BOOK - Advanced Pathology and Treatment of Diseases of Domestic Animals With Special Reference To Etiology, Signs, Pathology and Management 2008
BOOK - Advanced Pathology and Treatment of Diseases of Domestic Animals With Special Reference To Etiology, Signs, Pathology and Management 2008
Treatment of Diseases of
Domestic Animals
C.D.N. Singh
B.V.sc. &A.H., M.sc. (Vet.), Gold
Medalist, Ph. D., F.R.V.C.S.
(Sweden)
C.D.N. Singh
B.V.sc. &A.H., M.sc. (Vet.), Gold Medalist, Ph. D., F.R.V.C.S.
(Sweden)
Former University Professor-cum-Chairman of Pathology,
Bihar Veterinary College, Patna
ISBN 978-81-8189-134-1
Publisher
All Rights Reserved
Printed at:
Salasar Imaging Systems
C-7/5, Lawrence Road Industrial Area
Delhi -110 035
Tel. : 011-27185653,9810064311
Dedicated to
Lord Paw an Putr Hanuman Ji and
to the memory of Late Veena singh,
wife of the author
This Page is Intentionally Left Blank
~, -q-c;:rr
RAJ bHAVAN
PATNA, 800 022
23 February, 2007
MESSAGE
I am glad to note that the book "Advanced Pathology
and Treatment of Diseases of Domestic Animals" written by
Shri C.D.N. Singh will be usefull for veterinary students. The
user will find the book useful.
I wish success of the publication.
\\.~)
(R.S. Gavai)
This Page is Intentionally Left Blank
Advanced Pathology and Treatment of Diseases of
I
~ 23.12.2005
x-ewf-~, ~
This Page is Intentionally Left Blank
MESSAGE
K. R. Maurya
(Vice- Chancellor)
Rajendra Agricultural University,
Pusa (Samastipur) - 848 125
10-9-2005
This Page is Intentionally Left Blank
Preface
The book grew out of more than three decades of
teaching and the schematic structure of the text has been
designed to cater to the needs and problems of the students
in both undergraduate and postgraduate courses in the
veterinary colleges, diagnosticians and veterinary
practitioners engaged in the diagnosis and treatment of
animal diseases. The VCl syllabi followed in different
agricultural universities have been kept in view in preparing
the manuscripts of this book for inserting pertinent
pathological changes noticed in different animal diseases and
relevant information on the management and treatment
needed with the object of making this book of high value to
the students, teachers and veterinary practitioners. The book
has been written in a simple easy and lucid language with
more emphasis on the symptoms, lesions and treatment of
diseases. The material in the advanced pathology and
treatment of diseases of domestic animals is organized ill a
manner so that the students are introduced to symptoms and
lesions of diseases and their relevance to diagnosis,
chemotherapeutic and Prophylactic measures.
Different tables on symptoms and lesions of animal
diseases, veterinary drugs and vaccination schedules have
been incorporated in the book for quick diagnosis, treatment
on time and prophylactic steps against such
diseases. Molecular imaging is an important adjunct to today's
pathology and medicine helping the detection of disease
processes much earlier with information on the origins of
disease realated pathways, targets and adoption of proper
methods for treatment and management of the root cause of
diseases. It, thus, revolutionises the usual practice of treatment
through symptoms by adopting technology driven techniques
like PET, eT, SPECT, ultrasound, MRl and optical imaging
etc. in patients.
My indebtedness lies to various scholars and
pathologists whose views have been included in this book. I
am grateful to Dr. P.B. Kupuswamy, former Principal, Bihar
Veterinary College, Patna for help and encouragement in
writing this book. I lay no claim to any originalities and
welcome suggestions from users to improve its qualities. I
wish to thank Dr. S.P.Verma, Principal BVe, Patna. Bihar,
Dr. S.RP Sinha, University Professor, B.V.C Patna and Dr.
S.V Singh College of veterinary science, NDUAT, Kumar
Ganj, Faizabad, U.P in preparing the manuscript of the book.
My thanks are also due to Somya Raj, Shalini Raj, K-3, P.e.
Colony, Kankarbagh, Patna, Neha, West Ashok Nagar Road
No-I, Kankarbagh Patna-20 and Amit kumar, RM.5 Colony,
Kankarbagh, Patna-20 for its meticulous composing.
Pathology, an observational science, is combined with a live
demanding subject of medicine for making this book as
stimulating and exciting for the veterinarians.
C.D.N.Singh
CONTENTS
DISEASES 1
A. BACTERIAL DISEASES
1. Anthrax 10
2. Haemorrhagic septicaemia 15
3. Colibacillosis 21
4. Mastitis 24
5. Stangles 30
6. Navel- ill 31
7. Glanders 34
8. Leptospirosis 38
9. Nocardiosis 44
10. Tuberculosis 44
11. Johne' s disease 50
12. Salmonellosis 54
13. Actinomycosis 59
14. Actinobacillosis 62
15. Contagious bovine pleuropneumonia 65
16. Enterotoxaemia 68
17. Lamb dysentery 74
18. Black leg 76
19. Tetanus 78
20. Malignant oedema 82
21. Botulism 83
22. Braxy 85
23. Gas gangrene 86
24. Bovine bacillary haemoglobinuria 87
25. Abortion 88
26. Brucellosis 94
27. Swine erysipelas 98
B. VIRAL DISEASES
1. Foot and Mouth diseas e 120
2. Rinde rpest 128
3. Bovin e ephem eral fever 135
4. Pox diseas es 137
5. Africa n horse sickne ss 143
6. Equin e enceph alomy elitis 146
7. Blue tongu e 148
8. Scrapi e 151
9. Rabies 152
10. Canin e parvo virus infecti on
(haem orrhag ic gastro enterit is) 160
11. Infecti ous canine heptiti s (Ruba rth diseas e) 163
12. Canin e distem per 165
13. Swine fever 168
14. Pseud orabie s (Aujes ky's diseas e) 171
C. PROTOZOAL DISEASES
1. Babesiosis 203
2. Theile riasis 210
3. Surra 214
4. Anapl asmos is 217
5. Coccid iosis 219
6. Toxop lasmo sis 222
D. PARASITIC DISEASES
1. Fascioliasis 234
2. Amph istomi asis 237
3. Ancyl ostom iasis 239
4. Trichosh"ongylosis 242
5. Schist omias is 244
6. Ascari asis 247
E. DEFICIENCY DISEASES OF ANIMALS 263
F. PATHOLOGIC CHANGES AND
TREATMENT OF THE POISONING
CASES IN ANIMALS 278
G. MICELLANEOUS PATHOLOGICAL
CODITIONSjDISEASES
1. Pneumonia 290
2. Hepatitis 297
3. Gastritis 304
4. Enteritis 308
5. Nephritis 311
6. Oedema 322
7. Ruminal tympany 328
8. Viral diarrhea 329
9. Indigestion 332
10. Anaemia 333
11. Laminitis 336
12. Snake bites 337
13. Stings of bee, scorpion and wasp 339
14. Inpaction of omasum and abomasum 340
15. Shock 342
16. Treatment of some diverse pathological
conditions 344
H. SOME METABOLIC DISORDERS AND OTHERS
1. Milk fever 352
2. Ketosis 356
3. Magnesium deficiency 359
4. Azoturia 361
5. Post parturient haemoglobinuria 363
6. Photosensitisation 365
7. Equine colic 368
8. Table of different physiological values 372
I. APPENDIX
1 Common chemotherapeutic agents
and vaccines 373
2. Immunisation programme in animals 403
3. Patent preparations used animals 407
4. Post-mortem examination 429
Index 498
Chapter 1
Diseases
1
Advanced Pathology and Treatment of Diseases of Domestic Animals
2
Diseases
3
Advanced Pathology and Treatment of Diseases of Domestic Ammals
4
Diseases
5
Advanced Patlwlogy and Treatment of Diseases of Domestic Animals
6
Diseases
7
Advanced Pathology and Treatment of Diseases of Domestic Animals
8
Diseases
9
Chapter 2
Bacterial Diseases
Anthrax
It is a febrile and highly fatal septicaemic disease of
mammals (especially herbivores like cattle and sheep). The
infectious organisms are noticed in the blood films singly or
arranged in chains of twos or threes in the affected animals.
These organisms exist as an obligate parasites but they can
also exist in the soil which may remain infective for several
months. Humans handling the diseased animals or animal
products may be infected through cuts in the body with
development of malignant pustules in the skin or through
inhalation of spores into the lungs (woolsorter's disease).
Ingestion of the contaminated materials also leads to the
occurrence of anthrax in the animals. A few hours before
death, the state of bacteraemia is caused by these organisms
in the infected animals to be followed by the state of
septicaemia. A fulminant septicaemia is seen in cattle, sheep
and horses but swines, dogs and cats are resistant to anthrax
infection. In swines, the disease is localized and confined to
the regional lymph nodes e.g., cervical lymphnodes. The
anthrax bacilli fail to grow in the body due to lack of oxygen.
Organisms like Clostridium septique, Cl. sporogenes and
Cl.welchii grow rapidly in the dead bodies of animals after
entering from the gut and anthrax bacilli undergo
degenerative changes and disappear from the carcasses
within one to three days. While diagnosing anthrax in
animals, the anthrax bacilli must be differentiated from
putrefactive or other postmortem invaders which may form
very long chains in the stained films. Bacillus anthracis fails
to grow in long chains in the blood of the infected hosts before
death.
10
Bacterial Diseases
PATHOLOGY
Gross Appearance
Cattle
(i) A yellow gelatinous oedema in the abdominal or throat
region at the point of entrance of bacteria.
(ii) Haemorrhagic gastroenteritis, oedematous and
haemorrhagic serous membranes.
(ill) Haemorrhagic lymph nodes may have dark colour like
spleen.
(iv) Spleen is greatly enlarged (splenomegaly) with dark and
black pulp containing unclotted blood. It may be friable
or its capsule may rupture. There is a massive
haemorrage in the spleen. Spleen may be normal in rare
cases.
(v) Liver, kidneys and intestinal tract are congested, swol-
len and haemorrhagic.
(vi) Trachea and bronchi are filled with frothy blood stained
material.
(vii) Blood is dark in colour but does not clot firmly and rarely
a string or blood clot can be found in the case of an
anthrax.
(vill)Tarry blood discharge at the mouth and other body
openings.
11
Advanced PathologV and Treatment of Diseases of Domestic Animals
Sheep
The main changes are :
(i) Splenic enlargement is not a characteristic change.
(ii) Presence of gestroenteritis.
(ill) Rapid putrefaction in the carcass.
(iv) No throat lesions are found in the sheep
Equines
One can notice the following :
(i) Presence of throat swellings.
(ii) Oedematous fluid in the subcutaneous and inter-
muscular tissue.
(iii) Swollen and congested lymph nodes.
Pigs
The main changes seen in pigs are as under ;.
(i) Splenic enlargement is not seen.
(ii) Oedema and haemorrhage in the pharynx and cer-
vicallymph nodes. In old cases, lymph nodes may
be enlarged and firm in consistency.
Microscopic Appearance
Anthrax bacilli are large rod shaped organisms which
can be found in the blood and affected tissues. Splenic
architecture is not visible due to numerous red cells.
Trabeculae are visible amidst red cells and nuclear debris.
Splenic sinuses and cords of Bilroth are filled with red cells
and pulmonary oedema is noticed. Toxins produced by
anthrax bacilli are known to produce increased permeability
of the blood vessels. In pigs, there is focal necrosis surrounded
12
Bacterial Diseases
17
Advanced Pathology and Treatment of Diseases of Domestic Animals
18
Bacterial Diseases
19
Advanced Pathology and Treatment of Diseases of Domestic Animals
Control
Prophylactic vaccination in HS infection is advisable in
20
Bacterial Diseases
21
Advanced Pathology and Treatment of Diseases of Domes tic Animals
22
Bacterial Diseases
Treatment
Colibacillosis caused by E.coli is a severe disease of calves
(neonates). It is quite safe to make choice of antibiotics after
having report about sensitivity of E.coli strains affecting the
animals. The most important antibiotics are chloramphenicol,
neomycin, tetracycline, and streptomycin etc. There is a
severe development of dehydration in sick animals. Fluid
therapy can be given to dehydrated patients. In neonates,
the fluid should be administered in divided doses for a period
ending over 2 to 3 days. Streptomycin and chloramphenicol
can be given to patients with good results.
In order to have quick effect of drugs, parenteral
administration with oral preparation is advisable. Since
toxaemia is seen in white scour, administration of fluid
therapy is greatly helpful. Corticosteroids can also be given
to animal patients for quick response.
Sanitation and feeding management have got to be
improved and calves suffering from diarrhoea should be
given cold (previously boiled) milk.
In order to control colibacillosis, the calf feeding pan
should be thoroughly disinfected. Overcrowding of calves
should be avoided. There should be proper housing and
hygienic conditions. The calves must be given fresh water.
The calves during their first 7 to 10 days of life should be
given prophylactic medication with sulphonamides,
antibiotics or deworming agents. Newly born calves must be
fed colostrum within first twelve hours of life. The calves
should have milk at the rate of 10% of body weight till the
attainment of the age of three months. The calves may be
given 2 kg of colostrum depending upon their weights. This
practice imparts passive immunity to the newly born calves.
