Veterinary College, Bengaluru

Monthly e-Bullletin

Newsletter Date : 31st October 2013 Volume: 02 Issue: : 10

Dr. B. N. Nagaraja , Dr. A. S. Patil and Dr. Ramesh Rathod

Department of Veterinary Surgery & Radiology, Veterinary College Hebbal, Bangalore
settihallynag@rediffmail.com

Introduction:
Bursae are cavities lined by synovial membrane.
There are two types of bursae typical (present at
birth- Navicular, Bicipital, etc) and Atypical (acquired
after birth Atlantal, Subcutaneous, etc). A bursa serves
to reduce friction between moving parts, such as tendons,
ligaments, and muscles, or to cushion the effects of
excess pressure between these movable structures and
bony prominences. Therefore, pathologic changes in
bursae can be associated with changes in the adjacent
tendon, ligament, muscle, or bone.

Bursitis is an inflammatory reaction within a

bursa that can range from mild inflammation to sepsis.
Bursitis causes synovial effusions into the bursal cavity
resulting in painful swelling. It can be classified as true
or acquired. True bursitis is inflammation in a
congenital or natural bursa (deeper than the deep fascia),
eg, trochanteric bursitis and supraspinous bursitis
(fistulous withers). Acquired bursitis is development of
a subcutaneous bursa where one was not previously
present or inflammation of that bursa, eg, capped elbow
over the olecranon process, and capped hock over the
tuber calcaneus.

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Signs:
Bursitis may manifest as an acute or chronic inflammation.
Examples of acute bursitis include bicipital bursitis and
trochanteric bursitis in the early stages. It is generally characterized
by swelling, local heat, and pain. Chronic bursitis usually develops
in association with repeated trauma, fibrosis, and other chronic
changes (eg, capped elbow, capped hock, and carpal hygroma).
Excess bursal fluid accumulates, and the wall of the bursa is
thickened by fibrous tissue. Fibrous bands or a septum may form
within the bursal cavity, and generalized subcutaneous thickening
usually develops. These bursal enlargements develop as cold,
painless swellings and, unless greatly enlarged, do not severely
interfere with function. So the cronic bursitis is observed as cystic
form, proliferative form, fibrous form and hemorrhagic form.
Septic bursitis is more serious and is associated with pain and
lameness. Infection of a bursa may be hematogenous or follow
direct penetration.
Frequently encountered conditions:
Poll evil, Fistulous withers / Supraspinatous bursitis;
Bicipital bursitis; Capped elbow; Capped knee, Trochanteric
bursitis, Capped hock and Navicular bursitis.
Treatment:
The pain in acute bursitis may be relieved by application of
cold packs, aspiration of the contents, and intrabursal medication
(Gentamicin and Methyl Prednisolone). An elastic crepe bandage
roll should be used to prevent recurrence. Repeated injections
may result in infection. So take aseptic precautions.
The bursa may also be reduced in size by application of a
counterirritant or by ultrasonic or radiation therapy. Treatment of
choice for chronic bursitis is enbloc surgical excision. Application
of counter irritants like Bin Iodide of Mercury (one in eight),
needle point firing may be performed. In infected bursitis,
systemic antibiotics as well as local lancing and drainage
followed by application of irritant to its interior is required.

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 Dr.Muralidhara.A., Professor and Head
Dept. of TVCC, Hebbal,Bangalore
asoormurali@rediffmail.com
This includes the principles of diseases which occur during the first month of life in animals born
alive at term.
Prenatal disease
A) Fetal diseases: Diseases of the fetus during intrauterine life, e.g. prolonged gestation, congenital defects,
abortion, fetal deaths with resorption or mummification.
B) Parturient diseases: diseases associated with dystokia causing cerebral anoxia, injuries of skeleton and
soft tissues.

