard and soft
periodontal tissue after periodontal reconstructive
surgery. In this experiment five Beagle dogs were
used. The procedure was the following: 7 mm large
periodontal defects were created in the mandibular
vestibular face at the 4th premolar and the 1st. molar.
The root surfaces were then instrumented to remove
all cementum and the wounds immediately closed
by replacing and suturing the flaps just coronal to
the cementum-enamel junction. All the defects
were filled up with collagen, and during a period
836 of 4 weeks, 5 days a week, the teeth were treated
with soft laser only on experimental side. The dogs
were sacrificed 16 weeks postsurgery. Histometric
recordings included height and area of alveolar
bone regeneration, height of cement regeneration,
connective tissue repair, and junctional epithelium.
We evaluated the bone regeneration, the dental
cement regeneration, the new PDL, the collagen
sponges persistence, root resorption and/or
ankylosis histologicly. Group means, standard
deviations, and P values are shown (Student t test;
n=5 y χ2; n=2). The size of regeneration with laser
measured 1.8 ± 0.5 against 2.3 ± 0.8 on control
(ns). Bone-values with laser were 2.1 ± 0.8
against 2.7 ± 1.0 on control (ns). The regenerated

Back to contents

cement measured 1.7 ± 0.5 with laser against
2.8 ± 0.8 on control (p=0.006). The junctional
epithelium measured 2.7 + 1.1 with laser against
2.8 ± 0.1 on control (ns). The connective tissue
repair measured 2.2 ± 1.0 with laser against 1.6 ±
0.4 on control (p=0.04). Ankylosis was 0.0 ± 0.0
with laser against 0.0 ± 0.0 on control (ns). One
found root resorption on 11/18 with laser against
7/18 on control. The irradiated bone presents
architectural disorganization and an intense
CONCRETIONS IN EXOTICS. CLINICAL AND RADIOLOGICAL EVALUATION
J. Arnbjerg, M.L. Ruelokke, T. Iburg
Royal Veterinary University, Dyrlaegevej 32, Copenhagen, Denmark
Concretion is described in 9 guinea pigs out of
approx. 150 guinea pigs radiographed; High
density in the urinary bladder in 3 rabbits.
Case GP 1: A neutered male presented with pain
associated with defecation. Radiographs revealed
a urinary bladder calculus and irregular higher
density areas bilateral to the rectum. The urinary
calculus was removed but the animal still painful
during defecation. At post mortem both anal sacs
were found with hard concrements. Size, shape
and location were at the density observed on the
radiographs.
Case GP 2: A 4 years old male guinea pig had
dysuria and stranguria. Abdominal radiographs
showed a high density 6 x 14 mm around the os
penis. After content removed from the preputial
cavity normal radiological findings around the os
penis was observed and the animal had no clinical
symptoms.
Case GP 3 – 9: These 5 male and 2 female guinea
pigs were of different age but were radiographed
due to other reasons than urinary tract problems.
They showed minor concretions in their prepuce
cavity and urinary excretion system.
SEROEPIDEMIOLOGICAL INVESTIGATION OF VISCERAL LEISHMANIASIS IN
DOGS OF AHVAZ, IRAN
R. Avizeh, M. Mohebali, M. Sheikholeslami
Shahid Chamran University, Golestan, Ahvaz, Iran
Visceral leishmaniasis is a parasitic infectious
transmissible disease from dogs and canids
to human that is caused by protozoans of the
genus Leishmania. Infected dogs serve as
reservoirs of the disease in many countries.
Information on the prevalence of canine
leishmaniasis is necessary to define control
measures for zoonotic leishmaniasis. This
seroepidemiological survey was performed in
dogs from Ahvaz district using by DAT and
ELISA from October 2003 to March 2004. Blood
Back to contents
POSTERS
activity of bone remodelling. We could see some
empty osteocytes lacunes and some osteocytes
nucleus in picnosis or cariolisis. The PDL presents
a few density of functionally oriented periodontal
fibers and was poorly irrigated. We couldn’t find
collagenous vehicles in both the experimental
and the control groups. Our data suggest that
laser helps with the soft tissue cicatrization but it
stops the bone regeneration.
Case Rabbit 1 - 3: Three rabbits were presented
with coloured and opaque urine. No other
abnormal clinical signs. On radiographs their
bladders were visualized with varying but high
density.
Discussion: The urinary bladder stones in the
male guinea pig are located in the bladder, but in
the female, the stone can be located very caudally
in urethra. The existence of the Perianal Glands
is debated. We found Perianal Glands in male
Guinea Pigs only. Smegma is a normal fatty oily
substance, which some authors claims is produced
by the mucilaginous/sebaceous glands, Tyson’s
glands. The infection in relation to smegma
seems in animals to be mycobacterium, but no
specific organism was found in this material. The
Tyson Glands could not be found in these Guinea
Pigs. High density and opaque urine is due to an
excretion of surplus of Calcium.
Conclusion: In case of tenesmus in Guinea Pig
concretion-conditions should be considered.
In rabbits with high radiological density in the
urinary bladder the clinical symptoms can be
unspecific and due to excretion of calcium.
2006 World Congress WSAVA/FECAVA/CSAVA
was randomly collected in 38 pure or mixed
breed dogs presented to veterinary hospital
of Ahvaz Shahid Chamran university (urban
dogs) and 172 mongrel dogs of 10 villages
around Ahvaz city (rural dogs). A high level
of concordance (98%) was found between the
titers measured by DAT and ELISA then DAT
selected as valid and simple test. The detected
seroprevalences based on DAT were 2.6% and
16.3% in urban and rural dogs respectively. No
statistically significant difference was observed
837
POSTERS

between male and female seroprevalences in each
groups (P>0.05). Regarding age-groups of rural
dogs, the lowest of seroprevalence (5.3%) was
foun d in dogs younger than one year of age and
the highest (33.3%) in dogs older than seven years.
Only between of these two groups was statistically
significant difference (P<0.05). In rural dogs was
not statistically significant difference between
village seroprevalences (P>0.05). This study
revealed the importance of the dog as a reservoir
for visceral leishmaniasis in Ahvaz district. It
seems that seroprevalence of disease in rural dogs
from Ahvaz district is similar to Endemic area as
of Mediterranean countries.

ANTIBODY TITERS AGAINST CANINE DISTEMPER VIRUS IN UNVACCINATED

RURAL DOGS FROM AHVAZ, IRAN
R. Avizeh, M.R. Seifiabad Shapoori, N. Akhlaghi
Shahid Chamran University, Golestan, Ahvaz, Iran

Canine distemper is an acute to subacute contagious
febrile and often fatal disease with respiratory
gastrointestinal and CNS manifestations which
caused by canine distemper virus (CDV), a
morbillivirus in the paramixoviridae family.
The purpose of this study was to evaluate the
prevalence of antibodies to CDV in unvaccinated
rural dogs without known immunization status
and to assess risk factors for infection by means
of indirect immunofluorescent test (IFA), in Ahvaz
district, southwest of Iran. Serum samples were
randomly collected from 97 healthy dogs greater
than six months old from six villages around Ahvaz
city between 2004 and 2005. We considered titers
> or = 1:10 indicative of an adequate antibody
response. Dogs were grouped by age, sex, and
area to determine whether these factors were
associated with antibody titers, using fisher’s
exact test. Seroprevalence to CDV antibodies in
these dogs were 17.52% indicating that this virus
is present in the ecosystem. Also there is evidence
of previous natural exposure to CDV. Prevalence
of antibodies to CDV did not differ among various
regions or between sexes or ages (P>0.05). Rural
dogs are abundant in the ecosystem of area and
interact with other species of wild carnivores and
domestic animals in ways that could encourage
disease transmission. The prevalence of CDV
antibody-positive dogs do not indicates protection
against canine distemper, thus these dogs also may
be affected. Therefore we should direct future
guidelines for translocations, including quarantine
of seropositive dogs and preventing contact between
them and domestic pets. Also the role of rural dogs
in the epizootiology of CDV in both urban dogs
and wildlife needs to be further explored.

CLINICAL AND ELECTRODIAGNOSTIC EVALUATION OF TRAUMATIC DISEASE

OF BRACHIAL PLEXUS: 12 DOGS, 17 CATS
O. Besalti1, Z. Pekcan2, Y.S. Sirin3, E. Unlu4
1
Ankara University Faculty of Veterinary Medicine Department of Surgery, Diskapi, Ankara, Turkey; 2Kirikkale
University Faculty of Veterinary Medicine Department of Surgery, Yahsihan, Kirikkale, Turkey; 3Ankara University
Faculty of Veterinary Medicine Deapartment of Surgery, Diskapi, Ankara, Turkey; 4Ministry of Health Ankara
2006 World Congress WSAVA/FECAVA/CSAVA

Diskapi Education Hospital Department of Physical Therapy and Rehabilitat, Diskapi, Ankara, Turkey
The objective of the study was to present 76.47% respectively. The radial nerve was involved
electrodiagnostic and clinical findings of the in all cases individually or associated with other
traumatic disease of brachial plexus (TDBP). nerves. There were avulsion in radial nerve (n=11)
Dogs and cats that had clinical signs of TDBP and at the outside of vertebral canal or lower spinal
and diagnosed electrophysiologically were ganglion (n=4), and the other cases had multiple
reviewed. Standard motor nerve conduction nerve involvement in brachial plexus as in ulnar-
study and/or sensory nerve conduction studies, median, axial, musculocutaneous and suprascapular
H reflex, somatosensoric evoked potentials, and nerve in addition to radial nerve. The injured nerves
needle electromyography in both extremity and were found totally severed and lodged in fibrous
paraspinal muscles were employed for diagnosing tissues ventrally at the operation or necropsy.
the involved nerve and level of injury. Injured areas However in two surgically explored cats epineurium
were examined in three cases (1 dog, two cats) after remained partially intact. In conclusion, sensory
euthanasia and in 10 cases (4 dogs, 6 cats) during nerve action potentials, and needle EMG and H
operation at the lower part of brachial plexus by the reflex can be suggested in determining the avulsion
reflexion of the scapula laterally. The left side was of the brachial plexus, denervation potentials can be
predominant in both dogs and cats in 81.82 % and accepted as a clue to diagnose the involved nerve.
838
Back to contents
 POSTERS
THE EFFECT OF CHRONIC OTITIS EXTERNA–MEDIA ON BRAINSTEM AUDITORY
EVOKED RESPONSE IN DOGS
O. Besalti1, Y.S. Sirin2, Z. Pekcan3, O. Koskan4
1
Ankara University Faculty of Veterinary Medicine Department of Surgery, Diskapi, Ankara, Turkey; 2Ankara
University Faculty of Veterinary Medicine Department of Surgery, Diskapi, Ankara, Turkey; 3Kirikkale University
Faculty of Veterinary Medicine Department of Surgery, Yahsihan, Kirikkale, Turkey; 4Ankara University Faculty of
Agriculture, Diskapi, Ankara, Turkey

The objective of the study was to present normative
Brainstem Auditory Evoked Response’s (BAER)
data acquired by the both air conducted clicks
(30–100 dBHL) and bone conducted clicks
(100–130 dBHL) for normal dogs, and dogs
with chronic otitis externa–media. The data
were analyzed to acquire reference values of the
laboratory in 55 healthy dogs and to estimate the
degree of hearing impairment associated with
the disease. Fifty four dogs with chronic otitis
externa-media were divided into two groups. The
first group included dogs with severe chronic
otitis externa–media, candidate to surgery
(n=16), and the second group included dogs with
mild chronic otitis externa–media, candidate to
medical treatment (n=38). The appearance rate
of V. potential was found higher than the others
at the every stimulation level. Seventh potential
was not seen by the bone conducted click at the
all stimulation level, and also in cases with severe
chronic otitis externa–media by the air conducted
click. While fifth potential was seen more than 50
% at the 60 dBHL in severe otitis externa-media,
it was at the 30 dBHL in mild otitis externa. The
latencies of potentials (I-VII) acquired from
healthy dogs and interpeak latencies (I-III, I-V,
III-V) were compared between left and right side
there were no significant differences between
both sides except for the shorter latency of the
VI. potential in the left ear. Facial paralysis was
diagnosed in four cases with severe chronic otitis
externa-media. In conclusion, reference values
of the laboratory for BAER in healthy dogs were
obtained. Chronic otitis externa–media cause
increasing latency rather than total deaf. BAER
can be suggested as an ancillary diagnostic tool
in ear disorders.

SOME BIOLOGICAL AND IMMUNOLOGICAL STUDIES ON HYDATIDOSIS/

ECHINOCOCCOSIS IN EGYPT
A. Derbala1, A. Elmassry2, M. Mahmoud1, O. Elragehy1
1
National Research Centre, Parasitology & Anim. Dis. Departement, Tahrir Street, Giza, Egypt; 2Faculty of
Veterinary Medicine, Parasitology Departement, Gamea Street, Giza, Egypt

Hydatidosis or echinococcosis is caused by a
tapeworm, Echinococcus granulosus. It is still a
serious public health of zoonotic and economic
importance. The biological identification showed
several aspects between the adult worms. The
prepatent period was 55 days for camel strain
while that of Equine strain was 70 days. Marked
differences between the total length of worm; the
length and width of scolex, immature, mature and
gravid segments; total length and blade length
of rostellar hooks were observed. Regarding
the immunological studies, the hydatid fluid
(HF) and protoscoleces (P) antigens from both
animals were partially purified using gel filtration
chromatography. The crude and partially purified
antigens of HF and P of both origins were resolved
by SDS-PAGE. Electrophoretic pattern revealed
distinct variations among the used antigens.
ELISA was preformed twice to evaluate the crude
and partially purified antigens against their versus
sera. The second ELISA was preformed on PC p1
and HFD p2 antigens against sera obtained from
naturally infected animals with hydatidosis or
with other parasites. The sensitivity of ELISA was
100% using PC p1 and HFD p2 in serodiagnosis
of hydatidosis. The specificity of ELISA was
97.6% and 95.9% in both origins, respectively. 2006 World Congress WSAVA/FECAVA/CSAVA
Using of HFC p1 and HFD p1 antigens in the
first step of ELISA showed that these antigens
might contain diagnostic epitops for hydatidosis
in both origins, so both antigens could be used in
Immunoblot technique to identify the diagnostic
bands for each species. Western blot recognized
two bands at 80 and 150 KDa which might be
diagnostic bands in both intermediate hosts.
While the epitops at 21 and 59 KDa might be
specific for camel hydatidosis. The common
reactive band at the level of 138 KDa might be
specific for hydatidosis in donkyes. Two variant
subspecies from E. granulosus were recorded.
Identification of specific antigens may have a
value in diagnosis and vaccine candidates.

839
Back to contents
POSTERS

DOSE TITRATION STUDY OF ORAL PASTE, PRAZIQUANTEL IN THE TREATMENT

OF ECHINOCOCCUS GRANULOSUS IN DOGS
A. Derbala1, L. Frayssinet2, A. Elmassry3
1
National Research Centre, Parasitology & Anim. Dis. Departement, Tahrir Street, Dokki, Giza, Egypt; 2Virbac S.A.,
Research and Development Departement, Carros, Cedex, France; 3Faculty of Veterinary Medicine, Parasitology
Departement, Gamea Street, Giza, Egypt

A control study trial involving 36 selected
healthy vaccinated, experimentally infected
with Echinococcus granulosus (10000 viable
protoscoleces/2 successive days for each animal)
was carried out. The study was designed to
compare the efficacy of 4 tested drugs in a new
paste formulation and various concentrations
of praziquantel (2.5-10 mg PZQ/kg B.W.) and
Droncit® tablets as a reference drug, in treatment
of E. granulosus infection in dogs. A single or
fractionated administered dose of treatment
with these oral pastes or Droncit® tablets (5 mg
PZQ/kg B.W.) gave a similar degree of efficacy
(100% clearance) against immature forms of E.
granulosus. According the experimental design,
animals were examined after necropsy for worm
burdens at 5, 7 & 9 days post treatment. Adverse
reactions or side effects were not observed in the
treated dogs. No serious risk was involved in
administering the tested drugs. The administered
pastes given orally were well tolerated
without observable adverse effects. These new
pharmaceutical preparations of praziquantel were
effective and extremely convenient to administer
for treatment of E. granulosus infection in dogs.

BIOLOGICALCONTROLOF SOFTTICKS (ARGASIDAE) BYENTOMOPATHOGENIC

NEMATODES
A. Derbala1, M. Hassanain1, N. Abdelbarry3, M. Elsherif3, H. Elsadawy1
1
National Research Centre, Parasitology & Anim. Dis. Dept., Tahrir Street, Dokki, Giza, Egypt; 2National Research
Centre, Tahrir Street, Dokki, Giza, Egypt; 3Faculty of Agriculture, Gameaa Street, Giza, Egypt; 4Faculty of Agriculture,
Gameaa Street, Giza, Egypt; 5National Research Centre, Tahrir Street, Dokki, Giza, Egypt

Potential hazards of insecticides caused
environmental pollution, insect resistance and
disturbance of natural biological balance. The
possibility of infecting the Acari, Argas persicus
(tick bird) using two species of entomopathogenic
nematode: Steinernema carpocapsae and
Heterorhabditis bacteriophora was investigated.
Different concentrations: 12000, 9000, 6000,
5000, 4000, 3000, 2000 & 1000 infective
juvenile stages (IJS) of the two nematode species
were used in the experiment. The study revealed
that nymphs, male and females soft ticks were
2006 World Congress WSAVA/FECAVA/CSAVA
according to host stage, the nematode species
and concentrations of (IJS). It was of interest to
mention that the nematodes could invade, kill the
ticks but failed to reproduce inside the dead ticks.
The influence of infected and non infected tick
haemolymph on the development and migration
of nematode inside cotton leaf worm, Spodoptera
littoralis, the host choice of nematodes, was
investigated. Mortality percentage with different
values was observed after their injection with
infected and non infected Argas haemolymph.
Entomopathogenic nematode might be used as an

susceptible to the two used nematodes. The LD50 alternative useful, safe and effective biological
values were estimated for the two nematodes, control agent in the future.
respectively. Rates of mortalities differed

PROLAPSUS URETHRA IN A DOG: A CASE PRESENTATION

B. Dokuzeylül1, Y. Devecioğlu2, A. Akdoğan Kaymaz1, A. Uysal1
1
Department of Internal Medicine, Veterinary Faculty of Istanbul University, Avcılar Campus, Istanbul,
Turkey; 2Department of Surgery, Veterinary Faculty of Istanbul University, Avcılar Campus, Istanbul, Turkey

Prolapsus of the urethral mucosa is a very
rare condition that occurs in male especially
castrated dogs. A 7-year old male, neutered
Yorkshire Terrier was referred to Clinic of
Internal Medicine, Veterinary Faculty of Istanbul
University, constituted the material of this study.
As being informed by the patient’s owner lethargy,
840 stranguria and bleeding from the prepuce lasted
for the duration of 5 days and castrated 3 years
ago, was also mentioned. Physical examination
at the time of referral revealed discomfort at the
penis region and oversensitivity at the urinary
bladder. The urethral mucosa was seen as
prolapsed and the mucosa’s colour was bright red
to dark purple. During the urethral catheterization
it was easily passed through the center of the

Back to contents

tissue. Severe thrombocytopenia (56x103 µL)
and prolonged PT (11 sn) and APTT (21 sn)
were detected in haematologic analysis. BUN
and creatinine levels were seen in normal ranges.
In the urinalysis, pyuria and crystalluria were
POSTERS
detected. After the antibacterial and supportive
therapies prolonged for 10 days, bleeding from
the prepuce disappeared. The patient’s problems
had finished one month later after the treatment
and the prolapsed mucosa healed.

STUDY THE EFFECT OF L-CARNITINE ON APOPTOSIS IN THE ISCHEMIC –

REPERFUSED ISOLATED RAT HEARTS
Y. Doustar1, A. Garjani2, M. Najafi3
1
Islamic Azad University, Vally Asr, Tabriz, Iran; 2Faculty of Pharmacy, University of Medical Science, Daneshgah,
Tabriz, Iran; 3Faculty of Pharmacy, University of Medical Science, Daneshgah, Tabriz, Iran

Carnitine is a vital biologic substance for
transporting fatty acids into myocytes and
facilitates fatty acids β-oxidation for energy
production. There are not enough reports about
its anti-apoptotic effects during ischemia/
reperfusion. In this study, effects of L-Carnitine
on apoptosis in the ischemic isolated rat hearts
were investigated. Male Sprague-Dawley rats
(270-330g) were divided into 4 groups randomly
and were anesthetized by sodium pentobarbital
(50-60 mg/kg-ip). Heart was removed and
quickly mounted on a Langendorff apparatus and
perfused by a modified Krebs-Henseleit solution
under constant pressure at 37 ºC. In control group
(n=6), the hearts were perfused only by normal
Krebs -Henseleit solution at stabilization, 30 min
regional ischemia and 120 min reperfusion, while
in the test groups (1-3 groups, n=6 in each group),
during ischemia / reperfusion, the hearts were
perfused with 0.5,2.5 and 5mM of L-Carnitine
- enriched Krebs-Henseleit solution, respectively.
At the end of reperfusion, Immunohistochemical
detection of apoptotic cells was performed by
using an in situ apoptosis detection kit. The
number of TUNEL-positive cardiomyocytes was
counted in five random high-power fields in each
sample. Data represented as mean ±sem for each
group. In control group, the number of apoptotic
cells were 48 ±3 while in the test groups, addition
of L-Carnitine (0.5, 2.5 and 5mM) into the Krebs
solution during ischemia and reperfusion, reduced
the number of apoptotic cells to 6±1, 4±1 and 3±1,
respectively (p<0.001). There was no significant
difference between and within test groups using
ANOVA one-way. Considering these results, we
conclude that L-carnitine has a protective effect
against cardiac ischemic reperfusion injuries as a
reduction of apoptotic cardiomyocytes.

GROWTH PERFORMANCE, SURVIVAL RATIO AND BODY MEASUREMENTS

UNTIL WEANING AGE OF GERMAN SHEPHERD DOG
Ö. Elmaz1, O.A. Aksoy2, S. Dikmen3, A. Zonturlu4
1
Akdeniz University, Faculty of Veterinary Medicine, Burdur, Turkey; 2Gemlik Military Veterinary School and
Training Center, Bursa, Turkey; 3Uludag University, Faculty of Veterinary Medicine, Bursa, Turkey; 4Harran
University, Faculty of Veterinary Medicine, Şanlıurfa, Turkey
2006 World Congress WSAVA/FECAVA/CSAVA
This study was carried out to establish body weight, respectively. Birth weight was statistically affected
survival ratio and average body measurements of the by mother’s age. And tail length and wither height
German Shepherd Dogs raised under the condition at 24, 38 and 52 day age was affected birth type (6
at Gemlik Military Veterinary School and Training litter) (P<0.01). Body measurements before weaning
Center during suckling period. Live weight and body were not affected by sex (P>0.05) except for head
measurement records of 82 pure bred (54 female, circumference (P<0.01). Correlations between
28 male) puppies were used for determining growth live weight and body measurements were also
characteristics. Mean weights of puppies at 1st week determined. Correlations between live weight and ear
and weaning were 776 and 2614g, respectively. length were significant before weaning (P<0.001).
Mean live weight of male and female puppies were Correlation between live weight at 35 day age and
statistically different at 2-4 week of age. Survival rate all body measurements were statistically significant
of puppies at weaning was found 83%. At 52 day (P<0.001). In conclusion, it was determined that live
age, head length, head circumference, body length, weight and body measurements of German Shepherd
wither height, ear length, body circumference, rump puppies before weaning period should be a beneficial
height, cannon circumference, tail length and hind tool for selection.
leg wrist circumference were 14.76, 24.03, 22.97, Keywords: German Shepherd Dog, weaning age,
25.16, 5.93, 30.64, 24.16, 6.62, 15.51 and 5.99 cm, body measurements, growth curve, survival rate.
841
Back to contents
POSTERS

PREVALENCE AND SUSCEPTIBILITY OF EUROPEAN PATHOGENIC BACTERIA

FROM CANINE INFECTIONS SINCE 1994
D. Galland, F. Woehrle, B. Boisrame, M. Valle
Vetoquinol SA., BP 189, LURE, France

A network survey on pathogenic aerobic strains
from canine pathologies of otitis (44%), urinary
(17%), respiratory (9%) and dermatological
(30%) infections has been established by
Vetoquinol in Europe since 1994. The 1474
isolated strains showed that the main pathogenic
strains were Staphylococcus intermedius,
Staphylococcus aureus (between 40 and 64%)
and Pseudomonas aeruginosa (between 22 and
38%) from otitis and dermatological infections,
Bordetella bronchiseptica (39%) and Pasteurella
multocida (30%) from respiratory infections, and
Escherichia coli (61%) from urinary infections.
Activity testing (by antibiograms) of the main anti-
infectious drugs against these pathogenic strains
has shown that marbofloxacin was generally the
most active (82 to 100%), followed by amoxicillin/
clavulanic acid (1 to 100%), cefalexin (1 to 99 %),
doxycycline (1 to 100%) and clindamycin (0 to
84%). The main multiresistant strains (up to hexa-
R) were observed for Pseudomonas spp. strains
from otitis. Marbofloxacin MICs showed a very
high activity against P. multocida strains (MIC90
range: 0.025 to 0.413µg/ml), Staphylococcus
spp. (MIC90 range: 0.219 to 0.435µg/ml), E. coli
strains (MIC90 range: 0.014 to 8.574µg/ml) and B.
bronchiseptica (MIC90 range: 0.375 to 0.456µg/
ml) and a lower activity against P. aeruginosa
(MIC90 range: 0.478 to 12.126µg/ml). MIC90
variability was primarily due to the low number
of strains isolated. The marbofloxacin MIC
distributions were unimodal for Staphylococcus
spp., B. bronchiseptica and P. aeruginosa strains.
For the other strains, the distributions were
bimodal. Few resistances to marbofloxacin have
been observed and mainly for E. coli strains
(5%) and Pseudomonas spp. strains (8%), but no
significant increase of marbofloxacin MIC90 has
been observed excepted for Staphylococcus spp.
isolated from otitis since 1994. Consequently,
marbofloxacin appears to be effective against the
main canine infections even if a limited spread of
resistance was observed.

EXAMINATION OF CANINE MAMMARY TUMOURS BY USING MAGNETIC

RESONANCE IMAGING
R. Garamvölgyi1, Z.S. Petrási1, B. Lőrincz1, Á. Hevesi1, Ö. Petneházy1, I. Repa1, C.S. Jakab2
1
Institute of Diagnostic Imaging, University of Kaposvár, Guba Sándor u. 40, Kaposvár, Hungary; 2Szent István
University, Faculty of Veterinary Science, Department of Pathology, István u. 2, Budapest, Hungary
Magnetic resonance imaging (MRI) is a sensitive, breeds (4 German Shepherd, 2 Mongrel, 1 Giant
noninvasive diagnostic tool that helps to establish Schnauzer, 1 Foxterrier, 1 Mastino Napolitano,
accurate diagnosis in neoplastic patients and 1 Pointer, 1 Tervueren) were examined during
enables the staging of tumourous diseases. MR anoestrus. Average age was 10,2 years, the dogs
mammography is widely used in the human weighed between 7-52kg. Examinations were
2006 World Congress WSAVA/FECAVA/CSAVA

oncologic practice. Since the introduction of
contrast-enhanced MRI of the breast, this method
has gained increased acceptance because it offers
new and different information as compared with
other imaging modalities. The aim of this study
was to obtain the availability of the human
mammographic MR protocol in the routine
examination of canine mammary glands. Cancer-
induced angiogenesis is the main feature that can
be pictered in vivo by dynamic contrast enhanced
(DCE)-MRI, and it plays an important role in
the differentiation of benign mammary diseases
from malignant ones. We examined whether
this human characteristic could be applied to
describe canine mammary tumours (contrast
enhancement, morphological patterns and kinetic
curves). After the imaging procedure the tumours
were excised and typified by histopathological
842 examinations. Eleven intact bitches of different
performed with a Siemens Magnetom Vision Plus
and a Siemens Avanto, 1.5 Tesla MRI scanner.
The following sequences, adapted from the
human protocol, proved to be suitable for MRI
examination of the canine mammary glands:
– T1 SE (TR: 450 s, TE: 9.6 s, Aq.: 2 s, SL: 4 mm,
FoV: 350 × 200 mm) coronal, transversal planes;
– T2 SE (TR: 3800 s, TE: 110 s, Aq.: 2 s, SL:
4 mm, FoV: 350 × 350 mm) coronal, transversal
planes;
– STIR (short T1 inversion recovery; TR: 4500 s,
TE: 36 s, Aq.: 2 s, SL: 4 mm, FoV: 350 × 350 mm)
coronal, transversal planes;
– T1 GE (TR: 12 s, TE: 4.8 s, Aq.: 1 s, SL: 2 mm,
FoV: 320 × 320 mm) in a dynamic fashion,
coronal plane.
We found that using static sequences the neoplastic
mammary gland and the neighboring anatomical
structures could be examined in great detail

Back to contents

with optimal contrast conditions. We can typify
the morphological characteristics of neoplasms,
which can be compared to the histological
findings and help to plan the therapeutic
(surgical) method. All the eleven animals had
malignant lesions (malignant mixed tumours,
carcinoma simplex and carcinoma complex)
and the morphological patterns as well as the
WHAT INFLUENCE ON ORAL HEALTH IN CATS AND DOGS. RESULTS OF 2005
PET SMILE CAMPAIGN IN POLAND
J.P. Gawor1,2, K. Jodkowska1,3, G. Kurski1,4, A. Kurek3, J. Hylmarova5, M. Kaszyński5
1
Dental Working Group in Polish Small Animal Veterinary Association; 2ARKA Veterinary Clinic, Kraków;
3
SGGW Warszawa, Warsaw Agricultural University; 4ELWET Veterinary Surgery, Warszawa; 5Masterfoods Polska,
Kożuszki Parcel
The Dental group of the Polish Small Animal
Veterinary Association together with Masterfoods
Polska ran the third edition of the Pet Smile
Campaign (PSC) in 2005. The PSC Team
prepared materials for owners, instructions for
the veterinarians, posters and the questionnaires
for participating veterinary surgeons to fill in
based on examined pet’s oral health status.
Materials and methods: In 2005, members of
the Dental Working Group of the Polish Small
Animal Veterinary Association (PSAVA) and
representatives of Masterfoods Poland recruited
over 400 veterinary practices to provide free
oral examinations of pet cats and dogs. The
examination procedure consisted of three parts:
3 minutes dental/periodontal examination (no
sedation or GA applied), 3 minutes interview and
filling in the questionnaire with the owner, and 3
minutes presentation of diagnosis to the owner,
instruction for home oral hygiene methods, and
recommendation of professional treatment.
Each oral health check was documented in the
standardized chart which included following
parameters: age of the patients, their gender and
bodyweight, type of diet fed and extent of home
oral hygiene. Bodyweight was divided into 5
groups in dogs (<5, 5-10, 10-25, 25-40 >40) and in
2 groups in cats (<5kg >5kg). Dental examination
protocol consisted of: size of mandibular lymph
nodes evaluated on palpation, presence of
dental deposits, and presence of periodontal
disease. The size of mandibular lymph nodes
was determined as: normal, slightly enlarged, or
moderately to severely enlarged. The presence of
dental deposits was determined visually of the
most severely affected tooth and was recorded as
absent, up to 50% of the crown affected, or more
than 50% of the crown affected. The presence
of periodontal disease was determined visually.
Gingivitis was specified as inflammation of
gingival tissue, (abnormal reddening or bleeding
of the gums). Periodontitis was recorded when
a tooth had gingival recession or was mobile on
Back to contents
POSTERS
kinetic parameters proved to be satisfying for
the diagnostic work. The contrast accumulation
methods and curves prepared for human medicine
are of great promise in veterinary use but a highly
sensitive standard protocol should be completed.
In all cases we found malignant morphology, so
the method must be tested also on benign tumours
and on a large number of patients.
digital palpation. The scheme and scoring system
is presented in the table1.
Other parameters that were marked in the
questionnaire: diet (five options): dry food, dry
and tinned or other soft commercial food, mixed
home-made and commercial food, only home-
made food) and oral prophylaxis (five options):
daily teeth-brushing; daily dental chews, 2-3
times a week dental chew or brushing, seldom
dental chews or brushing, none. Breeds of the
examined patients were also recorded but the
results are not reported here.
The oral health index was defined as the
summation of scores obtained for the three
parameters: lymphadenopathy, dental deposits,
and periodontal disease, with 0 points indicating
optimal oral health, and 6 points indicating most
negative oral health status. A one-way analysis
of covariance was performed to adjust for age.
Significance was defined as p < 0.05. Statistical
analysis was performed using SPSS 12.0 software
(SPSS Inc., Chicago, IL).
Results: In 12344 evaluated animals 70.6% were
the dogs (8712) and 29.4% cats (3632). The
results regarding each of evaluated parameters 2006 World Congress WSAVA/FECAVA/CSAVA
are presented in Table 1 (cats) and Table 2 (dogs)
All parameters were adjusted to the mean age
that in cats was 4,801 yrs and in dogs 5,758 yrs.
The most significant influencing parameter on
oral heath status has the age. Bodyweight, oral
hygiene and diet also had significant influence on
oral health index, the most positive correlation
were: big size of the dog (over 25 kg)* and
smaller size in cats (less than 5 kg), dry diet and
daily oral prophylaxis in both species. There are
significant differences in oral health among the
animals fed different diets and having different
extent of oral hygiene. The cats fed dry, mixed
commercial and homemade food diet had
increasing oral health index respectively which
means decreasing oral health status. In dogs
was noted additional difference between soft
commercial and homemade food. 843
POSTERS