For successful treatment of colibacillosis, important
precautions to be kept in one's mind are alteration in the
diet of the calves, fluids, and intestinal protectants
antimicrobial therapy and proper management of the infected
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Advanced Pathology and Treatment of Diseases of Domestic Animals
24
Bacterial Diseases
PATHOLOGY
Gross Changes
1. The cardinal signs of inflammation i.e., heat, redness,
swelling, pain and loss of function (i.e., reduced milk
secretion) etc. can be seen in the inflamed udder. Clots,
flakes, blood, discolouration of milk and an excess of
leucocytes are important findings in the milk of mastitis
cases.
2. Cessation or reduction in the milk secretion. Exudative
fluid of abnormal colour or consistency can be milked
from the teat in place of usual milk. Warmth, diffuse
swelling and gangrene may be noticed in the mammary
glands in acute cases.
3. Firmness or shrinking in the quarters. When two or more
quarters are involved, the udder atrophy (marked by a
small quarter or small teat) is a more marked change.
The reason of the firmness in the udder is diffuse prolif-
eration of the fibrous tissue (fibrosis).
4. Old inspissated abscesses or lumps of firm tissue are
evident in the affected quarter and these can be pal-
pated.
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Microscopic appearances
Acute exudative inflammatory changes can be noticed
in the udder except the mucous inflammation (because of
udder being a non-mucus forming organ). Serous, purulent
and fibrinous changes occur in the lactating dairy animals
like cattle and buffaloes in the mammary glands.
Haemorrhagic inflammatory changes can be found rarely in
the udder. Fibrous proliferative changes are more marked in
chronic mastitis. (Fig. 1; p. 199) The exudative changes are
marked in the alveolar lumina and the intercellular spaces.
Dead or dying leucocytes (pus cells) can be found in the
alveoli of the udder. Scanty albuminous precipitate can be
seen in the alveoli indicating distension of the alveoli with
fluid. In such alveoli, the epithelial lining shows compressed
or vacuolated cells. Inflammatory cells like leucocytes,
neutrophiles, monocytes and lymphocytes can be noticed in
the adjoining alveolar stroma. The alveolar capillaries can
be found distended with blood. Clots of fibrin and leucocytes
are seen in the smaller ducts. Occlusion to the drainage of
the exudate leads to growth and spread of the infectious
organisms. In Streptococcus agalactiae infection of the udder,
there is hyperplastic thickening and cornification of the
epithelial lining of the lactiferous ducts and sinuses with
infiltration of the inflammatory cells beneath the hyperplastic
epithelial cells. The infection spreads to supporting stroma.
In virulent infections, the alveolar Epithelium is destroyed
and the alveolar walls may collapse against each other with
26
Bacterial Diseases
Bacteriological Examination
A loopful of well shaken milk sample is inoculated on
to an Edwards plate and an another loopful on to a blood
agar plate and the plates are incubated at 37C. The bacterial
sediments of the centrifused milk are used to make smears
27
Advanced Pathology and Treatment of Diseases of Domestic Animals
28
Bacterial Diseases
the cows are under dry state, the infusion of the udder is
done as a preventive measure at the end of the last milking
and also at the beginning of the first milking. The presence
of antibiotic residues in milk causes sensitivity in human
beings. It is better not to use the milk having residues of the
antibiotics.
There should be lapse of atleast ninty-six hours before
consumption of milk from infected quarters. The quarters of
lactating animal can be dried by using infusion of the
following preparation like 30 to 60 m1 (3% AgN03 soln or 20
ml of 5% copper sulphate soln) or 100 to 300 ml of 1:500
acriflavin solution. In case of visibility of reactions in other
tissues, the quarters should be milked out. The quarter of
the animals can be stripped after 10 -14 days of infusion.
Such two infusions may be required for rendering the udder
dry. If there is a suspicion of resistant strains of bacteria,
treatment of mastitis can be done only by obtaining report
on the antibiotics sensitivity test for organisms present in
the milk.
Mastitis due to fungi and yeast do not respond
satisfactorily to antibiotics and drugs nystatin may be used.
In order to control mastitis, it is advisable to remove the
sources of infection, reduce the susceptibility of mammary
glands and also prevent the spread of infection between
lactating quarters.
The milk from affected quarter is examined
bacteriologically and such infected cow should be separated
from healthy ones. As a general procedure, careful milking,
udder washing, disinfection of teats and cup etc., should be
followed strictly. The quarters of the udder, if fibrosed, can
not be restored to normalcy and any surgical interference in
such udder is not helpful. Cows and buffaloes etc., can go
on giving milk inspite of one or two functioning quarters for
whole of their life spans. Subclinical mastitis due to contagious
pathogens in cows can be treated by intramammary injection
29
Advanc ed Pathology and Treatment of Diseases of Domestic Animals
30
Bacterial Diseases
31
Advanced Pathology and Treatment of Diseases of Domestic Animals
33
Advanced Pathology and Treatment of Diseases of Domestic Animals
GLANDERS
It is a contagious bacterial disease primarily affecting
the solipeds like horses and now-a-days only sporadic
incidence of this disease is noticed. Man and members of the
cat family are also be affected. The obligate causative
organism is Pseudomonas mallei which produces an acute or
more usually a chronic disease in horses, mules and asses.
This disease ends fatally and fibro-caseous nodules are
formed in the upper respiratory tract, lungs and skin etc.
Pigs and cattle are immune to this disease. Ingestion of food
or water contaminated with discharges of excretion of the
infected animals produces it in healthy animals. Skin infection
through contamination of open wounds in the body may
occur in some cases. Infection by inhalation is unusual.
Incubation period ranges from 2 weeks to 2 or 3 months or
longer. Guinea pig is very susceptible to the glanders
organisms and nodules develop in their lymph nodes, spleen,
lungs and liver etc. The male guinea pig which is infected
with the organisms given intra peritoneally, develops pus
formation in the tunica vaginalis and orchitis is seen in 2 to 3
days. This is called Strauss test for glanders. Organisms are
found in the guinea pig's lesions and these can be isolated in
pure form from such lesions. The organisms are rodshaped,
Gram negative, non-sporulating and non-motile and are
isolated on glycerine-agar and potato etc.
Glanders can be divided into the following types:
(i) Nasal glanders
(ii) Pulmonary glanders
(ill) Cutaneous glanders
It may develop in either acute, sub acute or chronic form
in animals. The characteristic lesions in the glandered animals
are pneumonia, nodules or ulcers in the respiratory tract (e.g.,
larynx and trachea etc.), skin and subcutaneous tissues along
lymphatics. Vari-sized nodules in the subcutaneous tissues
34
- - - - - - - - - -
Bacterial Diseases
of hind limbs, neck, face and liver etc. are called farcy buds.
(i) Nasal Glanders
Submucosal nodules are found on the nasal septum and
these nodules break down to give rise to shallow, crater like
ulcers or erosions which liberate a thick, sticky or oily
yellowish brown discharge. Later, these ulcers turn into
stellate shaped scars. Swelling is noticed in regional lymph
nodes. The ulcers on the nasal septum may have
characteristic punched out appearance. There is an irregular
contour of these lesions with raised or eroded borders. Ulcers
can penetrate into cartilage to cause perforations. The
discharge from the ulcers may be often blood tinged in nature.
Usually isolated ulcers are found in the larynx and trachea.
Ulcers can also be found on the turbinate bones and in the
guttural pouches and Eustachean tubes.
(ii) Pulmonary Glanders
Greyish, firm round encapsulated nodules like tubercles
of Mycobacterium tuberculosis infection are found in the lungs.
Diffuse pneumonic changes may be present in such lungs.
The nodules can be found subpleurally like small shots in
the lung parenchyma. The nodules are red at the earliest
stages but later show yellowish centres projecting above the
surrounding red zone of hyperaemia. Later, yellowish grey
nodules are formed in the lungs from such lesions. Capsules
are found in the old lesions. Pleurisy is found with a covering
of fibrinous material. Bronchial and thoracic lymph nodes
may show degenerative changes or abscesses.
Microscopically, the lesions in the lungs show alveoli filled
with leucocytes and the alveolar walls can be seen
disappearing or disintegrating at places. The degenerative
necrotic changes occur in the affected tissues with
appearance of nuclear chromatin as fragmented or scattered
particles (phenomenon of karyorrhexis). At peripheral areas
of such changes, red cells and fibrinous material are found
35
Advanced Pathology and Treatment of Diseases of Domestic Animals
36
Bacterial Diseases
Diagnosis
It is based on the following :
(i) Symptoms, lesions and detection and isolation of P.
mallei from glanders lesions, nasal discharge, ulceration,
chronic cough, submaxillary lymphadenitis. Cutaneous
lesions help diagnosis of glanders in the affected ani-
mals.
(ii) Cultures from the lesions of glanders and performance
of Strauss test in the guinea pigs. These tests help its
diagnosis.
Mallein Test
It is done by subcutaneous, intradermo-palpebral,
ophthalmic and cutaneous methods. Intradermo-palpebral
mallein test is the most reliable one. 0.1 ml of concentrated
mallein is injected into the dermis of the lower eyelid about a
one- fourth of inch below the lashes. A voluminous oedema
develops in the positive cases. The oedema is very hot and
painful one.
Direct smears are made from a farcy bud and stained
by Gram's method after fixation over heat. Films are
examined for the presence of slender Gram negative rods.
For cultural examination, pus is inoculated on to blood agar
plates and the plates are examined after 3 - 4 days for the
growth of organisms. Animal inoculation is done to diagnose
glanders. Pus or contaminated material or culture is
inoculated into two male guinea pigs subcutanceously and
examination of guinea pigs is done for the development of
orchitis daily after 3 days. Complement fixation test confirms
its diagnosis.
Treatment/Management
The treatment of glanders is very costly one and in the
case of confirmation of glanders cases, the authorities should
be informed immediately, in fact, there is no effective
37
Advanced Pathology and Treatment of Diseases of Domestic Animals
Leptospi rosis
A bacterial disease of man and animals caused by
organisms of the genus Leptospira icterohaemorrhagiae. L.
canicola are the organisms affecting dogs. L. pomona and L.
grippohJphosa (bovis) infect cattle and swine etc. Several other
serotypes of Leptospira spp. have also been identified. The
organisms may be single, helical, flexuous or hooked. They
may have also curved ends.
The important types of leptospirosis are canine
leptospirosis, bovine leptospirosis and procine leptospirosis.
Canine Leptospirosis
Leptospira interrogans and serotypes as L. canicola and L.
ictero/zaemorrhagiae infect dogs. The important signs in these
animals are fever, vomiting, icterus, dehydration, bloody
diarrhoea, increase in E.5.R., albuminuria and debility etc.
The dogs develop nephritis with uraemia. Leptospira can be
found in the kidneys of dogs. The dogs show dehydration
and uraemic breath is recognized in them by smell. Ureamic
smell can be marked in the stomach contents or mucosae of
the mouth at autopsy of fatal cases.
Pathology
Leptospirosis occurs in acute and subacute phases in
dogs.
38
Bacterial Diseases
Bovine Leptospirosis
Leptospiral organisms have been noted in bovines
showing signs of mastitis, fever, icterus, emaciation,
haemoglobinuria, abortion (usually late abortions i.e. abortion
after 6 months), occasional anaemia, transient leucopenia
and death. The principal serotype of leptospira in cattle is
L. interrogans serovar pomana. 30 % of the pregnant infected
cows abort dead foetuses with yellowish brown
discolouration of the placenta. Gelatinous oedema may be
seen between allantois.
Pathology
Lesions
Acute septicaemic or chronic nephritic form of
leptospirosis has been noticed in cattle. The lesions are similar
to those of dogs. Icterus and swollen and yellowish liver with
petechiae are found in acute septicaemic form. Haemolytic
anaemia is seen in the diseased cattle. Microscopically, portal
lymphocytic infiltration with splenic haemosiderosis and
centrilobular necrosis are noticed in the livers of the affected
cattle. Hepatic cells dissociation, cholangitis, congestion and
haemosiderosis of the spleen are marked in cattle affected
with the Grippotyphosa serotype. Swelling and
disorganization of the convoluted tubular epithelium are
associated with the presence of bile and haemoglobin in the
tubular lumina. Greyish white focal lesions are seen in the
kidneys and these foci are discrete and scattered through
out the cortex. Microscopically, the epithelial cells of the
tubules are granular and swollen with vacuolated
cytoplasm. Fragmentation of the cytoplasm and detatchment
of the cells can be seen in the tubules. Leucocytes like
lymphocytes and plasma cells can be found around the
tubules. Syncytial giant cells of the Langhan's type can also
be found. Leptospirae can be demonstrated in the epithelial
cells of tubular lumina by silver impregnation method.
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Porcine Leptospirosis
Several serotypes of leptospira affect the pigs. Serotype
P01110na is a common type producing disease in the pigs. These
organisms can produce subclinical infection or acute lesions
or changes like hepatitis and icterus. Subacute chronic
nephritis, abortion, still birth or birth of the weak piglets can
occur in the leptospiral infections. Tubular degeneration and
intense focal lymphocytic infiltration can be found in kidneys.
Tubular epithelium and lamina also show leptospirae. The
organisms can be found in the nodules of the lymphocytic
infiltrations. Leptospirae are observed in the urine for some
time. Still born pigs and aborted foetuses are found in the
last third of gestation. The foetuses may be macerated. Focal
necrosis is found in the livers of still born or dead foetuses.
Diagnosis
Fresh material is used for diagnosis. Blood examination
is made in early febrile or septicaemic stage of the disease.