Postnatal diseases:
A) Early postnatal diseases: within 48 hours e.g. malnutrition due to poor mothering, hypothermia due to
exposure to cold, low vigor in neonates due to malnutrition, special disease (Naval ill and Colibacillosis).
(B) Delayed postnatal diseases: within 2 -7 days after parturition e.g. mammary incompetence resulting in
starvation, increased susceptibility to infection due to hypoglobulinemia such as lamb dysentery,
colibacillosis and foal septicemia.
(C) Late postnatal diseases: within 1 - 4 week of life e.g. white muscle disease, enterotoxemia. In summary,
the causes of mortality in newborn lambs are largely physical and environmental and occur immediately at
birth or shortly thereafter. In calves, the major causes of mortality are with dystokia and with neonatal
diarrhea in postnatal life. Meanwhile, lambs are susceptible to physical and environmental influences.

Congenital defects
Abnormalities of structure or function which are present at birth. They may be or may not inherited,
the inherited defects may not be present at birth. The effects of noxious agents in the pregnant female
during the three major periods of gestation are going as following:
A) Period of the ovum: causes deaths of the ovum and resorption e.g. vibriosis.

B) Period of the embryo and organogenesis: depending on dosage and duration of insult and may lead
either to:
Structural abnormality or functional deficit caused by vitamin A deficiency, toxic agent, infection.
Death of the embryo and resorption or abortion (vibriosis).
C) Period of the fetus and fetal growth: illness of fetus resulting in:
Abortion - Brucella abortus, IBR .
Mummification inherited, infectious and unknown.
Stillbirth , Dystokia, hypoxia, Weak neonate infection in last week of gestation
Weak neonate infection in last week of gestation.

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Causes:
1) Virus infection:
Only seven viruses are known to cause congenital defects in man and animals condition. They
include the viruses of :
Swine fever and Bovine viral diarrhea in animals
Blue tongue and Acabane disease in animals
A) Hog cholera virus:
Vaccination of sows with modified vaccine virus between 15 25 days of pregnancy produces
piglets with edema, deformed nose and kidney. Mean while natural infection causes cerebral hypoplasia in
piglets.
B) Blue tongue virus:
Vaccination of ewes with attenuated vaccine virus between 35 45 days of pregnancy causes
porencephaly in lamb.
C) Bovine viral diarrhea virus:
Natural infection causes cerebral hypoplasia in calves. Meanwhile exp, infection of pregnant heifers
causes cerebral hypoplasia, optic including cataract, retinal degeneration, hypoplasia and neuritis of nerve.
D) Acabana virus:
Infection of pregnant cow products arthrogryposis and hydroencephaly.

2) Nutritional deficiency:
There are numbers of congenital defects in animals which are known to be caused by deficiency of
specific nutrients in the diet of dam; such conditions include the following.
Goiter in all species due to iodine deficiency.
Enzootic ataxic in lambs due to copper deficiency.
Manganese deficiency which causes limb deformity in calves.
Vitamin D causes neonatal rickets.
Vitamin. A deficiency which causes eye defect, hairless in piglet.
Simple inanition or nutritional deficiency of protein do not cause congenital defects, but can increase
prevalence of stillbirth and abortions.
3) Chemical poisons:
A) Poisonous plants.
B) Farm chemical.
Parbendazole and cambendazole in sheep.
Organophosphorus compound (may be).
C) Miscellaneous chemical and drugs.
Cortisone in early pregnant.
Estrogen derivatives.
Bismuth, selenium, nitrogen mustard and tetanus toxin.
D) Physical insults.
Severe exposure to beta or gamma irradiation.
Hyperthermia.

4) Environmental influences.
The fetus is a sensitive biological indicator of the presence of some noxious influences in the
environment.

