174 DISC

Veterinary Dermatology 2000, 11, 133141

Diagnosis of canine claw disease a prospective study of

24 dogs
RALF S. MUELLER,* SUE FRIEND,{ MICHAEL A. SHIPSTONE 1 and GREG BURTON{
*Department of Clinical Sciences, Veterinary Teaching Hospital, Colorado State University, Fort Collins, CO
80523, USA, {Central Veterinary Diagnostic Laboratory, Mount Waverley, Victoria 3149, {Animal
Dermatology, Springwood, Queensland 4127, Australia
(Received 23 March 1998; accepted 7 April 1999)

Abstract The aetiology of claw disease in 24 dogs exhibiting only claw disease was investigated with
cytologic examination of claw exudate, complete blood count (CBC), serum biochemistry panel, urinalysis,
total thyroxine (tT4) concentration, antinuclear antibody (ANA) titre, bacterial culture and sensitivity testing,
fungal culture, histopathology of claw biopsy samples and elimination diet. Abnormalities on the CBC, serum
biochemistry panel and urinalysis were minor and nonspecic. Total T4 concentrations were within the
normal laboratory reference range. Fungal cultures and ANA titres were negative in all dogs. A bacterial
infection was present in approximately half of the dogs. On histological examination of claw tissue, a cell-poor
or cell-rich interface onychitis was seen in all but one dog. Evidence for an adverse reaction to food was
present in four dogs. One dog responded completely to antibiotic therapy. Interface onychitis seems to be a
histological reaction pattern of the claw matrix in the dog with various possible underlying aetiologies. In dogs
with claw disease as the only clinical sign, the recommended initial diagnostic evaluation includes cytologic
examination, bacterial culture and sensitivity, claw biopsy and an elimination diet.
Keywords: canine, claw, food adverse reaction, interface onychitis

INTRODUCTION
Diseases limited to the canine claw have received little
attention in the past. Most of the publications have
been anecdotal reports or retrospective studies.14
Onychodystrophy or onychodysplasia (abnormal
claw formation), onychomalacia (soft claws), onychoschizia (splitting or lamination of the claws),
onychorrhexis (spontaneous splitting of the claws)
and/or onychomadesis (sloughing of claws) may be
due to a variety of diseases. Trauma, bacterial and
fungal infections, immune-mediated diseases such as
pemphigus, systemic lupus erythematosus, cold agglutinin disease, drug eruption, vasculitis and a lupuslike syndrome as well as neoplasia have all been
reported as possible aetiologies.3,4 It has been
suggested that a complete evaluation of canine
patients with generalized onychodystrophy requires
numerous diagnostic procedures including biopsy of
the claw matrix.3,4 The purpose of this prospective
study was to evaluate the aetiology of claw abnormalities in dogs via a standard diagnostic approach to
obtain information helpful for the future selection of
diagnostic tests in patients with claw disease as the
only clinical sign.
Correspondence: Ralf S. Mueller, Department of Clinical Sciences,
Veterinary Teaching Hospital, Colorado State University, Fort
Collins, CO 80523, USA. E-mail: rmueller@vth.colostate.edu
# 2000 Blackwell Science Ltd

MATERIALS AND METHODS

Dogs
Only dogs with claw disease aecting multiple claws
and claw beds and no other dermatologic abnormalities were included in the study (Figs 1 & 2). The
breed incidence of dogs with claw disease was
compared by chi squared analysis with a hospital
population of a primary accession practice. A
detailed general and dermatologic history was taken.
After a recent American publication5 proposed
vaccination as a possible trigger for claw disease, it
was attempted to obtain vaccination history and
information about the time interval between vaccination and onset of disease. A thorough physical
examination was carried out to ensure that there
were no other dermatologic problems.
Laboratory testing
Urinalysis was performed using reagent strips to
evaluate proteinuria, pH and glucosuria (Multistix,
Bayer Diagnostics, Pymble, New South Wales,
Australia) and a refractometer to evaluate urine
specic gravity. Blood samples were taken for a
complete blood count (CBC) (Hematology analizer
CELL DYN 3500 R, Abbott Diagnostics, Lane
Cove, New South Wales, Australia), serum biochemistry panel (Hitachi 717, Boehringer Mannheim,
133

174 DISC
134

Ralf S. Mueller et al.

Figure 1. Loose claws shortly before

sloughing in dog #12.

Figure 2. Onychomalacia and

onychodysplasia in dog #2 after
onychomadesis of most claws.