Conclusions: observed in groups of large individuals (over

1. The age is the most important factor at oral
cavity condition.
2. Significant influencing factors are: diet,
bodyweight and oral hygiene.
3. The best results in dogs oral health index were
25 kg) fed with dry food, and with daily teeth-
brushing.
4. The best oral health index was presented in cats
less than 5 kg, fed with dry food and having daily
oral hygiene (teeth-brushing or daily chews)

Table 1 Cats. Relations between evaluated parameters and oral health index
Evaluated Number Ratio [%] LSM Logarithm Significant SE
parameter of individuals of Oral Health index +1 difference (Standardized error)

Gender
F= 0.32 P = 0.57
Female 1860 51,21 0,805 A 0,023
Male 1772 48,79 0,815 A 0,022
3632
Bodyweight
F= 20,96 P<= 0.01
>5 kg 2838 78,14 0,761 A 0,020
5-10,0 794 21,86 0,861 B 0,025
3632
Diet
F= 27,73P<= 0.01
Dry 823 22,66 0,638 A 0,024
Commercial mixed 1502 41,35 0,734 B 0,021
(dry and tinned)
Tinned 341 9,39 0,883 C 0,034
Mixed commercial 733 20,18 0,853 C 0,026
and homemade
Homemade 233 6,42 0,946 C 0,040
3632
Oral Hygiene
F= 24,15P<= 0.01
Daily teeth brushing 78 2,14 0,617 A 0,061
Daily chews 123 3,38 0,641 A 0,049
2-3 chews a week 219 6,03 0,856 B 0,037
Seldom 463 12,76 0,943 BC 0,027
No 2749 75,69 0,997 C 0,013
TOTAL 3632
2006 World Congress WSAVA/FECAVA/CSAVA

Age
F=1263,59 P<=0,01 3632 B = 0,095 0,003

Table 2. Dogs Relations between evaluated parameters and oral health index.
Evaluated Number Ratio [%] LSM Logarithm Significant SE
parameter of individuals of Oral Health index +1 difference (Standardized error)

Gender
F= 18,50 P<= 0.01
Female 4122 47,31 0,804 A 0,012
Male 4590 52,69 0,851 B 0,012
8712
Bodyweight
F= 51,62P<= 0.01
>5 kg 986 11,32 0,995 A 0,018
5-10,0 kg 2691 30,89 0,869 B 0,013
10,1-25,0 kg 2502 28,72 0,805 C 0,013
844
Back to contents
 POSTERS
25,1-40,0 kg 1883 21,04 0,753 D 0,015
>40,1 kg 650 8,03 0,715 D 0,022
8712
Diet
F= 49,42P<= 0.01
Dry 1793 20,58 0,696 A 0,014
Commercial mixed
(dry and tinned) 1454 16,69 0,768 B 0,015
Tinned 356 4,08 0,894 CD 0,028
Mixed commercial
and homemade 3704 42,52 0,854 C 0,012
Homemade 1405 16,13 0,926 D 0,017
8712
Oral Hygiene
F= 61,21P<= 0.01
Daily teeth brushing 208 2,39 0,606 A 0,035
Daily chews 438 5,03 0,757 B 0,024
2-3 chews a week 1050 12,05 0,820 B 0,016
Seldom 2362 27,11 0,970 C 0,012
No 4654 53,42 0,985 C 0,009
TOTAL 8712
Age
F=4528,0 P<=0,01 8712 B=0,097 0,001

DENTAL PROCEEDINGS IN BUSH DOG (SPEOTHOS VENATICUS) IN BRAZIL

M. Gioso1, R. Fecchio2, M. Gomes1, J. Rossi1
1
University of São Paulo, Av. Prof. Dr. Orlando Marques de Paiva, 87, São Paulo, Brazil; 2São Bernardo`s Zoo, Rua
Portugal, s/n, São Bernardo, Brazil

The Bush Dog (Speothos venaticus) is a South
American canid described by Lund in 1942 and
now is classified as in risk of extinction by IUCN
(1990), remaining only 26 captive animals in
Brazil. Their dental formula is different from other
canids by the absence of the seconds upper molars
(110 and 210) and of the third lower molars (311
and 411), presenting the following dental formula:
2x (3/3 1/1 4/4 1/2) = 38. Two females of Bush Dog
were chemically restrained for several procedures,
during which they were thoroughly examined,
including the oral cavity. One of the females, with
approximately 10 years of age, presented several
oral illnesses with lesions that included: fractures
with and without pulp exposure, tooth-version,
gingival hiperplasia, periodontal pocket, furcation
exposure, gingivitis and dental absence. The other
animal, with approximately 5 years, presented
dental fracture with pulp exposure of the left
lower canine tooth. During restraint, it was not
possible to accomplish the necessary treatment.
However all of the information regarding the oral
lesions were classified in specific clinical record
(dental chart). Later on the animals were directed
to the Laboratory of Comparative Dentistry,
of the Veterinary School of the University of
São Paulo, where the specific proceedings were
accomplished, which included: periodontic,
endodontic, exodontic and restorative dental 2006 World Congress WSAVA/FECAVA/CSAVA
treatments. One year later the animals are still
clinically healthy and new restrains were not
necessary. In the case of wild animals, the
treatment options are more restricted, because
the capacity of post-surgical attendance of the
oral cavity is more limited. Therefore, it should
be selected the therapy of longer trustiness, so
that it can be avoided other handlings of the
animals and new chemical restraints. Moreover,
it is indispensable the accomplishment of clinical
exam of the oral cavity wherever the animal be
anesthetized for any purpose, in order to have
early diagnostic of any related problem in the
oral cavity.

845
Back to contents
POSTERS

CLINICAL STUDY OF TYPE-I COLLAGEN CELL-BINDING (PEPGEN-P15®) IN

ADVANCED PERIODONTAL LESIONS IN DOGS
M.A. Gioso, D.G. Ferro
Universiadade de São Paulo, Av Prof Dr Orlando Marques de Paiva, 87, São Paulo, Brazil
The aim of this study is to evaluate the response
attachment loss, periodontal pocket and II
and III furcation lesion of tooth 3 and 6 month
after application of collagen cell-binding
peptide (PepGen P-15®). Twenty four dogs
from the FMVZ-USP Veterinary Hospital were
anesthetized in order to periodontal treatment
and 91 tooth faces with attachment loss was
treated. From it, 45% (41) received P-15 and
55% (50) constituted control group that received
conventional treatment (flap and root planning).
Eighth tooth had furcation lesions. Five received
the peptide and 3 do not. The procedure was
documented by radiography and photography
from the periodontal probing. After 3 and 6
month, the animals were re-anesthetized in
order to realize new photography, radiography
and periodontal probing exams. From furcation
tooth treated with P-15, two exhibit reduction
of furcation degree, two do not change it
condition and one had furcation enhanced after
6 month. The conventional treatment group
presents 1 tooth with furcation reduction and
no changes in 2 teeth. The 41 attachment loss
faces that received graft material exhibit 40% of
regeneration rate after 6 month. The control faces
do not change it attachment level. The palatal
face present the better regeneration rates (40%)
and the canines and molars were the better tooth
responses (57.14% and 65%, respectively). There
was no post-surgical infection related to oral
home care, despite the fact that just one owner
(4.16%) had reported diary tooth brush on his
pet. This data permits to conclude that the P-15
helps the more rapidly periodontal structures
re-attachment e regeneration, including alveolar
bone. Its application is easy and practical and
the post-surgical complications incidence is
poor. Nevertheless, more studies and researches
are necessary to evaluate the formed bone and
periodontal ligament amount and the quality.

EVALUATION OF SUPPRESSING EFFECT OF KETAMINE ORAL SPRAY WITH

ORAL KETAMINE ON CNS IN CAT
B. Habibi Asl1, E. Issabeagloo2, R. Kaffash Elahi3, J. Mahmoodi3
1
School of Pharmacy, Tabriz University of Medical Sciences, Daneshgah, Tabriz, Iran; 2Medical Sciences Faculty,
Islamic Azad University Of Tabriz, Manzariye-Soleymankhater, Tabriz, Iran; 3Veterinary Medicine Faculty, Islamic
Azad University Of Tabriz, Jadde Basmenj, Tabriz, Iran

Background: Ketamine is known to provide (above scores) for each dose. Peak scores for
anesthetic effects when is administrated each dose and the percentage of animals that
parentral. Ketamine has a low intestinal reached each peak score is given.
absorption in human (20 ± 7%). The aim of this Results: Animals accepted Ketamine
study was evaluation of suppressing effect of administered via the Oral spray route better than
2006 World Congress WSAVA/FECAVA/CSAVA

ketamine oral spray with oral ketamine mixed
with milk or meat on CNS in cat.
Methods: Ten cats received Ketamine in
mixed of milk or meat (30 gr) or oral spray.
Different doses of Ketamine (20, 40, 80, 120
mg/kg) in different route administrated. Each
animal was observed continuously by a winded
observer for CNS depression as graded on the
behavioral scale shown in under. Our scales
for CNS depression were: 0: Normal, 1: Slight
ataxia, 2: Marked ataxia, 3: Loss of righting
reflex, 4: Immobility, 5: No reaction to pain.
Quantal data were obtained by determining the
percentage of animals which lost the reflexes
that given other way. Different doses of ketamine
showed dose dependent effect. Oral spray use of
Ketamine lead to more and persistant depressive
effects. 100% of animals showed No reaction to
pain (score = 5) in ketamine (120 mg/ kg ) oral
spray way. Depressive effects of ketamine (20,
40 mg/kg) were weak in cat.
Conclusions: Ketamine as oral form (Syrup)
in mixed with milk is not appropriate for
cat, because of low PH and unpleasant taste.
Ketamine was taken oral spray was useful. Our
findings suggest that the ketamine oral spray
administration should be selected for anesthetic
effects in cat.

846
Back to contents
 POSTERS
EFFECT OF TYLOSIN ON THE QUALITATIVE COMPOSITION OF CANINE
JEJUNAL MICROBIOTA
J. Harmoinen, J. Björkroth, T. Spillmann, E. Westermarck
Faculty of Veterinary Medicine, Hämeentie 57, Helsinki, Finland

The indigenous intestinal microbiota forms a
dynamic ecosystem, the equilibrium of which is
essential for the host’s well-being. Disturbance
of the small intestinal microbiota have been
implicated as a risk factor of small intestinal
disease. Tylosin, a bacteriostatic macrolide
antibiotic, is commonly recommended for the
treatment of intestinal disorders such as small
intestinal bacterial overgrowth or tylosin-
responsive diarrhea in dogs. However, there are
only few data available about the influence of
tylosin on the composition of the small intestinal
microbiota. The aim of this study was to evaluate
the dynamics of the jejunal microbiota after
administration of tylosin at a dose corresponding
to routine therapeutic. Five healthy laboratory
beagles with permanent jejunal fistula located
approximately 60cm distal to the pylorus were
included into the study. Tylosin was administered
at a dose of 20-22 mg/kg/day for a period of 14
consecutive days. Samples of jejunal juice were
collected through the fistula on day 0 (before
tylosin administration), day 14, and day 28 (14
days after withdrawal of tylosin). For evaluation
of changes in the levels of total anaerobic and
lactic acid bacteria (LAB) in jejunal chyme,
samples were cultivated anaerobically on Brucella
and MRS media, respectively. From two highest
dilutions 20 colonies of LAB were randomly
selected, and identified to species level using
library based numerical analysis of 16 and 23 S
rRNA gene RFLP. Inter-individual variations in
the levels of both total anaerobic bacteria and LAB
were detected. LAB levels were not markedly
altered during tylosin treatment. However, the
administration of tylosin increased the proportion
of enterococci, particularly Enterococcus fecalis.
During tylosin treatment the proportion of
enterococci within all LAB was 98% compared
to 9.5% before and after tylosin administration.
The results support the concept that tylosin may
promote the growth of beneficial commensal
bacteria such as enterococci, i.e. strains that are
known to have probiotic characteristics.

FAILURE OF A SINGLE GNRH ANTAGONIST ADMINISTRATION TO PREVENT

ESTROUS INDUCTION BY A GNRH AGONIST IM
G. Hermo1, Y. Corrada1, D. Arias1, T. Trigg2, C. Gobello1
1
National University of La Plata., calle 60 y 118 S/N, La Plata, Argentina; 2Peptech Animal Health, Locked Bag
2053 North Ryde, Sydney, Australia

The combination of a short-acting GnRH
antagonist with a long-acting agonist could
prevent the gonadotropin “flare-up” at the
beginning of agonist treatment in other species.
The objective of this study was to evaluate the
efficacy and clinical safety of a single injection
of the GnRH antagonist, acyline, to prevent
post-GnRH agonist, deslorelin-estrous response
in anestrous bitches. Eight, postpubertal, 18 to
35 kg, anestrous bitches were allocated to one
of the following treatment groups: deslorelin
acetate (Suprelorin®, Peptech), 10 mg sc (DA; n
= 4) or deslorelin acetate (Suprelorin®, Peptech),
10 mg sc followed by acyline (NICHHD, NIH,
USA) 330mg/kg sc 72 hs later (DA&ACY, n
= 4). All the bitches were examined daily for
detection of post-GnRH agonist estrous response
and the appearance of systemic or local side
effects related to the treatments for one month.
In animals that presented an estrous response,
progesterone (P4) serum determinations were
carried out 3 wks after proestrus onset to test
ovulation (P4 > 5 ng/ml). The frequency of bitches
achieving estrous response, ovulation or side effects
in each treatment group were analyzed by PROC
FREQ. Days to estrous response were expressed
as least squares means (LSM) ± SEM (SAS®). 2006 World Congress WSAVA/FECAVA/CSAVA
Estrous response did not vary between treatment
groups (P > 0.05), as all (8/8) the animals
presented it. Ovulation occurred in all DA bitches
and in 3 of the 4 DA&ACY animals (P > 0.05).
None of the bitches presented local nor systemic
side effect related to the treatments. Estrous
response appeared 12.5 ± 0.1 and 5.2 ± 1.4 days
after implantation in the DA&ACY and DA
groups, respectively. It is concluded that, in this
preliminary study, a single administration of the
GnRH antagonist, acyline, failed to prevent post
GnRH agonist stimulation in anestrous bitches.
Further studies with repeated or higher doses of
antagonists are necessary before antagonist depot
formulations were available.

847
Back to contents
POSTERS

EVALUATION OF PERIOPERATIVE DESMOPRESSIN IN DOGS WITH

SPONTANEOUS MAMMARY GLAND TUMORS
G. Hermo1, P. Torres2, G. Ripoll1, D. Gomez1, D. Alonso1, C. Gobello3
1
Laboratory of Molecular Oncology, Department of Science and Technology, Roque Saenz Peña 352, Buenos Aires,
Argentina; 2Faculty of Veterinary Medicine, La Pampa National University, Calle 5 esq. 116, La Pampa, Argentina;
3
Faculty of Veterinary Medicine, La Plata National University, Argentina., calle 118 y 60, La Plata, Argentina

Desmopressin (DDAVP) is a synthetic DDAVP (1 μg/kg/dose), 30 min before and 24

vasopressin analog with hemostatic properties
that can be used to prevent bleeding in surgery.
Previously, we demonstrated that perioperative
administration of DDAVP dramatically
reduced lymph node involvement and lung
metastasis in a mouse model of mammary
tumor manipulation and surgical excision.
In this study, the effect of DDAVP was
evaluated in the surgical treatment of bitches
suffering from spontaneous mammary gland
tumors. Intact bitches with locoregionally
advanced mammary gland cancer (stages III
and IV) confirmed by deferred biopsy were
included. Tumors and regional lymph nodes
were excised. Treated animals (n=13) were
administered intravenously with two doses of
h after surgery. Control animals (n=13) received
the saline vehicle. Tumors were diagnosed
as carcinoma (n=11), osteosarcoma (n=1), or
carcinosarcoma (n=1) in the control group, and
carcinoma (n=11) or osteosarcoma (n=2) in the
DDAVP group. Six of 13 (46%) control bitches
had locoregional recurrence or metastasis within
the 3 months after surgery, while only 1 of 13
(7%) DDAVP-treated animals did (p=0.03;
chi2). The disease-free survival median time was
significantly higher in DDAVP-treated animals
(Control: 105 days versus DDAVP: >318 days;
p<0.05 log-rank test). These preliminary results
support the potential utility of the neoadjuvant
perioperative treatment with DDAVP in advanced
mammary tumors.

CLINICAL REPORT OF TRYPANOSOMA EVANSI IN THREE DOGS IN IRAN

M. Hosseini Nejad1, D. Shirani2, S. Nabian2, S.M. Nassiri2, R. Mazaheri2
1
Shahrekord University, Saman, Shahrekord, Iran; 2Tehran University, Azadi, Tehran, Iran

Three cross breed dogs; referred to the small
animal hospital of Tehran university. The most
important complaints were the anorexia and
sever emaciation. Corneal opacity was obvious
in two of these cases. Animals were pyretic
(T 40-41ºC) and other vital signs were normal.
Blood samples collected from the cephalic
veins of the dogs, using ethylene diamine
tetra acetic acid (EDTA) as anticoagulant
(1 mg/ ml). Complete blood cell count showed
2006 World Congress WSAVA/FECAVA/CSAVA
values of Alanin Aminotransferase, Aspartat
Amino transferase and total billirubin. Serum
analysis showed a polyclonal gammapathy and a
beta-gamma bridge in the electrophoresis of serum
samples of two dogs. The gamma fraction in one
of these dogs composed 36% and in another case
60% of the whole serum proteins. In these two dogs
the amount of increase in gamma2 region which
is mainly the region of IgG migration, was much
more than Gamma1, it can be resulted that these

a non regenerative anemia with low PCV, Hb,
RBC, MCV, MCH and MCHC. Thin smears
were made and stained by Gimsa method after
fixation in methanol and then examined under a
light microscope (100 X). Trypanosoma evansi
detected with 17-36 µ length (mean 25 µ). The
kinetoplasts of the parasites were subterminal,
the undulating membranes were well developed
and there was a substantial free flagellum. Serum
analysis showed hyperproteinemia and normal
dogs suffered from a chronic but active antigenic
stimulation of infection by Trypanosoma evansi.
Decrease in beta globulins was occurred in all of
the serum samples. Hypoalbuminemia occurred
in two cases as the result of extravasation of
albumin due to increased vascular permeability
in trypanosomiasi. After confirming the disease,
treatment started by Diminazen Aceturate (Brenil,
Intervet).

848
Back to contents
 POSTERS
COMPARISON OF TWO METHODS OF BLOOD PRESSURE MEASUREMENT IN
CONSCIOUS OUTPATIENT DOGS
T. Hsiang1, H. Huang1, Y. Lien2
1
Department of Veterinary Medicine, National Taiwan University, Taipei, Taiwan; 2Azu Clinics for Animals, Taipei,
Taiwan

The purpose of this study was to compare
two methods of blood pressure measurement
oscillometric sphygmomanometry and Doppler
ultrasonography in outpatient dogs in a
clinical setting. One hundred dogs admitted
to the National Taiwan University Veterinary
Hospital for various medical disorders were
randomly enrolled for the study. For each dog,
five consecutive measurements were taken for
each method. The mean (± standard deviation)
blood pressure measured using oscillometric
sphygmomanometry was 135 ± 35.3 mmHg;
whereas the mean blood pressure measured using
Doppler ultrasonography was 153 ± 36.3 mmHg.
The blood pressure readings measured using
these two methods were statistically different
(P<0.001). The coefficient of variance from five
consecutive measurements using oscillometric
sphygmomanometry was ranged from 2.6 to 51.4
(20.1 ± 9.9); whilst, the coefficient of variance
from five consecutive measurements using
Doppler ultrasonography was ranged 1.8 to 36.4
(9.2 ± 6.5). The coefficient of variance of both
methods was statistically different (P<0.001).
Based upon the results of this study, oscillometric
sphygmomanometry was lack of consistency to
obtain blood pressure readings, and tended to
obtain lower blood pressure readings in conscious
outpatient dogs in a clinical setting.

COMPARISON OF THE TRANSMUCOSAL ADMINISTRATION OF MIDAZOLAM

VERSUSE KETAMINE FOR CNS DEPRESSION OF CAT
E. Issabeagloo1, B. Habibi Asl2, A. Shabestary Asl3, J. Mahmoodi4
1
Medical Sciences Faculty, Islamic Azad University of Tabriz, Manzariye-Soleyman Khater, Tabriz, Iran; 2School of
Pharmacy, Tabriz University of Medical Sciences, Daneshgah, Tabriz, Iran; 3Veterinary Medicine Faculty, Islamic
Azad University of Tabriz, Jadde Basmenj, Tabriz, Iran; 4Veterinary Medicine Faculty, Islamic Azad University of
Tabriz, Jadde Basmenj, Tabriz, Iran

Background: Sublingual benzodiazepines,
including midazolam, are effective in humans.
Ketamine also has sublingual absorption in human.
The current study compared acceptance of and
behavioral responses to Transmucosal midazolam
and Ketamine administered via the sublingual
route in cat.
Methods: Ten mal mature freeroaming cats received
different doses of Ketamine (20, 40, 80, 120 mg/kg)
Or midazolam (0.3, 0.6, 1.2, 2.4, 4.8 mg/kg) under
the tongue with additional sugar. Each animal was
observed continuously by a winded observer for
CNS depression as graded on the behavioral scale
shown in under. Our scales for CNS depression
were: 1) no effect 2) impared gait, prancing
gait, some excitement 3) lowered head, braced
stance, hindquarter weakness 4) sternal or lateral
recumbency, some responsivness to repositioning,
unable to stand 5) lateral recumbency, no response
to movmentof limbs, no reaction to pain. Quantal
data were obtained by determining the percentage
of animals which lost the reflexes (above scores)
for each dose. Peak scores for each dose and the
percentage of animals that reached each peak
score is given.
Results: Animals accepted midazolam and
Ketamine administered via the sublingual.
Different doses of ketamine and midazolam
showed dose dependent effect in CNS depression.
Midazolam administration via the sublingual
in 1.2, 2.4, 4.8 mg/kg doses could induce only
immobility (score = 4) in 100% of animals but 2006 World Congress WSAVA/FECAVA/CSAVA
all of cats in any doses react to pain. 100% of
animals showed no reaction to pain (score = 5)
in ketamine (80, 120 mg/kg). Also onset of effect
in midazolam administration was dose dependent
but in regard with ketamine wasn’t in this order.
Conclusions: Sublingual administration of
ketamine is as effective and better suppressed
than sublingual midazolam as a sedative-hypnotic
in cats. Our findings suggest that the ketamine
subligual administration should be selected for
anesthetic effects in cat.

849
Back to contents
POSTERS

AN INTRANASAL KENNEL COUGH VACCINE ADMINISTERED AT 3 WEEKS OF

AGE IS ABLE TO STIMULATE PROTECTIVE IMMUNITY DESPITE THE PRESENCE
OF PASSIVE ANTIBODY
A.A.C. Jacobs, R.P.H. Theelen, D. Sutton, L. Van der Waart
Intervet International, Wim de Körverstraat 35, P.O. Box 31, 5830 AA Boxmeer, The Netherlands
Kennel cough, also called canine infectious
tracheobronchitis, is a common infectious
and highly contagious disease of dogs. A
number of different infectious agents, often in
combination, can be responsible for the disease,
however Bordetella bronchiseptica, and canine
parainfluenza virus are generally regarded as
the two most commonly implicated pathogens.
Although rarely fatal, the disease can cause
persistent, often severe, bouts of coughing
which can last many weeks and cause distress to
both dog and owner. Therefore many vaccines
have been developed in an attempt to prevent
clinical disease and reduce shedding of infection
following exposure. Although injectable vaccines
are available, and are often preferred by vets
because of the ease of administration, intranasal
vaccines are felt to offer a number of potential
advantages. In this respect, one of the often-
stated advantages of intranasal vaccination is that
it is less susceptible to interference by circulating
maternally-derived antibody (MDA) and therefore
can potentially be used to immunise very young
puppies. However a statement warning about
the possibility of MDA interference can be
found on the product literature for at least one
intranasal kennel cough vaccine and therefore
it may be that this generally accepted dogma is
not true – at least in the case of certain products.
This study therefore was instigated in order to
establish whether protection against Bordetella
bronchiseptica in the presence of significant
levels of passive antibody could be demonstrated
for one particular intranasal vaccine. Thirty three
2006 World Congress WSAVA/FECAVA/CSAVA
intranasally with Nobivac® KC plus (Intervet)
- a trivalent vaccine containing live attenuated B.
bronchiseptica strain B-C2, canine parainfluenza
virus strain Cornell and canine adenovirus 2
strain MH1 components, diluted to its minimum
authorised titre (106.5 CFU/dose) in respect of the
Bordetella component. The remaining 16 puppies
were kept as unvaccinated controls. At 96 hours
after vaccination the puppies were challenged
with virulent B. bronchiseptica. After challenge
the dogs were evaluated over a period of 25 days
for respiratory signs using a numerical clinical
scoring system. Just before challenge and at
regular times after challenge, nasal swabs were
collected for Bordetella isolation. After challenge,
both vaccinates and controls developed some
upper respiratory tract signs, as expected from
previous vaccine challenge studies. However the
total clinical scores were significantly lower in
the vaccinated group compared to the controls
(p=0.0022). Until four days post-challenge
the mean body temperature of vaccinates and
controls were nearly identical. However, from
day 5 post-challenge onwards the controls had
a significantly higher average body temperature
than the vaccinates (p=0.0155). On the day of
challenge, B. bronchiseptica was isolated from 8
of the17 dogs that were vaccinated with Nobivac
KC plus, but not from any of the control dogs. At
day three after challenge, the vaccinates still had
a higher re-isolation rate compared to the controls
– probably due to shedding of the live vaccine
strain. However from day 5 to 25 post-challenge,
the controls had a significantly higher overall

SPF puppies, both seronegative and culture
negative for Bordetella bronchiseptica, were
used in this study. At two days of age all puppies
were injected with Bordetella bronchiseptica-
positive antiserum to provide levels of passive
circulating antibody which was well above
the mean titre for adult dogs in the field. At
three weeks of age 17 pups were vaccinated
re-isolation rate than the vaccinates (P=0.0467).
From the results it can be concluded that Nobivac
KC plus at the minimum titre is effective in
reducing clinical signs and bacterial shedding
in passive antibody positive 3-week-old puppies
challenged with BordeteIla bronchiseptica, 96
hours after vaccination.

GASTRIC LESIONS IN CATS AND IT’S RELATION WITH HELICOBACTER

S.H. Jamshidi1, B. Akhtardanesh1, F. Sasani1, M. Mohammadi2, S. Bokaee1
1
Tehran University, Azadi ave, Small Animal Hospital, Tehran, Iran; 2Pasteur Institute, Pasteur square, Tehran, Iran

Gastritis is a common finding in dogs with 35%
of dogs investigated for chronic vomiting and
26% to 48% of asymtomatic dogs affected but the
true prevalence in cats is yet to be determined.
850 This study aimed to determine the prevalence of
chronic gastritis in domestic and stray cats. The
total rate was an estimated 66.6%. Thorough
histopathological studies revealed no significant
association between occurrence of chronic
gastritis with age and sex in both stray and domestic

Back to contents

animals. Gastritis was significantly more prevalent
in antrum than body and only chronic nonspecific
gastritis was diagnosed. The most common types of
chronic nonspecific gastritis were atrophic (26.6%),
lympho-plasmacytic (24.6%) and hypertrophic
(15.3%) respectively. In chronic gastritis cases,
fibrosis and lymphoid follicle was seen in 42.1% and
31.6% of the subjects respectively, but no significant
association between type of nonspecific chronic
gastritis, fibrosis and lymphoid follicle occurrence
POSTERS
was seen. The prevalence of gastric erosion and
ulcers in cats was 19.2% and 3.5% respectively
and there was no significant association between
chronic gastritis occurrence and gastric ulceration
& erosions syndrome. Cytology examination
showed GHLO infection rate of antrum and body
63.15% and 77.19% respectively, however there
was no correlation between presence and degree of
Helicobacter colonization and nonspecific chronic
gastritis.

HYPERTHYROIDISM ASSOCIATED TO A THYROID CARCINOMA IN A DOG

M. Jericó, R. Laurentino, C. De Biaggi, A. Nishiya, R. D´Angelino, M. Moreira, J. Guerra
Universidade Anhembi-Morumbi, Rua Conselheiro Lafaiete, 64, São Paulo, Brazil

Thyroid tumors in dogs are relatively uncommon,
representing around 1% to 4% of all neoplasias in
the species, with thyrotoxicosis, or hyperactivity,
being rare (<10% of cases). A female pinscher,
aged 8 yrs, was taken to the Veterinary Hospital
of Anhembi-Morumbi University, and presented
with a large volume increase in the cervical region,
a two-month evolution, dyspnea, coughing, and
was eurhythmic, in good general health status.
At radiological assessment, a decrease in the
rostral third of the tracheal lumen was observed,
adjacent or superposed in relation to the larynx,
with soft tissue increase in the ventral region of the
epiglottis and larynx. Considering the extension
of the finding, a complete surgical resection
was not possible, and an incisional biopsy was
performed. The histopathological evaluation
disclosed a small-cell carcinoma of the thyroid,
with infiltrative growth that invaded the adjacent
tissues. Laboratory assessment showed an increase
of thyroid hormones, characterizing a functional
follicular carcinoma of the thyroid [T4T =
= 4.59 μg/dL; T3T = 407.33 ng/dL; T4L= 4.8 ng/dL
(radioimmunoassay, Coat-a-count®, DPC, USA;
Laboratório Rhesus Veterinária, São Paulo)].
Chemotherapy with doxorubicin was started,
30mg/m²/IV every 3 weeks, and prednisone,
1mg/kg/PO/SID. There was a considerable
initial improvement; however, after two cycles
of chemotherapy, mass growth recurred, with
progressive dyspnea and dysphagia. At the X-
ray, an almost total occlusion of the trachea was
observed in its rostral portion, and at this moment,
a tracheotomy was performed. Despite the
procedures, the evolution remained unfavorable,
and the animal was sacrificed. The diagnosis of
follicular carcinoma of thyroid was confirmed by
a posterior anatomohistopathological assessment.
It is noteworthy the fact that this is a report
of a functional carcinoma, with consequent
thyrotoxicosis.