Diagnosis of these congenital defects:

1. Clinical signs and P.M. lesions.
2. Clinical laboratory findings.
3. Epidemiological investigation

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 Epidemiological investigation includes:
Pedigree analysis.
Nutritional history of dams of affected neonates.
Disease history of dams of affected neonates.
History of drugs of affected neonates.
Seasons and translocation.
Introduction of new comers to the herd.
Intrauterine growth retardation:
It is failure to grow properly and is distinct from failure to gain body weight. It is usually measured
by the crown to rump length. Dwarfism in cattle and ranting in pigs are most common disorders of retarded
intrauterine growths.

Diseases caused by physical and environmental influences:

1)Particular injury and intrapartum death:
As a result of dystokia, which may not be assisted by the farmers, there is a chance of physical
trauma to limb or rib cage. Damage of the brain by way of intracranial hemorrhage which causes death of
about ( 70% ) of neonates within days of life.
In causes of prolonged birth which leads edema of many parts of the body, especially head region
(tongue) may develop.
Intrauterine deaths may results in cause of prolonged birth from hypoxia of the fetus due to
impaired circulation through placenta.
2) Fetal hypoxia:
Normally, foals are born in a primary apnea state, but gasping respiration begins with 30 60
seconds.
Placental dysfunction or occlusion of the umbilicus during second stage of labor result in a state of
terminal apnea. It will be still born unless urgent and vigorous resuscitation is initiated immediately
including the following:
A ) Extending the head and clearing the nostrils from mucous.
B) Sealing one nostril by hand and breathing forcibly into the other, the chest wall to be moved only
slightly with each breathe.
C) I/V administration of 200 ml of 5% sodium. Bicarbonate solution to overcome acidosis.
D) Neonatal hypoxia usually occur in foals use than 325 days of fetal age, they are small size, reduced
body weight unable to rise and to suck and, suffering from respiratory distress.
E) Stomach tube feeding with mares milk or reconstituted by milk at dose rate of 80 ml/kg. B. wt. In
10 divided dose day.
Differential diagnosis:
1. Intrauterine infection in late gestation.
2. Exposure of neonate to cold environment.
3. Maternal deficiencies of the dam.

Environmental and nutritional factors:

There are two environmental factors which may predispose to infection, besides causing mortality
themselves, which are low: environmental temperature and deprivation of carbohydrate leading to
hypoglycemia.
Effects of temperature:
Piglets are more susceptible to hypothermia and hypoglycemia. The thermoregulation mechanism in
piglets is efficient in first 9 days of life after which it is not fully functional until 20 days of life.
The major causes of hypothermia in lambs are excessive heat loss, depressed heat production caused
by intrapartum hypoxia and immaturity, and starvation.
at 40 c and feeding of 100 200 ml colostrum.

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 Administration of glucose is necessary in such lambs at a dose rate of 2 gm / kg b wt. as 20% so-
lution injected intraperitioneally in addition to rewarming animal at 40 c and feeding of 100 200 ml
colostrum.

Effect of nutrition:
Nutrition of dams is so important in relation to the resistance of offspring. Newborn lambs, calves
and foals are much more capable of maintaining their blood glucose level than piglets when starved.
Hypoglycemic coma may be observed in lambs while calves are highly resistance to insulin deficiency
where produced hypoglycemia during first 48 hrs of life.
Malnutrition of lambs caused by:
Antipartum malnutrition of ewe which causes reducing of milk flow.
Inclement weather preventing lamb sucking or ewe mothering.
Inadequate maternal behavior.
Too old ewes low milk flow.
Too tired ewes low milk flow.

Inadequate mothering by ewe causes:

Malnutrition of lamb.
Lake of warmth and protection of lamb.

Reduced vigor of the lambs caused by:

Small lamb, especially during cold weather.
Intrauterine and postnatal infection.
Malnutrition.
Very cold or very hot weather.
Being one of multiple birth.

Neonatal infection:
Attention is currently devoted to both the virulence of the pathogens and the resistance of the host,
because of some of non-pathogenic microorganisms can cause the diseases if the immunological status of
the animal is not at an optimum level.