Dark ground microscopy is adopted to identify the organisms.
The main methods of diagnosiS are as follows :
1. Direct Examination - Deposits of blood collected at
height of the fever or deposits of fresh urine is exam-
ined by dark ground microscopy to detect leptospirae.
2. Fresh Kidney or Liver Tissue is examined by (i) Dark
ground microscopy and (ii) by Levaditi's methods.
Smears of liver of kidneys can be fixed and stained by
Levaditi method to identify the leptospirae.
3. Biological Examination White guinea pigs are inocu-
lated intraperitoneally with preparations from urine,
kidney or liver tissue. They are observed for 3 weeks.
These animals usually die within 8 to 12 days. Jaundice
and haemorrhage in the lungs, serous membranes and
muscles are found in the dead guinea pigs. Direct ex-
amination of liver and kidneys reveals leptospirae.
4. Cultural Examination For this, fresh kidney or liver
42
Bacterial Diseases
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Nocardiosis
It is a bacterial infection caused by Nocardia asteroides
in man and animals. Bovine farcy is produced by it. In cattle,
bovine mastitis is also caused by Nocardia spp . Infection of
the bovine foetus and placenta causes abortions in bovines.
Pathology
Lungs, pleura and skin are affected in the dogs and
the organisms are found to localize at places like peritoneal
and pleural cavities, brain and different visceral organs.
Tangled indistinct colonies of the organisms surrounded by
necrotic cellular debris, purulent exudate and granulation
tissue are seen in the lesions caused by Nocardia spp. The
organisms are Gram positive and have also acid fast staining
properties. In bovine farcy, there is a chronic suppurative
granulomatous inflammation in skin lymphatics draining
lymph nodes in the infected limbs. Infection can metastasise
in the organs like lungs, liver, spleen and internal lymph
nodes. Extensive granulomatous lesions are noticed in
nocardia I mastitis in cattle.
DiagnOSis
Symptoms, lesions and isolation of the organisms from
the lesions establish the infection in animals. The nocardial
organisms are also detectable in the stained sections of the
lesions in the tissues like mammary glands.
Treatment/Management
Sodium iodide can be used parenterally. The affected
limbs of cattle may be disinfected with proper drugs to control
this disease.
Tuberculosis
It is a bacterial disease of man and animals caused by
Mycobacterium tuberculosis. Koch (1882) demonstrated t)1.e
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Microscopic Appearance
Proliferation of plasma cells and endothelioid cells is
noticed in the mucosae of the intestinal lesions. There are no
changes in the muscular coat of the intestine. There is a
, disappearance of the normal cells and glands of the intestine
with increasing number of proliferated plasma cells etc., in
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Trematment/Management
Johne's disease is caused by a bacterium which resists
treatment by antibiotics etc. However, streptomycin at the
rate of 25 mg/lb body weight can be given for long period to
have some recovery. Since there is no absolute recovery from
this disease, and as such, an advocacy of Johne's disease
treatment is not economical for farmers. However,
symptomatic treatment can be given to check diarrhoea by
giving drugs like streptomycin and furazolidone etc. In short,
there is no significant and effective drug to treat JD in the
infected animals for the sake of recovery.
Treatment is not an encouraging suggestion because
other animals may get infection from the sick infected
patients. This disease rapidly spreads through contaminated
water and feeds etc., with the faeces of infected animals.
The best way to control Johne's disease is to test the
animals for its diagnosis and all the animals found positive
for the test should be segregated from non-reactors and the
positive animals for JD can be disposed of by sending them
into concentration camps. The method followed in Bihar is
to send the positive reactors into segregation camps. The
excreta or faecal material of sick animal is preferably
incinerated. The animals can be protected from Johne's
disease by adopting vaccination programm~. Proper hygienic
conditions must be maintained in farms to prevent spread of
the condition from animals to animals. Identification and
segregation of JD cases and rigorous vaccination programme
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Treatment/Management :
B.efore administration of antimicrobial antibiotics, it is
better to find out the drug sensitivity of the organisms in
question.
Antibiotics like ampicillin, oriprim and chloramphenicol
are found to be quite useful. In severe cases, one can
administer intravenously ch1oramph~nicol at the dose rate
of 20 mg per kg body weight six hourly in the animals like
cattle, horse, sheep and pigs.
Nitrofurazone at the rate of 20 mg per kg body weight
can be given daily for 5 days by oral route.
Demulcent and astringent preparation and fluid therapy
can be given in view of factors like dehydration and
imbalances of electrolytes.
Vit. B complex can also be given to patients for quick
recovery. It is very important to have strict hygienic
precautions. The houses should be well ventilated and there
should not be overcrowding in animal sheds. As recovered
cases may exist as carriers, steps should be taken to eliminate
such animals. It is advisable to vaccinate the cows in their
late pregnancy for giving passive immunity to the calves.
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The passive immunity lasts about six weeks. The calves must
be allowed adequate amount of colostrum from their mother
to control salmonellosis in animals. Identification of carrier
animals, restricted movement of animals, clear water supply
hygenic disinfection of buildings, disposal of contaminated
material and vaccination of livestock are important
preventive measures to control salmonellosis
Actinomycosis
It is also called lumpy jaw in cattle which is caused by
Actinomyces bovis. Cattle and pigs are commonly affected by
these organisms but its infection is rare in sheep and goats.
The organisms seem to enter inside the body of the host
through injuries in the mucosae of the alimentary tract.
Colonies formed by A bovis are gritty to the touch on the cut
surfaces of the lesions in bones or other tissues in the infected
animals. The most marked feature of lumpy jaw is a rarefying
osteomyelitis of jaw bones. Abovis lives in the mouth of cattle
and can also invade and grow in the visceral organs of the
affected hosts.
Pathology
The lesions in the tissues of animals infected with A
bovis are of a granulomatous kind and the organisms are
found embedded in the granulation tissue or found as
granules in the pus of suppurative lesions. The swollen lesions
may discharge sticky honey like exudates containing minute
hard yellowish white granules called sulphur granules.
In cattle, the jaw bones and its surrounding structures
show the granulomatous lesion or a painless bony swelling
on the mandible and maxillae. Involvement of the tongue is
an occasional incidence. The bones, particularly, the maxillae
and soft structures like gums, palate and tongue show
actinomycotic lesions characterized by granulomatous
reaction. The swellings on the bones are hard and immovable.
Lymph nodes in the vicinity get infected by direct extension.
There is no metastasis via the lymphatic channels as seen in
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Actinobacillosis
It is a chroni c infecti ous diseas e caused by Actinobacillus
lignieresi (an inhabi tant of alimen tary tract) occurr ing mainl y
in cattle . The chara cteris tic lesion in this diseas e is a
granu lomat ous one which occurs in tongue or soft tissues of
head and intern al organs . The organi sm A. lignieresi invade s
the injure d areas in the mouth , phary nx or intesti nes etc., to
enter differ ent kinds of tissue s (espec ially soft tissues ) to
produ ce the lesions. The granul omato us growt h of the tissue
marke d by inflam mation and absces sation in this infecti on
contai ns foci of pus having clubs radiat ing from the centre s
of the masse s called rosettes. Microscopically, these rosette s
are surro unded by giant cells, epithe lioid cells and
neutro philes . The tumou r like mass in the tongu e produ ces
seriou s disabi lity and leads to emaci ation and inanit ion in
the affecte d anima ls. Lingu al actino bacillo sis is notice d in
solipe ds like horses . Granu lomato us lesion s develo p in the
lips and cheek s of sheep infect ed with this organ ism and
may extend into the mucou s memb rane of turbin ates and
soft tissues of head and neck.
Pathology
The lesion s occur in the tongue , pharyn x, gums, palate
and neighb ouring lymph nodes of the affecte d anima ls. Other
organ s like stoma ch, intesti nes, lungs, liver and skin etc., also
show its lesions. There is an occasi onal involv ement of the
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Pathology
The following are the main lesions produced by Cl.
perfringens type D :
(i) Petechial and ecchymotic haemorrhages are seen sub-
epicardially and sub-endocc;trdially. Such haemorrhages
are also present on the serosal surfaces of the intestine,
abdominal muscles, diaphragm and thymus.
(ii) Hydropericardium.
(iii) Hyperglycemia, glycosuria, distension of the rumen,
retilculum, abomasum and lower intestine by gas.
(iv) Mild catarrhal gastroenteritis and presence of bloody
intestinal contents.
(v) Distended gall bladder as a sign of digestive
dysfuncition.
(vi) Pulpy kidneys. The kidneys of dead animals examined
soon after death show a blotchy appearance and con-
gested cortex. The kidneys, later, disintegrate and break
down into a soft pulpy mass (called pulpy kidneys). This
characteristic feature is valuable in the autopsy of dead
animals conducted a few hours after death. But a cau-
tious opinion is required on a carcass of a long dead
animal.
(vii) Nervous lesions i.e., lesions in the central nervous sys-
tem like malacia of the basal ganglia, substantia nigra,
thalamus and demyelination in subcortical white mat-
ter and cerebral peuduncles are found.
Diagnosis
(1) Examination of the stained thin smears of intestinal
contents, any inflamed or ulcerated areas by Gram's
method to detect presence of clostridial organisms.
(2) Mouse toxin test and demonstration of epsilon toxin.
Mice are injected I/V 0.03 m1 of the supematant material
or mixture of the suspected contents of the intestine. These
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Lamb Dysentery
(Cl.perfringens type B entero toxaem ia)
It is an entero toxaeI ria caused by Cl. perfringens type B.
Lambs less then two weeks of age are affected. Foals and
calves also suffer from it. Lambs are reluct ant to suckle , lie
down and show signs of abdom inal pain. Faece s are
semifl uid, brown ish and may have blood. Recum bency , coma
and death within 24 hours after the onset of sympt oms are
notice d in the diseas ed anima ls.
Patho logy
Presen ce of haemo rrhagi c enteri tis with ulcera tion,
petech iae and ecchy moses are seen on serous surfac e of
epica rdium and endoc ardiu m. Exces sive amou nt of
perica rdial fluid is also found . In acute diseas e, the conten ts
are blood staine d. In short, the main lesion s are haemo rrhagi c
enterit is and ulcera tion.
Cl. perfringens type C Enterotoxaemia
It is a type of entrot oxaem ia caused by Cl. perfringens
type C in adult sheep and is known as struck marke d by
sudde n death. Haem orrhag ic entriti s and ulcera tive chang es
are found in the mucos ae of the duode num and jejunu m.
Presen ce of perito nitis with a large volum e of clear fluid is
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Black Leg
Synonyms, Black quarter, Langari (Hind i)
It is a highly fatal and febrile bacterial disease caused
by Clostridium chauvoei in ruminants (particularly cattle) and
characterized by swollen and emphysematous or crepitating
lesions of the muscles and subcutaneous tissues in some
region in the bodies such as the shoulder or the hind quarter
of the affected animals. The infectious myositis is the most
marked lesion. The organisms exist in the soils and are also
found in large numbers in the local muscle lesions and
exudates around such lesions. Young cattle on high plane of
nutrition between the age of six months to two years are
chiefly affected by this disease. Grazing infected animals
suffer from lameness, depression, anorexia and ruminal stasis
etc. Outbreaks of black quarter have been found in sheep of
all ages after lambing, docking and castration etc., and this
disease occurs as an wound infection in the sheep. Horses
are refractory. Ruminants in good nutritional state fall victims
to this infection. Cl. chauvoei are Gram positive and may have
central or subterminal spores. BQ patients die of severe
toxaemia and myonecrosis of skeletal or cardiac muscles.
Signs
It occurs as an acute disease usually with a fatal ending.
Animals are found dead without showing signs of illness.
There is a characteristic extension of the limbs a short time
after death of the affected animals. Lameness is noticed in
the sick animals. High temperature (106F), increased pulse
rate (lOO-120/min.) are seen in the sick animals. Sheep reveal
myositis, lameness and depression in the cases of Cl. chauvoei
infection.
Pathology
The local lesions occur mainly in some muscular parts
of the body and these lesions are found in the shoulders,
hin~ quarters, neck, back and loins etc. Lesions of black
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Pathology
There are no specific lesions in cases of tetanus. Patches
of hyperaemia are noticed in the spinal cord, medulla and
along the peripheral nerves. Only local wounds as generation
sites of tetanus toxins can be found in patients.
Diagnosis
It is based on the following:
(i) Symptoms (almost similar symptoms noticed in all ani-
mals) and detection of Gram positive rods with termi-
nal spherical spores in the smears prepared from the
wounds.
(ii) Isolation of the organisms in culture from pus or wound
discharge and identification of the isolate.
(ill) Inoculation of mice or guinea pigs with material from
the wound or culture of the organisms. In this test, the
control is one which has been given a prophylatic dose
of antitoxin.
Treatment/Management
The tetanus is a toxaemic condition. It is very difficult
to treat it after the appearance of the symptoms. Horses and
sheep respond poorly to treatment but treatment leads to
recovery in cattle.
For treating tetanus, the steps adopted are the following:
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Botulism
It is a toxaemia called food poisoning in man and animals
characterized by the symptom of paralysis. This disease in
poultry is known as limberneck. A soluble exotoxin
(neurotoxin) is produced by it and the disease produced is
not an infection but a state of intoxication. Botulism in man
has been caused by eating sausages or decomposed animals
products. This organism exists in the soil or nature as a
saprophyte Cl. botulinum B, C and D are associated food
poisoning in animals.