CLINICAL EVALUATION OF OBESE DOGS

M. Jericó, A. Leonardi, V. Pereira, A. Tirapelli, M. Moreira, A. Provasi, C. Schaeffer 2006 World Congress WSAVA/FECAVA/CSAVA
Universidade Anhembi-Morumbi, Rua Conselheiro Lafaiete, 64, São Paulo, Brazil

Obesity, a multifactorial and polygenic common At the complementary examination, osteoarticular

nutritional disorder in dogs, brings harmful effects
to the health and longevity of the affected animals.
A dog is considered obese when it presents a
percentage of body fat > 20%. The presents study
reports the main clinical alterations observed in 38
obese dogs with no endocrinopathies, from the data
obtained through the identification, anamnesis,
physical examination, and routine laboratory
and imaging assessment. The most affected age
range was between 7 and 10 yrs, and they were,
mostly, female animals (79%), whose mean body
fat content was 37.87%. The man complaint of
animals’ owners were tiredness (82.8%) followed
by dyspnea (86.2%) and hyperexia (75.4%). It was
observed that 89% of them consumed several treats.
Back to contents
alterations were evidenced at the radiological
assessment (100% with varied arthropathies)
and 72% of them presented increased cardiac
silhouette. At the ultrasonographic assessment,
the main alteration observed was hepatomegaly,
present in 36% of the animals. Blood pressure
measurement showed that 50% of them were
hypertensive. The main laboratory alterations were
lipiduria (75.4%), as well as hypercholesterolemia,
hypertriglycemia, and hyperproteinemia, present
in 32.4% of the animals. We conclude that obesity
affects especially female dogs aged 7 to 10 yrs,
and is associated to morbid alterations such as
arthropathies, eating disorders, dyskeratosis,
cardiovascular and respiratory problems.
851
POSTERS

EFFECTS OF DIET AND PHYSICAL ACTIVITY IN THE CLINICAL EVALUATION OF

OBESE DOGS
M. Jericó, A. Silva, V. Pereira, A. Tirapelli
Universidade Anhembi-Morumbi /UNISA, Rua Conselheiro Lafaiete, 64, São Paulo, Brazil

The main treatment forms of canine obesity
are restriction diets and physical activity. In the
present study, the effects of diet and exercise were
analyzed in 30 obese female dogs, whose mean
age was 7.1 yrs. These animals were divided
in two groups: A (14 dogs treated with diet)
and B (16 dogs treated with diet and exercise).
Swimming was the physical activity of choice, for
20 min, twice a week. After six months, group A
showed a higher mean weight reduction (15.7%)
than group B (10.3%). On the other hand, body
fat decrease was higher in group B (16%) than
in group A (7.5%). Regarding blood biochemical
analysis, group A presented a mean reduction
of 33% in triglyceride levels, whereas group B
had 35.8%. Cholesterol concentrations remained
unaltered in group A and presented a decrease of
6.12% in group B. As for platelet count, group
A presented a reduction of 28.9% and group B,
31.85%. Systolic blood pressure (SBP) decreased
in 11.4% of dogs in group A and 13.5% in group
B. We conclude that, although weight loss was
higher in those dogs under diet, the diet and
exercise combination was more efficient for the
treatment of obesity, as it promoted a higher
body fat loss, greater reduction in cholesterol
levels and platelet count, as well as a significant
decrease in SBP.

USE OF PEDIATRIC TRANSFUSION BAGS FOR PRESERVATION OF CANINE

BLOOD
M. Jovanovic, M. Calic, M. Lazarevic
Faculty of Veterinary Medicine, Bul Oslobodjenja 18, Belgrade, Serbia

Blood transfusion is extremely important
therapeutical procedure that is widely used on the
small animal’s clinics. So far, in our practice we
have used transfusion bags for humans. Because
of their big volume (450 ml) it was sometimes
difficult to perform correct blood donation and
transfusion. Moreover, donors had to be only
dogs of the large breeds. Because of that, we
have explored a possibility for use of pediatric
transfusion bags for the preservation of the
canine blood and transfusion procedure.
During three weeks period of conservation we
followed the changes in some hematological
and biochemical parameters in the blood
2006 World Congress WSAVA/FECAVA/CSAVA
Bags were stored in the refrigerator at + 4°C.
Hematological and biochemical analyses were
performed on the day 0, 7, 14, 21, 28 day by
automatical analyzers (Arcus Diatron, Austria
and Basic Secoman, France). Prothrombine time
was measured by Reaplastin in vitro test (Reanal
Finechemical, Hungary). During the three weeks
period of storage we didn’t documented changes
in RBC and thrombocyte number, packed cell
volume, hemoglobin concentration, MCH and
MCHC values. Biochemical analyses in the
blood plasma revealed statistically significant
elevation of the free hemoglobin concentration,
total protein concentration and bilirubin

bags. Our investigations were conducted
on eight 2-3 years old, healthy bitches of
German shepherd breed. Blood was collected in
closed kits for transfusion (Blood bags, Jierui,
China) that contained 14 ml of CPDA (citrate,
phosphate, dextrose, and adenine) solution.
The amount of blood taken from every dog
was 86 ml to reach the final volume of 100 ml.
concentration from the day 21, while albumin
concentration remained the same. We have also
documented a significant prolongation of the
prothrombine time. We were able to conclude
that pediatric blood transfusion bags are suitable
for veterinary practice especially in small breeds.
Blood collected and preserved in this way can
be stored for 14-21 day.

FREQUENCY AND COMMON COMPLICATIONS OF BABESIOSIS IN DOG

M. Jovanovic, M. Calic, R. Resanovic
Faculty of Veterinary Medicine, Bul Oslobodjenja 18, Belgrade, Serbia

The study of incidence of this disease and of Veterinary Medicine of Belgrade, there were
complications occurred at dogs was performed included 2.865 dogs of various breed and age
in the period January-December 2005. At the categories. All the patients-suspects to have the
852 Clinics of Small Animals Diseases, the Facility babesiosis, on the basis of the clinical picture and

Back to contents

the anamnestic information, were submitted to the
complete haematological and biochemical blood
analyses, as well as urine examination. There
was also performed the blood smear, coloured
by Romanowsky method. At 128 dogs, or 4.46%,
there was established presence of Babesia
canis and erythrocytes, which, along with the
characteristic clinical picture, only confirmed
the suspicion of existence of this disease. There
was not established any breed inclination towards
this disease, while most of the dogs (38%)
were mix bred. As regards the haematological
anomalies, there was registered anaemia (86.5%),
eosinopoenia (32.1%), monocytosis (26.3%),
leucocytosis (53.7%), trombocytopoenia (68.3%).
After the diagnosis has been established, all
POSTERS
the dogs were subjected to a single treatment
with Imisol (imidokarb dipropionat). Most dogs
showed improvement of the general clinical state
as early as the following day and finally, after two
or three days of supportive therapy, the complete
healing. However, there were some complications
registered with 21 dogs (16.8%). All the dogs
were 6-12 years old. The complications that most
frequently accompanied the babesiosis of dogs,
included the acute renal failure occurred at
8 dogs (38.0%), icterus and hepatopathy at 6 dogs
(28.5%), acute respiratory distress syndrome at 3
dogs (14.2%), coagulopathy at 2 dogs (10.0%)
and cerebral babesiosis at 2 dogs (10.0%). Out
of this number, 16 dogs (76.1%) died despite the
administration of the adequate therapy.

THE FIRST CASE REPORT OF CANINE CHOLANGIOCARCINOMA IN IRAN

R. Kaffahsi Elahi1, Y. Doustar2, A. Adalat3
1
Department of Small Animal Internal Medicine, Veterinary Faculty, Islamic Azad University, Jade Basmenj,
Tabriz, Iran; 2Department of Veterinary Pathology, Veterinary Faculty, Islamic Azad University, Jade Basmenj,
Tabriz, Iran; 3Clinician, Valiasr, Tabriz, Iran

Cholangiocarcinoma (bile duct carcinoma)
has been reported in dogs, cats, sheep, goats
and frequently in cattle but not in swine. It is
relatively uncommon in all domestic species and
comprises less than 1% of all neoplasms in dogs.
The incidence of cholangiocarcinoma in dogs
estimated to be 1.6 per 100,000 dogs and 0.36%
of all neoplasms. This neoplasm arises within
the intrahepatic billiary system much more than
extrahepatic bile ducts or gall bladder. A 4.5 years
old mixed male German shepherd presented with
severe abdominal enlargement and vomiting.
Clinical examination showed depression, lethargy
and deep icterus, liver palpation was not possible
because of severe abdominal enlargement, but
confirmed presence of fluid in abdominal cavity.
Blood chemistry profile was the first laboratory
test performed; results showed severe hepatic
involvement (high level of hepatic enzymes,
hypoalbominemia). Abdominal radiography
showed ground glass appearance (figure-1).
Because of loss of owner companionship and
severe patient involvement (at the point of death),
we were not able to perform other compatible
diagnostic procedures, finally decided to
euthanize the patient. In necropsy (video-1) great
amounts of abdominal fluid drained and at first
glance a piknotic multinodular liver (firm) noted
(figures 2-12). Pathologic examinations showed
the cells that retained their resemblance to biliary
epithelium but with some pleomorfism and mitotic
figure abundance. Some acinar arrangements can
be detected among solid masses of neoplastic
cells. The epithelial components of neoplasm
were separated by fibrous connective tissue. And
mucin was present within the neoplastic tubules
or acini (figures 13-20). That all were evidences
of cholangicarcinoma.
Finally although this is a rare neoplasm but we
should bear it in our minds as one differential
diagnosis, and perform more concise (depends on 2006 World Congress WSAVA/FECAVA/CSAVA
availability of diagnostic instruments) diagnostic
approach. In this cases biopsy, ultrasonography
and clarifying metstatic state by radiography,
May lead us to a better and more concise decision
and saving more lives.

A CASE REPORT OF CANINE PULMONARY AND NASAL ASPERGILLOSIS IN IRAN

R. Kaffahsi Elahi1, A.A. Kave2, M. Sadeghi3
1
Department of Small Animal Internal Medicine, Veterinary Faculty, Islamic Azad University, Jadde Basmenj,
Tabriz, Iran; 2Department of Veterinary Obstetrics, Veterinary faculty, Islamic Azad University, Jadde Basmenj,
Tabriz, Iran; 3Department of Veterinary Microbiology, Veterinary Faculty, Islamic Azad University, Urmia, Iran
Aspergillosis is an opportunistic infectious is primarily a respiratory infection that may
disease caused by a number of aspergillus spp, become generalized; however tissue predilection
especially A. fumigatus. It is found worldwide, varies among species. The most common forms
in human being and almost all domestic animals are pulmonary infection in poultry and other
and birds as well as in many wild species. It birds, mycotic abortion in cattle, guttural pouch 853
Back to contents
POSTERS
mycosis in horses, and infections of nasal
and paranasal tissues of dogs. Pulmonary and
intestinal forms have been described in domestic
cats. A 5 years old mixed mesaticephalic native
dog (sarabian fight dog) presented with a history
of persistent nasal sanguineous discharge,
anorexia, depression, weight loss during past
1 year and rapidly getting breathless while
practice, with multiple non successful treatments.
Clinical assessments showed only mucopurulent
and sanguineous nasal discharge and pulmonary
wheezes. Minimum data base was collected and
there was no platelet deficiency, urine and liver
tested and all were normal except Mild neurophilia
and monocytosis. Radiographic evaluation
showed soft tissue density in nasal cavity (figure-
1) and severe lung involvement with cotton ball
like densities (figure-2). In the same time direct
AN MLV VACCINE ELICITS A PROTECTIVE SEROLOGICAL RESPONSE TO CPV
EARLIER THAN THREE OTHER VACCINES
T. Kanellos, A. Robinson, P. Chipanga, S. Thevassagayam
Pfizer Animal Health, Ramsgate Road, Sandwich, U.K.
Objective: Canine parvovirus (CPV) remains
one of the most significant and widespread
infectious pathogens that is associated with high
mortality rates in dogs and in particular in young
animals. Some commercial CPV vaccines have
shown to induce protective immunity in pups
however very little information is available on
the speed of onset of immunity. In this study the
onset of seroconversion to CPV after primary
vaccination in dogs using 4 different commercial
vaccines was measured.
Method: Forty-eight dogs were assigned to
four treatment groups of twelve animals each
according to a randomised block design with
blocking based on litter. Animals were between
51 to 60 days old when they received their 1st
2006 World Congress WSAVA/FECAVA/CSAVA
vaccination on study day 0 and between 79 to
88 days old when they received their booster.
All puppies were from vaccinated bitches and
had CPV antibody titres ≤ 1:10 pre-vaccination
on study day 0. The animals in the first group
(P) were vaccinated with Vanguard™ 7 (Pfizer).
The other 3 groups (M, V and I) were vaccinated
with three different commercial DHPPi+L
vaccines. Blood samples were collected from
all animals on study day 0 and -28 prior to
854
Back to contents
nasal samples collected and at the first glance
hyphae and some conidia were seen (figure 3-
6). Culture results showed aspergillus fumigatus
infection (figure-7). Tracheal wash samples also
showed the same results that mean pulmonary
fungal infection (figure-8). Treatment started
promptly with oral ketoconazole (10mg/kg bid
for 3 months) with broad spectrum antibiotics, vit
K, and nasal lavage with diluted chlorhexidine 4
times daily. Obvious recovery achieved after 50
days with 12 kg weight gain, treatment didn’t
stop, and continued with amphotricin B (3
times per week 0.15-1 mg/kg) for 60 days, but
ketoconazole was continued. At the end, the dog
successfully treated (no recurrence up to now,
7 months after stopping the treatment) and final
weight reached 62 kg. No nasal discharge and no
breathlessness while practice were seen.
vaccination, and then daily from study day 1 to
7 inclusive and on study days 14, 21, 32, 35, 39,
42, 49, 56 and 63. The samples were analysed by
haemagglutination inhibition (HAI) test for the
detection of antibodies to CPV.
Results: CPV antibody titres of 1:80 or greater
using HAI test are considered to be protective
(McCaw et al., 1998). Group P (Vanguard™ 7)
had a geometric least squares mean CPV HAI
antibody titre ≥ 80 within six days after the 1st
vaccination. Group M had a geometric least
square mean CPV HAI antibody titre≥ 80 within
21 days after the 1st vaccination. Group V and
Group I had a geometric least square mean CPV
HAI antibody titre ≥ 80 within 14 days after
the 1st vaccination. All animals that received
Vanguard™ 7 had protective CPV HAI antibody
titres within 14 days after the 1st vaccination,
before administration of the second vaccination
dose. All animals that received the other 3
vaccines only had protective CPV HAI antibody
titres within 35 days after the 1st vaccination.
Conclusion: Vanguard™ 7 induced a more rapid
CPV protective seroconversion compared to
three other commercial vaccines.

THE CORE ANTIGENS OF A MULTIVALENT CANINE VACCINE PROVIDE AT
LEAST 48 MONTHS DURATION OF IMMUNITY
T. Kanellos, A. Robinson, P. Chipanga, S. Thevassagayam
Pfizer Animal Health, Ramsgate Road, Sandwich, U.K.
Objective: This was a pivotal investigation to
determine the duration of antibody responses to
the viral antigens of Vanguard™ vaccine (Pfizer
Animal Health) in several field studies.
Method: A multi-centre serology study was
conducted using client-owned dogs from clinics
located in the USA (44), UK (14) and Canada (3).
Three hundred and seventy-five dogs of various
ages, breeds, sex, weights, lifestyles and time since
last vaccination were enrolled in the study. Dogs
were required to be healthy, with no history of those
viral diseases and should not have been vaccinated
for 12– 48 months. Additionally, dogs must have
received at least a priming vaccination series
Months Since 12-18 19-24 25-30
Last Vaccination
CPV 98.3% 100% 97.9%
CDV 99.2% 95.2% 100%
CAV1 96.6% 100% 100%
CPi 100% 100% 100%
Conclusion: Results from this study indicate
that dogs of high and low disease exposure
risk that have been previously vaccinated with
USE OF A MLV VACCINE IN 6 WEEKS OLD PUPPIES WITH CPV MDAS PREVENTS
CLINICAL DISEASE
T. Kanellos, A. Robinson, P. Chipanga, S. Thevassagayam
Pfizer Animal Health, Ramsgate Road, Sandwich, U.K.
Objective: A major problem with the immunization
of dogs against CPV is the persistence in pups
of varied levels of maternally derived antibodies
(MDA), which may strongly interfere with the
development of vaccine-induced immunity.
Hemagglutination inhibition (HAI) titres of >1:20
may interfere with an active immune response
after administration of some vaccines. This results
in a “immunity gap” as such titres do not prevent
infection with a virulent virus. Therefore, in this
study the efficacy of the canine parvovirus (CPV)
component of Vanguard™ 7 was evaluated in the
presence of moderate to high MDAs.
Method: Five puppies at 6 weeks of age with
CPV MDA levels of 1:40-1:80 as measured
by HAI and CPV negative were vaccinated at
6 weeks and 9 weeks. Two unvaccinated controls
with no MDA and CPV negative were enrolled in
the study. All seven puppies were challenged at
12 weeks of age with a virulent canine parvovirus
strain labelled CHSV Bio-1: CPV 12/1/04 (CPV
type 2a) and clinically monitored for 14 days after
Back to contents
POSTERS
approximately 2-7 weeks apart as a puppy and a
booster vaccination approximately 8-16 months
later. Dogs were considered to have antibody titres
indicative of a protective serological response if
their pre-vaccination serum levels were ≥1:16 for
CAV-1, ≥1:32 for CDV, ≥ 1:16 for CPi and ≥1:80
for CPV (CVDL Guidelines) or if they demonstrated
a 4-fold anamnestic response to revaccination.
Results: The pre-vaccination geometric mean
titres were above levels indicative of a protective
serological response for all viral antigens at all
time intervals. The percentage of dogs that were
classified as responders is shown in the table
below:
31-36 37-42 43-48 >48
96.6% 100% 90.9% 100%
96.6% 100% 100% 90.5%
98.2% 100% 100% 100%
98% 94% 90.9% 87.5%
Vanguard™ have protective antibody titers to the
core viral vaccines that persist up to and beyond
48 months.
the challenge according to the guidelines of the
relevant European Pharmacopoeia monograph.
In addition the White Blood Cell counts (WBC)
of the individual dogs were also monitored in 2006 World Congress WSAVA/FECAVA/CSAVA
order to evaluate the possible development of
leucopoenia. Animals were also monitored to
evaluate the shedding of virus in their faeces
post-challenge.
Results: Severe, clinical signs typical of CPV
infection and leucopoenia were observed in
the two control animals. The vaccinates were
100% protected against leucopoenia and the
manifestation of clinical signs of the disease.
Faecal viral shedding was very high in the
controls (>4096 HA) following challenge while
in only one of the vaccinates very low shedding
of the virus was detected (16 HA) on only one
occasion
Conclusion: The CPV fraction of Vanguard™
7 found to be 100% effective in the presence of
MDA and to induce almost sterilising immunity
when administered to puppies of 6 weeks of age. 855
POSTERS
VACCINATION OF PUPPIES AT 7 AND 10 WEEKS WITH A MULTIVALENT VACCINE
GIVES PROTECTIVE SEROCONVERSION
T. Kanellos, A. Robinson, P. Chipanga, S. Thevassagayam
Pfizer Animal Health, Ramsgate Road, Sandwich, U.K.
Objective: Early vaccination of puppies is very
desirable for owners especially when early
socialization of puppies is expected. Although
the immune system of dogs at 7 weeks is mature
enough to respond to the vaccine stimulus, the
presence of MDA can impede the development
of protective immunity. Vanguard™ 7 (Pfizer) is
a core multivalent vaccine and the recommended
vaccination schedule is a two-dose regimen with
the first dose at 9 weeks of age and the final dose
at 12 weeks of age. This study was designed to
compare the serological responses of the viral
fractions to administration of Vanguard™ 7
vaccination at 9 and 12 weeks of age with an ‘early
finish’ regimen, where pups were vaccinated at 7
and 10 weeks of age.
Method: Twenty-nine pups from vaccinated dams
were randomly allotted into two treatment groups:
14 were allocated to T1 (vaccination at 9 and 12
weeks) and 15 were allocated to T2 (vaccination
at 7 and 10 weeks). Blood samples were taken
throughout the study and were analysed by virus
neutralisation for antibodies to CDV, CAV and
CPiV and by haemagglutination inhibition for
COMPARATIVE PALATABILITY OF TWO FEED SUPPLEMENTS FOR SKIN & COAT
CONDITIONS
J. Ketzis
Charles River Biolabs, Carrentrila, Ballina, Co. Mayo, Ireland
Products with essential fatty acids have become
popular feed supplements for dogs to improve
the condition of the skin and coat. The available
products come in various forms: liquids,
2006 World Congress WSAVA/FECAVA/CSAVA
powders, and tablets. Quality and palatability of
the products are primary concerns. In this study,
the palatability of two brands (a powder produced
by Oystershell and a liquid produced by Virbac)
of essential fatty acid feed supplements were
compared; the Oystershell product also was tested
separately. In each trial, 20 dogs (pointers) were
used and Purina Dog Chow (dry) was offered as
the feed. The supplements were added directly
to the feed. In trial 1, the palatability of the two
products was compared using a preference test.
Two bowls of feed with 1000 g of feed each were
prepared for the dogs. In each bowl, either the
powder or liquid product (at the label rate) was
mixed with the feed. The bowls were then placed
in the dog pen (one on each side) and then the dog
856
Back to contents
antibodies to CPV. The antibody titers to CDV,
CAV, CPV and CPiV in blood samples taken
two weeks after the second vaccination and
were compared using a mixed linear model to
determine non-inferiority.
Results: The antibody titres for all four of the
viral fractions of Vanguard™ 7 in T2 were non-
inferior to T1 i.e. the lower confidence limit for the
log2 difference between treatments was greater
(more positive) than –2: CDV (-1.5186), CAV
(0.3474), CPV (-1.6684) and CPiV (-0.9305).
Furthermore, categorization of animals
according to their serological status at the start
of the study demonstrated that even animals
with high maternally derived antibody titres
before vaccination developed protective titres
post-vaccination in both treatment groups.
Conclusion: This study demonstrated that in pups
born to fully vaccinated dams vaccination at 7 and
10 weeks of age provided protective serological
responses to the viral fractions of Vanguard™
7 and that were non-inferior to the serological
responses obtained when pups were vaccinated at
9 and 12 weeks of age.
was led into the pen and allowed to eat for 1 h.
The position of the bowls with each product was
altered daily (left or right side of the pen). Which
bowl the dog approached first was noted, which
bowl the dog ate from first was noted, and the
total consumed from each bowl was measured.
The two bowls were offered for four days. In
trial two, an acceptance test was used to test the
palatability of the Oystershell product. The same
dogs were not used in the two studies. Data from
both trials were analyzed using a paired one-
tailed t-test. Both products were accepted by
the dogs and there was no preference for either
product. In addition, the Oystershell brand was
tested for consistency in fatty acid content. Based
on the analysis of 8 samples, consistency from a
single production run was relatively high (64.7%
(arithmetic mean; StDev 0.4) and 16.9% (StDev
0.6) poly- and mono-unsaturated fatty acids,
respectively).
 POSTERS
THE SAFETY OF A PLANT-BASED NUTRACEUTICAL FOR BEHAVIOUR IN CATS
AND DOGS
J. Ketzis1, T. Griffiths2, M. Reichel3
1
Charles River Laboratories, Carrentrila, Ballina, Ireland; 2Novartis Animal Health Australasia Pty. Ltd., 245
Western Road, Kemps Creek, Australia; 3Novartis Centre de Recherche Sante Animale SA, St. Aubin, Switzerland
PID 02027010 (Oystershell NV, Belgium) is one did not cause any adverse events. Some changes
of the many nutraceuticals available for dogs in clinical laboratory chemistry were observed,
and cats. It has been shown to have an impact on but remained within normal ranges and were not
the behaviour of dogs and cats and is marketed considered clinically relevant. In Study 2, single
as a complement or alternative to behaviour high doses (5 and 10 ml) were tested in 3 cats (m
treatments. The standard dose rate is 0.5 to 1 ml/ and f; average weight of 5 kg) to assess safety
kg bodyweight (BW), and treatment needs to be and determine if single high doses could have
for at least 3 consecutive days before there is an an impact on behaviour. The 5 ml dose had no
effect. Two studies were conducted to determine impact on behaviour and there were no adverse
the safety of the product. The tolerability in dogs events. The 10 ml dose resulted in a mild sedative
was assessed in a blinded, randomized, placebo- effect for approximately 2 h in two of the three
controlled study (Study 1). Twenty-four dogs cats treated. One cat had diarrhea after treatment.
(16 m and 8 f; divided into 4 groups of 6) were Based on these studies, the product was safe if
treated for 15 d with either a placebo (5x the used at the label rate. However, further work is
labeled dose rate of PID 020270101) or 1x, 3x, required to confirm safety when used over longer
or 5x the labeled dose rate for 15 d consecutively. periods of time. Also, reformulation would be
Based on daily observations, body weight, required if a high dose for immediate effect is
clinical laboratory parameters, and clinical desired.
examinations, the product was well tolerated and

IN VITRO ANTI-FUNGAL ACTIVITY OF THE ESSENTIAL OIL AND PLANT EXTRACT

MIXTURE OF A SKIN CREAM
J.K. Ketzis1, N. Nolard2
1
Charles River Biolabs, Carrentrila, Ballina, Co. Mayo, Ireland; 2Scientific Institute of Public Health, rue Juliette
Wytsman, Brussels, Belgium

The investigational skin cream (PID 02027030,
produced by Oystershell, Belgium) is sold as a
cosmetic product for dogs, cats, and horses to be
used on skin abrasions, hot spots, etc. It contains
a mixture of essential oils and plant extracts
(8.25% v/w) in a non-natural base. To determine
if the product could be useful in promoting
healing in the case of skin infections, an in vitro
study was conducted to determine the anti-fungal
activity of the cream. Due to difficulties of using
the formulated cream in a water-based test, the
mixture of oils and extracts were used. A broth
microdilution method was used to determine
the minimum inhibition concentration (MIC)
(read visually and with a spectrometer) and
minimum fungicidal concentration (MFC)
of the oil/extract mixture against three
strains each of Candida albicans, Malassezia
pachydermatis, Microsporum canis, and
Trichophyton mentagrophytes. Each test was
repeated 3 times. The MIC 80% values ranged 2006 World Congress WSAVA/FECAVA/CSAVA
from 0.032 to 1% concentration (visual) and
0.032 to 2% concentration (spectrometer), with
more activity against C. albicans. The MFC
values ranged from 0.25 to >2% concentration
with more inhibition against M. canis.

TRAUMATIC BLEEDING OF THE PENIS DUE TO SELF-MUTILATION AS AN

UNUSUAL SIGN OF SEPARATION–RELATED PROBLEMS IN A CROSS-BRED
DOG
N. Khorami2, M. Selk Ghaffari1, S.J. Aledawod2
1
Department of Clinical Science, Faculty of Veterinary Medicine, Islamic Azad University, Karaj, Iran; 2Department
of Clinical Science, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran

Separation anxiety is a common behavioral being left alone, by rewarding calm, relaxed
problem in dogs. Treatment is based on developing behavior (Lem 2002) the presenting complaints
a behavior modification protocol that gradually varied. These are included: inappropriate
desensitizes and counter-conditions the dog to urination, excessive vocalization, fearful behavior, 857
Back to contents
POSTERS

trembling, vomting, diarrhea, excessive licking,
self-mutilation, overactive greetings, excessive
attention seeking, and aggression at departures
(Beaver 1999). This article descries a case of
genital self-mutilation as an unusual clinical
manifestation of separation anxiety, and is, to the
author’s knowledge, the first such case reported
in veterinary medicine. A two-year old sexually
intact male cross-bred dog was presented for
evaluation of hemorrhagic preputial discharge.
The owner had noted excessive vocalization and
intermittent episodes of licking of the penis, when
it left alone. The owner had reported that he had a
car accident and hospitalized, so he had no chance
to meet the dog. During this time, the behavior
then would progress to frequent episodes of
licking and biting of the penis. The dog lick, bite
and severely self-mutilate his penis resulting in
ulcers with secondary bacterial infection. Three
weeks of treatment with Amitriptyline appeared
to produce a considerable degree of improvement.
Episodes of biting behavior were reduced and
wounds healed gradually. Owner-recorded
audiotape tried concomitant to Amitriptyline
therapy in the first week of treatment. In the
second week after beginning of treatment the
dogs brother who kept in another apartment, had
brought to the dogs living place. It seemed to be
more effective and reported behavior occurred
less than first week of treatment.

A CASE OF CARNASSIAL ABSCESS FOLLOWING COMPLICATION WITH

CELLULITIS IN A YOUNG DOG
J.-H. Kim, J.Y. Lee, T.-S. Han, G. Kim, S.H. Choi
Veterinary Medical Center, San 12 Gaeshin-dong Heungduk-gu, Cheongju, South Korea

Periapical abscess is a common condition, investigation to the Veterinary Medical Center,

which usually developed as a complication of
the infection of the root of the tooth. The cases
originated from periodontal disease have been
reported. Facial injury may also cause tooth root
infections. The clinical presentation is seen as a
swelling or drainage tract near the involved root
of the tooth. Diagnostic methods available for
evaluating periapical abscess include physical
examination, dental examination and X-ray.
Most periapical abscess is treated with extraction
of the involved tooth. In some cases, endodontic
procedure may also be used. Prompt diagnosis
and treatment are necessary to allow drainage and
prevent recurrence of infection. An 11 months old,
female Maltese dog with recurrent facial cellulitis
below the left eye was referred for further
2006 World Congress WSAVA/FECAVA/CSAVA
Chungbuk National University. There were no
visible dental problems, but left maxillary third
and fourth premolars showed periapical bone
lyses on extraoral radiographs. In this case, the dog
was young and had no clinically significant dental
problems like, gingivitis or periodontal pocket. It
could be suspected that carnassial abscess might
be secondary to cellulitis. Left maxillary third
and fourth premolars were extracted by the closed
extraction technique. Communication between
some extraction sockets and the facial lesion was
confirmed using periodontal explorer. The facial
lesion was treated as open wound. During the
follow-up of 3 weeks, the extraction site and the
lesion reveal normal healing after procedure.