Etiology:
The common neonatal infections among the domestic farm animals are:
Cattle:
Bacteremia or septicemia caused by E. coli, listeria monoytogenes, pasteurella spp., Streptococcus,
salmonella spp.
Enteritis caused by pathogenic E. coli, salmonella spp, rotavirus, corona virus, cryptosporidia,
clostridium.
Respiratory tract diseases caused by IBR, Pl3 viruses.
Horses:
Septicemia with localization especially in joints, caused by E. coli, Salmonella typhimurium,
Sterpt.Pyogenes.
Septicemia with localization particularly in lungs caused by C. equi.
Enteritis caused by Clostridium perfringens and rotavirus.
Sheep:
Bacteremia with localization in joints caused by Strept. micrococci, E. insidiosa.
Gas gangrene of the navel caused by CI. septicum, CI. edematus.
Lamb dysentery caused by Cl. Perfringens type B.

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Epidemiology:
1. Portal of infection:
It could be intrauterine or postnatal. If it is intrauterine the infection gains entrance via the placenta, and
probably by means of placentitis due to a blood born infection or an existing endometritis.
Thus disinfections of the uterus is so important and disinfections of the environment may have little
effect on the incident of the disease.
If the disease is postnatal the portal of infection may be through the navel or by ingestion.
Contamination of the environment can occur from soiling of the udder or bedding by uterine discharges
from the dam, from previous parturition, or from discharge of other affected neonates.

2. Resistance to infection:
All newborn farm animals are more susceptible to infection than adults due to:
They are a gammaglobulinemic and possess no resistance to infection until after they have ingested
colostrums. The immune system of the newborn animal is less mature than adult and dose not respond
effectively to antigens as the adult.
The fetal lamb produce large quantity of corticosteroides beginning 810 days before birth (also fetal
calves) result in lymphopenia decrease phayocytic activity decreased cellular immunity and decreased
resistance.
There are four recognizable immunological deficiency states in newborn foal which are:
(1) Combined immunodeficiency (CID):
Which is inherited as an autosomal recessive trait in Arabian horses. There is marked lymphopenia,
absence of lymphocytes from all lymphoid organs, hypo-or a gammaglobulinemia and death at 2-20 weeks
of age.
(2) Primary a gammaglobulinemia:
Animals are usually affected with chronic infection. Serum concentration of IgG and IgM are low and may
not be detectable. There is failure of antibody production following injection of foreign antigens, but tests
for cell mediated immunity may be positive.
There is complete absence of B-lympocytes and immunoglobulins but normal T-lymphocyte counts.
(3) Hypogammaglobulinemia:
Following inadequate transfer of clolstral immunoglobulins from dam to foal; it is most common in foals
and associated with high incident of infection influence.
(4) Selective immunoglobulin M deficiency (IgM):
It is associated with infection 4-8 months of age.
(5) Passive immunity:
There are many important factors which influence the level of serum immunoglobulins achieved by the
newborn and they are:
(1) Insufficient ingestion of immunoglobulins due to:
Insufficient amount of colostrums produced by dam for many reasons as poor husbandry, malnutrition.
Low concentration of immunoglobulin in the colostrums.
Insufficient amount of colostrums ingested by the newborn due to:
- Poor mothering behavior which may prevent newborn from sucking.
- Poor udder or teat conformation.
- Weak and traumatized calf.
- Failure to allow the newborn to ingestion.

(2) Insufficient absorption of immunoglobulin from colostrums:

Delayed ingestion of colostrums.
Interference with the efficiency of absorption of immunoglobulins from colostrums.

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Clinical finding of newborn infection:
The clinical finding depend on the rapidity of infection.
Slow spreading: Omphalophlebitis, fever, depression, anorexia, leucocytosis and signs referable to the
localization as :
a. Endocarditis with heart murmur.
b. Panophthalmitis with pus in the anterior chamber of the eye, meningitis with rigidity, pain and
convulsions.
c. polyarthritis with lameness and swollen joints.
When the spread is more rapid:
Fever, prostration, coma, petechiation of mucosa, dehydration, acidosis and finally death.