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(6) Trauma
Traumatic injury can lead to death of the foetus which
is expelled later.
(7) Mummified Foetus
A dead foetus is an irritating foreign substance in the
uterus and is soon expelled. Putrefactive or pathogenic
bacteria invade the dead foetus and the state of maternal
infection and septicaemia is produced. When the cervix is
closed, the uterine contents are sterile and the foetus
undergoes postmortem autolysis and may not get expelled.
The soft tissues are liquified and the liquid formed is absorbed
by the maternal blood or lymph. The foetus is, then, expelled
as a mass of bones with the shrunken or wrinkled skin. The
foetus looks like a dried or shrivelled mummy.
Hydatiform Mole
Small bits of chorion remain even attached to the
endometrium and derive nutrients. The cells of the chorionic
villi proliferate to produce an irregular mass of cystic
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Hydrops Amnii
It means an oedema of the amnion i.e., presence of two
much fluid in an amniotic cavity (upto 3 to 6 litres in mare
and cow). 6 to 15 litres of fluid can be found in the allantoic
cavity. Rotation of uterus or twist of the umbilical cord can
give rise to the state of hydrops amnii. Oedema arises on
account of the compression of the veins. This condition may
last in cow until parturition. The foetus may die and is then
expelled from the body.
Diseases or disorders of the uterus causing abortions
and placentitis (inflammation of placentitis) in the animals.
Placentitis is caused by several infectious agents. It ends
in abortion (expulsion of the foetus). Granulomatous
inflammation in the chorionic villi is caused by tuberculous
bacilli. The foetus dies before the development of the tubercles
on the chorion and it gets expelled by the uterus.
The following are the important diseases causing
abortions in the animals :
(1) Brucellosis
Brucella spp. causes placentitis. Bang's diseases is caused
by Br. abortus in cattle. In acute brucellosis, there is an
extensive formation of seropurulent exudate between the
chorion and endometrium in the interplacental areas
(chorionic leaves). This leads to separation of the surfaces
with subsequent expulsion or abortion. Chorion shows
inflammatory oedema and there is also infiltration of
reticuloendotheial cells, lymphocytes, plasma cells and
neutrophiles. Chorionic epithelium is rich in bacterium.
Necrosis extends in the allantochorion which undergoes
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Vibriosis
In this disease, there is placentitis caused by Vibrioi spp.
Necrosis and cellular infiltration are noticed in the placental
structures and there is formation of serofibrinous exudate in
the inter-placental areas. The smears prepared from
placentomes show Gram negative curved organisms. Foetus
is killed in vibriosis in ewes about one month before full term
and no permanent injuries are found in the foetus. The foetal
liver is discoloured and changes like necrosis and perivascular
infiltration of neutrophiles and eosinophiles are found.
Vaginitis, metritis, infertility and abortions are some
important findings in vibriosis.
Trichomoniasis
It is an important disease of cattle caused by Trichomonas
foetus. T. foetus infection spreads from infected vagina to'
uterus which show endometritis and placentitis. Copious
pyometra and a mild purulent reaction in the endometrium
is produced. In chronic cases of trichomoniasis, the foetal
membranes are retained usually following abortion during
the 1st half of gestation. The organisms are noticed in foetal
membranes.
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per cent of the infected cows abort only once. Affected bulls
show enlarged seminal vesicles, become sterile, and scrotum
may be swollen. Br. abrotus is a Gram negative, non acid
fast and non sporulating rod like organism.
Pathology
The main lesions are :
(1) Placentitis leading to abortion of the foetus and necrotic
granulomatous changes in the placenta.
(2) Discharge of yellowish brown slimy flocculent aborted
odourless discharge from the vagina in the aborted cases.
(3) A yellow necrotic appearance of the foetal membranes
or uterine cotyledous. The chorion becomes thick and
the intercotyledonary areas present a leather like wrin-
kling. Br. abrotus is found in the scrappings of such tis-
sues. The placenta may be dull or granular.
(4) Endometritis and retention of the foetal membrane.
(5) Presence of subacute or chronic inflammatory changes
in foci in the alveoli, inter-alveolar tissue and lactifer-
ous ducts of the infected mammary glands in the cattle
(6) Presence of orchitis, epididymitis and vesicullitis in the
infected bulls. Scrotal lymph nodes may show inflam-
matory changes.
(7) Synovitis and hygroma are also seen in the cattle.
(8) Phagocytic cells are attracted towards the Brucella or-
ganisms which are engulfed by them. The organisms
grow and multiply in the cytoplasm of these cells. Later,
epithelioid cells accumulate at these sites. The early mi-
croscopic lesion in the tissues infected with such organ-
isms is a tiny nodule of epithelioid cells surrounded by a
narrow zone of lymphocytes. Later, caseous necrosis can
occur at the centres of such lesions which may be sur-
rounded by a fibrous capsule formed at the periphery.
Neutrophiles and lymphocytes get attracted towards
such necrosed cells. Frank abscesses and nodules or frank
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Treatment/Management
The attempt for treating brucellosis in animals is usually
not made. But, however, sulpha drugs and antibiotics can
be used. Streptomycin and chloramphenicol can be given to
the cases of brucellosis. There can be intraperitoneal injection
of teteracycline in a single dose of 10 mg and it can be repeated
after 3 days.
For control of brucellosis, specific programme of testings
like serological agglutination test can be adopted and the
reactors can be segregated from healthy stock. Hygienic
methods are very much useful in controlling brucellosis. This
includes isolation and segregation of infected animals, proper
disposal of aborted foetuses, placenta and uterine discharges
etc. Cattle sheds and premises are thoroughly disinfected.
The infected animals can be isolated for thirty days and
retested.
For controlling brucellosis, vaccination of tlle animals
with Brucella abortus strain 19 living vaccine is quite useful.
This vaccine protects the healthy animal from contacting
infection in contaminated environment. For any control
programme, the method of isolating and disposing of infected
ones is very useful one. Calves getting infection after birth
remain infected till they are adult.
The vaccination of female calf can be done between 4 to
8 months of age. If adult cattle are vaccinated, abortion rate
comes down but this is not advisable. Bulls and pregnant
animals are not vaccinated. Cows vaccinated in the
advanced stage of pregnancy may abort. Reactions of
vaccination are seen in the form of high fever,anorexia,
decrease in milk yield and local reaction.
There is a single 5 m1 dose of Brucella abortus strain 19
which is given si c at the age of six months in calves. The
immunity conferred in calves is adequate one for five or more
lactations.
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Swine Erysipelas
It is a bacterial disease caused by Erysipelothrix
rhusiopathiae (E. insidosa) in pigs. The organisms are Gram
positive, non-sporing and non-motile. In less severe form of
the disease, rhomboid - shaped areas of erythema are seen
in the skin and the disease is so called as diamond skin disease.
Acute and chronic forms of the diseases in animals are
noticed. Septicaemia, skin discolouration, high fever (upto
108F) and gastroentritis are seen in the acute infections. The
chronic form is recognized by unthrifitines, endocarditis and
lameness due to arthritis. Human beings handling the
infected pigs show cutaneous lesions (erysipeloids) on the
hands, face or over the body. Pigs between 3 to 9 months of
age are affected and those over one year of age are resistant
to it. Ingestion of contaminated food or water produces
infection of the disease in pigs. Carrier stage is also seen in
the pigs. Incubation period varies from 1 to 5 days. This
organism also infects birds like turkeys, chickens, ducks and
geese etc.
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Signs
Pyrexia, inappetence, thirst, vomiting, conjunctivitis and
prostration are seen in the affected pigs. Bright or dark red
patches are present over the ears, neck, abdomen and inside
the thigh and forelegs. These patches get covered with scabs.
Tips of ears and tail are necrosed and sloughs of dead tissues
are cast off. Eighty per cent of the affected pigs die within 2
to 3 days.
2. Urticarial or Diamond Forms
This form of the disease is mild in nature. Loss of
appetite, dullness, stiffness, characteristic quadrangular, deep
red or purple patches or blotches with a paler centre on the
sides, back and buttock are noticed in the affected pigs. The
skin lesions vary from an inch to 2 inches in size. These
patches become swollen and covered with crusts which are
later thrown off. The skin lesions like diamond shaped'
plaques in infected pigs are considered pathognomonic.
(3) Chronic form (Cardiac form)
It is usually sequel to acute form or may arise
independently. Cardiac insufficiency from chronic valvular
endocarditis marked by vegetations on the cardiac valves in
pigs may cause death. Dyspnoea, stunted growth, coughing
and dark red discolouration of skin and extremities are quite
marked signs. Chronic venous congestion may be seen in
the lungs and livers of infected pigs. The lungs may be
odematous in such cases.
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Diagnosis
It is based on the lesions and demonstration and isolation
of organisms from cardiac and valvular or joint lesions. Acute
form of the disease is marked by early leucocytosis. Later,
leucopenia and monocytosis are noticed.
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Treatment I Management
In infected cases, treatment is not much effective. Long
acting penicillin (Penidure) can also be given.
Use of cortisone is also suggested in cases of arthritis. In
skin lesions on the bodies of pigs, topical applications (Himax
or beta dine lotion) can be given. Since this disease may appear
as an acute septicaemic form, use of an antipyretic and
supportive treatment may be applied. For the sake of
controlling swine erysipelas, it is advisable to adopt general
hygienic conditions and affected pigs should be isolated and
disposed of at the earliest. Eradication becomes a difficult
problem on account of existence of EnJsipelotlzrix rlzusiopntlzine
as soil borne bacterium. Animals with arthritis and
endocarditis must not be allowed to mix with healthy ones.
Steps should be taken to immunize animals against swine
erysipelas. Immune serum and virulent culture live vaccine
using a virulent stain of E. rhusiopathiae and inactivated
bacterium can also be given. The method followed in U.5.A.
for control of swine erysipelas is as follows:
(i) Use of the autogenous killed vaccine.
(ii) Use of immune serum simultaneous with virulent cul-
ture.
(ill) A virulent culture alone.
(iv) Immune serum alone.
Immunity is quite durable in pigs (aged 5 to 8 weeks).
The infected animals and new or fresh animals should be
kept in quarantine. New or fresh animals should be only
acceptable after, keeping them in the quarantine for about
fortnight and they should be vaccinated before being added
to the herds. Yearly vaccination is followed. There should a
thorough disinfection of the premises, utensil etc. Caustic
soda, carbolic acid or copper sulphate solution or even hot
house soap should be used as disinfectant.
The main symptoms and lesions of different bacterial
diseases in animals are given in table 10.
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3. Clostndillm Alphatoxin
An acute infectious 1. Based on
Blackquart cJzauvoei s, febrile disease of cattle symptoms
er (BQ) Affected betatoxins
and buffaloes and lesions and
Hi.ndi animals are (a DNase)
marked by swollen, isolation of Cl.
(langari) cattle and gammatoxi
painful emphysematous challvoci
bllffaloes n (a and crepitating lesions 2. Increase in
Sheep and hyaluronid
in the muscles of young the levels of
horses also ase) andanimals (4 months to 2 SGPT,SGOT
sllffer frOIll delatatoxin
years of age) or animals and lactic
it. (a in good condition The dehydrogenase
haemolysi
muscular lesions are dry myositis
n) and infiltrated with gas
bubbles. The affected
muscles emit rancid
odour and produce
crackling sound on
being pressed with
fingers. The
characteristic signs are
fever, lameness and
depression. Cardiac
muscles are pale and
friable and show
myositis in the dead
calves. Shearing
docking, castration and
lambing may cause out
breaks of BQ in sheep.
Quick development of
bloating and
putrefaction are also
noticed. In the cases of
bovines, body cavities
reveal the excess of
fluid.
4. Botulism Clostndlllm 1.A A serious intoxication in 1. Based on the
(food botulilllllll powerful animals and birds symptoms and
Anil1lals lleurotoxin following ingestion of isolation of
intoxicatio sllceptable: infected, spoiled or neurotoxins,
n or food Cattle, decomposed or spoiled the causative
poisioning) sheep and food. agent from gut
horses and contents of the
man.
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and animals recovered from the attack of one type are fully
susceptible to infection with another types. Cattle, pigs, sheep
and goats are susceptible to it. The disease is transmitted by
direct contact between healthy and diseased animals. Tissues
and discharges have high infectivity. Airborne droplets of
saliva or discharges from infected cases of FMD lead to spread
of infection. Animals in good fat conditions are more severely
affected than lean animals. Immune status of the population
affected also influences the severity of FMD outbreak among
cattle and other susceptible animals. In enzootic areas,
animals are partially immune. A malignant from of FMD
occurs in the young stock of cattle with severe heart damage
because of degenerative changes in the heart muscles. Several
calves die of cardiac lesions marked by subendocardial
yellowish streaks and foci with a high rate of mortality. 50%
glycerine in normal sline is a good preservative of this virus
in vesicle fluid or epithelium.
Signs
Inappetence, loss of condition, ulcers in the mouth and
feet and severe lameness are important symptoms of the
disease in animals. Superficial erosions of the feet can be seen
with loss of horny covering of the hoof. Degenerative lesions
develop in the myocardium of the infected young animals
(like calves).