ANTIOXIDANT EFFECTS OF ASCORBIC ACID ON RENAL ISCHEMIA-

REPERFUSION
M.C. Kim1, J.M. Kim1, C.S. Park2
1
Coll. of Vet. Med., Chungnam Natl. Univ., 220 Kungdong, Yoosung-gu, Daejeon, South Korea; 2Div. of Animal
Sci. & RCTCP, Chungnam Natl. Univ., 220 Kungdong, Yoosung-gu, Daejeon, South Korea

Introduction: Tissue subjected to a period of clamped with an atraumatic vascular clamp.

ischemia undergoes damage (1,2). The purpose
of the present study is to clarify the effects of
ascorbic acid on renal I/R injury in rabbits.
Materials and methods: Fifteen New Zealand
white rabbits weighing 2-4 kg were used for the
experiments. In group 1 (n = 3), only the right
kidney was removed. In group 2 (n = 3), the
left kidney was freed from the perirenal tissue
and fat after the right nephrectomy. A bolus of
150 IU/kg of heparin was given IV 3 minutes
858 before ischemia and the left renal vessels were
After ischemia for 30 minutes, the clamp was
removed and the blood reflows. In group 3
(n = 3), ascorbic acid 50 mg/kg IV before the
operation. After ischemia during 30 minutes,
then the renal vessels were unclamped. The right
nephrectomy was performed. In group 4 (n = 3);
ascorbic acid 100 mg/kg IV before the operation.
In group 5 (n = 3); ascorbic acid 200 mg/kg IV
before the operation.
Results: The levels of SOD were significantly
increased in the group 4 and 5 at the 24 hours

Back to contents

after reperfusion compare to group 2. The
levels of GSHPx activities (nmol/min/ml) were
measured. They were 143.20 ± 12.23 (group 1),
118.01 ± 2.81 (group 2), 125.268 ± 15.80 (group
3), 150.24 ± 13.77 (group 4) and 163.76 ±13.28
(group 5) followed by 24h reperfusion. The levels
of CAT activities (nmol/min/ml) were measured.
They were 9.19 ± 0.74 (group 1), 4.15 ± 1.49
INTERSEX ANOMALIES IN THREE DOGS
N.S. Kim1, M.R. Alam1, Y.G. Cho2, I.S. Kim1, S.H. Shin1, J.H. Kim1, K.C. Lee1, I.H. Choi1
1
College of Veterinary Medicine, Chonbuk National University, Jeonju, South Korea; 2Medical School, Chonbuk
National University, Jeonju, South Korea
Three Cocker Spaniel dogs, 2-3 moths old
weighing 3-4 kg were presented to the Animal
Medical Centre, Chonbuk National University
with intersex anomalies. Physical, radiological,
gross, histological, hormonal and cytogenetic
studies were performed. Physical examination
of the external genitalia revealed dogs possessed
vulva with an enlarged clitoris protruding
from the vulvar juncture and the scrotum with
an undescended testis in case 1 and 2, and
both testes remained undescended in case 3.
Hyperestrogenemia and low testosterone serum
LIVER DISEASES IN PETS AND THE HOMEOPATHIC REMEDY CHELIDONIUM
MAJUS
G. Kirkilesi, K. Loukaki
Private Veterinary Clinic, Protopapa 29, Helioupolis, Athens, Greece
The liver is the largest organ that is located in the
body, a testament to its importance. It is involved
with almost all biochemical processes and
there are many different diseases that affect it.
Nevertheless the liver has the ability to regenerate.
This regenerative ability allows a diseased liver
to return to normal function in some cases.
Homeopathy is a complete diagnostic and
therapeutic method. Homeopathic remedies are
made from over 2000 substances derived from
plants, minerals and animals. The process of
producing the homeopathic remedies is called
potentisation and includes serial dilution and
succussion. The basic principle of homeopathy is
the law of similars, which states that a substance,
which produces symptoms in a healthy organism,
can cure these symptoms in a sick organism, if
it is prepared and administered as a homeopathic
remedy. Chelidonium majus is a plant, which
belongs to the Papaveraceae family. As a
homeopathic remedy it acts mainly on the liver and
Back to contents
POSTERS
(group 2), 5.74 ± 1.10 (group 3), 8.06 ± 0.77
(group 4) and 10.80 ± 1.79 (group 5) followed by
24h reperfusion.
Conclusion: Antioxidant enzyme activity suggests
that premedicated ascorbic acid alone may have
roles on the attenuation of I/R injury and recovery
of renal function in rabbits.
concentrations were found. Laparotomy revealed
persistant Müllerian ducts (PMD) in case 1
and 2, and abdominally located testicle(s) in
all the cases. Histological examination of the
gonads revealed inactive seminiferous tubules.
Cytogenetic analysis showed a 78XY male
karyotype in case 1 and 2, whereas case 3 showed
79XX female karyotype. The congenital defects
were diagnosed as male pseudohermaphroditism
(MPH) and PMD in case 1 and 2, and XX sex
reversal MPH in case 3.
on the gallbladder. In 10 cats and dogs with liver
disfunction caused by various agents (Ehrlichia
canis, Leishmania, cancer, hepatic lipidosis,
conventional medicines like phaenobarbital,
carprofen) one capsule of Chelidonium majus
30CH was given per os every 7-14 days. The
results were: improvement of the clinical signs 2006 World Congress WSAVA/FECAVA/CSAVA
(anorexia, vomiting, diarrhea, emaciation) and
of the biochemical values in different degrees.
The most important was the improvement of the
animals’ quality of life despite the serious and
sometimes incurable diseases, from which they
were suffering. The use of Chel. majus in dogs
and cats with liver diseases has given encouraging
results. Further research is needed to investigate
the efficacy of Chel. majus in comparison and in
combination with the idiosyncratic (constitutional)
homeopathic remedy, the efficacy of lower and
higher potencies, the combination of its use
together with special diets and other conventional
or/and alternative therapeutic methods.
859
POSTERS

ENDOSCOPIC DIAGNOSTICS AND SURGICAL TREATMENT OF FOREIGN

OBJECTS IN STOMACH AND DUODENUM IN CANINES
V. Krstic, S. Filipovic, M. Calic
Faculty of Veterinary Medicine, Bulevar Oslobodjenja 18, Belgrade, Serbia

Foreign objects in stomach may be found in
canines of all age groups. Most frequently those
are bones, stones, balls, plastic objects and
cellophane bags. A four-year male Labrador
was taken to the dispensary of the Belgrade
School of Veterinary Medicine. For several
days, the dog vomited everything eaten. The
semi-digested food contained plenty of whitish
mucus. The general examination did not show
any deviation of the triad from physiological
range. Abdomen palpation in the epigastria
region showed tenderness with marked muscular
rigidity. As a foreign object was suspected to be
in the stomach, gastroscopy was carried out. The
endoscopic examination of the stomach showed
hyperemic and edematous mucosa with small
dotted strongly manifested hyperemic fields. A
foreign item which fully closed the pylorus was
noted in the pyloric part of the stomach. It could
not be taken out by means of any accessorial
instruments used in endoscopy so that the surgery
was performed. The dog was anesthetized and the
surgery started. The initial incision on the skin
was made in the region of linea albi, from the
xyphoid to umbilical region. After the incision
of the stomach, two sutures were placed on
each side in order to lift the stomach from the
abdominal cavity. The foreign object was taken
from the stomach by means of tongs for foreign
objects. After gastrotomy, the initial incision was
extended to the pubic region. Palpation detected
a foreign object within the duodenum lumen,
too. Therefore, enteretomy was performed and
the foreign object (a cellophane bag with bones
leftovers) removed. Intestines and abdomen were
then closed as per standard surgical procedure.

DIAGNOSTICS AND SURGICAL TREATMENT OF PERSISTENT RIGHT AORTIC

ARCH IN DOGS – A CASE REPORT
V. Krstic, N. Krstic, M. Macanovic-Lazarevic, V. Magas, D. Ristanovic, R. Srejic, T. Stefanovič
Faculty of Veterinary Medicine, Bulevar Oslobodjenja 18, Belgrade, Serbia

A four-month old female dog, an Epagneul
Breton, was taken to the out-patients dispensary
of the Small Animals Clinic with the Belgrade
School of Veterinary Medicine. The dog breathed
heavily, coughed occasionally and regurgitated
undigested food from esophagus. These symptoms
were more obvious after intake of solid pelleted
food. X-ray test result: the special neck and thorax
x-ray showed round, baggy shadow of barium
mush, size of lemon. Endoscopy test result: The
2006 World Congress WSAVA/FECAVA/CSAVA
was noted, and then incision of esophagus carried
out followed by preparation of esophagus at the
stricture, insulation of lig. arteriosum and its
ligating. The surgery ended in routine procedure
of closing the chest cavity and placing a thoracic
drain. The endoscopic finding in the course of
the surgery: The endoscope tip passed through to
cardia and entered the stomach rather easily. The
x-ray test result ten days after the surgery: still
shows a contrast path, immediately in front of the

tip of the endoscope could not pass through this
dilation towards cardia due to severe esophageal
stricture. We decided to perform the surgery: after
the preparation the operative field, thoracotomy
was done in the area of the fourth intercostal
space on the left side. Esophagus diverticulum
heart shadow, the size of a plum. X-ray test result
30 days after the surgery: diverticulum filled
with contrast, anterior to the heart shadow, is still
noticeable. The contrast meal is passing posterior
towards the stomach.

STRATEGIES OF DOGS IN OBJECT HIDDEN FOOD TASKS

F. Kuhne
Institute of Animal Welfare and Behaviour, Veterinary Department, FU Berlin, Oertzenweg 19b, 14163 Berlin, Germany

The strategies of dogs to get food, when an, until (Figs. 1-3). Dogs had to scratch the objects in
then, unknown object hiding the food is used, was the first 2 tests and pull a wooden stick with their
taken into account in this study. 16 dogs took part mouth in the third test.Each test was repeated in
in this study. The food was hidden in three tests a series of 5 trials. The dog owner attended the
by a “Pylon”, a “Knepig”TM and a “Klurig”TM experiment.
860
Back to contents
 POSTERS
Fig.1: Pylon Fig.2: KnepigTM Fig.3: KlurigTM

The whole test was videotaped. The main
parameters were the preferred strategy and
latency of reaching the food, the frequency and
duration of looking at and making contact with the
experimenter or owner, as well as the frequency of
coping strategies. The average latency of reaching
the food in the five trials improved from 93 - 7 s.
The dogs were not necessarily faster in the last
of the five trials. Nevertheless, the correlation
between the mean time of reaching the food and
the trial number was negative for all three tests;
but just for the “Pylon” significant (Spearman,
p=-1.0, P<0.000). Sniffing at the experimenter
hands was shown by the dogs in each trial once.
The frequency of looking at and making contact
with the experimenter was exhibited significantly
different by the dogs among the tests (Friedman,
P<0.05). On average the dogs made contact with
the experimenter 0.33 - 2 times in the trials.
The duration of looking at and making contact
with the experimenter varied from 0.52 - 7.57
s. The longer the whole experiment went on,
the more direct contact the dogs tried to make
with their owners. Blinking and licking of the
own nose and mouth were behaviour patterns
which the dogs displayed only in interaction
with the experimenter or owner. Sniffing and
looking around as less effective problem-solving
abilities reached from 4.67 - 0.33 times with an
average duration from 0.81 - 16.72 s in the single
tests. The dog owner attendance was chosen in
dependence on the need of dogs to look at their
owners when they encounter difficulties. Positive
affiliation behaviour with the experimenter was
mainly displayed by the dogs because the owner
was sitting passively on a chair. Dogs which were
able to solve all three hidden food tasks rapidly
have excellent relearning abilities and a high
frustration tolerance level.

FELINE IMMUNODEFICIENCY VIRUS (FIV): DEVELOP OF QUANTITATIVE

COMPETITIVE POLYMERASE CHAIN REACTION (QC-PCR) TO EVALUATE
VIRAL LOAD DURING ASYMPTOMATIC CARRIER AND AIDS STAGE
J.C. Lalia, M.A. Gisbert, A.C. Bratanich, M.J. Huguet, N.V. Gomez
Buenos Aires University, Chorroarin 280, Buenos Aires, Argentina

Feline Immunodeficiency Virus (FIV) infection
in domestic cats results in an acquired
immunodeficiency syndrome (AIDS) similar to
that caused by Human Immunodeficiency Virus
(HIV) infection in humans. The infection stages,
disease progression and therapy efficacy are
monitored based on CD4+ cell counts in blood
samples by use of flow cytometry. In Argentine,
FIV-infected cats are treated with oral Zidovudine
(AZT) and Valproic Acid because using drug
cocktails enhances the therapy efficacy. The
aforementioned therapy showed statistically
significant differences in infected cats, with
regards clinical parameters and increase of the
CD4+ cells counts. FIV antiviral therapy in
Argentine is limited due to the unavailability
of adequate techniques to evaluate in vivo viral
kinetics. We developed and optimized a qc-
PCR for the quantitative detection of FIV. This
method consist of the reverse transcription and
Back to contents
amplification in the same tube of two similar
RNA templates, the wild-type template and a 2006 World Congress WSAVA/FECAVA/CSAVA
known internally deleted synthetic template,
both with identical primer recognition. In gel
electrophoresis, the two targets must be clearly
distinguishable to allow densitometric evaluation
and further quantitation of the relative band
intensities. In this work, a 594 bp fragment (wild-
type template) of the highly conserved FIV gag
gene, was amplificated by primers FIV-771-f
(AGAACCTGGTGATATACCAGAGAC) and
R2-r (TCTGCTTGTTGTTCTTGAGTT) from
blood samples of a naturally FIV-infected cat. The
synthetic template (competitor) was constructed
by deleting 100 bp from the internal sequence of
wild-type template. Both templates were inserted
into a plasmid vector and in vitro transcribed.
The RNA concentrations were determined by
measuring absorbance at 260 nm in a Gene
Quant spectrophotometer. Serial dilutions of
861
POSTERS
both RNA templates were submitted to qc-PCR
amplification, starting at 106 copies/ml and
ending at 109 copies/ml. We detected a analytical
sensitivity of approximately 106 copies/ml for
494 bp template (competitor) and 108 copies/ml
for 594 bp (wild-type template). The sensitivity of
this technique in our hands allows us to distinguish
DETECTION OF MICROSPORIDIA SPORES IN STOOLS AND URINE OF DOGS
M.A. Lallo, E.F. Bondan
University Paulista, Rua Caconde 125/51, São Paulo, Brazil
Dogs may play an important role on the emergence
and dissemination of zoonotic parasitic diseases,
including microsporidiosis. Microsporidia have
emerged as important opportunistic protozoan
parasites in immunocompromised individuals,
such as HIV-positive patients. In this study, we
performed a survey of occurrence of Microsporidia
species in faecal and urine samples of dogs
(n=250) from São Paulo city, Brazil. The samples
were ramdomly selected from dogs housed in a
university veterinary hospital (group I, n=150)
and private kennels (group II, n=100). Urine
sediment was obtained by centrifugation (1,000g
for 20 minutes). Thin smears of stool and urine
were screened for the presence of microsporidian
spores by using Gram-Chromotrope. Futhermore,
the presence of microsporidia was confirmed by
their typical staining pattern with use of Weber´s
THE USE OF CYCLOPHOSPHAMIDE AND LEVAMISOLE IN THE TREATMENT OF
CANINE MALIGNAT MAMMARY TUMOURS
M.A. Lallo, E.F. Bondan
University Paulista, Rua Caconde 125/51, São Paulo, Brazil
Previous studies showed that various imune
stimulants in CaD2 mammary adenocarcinomas
were effective in controlling tumour growth. The
2006 World Congress WSAVA/FECAVA/CSAVA
objective of this study was to evaluate the efficacy
of cyclosphophamide (CY) in combination
with levamisole (LE) as an adjuvant therapy to
surgical resection of canine mammary tumours.
Thirty bitches of various breeds presenting
malignant mammary tumours were attended at a
public veterinary hospital (São Paulo, Brazil) and
randomly divided into 2 groups - those submitted
to surgical procedure alone (group I, n=15)
and those in which was used the association of
surgery and a combination of CY and LE (group
II, n=15). Mammary tumours were assigned based
on the WHO Tumour-Node-Metastasis (TNM)
classification. Depending on the specific case,
the surgical procedure consisted of regional or
complete unilateral mastectomy. Chemotherapy
was done using CY (50mg/m2, twice a week,
v.o.) and LE (2,5mg/kg, three times a week, v.o.)
862
Back to contents
the transition from the asymptomatic carrier stage
to the AIDS stage, according to studies reported
by other authors. In summary, this methodology
allow determinate viral load, disease progression
and therapy efficacy in advance stages of the FIV
infection.
modified Chromotrope-based stain. A smear was
considered positive only if microsporidian spores
were identified by both staining methods. It was
observed 5 positive cases for microsporidia
from faecal specimens, 3 from group I and 2 for
group II. Using the polymerase chain reaction
(PCR) technique, the spores were identified as
Encephalitozoon cuniculi spores. No parasites
were found in urine samples. By light microscopy,
microsporidia spores were seen as purple and
ovoid structures, in a green background, ranging
from 2.4–3.2 micrometers of length to 1.0-1.6
micrometers of width. In this investigation, a
prevalence of 2% for microsporidia was found
in canine stools, showing that pets like dogs
could be a potential source of these protozoans
to humans.
during 2 months. For a period of 2 years each
bitch was regularly monitored by laboratory tests
and clinically for local recidives and metastases.
In all cases, mammary tumours were detected by
the owner one month to one year before the first
clinical examination. The mean age of the dogs
at diagnosis was 9 (±1,5) years and there was
no statistical association between these tumours
and history of pseudopregnancy, parity, estrus
irregularity and anticonceptional therapy. Group
I presented 4 bitches with tumours assigned as
TNM stage I, 8 with TNM stage II and 3 with
stage III. Histopathological classification of these
tumours resulted in 9 cases of tubulopapillary
carcinomas and 6 cases of solid carcinomas.
Lymph node or lung metastases were not found
in none of these patients before surgery, but one
year after surgical resection, 7 animals (46,7%)
presented local recurrences and metastases, and
euthanasia was demanded by the owner. In group
II, 3 bitches had tumours with TNM stage I, 9 with

stage II and 3 with stage III. Histopathological
analysis showed 10 tubulopapillary carcinomas
and 5 solid carcinomas. One female dog presented
severe leucopeny, demanding the interruption of
treatment. Only 2 animals (14,3%) presented local
EPIDEMIOLOGICAL ASPECTS IN TOXOPLASMOSIS IN DOGS FROM A SMALL
COMMUNITY OF SÃO PAULO STATE, BRAZIL
H. Langoni, L.C. Souza, B.D. Menozzi, R.C. Silva
São Paulo State University, Distrito de Rubião Júnior, s/n, Botucatu, Brazil
Toxoplasmosis is a parasite zoonosis caused by
Toxoplasma gondii, a coccidian protozoan, whose
life cycle alternates between an intermediate and
definitive host. In intermediate hosts, herbivorous
or omnivorous, the parasite multiplies in several
cell types, forming tissue cysts. In definitive
host, species of Felidae family the sexual phase
causes the formation of oocysts in the gut. The
aim of this study was to verify the seroprevalence
of anti-T.gondii antibodies in sera samples of
dogs from Vitoriana, a small community from
São Paulo state, Brazil, and the correlation of
some epidemiological variables. A total of 245
sera samples of dogs was collected and tested in
Laboratory of Zoonosis Diagnosis, and assisted
by Botucatu City Hall. Sera were tested for
Indirect Fluorescent Antibody Test (IFAT) to
research of anti-T.gondii IgG antibodies, using
a canine anti anti-IgG antibody conjugated to
fluoresceine isothiocyanate, kindly supplied by
Center of Zoonosis Control of São Paulo City
Hall. The reading was realized in fluorescent Zeiss
SURGICAL THREATMENT OF FEMORIS DISTAL FRACTURES IN YOUNG CATS
USING TWO HYPODERMIC NEEDLES
A. Lavrenčič, J. Koren, I. Princes
Vet. ambulance Vipava, Gradiška cesta 10, Vipava, Slovenia
The distal fractures of femoris frequently happen to
young animals. Due to spacing between the fragments,
a surgical treatment is necessary. In our work, we
describe a simple technique of fixation supracondilar
fractures of femoris using two hypodermic needles.
The easiest access to the distal side of the femoris is
from the lateral side, the orientation points being femur,
patela in tuberositas tibiae. After anatomical reposition
we did osteosynthesis using two hypodermic needles
with the perimeter 1,2mm X 38mm. The hypodermic
needles were inserted in way from the trochanter area
by manually pushing to the plastic part of the needle
in the direction of the diaphfisis area. We pushed one
needle from the lateral and the other fromthe medial
side, thus they intersected. Then we pinched off the
plastic part and the rest of the needle we pushed in
the periost. After that we closed the wound in the
routine manner. We let the bandages on all the cats for
Back to contents
POSTERS
recurrences and metastases. Thus the present study
showed that a combination of surgery and use of
CY/LE revealed to be a better method of therapy
for malignant canine mammary neoplasms than
tumour resection alone.
microscope, SH 250 model, considering positive
the sera reacting at dilutions equal or higher than
1:16. In positive cases, some epidemiological
variables were studied, like breed, age, sex,
access to the street and ingestion of homely food.
From 245 sera samples, 98 (40.00%) showed anti-
T.gondii antibodies. The most frequent titer was
16, in 70 (71.43%) dogs, followed by titer 64, in
27 (27.55%), and titer 256, in 1 (1.02%) dogs.
From positive dogs, 76 (77.55%), ingest homely
food fact that can be considered as an infection
route to this disease, and 45 (45.92%) dogs
had access to the street, where they can ingest
oocysts from feces of infected cats, presents in
environment, or contaminated water. Thus, we can
affirm that toxoplasmosis is present in Vitoriana,
characterized for a high consumption of homely
food for these animals or the contact with the
agent from soil or contaminated water, being
necessary sanitary and health education about the
importance of food sanity and the prevention of
these and others important diseases.
2006 World Congress WSAVA/FECAVA/CSAVA
three weeks after the treatment. Using this approach
we performed osteosynthesis to eight cats of the age
between five and seven months. The cats did not use
the operated leg for two weeks after the operation,
they started to use the leg in a normal way between
the sixth and the eight week after the treatment, when
the pain in the handicapped joint diminished. Only
in one case, the needle could be felt through the skin
in the area of the knee joint; we removed this needle
from the medial side of the knee. In all other cases
we did not remove the needles. Due to its simplicity,
speed, and success of the treatment, we propose to
use this technique to treat the supracondilar fractures
of femoris in young cats until the age of seven moths.
We propose not to use this technique during the
treatment of older cats, since the bone tissue is too
hard, which makes the manual fixation of the needles
in the broken fragments too difficult. 863
POSTERS

WHAT HAPPENED TO RODENTS DURING RENOVATION OF AN ANIMAL

FACILITY?
B.H. Lee, H.D. Jung, B.N. Lee, K.S. Park, D.H. Kim
Laboratory of Animal Research, Asan Institute for Life Sciences, Asan Medical Center, Seoul, Korea

Rodent animals are adversely affected by noisy
environments of construction work. The 16-year-
old laboratory animal research facility at Asan
Institute for Life Sciences was remodeled. The
institute is 5-story building and the facility was
on the top floor. The renovation was designed to
improve the old facility on the fifth floor (1,386 m2)
partially and to expand a new animal facility on the
fourth floor area (1,162 m2) which had been in use
as in vitro laboratories previously. The fifth floor
consisted of SPF zone (247.5 m2) and Semi-SPF
rooms (181.5 m2) for rats and mice only, and the
forth floor BioSafety Level 3 Laboratory (139.9
m2), middle to large animal rooms (155.4 m2) and
small animal rooms (123.8 m2). However, users
of the old facility did not want to stop studies with
animals during the renovation. For this reason,
the expansion work for the new facility on the
fourth floor had been given priority. After finished
the work, housed animals on the fifth floor moved
to the fourth floor, and then the remodeling to the
old facility started. Therefore, the remodeling had
divided by two stages. During the remodeling,
the noise, vibration and dust of construction by
drilling and hammering concentrated in the early
of every stage. The noise levels ranged from
50-90 decibels (dB) (A) (average: 70-80 dB).
Housed rodent animals were adversely affected
by the construction environment. Some users
expressed complaints about increase of skin
injuries by self-biting, mortality, killing and
eating young, blood sugar levels and infertility,
and decrease of litter sizes. The complaints were
localized when remodeling on the fourth floor.
In conclusion, an animal facility where planning
renovation need to start construction work after
moving housing animals to a safety area for
preventing from a construction environment,
and if not, the facility should begin the work
after stopping all of animal experiments.

CHANGES OF TARTRATE-RESISTANT ACID PHOSPHATASE IN SYNOVIAL FLUID

IN THE DOGS WITH RUPTURE CCL
H.B. Lee1, M.R. Alam1, S.Y. Park2, J.H. Kim1, S.Y. Heo1, Y.H. Lee3, I.S. Kim2, H.S. Kang2, K.C. Lee1,
N.S. Kim1
1
College of Veterinary Medicine, Chonbuk National University, Jeonju, South Korea; 2Center for the Development
of Healthcare Technology, Chonbuk National University, Jeonju, South Korea; 3School of Dentistry, Chonbuk
National University, Jeonju, South Korea

Objective: The objective of this study was to
determine whether activity tartrate-resistant acid
phosphatase (TRAP) in synovial fluid (SF) and
serum is a useful marker for induced osteoarthritis
(OA) secondary to experimental rupture cranial
2006 World Congress WSAVA/FECAVA/CSAVA
synovium and CCL were identified by enzyme
histochemistry.
Results: The activity of TRAP in SF of induced
OA was increased when compared with SF of
normal dogs during 3 month (p<0.05), but there

cruciate ligament in the dogs. is not significant in serum. Macroscopically

Methods: Ten skeletally mature beagle dogs
underwent unilateral surgical transection of cranial
cruciate ligament, medial collateral ligament and
medial menisectomy. 23 normal dogs served as
controls. SF was collected from the femoropatellar
compartment of the affected stifle joint by direct
arthrocentensis every a month during 4 month.
The TRAP activity in stifle joint SF and serum
was determined using spectrophotometer with
p-nitrophenylphosphatate (pNPP) substrate. An
addition, the presence of TRAP positive cell in
visible surface fibrillation, cleft and focal
erosions appeared 1 month after postoperative
in the femorotibial joint; predominantly on
the medial tibial plateau and medial femur. On
histochemistry, increased cellular of TRAP
positive cell was detected in synovium and cranial
cruciate ligament.
Conclusion: In this induced OA, activity of TRAP
in SF appears to provide a useful marker of the
degenerative changes.

864
Back to contents
 POSTERS
ORTODONTIC CORRECTION OF INCISORS POSITION BY DURABLE ARCH AND
COMPOSITE LOCKS
Z. Lonsky
Veterinární Ošetřovna, Počátecká 5, 140 00, Praha, Czech Republic

What is goal of this orthodontic method? There is
manipulation by incisors to demanding position.
Incorrect positioning of incisors is one of the
most often defects, limited demonstration dogs
at the dog show. Not always is this fault cause
by hereditary factors and such handicapped
individual is layed off breeding without rational
arguments. Just thinking about faults caused by
positioning of teeth, not by length and width of
dog jaws.
About method: This method is built on action
of mechanical forces between tooth and durable
arch, transmitted by rubber puller. Basicly we can
use this method for moving incisors labialy or
lingualy on maxilla and mandibula too. It means
we use four types of durable arches for two jaws
and two directions of movement. Placement of
composit locks can be on labial or lingual surface
of incisor. For the start of procedure is essential
make a precise imprints of both jaws. Author is
used make imprints so called „from hand method“,
convenient for majority sizes of jaws. Next step is
laboratory work. This part of procedure consider
very important and needs skilled laboratory,
because methods using durable archs are not
usually used in present human orthodontics. Step
number three is fixing arch on canines and marginal
incisors, creation of composite locks on incisor
or incisors and apparatus completing by rubber
puller. Active phase of orthodontic moving needs
regular checking by vet and owner too. Passive
phase necessary for remodelation of alveolar bone
should take minimum two times longer time than
active phase. Usual time of whole procedure can
take about two month. Procedure lasting is depend
on many factors like age and size of dog, pulling
power, homecare and possibility of checking
by veterinarian. Author uses this orthodontic
minimum invasive method several years with
great success. More you can see at photos.

MR IMAGING OF SYRINGIMYELIA: THREE CANINE CASES

B. Lörincz, R. Garamvölgyi, Z. Petrási, Á. Hevesi, Ö. Petneházy, Z. Vajda, I. Repa
Institute of Diagnostic Imaging and Radiation Oncology, University of Kaposvár, Guba S. u. 40, Kaposvár, Hungary

The term syringomyelia means the formation of
syrinx (i.e. cavitation) in the spinal cord. Although
several mechanisms for the development of syrinx
have been postulated, the exact pathogenesis is
still unknown. Syringomyelia can be associated
with congenital malformations of the skull base,
or can be secondary to lesions involving the
spinal cord, such as tumor, trauma or infections,
resulting in corticospinal-fluid (CSF) flow
obstruction. The symptoms are variable, according
to the location of the syrinx in the spinal cord.
Among others chronic pain, increased sensitivity
to touch, scoliosis, hindlimb weakness, ataxia,
facial nerve paralysis, deafness, seizures and/or
loss of bowel/bladder control might be present.
Nonsymptomatic cases are reported as well.
The diagnosis is based on Magnetic Resonance
Imaging (MRI). Conservative therapy includes
the use of analgesics, corticosteroids and drugs
reducing CSF production. In the veterinary
practice, surgery is rarely a therapeutic option. In
this study, we present three cases of syringomyelia:
a 7 years old Cocker Spaniel and two Yorkshire
Terriers, aging 2 and 2,5 years. The patients
presented with different symptoms (multiple
neurological deficits, ataxia, hindlimb weakness, 2006 World Congress WSAVA/FECAVA/CSAVA
epilepsy). In all three cases, syringomyelia was
diagnosed by using a 1,5 T Siemens Magnetom
Vision Plus, and Siemens Magnetom Avanto
MRI scanner. To our knowledge, this is the first
report in Hungary on the diagnosis of canine
syringomyelia using MRI.