Laboratory findings:
Determination of serum immunoglobulin through:
(1) Indirect method:
Refractometer measures total protein.
Zinc sulphate turbidity test.
(2) Direct method:
Paper electrophoresis.
Radial diffusion test Ig. subclasses.
Other evaluation as that of adult.

Diagnosis:
History
Clinical signs.
Laboratory findings.

Special investigation of any neonatal deaths (illness):

Determination of pregnancy duration to ensure that the newborn animal was born at term.
Collect epidemiological information on prevalence in a group, maternal, paternal, nutritional,
vaccination etc
Conduct a postmortem examination of all available dead neonates.
Laboratory examination of specimens of fetal tissues and placenta.
Investigate management practices operating at the time.
Ensure that the dam has a milk supply.

Principles of treatment of infectious diseases in newborn animals:

Obtaining of etiological diagnosis if it is possible.
Drug sensitivity of the causative microorganisms. Should be obtained before treatment.
Choose the antibacterial agents.
Individual treatment is necessary to maximize survival rate.
Supportive treatment is usually necessary.
Provision of antibodies to sick and weak newborn animals through the use of transfusions or
hyper immune serum.
Whole blood 10-20 ml / kg body weight. I /V.
Equine plasma 20 ml / kg body weight. I /V.
Good nursing care is also necessary.

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 Sudha G
Assistant Professor, Department of Gynecology and obstetrics
Veterinary College, KVAFSU, Bangalore
dineshtumkur@gmail.com

ANOESTRUS- ESTRUS IS NOT EXHIBITED OR ESTRUS IS NOT OBSERVED

Possible causes
1. Undetected heat symptoms in normal cow.
a. Failure to properly observe for estrus.
b. Failure to keep adequate records.
c. Failure to turn cows out of barns.
d. Few open cows within a group that are available to detect heat in other open cows pregnant cows and
cows in midcycle are much less likely to mount cows in or near heat.
e. Feet and leg problems, lameness.
f. Slippery footing.
g. Unfamiliarity with symptoms of estrous behavior.
h. Quiet heats or silent heats (normal ovulation with little or no sign of heat).

2. True anestrus: estrus is not occurring.

a. Energy deficiency, cows losing large amounts of flesh due to high milk production and/or
underfeeding and low dry matter intake.
b. Anemia, often from inadequate protein, iron, selenium or vitamin E.
c. Phosphorus deficiency, especially in heifers or excess phosphorus.
d. Poor endocrine tone from stored forage only, no fresh forage; lack of fat-soluble vitamins, plant
hormones and antihormones.
e. Pyometra and severe uterine infection.Cows may or may not show discharge and generally do not
cycle.
f. Pregnancy.
g. Cystic ovarian disease70% of cystic cows are anestrus.

Suggestions
1. Examine suspect cows to determine whether they are truly anestrus, i.e., absence of ovarian structures,
cysts, pyometritis, etc.
2. Maintain adequate reproductive records and use heat expectancy chart. Milk Progesterone Testing can
be used to evaluate heat detection.
3. Closely observe cows for heat for at least 20 minutes each time. More heats will be shown in evening
and early morning than at mid-day. Provide good footing in heat detection area.
4. In conventional housing situations, turn cows out at least daily. Determine which cows are pregnant and
concentrate efforts on open cows.