Nunawading, Victoria, Australia), total thyroxin

concentration (tT4) and antinuclear antibody titre
(ANA). The tT4 was measured by a commercially
available radio immunoassay (Chiron Diagnostics,
Ferntree Gully, Victoria, Australia).
Diagnostic samples from claws
Patients were anaesthetized with ketamine hydrochloride (5 mg kg71) (Ketamine, Parnell Laboratories,
Alexandria, New South Wales, Australia), diazepam
(0.1 mg kg71) (Pamlin, Parnell Laboratories, Alexandria, New South Wales, Australia) and xylazine (0.2
mg kg71) (Ilium Xylazil-20, Troy Laboratories,
Smitheld, New South Wales, Australia) intravenously. If analgesia was needed, buprenorphine
hydrochloride was administered intravenously at 0.01
mg kg71 (Temgesic, Reckitt & Coleman Pharmaceuticals, West Ryde, New South Wales, Australia).
Cytologic samples were taken by impression
smears from the exposed dermis as proximal as
possible from the point of avulsion of a lifted claw. If
loose claw plates were not present, samples were
obtained from claw bed discharge or by pressing
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

slides onto the claw fold directly adjacent to the claw.

Bacterial culture samples were obtained in a similar
fashion. Culture swabs were stored at 4 8C for less
than 20 h and then transported by courier to the
laboratory and cultured within 20 min. A Gram stain
was performed on each sample and cellular, bacterial
and yeast organisms were identied and numbers
graded as low, moderate and high. Samples were
cultured aerobically on horse blood and MacConkey
agar and cultured anaerobically on horse blood agar
for 48 h at 3637 8C. Gram positive organisms were
identied using conventional methods, streptococci
by streptococcal grouping and staphylococci by
coagulase kits (Oxoid, West Heidelberg, Victoria,
Australia). Gram-negative organisms were speciated
using API 20E and 20NE identication methods
(bioMerieux, South Melbourne, Victoria, Australia).
Proteus spp. were identied using spot indole and
maltose peptone water tests.
The proximal part of avulsed claws was cultured
for dermatophytes on Sabouraud agar and dermatophyte test medium (Oxoid, West Heidelberg, Victoria, Australia) at 22 8C. If none of the claws were

174 DISC
Canine claw disease
avulsed, scales were obtained by scraping both the
aected proximal claw fold and claw and submitted
for fungal culture. If there was no growth after 21
days, cultures were considered negative. If growth
was observed, the culture was evaluated microscopically for hyphae and macro-and microconidia.
Two biopsy specimens of haired skin, claw and
bone of the ungual process were taken as previously
described6 and xed in 10% neutral buered formalin
for 1248 h. Bone samples were decalcied in formic
acid for 1248 h as required, then trimmed, processed, paran-embedded, sectioned at 35 mm and
stained with haematoxylin and eosin (Fig. 3).
Further proceedings
To assess the possibility of claw disease due to a drug
reaction, current heartworm preventatives were
changed to another preparation and nonavoured
products were used. Any avoidable systemic medications such as deworming or ea control products
were discontinued for 23 months.
To evaluate possible adverse reactions to food or
drug reactions caused by food preservatives or additives,
a home-cooked elimination diet was fed to each
patient with the exception of the rst dog in the study.
A novel protein and a novel carbohydrate source were
fed exclusively to each dog for at least 68 weeks.
Typically, potato was used as a carbohydrate source
and kangaroo, rabbit, emu or deer as a protein source.

Figure 3. Histopathological demonstration of the claw matrix (H

& E, 640).