Pathology
Necrotic lesions are found in the stratified epithelium of
the tongue, buccal mucosae, rumen and coronary bands or
teats. Vesiculation in such tissues occurs with loss of the
epithelium covering at a later stage. Ulcers may heal with
presence of very little scarring. There is an extensive
denudation of epithelial cells because of rupture of the vesicles
in the mucosa of tongue. The virus multiples in the stratum
germinativum of the epithelium which develops degenerative
changes (ballooning of the cells with swelling and pyknosis
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Table 12. DNA and RNA viruses their genetic and some
other features
Viruses Families Sites of Species/virus Genome
Viral types
replication
A.DNA
Viruses
(i) Double
stranded (ds)
DNA
Enveloped i. Poxviridae Cytoplasm Cow pox, small A linear
(ds) DNA (+/- (enveloped) pox, swine pox double
) and fowl fox . stranded
viruses DNA
molecule
(dsDNA)
ii. Nudes Pseudorabies do
Herpesviridae and Mareks
I(enveloped) diseases viruses
N onenvelope i. Adenoviridae do Bovine do
d (non- adenovirus and
enveloped) canine
adenovirus-l
(Rubarth
disease virus)
ii. do Bovine, canineCircular
Papovaviridae and Shope super
(non- papilloma double
enveloped) standed
viruses (rabbits)
DNA
molecule
Single Parvoviride do Feline A linear
stranded (ss) panleucopenia single DNA
DNA virus and molecule
Nonenvelope canine (ssDNA)
d (ss) DNA parvovirus-2
(+/-)
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(iii) do
molecu le
I(+ssRNA)
Astrovi ruses do
Astrovi ridae
(iv) Togavir idae do Equine do
(envelo ped) encepha litis
virus
(v) Flavivir idae do Hogcho lera do
virus and
Bovine and
viral
diarrho ea
virus
CaIcivi ridae do Vesicul ar do
(non-en veloped ) exanthe ma
virus of
swine
c. DNA and Hepadn avirida e Nucleus Hepatit is B A circular
RNA (non envelop ed) virsus double
reverse transcri (Orthoh epad strande d
bing virsues na virus) DNA
partly double Duck molecu le
strande d (ds) hepatiti s (ss/ds DNA)
DNA/p artly virus
single strande d (Avihep adna
(ss) DNA virus)
DNA
I(nonenv eloped)
Single strande d Retrovi ridae do Bovine Diploid linear
(ss) RNA or ss (envelo ped) leukaem ia Single
RNA (+) strande d
DNA step in virus, feline RNA
replicat ion (non leukaem ia molecu le
envelop ed) virus and
avian leucosis
virus
Note :- Subviral agents These are self replicating proteins with no known
nuclic
acid and are known as prions (PrP)-a protein associated with scrapie.
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Rinderpest
It is an acute contagious febrile disease caused by a
filterable virus known as rinderpest virus of the genus
Morbillivirus. Cattle and buffaloes are very susceptible to it
and the virus of cattle plague (RP) is present in all the
secretions and the excretions of the body. The viral position
is intraleucocytic in the blood and the virus is not available
in the serum of the patients. Many other ruminants (like
cattle and buffaloes) and pigs are also susceptible to
rinderpest. Food, water, utensils, hides etc., contaminated
with the virus of RP infect the healthy animals. The virus
penetrates through the alimentary tract to enter inside the
body. There is a natural transmission of disease by direct
contact between infected and susceptible animals. Incubation
period of RP varies from 3 to 9 days. R.P. runs a milder course
in sheep, goat and camels than in cattle but causes an
explosive out break in Asiatic countries.
Signs
Affected animals show fever (104 to 105F), profuse
diarrhoea and inflammation of mucous membranes in the
alimentary tract and small ulcers or erosions are found in its
mucosae. In India, RP is an enzootic disease and indigenous
cattle suffer from a mild course and the mortality in them is
also low, but RP is a serious disease in imported exotic cattle
(Le., foreign breeds or crossbred animals) and mortality in
them may exceed over 90 per cent. The disease in the infected
animals lasts over 2 to 9 days and these animals usually die.
Marked leucopenia is found is RP cases. The body
temperature rises to 105F or higher and remains high for 3
to 10 days before becoming normal. The peak of the fever in
RP reaches on the 3rd to 5th day but there is an abrupt drop
with the onset of diarrhoea. Lesions within the oral mucosa
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are seen on the 2nd or 3rd day of fever. The RP cases show
proshation, subnormal temperature and death after a course
of 6 to 12 days. High temperature, congested mucous
membranes, watering of the eyes, erosions in the mouth,
nasal discharge and diarrhoea are important signs to suspect
RP in a herd of cattle and buffaloes. The muzzle and mouth
are hot. Diarrhoea and arching of back are seen at the later
stages. Red spots can be seen on the inner aspects of the lips,
cheeks, gums, hard palate and the sides of the tongue.
Inflammatory changes are present in the papillae of the cheek
and the commissures of the mouth. Greyish yellow necrotic
areas replace the red spots on the mouth and nostrils and on
being sloughed off, these spots give rise to red ulcers which
may be deep or bleeding. The discharges from the mouth are
offensive and the breath is foetid. Weakness, exhaustion,
sunken eyes, fever and dehydration due to diarrhoea are very
important signs of RP patients. In epizootics of R.P., numerous
cases of rinderpest are seen all at once in many places but in
enzootic cases, the symptoms are less intense and are not so
violent as seen in the epizootics of this disease. Restlessness,
dryness of the muzzle and constipation can be seen in cattle
with the onset of rinderpest, but after a day or two, nasal
discharge, larcrimation, photophobia, depression, excessive
thirst, retarded rumination, anorexia and excessive salivation
(drooling of saliva) can be noticed in the rinderpest cases.
Lesions in the oral mucosa occur on the third day of infection
and severe diarrhoea develops at later stages.
Pathology
The bodies of the RP patients are dehydrated and
emaciated due to rapid loss of condition. Haemorrhages,
small papules or pustules can be found in the skin of udder
or scrotum ett\. The mucous membrane in the rectum is
swollen and congested and blood stained foetid faeces can
be found around the anal region. Conjunctivitis may be
present. Crusts of discoloured mucopurulent discharge are
found in the areas around eyes, nostrils and mouth and
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Treatment/Management
As applicable for all viral diseases, there is no specific
treatment of rinderpest in animals. However, symptomatic
treatment is given and in order to check diarrhoea and
superimposed infections (secondary complications),
administration of sulpha drugs and antibiotics is advisable.
In early cases of rinderpest, hyper-immune serum can be
given for the first few days (200 to 500 cc. of the immune
serum can be given s/ c or i/v). To check the acute
dehydration in the suffering animals, fluid therapy (5%
dextrose saline) at the dose rate of 50 to 100 mljkg body
weight can be given. In convalescent animals vit. B-complex
may be given for 5 to 7 days. Antipyretics can be given in the
early stage to lower down the high temperature in developing
rinderpest infection. There is no specific therapy for
rinclerpest but surveillance and annual vaccination with
tissue culture or other vaccine is advisable in the endemic
areas.
In order to control rinderpest in cattle, the steps followed
are as under :-
(i) There should be compulsory vaccination of all suscepti-
ble animals. Legislation can be passed for compulsory
vaccination.
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Pathology
The main lesions in the animals are generalized vascular
engorgement, oedematous lymph nodes, hydropericardium,
hydroperitoneum, oedema of the lymph nodes, rhinitis,
tracheitis and pulmonary emphysema. Fasciculitis,
tendovaginitis, cellulitis and focal necrosis in the muscles are
also found. The blood vessels are seen surrounded by oedema
and leucocytic infiltration and endothelial proliferation are
also present. Blood vessels can be thrombosed and necrotic
changes are found in their walls. Haemosiderosis of spleen
and lymph nodes can be found. Haemorrhages in the trachea
and heart muscles are seen. When the throat muscles are
involved, drenching can produce inhalation pneumonia due
to improper entry into trachea.
Diagnosis
It is based on the symptoms, lesions and isolation and
identification of the viral agent i.e., a vesiculovirus. Sudden
onset of illness (fever) and short course are characteristic signs
of the disease. Other diagnostic tests are blocking ELISA,
agargel immunodiffusion (AGID), serum neutralization and
fluorescent anti-body test etc.
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Treatment/Management
Ephemeral fever in cattle is a viral infection and no
specific treatment is given for this disease. The principle of
symptomatic palliative treatment is followed. Animals
suffering from constipation are given purgative or an enema.
Saline and diuretics may also be given. The sick animals
should have an access to plenty of water. The body of animal
is protected from cold and heat.
Analgesic (Novalgin) 10-20 rnl (i/m B.LD.) can be given
to animals to reduce temperature and stiffness of the body.
Antibiotics can also be given to check secondary infection in
the lungs and other organs. Non steroidal anti-inflammatory
drugs and calcium borogluconate in the cases of
hypocalcaemia are beneficial in the sick animals.
Pox Diseases (Variolae)
These diseases refer to an acute viral diseases affecting
man, animals and birds. The viruses of pock or pox diseases
are basically similar and belong to the family Poxviridae but
under natural conditions, different species of animals are
attacked by the pox viruses. All strains in man, animal or
birds produce cross immunity against each other but the fowl
pox and swine pox viruses are quite distinct from each other.
Typical lesions in the skin and mucous membranes are found
in these diseases.
The lesions are as follows :
1. Macules: These are small red spots like flea bites
which are formed in the roseola stage. This stage in noted
after an incubation period of 3-6 days in cattle.
2. Papules: These small spots (macules)are converted
into small red, swollen areas or nodules due to prolif-
eration of cells. These lesions are found in papular stage.
Raised papules have a zone of hyperaemia around their
bases.
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Cow POX
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Goat Pox
It resembles sheep pox and is a very contagious disease.
A viral dermatitis resembling goat pox occurs as an acute
fatal disease in the goats in India. Pneumonia developing in
goats is usually of a fatal type. The lesions in the skin develop
in the hairless parts like axillae, inside the thigh, nose, chick
and lips. In goat, the pox is less severe than in sheep.
Horse Pox
The virus of horse pox is similar to that of cow pox.
There is a cross immunity between the viruses of horse and
cow pox which transmit immunity to non-vaccinated human
beings. This fact led to development of vaccines for use in
the human beings.
Two kinds of horse pox are:
1. Skin Type :The flexor surfaces of joints in the lower
part of the legs are attacked by the virus. Very greasy
painful crusts are formed. Nodules, vesicles, pustules
and scabs are noticed on the back of the pastern. Sick
horses suffer from pain and lameness with formation of
nodules, vesicles and pustules etc.
2. Mouth Type: The lesions develop in the buccal mucous
membranes, lips, gums, tongue, nose and cheek etc. Fe-
ver is present in the sick horses. Drooling of saliva from
the mouth and loss of appetite are seen in the affected
horses. Death may occur in foals. Recovered horses get
lifelong immunity. Healing of lesions occur in 2-4 weeks.
Buffalo Pox
It is a contagious disease of water buffaloes caused by a
virus very similar to vaccinia virus. Lesions develop on the
teats and udders of milking buffaloes. Necrotic nodules are
formed in an experimental infection in mice.
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Viral Diseases
Swine Pox
1. Swine pox caused by swine pox virus of the genus
Suipoxvirus. Typical lesions appear on the ventral sur-
face of the abdomen of the affected pigs. A solid immu-
nity is a sequel to viral infection in swines. It can occur
as a sporadic or epizootic disease in pigs.
The virus affects usually the young pigs and the lesions
like eruptions of pox are found on skin, mouth and pharynx.
The lesions in the lungs cause a lot of mortalities. Black
pustular crusts are found on the abdomen, inside the thighs
and arms. Hamatopinus suis transmits the virus to pigs. Lesions
like vesicles and scabs heal and drop off at the end. Young
pigs are very susceptible to this virus which may be
transmitted by mosquitoes and flies etc. There is no cross
immunity with either cow pox vaccine or with other types
of swine pox.
Fowl Pox
A virus infection of birds characterized by development
of wart like nodules on the skin, a watery or mucopurulent
discharge from the eyes and nose and presence of diphtheritic
growths in the oral cavities. The poxes in all birds are closely
related. The causative agent is a fowl pox virus of the genus
Avipoxvirus. Skin lesions are noticed on combs, eyelids and
wattles of chickens. The lesions are marked as hyperplastic
epidermis, thick layers of keratin, oedema in dermis and
inclusions (called Boolinger bodies) in epithelial cells.
Treatment/Management
Since pock (pox) diseases are caused by viruses, only
palliative treatment is advisable. Antiseptic cream or a
stringent lotion can be used before milking. Control of the
pock disease is a very difficult task. However, milking
machine and udder cloth should be disinfected to avoid
spread of infection to healthy animals. For washing teats,
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Diagnosis
Its diagnosis is based on the symptoms, leucopenia and
lesions. The immunological type of the virus infecting the
horse is also identified. Other tests are detection of the virus
by culture and reverse transcriptase - polymerase chain
reaction (RTPCR) in blood or tissues.
Oedema of head and neck (especially supraorbitalfossae)
along with fever, hydrothorax and pulmonary oedema are
important signs of the disease. In cases, horses are found
dead, the diseases like piroplasmosis and anthrax should be
eliminated before diagnosing it as a cause of death. Agar gel
immunodiffusion (AGID), indirect fluorescent antibody (IF A),
complement fixation (CF), virus neutralization (VN) and
ELISA test are advisable to confirm its diagnosis.