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5. Check problem cows for anemia:
a. Run CBC, which includes hemoglobin, packed cell volume, red and white blood cell counts.
b. Submit unclotted samples from 12 to 21cows, including dry cows and early lactation cows.
7. Check serum mineral, protein and BUN or MUN levels. Submit 2 tubes of clotted blood per cow or 10
cc of serum per cow. Sample about 12 to 21 cows. Do not sample treated cows, those within one week
of expected calving or those fresh less than three weeks. Forward samples to an animal diagnostic
laboratory.
8. Submit forage and/or TMR samples for standard analysis and mineral tests.
9. Submit feed program for evaluation. Carefully examine protein, mineral and vitamin levels.
10. Examine cows for uterine infection. Prevent retained placenta and reproductive tract infections as given
on pages 3 and 4.
11. Whenever possible, have cows in a gaining condition as desired breeding time approaches.
12. Control periparturient disease problems, especially ketosis.
13. Provide cows with adequate amounts of fresh forage for at least four to six weeks each year.
14. Ensure pregnancy exams are conducted routinely, 40 to 50 days after breeding.
15. Treat for anemia if determined to be a problem.

Dr. Madhukar* and Prof. H. A. Upendra#

*
Assistant Professor, #The Director, Institute of Wildlife Veterinary Research, KVAFSU,
Doddaluvara, Kodagu 571232.
madhukar262@gmail.com
Sometimes elephant calves need to be hand reared
due to various reasons. Elephant claves may get separated or
rejected from the herd due to death of the mother or injury to
the calf. Calves may get lost when herd moves fast in case
of dangers. Sometimes calves may follow buffalo herds and
enter human habitats which may permanently separate it
from its mother. All these situations put the calf in serious
danger as it necessitates immediate and special attention.
Such calves should be given full attention with special
considerations for its anatomical, behavioural and
psychological uniqueness. On the contrary, some mothers,
mostly in captive conditions, may also reject calf due to
unknown reasons. Hence, most of the times such calves will
be very young.

Figure1: Orphan elephants need someone to bond with like its real mother. Picture from Understanding
The Elephant Orphans' Project.

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 Immediately on finding an abandoned calf, the veterinarian has to thoroughly check for injuries and
health condition. First, a caring and responsible caretaker should be assigned to manage the calf, then a
strict and regular feeding schedule has to be developed considering following aspects:
Avoid overfeeding of calf at initial stages. Instead keep it on optimal or suboptimal feeding to get it
accustomed to the new feeds and regimen.
It should be given fresh food and hygienically prepared food
For first 6 to 7 weeks it should be fed only milk.
Elephant milk is very low in lactose, high in fat and fat globules are small. Hence, cow milk or cow
milk based infant formulas are not suitable option and should be avoided.
Some commercially available formulas recommended specially for elephant calves are Grober
Elephant, Gro African and Asian elephant formulas.
Goat milk is a suitable option.
In case these options are not available, milk powders like AmulSpray can be used.
Calves express hunger by cries.
Calves can be fed at least 1 litre of milk during 5 AM to 10 PM, with an interval of 1 to 2 hours,
during first 2 months of age. By the age of one year the calf can be fed 5 to 6 times by gradually
increasing the feeding interval.
Although volume of food depends on the milk/formula used, a calf typically consumes 10-15% of its
body weight.
A 100 kg calf requires 6000 to 8000 kcal/day whereas 200 kg calves require 16000-20000 kcal/day.
Food quantity can be adjusted based on this requirement.
Enema cans may be used to feed the calf, as it is easy to clean and flow can be regulated. Bottle
feeding can be time consuming and calves may get frustrated due to small nipple openings.
If the mother who has rejected the calf is in captivity, its milked to feed the calf.
Milk powder concentration should be increased slowly, with a starting value of 50 gms/litre during
first few weeks.
A healthy calf will rest between feedings, urinate 10 to 12 times a day, and pass semisolid faeces
twice in a day.
Calves can be introduced slowly to semisolid concentrates after 55 to 65 days.
Fine powder prepared by cleaning, sprouting and drying of ragi is commonly used for Indian ele-
phant calves.
Solid food can be introduced after 6 months.
Milk quantity can be reduced to 1 litre per day at the end of first year.
Fresh dung collected from a healthy cow elephant, diluted in water can be fed to the calf around 2 to
3 months of age to establish the natural microbial flora of the gut which will aid in the digestion of
green fodder.
By the age of 9 months, calves should be taking 35 to 40 kg of fodder per day.
Captive calves can be given carminatives and gastric stimulants to aid in the maintenance of
digestion.
Mineral and vitamin supplements, especially calcium should be regularly included at this age.