135

RESULTS
Dogs
Twenty-four dogs were included in the study. Six
German Shepherd dogs, two Border Collies, two
Rhodesian Ridgebacks and two Terrier cross breeds
were presented with claw problems, all other breeds
were represented only once. There were 321 German
Shepherds in the reference hospital population of 4394
dogs. Thus German Shepherd Dogs were signicantly
over-represented, compared with the reference hospital
population (P 5 0.05). The age range was from 18
months to 10 years with a mean of ve years and a median of six years. Ten dogs were male (four of which were
neutered) and 14 female (12 of which were spayed).
The age of onset varied from one to 10 years with a
mean and a median of ve years. Most dogs were
presented within 812 weeks of disease onset. One
dog (#17) had a history of constant onychomadesis of
dierent claws for seven months prior to referral,
another dog (dog #7) had had claw problems for ve
years. Onychomadesis and onychomalacia were present in all dogs, onychorrhexis in two patients and
two others exhibited onychoschizia.
Onset of clinical signs post vaccination was
variable: (30 days n = 2, 23 months n = 3, 46
months n = 5, 69 months n = 3, 912 months n = 4
and 4 12 months n = 2). Vaccinations typically contained live attenuated distemper virus, live attenuated
canine adenovirus type 2 and live canine parvovirus
type 2. Some dogs additionally received attenuated
live parainuenza virus and in some dogs inactivated
Bordetella bronchiseptica was included as well. In ve
patients, a vaccination date could not be veried.
Laboratory testing
With one exception, abnormalities on the CBC were
limited to a mild increase in packed cell volume,
haemoglobin and mean corpuscular haemoglobin in 7
of 24 dogs. One dog (#8) had leukopenia (3.60 6 109
L71, normal range 617 6 109 L71) and neutropenia
(2.23 6 109 L71, normal 311.50 6 109 L71). The CBC
repeated one week later revealed a white bloodcell
count (WBC) of 4.90 6 109 L71 with lymphopenia
(0.49 6 109 L71, normal 14.80 6 109 L71) and monocytopenia (0.1 6 109 L71, normal 0.151.35 6 109 L71).
Eleven patients showed abnormalities on the biochemistry panel. Cholesterol was mildly increased in
three dogs (7.810.3 mmol L71, normal range 3.97.8
mmol L71), serum globulins were elevated in 3 dogs
(4346 g L71, normal range 2842 g L71), lactic
dehydrogenase (LDH) was increased in three dogs
(410519 IU L71, normal range 50400 IU L71).
Bilirubin was increased in 1 dog (16 mol L71) and
decreased in 3 dogs (1 mol L71, normal 215 mol L71).
The antinuclear antibody titre was 5 1: 20 in all
cases. Titres below 1: 20 are considered negative in
our laboratory. The total T4 concentrations ranged
from 22 to 70 nmol L71 with a mean of 41 nmol L71
(normal 1840 nmol L71).
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

174 DISC
136

Ralf S. Mueller et al.

Diagnostic samples from claws

Cytology and cultures. Cytologic samples revealed
neutrophils with extra cellular and intra cellular cocci
in eight cases. Rod-shaped organisms were identied in another three dogs, always in association
with cocci.
Bacterial cultures were positive in 12 dogs. Mixed
infections were present in 6 dogs, S. intermedius was
the sole isolate in 5 dogs and Pseudomonas aeruginosa
in one patient. S. intermedius was identied in 10
dogs. The isolates were uniformly sensitive to
erythromycin, cephalexin, clavulanic acid/amoxycillin, tetracycline and cloxacillin, but resistant to
penicillin and amoxycillin in six of 10 cultures and
to trimethoprim/sulphonamide in eight of 10 cultures. Dermatophytes or other pathogenic fungi were
not identied in any of the dogs.
Six of the dogs had evidence of infection cytologically (neutrophils and extra and intra cellular cocci)
and a positive culture, six had pathogens isolated on
culture, but no evidence of infection cytologically. In
ve dogs neutrophils and intracellular cocci were
found on impression smears, but no micro-organisms
could be grown on culture.
Histopathology. Details of the histopathological
features are summarized in Table 1. Nineteen of the
24 cases revealed cell poor (n = 5) or cell rich (n = 14)
interface dermatitis. The epidermis was hyperplastic
with orthokeratotic hyperkeratosis. Hydropic degeneration of the stratum basale and a thickened
basement membrane zone were noted in 18 of 24
dogs (75%) (Fig. 4 and 5). Apoptotic cells (Fig. 6)
and pigmentary incontinence (Figs 5 & 7) were
evident in 10 (42%) and 11 patients (46%), respectively. Focal separation of the claw matrix from the
underlying tissue was present in 9 dogs (38%), brin
exudation and haemorrhage were seen in some of the
clefts. In 23 dogs (96%), there was a diuse mononuclear inltrate in the dermis underlying the claw
matrix consisting of predominantly lymphocytes with
some histiocytes and plasma cells (Fig. 8). Dermal

oedema, increased vascularity and vascular dilation

was present in four dogs (17%).
Biopsies of four patients showed a chronic active
inammation with prominent plasma cells and
neutrophils as part of the dermal inltrate. In one
case neutrophilic exocytosis into the claw epithelium
was present. Three of these four dogs had cytological
evidence of infection and cultures yielding bacteria.
In one dog, neither cytology nor culture revealed
evidence of bacterial infection. One biopsy showed
folliculitis and furunculosis in the haired epidermis
Table 1. Histopathological ndings of 24 dogs with claw disease
Abnormality