Treatment/Management
African horse sickness is a viral disease with fever
respiratory and cardiac trouble. Symptomatic treatment in
view of the lesions can be given to horses. Antibiotics can be
administered to check bacterial infection. Cough electuary
and expectorants can also be given. Diruetics and cardiac
tonics are also given in cardiac form of African horse sickness.
Proper managemental care should be taken in stable and
freeze dried polyvalent attenuated vaccine can be used in
doses of 5ml by subcutaneous route. The horses are given
rest for three weeks and immunity caused by this vaccine
lasts a year. The horses should be protected from the bites of
insects and flies by providing fly proof stables. Vaccination
and reduction of exposure of horses to bites of insects are
very important steps to control African horse-sickness. Foals
(aged 3-4 months) are also vaccinated. An immunity
following vaccination lasts a year in the vaccinated horses.
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Equine Encephalomyelitis
It is a viral disease caused by the arthropod borne alpha
viruses affecting the central nervous system of the horses.
The virus belongs to the genus Alphavirus of the family
Togaviridae. The three immunologic ally distinct strains of
equine encephalomyelitis are:
1. Western strain or Western equine encephalitis virus.
2. Eastern strain or Eastern equine encephalitis virus.
3. Venezuelan strain or Venezuelan equine encephalitis
virus.
Mosquitoes are the main vectors of the virus of equine
encephalomyelitis. Human beings and other animals like pigs
are also affected by these viruses. Incubation period varies
from strain to strain as given below :
EEE - 1 to 3 days
WEE - 2 to 4 days
VEE- 1 to 6 days
Signs
Loss of awarness of the surroundings, tremors of
shoulders, facial muscles, aimless wandering, continuous
walking in circles, unresponsive to commands, mental
depression and collision with different objects are some of
the main signs of equine encephalomyelitis. Fever occurs at
the outset of the disease and paralysis of the various groups
of muscles occurs. The sick horses lie down and are unable
to stand and soon die or relapse into a state of somnolence.
Pathology
The neurons are attacked by the virus of equine
encephalomyelitis and are greatly damaged. Neurons show
degenerative or necrotic changes. There is a dissolution and
loss of tigroid substance (tigrolysis) and chromatin
(chromatolysis) in the neurons. The neurons, later, undergo
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Diagnosis
It is based on the symptoms and lesions. Fever, lameness,
swollen and hyperaemic conditions of the lips, cyanosis of
the tongue, ulceration in the mouth, foot lesions, stiffness
and nasal discharge etc. helps in its diagnosis. The petechiae
in the trapezius muscle is quite suggestive of the disease.
Suspected blood collected during febrile stage in sick sheep
is inoculated into healthy and immune sheep to confirm its
diagnosis. Virus isolation, detection of viral nucleic acid
complement fixation, AGID, ELISA and virus neutralization
(VN) tests are carried out to confirm the blue tongue infection
in sheep.
Treatment/Management
No specific treatment is available for blue tongue.
Antibiotics are used to control secondary bacterial infections.
Vitamin A (prepalin) or Vit.C (Redoxone) can be used as
supportive drugs. Egg-attenuated polyvalent virus vaccine
is used in South Africa and the immunity lasts in the sheep
for a year. Use fly repellants in the sheep dwellings and ,
control insect population by spraying. A void the risk of
exposure to control the insect vectors. Timely annual
vaccination in sheep is recommended and immunity develops
in 10-15 days following vaccination in sheep. Import of sheep
from infected countries or zones is prohibited to prevent
spread of blue tongue.
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Itchy Variety
There is an intense pruritus (itchiness) or scraping of
the skin with loss of flesh and abnormalities of gait. The sheep
get emaciated and show extreme debility and loss in weight.
There is an increasing weakness with fixed stare or listening
attitude and twitching of the ears and eye lids. Sheep are
restless and affected cases may live from weeks to months. 5
to 20 per cent of the affected sheep die. Sheep show
restlessness and a startled look and the pupils are dilated in
the sick sheep. The skin irritation commences in the lumbar
region and the affected sheep scratch the back with grinding
of the teeth.
Trotting Variety
Itchiness and scratching or scraping of the skin is seen.
Sheep trot with flopping ears. There is an emaciation in the
body. Nervous twitchings are seen in the sheep. Grinding of
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ratories.
Treatment/Management
Rabies is a disease which defies treatment, in case,
symptoms of rabies are evident in the animals. And as such,
preventive or timely steps are essential to ward off danger of
rabies infection. The sites of bite-wounds in the body of
animal should be washed with dettol solution or ordinary
soap solution within a few minutes i.e., just after the dog
bite. Wound can be very well washed with ordinary cloth
soap (i.e., 20% soft soap solution) without producing deep
scratches at the bite site. The site of dog bite must be washed
immediately. A solution of zephiran may be used to irrigate
the site of the wounds.
Vaccination against rabies cases showing symptoms is
useless, because the animal usually dies before onset of
immunity. If the human beings had been bitten by rabid
animals like dogs, these animals should not be deshoyed and
rather advised to be kept under observation in cages for 7 to
10 days. In positive case of rabies infection, animals invariable
die within 7 days. In animals, alike human beings, post
vaccination paralysis develops after vaccination with rabies
vaccine. The rabid cases may show unsteady gait and
hypersensitiveness. The symptoms may be treated with
cortisones, and sedatives. Immunity does not develop
effectively in the animals, which are under three months of
age (and in the case of cat under six month of age).However
there are vaccines which can be innoculated under three
months of age.
In order to protect the pet dogs and cats, it is always
advisable to keep them in chains. All unprotected street dogs
and cats (without owners) should be destroyed or sterilised
for reproduction, if possible. Such canines or felines pose
threat to human beings under the spell of rabies. To eradicate
rabies, practice of keeping animals in chains is highly
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rhagiaae**) with
NB Live normal
attenuated tempera
viruses* t-ure
Inactivated and free
antigens** from
Biocan-L parasitic
inj.(primovac inf-
cinated dogs estation
at the age of Megava
8/9 weeks) c-
revaccinated product
after 14 to 28 s of
days Nobi Indian
vac puppy immuno
DP I-ogicals
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Treatment/Management
There is no specific treatment of canine hepatitis. Steps
for prophylaxis and control are adopted. Recovered dogs
develop solid immunity. Symptomatic treatment can be given.
It is better to vaccinate the susceptible dogs. Supportive
treatment must be given in view of degenerative changes in
livers of the patients. Corneal opacity should be treated with
ointment containing corticosteroids. Combined distemper
hepatitis vaccine is available for controlling the canine
distemper and Rubarth disease. Important guide lines are
given for preparing vaccination schedule of canines.
(table 14). Rabies and leptospirosis are very serious zoonosis
for humans. Even the parainflunza and influnza viruses are
also pathogenic for humans. And as such, immunisation
against these viral infections is also included in vaccination
regimen. Multicomponent vaccines for providing
simultaneous immunisation against four or five viral diseases
like canine distemper, rabies, canine leptospirosis (its two
types), and viral hepatitis (Rubarth disease) are administered
to dogs
Canine Distemper (Abbreviation CD)
It is a viral disease caused by the species of the ~nus
Morbillivirus which affects dogs, ferret, fox and mink etc.
Most of the dogs may get infected with it before the
attainment of the age of one year. The virus of canine
distemper is present in the blood (in the initial febrile stage),
secretions and excretions etc.
Disease is transmitted from infected animals to healthy
ones through contaminated discharges, secretions, food or
air droplets etc. The secondary bacterial invader in canine
distemper is Brucella bronchiseptica- an organism usually
recovered from pneumonic lesions in CD cases.
Signs
Incubation period of canine distemper is about four
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the spleen . The embry os in the pregn ant swine s are de-
stroye d by the virus to produ ce the state of still birth.
Precap illarie s and capilla ries may be dilated or closed
in the infect ed organs . In the centra l nervo us system ,
periva scular accum ulatio n of lymph ocytes , mono nu-
clear cells and plasm a cells can be found in the Vircho w
Robin spaces . Haem orrhag es are seen in the brain and
spinal cord. Prolife rated microg lia can be presen t in the
white matter of the brain. The neuro ns show degen era-
tive or necrot ic chang es (Le., tigroly sis of the cytopl asm
and fragm entatio n of the nuclei). Neuro nopha gia and
satelli tosis can be seen in the grey masse s of the brain.
Intran uclear inclus ions have been notice d in the neu-
rons. These inclus ions are found to be homog enious and
acidop hilic in appea rance.
Diagnosis
It is based on the sympt oms, lesion s and isolati on of the
virus. Fluore scent antibo dy stainin g is done to confir m the
diagno sis. Diagn osis can also be made by inocu lation of
infect ed food or tissue filtrate into both health y suscep tible
pigs and pigs (controls) which have receiv ed a large dose of
antich olera immu ne serum . The unpro tected pigs die but the
immu nized ones show no chang e in their health . Antige n-
captur e ELISA and agar gel precip itation tests are helpfu l in
confir ming the diagno sis of the cases of swine fever.
Treatm ent/M anage ment
Since it is an acute septic aemic diseas e, sympt omati c
treatm ent can be given. Analg esics should be used to lower
down the tempe rature . Antibi otics are not effective becaus e
of the viral origin of the diseas e. To preve nt secon dary
bacter ial compl ication s, antibio tics can, howev er, be used.
In order to contro l swine fever, hyper immu ne sera and
vaccin es are used. 50 to 150 m1 serum can be given to sick
pigs. It is better to eradic ate swine fever by slaugh ter of all in
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Lesions
These are as follows:
(i) No typical gross lesions in the dead animals.
(ii) Extensive damage to local areas of skin and extensive
subcutaneous oedema in infected animals with a his-
tory of pruritus.
(iii) Reddened and abraded skin is seen in animals like cat-
tle. Excess fluid with the pericardial sac and subendo-
cardial haemorrhages in the carcasses.
(iv) Some splenomegaly, meningitis and excess pericardial
fluid in pigs. Foci of necrosis in livers of the aborted
foetuses.
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Diagnosis
It is based on symptoms, lesions and serological test etc.
Detection of virus in tissues and inclusion bodies in nervous
tissue and respiratory tract are carried out for diagnostic
confirmation. Serum- neutralization (SN) and ELISA are done
to confirm preudorobies in infected animals.
Treatment/Management
There is no specific treatment for pseudorabies. The
reproduction ratio is kept in view in control and eradication
of pseudorabies. Control and eradication of pseudorabies
depend on reproduction ratio (i.e., Ra-to average number of
new infections caused by one typical infection in animals. A
ratio greater than one (Ro>l) indicates the potentiality of
spread of pseudorabies. A ratio less than 1 indicates the end
of infection. Depopulation and repopulation of the herd is
practiced when the herd infection is above 50%. But
depopulation is Cl very extensive method. Subunit vaccines
which distinguish between infected and vaccinated pigs are
also used to control this disease. Infected swines are
segregated from healthy cattle herds.
Some important details about viral diseases and their
viral genomes are given in Table 16.
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Table 16. Viruses, their genetic features, signs and pathological changes (lesions) etc.
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
A DNA viruses Poxvlridae i.Orhtopox a. Vaccima Cow Humans Cow pox or Pock Diseases Pock 1. Based on the
Double stranded virus vIrus Buffaloes Pigs Variola vaccina diseases are called symptoms and
(ds) DNA viruses 1. (vaccinia) variolae. Pox is spread lesions in the
Poxviruses Pox by contact, abrasions affected
b. Cowpox C"ttle Cowpox
viruses (poc= etc. Dogs and cats do animals. 2.
vinls humans and
pustule) marked by not suffer from it. Detection of
elephants
a SIngle linear Human beings, cattle inclusion bodies
molecule of double c. Camel pox Camels Camel pox and sheep are affected in the epithelial
stranded (ds) DNA, virus by it. Cow pox lymph cells. 3.
replication and protects humans Eruptions on
assembly within the againstsrnallpox.The the skin in the
ii. Capri pox a. Sheep pox Sheep & goat Sheep pox
cytoplasm, releasing important stages of affected animals
VIrus virus
of enveloped pox are as follows (1) are considered
virions by budding Do b. Goat pox Goat & sheep Goat pox Roseola stage - characterishc
and non-enveloped virus Marked by small red lesions.
virions released by iii. Suipox c. Swmepox Pigs Swine pox spots and measles (2)
cell lysis and VIruS virus Papular stage - Small
formation of red areas formed in
intracytoplasnuc iv. AVlpox Fowl pox virus Fowls Fowl pox the skin due to
inclusions (called virus proliferation of
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
Guarnieri bodies epithelial cells. (3)
and Bollinger bodies Vesicular stage -
in cattle and fowls Accumulation of fluid
respectively). An in papules is the main
example of change. (4) Pustular
enveloped DNA stage - Conversion of
virus. lymph in vesicles into
a purulent material in
about 10 days. (5)
Desquamative stage-
Dessication of the
exudate in the
pustule, formation of
scabs and final
desquamation in
about 21 days
Fever, fall in the milk
yield and pox like
lesions are seen on the
teats and udders of
cows affected with
cow pox. leSIOns of
Ipox are noticed on the
Genetic Features Family/Sub Genus Species,! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
lips, muzzle and
around the nostrils in
calves. Cow pox VIrUS
is distinguishable
from the vanola and
vaccinia virus. Variola
causes small pox in
man but vaccinia (a
created laboratory
virus) is used for
immunising human
beings.