PELVIC

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 Healthy calves weigh about 100 kgs at birth and grow up to 2 inches in height every year.
The tethering area should be clean, dry, free from materials like plastics, papers and rubbers etc.
Calves can be housed near kitchen or in mahouts house to provide them warmth during night times.
Health should be regularly monitored to adjust the quantity and quality of food during hand rearing.
Naturally, elephant calves are not weaned up to 3-4 years, whereas captive, orphaned or hand reared
calves are weaned at 15-18 months of age.

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PELVIC

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 APPEAL
Dr. K. Trivikrama Rao is nearest and dearest to all his students. He was one of the teachers known
for simplicity of expression, precision, and was able to make the subject understandable even to the dullest
of the students. Thus he was a great motivating force to the students and building confidence in them. No
doubt his students still remember the Splanchnology course taught by him. He was always considerate and
compassionate to the below average students and helping them in their learning which was reflected in
their performance in the examinations.

In later part of his career he served as the Director of Instructions (Vety) and undertook many of the
activities. Under his stewardship Dairy Science College was started at Bangalore by erstwhile UAS. Many
teachers were benefited by being appointed in various cadres in KDDC scheme. Subsequent to winding up
of KDDC, Dr. K.T. Rao strived hard to relocate the staff into the university with due weightage given to
their cadres in KDDC.

For his kind heartedness and noble personality, consequent to his demise, like-minded veterinarians
who have great respect for Dr. K.T. Rao joined and thought of perpetuating the interest and philosophy of
Dr. K.T. Rao. In this direction DR TRIVIKRAMA RAO MEMORIAL VETERINARIANS FORUM
was founded in the month of September 2012.
Mandates of the forum:
Initially a fellowship to an economically weaker meritorious student of I BVSc. & AH Programme
of Veterinary College, Bangalore will be awarded and a lump sum of Rs. 15,000/- per year will
be paid for covering the expenses of tuition fees.
II year MVSc. Student majoring in Veterinary Anatomy will be provided a research grant of Rs.
5,000/- from the year 2013-14.
For this activity an appeal is made to all the Veterinarians who are ardent disciples of Dr.
K.T. Rao to donate liberally for this noble cause. An amount of not less than Rs. 1000/- can be do-
nated as per the details given below:
Cheque/DD drawn in favour of DR
Account No: 0425101053233 TRIVIKRAMA RAO MEMORIAL VET-
Canara Bank, Hebbal Branch, ERINARIANS FORUM sent to The
Bangalore 560 024. Secretary Dr. R.V. Prasad, Professor
IFSC Code : CNRB0000425 and Head, Department of Anatomy,
MICR Code: 560015021 Veterinary College, Hebbal, Banga-
With an Intimation to Secretary by lore 560 024.
mail/letter e-mail: rvprashwin@gmail.com
Phone: 09449855893

monthly e-Bulletin
Published and circulated by Veterinary College, Hebbal Bengaluru

Editor: Associate Editior:

Dean, Veterinary College, Hebbal, Bengaluru Head,Dept of Vety & Animal Husbandry Extension Education
Dr.S.Yathiraj (Ex-Officio) Dr.K.Satyanarayana (Ex-Officio)

Contact :
Dept of Veterinary and Animal Husbandry Extension Education
Veterinary College, Hebbal Bangalore
email: pashubandhavch@gmail.com

PELVIC

Pashubandha 2013
2012 Volume No : 2
1 Issue : 10
07