Severity*

Number
of dogs{

%{

Basal cell vacuolization

mild
moderate
severe
mild
severe
mild
moderate
severe
mild
moderate
moderate
severe
mild
moderate
severe
mild
moderate
severe
mild
moderate
severe
mild
moderate
mild
moderate

8
9
1
9
1
2
6
1
1
1
8
3
9
7
7
3
5
3
2
1
1
1
3
2
2

33
38
4
38
4
8
25
4
4
4
33
13
38
29
29
13
21
13
8
4
4
4
13
8
8

Dyskeratotic keratinocytes
Dermo-epidermal clefting
Thickening of BMZ}
Pigmentary incontinence
Lymphocytic inltrate
Plasmacytic inltrate
Neutrophilic inltrate
Dermal oedema
Dermal haemorrhage

Severity *, as judged subjectively, mild changes were considered

marginally more than normal, moderate changes were immediately
noticeable on low power; Number of dogs {, number of dogs
aected; % {, percentage of dogs aected; }BMZ, basement
membrane zone

Figure 4. Thickening of the basement

membrane zone and exocytosis of
inammatory cells into the claw matrix
of a dog with idiopathic
onychomadesis (H & E, 6100).
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

174 DISC
Canine claw disease

137

Figure 5. Pigmentary incontinence and

interface dermatitis with vacuolization
and separation of the epidermis from
the dermis (arrow) (H & E, 6400).

Figure 6. Civatte body formation and

satellitosis in the claw matrix of a dog
with idiopathic onychomadesis (H & E,
6200).

adjacent to the claw matrix in addition to the

interface dermatitis described above. The biopsy of
dog #8 was very atypical. There was extremely mild
vacuolization of the stratum basale of the matrix
(which is frequently observed in claws of normal
dogs6) with very mild mononuclear exocytosis. The
prominent changes were found in the mid and deep
dermis. There was severe mucinosis with a moderate
inltrate of plasma cells and lymphocytes. Hemosiderin-lled macrophages were prominent in the mid
and deep dermis of adjacent haired skin.
Further proceedings
Elimination diets. Four dogs (#2, 17, 20 and 22)
showed partial or complete resolution of clinical signs
after being fed an elimination diet. Two dogs relapsed
within two days upon provocative challenge with the
original diet and recovered again when the elimination diet was reintroduced. During sequential rechallenge with individual allergens (beef, mutton, wheat,
chicken and dairy products) one dog (#20) developed

clinical signs within a few days of exposure to beef

and later was reintroduced to milk. Clinical signs
resolved when the elimination diet was reintroduced.
This dog remained in clinical remission for more than
two years with the exception of one short relapse
after exposure to beef bones. The second dog (#2) did
not undergo a systematic sequential provocative
challenge and has been in remission for over 12
months on beef and a dierent dry food (Pal Mince
and Vegetables, Waltham, Wodonga, Victoria, Australia). Dogs #17 and 22 have been in incomplete
remission for 10 and four months, respectively, on a
home-cooked diet containing beef, lamb, vegetables
and rice. There was still mild onychomalacia of some
claws, but no pain, lameness or onychomadesis.
Neither owner was willing to perform a provocative
challenge with the previous diet.
Antimicrobial treatment. Eight dogs were treated
with antimicrobial therapy, six based on the results of
the culture and sensitivity and two empirically after
cytology had revealed neutrophils and intra cellular
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

174 DISC
138

Ralf S. Mueller et al.

Figure 7. Interface onychitis with

vacuolization of the basal cells and
severe pigmentary incontinence in a
dog with idiopathic onychomadesis
(H & E, 6100).

Figure 8. Cellrich mononuclear

interface dermatitis with hyperplasia
of the claw matrix in a dog with
idiopathic onychomadesis (H & E,
6100).

cocci. One of these dogs completely responded to a

six week course of clavulanic acid/amoxycillin at
12.5 mg kg71 orally twice daily and has been in
remission for more than two years with no further
therapy. The other seven dogs only responded partially
or not at all to therapy. Other antibiotics used were
cephalexin at 20 mg kg71 orally twice daily, enrooxacin at 5 mg kg71 orally once a day and clindamycin
at 5 mg kg71 orally twice daily for at least three weeks.
DISCUSSION
Etiologic causes of claw disease are reported to be
quite variable.3,4 In this study we attempted to
dene the aetiology of the claw disease in 24 dogs
using a standard diagnostic battery of tests. We also
evaluated a wide range of laboratory tests to assess
their usefulness in the diagnostic evaluation of
claw disease.
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