2.Herpesviruses A Herpesvmdae 51lidherpes or Pigs and A generalized Pseudorabies 1. It is based on
single molecule of Alpha herps- Porcine cattle disease and Pseudorabies is a the symptoms
linear double virinae (a sllb- herpes-vims 1 abortion in highly fa tal disease in of pruritus,
stranded (ds) DNA Ifamily) (5HV-l) pigs and swims. Pharyngeal lacerations, torn
i.e. a monopartJte Gam111aher pseudorabies paralysis, salivation areas in the
genome. An pesvirinae (a in second-dary mania, bellowing and skin of the sick
example of ds DNA subJamzly) hosts convulsions are animals and
enveloped virus noticed in cattle. intranuclear
Cattle die within 24 inclusions in the
hours. Intense itching, capillary
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
local irritation, endothelium
necrosis, hyperaemia and nerve cells.
and oedema in the 2. Experimental
skm. 2. Neuronal productIOn of
degeneration, mad itch in the
proliferation of susceptible
capsule and glial cells animals helps
3. Intranuclear its diagnosis in
inclusions in the the patients.
nerve cells, glial cells, It is based on
capillary endothelium signs and
and sarcolemmal lesions and
cells, etc. Lesions are acidophilic
noticed on flank or cytoplasmic
hind limbs of affected inclusions
cattle. Pigs do not D.3/0.5 micron
show pruritus, in diameter in
become prostrate and the affected
die in 12 to 24 hours. neurons
Suhcutaneous,
Bovine herpes- Cattle Infectious
virus 1. oedema,
pustular vulvo
haemorrhages on the
vagi-nitis and . .~.
, .u. .~
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
,
1 2 3 4 5 6 7 8
abortion oedema of the lungs
seen in the animals
Bovine herpes- Cattle & Bovine
virus 2. showing symptoms of
sheep mammalitis
pruritus. Malignant
Gal/id herpes Frls Infectious catarrhal fever (MCF)
viurs 1 larynggo Malignant catarrhal
tracheitis of fever (malignant
fowls catarrh) is marked by
Galid herpes Fowls Marek's fever, depression, loss
virus 2 disease of condition,
leucopenia,
(a) Alcela Cattle AHV-1 neutropenia and
phine herpes associated with weakness. Three
virus 1- AHV- bovine clinical types are (1)
1 malignant head and eye (2)
catarrhal fever abdominal and (3)
(b) Ovine Sheep Catarrhal cataneous forms.
herpesvirus 2 fever(MCF)of Catarrhal
(a sheep sheep inflammation of the
associated mucosae of the
MCFvirus) respiratory and
digestive tracts
leadinz_ to congestion
Genetic Features Family/Sub Genus Species,' Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 - 2 3 4 5 6 7 8
of the mucous
membranes and
formation of catarrhal
exudate, presence of
ulcers on the gums,
checks and dental
pad. Nodules of pea
size turning into
pustules and
ulcerated areas.
Swollen and closed
eyes with catarrhal
conjunctivitis.
Adenoviruses Adenaviridae (a)Aviadenavi (i) (Fowl Fowls Egg drop Bovine adenoviral It is based on
Double stranded rus adenovirus-l) syndrome infection Symptoms the symptoms,
(ds) DNA viruses in bovines arising lesions
linear A single from infection of inclusions in the
molecule of linear respiratory and enterocytes and
double stranded gastrointestinal tract. isolation and
(ds) genome. An Presence of oedema, identification of
example of non- haemorrhage around the adenovirus.
enveloped DNA the joints,
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
virus. keratoconjunctivitis,
lymphangitis, colic
and diarrhoea etc. are
seen in the infected
bovines. Both the
mobidity and
mortality are low in
the patients.
Haemorrhage,
oedema congestion,
and consolidation in
the lungs and
inclusions in the
enterocytes are other
changes in diseased
animals.
1 2 3 4 5 6 7 8
anorexia,intense
thirst, vomiting
diarrhoea abodorninal It is based on
pain high temperature signs lesions
with the onset of and basophilic
illness. The main intranucler
lesions are congested inclusions in the
and larged hepatocytes and
oedematous and endothelial
thickened gall cells.
bladder,haemorrhage
s in the lungs and
serosal surfaces,
characteristic
basophilic inclusion
bodies in hepatocytes
and endothelial cells.
Papovaviruses Papovaviridae 1. Polyoma (a) Murine Murines Murine The tumours look like
(papova-Pa= virus polyoma virus polyoma warts or papillary
papilloma, Po= growths and reveals a
polyoma and Va= fibrous core with a
vacuolating) A laver of stratified
Genetic Features Family/Sub Genus Species,' Animal Diseases Signs and Diagnosis
Family Virus Types Mfected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
single molecule of squamous epithelium
circular super coiled withhyper
dsDNAAn keratinisation in the
example of non- outer epithelial layer
enveloped DNA in the stained
virus.Transcription sections. Spontaneous
to form m RNA(+) regression noticed in
tumours after
2. PapIlloma (b) Papilloma Papillomas
virus viruses persistence of 4~
caused in
canines, ovines months.
and bovines
(c) Bovine pap- Bovines Cutaneous
. illoma virus 1-
2
fibro papilloma
1 2 3 4 5 6 7 8
rabbIt papilloma
papilloma
virus
Single stranded Parvoviridae Parvovirus 1. Canine Dogs Haemorrhagic Canine parvovirus (1) Based on the
DNA viruses parvovirus2 gastroenteritis infection (related to symptoms and
Parvoviridae A (Canine feline pan lesions and intra
linear single parvovirus aeukopenia) Two nuclear
stranded DNA, non- infection) forms of inclUSIOns in the
enveloped virus of haemorrhagic intestinal
negative or positive gastroententis are as epithehal cells.
Diarrhoea
sense. under. (i) Intestinal
form A very rare
2. Bovine infection in pups and
dogs of all ages
Calves affected and marked
by vomiting,
diarrhoea,
parvovlrus Still birth, dehydration, fever
abortion and and loss of condition.
foetal death Intestinal mucosae
3. Porcine
parvovirus congested. Nuclear
inclusions are found
ill me e p unellum or
\
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
intestinal mucosae.
Pigs (ii) Cardiac form seen
in puppies in the age
4. Feline pa- Members of Panleukopenia group of 2 to 6 weeks
nleukopenia Felidae and enteritiss Dyspnoea and
virus
respiratory distress
are the main signs.
Necrotic changes
along with infiltration
of mononuclear cells
are noticed in the
myocardium of the
dead pups.
B. DNA and RNA (a)Hepadnaviri 1.0rthohepad Hepatitis B Human Hepatitis
reverse transcribing dae na virus vzrus beings
viruses DNA
reverse transcribing
virus Ut is marked
by DNA reverse
transcribing features
and a single
molecule of circular
double stranded
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
DNA with a region
of a single stranded
DNA An example of
non-enveloped virus
2 Single stranded
RNA of positive
sense
2.Avihepa dna Duck Ducks Duck
virus hepatitis
(b) i.Alpha Avian leUCOSIs Fowls Avian leucosis
Retrovlridae retrovirus virus Cattle . and Rous
sarcoma
li. Delta Bovine Bovine
retrovirus leUCOSIs virus leukemia
C. RNA viruses Paramyxovmd Rinderpest Cattle and 1. It is based on
Single standed (ss) ae buffaloes of all ages the symptoms
RNA virus with and swines are and lesions 2.
negative sense affected by RP VIruS. Challenge or
genome A Inoculation of
immune and
"~_""j a"u",u~
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Mfected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
Paramyxoviruses contagious highly with suspected
febrile disease (1080 F) material from
with mortality upto RP cases. ELISA
Paramoyxovlru Morbilli virus i Rinderpest Buffalo of all Rinderpest 90%. Related to the and AGID agar
ses virus ages, cattle virus-causing peste gel immunodif-
and wild des petitis ruminants. fusion tests are
ruminan Hill cattle more performed to
ts. susceptible to RP confirm the
ii. Peste des Goats and Peste des virus than the plains diagnosis of RP.
petitis less often petitis cattle. Excessive Canine
ruminants sheep ruminants (a salivation with nasal parainfluenza is
virus (related disease alike discharge. A marked by
toRPandCD RP) generalised disease cough, nasal
virus) with greyish white discharge, retch,
elevations like rhinitis,
deposits of bran tracheitis,
Single standed RNA Paramyxovirin Rubula virus iii. Canine Dogs Canine (small discrete bronchitis and
with non-segmented ae(sub famIly) distemper distemper necrotic areas on the bronchopneumo
negative (-) sense virus i.New lips, gums and dental nia. These
genome. castle disease pad of the sick changes and
Ranikhet
virus or Avian Fowls aninlllls). Erosions or viral
paramyxo disease
ulcers seen on the identification
VIruS 1 i.e
-r
Genetic Features Family/Sub Genus Specie Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
PM V-I Abomasal and diagnosis of this
intestinal mucosae disease.
ll. Canine Dogs Parainfluensis
congested and
parainjluenza (Kennel cough
ulcerated or eroded
virus-2 SV-5 syndrome)
(erosions or ulcers
formed). Linear
brightened stripes in
the colonic and rectal
mucosae called Zerba
markings are the
characteristic lesions
of RP. Necroses or
ulcerated areas are
noticed in the Peyer's
patches of the
intestinal mucosae.
High fever seen
round about 3rd day
of infection followed
by fall in temperature,
diarrhoea and faecal
matter coated with
mucus or blood are
Genetic Features Family/Sub Genus Species,' Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
strong indIcations of
RP infection.
Rhabdoviruses(Rha RlJabdovlridae The main All waml Rabies 1. It is based on
bdo=rod) Genus types blooded A dIsease marked by the symptoms
Enveloped negative are animals lesIOns in the nervous and presence of
(-), non segmented system of all warm Negn bodies in
single stranded blooded animals and the neurons of
RNA genome caused by the bItes of hippocampus
infected rabid major in
1.Lyssa VIruS Rabies VIIUS e.g. Cattle Rabies
aninlals. ReservOirs of carnivores and
and horses
rabies are wolves, in the neurons
etc
mongooses, bats of cerebellum of
2. Vesiculoviru Vesiculostoma Horse, cattle Vesiculo (vampire) and bovines.2.
s litis virus and swines stomatitis squirills etc. The seller's stain is
3.EpiJemerovir Bovine Bovine furious and dumb used to stain the
Cattle
us ephemeral ephemeral forms are its two mclusion bodies
fover VIruS fever (an kmds of rabies. in to neurons of
Arthopod Tendency to attack, mfected brains.
borne enzootic mania, paralysis of 3. A suspected
disease in the tongue and limbs, aninlal of rabies
tropical excessIVe salivation dies within a
countries. are important signs of week in pOSItive
Genetic Features Family/Sub Genus Species,! Animal Diseases Signs and Diagnosis
Family Vh-us Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
furious rabies. Some cases, when it is
50 passages of the kept in cages
rabies virus through InclUSIOn bodIes
rabbits turns it into a are usually
fixed virus capable to noticed in such
produce symptoms of cases when
rabies and paralysIs sufficient time is
as early as 30 days in given for
the rabbits consequent formation of
to inoculation of such inclusions.
fixed virus. Street Immunofluoresc
virus is noticed in the ent antibody
wild carnivores and testing on the
street dogs etc. Rabies bram material
virus is present in the to confirm its
milk, fetus and many diagnosis
organs of the infected
cases. The dumb form
of rabies is marked by
paralysis of the
muscles of head and
neck and mandible
causing inability to
Genetic Features Family/Sub Genus SpecieIV' Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
swallow water or
chew food given to
the patients. Broken
teeth, foreign bodies
in the stomach,
encephalitis,
proliferation of
capsule cells around
the ganglion or glial
cells and inclusion
bodies (called Negri
bodies) in the neurons
are pathognomonic
lesions of rabies
infection in animals.
Double stranded 1. Reovindae Orbivirus (a) Blue Sheep, cattle Bluetongue It is a 1. It is based on
(ds) non-enveloped tongue virus and deer highly febrile viral symptoms and
RNA viruses (BTV) 1-25 disease of sheep lesions 2.
Reoviruses Marked serotypes of transmitted by Isolation and
by segmented BTV recorded) Culicoides. identification of
genome, linear (b) African Horse, African horse Inflammatory changes Blue tongue
double stranded horse sickness donkey mules sickness (an are noticed in the virus (BTV) 3.