EVALUATION AND COMPARISON OF CLINDAMYCIN AND MONENSIN ON

OOCYST SHEDDING IN EXPERIMENTALLY TOXOPLASM
A. Malmasi1, B. Mosallanejad2, M. Mohebali3, A.H. Tabatabaie4
1
Tehran University, Azadi, Tehran, Iran; 2Shahid Chamran Ahvaz, Golestan, Ahvaz, Iran; 3Tehran University, Azadi,
Tehran, Iran; 4Tehran University, Azadi, Tehran, Iran

Toxoplasma gondii is an obligate intracellular Domestic cats and other Felidae are the definitive
coccidian parasite that can infect virtually all hosts. All nonfeline hosts are intermediate
species of warm-blooded animals and humans. hosts. The importance of this parasite is due to
865
Back to contents
POSTERS
the fact that it causes congenital toxoplasmosis,
abortion and mortality in both human and
animals. Toxoplasmosis is a major cause of
death among patients with AIDS. The efficacy
of Clindamycin and Monensin were evaluated
in the prevention of oocyst shedding of kittens
with Toxoplasma gondii (Tehran strain). In this
study 28 healthy kittens aged 1.5 – 2 months
old divided randomly into 4 groups of seven. In
group 1, that fed infected brain tissues of mice,
all of seven kittens (100 %), shed oocyst, nearly
1 week after infection, which lasted for 8 to 9
days. In group 2, which fed infected brain tissues
DETERMINATION OF CONJUNCTIVAL MICROBIAL FLORA IN CLINICALLY
NORMAL FELINE CONJUNCTIVA
S. Mashhady Rafie
Islamic Aazad University, Science and Research Branch, Poonak, Tehran, Iran
Introduction: This study focused on the
determination of conjunctival microbial flora in
normal cats for investigating relations between
factors like old, environment and breed that
predispose conjunctivitis.
Material and Methods: Samples were obtained
from both conjunctival sacs of 35 household
cats for aerobic and anaerobic cultures by moist
sterile swabs. Any cats suffered from eye diseases
previously.
Results: No bacteria were seen in 45/7%, while
a single isolate was obtained from 17% and in
31/5% of cases two species and in 5/8% of cases
three kind of bacteria were isolated. These bacteria
were include: Staphylococcus epidermis 47%,
Staphylococcus aureus 23/5, Staphylococcus
EFFICACY OF CEPHALEXIN TABLETS IN THE TREATMENT OF LOWER URINARY
TRACT INFECTIONS IN CATS
2006 World Congress WSAVA/FECAVA/CSAVA
L. Maynard1, A. Sanquer1, C. Medaille2, I. Villard1
1
VIRBAC, 13e rue LID, Carros, France; 2VEBIOTEL, 41bis avenue Aristide Briand, Arcueil, France
A study was performed to evaluate the clinical
and bacteriological efficacy of Cephalexin tablets
on cats which were presented with a lower
urinary tract infection (UTI) clinically diagnosed
and confirmed by positive cytobacteriological
urine examination (CBUE) on D0 (bacterial
counts >1,000 CFU/ml for cystocentesis or
urethral catheterisation, >10,000 CFU/ml for
palpation-pressure). Cephalexin-based tablets
(Rilexine®, Virbac) administered at a dosage of
15 mg/kg body weight twice daily for 10 days
were compared to Amoxicillin-Clavulanic acid
866
Back to contents
of mice and Clindamycin at dose of 20 mg/kg
from day -3 to + 21 after infections, none of
seven kittens, shed any oocyst. In group 3, that
fed Clindamycin at dose of 10 mg/kg, same as
group 2, two of 7 kittens (28/6%), began to shed
oocyst from day 11 to 18 after infection. Kittens
of group 4 that fed Monensin at dose of 0.02%
incorporated in dry food didn’t shed any oocyst.
Data analysis revealed that Clindamycin 20mg/
kg and Monensin 0.02% had a 100% inhibitory
effect against Toxoplasma gondii (Tehran strain).
No adverse reactions were observed during the
experimental period.
saprephyticus11/7% unknown Staphylococcus
17/8%, alpha hemolytic Streptococci 21%, beta
hemolytic Streptococci 11%, non hemolytic
Streptococci 10/5%, Corynebacterium Spp.
10/5%, Coliform 15/8%, Bacillus spp. 10/5% and
Moraxella catarhalis 5/2%. No anaerobic was
isolated in this study.
Conclusion: No significant difference was seen
between both eyes. The most accumulation
of bacteria was seen in mixed cats (66%) and
minimum level was in Siamese (20%). Also in
regard to keeping manner, the great number of
bacteria was seen in cats can go to garden (83.3%)
Also the most number of bacteria was seen in cats
above 2 years old (97%).
(ACA) tablets (Synulox®, Pfizer) administered
at a dosage of 12.5 mg/kg twice daily for 10 days.
Cats were examined on 3 days: D0, D7 and D14
(5 days after the end of treatment). At each visit, a
total clinical score (CS) was calculated by adding
the severity scores of 11 different clinical signs.
On D10, a second urine sample for CBUE was
performed. Efficacy of each product was assessed
by the percent bacteriological recovery calculated
on D10 (bacterial counts lower than the reference
threshold value of the urine sampling method)
and the percent reduction of the CS on D14.
 POSTERS
EFFICACY OF CEPHALEXIN TABLETS IN THE TREATMENT OF LOWER URINARY
TRACT INFECTIONS IN DOGS
L. Maynard1, A. Sanquer1, C. Medaille2, I. Villard1
1
VIRBAC, 13e rue LID, Carros, France; 2VEBIOTEL, 41bis avenue Aristide Briand, Arcueil, France

A study was performed to evaluate the clinical and
bacteriological efficacy of Cephalexin tablets on
dogs which were diagnosed with a lower urinary
tract infections (UTI) clinically diagnosed and
confirmed by positive cytobacteriological urine
examination (CBUE) on D0 (bacterial counts
>1,000 CFU/ml for cystocentesis, >10,000 CFU/ml
for urethral catheterisation, >100,000 CFU/ml
for palpation-pressure). Cephalexin-based tablets
(Rilexine®, Virbac) administered at a dosage of
15 mg/kg twice daily for 10 days were compared
to Amoxicillin-Clavulanic acid (ACA) tablets
(Synulox®, Pfizer) administered at a dosage of
12.5 mg/kg twice daily for 10 days. Dogs were
examined on 3 days: D0, D7 and D14 (5 days
after the end of treatment). At each visit, a total
clinical score (CS) was calculated by adding the
severity scores of 11 clinical signs. On D10, a
second urine sample for CBUE was performed.
Efficacy of each product was assessed by the
percent bacteriological recovery calculated on
D10 (bacterial counts lower than the reference
threshold value of the urine sampling method)
and the percent reduction of the CS on D14.

CLINICAL EFFICACY OF CEPHALEXIN TABLETS IN THE TREATMENT OF

CUTANEOUS WOUNDS AND ABSCESSES IN CATS
L. Maynard1, V. Skowronski1, A. Sanquer1, C. Medaille2
1
VIRBAC, 13e rue LID, Carros, France; 2VEBIOTEL, 41bis avenue Aristide Briand, Arcueil, France
A multicentre, controlled, randomised field trial
was performed in France to evaluate the efficacy
of Cephalexin administered per os at a dosage of
15 mg/kg twice daily for 5 days in the treatment of
cutaneous and subcutaneous infections in the cat.
A total of 114 cats were included in the study. Fifty-
seven cats were treated with Cephalexin-based
tablets (Rilexine®, Virbac) at the recommended
dosage; 56 cats were treated with Marbofloxacin-
based tablets (Marbocyl® P, Vetoquinol) at the
recommended dosage of 2 mg/kg body weight
SID. Both treatments were administered for 5
days. Cats were clinically observed on 3 days:
D0, D5 and D0 (5 days after end of treatment).
On D0, a cutaneous swab was taken from each
enrolled animal for bacteriological analysis.
Efficacy of the products was assessed by the
percent clinical recovery (total disappearance of
local signs: suppuration, oedema, pain, redness/
heat) on D10 and percent relapses. On D0, there
was no significant difference between groups
for demographic characteristics, clinical signs
or for bacteriological results. Approximately
68.1% of enrolled cats presented with an abscess;
21.2% presented with an infected wound; 10.6%
presented with both a wound and abscess.
Pasteurella multocida represented 42.9% of
the isolated pathogens. Gram-negative bacteria
represented 67.2% of the total isolates and
Gram-positive bacteria (Staphylococcus spp,
Streptococcus spp) represented 32.8%. Out of the
113 cats treated on D0, 78 (69.0%) no longer had
local clinical signs after treatment (41 (71.9%)
in the Cephalexin-treated group and 37 (66.1%)
in the Marbofloxacin-treated group (p=0.5007)).
Only one cat from the Cephalexin-treated group
relapsed. (p=1.0000). Based on these results,
Cephalexin administered orally at a dosage of
15 mg/kg twice daily for 5 days is at least as 2006 World Congress WSAVA/FECAVA/CSAVA
effective as Marbofloxacin administered at the
recommended dosage of 2 mg/kg once daily for
5 days in the treatment of cutaneous wounds and
abscesses in cats.

CLINICAL EFFICACY OF MILTEFOSINE ORAL SOLUTION IN THE TREATMENT

OF CANINE LEISHMANIASIS
L. Maynard1, V. Woerly1, A. Sanquer1, C. Medaille2
1
VIRBAC, 13e rue LID, Carros, France; 2VEBIOTEL, 41bis avenue Aristide Briand, Arcueil, France
This study was performed to evaluate the efficacy included in the study with a canine leishmaniasis,
of a recent oral antiprotozoal agent, Miltefosine, based on clinical examination and confirmed
in the treatment of canine leishmaniasis due to by positive serology, myelogram and/or PCR
Leishmania infantum. A multicentre field trial analysis. Dogs were treated with a Miltefosine-
was conducted in 20 veterinary practices in based oral solution at 2 mg/kg body weight once
France, Spain and Italy. Eighty-two dogs were a day for 28 days. They were clinically observed 867
Back to contents
POSTERS
6 times: V1 (pre-inclusion and sampling), V2-
Day 0 (inclusion and start of treatment), V3-Day
14, V4-Day 28 (end of treatment and sampling),
V5-Day 42 and V6-Day 56. Efficacy was assessed
by the percent reduction of the clinical score,
veterinarians’ opinion, the time course of the
clinical score, the percent parasitological cure, the
albumin/globulin ratio and serology. On average,
Miltefosine treatment reduced the clinical score
by 61.2 ± 44.9% in 8 weeks. In 82.7% of cases,
veterinary investigators considered treatment
with miltefosine retrospectively as or more
effective than conventional antileishmanial
treatment (Meglumine antimoniate – Allopurinol
association). The clinical score decreased
EVALUATION OF CYTOKINES CONCENTRATION AND PERCENTAGE OF
SURVIVAL OF RABIES VIRUS INFECTED MICE
J. Megid1, C.M. Appolinario1, A.M. Mazzini1, M.F. Almeida2
1
UNESP, School of Veterinary Medicine, Botucatu -SP, Brazil; 2Center of Zoonosis Control, R. Santa Isabel, 181,
São Paulo -SP, Brazil
High percentage of survival correlated with low
IL6 serum concentration in mice submitted to
2006 World Congress WSAVA/FECAVA/CSAVA
post exposure treatment with Fuenzalida Palacios
Vaccine associated to Propionibacterium acnes
was described in previous works. Considering
the substitution of Fuenzalida Palacios by
Vero antirabies vaccine in almost all countries
the objective of this work was to evaluate the
percentage of survival and cytokines serum
concentration of rabies virus infected mice
treated with P. acnes associated or not to
antirabies VERO vaccine in different post
exposure treatment protocols. For this swiss mice
were experimentally infected with street rabies
868
Back to contents
significantly over the 2-month follow-up period
(p<0.0001). Clinical response was markedly
visible during the 4 weeks of treatment and
continued to improve in the 4 weeks after
completion of treatment. 51.5% of dogs were
parasitologically cured on Day 56 according to the
myelogram. In 24.1% of cases with an albumin/
globulin ratio Ł 0.7 at V1, the ratio became > 0.7
at V6. A decrease of at least one dilution in IFAT
titres was recorded in 37.2% of dogs over the 8-
week follow-up period. Miltefosine given orally
at 2 mg/kg once a day for 28 days proved to be an
effective and convenient new alternative to treat
canine leishmaniasis.
virus and submitted or not to VERO antirabies
vaccine and P. acnes as immunomodulator.
Animals were killed at different times and serum
was collected in order to evaluate cytokines
concentration. Highest percentage of survival
was observed in animals submitted to P. acnes in
one or two doses followed by animals submitted
to antirabies vaccine alone or with three doses
of P. acnes. The group that presented the higher
percentage of mortality also presented the higher
IL6 concentration on the 10th day correlated with
clinical symptoms of the animals. These results
reinforce the importance of IL 6 concentration on
rabies virus pathogenesis.
 POSTERS
EVALUATION OF DIAGNOSIS METHODS IN DOGS EXPERIMENTALLY INFECTED
WITH LEISHMANIA INFANTUM
J. Miret1, J. Nieto1, E. Carrillo1, J. Saugar1, M. Flores1, F. González2, J. Moreno3
1
Centro Nacional de Microbiología, Instituto de Salud Carlos III, Ctra de Majadahonda-Pozuelo Km 2, 28220
Majadahonda (Madrid), Spain; 2Department of Toxicology and Pharmacology, Faculty of Veterinary, Universidad
Complutense de Madrid, Avda Puerta de Hierro s/n, 28040 Madrid, Spain; 3Centro de Investigaciones Biológicas,
CSIC, Ramiro de Maeztu, 9, 28040 Madrid, Spain
Dogs are the main reservoir of Leishmania Leishmania antibodies could be detected in the
infantum, the causative agent of zoonotic all dogs from the first month. It was observed
visceral leishmaniasis (ZVL). Early diagnosis high levels of antibodies by IFAT and SLA and
constitutes a good strategy to control ZVL. In rk39 ELISA in the dogs; the symptomatic dogs
order to compare different diagnostic techniques showed higher levels of antibodies by rk39
for canine leishmaniasis we have carried out ELISA during the follow-up. All the dogs showed
the experimental infection of beagle dogs and lymphoproliferative response to SLA at the first
follow up the infection by immunological and month after the infection. Parasites were found
parasitological methods. Six beagle dogs were in five out of six dogs by culture and Ln-PCR
infected intravenously with 108 L. infantum (83.3%) at the fifth month. The clinical signs
promastigotes and the clinical, immunological of diseases: exfoliative dermatitis, ulcerations,
and parasitological status of the animals were peripheral popliteal lymphadenopathy, dry
monitored monthly during a period of 32 weeks. hair, weight loss, onychogryphosis, hepato and
Leishmania infantum specific serum levels splenomegaly, ocular symptoms were observed
of antibodies were measured by the Indirect from the third month of the infections in 66.6%
Immunofluorescence Antibody Test (IFAT), of dogs. This experimental model of infection has
and the soluble Leishmania antigen (SLA) and proved to be useful to study the evolution of the
rk39 ELISA (IgG, IgG1, IgG2); the cellular disease, for the establishment and standardization
immunological response was studied by the in of early diagnosis methods, and the development
vitro lymphoproliferation assay with SLA antigen. of control strategies against ZVL Funded by
The parasitological status were determined by ISCIII (MPY-1014).
the lymph node, bone marrow aspiration, spleen Jorge Miret holds a fellowship from MAE-AECI,
aspiration helped with a ecography, skin biopsy Javier Moreno is supported by a RyC contract
and peripheral blood mononuclear cell subsets by from MEC
culture in NNN medium and Ln-PCR. Specific

A HISTOPATHOLOGICAL STUDY ON THE SIDE EFFECTS OF LARGE DOSES OF

DEXAMETHASONE ON DOG’S KIDNEY
D. Mohajeri, A. Samavatian
Veterinary Faculty, Islamic Azad University, Tabriz, Iran

In this limited study a total of 18 stray dogs divided
into one control (n=6, 3 male and 3 female)
and two experiments groups (n=6). The two
experiments groups were administrated daily dose
of 40 and 125 microgram/kg bw of Dexamethasone
intramuscularly for 16 weeks, respectively. In order
to eliminate probable pathologic lesions, animals
of less than a year old were used. The nutritional
conditions and care were similar for all the dogs.
During the treatment no changes were observed
on food intake. Decreased body weight gain was
observed in all treated dogs. One of the low dose
treated dog died during the study (not related to
treatment). At post-mortem examination extreme
macroscopic changes including inflammation 2006 World Congress WSAVA/FECAVA/CSAVA
and paleness of kidneys were seen in dogs
receiving a dose of 125 micrograms/kg bw.
The renal specimens were prepared for routine
histopathological study after fixation (in formalin
10% and alcohol) and staining by H&E and
P.A.S method respectively. Microscopically,
glomerular lesion including of mild mesangial
hypercellularity, synechiae, thickened basement
membranes were seen. The cause of this lesion is
unknown; however, hypertension, because of its
occurance due to increased plasma glucocorticoid
concentrations has been postulated.

869
Back to contents
POSTERS

FAILURE OF CRYOSURGICAL TREATMENT FOR PERIANAL GLAND ADENOMA

IN HYPER-ADRENOCORTICISM CONDITION
S. Mohit Mafi
Faculty of Veterinary Medicine, Islamic Azad University, Karaj branch, Karadj, Tehran, Iran

Cryosurgery is an effective method for treatment suppurative inflammation, exuberant granulation

of perianal gland adenoma (PAGA) and we had
several successful treatments in our teaching
hospital using this method. However, this
article reports a failure of cryosurgical treatment
of PAGA and severe complications in a dog
suffering from hyper adrenocorticism.”Pooh
Pooh” was a nine year old intact male standard
poodle taken to veterinary teaching hospital with
signs of constipation and dyschezia. The owner
reported a firm lump near by anus which bleeds
occasionally. Clinical examination reveals an
obese animal with slightly poor hair coat having
a large multi focal and two smaller tumors
around the anus. Biopsy was taken from lesions
and after histopathology confirmation of PAGA,
cryosurgery was done using a Liquid nitrogen
spray apparatus and three freeze-thaw cycle
performed on the lesions. Tissue temperature
were monitored using Needle Thermocouples
and Electronic Tissue Temperature Indicator.
Classic sequences of cryo-lesions healing process
were observed on follow up examinations during
the first week. But in second week, abnormal
exuberant granulation tissue, purulent discharge
and soft tissue swelling were seen. Histopathology
report for second biopsy specimen showed
tissue and hepatoid texture of tumoral cells in
several sites. After antimicrobial therapy the
second cryosurgical operation was done but
regrowth of abnormal exuberant granulation
tissue and exacerbation of swelling and severe
cellulitis were seen again. Review of the history
and clinical findings led us to probable systemic
disorders affecting wound repair process and Para
clinic test results evidenced that “pooh pooh” is
suffering from hyper adrenocorticism. The owner
had no agreement with further tests and treatments
and “pooh pooh” had put on sleep by his owner
request. Three sequential phases (Rapid, Delayed
and Immunological) are described for tissue cell
death mechanism in cryosurgery. Laboratory
animal studies have shown importance of
immunological phase in tumors cryosurgery
and some clinical reports have shown failure
of cryosurgery in animals receiving exogenous
corticosteroids, simultaneosly. However, in this
case, it seems endogenous corticosteroids not only
had a negative effect on wound healing process
but also affect the cryobiological behaviors of
tumoral tissue exposing to cryogenic substance
and led into failure of cryosurgical treatment.

COMPARATIVE STUDY OF THE PITUITARY-ADRENAL AXIS IN CATS INFECTED

WITH FELINE IMMUNODEFICIENCY VIRUS (FIV)
C. Moltedo, A. Fontanals, V. Castillo, M. Gisbert, A. Suraniti, A. Márquez, N. Gómez
Buenos Aires University, Chorroarín 280, Ciudad de Buenos Aires, Argentina

The neuroendocrine and immune systems are FIV along 6 months of antiretroviral therapy.
2006 World Congress WSAVA/FECAVA/CSAVA

bidirectionally communicated.The neuro-immune-
endocrine interface is mediated by cytokines such
as IL1, TNFα and IL6. These cytokines play
a variety of roles in stress, behaviour; sensory
processing and cognition. The immune system is
partially regulated by the hipothalamus pituitary
adrenal axis (HPA) and the sympathetic nervous
system. Cortisol is the key effector glucocorticoid
synthesized via the HPA axis. This hormone has
been associated with the development of several
retroviral diseases and their pathogenesis, such as
Feline immunodeficiency. FIV is a lentivirus that
causes a progressive disruption of the immune
function in cats.
Objective: The main objective of the present
study is to compare neuro-immune-endocrine
parameters (ACTH, Cortisol, AGP and
Evoqued potentials) in cats infected with
870
Back to contents
Material and Methods: Sera and plasma of cats
were analyzed for: IL1 (Elisa, Lehmann, 1992),
Acute Phase Protein (Alpha-Glycoprotein acid)
(Immunoprecipitation, Ecos, Japan), endogenous
ACTH (RIA), and cortisol (RIA). In addition,
neurological manifestations of the patients were
studied through auditory and visual evoked
potentials (AEP; VEP). FIV infection was
confirmed by nested PCR. The samples were
obtained at two times: one in the beginning of
therapy and the other after six months of treatment
with antiretrovirals: Zidobudine (AZT 5mg/kg/
day) and Valproic acid: 10 mg/kg/day). Statistical
results were analyzed with Mann-Whitney test (p
<0.05). In order to compare IL1, ACTH and AGP,
Chi-Square test and Contingency tables were
used. Correlation was estimated with Pearson-
test.

Results:
References: Values are represented as median and
range. Mann-Whitney test significance p<0.05.
There were not significant differences in cortisol
levels and there were not correlation between
ACTH and cortisol. IL1 decreases significantly
after 6 months of treatment (p 0.03). Correlation
between IL1 vs ACTH and IL1 vs AGP was found.
VEP showed latencies higher than 162 mseg in
the p100 in 75% of cats. Alterations of AEP were
observed only in 30% of the patients and there
were not significant differences between both
times of evaluation.
Discussion: The results at the beginning of
the therapy showed a compromise of the
neuroimmune-endocrine axis. High levels of
ACTH, IL1 and AGP were observed, due to
chronic stress, inducing an alteration of normal
regulation of the HPA axis. The comparison with
the results after 6 months of treatment showed
a lesser activation of axis. Positive correlation
beteween IL1, ACTH and AGP is related to the
improvement of the disease. It is well known that
RADIOGRAPHIC FEATURES OF ACEPROMAZINE – INDUCED SPLENIC
ENLARGEMENT AND ITS RELATIONSHIP WITH HEMATOCRIT AND TOTAL
PROTEIN CHANGES IN CATS OF IRAN
B. Mosallanejad, R. Avizeh, A. Ghadiri, M. Ezzati
Shahid Chamran University, Golestan, Ahvaz, Iran
Splenomegaly is commonly seen as a consequence
of sedation or anesthesia, Portal hypertension, or
splenic vein thrombosis. Splenic enlargement can
be sever, because up to 30% of the blood volume
can be pooled in the spleen. This research attempted
to verify and quantify size changes associated
with acepromazine splenic enlargement in cats.
Radiographic images of the spleen in normal
cats were collected to determine the maximum
diameter in the minimum dimension prior to, and
15 min after, administration of acepromazine in
cats. In this study 5 cats (DSH), 4-6 months of age
and weighing 0.8 – 1.1 kg were used. Significant
splenic enlargement was seen after administration
of acepromazine (P<0.01). Acepromazine was
injected to cats with dosage 3 mg/kg IM. These
Back to contents
POSTERS
IL1 stimulates the axis, with other cytokines,
and induces liberation of Acute Phase Proteins
(AGP). The therapy, as the present results show,
could produce an improvement of the disease,
diminishing IL1 levels and consequently ACTH
and AGP levels slow down. There were not
correlation between Cortisol and ACTH levels
and this could be explained because of the
abnormal regulation of the axis in this patients.
Conclusions: Feline Immunodeficiency produced
by a Retrovirus, Lentivirus, causes a similar
condition to Human Immunodeficiency (AIDS)
and it is being intensively studied worldwide. It is
particularly relevant to study auditory and visual
evoked potentials, since FIV produces a slowing
down of the conduction of the nervous impulse
but this al least did not showed amelioration
after six month of therapy. The treatment of
the disease with Zidobudine and Valproic acid
during 6 months shows in the present results
a normalization of HPA axis, diminishing the
chronic stress
2006 World Congress WSAVA/FECAVA/CSAVA
results indicate that measurable splenomegaly
occurs after acepromazine administration and a
condition causing measurable diffuse increased
attenuation in the spleen of cats. Also, hematocrit
and total serum protein (TSP) were measured
before and after induction. Hematocrit decreased
significantly in all cats after induction, but
changes of Total protein were no significant.
Correlation between decrease of hematocrit and
increase of spleen size following the anesthetic
protocols studied suggests sequestration of
red blood cells in splenic sites. In this survey,
prominence of spleen and prevention of diagnosis
mistakes following prescription of tranquillizer
were confirmed.
871
POSTERS

PARVOVIRUSASAPREDISPOSING FACTOR FOR INTESTINAL INTUSSUSCEPTION

IN 3 DOGS OF IRAN
B. Mosallanejad, R. Avizeh, A. Ghadiri, A. Moarrabi
Shahid Chamran, Golestan, Ahvaz, Iran
Parvovirus is a serious, deadly threat to the
unvaccinated dog population. Parvovirus is
capable of causing two different sets of clinical
problems. The first to be recognized, and most
common, is the “intestinal” form, which is
manifested by diarrhea; often bloody vomiting,
loss of appetite, depression, fever, and sometimes
death. The second syndrome, the “cardiac” form,
occurs in very young pups and is manifested
by an acute inflammation of the heart muscle.
Parvovirus can be caused illeus in dogs. In this
study intestinal intussusceptions were diagnosed
in 3 dogs with hemorrhagic gastroenteritis, due to
canine parvovirus. They were with age of 1 – 2
years and their breeds were Doberman pinscher
(2) and German shepherd (1). In history, they were
affected to Parvovirus in 3 – 6 months. As the other
causes of the disease were excluded, Parvovirus
was considered to be the most likely predisposing
factor for the intestinal intussusception. Ileocolic
intussusception was found in all of dogs. Of the
3 dogs that underwent surgical resection and
anastomosis of the intestine, 2 dogs recovered
completely and one died due to complications.
CBC was abnormal (Leucopenia and Neutrogena)
in dogs. Supportive treatments were done for
them. The objective of this investigation was to
detection whether Parvovirus in young dogs can
be a predisposing factor for intussusception in
higher ages.

RELATION OF CLINICAL INFECTION DEVELOPMENT IN DOG-TO-DOG BITE

WOUNDS WITH BACTERIAL CONTAMINATION
S. Mouro1, C.L. Vilela1, L.M. Cavaco2, M.M.R.E. Niza1
1
CIISA/FMV, Faculdade de Medicina Veterinária, Av. Universidade Técnica, Lisboa, Portugal; 2Presently at KVL
University, Institut for Pathobiology, Copenhagen, Denmark

This study aimed at relating the development of
clinical infection in dog-to-dog bite wounds with
the type of bacterial contamination present, from
environmental, oral or skin microbiota sources.
The study comprised 48 untreated dog bite
wounds, 23 of which clinically infected (48%).
Infection identification was based on the presence
of pus, fever, leukocytosis or when 3 or more
of the following minor criteria were present:
erythema, oedema, subcutaneous emphysema,
tissue necrosis, and malodor. Samples, collected
before any wound manipulation, with cotton
2006 World Congress WSAVA/FECAVA/CSAVA
from infected wounds were streptococci (23.2%),
Enterobactereaceae (20.3%) and P. multocida
(17.4%). Anaerobic cultures were positive in 26%
of infected wounds, being Clostridium perfringens
present in 3 samples. The most common isolates
from non-infected wounds were Gram-negative
oxidase-positive bacilli (42.8%), including P.
multocida (19.6%), and staphylococci (21.4%).
The results suggest that both environmental and
animal microbiota contamination occur in dog-
to-dog bite wounds. Environmental pathogens
may represent an important source of infection.

swabs or by needle aspiration, were submitted to
bacteriological analysis. All wounds bear aerobic
bacteria: from a total of 125 isolates, the most
frequent isolates were Pasteurella multocida
(16.8%) and Staphylococcus intermedius
(14.4%). Strict anaerobes were only isolated from
infected wounds. The most common isolates
The presence of skin and mouth microbiota of
dogs, frequently found in both types of wounds,
may also represent an important factor for the
development of infection. Further studies are
required on microbiota virulence factors, in order
to deeply understand their role in the outcome of
wound contamination.

DOG BITES TO CHILDREN IN THE CZECH REPUBLIC - A SURVEY

J. Náhlík1, E. Baranyiová1, M. Tyrlík2
1
University of Veterinary and Pharmaceutical Sciences, Palackého 1-3, Brno, Czech Republic; 2Faculty of Arts,
Institute of Psychology, Masaryk University, Arne Nováka 1, Brno, Czech Republic

The aim of the survey was to study the
circumstances of dog bites to children, and
their outcomes in terms of medical help sought.
Data were obtained from a questionnaire
872 completed with children. A total of 103 bites
were documented; 58 were inflicted on boys and
45 on girls. Results were evaluated using chi2
and F tests. Family dogs bit at home (57.6%),
dogs belonging to friends bit outside (62.2%),
and unknown dogs bit only outside (100.0%),

Back to contents

(chi2=24.796, df=2, p<0.001). Bites by small
dogs were more frequent at home (51.5%),
those by medium size (73.1%) and large dogs
(80.5%) outside (chi2=9.022, df=2, p<0.011). Of
101 responses, 32 bites happened at home; in 2
cases (6.3%) medical assistance was sought; 69
incidents happened outside, 21 of them (30.4%)
were treated. Assistance was sought when the
bite occurred outside (91.3%) rather than at
home (8.7%), (chi2 =7.271, df=1, p<0.009).
The age of children bitten and medically treated
was 2-11 years, mean age 5.6 years (F = 11.155,
df=1, p<0.001). Of 102 responses, broken skin
and bleeding was in 58 cases, of which 23 were
treated (39.7%). Medical help was related to the
type of injury (chi2 =22.528, df=2, p<0.001). Of
the bites 57 were inflicted on boys, 7 were given
A SURVEY ON HELMINTHIC INFECTION OF GASTROINTESTINAL TRACT IN
STRAY DOGS AT URBAN AREAS IN TABRIZ
A. Nematollahi
University of Tabriz, 29 Bahman, Tabriz, Iran
This study was done to determine the prevalence
of gastrointestinal helminthes infection of stray
dogs in Tabriz. Within eight months in six areas
susceptible to infection in the vicinity of Tabriz,
one hundred and two stray dogs (between 1-4
years old) were caught by strychnine poisoned
meat and were necropsied. Fifty nine dogs were
male and forty three dogs were female. For
preventing to zoonotic aspects, after necropsy,
digestive system of the dogs (from esophagus
to rectum) were separated from body and were
placed in formalin for three months. All of
parasites in their digestive system were isolated.
After fixation of the samples in 10% formalin
their identification were performed based on
parasitological characteristics. Total infection
rate in stray dogs was 64.5%. In parasitological
study four nematode: Toxocara canis (26.9%),
CONTROL STRATEGIES AGAINST GIARDIA INFECTION IN KENNELS
A. Ortuño, J. Castellà
Facultat de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain
Giardia is a protozoan flagellate which is found
in the intestinal tract of human and animals. It is
one of the most common parasites in dogs. The
infection is clinically important due to its high
prevalence, clinical symptoms - especially in
puppies-, its difficulty in control and its zoonotic
potential. Giardiasis can be transmitted by direct
contact or by fomites. Cysts are passed from
the host to the environment through feces. One
particular condition of Giardia is that cysts are
intermittenly shed in the feces. Outside, cysts
Back to contents
POSTERS
medical help (12.3%); among 45 girls bitten
help was given to 16(35.6%) of them. Girls were
treated more often (69.6%) than boys (30.4%),
(chi2 =7.8, df=1, p<0.008). Children were more
often treated when an adult was present at the time
of incident (56.5 %). In 66.7% cases no medical
help was given despite the presence of an adult at
the moment of the incident (chi2 = 4.029, df=1,
p<0.054). Most bites in the head area were by small
dogs (boys 80.0%, girls 50.0%); (boys, chi2=4.302,
df=2, p<0.122; girls chi2 =6.2, df = 2, p<0.038).
Dog bites to children seem underestimated in
terms of medical care given. Bites at home were
rarely treated, bites with broken skin in less than
a half of the incidents, and bites inflicted on boys
were treated less frequently than those inflicted on
girls.
Ancylostoma caninum(0.8%), Toxocara
leonine(20%) and Uncinarian stenocephala
(35.6%) and two cestod: Echinococcus granolosus
(48%) and Taenia hydatigena (3.6%) and one
Acantocephal: Macrocanthorynchus hiradinaceus
(13.9%) were identified. Maximum number of
parasites in one animal belonged to Echinococcus
granolosus (23.2 worms). There was not any
significant difference in infection rate between
males and females. However, with regard to
age, it seem that older animals are more prone to
acquire the infection. Furthermore, results of the
study showed that because of high prevalence of
digestive helminthes in stray dogs and the risk of
human and livestock animal’s infection a control
program must be carried out for controlling and
collecting of these animals to improve hygiene. 2006 World Congress WSAVA/FECAVA/CSAVA
survive for months in moist conditions but are
extremely susceptible to drying. This parasitoses
occurs far more frequently in kennels or shelters
since young animals and crowded environments
constitued important risk factors. Protection
against Giardia in kennels needs more complex
measures than in household with individually kept
dogs. In this report, it is presented two cases of
giardiasis in kennels: The first one was a breeding
kennel where puppies where clinically affected,
showing diarrhea, weight loss and growth
873
POSTERS

retardation; adult dogs were assymptomatic. The
other one was a shelter, where most dogs were
adults with chronic diarrhea. In some animals,
feces were malodorous and steatorrheic. Faecal
specimens were collected and were analised using
zinc sulphate flotation/centrifugation technique.
In some cases, at least three fecal fresh samples
had to be examined due to intermitent shedding
cysts. The main approaches to control giardiasis
were focused on environmental decontamination
and detection of carrier dogs. Environmental
disinfection with quaternary ammonium, decrease
environmental humidity, treatment of all animals
- even assymptomatic since they may continue to
shed cysts - with fenbendazol (50 mg/kg), fomites
control and routinely coprological controls of
all animals, especially those that were newly
acquired or incoming dogs, constitued the main
strategies followed up in both communities.
Acknowledgments: This study was partially
financed by Servei de Salut Pública i Consum de
la Diputació de Barcelona, Spain.