Scott found that German Shepherd dogs were

signicantly over-represented with claw disease when
compared to the hospital population.7 Harvey recently
evaluated the mineral composition of claws from dogs
with idiopathic onychomadesis and also reported an
over-representation of German Shepherd dogs in his
population of patients.8 Our results further support
the predisposition of this breed for onychomadesis.
Vaccination has been proposed as a possible trigger
for claw disease and vaccination history could be
obtained from 19 dogs.5 The time interval between
vaccination and onset of disease varied widely
between the cases in this study. We could not detect
a consistent or causal relationship between vaccination and the onset of clinical signs. Therefore, it
seems unlikely that vaccines were involved in triggering claw disease in the patients included in this study.
Vasculitis reactions have been described in dogs
secondary to rabies vaccination. Detection of rabies
antigen in blood vessel walls was described.9 It may

174 DISC
Canine claw disease
be conceivable that rabies vaccination is able to
induce other types of reactions such as onychomadesis. Australia is a rabies-free country and thus
vaccines against rabies are not routinely administered
to pets and were not given to any of the dogs
involved. The possibility of rabies vaccines triggering
claw disease in patients elsewhere cannot be excluded
based on this study.
Cytologic evidence of bacterial infection was noted
in 11 of the 24 dogs (46%). In ve dogs, no growth
was observed on culture after 48 h despite cytologic
evidence of suppurative inammation and bacteria.
This may be due to inadequate sampling or a delay of
up to 20 h between sampling and culturing.
Based on our results, bacterial infection is seen
commonly in dogs with exclusive claw disease and
antimicrobial therapy may be an important part of the
initial therapeutic protocol in these dogs. However, a
positive culture does not necessarily indicate active
infection nor can it be used to predict the response to
therapy. When infection was present, it appeared to be
secondary to an underlying disease in the majority of
cases. Only one dog responded completely to antibiotic therapy and has remained in remission for more
than two years without further treatment.
In several patients, mild changes in the blood count
or serum biochemistry were found and considered to
be of no clinical relevance. Based on the ndings in
this study, a complete blood count and a biochemistry panel did not oer signicant diagnostic value in
dogs with claw disease as their only abnormality.
Determination of total T4 is not the test of choice
for diagnosing canine hypothyroidism but was
elected as an initial screening test in this study for
nancial and practical reasons. Diagnostic dilemmas
are most commonly encountered when dierentiating
the low tT4 of euthyroid sick individuals from those
who are hypothyroid. A TSH stimulation test, an
endogenous TSH assay, measurement of free T4 by
equilibrium dialysis or a combination thereof may be
needed to conrm the clinical diagnosis. None of the
dogs included in this study had decreased tT4
concentrations. However, the tT4 in hypothyroid
dogs can occasionally be in the normal range. Three
of 24 hypothyroid dogs in a recent study showed
values above 22 nmol L71 (28, 30 and 30 nmol L71,
respectively), the normal range for the referral
laboratory was 1945 nmol L.71 10 In another study
including 51 hypothyroid dogs, the highest concentration of tT4 was 19.3 nmol L71 (normal lower limit
for this laboratory was 19 nmol L71).11 In the light of
no other clinical and laboratory changes, we did not
perform a TSH stimulation test on the six dogs with
tT4 values in the low normal range (between 22 and
30 nmol L71). Anti-thyroxin antibodies in dogs with
hypothyroidism can lead to falsely increased T4
concentrations with commercial radioimmunoassays.12 A number of dogs had T4 concentrations
slightly above the normal range for the referral
laboratory and two samples were moderately in-