EFFICACY OF ANTIANGIOGENIC PHOTODYNAMIC THERAPY WITH BPD-MA IN

19 DOGS WITH HEAD TUMORS
T. Osaki, S. Takagi, Y. Hoshino, M. Okumura, T. Kadosawa, T. Fujinaga
Graduate School of Veterinary Medicine, Kitaku, Kita 18, Nishi 9, 060-0818 Sapporo, Japan

PDT was effectively able to treat locally solid
tumors without any serious side effects. The
purpose of this study was to assess the efficacy of
antiangiogenic PDT using BPD-MA in nineteen
dogs with head tumors. The tumor was irradiated
with 690-nm laser light at 15 minutes after
initiating the intravenous infusion of 0.5 mg/kg
BPD-MA. In cases that were followed up for
more than 1 year after PDT, the median survival
time of 6 dogs with oral tumors was 423 days
(range, 300–743 days) and the 1-year survival rate
was 67%. In 5 dogs with nasal cavity tumors, the
values were 533 days (range, 129–694 days) and
60%, respectively. The CT enhancement values
before and after PDT were significantly different
(p < 0.001) and were 54.3 ± 25.8 Hounsfield units
(HU) (21 treatments in 15 dogs) and 5.5 ± 5.7 HU
(18 treatments in 11 dogs), respectively. The mean
CT enhancement value of the tumors in which 19
treatments was effective was 57.2 HU and the one
for tumors in which 2 treatments was ineffective
was 27.5 HU. The main side effect was temporary
edema around the treated area for 1 week after
PDT; however, it did not require any particular
treatment. Antiangiogenic PDT is a promising
method for canine solid malignant tumors without
any serious side effects. Angiographic CT plays a
useful role in selecting antiangiogenic PDT cases
and in determining the therapeutic effect after
antiangiogenic PDT. Conversely, antiangiogenic
PDT using BPD-MA could be finished at short
times and performed repeatedly because of BPD-
MA rapid clearance and low accumulation in
tissues. It is concluded that antiangiogenic PDT
was effectively able to treat locally solid tumors
without any serious side effects.

A CASE REPORT OF EXOCRINE PANCREATIC ADENOCARCINOMA IN A TOY

BREED DOG
2006 World Congress WSAVA/FECAVA/CSAVA

K. Oskouizadeh
Faculty of Veterinary Medicine, Tehran University, Azadi, Tehran, Iran
A 4-year-old female miniature pincher with
a 40-days history of weight loss, lethargy and
vomiting was referred to Small animal hospital,
Faculty of veterinary medicine, University of
Tehran. The case also had severe jaundice,
chronic diarrhea and steatorrhea. All of the
efforts for saving the life of the case were not
successful and finally the signs deteriorated and
animal died because of hypovolemic shock and
electrolyte imbalances. At necropsy, the body
was cachectic, edematous and severely icteric.
A bloody ascetic fluid, lacking fibrin strands
was also noticed in the abdominal cavity. Firm
tumor masses originated from pancreas were
seeded to peritoneum with multiple attachments
to duodenum. There were also some points of
metastasis in regional lymph nodes and liver. On
the basis of histopathologic characteristics of
the tumor, the mass was diagnosed as relatively
well-differentiated exocrine pancreatic
adenocarcinoma.

874
Back to contents
 POSTERS
STUDY IN PREVALENCE AND DETECTION OF BARTONELLA HENSELAE (CAT
SCRATCH DISEASE AGENT) FROM DOMESTIC CAT IN IRAN
K. Oskouizadeh
Faculty of Veterinary Medicine, Tehran University, Azadi, Tehran, Iran

Bartonella henselae is the causative agent of
cat scratch disease (CSD) in human. Cat is
considered the reservoir of the bacterium. Blood
samples were collected between April-September
2005. From 100 domestic cat (indoor-outdoor)
living in Tehran-Iran tested for Bartonella
henselae bacteremia&seroprevalence. Cultural
and IFA method for serology were used. The IFA
cutoff titer was ≥1:64. All blood samples from
cats were cultured on fresh sheep blood agar
for 4 weeks. For the comparison seroprevalance
between groups, SPSS12 software and pearson
Chi-square were used with CI=95% and odd
ratio determination. Bartonella was not isolated
from these cats and no bacterial growth were
seen. 23% (23 of 100) of cats had antibodies to
B. henselae, detected by IFA at a titer ≥1:64.In
our study there were no significant differences
statistically in seroprevalence between cats and
their owner. 18% of cat owners had antibodies
to bartonella henselae. Seroprevalence in control
group (individuals which own no cat) was 5%, and
in statistical comparison between cat owner and
control group there were significant differences.
Seroprevalence in cats more than 6 months and
in outdoors cats were higher than the cats under
6 months and indoor cats. Our study confirm
that indoor cats are less frequently infected
than outdoor or stray cats and seroprevalence in
cats as compare with their owner showed that
contact with cats is a risk factor to infected with
Bartonella henselae.

EFFECT OF VITAMIN C AND E ON RENAL INJURY IN PIG AUTOTRANSPLANTATION

MODEL
C.S. Park1, M.J. Kim2, M.H. Jun2, J.Y. Lee2, S.W. Cho2, S.M. Jeong2, M.C. Kim2
1
Div. of Animal Sci. & RCTCP, Chungnam Natl. Univ., 220 Kungdong, Yoosung-gu, Daejeon, South Korea; 2Coll.
of Vet. Med., Chungnam Natl. Univ., 220 Kungdong, Yoosung-gu, Daejeon, South Korea

Introduction: Ischemia-reperfusion (I/R)
injury is a major cause of renal failure and
renal graft rejection (1,2). The purpose of
this study is to determine that antioxidants
vitamin C and E therapy provides protection
against I/R injury in pig kidney during kidney
transplantation.
Materials and methods: In control group
(n=3), after the left kidney was removed,
all arteries are perfused using hepa-saline
(heparine 1000 IU + saline 500 ml) followed
by autotransplantation. And then right
nephrectomy performed. In treatment group
(n=3), vitamin C (1,000 mg/head/day, IM) and
vitamin E (100 IU/head/day, PO) combination
were given for 2 days before operating. After
the left kidney was removed, all arteries are
perfused using hepa-saline including vitamin
C 1,000 mg. After implantation of the renal
autograft, right kidney was removed.
Results: The level of BUN increased to 81.0±5.57 mg/
dl at day 1 the control group, and then increased
gradually and was not normalized until 7 days
after renal autotransplantation. While in the
treatment group, the level of BUN went up to
53.50±16.23 mg/dl at day 1 and then slightly
decreased. In the control group, serum creatinine
levels increased to 6.80±2.22 mg/dl after 1 day
of renal autotransplantation and then decreased
slightly and were not normalized until 7 days of
operation. The serum creatinine level in the
treatment group increased 4.00±0.28 mg/dl
after 1 day of renal autotransplantation and
then slightly decreased to 3.05±0.07 mg/dl 2006 World Congress WSAVA/FECAVA/CSAVA
by 7 days of operation.
Conclusion: It was considered that antioxidants
vitamin C and E therapy may have roles on the
attenuation of I/R injury and recovery of renal
function in the renal transplantation model in
growing pigs.
References
1. Casanova D et al. 2002. Transplant Proc 34:
45-46.
2. Sarin PK et al. 2003. Transplant Proc 35: 35-36.

875
Back to contents
POSTERS

REPLANTATION OF COMPLETELY AMPUTATED PENIS IN A DOG

J. Park, K.-R. Cho, T.-S. Han, D. Chang, S.H. Choi, G. Kim
Veterinary Medical Center, College of Veterinary Medicine, Chungbuk National University, 12 Gaeshin-dong
Heungduk-gu, Cheongju, Chungbuk, South Korea

Objectives: To report a rare case of replantation
of traumatically amputated penis in a dog and
experimentally to elucidate the importance of the
anastomosis of the dorsal veins of the penis by
performing cavernosography.
Materials & Methods: A 2-year-old, mixed-breed
hunting dog was presented with the history of
penile amputation and laceration of femoral
and inguinal area during wild boar hunting.
Replantation of the penis was done by performing
anastomoses of the urethra, cavernous body, and
the left and right dorsal veins of the penis. The
other injuries were treated with the routine surgical
treatment. To identifying the dorsal veins of the
penis, as the main venous drainage vessels from
the bulbus gladis, experimental cavernosograms
were done on 3 beagle dogs.
Results & Discussion: The continuity of the
transected penis was recovered anatomically
and functionally. Postoperatively, there were no
evidences of necrosis and edema at the distal
portion of the penis. In addition to, no fistulas and
stenosis were found on urethrogram 20 days after
the surgery.
On the experimentally performed cavernosograms,
the contrast media (iohexol) which was injected
into the bulbus glandis drained by the left and
right dorsal veins of the penis, then converged
into one vessel at the ischial arch and diverged
into the left and right internal pudendal veins.
Conclusion: The reanastomosis of the left and
right dorsal veins of the penis in transected
canine penis is important factor to improve the
postoperative prognosis.

EFFICACY OF A RECOMBINANT FELINE OMEGA INTERFERON IN THE

PREVENTION OF INFECTIONS IN KITTENS
D. Pechereau1, L. Gardey2, K. de Mari2, P. Mahl2
1
Veterinary Clinic des Pyrénées, Pau, France; 2Virbac SA, Carros, France

Vaccines generally are not protective before 7
to 20 days after administration. Morbidity and
mortality due to viral infections may be recorded
in kittens during this period and represent major
risks in crowded shelters. The efficacy of a
recombinant feline omega interferon (rFeIFN)
was evaluated for the prevention of infections in
kittens recently introduced into a shelter. Recently
vaccinated kittens were allocated into 2 groups:
36 cats were injected with 1 MU of rFeIFN (group
T), while 52 cats remained untreated (group C).
2006 World Congress WSAVA/FECAVA/CSAVA
using the Wilcoxon rank sum test. The percentage
of diseased cats was compared between groups
using Fisher’s exact test. At V1, the 2 groups did
not differ for any of the parameters. After 15 days,
10 cats had shown clinical signs of infection.
Four cases of panleucopenia confirmed by PCR
(with 1 fatal outcome) and 3 cases consistent with
a coryza-like infection were observed in group C.
Only 1 cat showed signs of coryza in group T.
Fewer infectious episodes were thus recorded
after rFeIFN preventive treatment (p=0.0429).

The cats were observed over a 15-day follow-
up period. Treatment preventive efficacy was
evaluated from morbidity over 15 days following
the 1st veterinary consultation (V1). Animal
characteristics were compared between the groups
These results show the interest of rFeIFN in
reducing the risk of viral infection in the few days
following vaccine injection, while the animal is
not yet protected by the immune response.

PERIANAL NEOPLASIA IN DOGS: 23 CASES

Z. Pekcan1, O. Besalti2, S.A. Vural3, Y.S. Sirin2
1
Kirikkale University Faculty of Veterinary Medicine Department of Surgery, Yahsihan, Kirikkale, Turkey; 2Ankara
University Faculty of Veterinary Medicine Department of Surgery, Diskapi, Ankara, Turkey; 3Ankara University
Faculty of Veterinary Medicine Department of Pathology, Diskapi, Ankara, Turkey; 4Ankara University Faculty of
Veterinary Medicine Department of Surgery, Diskapi, Ankara, Turkey
The aim of the study was to present clinical, neoplasia were included. The breed dispersion
surgical and histopathological results of the of the dogs were Terriers (n=12), Mixed (n=4),
perianal neoplasia. Twenty four dogs presented Cocker (n=2), Boxer (n=1), Shitzu (n=1), Collie
at Department of Surgery Faculty of Veterinary (n=1), Tibetian Spanial (n=1) and Pekingese
876 Medicine Ankara University with perianal (n=1). The ages were between 6 and 15 years old.

Back to contents

Two of the 23 dogs were female and the others
were male. Perianal swelling, faecal tenesmus,
itching, hemorrhage, pain and dyschezia were
the clinical symptoms. Three of them had
tumors in tail, one had in abdomen and one had
in auricula in addition to perianal mass. Except
for cytoreductive surgery in one cases complete
resection were carried out in the operation.
Orchiectomy was performed in all male dogs.
Perioperative analgesia was achieved by epidural
morphine preoperatively. In histopathologic
examination perianal gland adenoma (n=11),
hepatoid gland epithelioma (n=3), lipoma
(n=2), squamose cell carcinoma (n=2),
POSTERS
rhabdomyosarcoma (n=1), sebaseose carcinoma
(n=1), fibromyosarcoma (n=1), perianal gland
adenocarcinoma (n=1) and rhabdomyom (n=1).
Lipoma was the histopathologic results of the
females. Circular resection was carried out in
2 cases with mucocutaneus involvement. Tail
amputation were performed in cases had tail
neoplasia addition to perianal masses. Recurrence
were seen in three cases which were diagnosed
as fibromyosarcoma, sebaseose carcinoma and
perianal gland adenocarcinoma and permanent
faecal incontinence were seen in none of the
dogs. In conclusion surgical management was
found favourable in this case series.

MULTIFACTORIAL TREATMENT TO OBSESSIVE-COMPULSIVE DISORDERS IN

DOGS
M. Pifarré i Olivé, L. Centrich i Pons
ETOVET S.C., C/ Francesc Jofre, St. Feliu de Guíxols, Spain

Poor welfare can cause the execution of abnormal
behaviour and it can appear compulsive disorders.
They are more difficult to solve when they are
chronic, when the animal spends many time
carrying out the abnormal behaviour, when the
environmental attention is reduced or when it
separates the abnormal behaviour from the initial
trigger. Usually, the treatment of these disorders
is symptomatic because in many cases we don’t
know the trigger or if we know them, we can’t
remove them. To treat these cases we propose
five points where we can make an incision in:
(1) Pharmacologic treatment: it can help us to
maintain the dog less reactive to exterior trigger
stimuli. (2) To prevent the conflict situation:
the approach of the cause, the hour of the day,
the place, the previous behaviour and change
the situation. (3) To stop conflicting situations:
adverse stimuli or stimuli which hinder the
abnormal behaviour. (4) Don’t promote conflicting
situations: prevent the relation between abnormal
behaviour and positive stimuli. (5) General
habits: to create a fixed routine of life, stable life
environment, walk and food habits. To optimize
the treatment of obsessive disorders the trigger
should be removed. As this can’t be possible,
we can see results in the interaction between all
the parts of the palliative treatment. In chronic
cases the application of just one point doesn’t
cause long-term improvement. For this reason
the owner’s implication is essential to carry out
the conjunction of all the points, otherwise the
treatment is doomed to fail.

CANINE IATROGENIC HYPERADRENOCORTICISM AS COMPLICATION IN 2006 World Congress WSAVA/FECAVA/CSAVA

HYPOTHYROIDISM OF THE DOG
S. Počta
Specializovaná veterinární ambulance Nové Město nad Metují, Czech Republic

In one year old dog was diagnosed
hypothyroidism. The treatment lasting for two
months was finished as a result of an owner’s
decision. He changed the veterinarian and we
haven’t had any information about this dog for
a long time. The patient appeared in our office
again in the age of five years. Dog was suffering
from an extensive alopecia, pendulous abdomen,
polydipsia, polyuria and calcinosis cutis as a
result of prolonged corticosteroid administration
(0.9 mg/kg SID for a period of three years). The
result of this treatment was iatrogenic Cushing’s
syndrome.

877
Back to contents
POSTERS
STUDY ON CARDIAC IMAGES FOR DIAGNOSIS OF DIROFILARIA IMMITIS
S. Ranjbar-Bahadori1, A. Veshgini2
1
Veterinary Collage, Islamic Azad University, Garmsar Branch; 2Clinical Sciences of Veterinary Collage, Tehran
University
Diagnosis of heartworm disease in dogs may
be made by identification of microfilaria
in the blood, by observation of thoracic
radiographic abnormalities and two-dimensional
echocardiography can project images of adult
heartworms.
Two hundred of stray dogs were studied by
modified Knott method for Dirofilaria immitis
and six dogs were infected. Results of CBC
indicated absolute eosinophilia (4254/µl) and
results of serum biochemical analysis were
normal. Radiographic signs included enlargement
LABRADOR RETRIEVERS’ PROBLEM-SOLVING STRATEGIES: A COMPARISON
BETWEEN THEIR 8TH AND 16TH WEEK OF LIFE
N. Reitz, F. Kuhne
Institute of Animal Welfare and Behaviour, Veterinary Department, FU Berlin, Oertzenweg 19b, Berlin, Germany
The problem-solving abilities of Labrador
Retrievers at 2 different life stages were taken into
account. The dogs had to solve 2 test sequences
of 5 hidden food/ toy tasks. The development
of behaviour patterns between the end of the
weaning and socialisation phase were assessed.
25 Puppies at their 8th and 16th week of life from
5 litters took part. The food was hidden by diverse
objects: under a wheeled wooden board, a pylon,
a “Knepig”TM, behind chairs and in the hand of the
experimenter. The puppies had to find out by their
own, how they could reach it in 4 trials. The tests
were videotaped and analysed frame-by-frame.
The main documented parameters were coping
strategies, e.g. licking or yawning, the latency of
reaching the food as well as the strategies which
2006 World Congress WSAVA/FECAVA/CSAVA
the dogs used to solve the hidden food task. The
frequency and duration of these parameters were
analysed. The puppies at the age of 8 weeks have
shown the tendency of fewer problem-solving
strategies. The average latency of reaching the
food in the 4 trials of the test with the wooden
board improved with each attempt. The dogs
were not necessarily faster in the 4th trial. Thus,
the correlation between the mean time of reaching
the food and the trial number was negative or
878
Back to contents
of right side of heart and mix alveolar and
interstitial densities in the caudal lobes of the
lungs. Echocardiography revealed the presence of
heartworms as hyperechoic densities within the
right atrial and ventricular cavities. Adult worms
were easily identified as parallel echogenic lines
separated by a hypoechoic region. Therefore
echocardiography appears to be a sensitive
procedure, which can be used in combination
with thoracic radiography to improve accuracy of
diagnosis of heartworm disease in dogs.
positive for all 5 tests; but just for the wheeled
wooden board test significant (Spearman, p= -
0.9, P<0.000). The problem-solving strategies in
the 8th and 16th week were tendential equal, but
the older puppies have shown behaviour patterns
characterised by more persistence. Dogs which
mainly reached the food through a problem-
solving strategy also preferred these behaviour
patterns at the age of 16 weeks. Licking intentions
and yawning etc. were behaviours which were
assessed with a huge individual diversity. When
the dogs solved the task in the 1st or 2nd attempt,
the object which hid the food was fixed more.
Thus, the correlation between the mean time
of reaching the food and the trial number was
sometimes negative or positive.
Dogs of the same litter have mainly borne
resemblance in the behaviour patterns while
the comparison of dogs of different litters has
revealed a huge diversity. This diversity was
mainly assessed for motivation and problem-
solving abilities as well as for displacement
activities. The motivation problems of the puppies
at the age of 8 weeks led to the assessment that
behavioural tests of dogs have to begin later at the
end of the socialisation phase.
 POSTERS
EFFICACY OF STABLE SAME TOSYLATE TABLETS TO REDUCE SIGNS OF AGE-
RELATED BEHAVIOUR PROBLEMS IN DOGS
C. Rème1, V. Dramard2, L. Kern3, J. Hofmans4, C. Halsberghe5, D. Vida Mombiela6
1
Medical Department Virbac SA, 13e rue LID, Carros, France; 2Veterinary Clinic, 16 rue Jeanne d’Arc, Lyon,
France; 3Veterinary Clinic, 6 place Léon Deubel, Paris, France; 4Veterinary Clinic, Avenue des Martyrs 173, Fléron,
Belgium; 5Veterinary Clinic, Deken Camerlyncklaan 14, Kortrijk, Belgium; 6Veterinary Centre Poble Sec, Passeig
de Montjuic 26, Barcelona, Spain

A double-blind placebo-controlled trial evaluated disorientation, learning deficits, decreased

whether oral stable S-adenosylmethionine tosylate
(NoviSAMeTM) supplementation (Novifit®
tablets, Virbac) could be useful in the management
of age-related mental decline in dogs. Thirty-six
dogs over 8 years that had displayed for at least
1 month signs of cognitive dysfunction were
included in the study. Exclusion criteria were
incapacitating disease, hypothyroidism, recent
administration of psychotropic drugs. The dogs
were administered NoviSAMeTM 18 mg/kg (n=17)
or identical placebo tablets (n=19) for 2 months.
Concurrent behavioural treatment was forbidden.
Examinations were performed on D0, D30 and
D60. A codified grid with 12 items evaluated
awareness or activity, social interactions, altered
sleep-wake cycle, inappropriate toileting and
anxiety. The scores were added together to give a
Standardised Geriatric Behaviour Score (SGBS).
Ability of the dogs to perform 4 observable daily
activities selected by owners was rated every
2 weeks to give a Case-Specific Disability Score
(CSDS). Decreased purposeful activity (75% of
dogs), diminished reaction upon verbal command
(77.8%) and increase of the period of sleep over
24h (83.3%) were the most frequent signs on
D0.Greater SGBS reduction was recorded with
NoviSAMeTM than with the placebo (P=0.016 on
D30, P=0.037 on D60) Fig1

Eleven (64.7%) and 7 dogs (36.8%) responded
favourably to NoviSAMeTM and placebo therapy
respectively.NoviSAMeTM supplementation
produced clinically meaningful improvement in
the level of activity (57.1%), awareness (59.5%)
and elimination disorders (57.1%). NoviSAMeTM
proved more effective than placebo to reduce the
CSDS as scored by owners (P=0.004 on D30,
P=0.013 on D60) Fig2 2006 World Congress WSAVA/FECAVA/CSAVA

Tolerance to the supplementation was recorded as effective to improve signs of age-related mental
good in 16/17 dogs. One dog exhibited transient decline in dogs.
diarrhoea. Novifit® tablets proved safe and 879
Back to contents
POSTERS

THROMBOEMBOLISM DUE TO ANTITHROMBIN III DEFICIENCY IN A DOG

WITH LEISHMANIASIS ASSOCIATED TO NEPHROTIC SYNDROME
M.M. Rodeia Niza, N. Felix, S. Mouro, C.L. Vilela, M.C. Peleteiro, A.J.A. Ferreira
CIISA/Faculty of Veterinary Medicine, Rua Prof. Cid dos Santos, Lisbon, Portugal

A 3-years-old male Boxer was referred with a
history of weight loss, anorexia and lethargy for
two weeks. On admission the dog was lethargic,
thin, anorectic, showing pd/pu. Laboratory
abnormalities comprised leucocytosis, total
protein increase, hypoalbuminaemia and
hyperglobulinaemia, high values for BUN,
creatinine, cholesterol, phosphorus and potassium,
and proteinuria. Leishmaniasis was diagnosed by
IFI and bone marrow aspirate. Urine protein-
creatinine ratio was elevated. The dog was
medicated with intravenous fluid, amoxicillin/
clavulanic acid, cimetidine, prednisolone
and alopurinol. On day 3 the animal showed
lumbar pain and paraparesis, absent femoral
pulses, cold extremities and hindlimb pain.
Ultrasonography showed a thrombus in the aortic
bifurcation. Aortic thromboembolism associated
to leishmaniasis with nephrotic syndrome
was diagnosed. Antithrombin III was severely
diminished and fibrinogen increased. Heparin was
then associated to the therapy. Fifteen days later,
an extensive necrosis developed from both hind
limb extremities, and owner request euthanasia.
Necropsy revealed extensive thrombus, from
distal aorta, through the iliac bifurcation, the right
iliac artery until both femoral arteries. Another
thrombus extended from the posterior vena cava
to the femoral vena. Histology revealed lesions
of glomerulonephritis. Aortic thromboembolism
leading to occlusion of the distal aorta and often
the iliac and femoral arteries with subsequent
ischemia of hindlimbs is a cause of posterior
paresis and paralysis rarely observed in dogs. In
visceral leishmaniasis, renal failure is a common
feature, being nephrotic syndrome associated to
thromboembolism very rare. Nephrotic syndrome
leads to urinary antithrombin III losses, due to
its low molecular weight, and consequently to
thromboembolism. Aortic thromboembolism
should be added to the list of leishmaniasis
complications.

LEPIDOPTERISM IN A DOG – AN UNUSUAL TWO-STAGE DEVELOPMENT OF

LESIONS
M.M. Rodeia Niza1, R.L. Ferreira2, I.V. Coimbra2, H.M. Guerreiro2, C.L. Vilela1
1
CIISA/FMV, Faculty of Veterinary Medicine Lisbon, Rua Prof. Cid dos Santos, Lisbon, Portugal; 2AZEVET,
Clínica Veterinária de Brejos de Azeitão Lda, EN10 nº453, Brejos de Azeitão, Portugal

Exposure to larvae of pine processionary
caterpillar (Thaumetopoea pityocampa), usually
by direct contact, leads to a rapid and exhuberant
allergic response to caterpillar’s hairs, rich in
thaumetopoein. In dogs, clinical signs include
lingual, sublingual and submandibular oedema,
2006 World Congress WSAVA/FECAVA/CSAVA
By the third day, the necrotized portion of the
tongue was lost and the animal apparently
recovered, eating normally. By the fourth day,
she stopped eating and lesions of labial and
mentum necrosis were noticed, accompanied by
conjunctival hyperemia and corneal ulceration.

facial pruritus, ptyalism, vomiting, and sometimes
ocular signs. The most frequent sequel is partial
lost of the tongue, following a necrotizing
process. In the present case, the lesions developed
in two-stages, with 4-days interval. A 10-months
old bitch was presented five hours after contact
with Thaumetopoea pityocampa with a history of
sudden ptyalism, vomiting and facial pruritus. She
showed lingual necrosis and severe discomfort.
Oral cavity was flushed with pressurized water,
to eliminate the majority of urticating hairs.
Methylprednisolone sodium succinate and
amoxicillin/clavulamic acid were administered.
Muzzle clipping and local disinfection were
performed, treatment was maintained and the
animal was fed through a nasogastric tube. A
topical ointment of chloramphenicol was applied
TID in the eye. Necrotized tissues were gradually
eliminated. The animal was discharged 5 days
later, with labial and lingual lost. This case’s
evolution is very atypical, with lesions developing
in two-stages, with a 4-day interval. The late labial
and mentum involvement is consistent with a
continuous liberation of thaumatopoein persisting
in the long hair of the animals’ muzzle.

880
Back to contents
 POSTERS
DIAGNOSTIC TOOLS IN RENAL DYSFUNCTION IN GUINEA PIGS
M.L. Ruelokke, J. Koch, A.L. Jensen
Dept. of Small Animal Clinical Sciences, Dyrlaegevej 16, 1870 Frederiksberg C, Denmark

20 guinea pigs, 10 of which were reported
polydipsic by the owners (PD group) and 10 with
normal water intake (C group) were examined
for renal disease. After clinical examination the
guinea pigs were anaesthetised, blinded and
randomized and underwent renal ultrasonography,
urine and blood sampling. The ultrasonographic
findings were classified as 0 for no abnormalities
indicative of renal dysfunction and 1 for
abnormalities indicative of renal dysfunction. The
C and PD group were subdivided into a C0, C1,
PD0 and PD1 group according to these findings.
Blood was analysed for urea, creatinine, glucose,
fructosamine and PCV. Urine was analysed on
urine dipstick for pH, blood, protein, glucose and
density and a microscopic examination was done.
The results were analysed and the groups were
tested against each other for statistic significance
by a Kruskal-Wallis and a Dunn’s test (p<0.05). 2
animals from the PD group were euthanised and
the kidneys sent for histopathology. 4/10 animal
had renal changes on ultrasonography, all from
the PD group, giving 3 groups: C0 (n=10), PD0
(n=6) and PD1 (n=4). Blood test results showed
no stastistic significance between groups for all
tested parametres. Urine test results showed pH
>8.5 and no glucose in 20/20 samples. For density
and protein no statistic significance between
groups were found. Blood was found on dipstick
in 12/20 urine samples evenly distributed between
groups. On microscopy red blood cells were found
only in 4/20 samples, all 4 were positive for blood
on dipstick. Histopathology of kidneys showed
bilateral chronic nephrosclerosis in both cases,
which correllated well with the ultrasonographic
findings. In conclusion blood and urine tests do
not seem as good diagnostic tools as in dogs and
cats. Other parameters as serum amylase could
be considered. Ultrasonography seems useful
for diagnosing renal disease in guinea pigs, but
further investigation is needed.

SEROPREVALENCE OF TOXOPLASMA GONDII ANTIBODIES IN CATS

S. Savic-Jevdjenic1, B. Vidic1, Z. Grgic1, E. Misic2
1
Scientific Veterinary Institute “Novi Sad”, Rumenacki put 20, Novi Sad, Serbia; 2Private practice “Misic”, MAtice
Srpske 16, Novi Sad, Serbia

Cats are the only species that pass the
environmentally resistant oocyst in feces and
sporulated oocysts are infectious to humans
and other animals. This is the reason why cats
were always accused to be the main source of
Toxoplasma gondii infection and very often they
have no clinical signs. A seroprevalence study
of Toxoplasma gondii antibodies was performed
in household and stray cats (92 cat sera were
examined: 60 household cats and 32 stray cats).
The survey for the determination of antibodies
for Toxoplasma gondii was done by the usage of
complement fixation test technique. The overall
seroprevalence was 17.3%. The infection rate in
stray cats was higher (35.8%) than in household
cats (15.2%). Last serum positive dilutions varied
from 1:40 to 1: 640, for the both groups of cats.
All of the cats were adult ones, so the correlation
between the age and the rate of infection was
not observed and most of them were females
(90%), so the difference between sexes was not
significant. None of the cats had any clinical 2006 World Congress WSAVA/FECAVA/CSAVA
signs. Gained seroprevalence results among the
cats are significant, especially among stray cats,
since they usually live close to humans or other
animals, and can be the source of toxoplasmosis.

AN UNUSUAL CASE OF CONCURRENT METAPLASTIC OSSIFICATION

ASSOCIATED WITH SERTOLI CELL TUMOR AND PARAPROSTATIC CYST IN A
GERMAN SHEPHERD DOG
M. Selk Ghaffari1, N. Khorami3, O. Dezfolian2, M. Massodifard3
1
Department Of Clinical Science, Faculty of Veterinary Medicine, Islamic Azad University Karaj-Branch, Karaj,
Iran; 2Department of Veterinary Medicine, Faculty of Agriculture, Lorestan University, Khoramabad, Iran;
3
Department of Clinical Science, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran
A 9–year–old male German shepherd dog was laboratory tests performed. Hyperestrogenism
referred for investigation of a two- months was the main paraclinical finding. Based on
history of progressive straining during defecation, plain and Contrast radiographic studies, a
and intermittent hematuria. Complete series of provisional diagnosis of paraprostatic cyst was 881
Back to contents
POSTERS

made. Exploratory laparotomy was performed.
Histopathologic examination of specimens
obtained following the surgery confirmed an
exceptional finding of bone metaplasia in sertoli
cell tumor and paraprostatic cyst.Although osseous
metaplasia has been reported in paraprostatic
cyst, but concurrent similar metaplastic changes
associated with sertoli cell tumor have not been
described in veterinary literature.

EFFECTS OF A FASCIAL REPLACEMENT TECHNIQUE FOLLOWING

INTERCONDYLAR NOTCHPLASTY IN DOGS
A.L. Selmi, J.G. Padilha Filho, B.T. Lins, G.M. Mendes, J.P. Figueiredo
Universidade Anhembi Morumbi, Rua Conselheiro Lafaiete, Sao Paulo, Brazil

Rupture of the cranial cruciate ligament (RCCL)
is a common orthopedic problem in dogs.
Several techniques have been described for the
treatment of stifle instability following RCCL,
but scarce information is available concerning
the effects of intercondylar notchplasty (IN) on
intra-articular fascial replacement of the cranial
cruciate ligament. Eighteen stifle joints were
operated, where 9 joints comprised the control
group and 9 joints were submitted to IN. Dogs
were evaluated prior to surgery and at days 1, 30,
90 and 180 postoperatively regarding the degree
of lameness, stifle stability, thigh circumference,
and degree of extension, flexion, range of motion,
tibial rotation and degree of degenerative joint
disease (DJD). Data were analyzed by means
of ANOVA for repeated measures followed by
an appropriate post-hoc test. Lameness was
significantly greater following surgery in both
groups, and decreased thereafter. Thigh muscle
circumference was significantly decreased at
days 30 and 90 post-op in both groups when
compared to pre-op values, however at 180 days,
thigh circumference was similar to pre-operative
values in both groups. Stifle stability increased
over time in both groups following surgery,
however during stifle flexion, an equal number
of joints showed some degree of instability.
Maximum degree of extension, flexion, range
of motion and tibial rotation was not affected by
surgery in any group. Radiographic signs of DJD
increased in both groups after surgery, however
statistical significance was not observed between
groups. It is concluded that IN does not cause any
detrimental effect on stifle joint following intra-
articular repair.

INTERCONDYLAR STENOSIS AFTER FASCIAL REPLACEMENT IN DOGS WITH

CRANIAL CRUCIATE LIGAMENT RUPTURE
A.L. Selmi, J.G. Padilha Filho, BT. Lins, G.M. Mendes, J.P. Figueiredo
Universidade Anhembi Morumbi, Rua Conselheiro Lafaiete 64, Sao Paulo, Brazil

Rupture of the cranial cruciate ligament is a were significantly greater, both radiographic and
common orthopedic condition in dogs treated macroscopically, when compared to CG at any
by several different surgical techniques. Stenosis given time. Stifles in GC presented a progressive
2006 World Congress WSAVA/FECAVA/CSAVA

of the intercondylar notch following transection
of the cranial cruciate ligament has been
studied in dogs but the effects of intercondylar
notchplasty (IN) following intra-articular
stabilization of the stifle has not been described.
We determined the effects of IN prior to intra-
articular stifle stabilization in dogs. Macroscopic
and radiographic indexes for intercondylar notch
width and notch height were evaluated in 18 stifle
joints, where 9 joints comprised the control group
(CG) and 9 joints were submitted to IN. Dogs
were evaluated radiographically prior to surgery
and at days 1, 30, 90 and 180 postoperatively.
Data were analyzed by means of ANOVA for
repeated measures followed by an appropriate
post-hoc test. Following IN, notch width indexes
decrease in notch width indexes; however this
was not statistically significant when compared
to baseline values. In the stifles undergoing IN,
a decrease in notch width index was observed
over time from day 1 through 180, however mean
values were significantly greater at any time in
comparison to preoperative values. Notch height
indexes did not vary over time in any group. It
is concluded that IN caused an increase in notch
width indexes following intra-articular fascial
repair, although stenosis of the intercondylar
fossa was not observed in the control group,
which suggests that stability might be responsible
for prevention of stenosis in the cranial cruciate
ligament-deficient stifle.

882
Back to contents
 POSTERS
IS BRUSH CYTOLOGY TRUSTABLE METOD FOR DETECTION OF DOG’S
HELICOBACTER LIKE ORGANISMS?
A. Shabestari Asl1, A. Bahadori2, M.H. Soroush3, A.T. Eftekhar Sadat4
1
Islamic AZAD University Tabriz branch, Tabriz, Iran; 2Islamic AZAD University, Tabriz, Iran; 3Tabriz University,
Tabriz, Iran; 4Tabriz EMAM med hospital, Tabriz, Iran

Helicobacter are spiral-shaped or curved Gram
negative bacteria that inhabit the glands, parietal
cells and mucus of the stomach. The large
gastric HLO in dogs are indistinguishable by
light microscopy, where they are seen as large,
5 -12µ long spirals. H. felis, H. bizzozeronii, H.
salomonis, H. heilmannii have been found in
the gastric mucosa of dogs. The prevalence of
HLO infection in dogs is 67 to 86% of clinically
healthy pet dogs, 74 to 80% of dogs presented
for investigation of recurrent vomiting, and 100%
of healthy laboratory beagles. In this research,
we examined 40 healthy stray dogs randomly.
Twenty of them were females and 7 of them were
immature (table 1). All dogs were healthy and
have good appetite. CBC was normal (see table
2). Endoscopic examination was established for
taking of brush cytology after 16 hours fasting.
All gastric specimens were taken from body and
antrum area. They were examined by Gimsa’s
and gram’s staining at the same time by light
microscope. HLO were seen in many of these
specimens (table3). The percentage of infection
was high and even was seen in the immature stray
dogs (table 4). By light microscopic taxonomy
evaluation, different shapes and co-infection
of gastric HLO were detected (figure 1-5). The
aim of this study was detecting the rate of gastric
HLO infection in dogs with brush cytology.
Brush cytology appears an effective method
to detection of HLO. This method is safer than
biopsy and available. Determination of HLO
with this method is simple and seems have a
correct results because of large spiral shape of
these organisms. But this method only shows the
existence of these organisms and we dont able to
confirm the presence of ulcers and erosions that
will produced by these organisms.

PREVALENCE OF GASTRIC HELICOBACTER LIKE ORGANISMS (HLO) IN

IRANIAN STRAY DOGS WITH BRUSH CYTOLOGY
A. Shabestari Asl1, A. Bahadori2, M.H. Soroush3, A.T. Eftekhar Sadat4
1
Islamic AZAD University Tabriz branch, Tabriz, Iran; 2Islamic AZAD University, Tabriz, Iran; 3Tabriz University,
Tabriz, Iran; 4Tabriz EMAM med hospital, Tabriz, Iran

Helicobacter are spiral-shaped or curved Gram
negative bacteria that inhabit the glands, parietal
cells and mucus of the stomach. The large gastric
HLO ie, H. felis, H. bizzozeronii, H. salomonis,
H. heilmannii have been found in the gastric
mucosa of dogs. The reported prevalence of
HLO infection in pet dogs is about 67 to 86%.
However, this study is first report of natural
infection of gastric HLO. In this research, we
examined 40 healthy stray dogs randomly.
Twenty of them were females and 7 of them were
immature (table 1). All dogs were healthy and
they have good appetite. CBC was normal (see
table 2). Endoscopic examination was established
for taking of brush cytology after 16 hours fasting.
All gastric specimens were taken from body and
antrum area. They were examined by Gimsa’s
and gram’s staining at the same time by light
microscope. Specimens also used for urease test
too (table 3). HLO were seen in many of these
specimens (table 4). The percentage of infection
was high and even was seen in the immature
stray dogs (table 5). By light microscopic
taxonomy evaluation, different shapes and co-
infection of gastric HLO were detected (figure
1-5). The occurrence of gastric HLO infection
was similar to the prevalence of these organisms
in the pet dogs (table5) that suggested for pets
in references books. The aim of this study was 2006 World Congress WSAVA/FECAVA/CSAVA
detecting of the prevalence of natural infection
of gastric HLO in stay dogs with brush cytology.
With attention to the result; presence of HLO is
similar to pet animals (table5). Brush cytology
appears an effective method to detection of HLO.
This method is safer than biopsy and available.
Determination of HLO with this method is simple
and seems have a correct results because of large
spiral shape of these organisms. Further more,
the prevalence of HLO in our stray dogs is high
and there are no differences between prevalence
of HLO healthy pet dogs (as reported in the
references) and our study.

883
Back to contents
POSTERS
DIAGNOSIS OF MALIGNANT NASOPHARYNGEAL HISTIOCYTOMA IN A
DOMESTIC SHORTHAIR CAT
S. Shibly1, R. Hirt2
1
Institute of Pathology and Forensic Veterinary Medicine, University of Veterinary Medicine Vienna, Veterinärplatz 1,
Vienna, Austria; 2Clinic of Internal Medicine and Infectious Diseases, University of Veterinary Medicine Vienna,
Veterinärplatz 1, Vienna, Austria
Malignant histiocytic tumors are rarely seen in
cats. To the author´s knowledge, this is the first
report of malignant nasopharyngeal histiocytoma
in a cat. A 12 years and 10 months old female
spayed domestic short hair cat was presented
with a history of coughing, retching and loss of
appetite. Apart from mildly reduced skin turgor,
the clinical examination was unremarkable.
Blood tests revealed elevated total protein, all
other parameters were within normal limits. X-
rays of the skull were taken and showed increased
opacity and widening of the nasopharynx (Fig.
1). Retrograde rhinoscopy was performed and a
nasopharyngeal tumor located at the level of the soft
palate was discovered (Fig. 2). Multiple biopsies
were obtained. For the histologic examination
the biopsies were fixed in formalin, embedded
in paraffin wax, sectioned and stained with H &
E. Besides inflammatory infiltration a neoplastic
cell population resembling atypic histiocyts
could be demonstrated (Fig. 3). Neoplastic cells
1 2
4 5
2006 World Congress WSAVA/FECAVA/CSAVA
EXAMINATION OF SIDE EFFECTS OF SULFANAMIDE DRUGS CAUSING
KERATOCONJUNCTIVITIS SICCA IN RABBIT
D. Shirani1, A. Ali Asgari2
1
Department of Clinical Science, Faculty of Veterinary Medicine, University of Tehran, Azadi, Tehran, Iran; 2Private
Clinic, Char Bag, Esfahan, Iran
The sulfanamides are one of the oldest
recognized group of antibactrial agents. During
the recent years sulfanamides have been used in
combination with asynergistic compound called
trimethoprim to potentiate their antibacterial
884
Back to contents
stained negative for Cytoceratine-Ag, S-100-Ag
and Toluidin-Blue. Positive Vimentin- and HLA-
immunostaining confirmed the mesenchymal and
histiocytic nature of the neoplasm (Fig. 4, 5). The
application of immunohistochemical methods
assisted the diagnosis of malignant histiocytoma
in this case as routine H & E – staining did not
yield distinct results.
Conclusions:
•As nasal neoplasia is a common finding in cats,
importance has to be placed on accurate and
early diagnosis in order to balance prognosis and
therapy.
•Tentative diagnosis of nasal neoplasia demands
the application of imaging techniques.
•Endoscopy features the advantages of a low
stress procedure combined with high visibility
and the possibility to obtain biopsy samples.
•Immunohistochemical stainings can be very
useful in identification of poorly differentiated,
high-grade malignant and uncommon tumors.
3
action. These potentiated sulfanamids belong to
the category of bactricidal drugs. Sulfanamides
are used in the treatment of pet animal disease
and are among the most commonly used drugs.
When there is a renal disorder, the clinical side

effects are sedimentation and urinary crystals in
dogs. Other side effects are cystic calculus as in
dog, renal insufficency and azotemia in cats. One
of the most common diseases caused by the long-
time use of this drug is kerato conjunctivitis sicca
in dogs. The main reason of which is low tear
production. This dryness causes conjunctivitis
and as a result corneal ulcer and blindness.
Material and method: In this study a number of
35 rabbits with an average age of one year were
studied in three groups of ten and one group of
five as a case control group. Co-trimoxazol is
used as 200mg/5cc oral suspension. The first
POSTERS
group were treated with a dose of 30 mg /kg for
7days, the second group with 60 mg /kg dosage
for 7 days, and third group with 30 mg /kg for 14
days. Schirmer tear test was used to measure the
tear volume. Discussion and Result: the statistical
test shows the two by two difference of average
in all the cases of which there is a significant
diffrence between the two averages with a 99%
level of confidence and an error probability of
1% increased duration of drug adminstration
from 7 to 14 days, caused a significant drop in
tear secration rate.

EFFECTS OF CELECOXIB ON GASTRIC MUCOSA, HAEMOGRAM AND BLEEDING

TIME IN DOG
A. Shojaee Tabrizi1, A. Kamrani2, H. Kazerani3
1
Small Animal Department, University of Tehran, Azadi, Tehran, Iran; 2Small Animal Department, University of
Mashhad, Azadi, Mashhad, Iran; 3University of Mashhad, Azadi, Mashhad, Iran

Nonsteroidal antiinflammatory drugs (NSAIDs)
exert their antiinflammatory, analgesic and
antipyretic effects by reducing synthesis of
prostaglandins via cyclooxygenase (COX)
inhibition. Despite the extensive applications
of NSAIDs, both in human and in veterinary
medicine, the use of these drugs is limited due to
their sever adverse effects especially on gastric
mucosa. Classic studies attribute the therapeutic
and the adverse effects of NSAIDs to the
inhibition of COX-2 and COX-1 respectively.
Celecoxib, a COX-2 specific drug, has caused
less gastric effects compared to the classic non-
specific NSAIDs. However, to the best of our
knowledge, gastric effects of this drug has not
been studied yet. In this research, dogs (mixed
Iranian breed) in groups of 5, received either
celecoxib (3mg/kg; twice a day) or placebo
(control) orally for 14 days. The haemogram
was studies during the treatment and 3d after
cessation of celecoxib (day 17). The lesions of
gastric mucosa were also graded at days 0, 7 and
14 using standard gastroscopy according to the
modified method of Murtaugh and his colleagues.
The haemogram results (WBC, RBC and platelet
counts as well as the levels of PCV, hemoglobin,
MCV, MCH and MCHC) were not statistically
different between the two groups. However,
celecoxib increased the bleeding time 3d after
cessation of the treatment. Besides, significant
lesions were observed on gastric mucosa of
celecoxib receiving dogs especially at day 14.
These results suggest that celecoxib, due to its
potential sever gastric effects, should be used
cautiously in dogs.

2006 World Congress WSAVA/FECAVA/CSAVA

A CANINE PARVOVIRUS TYPE 2 VACCINE PROTECTS DOGS FOLLOWING
CHALLENGE WITH A RECENT TYPE 2C STRAIN
N. Spibey1, N. Greenwood1, I. Tarpey1, S. Chalmers1, D. Sutton2
1
Intervet UK Ltd, Walton Manor, Walton, Milton Keynes, MK7 7AJ, U.K.; 2Intervet International, Wim de
Körverstraat 35, P.O. Box 31, 5830 AA Boxmeer, The Netherlands

Since the emergence of canine parvovirus type 2
(CPV2) in the 1970s, the virus has been evolving.
The first variant which appeared was called type
2a, subsequently a second variant appeared and
was called type 2b. The original type 2 virus
now appears to have been replaced in the field
by the type 2a and 2b variants. There is evidence
that this evolution is continuing and reports of
the emergence of a new variant - type 2c – have
appeared over the last few years. The initial
canine strain vaccines were based on the original
type 2 virus. Concern has already been expressed
Back to contents
as to whether these vaccines protect as effectively
against the 2a and 2b variants, and the more recent
appearance of CPV type 2c has again raised this
question. One of the original live attenuated
vaccines which is still widely used today was
based on a type 2 field strain isolated in the UK
(Nobivac® Parvo-C – Intervet). This vaccine has
already been shown to protect dogs from both
clinical disease and virus shedding following
challenge with CPV type 2, 2a and 2b. The
following study was set up to investigate whether
this type 2 vaccine could also successfully protect
885
POSTERS

against challenge with a field isolate of the new
type 2c variant. Twelve seronegative beagle dogs
were divided into two equal groups. One group
was vaccinated with Nobivac Pi and Nobivac
Lepto at 8-10 weeks of age and Nobivac DHPPi
and Nobivac Lepto three weeks later. The control
group received no vaccinations. Four weeks
following the second vaccination both groups of
dogs were challenged with a recent field isolate
of canine parvovirus type 2c. Blood samples, in
order to monitor antibody response and leucocyte
numbers, and rectal swabs, in order to detect
any viral excretion post challenge, were taken
at various intervals. Dogs were also clinically
monitored from two days prior, to 14 days post
challenge. In the unvaccinated control group all
the dogs became severely ill. Three of the six
control dogs had to be euthanised and although
the three remaining control dogs survived they
required supportive oral administration of
electrolytes. In addition all of the unvaccinated
control dogs shed parvovirus in their faeces for
at least four days post challenge. In contrast all
the vaccinated dogs remained clinically normal
throughout the course of the study and no virus
could be isolated from rectal swabs at any stage
post challenge. This study demonstrates that a
single dose of the Nobivac CPV vaccine is able
to successfully protect against clinical signs of
disease and prevent shedding of virus, following
challenge with the recent type 2c variant of canine
parvovirus.

EVALUATION OF SURGERY IN DOGS WITH DEGENERATIVE LUMBOSACRAL

STENOSIS BY FORCE PLATE AND QUESTIONNAIR
N. Suwankong, B.P. Meij, N.J. van Klaveren, S. de Boer, E. Meijer, W.E. van den Brom, H.A. Hazewinkel
Department of Clinical Sciences of Companion Animals, Utrecht University, Yalelaan 8, Utrecht, The Netherlands

Introduction: Degenerative lumbosacral stenosis
(DLS) in dogs results in compression of the
cauda equina. The main clinical signs are low
back pain and pelvic limb lameness. Treatment
may consist either of rest and anti-inflammatory
drugs or of decompressive surgery. Evaluation
of the result of surgery can be done subjectively,
through interviews with the owner, or objectively,
by force plate analysis (FPA) of the gait of the
dogs.
Aim of study: The aim of this study was to
investigate the long term follow up after
decompressive surgery in dogs with DLS using
FPA and questionnaires to owners.
Materials and Methods: Thirty-one dogs with DLS
underwent decompressive surgery consisting of
dorsal laminectomy. FPA was performed before,
and 3 days, 6 weeks, 6 months and ≥ 1.5 years
2006 World Congress WSAVA/FECAVA/CSAVA
force of the pelvic limbs and that of the thoracic
limbs (P/Tfy-) was calculated.
Results: The Fy- of the pelvic limbs and the ratio
P/Tfy- were significantly smaller in dogs with
DLS than those in the control group. The Fy- and
P/Tfy- were significantly decreased at 3 days after
surgery, and the values increased from 6 weeks
to 6 months after surgery. The questionnaires
reported significant improvement at 6 months
and at ≥ 1.5 years compared with questionnaires
before surgery. The majority of owners were
satisfied with the results of surgery.
Discussion: Decreased propulsive forces in dogs
with DLS and at 3 days after decompressive
surgery may be the result from impairment of
neural tissues. The Fy- and P/Tfy- increased over
a 6 months follow-up period, but remained smaller
than those in control dogs. Owners’ questionnaires

after surgery. Questionnaires were answered by
owners before and at 6 months and ≥ 1.5 years
after surgery. Force plate data were analysed
using the peak braking force (Fy+), the peak
propulsive force (Fy-), and the peak vertical force
(Fz+). The ratio between the total propulsive
illustrate that decompressive surgery reduces
the pain and restores normal companion animal
function as experienced by owners. It is concluded
that surgical treatment of dogs with DLS may
result in restoration of propulsive force of pelvic
limbs over a period of 6 months.

DIROFILARIOSIS - NEW DISEASE IN DOGS IN THE CZECH AND SLOVAK REPUBLIC

V. Svobodova1, Z. Svobodova1, V. Beladicova2, D. Valentova2, P. Forejtek3, M. Svoboda1
1
Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Sciences, Czech Republic; 2State
Veterinary and Food Institute, Slovak Republic; 3Institute of Wildlife Ecology University of Veterinary and
Pharmaceutical Sciences, Czech Republic

The incidence of canine filariosis in Central We investigated occurrence of dirofilariosis

Europe in the past was rare and associated with in the Czech and Slovak Republic. Finding of
import. Movement of dogs across countries has microfilariae in blood of two dogs from Slovakia
contributed to spreading of filariae to new areas. on occasion of haematological testing in May
886
Back to contents

2005 became an impetus for taking and analysing
blood samples of other dogs. In Czech Republic
we started investigation in December 2005 and
January 2006. Slovak group consisted of 21 dogs
and Czech group of 30 dogs. Microfilariae were
detected using the Knott test and determinated
with the histochemical method based on the
activity of acid phosphatase. For serological
detection of D. immitis antigen we used the
PetChek® kit. In Slovak group we found positive
12 out of 21 dogs. We identified microfilariae
of D. repens in 12 dogs and D. immitis in two
dogs simultaneously with D. repens. Serological
testing detected D. immitis antigen in 3 dogs. In
IMPORTED EMERGING INFECTIONS OF TRAVELLING DOGS IN THE CZECH
REPUBLIC
Z. Svobodova1, V. Svobodova1, E. Nohynkova2, M. Svoboda1
1
Faculty of Veterinary Medicine, University of Veterinary and Pharmaceutical Science, Brno, Czech Republic;
2
Department of Tropical Medicine, Bulovka Faculty Hospital, Prague, Czech Republic
In the Czech Republic, vector borne diseases
- leishmaniosis, dirofilariosis, babesiosis and
ehrlichiosis are classified as serious imported
infections of dogs. In order to identify the risk of
travelling and imported dogs to become infected
we have examined a group of 97 (Group 1) dogs
which were potentially at risk because they
either travelled to or were imported from foreign
countries endemic for these infections. The second
group (Group 2) was set up from 80 non-travelling
dogs living in areas of the Czech Republic with
a potential risk of Dirofilaria immitis, D. repens,
Babesia canis and Anaplasma phagocytophilum
transmission. Vectors of these pathogens are
commonly found in Czech Republic. The study
was carried out from November 2003 to May
2006. For laboratory tests, samples of whole
blood, blood serum and 2 fresh blood smears
were obtained from each dog. As the vectors
of leishmaniosis are not found in the Czech
Republic, only dogs from the first group were
examined. 10 (10.3%) out of 97 dogs from Group
1 examined for leishmaniosis were serologically
positive using indirect hemagglutination test.
Microscopical examination of stained smears
from lymph node or bone marrow fine needle
aspiration revealed the amastigotes of parasites in
7 dogs serologically positive the other three were
free of amastigotes. Seven dogs, which were
found positive during microscopical examination
of lymph node aspiration, were suffering from
serious clinical signs. The mosquito vectors of
dirofilariosis are endemic in our country, so not
only imported or travelling dogs (Group 1), but
also dogs living only in the Czech Republic
(Group 2) were examined. No animal out of
a total of 97 dogs from Group 1 examined for
Back to contents
POSTERS
Czech group we found positive 7 out of 30 dogs.
Microfilariae were detected by the Knott test in 4
dogs but only in 1blood smear where agreed with
D. repens. Serological detection of D. immitis
antigen was positive in 3 dogs. No microfilariae
D. immitis were detected. The intensity of
infection of dirofilariosis has been still lower than
in Slovakia. Dogs were without specific clinical
signs only 1 of them from the Slovak Republic and
D. immitis positive manifested higher weariness.
Conclusions: Dirofilaria repens and Dirofilaria
immitis have colonized the Czech and Slovak
Republic.
dirofilariosis was positive. Seven animals (8.8%)
out of a total of 80 dogs from Group 2 examined
for dirofilariosis were positive. Acid phosphatase
staining identified D. repens species in all the
samples. PCR definitely confirmed D. repens
diagnosis in these samples. 13 dogs (7.3%)
out of 177 dogs examined for babesiosis were
positive. All positive dogs were from the Group1.
None of 80 dogs living in the area of the Czech
Republic, where Dermacentor reticulatus ticks
with a vector potential occur, was positive
for babesiosis. Rhipicephalus sanquineus is
a vector of E. canis which does not occur in
the Czech Republic. None of the dogs (Group
1) examined for ehrlichiosis was positive.
Intracellular morulae of Ehrlichia canis were
not microscopically found and serologic tests
(IFAT) were also negative in all animals. Ixodes
ricinus transmits the agent of canine granulocytic 2006 World Congress WSAVA/FECAVA/CSAVA
ehrlichiosis/anaplasmosis - A. phagocytophilum
in Europe. It is the most common tick in the
Czech Republic. Only animals from the Group
1 were tested for A. phagocytophilum using both
IFAT and microscopic examination. 8 (10%)
out of 80 dogs examined for anaplasmosis were
serologically positive. Intracellular morulae of
A. phagocytophilum were not microscopically
found. All positive animals showed serious
clinical signs of the respective disease and
were treated accordingly. From our data we
conclude that exotic diseases of travelling dogs
seem to be important emerging infections in
our country which veterinary practitioners
must deal with. Methods of diagnosis,
treatment and prevention must be discussed
to avoid increasing risk of these infections in
new regions.
887
POSTERS

BABESIOSIS IN FALCONS
W. Tarello
Al Wasl Veterinary Clinic, Al Wasl Road, Dubai, United Arab Emirates

Babesia shortti causes a disease in falcons
showing signs such as anorexia, somnolence,
weight loss, vomiting, neurological symptoms
and blood in stool. Results obtained following
imidocarb dipropionate therapy performed on
captive falcons from Kuwait and Dubai indicates
that Babesia shortti is pathogenic, largerly
present in the local population and responsive to
imidocarb dipropionate.

TREMATODOSIS IN FALCONS IN THE MIDDLE EAST

W. Tarello
Al Wasl veterinary Clinic, Al Wasl Road, Dubai, United Arab Emirates

Strigea falconispalumbi is the causative agent of reports the results of a survey on 1706 captive
trematodiasis in falcons. However, little is known falcons from Kuwait, including the response to
of its incidence and pathogenicity. I therefore therapy with ivomec super.

DOPPLER IMAGING OF THE ORBITAL VASCULATURE OF THE NORMAL

DOMESTIC SHORT HAIR CATS
D. Vosough, M. Masodifard
Faculty of Veterinary Medicine, University of Bahonar, Kerman, Iran

Introduction: Blood velocity parameters of the
orbital and ocular vasculature can be no invasively
assessed and measured by Doppler imaging.
The purpose of this study was to blood velocity
measurement in orbital vasculature.
Methods: A total of 4 (male) previously healthy
DSH cats were selected. General Electrics Voluson
730-Pro ultrasound equipment with linear trapezoid
5-12 MHz transducer was applied for all the
examinations. Vessels identified a majority of the
time, include: external ophthalmic artery (EOA), and
internal ophthalmic artery (IOA) and the following
Doppler parameters were measured, peak systolic
velocity (PSV) and diastolic velocity (EDV).
2006 World Congress WSAVA/FECAVA/CSAVA
Results: Mean PSV, EDV, at the EOA were 13.3,
6.1, and the mean PSV, EDV, at the IOA were
12.8, 6.5, and 0.607.
Discussion: Doppler imaging has the potential for
determining no invasively and consecutively the
blood velocity parameters found in orbital and
ocular diseases, including orbital inflammations
and neoplasia; intraocular inflammations and
neoplasia; vascular diseases including systemic
vascular disease (hypertension) vasculopathies,
and anemia; the glaucoma; and document able
follow-up after medical and surgical treatment of
these diseases.

POSSIBILITY OF THE USE OF THREE DIMENSION ULTRASOUNDS AND

MEASURMENT OF OPTICAL LONG AXIS OF MIX BREED DOG
D. Vosough, M. Molaei, M. Masodifard
Faculty of Veterinary Medicine, University of Bahonar, Kerman, Iran

Introduction: The purpose of this study was to
evaluate the possibility of taking three dimensional
(3D) ultrasound images for better visualization of
canine eye and also taking the normal values of
the optical a long axis by using this technique.
Methods: A total of 16 (8 males and 8 females)
previously healthy 2 years old mix breed dogs.
General Electrics Voluson 730-Pro ultrasound
equipment with “3D small parts” option of a 3D
and 4D linear trapezoid 5-12 MHz transducer
was applied for all the examinations. Ultimately
888
Back to contents
the normal values of the optical long axis were
measured from a line between cornea and optic
disc in males and females, lefts and rights. All the
obtained data were analyzed by paired sample T-
Test statistically
Results: The 3D ultrasonography method was
found to be suitable for ophthalmic purposes. The
relationships and connections between vitreous
membranous, retina, and ocular wall are finely
displayed and due to the stored 3D ultrasound
tissue information, The values of the optical long

axis in obtained 3D images were measured. There
was a significant difference between male and
female dogs but there was not any between left
and right eye as it was expected (p<0/05).
Discussion: It was so fast that a real-time 4D
reconstruction could be performed too. Axial
A RARE CASE REPORT OF BILATERAL PATTELAR LUXATION IN A PERSIAN CAT
D. Vosough, M. Molazem
Faculty of Veterinary Medicine, University of Kerman, Kerman, Iran
Introduction: Patellar luxation may result
from malformation of the femoral trochela,
poor alignment between the distal femur and
the proximal tibia or rotation of the proximal
extremity of the tibia. This abnormality results
in the patellar straight ligament being out of line
with the trochlear groove. Lateral luxation of the
patellar is occasionally seen in large dogs with
valgus deformity(2). In cat patellar luxation is a
very rare event and bilateral luxation of that is
much more rare(3).
Case report: 5 months old, male DSH cat was
refferd to the Small animal Clinic of University
of Tehran, which had a history of lameness of
both hind limbs. The prior history was unknown
but after clinical examination abnormality in
both stifles was highly suspected, it also had a
painful stifle joint on deep palpation of pattelars.
In clinical examination; the patella will often
spontaneously relocate when the problem resolves
immediately. Then radiography was taken on
craniocaudal, mediolateral, and skyline views
of both stifles and these radiographs revealed:
RADIOLOGICAL AND PARASITOLOGICAL DIAGNOSIS OF OTITIS MEDIA IN A
DOMESTIC SHORT HAIR CAT (DSH)
D. Vosough, S. Norolahifard
Faculty of Veterinary Medicine, University of Kerman, Kerman, Iran
Mange was diagnosed in a male two years old
DSH cat with clinical signs of, fever, Anorexia,
vomiting, restlessness, ataxia, sever pruritus,
tilting of head to right side, popular lesion in ear
margin and face and thick mucosal malodorous
exudates from right ear referred to Department
of Small animal, school of veterinary medicine,
Shahid Bahonar University of Kerman. In
Paraclinical examination Leococytosis and
Eosinophilia was observed. In Ventro-Dorsal
position of head and Rostro-Caudal- open
mouth radiography an increase of opacity of
tympanic bulla and ring of calcification was
obvious in right ear. External otitis in left ear
Back to contents
POSTERS
ocular length is significantly longer in the
human male than the female. In veterinary
medicine, ocular biometry can be used in
establishing lens implant size, calculating lens
power, and estimating prosthetic globe size after
enucleation.
Medial patellar luxation was more in the left
stifle than the right one. Left and right stifle
showed grade four patellar luxation according
to Anderson’s classification(1). Developmental
medial patellar luxation is associated with other
anatomical abnormalities of the medial bowing
of the proximal tibia and medial rotation of the
tibia tuberosity. After final diagnosis the case was
refferd to surgical treatment.
References:
1-Collinson. R. (1994): Manual of small animal
arthrology. The stifle. Editted by G. Anderson.
BSAVA. pp: 275-277
2-Donald E. Thrall, Text book of veterinary
diagnostic radiology. 4rd. Ed. W.B. Saunders
Company. Philadelphia, pp: 189-191
3-Houlton, J.E. F and Meynink S.E. (1989):
Medial patella luxation in the cat. Jurnal of small
animal practice, 30, 349-352
4-Kevin Kealy J. (2000): Diagnostic radiology of
the dog and cat. 2rd. ed. W.B. Saunders Company.
Philadelphia, pp: 363
2006 World Congress WSAVA/FECAVA/CSAVA
was not remarkable in compare with right ear.
In parasitological examination the mites were
identified morphologically as Notoedred cati
in exudates after examination microscopically
in 10% KOH solution to detect the presence of
mites. For treatment Prednisolone, Ivermectin
with dose of 400 microg/kg subcutaneously
applied together with antimicrobial therapy with
chloramphenicol topically and a pre wash of the
entire skin surface with sulfurated soap.
References: 1-Isingla LD, Juyal PD, Gupta
PP(1996) Therapeutic trial of Ivermectin against
Notoedres cati var. cuniculi infection in rabbits.
Parasite. 1996 Mar; 3(1): 87-9.
889
POSTERS

THE HYDATID CYST OF THE LUNG IN A MONKEY - A CASE REPORT

D. Vosough, S. Nourollahi Fard
Faculty of Veterinary Medicine, University of Kerman, Kerman, Iran

A male three years old monkey with clinical
signs of, respiratory dyspnea, hemoptysis,
cyanosis, anorexia, and diarrhea, referred to
Department of small animal, school of veterinary
medicine, Shahid Bahonar University of Kerman,
in clinical examination respiratory rales in
auscultation of respiratory sounds was heard
in right and left cranial and caudal lobs of lung
because of Bronchpulmonary infection. The
diagnosis of pulmonary cysts was established
with radiography. In Ventro-Dorsal and Lateral
position of thoracic and peritoneal region an
increase of opacity of lobular nodules was
obvious in cranial and caudal lobes. There was
a distention of stomach and intestine by gas. The
case died because of severe respiratory dyspnea.
In mortem examination of respiratory system
diagnosis of pulmonary hydatid cyst confirmed
by parasitilogical examination and detection of
protoscolex in cyst.