139

creased (62 and 70 nmol L71). Although these results

may indicate interference of T4 autoantibodies with
the assay, it seemed unlikely based on the authors'
clinical experience with this assay over the last six
years in the diagnosis of hypothyroidism. We use this
assay routinely in our practice. In the few hypothyroid dogs with T4 autoantibodies we noted T4
concentrations above 100 nmol L71. Based on these
results, thyroid evaluation in a dog with claw disease
and with no evidence for endocrine disease may not
be an essential part of the initial diagnostic work-up.
Systemic lupus erythematosus may cause claw
disease.4 In humans, increased ANA titres are present
in over 95% of SLE patients.13 A positive ANA titre
is seen in 7590% of dogs with SLE.14,15 All dogs in
this study had an ANA titre 5 1 : 20 which is
considered negative in our laboratory. Because there
was no other clinical or pathological evidence of
systemic lupus erythematosus, we felt that ANA titres
in dogs with claw abnormalities in the absence of
other signs of systemic disease are not cost-eective.
In four patients (#2, 17, 20 and 22), complete or
near complete remission was observed when an
elimination diet was instituted. In two of these
patients, adverse food reaction was conclusively
identied as the cause for the claw disease. In the
other two dogs, the role of an adverse reaction to
food is only speculative. All four patients had the
histopathological changes typical of other dogs in this
study. An elimination diet appears to be a worthwhile
diagnostic test for patients with claw disease alone.
With the exception of case #8, biopsy changes were
very similar, although individual features varied in
severity. Epidermal hyperplasia, basal cell hydropic
degeneration, degeneration and/or apoptosis of
individual keratinocytes in the basal cell layer,
pigmentary incontinence and a lichenoid band of
plasma cells and lymphocytes have been reported as
suggestive of discoid or systemic lupus erythematosus
in the dog.1618 Most of these changes were present in
the patients in this study with the exception of dog
#8. The complete response to therapy in case #10
indicates that bacterial infection without an underlying immune-mediated disease may lead to interface
dermatitis of the claw matrix. Similar histopathological lesions were seen in patients with adverse food
reactions. Both the dogs with adverse food reactions
and the dog with bacterial infection are in complete
remission eight months to two years after appropriate
treatment of the diagnosed disease. Thus the histopathological changes seen in the claw matrix of dogs
with exclusive claw disease may be compatible with,
but not exclusive for, immune-mediated disease.
Instead, they appear to mirror a reaction pattern of
the claw matrix to a variety of inuences similar to
the lichenoid inltrate observed in biopsies from
mucous membranes.16,17 Subepidermal clefts and
vacuolar changes in the keratinocytes have been
reported to occur in normal claw matrix.19 Apoptosis
may be the only specic feature pointing to immune# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

174 DISC
140

Ralf S. Mueller et al.

mediated disease. Interestingly, three of the four dogs

with suspected or conclusive food adverse reactions
and the dog with complete response to antibiotics
lacked apoptotic cells. Scott's proposed term for
these interface changes was lichenoid onychodystrophy.7 Lichenoid dermatitis is characterized by a
dense, band-like inammation within the supercial
dermis.16 The inltrates identied in our study were
not always dense and band-like. In almost 40% of
our patients the inltrate was mild and in approximately 30% it was moderate. We propose a clearly
descriptive term such as a cell rich or cell poor
interface onychitis for description of the histopathological changes. How many of the patients without
nal aetiologic diagnosis actually have immunemediated disease is unclear as the pathogenesis of
their claw disease is unknown. It is possible that other
aetiologies not evaluated by the studies undertaken so
far may cause identical clinical and histopathological changes.
Idiopathic onychomadesis or onychitis is our
proposed clinical descriptive term for dogs in which
a thorough diagnostic work-up has not identied the
cause of the disorder. Recommended cost-eective
initial diagnostic procedures for a dog presenting
with claw disease only are cytology, bacterial culture
and sensitivity, biopsy and elimination diet. Appropriate antibiotic therapy may be the best way to rule
out bacterial claw disease. Biopsy may be benecial in
ruling out several possible rare aetiologies such as
pemphigus foliaceus or dermatophytosis. However,
interface onychitis may not always be due to immunemediated disease. Despite the use of many diagnostic
procedures, the aetiology of the claw disorder could
only be identied in a small number of dogs.
ACKNOWLEDGEMENTS
We would like to thank our referring veterinarians
for encouraging their clients to join this study. Kerrie
Lay kindly supplied the information on breed incidences in a control hospital population. We also owe
her thanks for suggestions regarding the manuscript.
The study was nancially supported by the Animal
Skin & Allergy Clinic and Central Veterinary Diagnostic Laboratory.

REFERENCES
1. McEwan, N.A. Nail disease in small animals.
Veterinary Dermatology News 1987; 11: 1820.
2. Foil, C.S., Conroy, J. Dermatoses of claws, nails and
hoof. In: Von Tscharner, C., Halliwell, R.E.W. eds.
Advances in Veterinary Dermatology. Philadelphia:
Bailliere Tindall, 1990: 4202.

# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141

3. Scott, D.W., Miller, W.H. Disorders of the claw and

clawbed in dogs. Compendium of Continuing Education
1992; 14: 144858.
4. Rosychuk, R.A.W. Diseases of the claw and claw fold.
In: Bonagura, J.D. ed. Kirk's Veterinary Therapy XII.
Philadelphia: W.B. Saunders, 1995: 6417.
5. Boord, M.J., Grin, C.E., Rosenkrantz, W.S.
Onychectomy as a therapy for symmetric claw and
claw fold disease in the dog. Journal of the American
Animal Hospital Association 1997; 33: 1318.
6. Mueller, R.S., Olivry, T. Onychobiopsy without onychectomy: Description of a new biopsy technique for
canine claws. Veterinary Dermatology 1999; 10: 559.
7. Scott, D.W., Rouselle, S., Miller, W.H. Symmetrical
lupoid onychodystrophy in dogs: a retrospective
analysis of 18 cases (198993). Journal of the American Animal Hospital Association 1995; 31: 194200.
8. Harvey, R.G., Markwell, P.J. The mineral composition
of nails in normal dogs and comparison with shed nails
in canine idiopathic onychomadesis. Veterinary Dermatology 1996; 7: 2934.
9. Wilcock, B.P., Yager, J.A. Focal cutaneous vasculitis
and alopecia at sites of rabies vaccination in dogs.
Journal of the American Veterinary Medical Association
1986; 188: 11747.
10. Paradis, M., Lepine, S., Lemay, S., Fontaine, M.
Studies of various diagnostic methods for canine
hypothyroidism. Veterinary Dermatology 1991; 2:
12532.
11. Nelson, R.W., Ihle, S.L., Feldman, E.C., Bottoms,
G.D. Serum free thyroxine concentration in healthy
dogs, dogs with hypothyroidism and euthyroid dogs
with concurrent illness. Journal of the American
Veterinary Medical Association 1991; 198: 14017.
12. Feldman, E.C., Nelson, R.W. Canine and Feline
Endocrinology and Reproduction. Philadelphia: W.B.
Saunders, 1996: 68118.
13. Harley, J.B., Scoeld, R.H. Systemic lupus
erythematosus: RNA protein autoantigens, models of
disease heterogeneity and theories of etiology. Journal
of Clinical Immunology 1991; 11: 297316.
14. Gorman, N.T., Werner, L.L. Diagnosis of immunemediated diseases and interpretation of immunologic
tests. In: Kirk, R.W. ed. Current Veterinary Therapy
IX. Philadelphia: W.B. Saunders, 1986: 42735.
15. Fournel, C., Chabanne, L., Caux, C. et al. Canine
systemic lupus erythermatosus. I. A study of 75 cases.
Lupus 1992; 1: 1339.
16. Gross, T.L., Ihrke, P.J., Walder, E.J. Veterinary
Dermatopathology: A macroscopic and microscopic
evaluation of canine and feline skin disease. St. Louis:
Mosby Year Book, 1992: 1436.
17. Yager, J.A., Wilcock, B.P. Colour Atlas and Text of
Surgical Pathology of the Cat and Dog. London: Wolfe
Publishing, 1994: 923.
18. Scott, D.W., Walton, D.K., Manning, T.O., Smith,
C.A., Lewis, R.M. Canine lupus erythematosus. II.
Discoid lupus erythematosus. Journal of the American
Animal Hospital Association 1983; 19: 4818.
19. Mueller, R.S., Sterner-Kock, A., Stannard, A.A.
Microanatomy of the canine claw. Veterinary
Dermatology 1993; 4: 511.