IMMUNOGENOUS AND PROTECTIVE ABILITIES OF RECOMBINANT VACCINE

AGAINST CANINE BORRELIOSIS
V. Vrzal1, J. Tuháčková1, J. Nepeřený1, J. Chumela1, E. Weigl2
1
Bioveta, a.s., Komenského 212, Ivanovice na Hané, Czech Republic; 2Faculty of Medicine, Palacky University,
Hněvotínská 3, Olomouc, Czech Republic

Ten dogs were vaccinated using an experimental
vaccine containing recombinant OspA and OspC
proteins of serospecies Borrelia burgdorferi,
Borrelia afzelii and Borrelia garinii. Two dogs
without vaccination were used as controls. A
challenge test was accomplished using the natural
way of contact (with infected common ticks
– Ixodes ricinus). Blood samples for serological
examination were collected after the immunisation
prior to and after the challenge. An autopsy was
performed 2 months after the challenge and
samples were collected for the culture detection
of borrelia from the predilection organs. Culture
detection was performed also after the challenge
prior to autopsy from biopsy skin samples. It
was verified that the experimental recombinant
vaccine induces specific antibodies against OspA
and OspC proteins and results in protection
against borrelia during natural infection from
common ticks – Ixodes ricinus. Results from
project of MPO - FD-K3/100 were used in the
presentation.

CASES OF POISONING IN OUR CLINICAL PRACTICE

I. Vucicevic, M. Jovanovic
1
Faculty of veterinary medicine, Bul. oslobodjenja 18, Belgrade, Serbia

During two years of my practice in hospital the range of pets, because we had two cases
2006 World Congress WSAVA/FECAVA/CSAVA

for the small animals on Faculty of veterinary
medicine in Belgrade there were 25 cases
of dogs poisoning. In 13 accidents the cause
of intoxication were rodenticides (Warfarin,
Brodifacoum). Anticoagulant rodenticides
caused internal bleeding. The poisoned dogs had
symptoms of bleeding from anus and gums were
paled. Sometimes bloody urine or stool is evident
or nose bleeding may be seen. Six of the dogs were
poisoned with creosol (4,6-dinitro-o-cresol) and
their body temperature was over 40 °C. We noticed
two cases of poisoning with ethylene-glycol.
Dogs exhibited vomiting due to gastrointestinal
irritation, polydipsia and polyuria, and neurologic
signs (depression, ataxia, etc.). One patient who
consumed thinner had a serious injury of tongue
and oral mucosa. Drugs should be kept out of
of ibuprofen toxicosis and one antidepressant
drug overdoses. Vomiting, abdominal pain,
hematemesis and diarrhea can be seen within
24 hour of ibuprofen ingestion. Antidepressant
drug overdose may cause hypotension, ataxia,
restlessness, arrhythmia, respiratory depression
and coma. Mentioned in all cases the owners saw
when their dogs had taken those poisons. In few
cases dogs had symptoms of poisoning, but the
owners weren’t sure if they had eaten something
that could be toxic. In this cases the a suspicion
of poisioning was diagnosed. The patient had
recovered succsesfuly after they got apropriate
therapy, except two dogs who passed away
because of consecvenses of cresol poisoning. Dog
owner education is the most effective method to
prevent toxicosis in dogs.

890
Back to contents
 POSTERS
EFFECT OF BENAZEPRIL ON SYSTEMIC BLOOD PRESSURE IN DOGS WITH
HEART FAILURE
S.Y. Wu, H.P. Juany
Department of Veterinary Medicine, National Taiwan University, Roosevelt road, Taipei, Taiwan

The aim of this study was to evaluate the effect
of benazepril on the systemic blood pressure in
dogs with heart failure. Twenty client-owned
dogs presented with clinical signs related to heart
failure were investigated. The diagnosis of heat
failure of these 20 dogs was based on clinical
signs, chest radiographs, electrocardiography, and
echocardiography. The systemic blood pressure
was measured using by Doppler ultrasonographic
sphygmomanometry. For each dog, the systemic
blood pressure was measured before and after
benazepril administration regularly at 1 to 2 week
intervals for 16 weeks. During these 16 weeks
(benazepril 0.1 mg/Kg, q 12 hours), improvements
of clinical signs, including cough, tachypnea,
appetite, and exercise endurance, were evaluated
by both the clients and veterinarians regularly.
Clinical improvement was clearly recognized
toward the end of 16 week-course of benazepril
administration in all 20 dogs. The mean systemic
blood pressure before benazepirl administered
was 142.1 ± 22.6 mmHg. The mean blood pressure
after 16 week-course of benazepril was 139.6 ±
± 17.1 mmHg. No significant difference of the
mean blood pressure before and after benazepril
(P=0.54) was observed. No substantial changes
of systemic blood pressure were found to be
related to benazepril doses (P = 0.36). The result
of this investigation indicated that benazepril
(0.1 mg/Kg, q 12 hours) did not affect the systemic
blood pressure in dogs with heart failure.

EMERGENCE OF MYCOPLASMOSIS IN DOGS

S. Yadav
Dept. of Epidemiology & Veterinary Preventive Medicine, AGRA ROAD, Mathura, India

In a study on dog mycoplasmas 61 samples
collected from 28 street dogs, out of which
15 are normal, 2 were suspected for arthritis,
5 for pneumonia, 3 were infertile and 2 were
parvovirus suspected. Samples from 33 domestic
dogs were also collected out of which 11 were
from infertile dogs, 7 were from pneumonia,
8 were parvo virus suspected, 3 were from
fever and digestive problems and one each was
suspected for paralysis and abortion. These
samples were tested for possible presence of
pathogenic mycoplasmas causing pneumonia,
arthritis, infertility and abortions. Out of 61
samples two species of mycoplama were detected
in present study from german shepherds dogs
having genital problems. These mycoplasmas
were able to reproduce the disease in control dogs
and produced death in control pups. The study
also showed the importance of mycoplasmas in
breeding and rearing practices in canines.

CLINICAL EFFECTIVENESS OF LLLT IN 100 CANINE PATIENTS WITH

ORTHOPEDICS 2006 World Congress WSAVA/FECAVA/CSAVA
A. Yasukawa1, T. Satoh2, M. Kaneko3, Y. Koyama1, M. Nagai1, K. Takakuda1
1
Institute of Biomaterials and Bioengineering, 2-3-10 Kanda Surugadai, Chiyoda-ku, Tokyo, Japan; 2Nishiogi
Veterinary Medical Hospital, 4-4-5 Nishiogi-kita, Suginami-ku, Tokyo, Japan; 3Kamishakujii Veterinary Medical
Hospital, 1-4-13 Sekimachi-higashi, Nerima-ku, Tokyo, Japan

Following the world’s first successful laser
emission by Maiman in 1960. Laser technology
was first applied to medicine in 1961 for the
photocoagulation of detached retinal lesions.
Since then, lasers have been used in a variety
of clinical fields including selective resection
and vaporization of tumor tissues, lithotripsy,
vascular anastomosis, irradiation of local
infectious agents, pain and inflammation control,
photostimulation of nerve fibers and local blood
circulation. Clinical applications of lasers are
largely divided into thermodestructive therapy
Back to contents
and nonthermal phototherapy [6]. The former,
generally referred to as high reactive-level laser
treatment (HLLT), uses laser-generated heat to
obliterate target tissues. On the other hand, the
latter low reactive-level laser treatment (LLLT) is
based on biostimulation or bioactivation by laser
light, although the mechanism of bioactivation
by LLLT has not been clearly understood. In
veterinary medicine, HLLT has been used for
the surgical resection of tumors since the 1980s,
while LLLT has become clinically applicable
since the early 1990s for pain relief, inflammatory
891
POSTERS
control and rehabilitation in various surgical and
orthopedic disorders, especially wound healing,
hip dysplasia, patellar luxation, spondylosis
deformans, osteoarthritis, intervertebral disc
herniation, bone fracture, contusion and other
TREATMENT OF CANINE DIABETES MELLITUS USING MOMORDICA
CHARANTIA CAPSULE WITH INSULIN HORMONE
S. Yibchok-anun, P. Pusoonthornthum, K. Thungrat, K. Ousilamongkol, L. Chaiyahong
Chulalongkorn University, Henridunant, Bangkok, Thailand
Objectives: The purpose of this study was to
determine the effect of the Momordica charantia
capsule, combined with insulin hormone on the
treatment of naturally occurring diabetes mellitus
dogs.
Materials & Methods: Twelve client-owned
dogs with naturally occurring diabetes mellitus
at Small Animal Hospital, Chulalongkorn
University were entered into the study. All dogs
received subcutaneous insulin therapy and they
were fed with a commercially available low-
carbohydrate canned canine diet. Eight dogs
which were randomly assigned into a treatment
group received 1000 mg/10 kg body weight of
Momordica charantia capsule orally every 12 hour
with meals for three months and increased dose to
2000 mg/10 kg body weight for the next 2 months
later. Other 4 dogs were randomly assigned into
a control group and did not receive Momordica
charantia capsule. Monthly fasting blood glucose
2006 World Congress WSAVA/FECAVA/CSAVA
892
Back to contents
types of luxation. In this report, we conducted
a double-blind trail of LLLT in 100dogs with
orthopedic conditions to examine the clinical
significance of laser phototherapy
and serum fructosamine concentration were
obtained, and used to adjust insulin dosage for
individual requirement.
Results: In treated dogs, serum fructosamine
concentrations were slightly decreased from
596.00 ± 94.49 µmol/l to 520.88 ± 151.91 µmol/
l after receiving 1000 mg/10 kg of MC capsule
for three months and they were significantly
decreased to 465.75 ± 171.16 µmol/l, after
receiving 2000 mg/10 kg of MC capsule for
two months. However, the fasting blood glucose
concentration was not significantly different in
both treatment and control groups. In addition,
the MC capsule could not help to decrease the
dosage of insulin requirement.
Conclusion: The use of MC capsule improved
glycemic control in naturally occurring diabetes
mellitus, but could not reduce or replace the
exogenous insulin hormone.
POSTERS

2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

AUTHOR
TH AUTHOR
INDEX INDEX
POSTERS
2006 World Congresss WSAVA/FECAVA/CSAVA
CSAVA

POSTERS
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

AUTHOR
TH AUTHOR
INDEX INDEX
POSTERS

POSTERS

AUTHOR INDEX -
POSTERS
A
Abdelbarry, N. ............................. 838
Abdi, M. ...................................... 830
Acar, S.E. .................................... 827
Adalat, A. ..................................... 851
Adamiak, Z. ................................. 827
Agudelo Ramirez, C.F. ................. 827
Ahmed, C. .................................... 828
Akdogan Kaymaz, A. ................... 828
Akhlaghi, N. ................................ 836
Akhtardanesh, B. ......................... 848
Aksoy, O.A. .................................. 839
Alam, M.R. ................... 829, 857, 862
Albeniz, I. .................................... 828
Albouy, M. ................................... 829
B
Bahadori, A. ............................... 881
Baranyiová, E. ............................ 870
Beladicova, V. ............................ 884
Besalti, O. ................... 836, 837, 874
Björkroth, J. ................................ 845
Boer, S.de .................................. 884
C
X Calic, M. ............................ 850, 858
Carrillo, E. .................................. 867
Castellà, J. ................................... 871
Castillo, V. ................................... 868
Cavaco, L.M. .............................. 870
Centrich i Pons, L. ..................... 875
Chaiyahong, L. ........................... 890
Chalmers, S. ................................ 883
Chang, D. ................................... 874
Chipanga, P. .................. 852,853, 854
D
D´Angelino, R. ........................... 849
De Biaggi, C. ............................. 849
Derbala, A. ........................ 837, 838
Devecioğlu, Y. ............................ 838
Dezfolian, O. .............................. 879
Dias, M.I.R. ................................ 834
Back to contents
INDEX − POSTERS
Aldavood, S.J. .............. 830, 831, 832
Aledawod, S.J................................ 855
Ali Asgari, A. ............................. 882
Allix, V. ....................................... 832
Almeida, M.F. .............................. 866
Alonso, D. .................................... 846
Andrade, A.L.................................. 833
Andric, N. ............................. 833, 834
Antunes Viegas, C.A. ................... 834
Appolinario, C.M. ....................... 866
Arias, D. ...................................... 845
Arnbjerg, J. ................................. 835
Avizeh, R. ........... 835, 836, 869, 870
Boisrame, B. ............................... 840
Bokaee, S. ................................... 848
Bondan, E.F. ................................ 560
Bratanich, A.C. ............................. 859
Brom, W.E.van den ..................... 884
Cho, S.W. .................................... 873
Cho, K.-R. ................................... 874
Cho, Y.G. .................................... 857
Choi, I.H. ..................................... 857
Choi, S.H. ............................ 856, 874
Chumela, J. .................................. 888
Coimbra, I.V. ............................... 878
Curcic, M. ................................... 833
2006 World Congress WSAVA/FECAVA/CSAVA
Corrada, Y. .................................. 845
Dikmen, S. .................................. 839
Djurdjevic, D. ............................. 834
Dokuzeylül, B. ............................ 838
Doustar, Y. ........................... 839, 851
Dramard, V. ..................................877
895
INDEX − POSTERS
E
Eftekhar Sadat, A.T. .................... 881
Elmassry, A. ........................ 837, 838
Elmaz, Ö. ................................... 839
Elragehy, O. .................................837
F
Fecchio, R. ................................. 843
Felix, N. ...................................... 878
Fernandes, M.A.R. ..................... 833
Ferreira, A.J.A. .............................878
Ferro, D.G. .................................. 844
Figueiredo, J.P. ............................. 880
G
Galland, D. ................................. 840
Garamvölgyi, R. .................. 840, 863
Gardey, L. ................................... 874
Garjani, A. ...................................839
Gawor, J.P. ................................... 841
Ghadiri, A. ......................... 869, 870
Gioso, M.A. ................................ 843
Gisbert, M.A. ..................... 859, 868
Gobello, C. ......................... 845, 846
Gomes, M. ................................. 843
Gomez, D. ................................. 846
H
Habibi Asl, B. ..................... 844, 847
Haddad, S. ................................... 828
2006 World Congress WSAVA/FECAVA/CSAVA
Halsberghe, C. ............................ 877
Han, T.-S. ............................ 856, 874
Harmoinen, J. ............................. 845
Hassanain, M. ............................. 838
Hazewinkel, H.A. ........................ 884
Heo, S.Y. ............................. 829, 862
Hermo, G. .......................... 845, 846
Hesaraki, S. ................................ 831
I
Iburg, T. .................................... 835
896
Back to contents
Elsadawy, H. ................................838
Elsherif, M. ...................................838
Eugênio, F.R. ................................833
Ezzati, M. .....................................869
Filipovic, S. ................................. 858
Flores, M. .................................... 867
Fontanals, A. ................................ 868
Forejtek, P. .................................. 884
Frayssinet, L. ............................... 838
Fujinaga, T. ................................ 872
Gomez, N.V. .............................. 859
Gómez, N. .................................... 868
González, F. .............................. 867
Gool, F.van ................................. 828
Gorgin, E. .................................... 832
Greenwood, N. ........................... 883
Grgic, Z. ..................................... 879
Griffiths, T. ................................. 855
Guerra, J. ..................................... 849
Guerreiro, H.M. ......................... 878
Hevesi, Á. ........................... 840, 863
Hirt, R. ........................................ 882
Hofmans, J. ................................ 877
Hoshino, Y. .................................. 872
Hosseini Nejad, M. ..................... 846
Hsiang, T. ................................... 847
Huang, H. ................................... 847
Huguet, M.J. ............................... 859
Hylmarova, J. ............................. 841
Issabeagloo, E. .................... 844, 847

J
Jacobs, A.A.C. ...........................
Jakab, C.S. .................................
Jamshidi, S.H. ............................
Jensen, A.L. ...............................
Jeong, S.M. ................................
Jericó, M. ........................... 849,
K
Kadosawa, T. .............................. 872
Kaffash Elahi, R. ............... 844, 851
Kalinowska, K. ........................... 827
Kallel, F. ..................................... 828
Kamrani, A. ................................ 883
Kaneko, M. ................................ 889
Kanellos, T. ................. 852, 853, 854
Kang, H.S. ......... ............... 829, 862
Karegar, A.R. ........... ................. 830
Karimi-Nejad, M.H . ................. 832
Kaszyński, M. ............................ 841
Kave, A.A. ................................. 851
Kazerani, H. ................................ 883
Kern, L. ....................................... 877
Ketzis, J. ............................ 854, 855
Keyhani, P. ..................................830
Khorami, N. ..................... 831, 855,
Kim, D.H. .................................. 862
Kim, G. .............................. 856, 874
L
Lalia, J.C. ..................................
Lallo, M.A. .................................
Landolsi, F. ..................................
Langoni, H. ................................
Laranjeira, M.G. .........................
Laurentino, R. ............................
Lavrenčič, A. .............................
Lazarevic, M. ..............................
Lee, B.H. .....................................
Lee, B.N. ...................................
Lee, H.B. ........................... 829,
INDEX − POSTERS
848 Jodkowska, K. ........................... 841
840 Jovanovic, M. .................... 850, 888
848 Juany, H.P. ................................. 889
879 Jun, M.H. .................................... 873
873 Jung, H.D. ................................... 862
850
Kim, I.S. .................... 829, 857, 862
Kim, J.-H. .................. 856, 857, 862
Kim, J.M. ............................. 856, 873
Kim, M.C. .......................... 856, 873
Kim, N.S. .................... 829, 857, 862
Kirkilesi, G. ............................... 857
Klaveren, N.J.van ...................... 884
Knezevic, M. .............................. 834
Koch, J. ....................................... 879
Koren, L. ..................................... 861
Koskan, O. .................................. 837
Koyama, Y. ................................ 889
Krstic, N. .................................. 858
Krstic, V. .................................... 858
Kuhne, F. ............................ 858, 976
Kukolj, V. .................................... 834
Kurek, A. .................................... 841
Kurski, G. ................................... 841
859 Lee, J.Y. ............................. 856, 873
560 Lee, K.C. .............................857 , 862
828 Lee, Y.H. ..............................829, 862 2006 World Congress WSAVA/FECAVA/CSAVA
861 Leonardi, A. ................................ 849
833 Lien, Y. ........................................847
849 Lins, B.T. .....................................880
861 Llorens, P. ....................................834
850 Lonsky, Z. .................................... 863
862 Loukaki, K. .................................857
862 Lőrincz, B. .......................... 840, 863
862 Luvizotto, M.C.R. ....................... 833
897
Back to contents
INDEX − POSTERS

M
Macanovic-Lazarevic, M. ............858 Meijer, E. .................................. 884
Magas, V. ................................... 858 Mendes, G.M. ............................ 880
Mahl, P. ...................................... 874 Mezzasalma, T. ......................... 832
Malmasi, A. ................................ 863 Miret, J. ...................................... 867
Mari, K.de .................................. 874 Misic, E. .................................... 879
Márquez, A. ................................ 868 Moarrabi, A. .............................. 870
Masodifard, M. ........................... 886 Moghadami, A. .......................... 830
Mazzini, A.M. ............................ 866 Mohajeri, D. ............................... 867
Menozzi, B.D. ............................ 861 Mohebali, M. ..................... 835, 863
Mohammadi, M. ......................... 848 Mohit Mafi, S. .......................... 868
Mahmoodi, J. ..................... 844, 847 Mokaram, S. ...................... 830, 831
Mahmoud, M. ............................. 837 Molaei, M. ............................... 886
Matic, M. .................................... 833 Molazem, M. ............................. 887
Mashhady Rafie, S. .................... 864 Moltedo, C. ................................ 868
Massodifard, M. ......................... 879 Moreira, M. ................................ 849
Maynard, L. ................ 832, 864, 865 Moreno, J. ................................. 867
Mazaheri, R. .............................. 846 Mosallanejad, B. .............. 869, 870
Medaille, C. ....................... 864, 865 Mosallanejad, M. ....................... 863
Megid, j. ...................................... 866 Mouro, S. ........................... 870, 878
Meij, B.P. .....................................884

N
Nabian, S. ................................. 846 Nieto, J. ..................................... 867
Nagai, M. ................................... 889 Nishiya, A. ................................ 849
Náhlík, J. .................................... 870 Niza, M.M.R.E. ......................... 870
Najafi, M. ................................... 839 Nohynkova, E. .......................... 885
Nassiri, S.M. .............................. 846 Nolard, N. ................................. 855
Nematollahi, A. .......................... 871 Norolahifard, S. ................. 887, 888
Nepeřený, J. ............................... 888

O
Okumura, M. ............................... 872 Oskouizadeh, K. ................ 872, 873
2006 World Congress WSAVA/FECAVA/CSAVA

Ortuño, A. .................................. 871 Ousilamongkol, K. ................... 890

Osaki, T. ...................................... 872

P
Padilha Filho, J.G. ...................... 880 Pereira, V. ......................... 849, 850
Park, C.S. ........................... 856, 873 Petneházy, Ö. .................. 840, 863
Park, J. ........................................ 874 Petrási, Z.S. ........................ 840, 863
Park, K.S. ................................... 862 Pifarré i Olivé, M. ...................... 875
Park, S.Y. ............................ 829, 862 Počta, S. ................................... 875
Pechereau, D. .............................. 874 Princes, I. ................................... 861
Pekcan, Z. ................... 836, 837, 874 Provasi, A. ................................. 849
Peleteiro, M.C. .......................... 878 Pusoonthornthum, P. ................. 890

898
Back to contents

R
Ranjbar-Bahadori, S. .................. 876
Reichel, M. ................................. 855
Reitz, N. ..................................... 876
Rème, C. ..................................... 877
Repa, I. .............................. 840, 863
Resanovic, R. ............................. 850
Ripoll, G. ................................... 846
S
Saberi, M. ........................... 830, 831
Sadeghi, M. ................................ 851
Sadalak, D.J. .............................. 827
Salari Seddigh, H. ...................... 830
Samavatian, A. ........................... 867
Sanquer, A. .................. 829, 864, 865
San Román, F. ............................. 834
Saroglu, M. ................................ 827
Sasani, F. .................................... 848
Satoh, T. ..................................... 889
Saugar, J. ................................... 867
Savic-Jevdjenic, S. ..................... 879
Schaeffer, C. .............................. 849
Scheer, P. .................................... 827
Seifiabad Shapoori, M.R. ........... 836
Selk Ghaffari, M. ............... 855, 879
Selmi, A.L. ................................. 880
Shabestari Asl, A. ....................... 881
Shabestary Asl, J. ....................... 847
Sheikholeslami, M. .................... 835
Shibly, S. ................................... 882
Shin, S.H. .................................. 857
T 2006 World Congress WSAVA/FECAVA/CSAVA
Tabatabaie, A.H. ......................... 863
Takagi, S. .................................... 872
Takakuda, K. ............................... 889
Tamer, Ş ..................................... 828
Tarello, W. .................................. 886
Tarpey, I. .................................... 883
Thams, U. .................................. 834
Theelen, R.P.H. ......................... 848
Back to contents
INDEX − POSTERS
Ristanovic, D. ............................. 858
Rmili, M. .................................... 828
Robinson, A. ................ 852, 853, 854
Rodeia Niza, M.M. ..................... 878
Rodrigues, J. ............................... 834
Rossi, J. ...................................... 843
Ruelokke, M.L. ................... 835, 879
Shirani, D. .................. 831, 846, 882
Shojaee Tabrizi, A. ..................... 883
Sillon, M. .................................. 832
Silva, A. ...................................... 850
Silva, R.C. .................................. 861
Sirin, Y.S. ................... 836, 837, 874
Skowronski, ............................... 865
So, K.M. ..................................... 829
Soroush, M.H. ........................... 881
Souza, L.C. ................................ 861
Spasojevic, S. ............................ 833
Spibey, N. .................................. 883
Spillmann, T. ............................. 845
Srejic, R. ..................................... 858
Stefanovič, T. ............................. 858
Suraniti, A. ................................ 868
Sutton, D. .......................... 848, 883
Suwankong, N. ............................ 884
Svoboda, M. ...................... 884, 885
Svobodova, V. .................... 884, 885
Svobodova, Z. ..................... 884, 885
Thevassagayam, S. ....... 852, 853, 854
Thungrat, K. ................................ 890
Tirapelli, A. .......................... 849, 850
Torres, P. ..................................... 846
Trigg, T. ..................................... 845
Tyrlík, M. ................................... 870
Tuháčková, J. ...............................888
899
INDEX − POSTERS

U
Unlu, E. ...................................... 836 Uysal, A. ................................... 838

V
Vajda, Z. .................................... 863 Vilela, C.L. ........................ 870, 878
Valentova, D. ............................. 884 Villard, I. ............................ 864, 865
Valle, M. .................................... 840 Vosough, D. ............... 886, 887, 888
Van der Waart, L. ....................... 848 Vrzal, V. ...................................... 888
Veshkini, A. ........................ 832, 876 Vucicevic, I. ............................... 888
Vida Mombiela, D. ..................... 877 Vural, S.A. ................................. 874
Vidic, B. ...................................... 879

W
Watzek, G. ................................ 834 Woehrle, F. .................................. 840
Weigl, E. .................................... 888 Woerly, V. ................................. 865
Westermarck, E. ........................ 845 Wu, S.Y. ....................................... 889

Y
Yadav, S. ..................................... 889 Yibchok-anun, S. ....................... 890
Yasukawa, A. ............................ 889

Z
Zonturlu, A. ................................ 839
2006 World Congress WSAVA/FECAVA/CSAVA

900
Back to contents
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

AUTHOR
TH AUTHOR
INDEX INDEX
STATE OF THE ART LECTURES
AND INVITED LECTURES

STATE OF
 2006
WORLD
CONGRESS
WSAVA/FECAVA/CSAVA

AUTHOR
TH AUTHOR
INDEX INDEX
STATE OF THE ART LECTURES
AND INVITED LECTURES

STATE OF
 INDEX − LECTURES
AUTHOR INDEX -
STATE OF THE ART LECTURES
AND INVITED LECTURES

A
Ackerman, L. ............. 491, 494, 497 Arnold, S. ..................... 690, 783, 806
Amat, M. ............................ 130, 152

B
Baneth, G. ................... 479, 481, 487
Beale, B. ........ 81, 83, 623, 626, 628
Bedford, P. ......... 601, 609, 611, 616
Beránek, J. .......................... 595, 612
Bernaud, J. ................................. 461
Biller, D.S. .......... 279, 281, 283, 289
Bjerkås, E. ................. 606, 613, 615,
Bonnefont-Rebeix, C. ................. 461
Brown, C. ................ 8, 793, 796, 799
Brown, S. ................ 8, 793, 796, 799
Butcher, R. .................. 507, 820, 825

C
Carlotti, D.N. ................ 31, 211, 223
Carpenter, J.W. ........... 321, 324, 330
Center, S.A. .......... 43, 419, 423, 430
Chabanne, L. ..................... 456, 461,
Chambreau, Ch. ................... 118, 121
Chaves, G. .................................. 154
Church, D. ....................... 36, 39, 167
Coyne, K.P. ...................................343
Crispin, S. .................................. 598,
Crossley, D. .....253,256, 263, 253, 257

D
X Daminet, S. ...................299, 309, 312
Dawson, S. ................................. 343
Day, M.J. ................... 451, 460, 463

E
De Keuster, T. ........................822, 825
Distl, O. ...................................... 443
Dobias, P. ....................................... 24
2006 World Congress WSAVA/FECAVA/CSAVA

Elliott, D. ............. 379, 390, 396, 407

F
Faldyna, M. ................................ 452 Fox, P.R. .............................. 173, 177
Fatjó, J. .............................. 130, 152 Faschen, F. .................. 398, 401, 404
Fontbonne, A. ........... 679, 683, 721
Fossum, T.W. ............ 12, 94, 97, 739
742,745, 755, 758 903
Back to contents
INDEX − LECTURES

G
Gaschen, R.M. .............................. 343 Griffin, C. .................99, 101, 236, 763
German, A. ................... 15, 109, 377 Griffon, D.J. .............. 630, 634, 643
Giger, U. ............................ 102, 104 Gunn-Moore, D. ......... 707, 714, 723

H
Heiblum, M. ..... 72, 74, 129, 145, 154 Hubler, M. ................. 691, 783, 806
Holt, P. ............... 86, 785, 791, 808, Hulse, D. ..................... 619, 625, 641
Horzinek, M.C. .......................... 465,

I
Ihrke, P.J. ............ 32, 218, 227, 241 Indrebø, A. ................................ 439

J
Jekl, V. ....................................... 337

K
Kirpensteijn, J. .... 549, 566, 570, 572 Kohn, B. .............................. 368, 373
579, 748, 751, 752 Kooistra, H.S. ....... 18, 296, 306, 318
Knotek, Z. .......................... 334, 337
Knotková, Z. .............................. 334

L
Labastida, R. .............................. 154 Legendre, L. ....................... 259, 261
Lake, T. .............................. 508, 510 Lloyd, D. ................... 215, 232, 238
2006 World Congress WSAVA/FECAVA/CSAVA

Lamb, C.................................... 21, 276 Lobetti, R. ................. 468, 471, 484

Lang, J. ....................... 267, 272, 287 Lombard, C.W. .................... 23, 165
Lappin, M.R. ............... 50, 474, 477 Lumeij, J.T. ........ 113, 127, 333, 340
LeCouteur, R.A. ..76, 78, 521, 530, 540

M
Malm, S. ..................................... 446 Meints, K. .................................. 822
Manteca, X. ........................ 130, 152 Moise, S. ..................... 179, 181, 184
Mardell, E.J. ................................ 371 Moore, A. .... 558, 562, 566, 570, 572, 581
Mason, D.E. .............................. 106 Moreau, P. .......................... 501, 503

N
904 Nečas, A. ............................. 637, 639

Back to contents

O
Ofri, R. ......... 585, 588, 590, 593, 603
Ogilvie, G.K. ......... 88, 91, 555, 566
570, 572, 575
P
Pavlica, Z. .......................... 247, 250
Pikula, J. .................................... 327
R
Radford, A. ......................... 343, 347
Raskin, R.E. .................. 651, 654, 656
659, 661, 664, 667, 670
Read, R.A. .......... 727, 730, 733, 736
Rebar, A.H. ................. 647, 649, 654
656, 659, 661, 664
S
Senior, D. ............................ 788, 803
Schaer, M. ..... 52, 55, 187, 202, 205
Simpson, K.W. ..... 382, 392, 411, 416
Sommerfeld-Stur, I. .................. 693
T
Tasker, S. ................... 357, 361, 364
Teheda, A. .................................. 154
Tello, L.H. .......... 190, 196, 512, 516
Ter Haar, G. ................. 766, 775, 780
V
Venker-van Haagen, A.J. ............ 769
772, 778
W
Weingart, Ch. ........................... 368
Back to contents
INDEX − LECTURES
Otero, P. ..................... 192, 199, 207
Overall, K.L. ................ 60, 132, 148
158, 811
Platt, S.R. ................. 523, 532, 542
Porter, C. .................................... 343
Reichler, I. ................. 691, 783, 806
Reusch, C.E. ....................... 293, 302
Rigal, D. ..................................... 461
Rijnberk, A. ................................ 114
Romagnoli, S. ...... 673, 683, 696, 701
Rothuizen, J. ............... 427, 429, 435
Sparkes, A.H. ............... 351, 354, 371
Steiner, J.M. .................................. 58
Surdyk, K. .............. 9, 793, 796, 799
Thiry, E. ..................................... 465
Toman, M. ................................... 452
Trnková, Š. .................................. 334 2006 World Congress WSAVA/FECAVA/CSAVA
Wheeler, S. ......................... 526, 528
905
PROCEEDINGS