174 DISC
Canine claw disease

141

Resume Le diagnostic etiologique d'une atteinte exclusive des gries a ete realise chez 24 chiens par examen
cytologique de l'exsudat obtenu au niveau du lit de la grie, numeration-formule (NF) sanguines, analyses
biochimiques, analyse d'urine, mesure de la concentration en thyroxine totale (tT4), dosage des anticorps
antinucleaires (ANA), culture bacteriologique et antibiogramme, examen histopathologique de biopsies
ungueales et regime d'eviction. Les anomalies observees a l'examen de la NF, des analyses biochimiques et
d'urine etaient mineures et peu speciques. Les mesures de tT4 etaient dans les normes usuelles. Les cultures
fongiques et les dosages d'ANA etaient negatifs pour tous les chiens. Une infection bacterienne etait presente
dans environ la moitie des cas. L'examen histopathologique a montre une onychite d'interface, riche ou
pauvre en cellules, pour tous les animaux sauf un. Une intolerance alimentaire a ete mise en evidence dans 4
cas. Un chien a completement gueri avec un traitement antibiotique. Une onychite d'interface semble etre une
modalite de reaction histologique des lesions de la matrice ungueale chez le chien, pouvant correspondre a
plusieurs causes. En cas d'atteinte exclusive des gries chez le chien, l'examen dermatologique devrait
comprendre une analyse cytologique, une culture bacteriologique avec antibiogramme, des biopsies des gries
et la realisation d'un regime d'elimination. [Mueller, R. S., Friend, S., Shipstone, M. A. et Burton, G.
Diagnosis of canine claw disease a prospective study of 24 dogs. (Diagnostic des maladies des gries chez le
chien une etude prospective de 24 cas.) Veterinary Dermatology 2000; 11: 133141.]
Resumen Se investigo en 24 perros la etiolog a de la enfermedad ungueal que presentaban como afeccion
unica, mediante examen citologico del exudado, hemograma completo (CBC), bioqu mica serica, urianalisis,
concentracion de tiroxina total (tT4), t tulo de anticuerpos antinucleares (ANA), cultivo bacteriano y pruebas
de sensibilidad, cultivo fungico, histopatolog a de biopsias de la una y dieta de excusion. Las anormalidades
en el CBC, la bioqu mica serica y el urianalisis fueron m nimas e inespec cas. Las concentraciones totales de
T4 se encontraban en el rango normal de refernecia del laboratorio. Los cultivos fungicos y los t tulos de ANA
fueron negativos en todos los perros. En aproximadamente la mitad de los perros exist a infeccion bacteriana.
El examen histologico del tejido de las unas mostro una oniquitis de la union (de interfase) rica o pobre en
celulas en todos menos uno de los perros. Exist a evidencia de reaccion adversa a los alimentos en cuatro
perros. Un perro respondio completamente a terapia antibiotica. La oniquitis de interfase parece ser un
patron de reaccion histologica cutanea de la matriz de la una en el perro, con varias posibles etiolog as
subyacentes. En los perros con enfermedad ungueal como unico s ntoma cl nico, el estudio diagnostico inicial
recomendado incluye el examen citologico, cultivo y sensibilidad bacteriana, biopsia y dieta de exclusion.
[Mueller, R. S., Friend, S., Shipstone, M. A. y Burton, G. Diagnosis of canine claw disease a prospective
study of 24 dogs. (Diagnostico de la enfermedad ungueal canina estudio prospectivo de 24 perros.)
Veterinary Dermatology 2000; 11: 133141.]
Zusammenfassung Die Atiologie von Klauenerkrankungen bei 24 Hunden wurde durch zytologische
Praparate von Klauenexudat, Blutuntersuchungen, Harnanalyse, Thyroxinbestimmung, antinukleare
Antikorper-(ANA) titer, bakterielle Kultur, Pilzkultur, Histopathologie von Klauenbiopsieproben und
Eliminationsdiaten untersucht. Abnormale Werte der Blutuntersuchungen und Harnanalyse waren
unspezisch und nicht wesentlich. Thyroxinkonzentrationen lagen innerhalb der normalen Referenzwerte.
Pilzkulturen und ANA Titer waren bei allen Hunden negativ. Bei der Halfte der Hunde wurde eine bakterielle
Infektion festgestellt. Bis auf einen Hund ergab die histologische Bewertung der Klauenproben bei allen
Hunden eine zell-arme oder zell-reiche Onychie der dermo-epidermalen Grenzzone. Anzeichen einer
Futterreaktion wurden bei 4 Hunden festgestellt. Ein Hund sprach vollstandig auf Antibiotika an. Die
Onychie der dermoepidermalen Grenzzone scheint beim Hund ein histologisches Reaktionsmuster der
Klauenmatrix mit mehreren moglichen Ursachen zu sein. Bei Hunden mit Klauenveranderungen als einzigem
Symptom wird zur anfanglichen diagnostischen Aufarbeitung Zytologie, bakterielle Kultur, Klauenbiopsie
und Eliminationsdiat empfohlen. [Mueller, R. S., Friend, S., Shipstone, M. A. und Burton, G. Diagnosis of
canine claw disease a prospective study of 24 dogs. (Diagnose von Klauenerkrankungen beim Hund eine
prospektive Studie von 24 Hunden.) Veterinary Dermatology 2000; 11: 133141.]

# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 133141