Genetic Features Family/Sub Genus Species! Animal Diseases Signs and Diagnosis
Family Virus Types Mfected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
RNA VIrus (AH5V) and zebras Arthopod mucous membrane of ELISA and Agar
Birnaviridae a. Non- borne lips, tongue, cheeks gel
enevloped infectious and gums i.e. immunodiffusio
bisegmented ds disease) occurrence of chelitis, n test (AGID) It
RNA virus Single (c) Rota virus Almost all stomatitis, rhinitis and is based on the
Enteritis
stranded (ss) RNA enteritis etc. Swollen signs and
animals
enveloped viruses oedematous and lesions and
Coronaviruses Orthoreo Avian Chickens, Viral arthritis cyanotic tongue, isolation of
Marked by a single VIruS reoviruses-1- turkeys and of fowls,CRD sloughing of tissues immunilogically
molecule of positive 11 geese and noticed in the oral distinguished
(+) sense RNA myocarditis mucosae. Congested viral types.
genome. An patches in the
enveloped virus 2.Birnaviridae AVlbirna virus Infectious Fowls Infectious mucosae of stomach
Togaviruses bursal disease bursal disease and intestine and
(Toga=cloac) Linear virus inflammatory changes
single stranded (ss) 1. Coronavirida Coronavirus Avian Fowls Avian in the coronary band
RNA (+) sense e infectious infectious of the foot. African
genome marked by bronchitis bronchitis horse sickness It is a
direct transcription. virus (at least virus febrile (105 F) viral
0
1 2 3 4 5 6 7 8
Alphavirus Camne Dogs Enteritis midges etc. Mortality
coronavirus (a) upto 90%. Dikkop and
Dunkop (pulmonary)
are the two forms of
Alphavlrus Canine Dogs Enteritis (u) african horse sickness.
coronavlrus Dikkop (i.e. thick or
2. Togaviridae (a) Eastern Horse Eastern equine cardiac form) is
equine encephalo marked by oedema of
encephala myelitis the head, neck and
myelitiS VIruS face,
hydropericardium
(b) Western (b) Western and degenerative
equine equine changes in the
encephalamyelz encephalomyel myocardium In
lis virus itis Dunkop (pulmonary
form), hydrothorax,
oedema of lungs,
(c)Venezllelan (c)Venezuelan
dyspnoea and
equme equine
discharges from the
encephalomyeli encephalomyel
nose are the main
tis virus itis
changes.
Genetic Features Family/Sub Genus Specie!, Animal' Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
Astroviridae A Astroviridae Astrovirus Several Self limiting
single molecule of animal gastro enteritis
linear single species
stranded RNA virus
having positive (+)
sense genome
Picornaviruses Picomaviridae I.Enterovirus 1. Swine Pigs Swine Foot and mouth (1) It is Based on
Direct transcription vesicular vesicular disease It is a febrile the symptoms
A single molecule of disease virus disease viral disease of many and lesions (2)
linear single cloven footed Injection of the
stranded (ss) RNA, animals. Excessive suscepted
positive sense and a 2.Avian Chicken Avian salivation, anorexia material in to
non-enveloped virus entroviruses s Ducks and encephalomyel due to mouth sore, guinea pigs (3)
turkeys itis lameness. Severe Performance of
3.Poliovirus Man Hepatatis depression and the compliment
1,[[ and III Poliomyelitis sudden death in fixation test.
calves arising from
Aphthovirus Foot and Cattle, sheep, Foot- and- mycardial
mouth disease goats pigs mouth disease degenerahve changes
virus The and wild The characteristic
viral types are rumints lesion is an aphthous
0, A, C,SAT- or vesicle formation.
1,SAT-2,
Genetic Features Family/Sub Genus Specie!, Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
SAT-3and A vesicle is a
Asia-l circumscribed cavity
Hepata VIruS Hepatatis A Man Hepatatis containing fluid. A
virus Aphthae are noticed
on lips, dorsum of
Calavmdae Ca/civirus Pigs Enteritis tongue, palate and in
Vesicular Pigs Vesicular the skin near the
Calciviruses Direct exanthema lesions in coronary band, teat,
transcription A virus epithelial cells vulva and udder.
single molecule of of lips, tongue, Ballooning
linear single nostrils and degenerative changes
stranded (ss) RNA. snouts. in epithelial cells in
Non enveloped the form of pyknosis,
Mucosal
Flaviviruses Direct fragmentation leading
disease to appearance of
transcription A
single molecule of Flaviviridae i.Pestivirus Bovine viral Cattle and vesicles (aphthae) on
linear single dlarrhea virus calves the lips and tongue
stranded RNA, etc. Degenerative
Swmefever/ Pig Hog cholera
positive sense changes in the
Hog cholera (Swine fever)
genome sensitive laminae of
virus
the foot causes
1l.Flavivirus Japanese Swine man Abortion and shedding of the hoof
e~cephalitis and birds encephalitis in cattle or claws in
Genetic Features Family/Sub Genus Specie"" Animal Diseases Signs and Diagnosis
Family Virus Types Mfected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
VIruS sheep and goat.
Mosquitoes act
as its vectors
Bronaviridae Single Bornaviridae Bornavlrus Borna disease Horses Borna disease
stranded RNA with virus
negative (-) sense
genome.
1 2 3 4 5 6 7 8
ViruS C swinesand fowl plague)
fowls.
Bunyaviruses Single Bunyaviridae Bunya virus Bunyawera Sheep and Arthrogryposis
stranded negative (-) virus cattle and
genseRNA hydranenceph
segmented genome aly
Nairovirus Nairobi sheep Sheep and Nairobi sheep Marked by acute
disease virus goats disease haemorrhagic
gastroentrltis
Phlebovirus Rift valley Sheep cattle Rift valley
ltevervlrus and buffaloes fever
NB Prions (self Cattle (i) Bovine a.Marked by neuronal
replicating Sheep and spongy form degeneration
infectious or rogue occasionally encaphalopath b.Spongiform
proteins with no goat y (ii) degeneration ID the
nucleic acid) Scrapie grey matter of brain,
Aminoacid astrological
sequences of many proliferation and
prions or variants hypertrophy are the
are known but marked changes in
information about bovine spongiform
Genetic Features Family/Sub Genus Specie!, Animal Diseases Signs and Diagnosis
Family Virus Types Affected caused Pathological Changes
Humans etc.
1 2 3 4 5 6 7 8
their families, encphlopathy. a.
genetics and species Neuronal vacuolation
is lacking. and degeneration
with astrocytic
hypertrophy,
hyperplasia,
neuronophagia and
perivascular cuffing
are the marked
lesions in the cases of
5(.Tapie.
Advanced Pathology and Treatment of Diseases of Domestic Animals
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Viral Diseases
199
Advanced Pathology and Treatment of Diseases of Domestic Animals
200
Viral Diseases
201
Advanced Pathology and Treatment of Diseases of Domestic Animals
202
Chapter 4
Protozoan Diseases
Babesiosis (Piroplasmosis)
It is a febrile protozoan disease caused by
intraerthrocytic organisms of the genus Babesia spp. or
piroplasms capable to multiply into two or four by means of
binary fusion inside the red blood cells of the hosts like cattle
and buffaloes etc. Pear shaped structures are formed by the
causative prototozoa inside the erythrocytes. These forms are
pathogenic asexual structures and are transmitted by blood
sucking ticks. A piroplasm or a typical babesia consists of
three parts :
(i) A thin envelope containing protoplasm.
(ii) A dot of chromatin.
(iii) A vacuole.
The newly divided forms of piroplasms are held together
be means of stalk and the affected red cells, later, disintegrate
releasing haemoglobin into circulation. Excessive amount of
haemoglobin so formed passes into urine through glomeruli
to give rise to a condition of haemolytic jaundice and
haemoglobinuria. These protozoa attack healthy red cells and
cause them to disintegrate. In B. callis infection, the division
or subdivisions of parasites give rise to more than two
piroplasms inside the red cells with the result of crowding
inside their bodies. Such red cells, later, disintegrate or get
haemolysed to produce anaemia, haemoglobinuria and
jaundice etc. The reticuloendothelial cells in the liver, spleen
and bone narrow dispose of the excess of released
haemoglobin from lysed red cells. But in the case of massive
destruction of red cells, excessive haemoglobin formed in the
203
Advanced PathologlJ and Treatment of Diseases of Domestic Animals
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Protozoan Diseases
205
Advanced Pathology and Treatment of Diseases of Domestic Animals
206
Protozoan Diseases
207
Advanced Pathology and Treatment of Diseases of Domestic Animals
209
Advanced Pathology and Treatment of Diseases of Domestic Animals
210
Protozoan Diseases
211
Advanced Pathology and Treatment of Diseases of Domestic Animals
213
Advanced Pathology and Treatment of Diseases of Domes tic Animals
Treatment/Management
There is no suitable or reliable drug for absolute
treatment of theileriasis. However, drugs like Berenil, steclin
and supportive medicine can be given to sick animals. Berenil
is to be given @ 0.8 to 1.6 gm/lOO kg. body weight I/M to
cattle. Recently, a drug called Butalex has been found to be a
specific drug of choice for treating theileriasis. Tetracyclines
show moderate efficacy in sick cattle.
Supportive therapy by way of administration of
haematinics, B-complex and inferon etc., may be used. Blood
transfusion can also be done. 10 ml of 3.8% soln. of sodium
citrate is added to 100 ml of blood for the sake of transfusion
through i/v routes. 5% dextrose saline may also be given
through i/ v in sick animals. Halofuginonelactate and
parvaquone are found to give good results in the cases of
theileriasis.
The disease can be controlled by destroying the ticks by
hand picking or application of acricide externally. Recovery
of animals is followed by a solid immunity in them.
Surra (Hindi for Rotten)lTrypanosomiasis
It is a protozoan disease of cattle, buffaloes, horses,
elephants, donkeys, mules and dogs etc., and is caused by
TnJpanosoma evansi. Tabinidae (Tabnid files) spread T.evansi
infection mechanically to healthy animals from diseased ones
by their bites. Ruminants like cattle exist mainly as reservoirs.
Surra is an endemic disease of cattle, horses and camels etc.
in tropical countries like India.
Signs
There is a loss of glycogen from the liver and muscles in
the affected anim&ls due to its rapid utilization by the T.evansi
and the animals become weak and emaciated inspite of good
appetite. In horses, emaciation and oedema are important
signs .of the disease. Urticarial plaques are seen on the neck
214
Protozoan Diseases
215
Advanced Pathology and Treatment of Diseases of Domestic Animals
216
Protozoan Diseases
There are many drugs which were used in the past but
now-a-days triquine, triboxine and trypnil etc. are found to
be more effective. Since surra is a disease of cattle, buffalo
and horse etc., it is very important to recommend supportive
therapy in such cases. Haematinics, B-complex inj. and 5%
dextrose solution can be given to sick animals.
In severely anaemic patients, blood transfusion can be
done. Blood transfusion can be done after having
compatibility report or necessary precautions in view about
the blood groups of the donors and recipients to avoid
transfusion reactions. Berenil (diminazene and
quinapyramine sulphate) are also effective in treating surra
cases.
217
Advanced Pathologlf and Treatment of Diseases of Domestic Animals
infection and from six weeks to 3 months after the bite of the
infected ticks. There is dullness, emaciation, pallor of the
tissues depression and loss of condition in the affected
animals. Anaemia is a very important feature of this disease
and red cells count drop to one to 2 millions per cu. mm. and
the blood becomes thin and watery Anisocytosis, punctate
basophilia, polychromasia and nucleated red cells are noticed
in the blood films. There is usually no haemoglobinuria and
jaundice may be noticed in the later stages. Death in the
imported cattle rises to 80%. The affected animals show rise
in temperature upto 107P. The temperature may become
normal or subnormal before the death of the animals.
Breathing is accelerated and animals show depraved
appetite, exhaustion and lack of rumination or appetite. The
skin and mucous membranes become yellow and anaemic.
There is a presence of stiff and unsteady gait in the sick
animals. There is also no change in the colour of urine.
Constipation can be noticed in them and the animals pass
blood stained faeces covered with mucus. Death occurs within
24 hours in the acute cases. Chronic cases are marked by
anaemia. There is very slow recovery and also practically no
mortality in enzootic areas.
Pathology
There is an emaciation and icterus in the body. The
lymph nodes are enlarged and oedematous. Enlargement of
heart with marked petechial haemorrhages is noticed. The
blood is thin and watery and does not stain the fingers. There
is presence of gastroenteritis and the lungs are anaemic with
changes like emphysema. The liver is enlarged, brownish
yellow or deep orange in colour and saturated with bile and
the gall-bladder is distended with dark green bile. The spleen
is enlarged and has a soft pulp. A yellowish discolouration
may be found throughout the viscera. Excess of fluid is found
in the body cavities. The kidneys are congested and
myocardial haemorrhages are seen in the dead animals.
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Treatment/Management
Since coccidiosis is a selflimiting disease, proper
administration of drugs successfully controls outbreaks. The
infection of birds with coccidia needs to be checked by all
means. The drugs to be used to treat coccidiosis, are
sulphadimidine, thalazole and nitrofuran etc., in domestic
animals and birds e.g., cattle, calves, sheep and goats and
poultry. It is worthwhile to mention that sulpha drug is a
drug of choice to treat coccidiosis in the animals. Amprosol
20% @ 30 gm in 100 litre water is very useful in coccidiosis
and can be given to minimize dehydration and anaemia etc.
Blood transfusion in young stock may also be advisable. The
severe straining in coccidiosis can be reduced by giving
intestinal sedatives or epidural anaesthesia. Injection of
prep aline forte and B-complex with liver extract can be
recommended in large animals.
Toxoplasmosis
Toxoplasmosis is an infectious disease of domesticated
and wild animals, which is caused by Toxoplasma gondi. It is
a universal systemic coccidian of the suborder Eimeriilla. T.
gondi is a specific parasite of the members of the family
Felidae,. which are defiinitive hosts of T. gOlldi.
Three infective stages are :
Infective stages Intermediate hosts (farm animals)
1. Tachyzoites Multiplying forms in the body of
intermediate hosts.
2. Bradyzoites Forms present in the tissue cysts in
intermediate hosts
3. Oocysts (containing Forms present in the faeces of
sporozoites) intermediate hosts.
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Diagnosis
Treatment/Management
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Chapter 5
Parasitic Diseases
FASCIOLASIS (Distomiasis)
Distomiasis is caused by species of the families like
Fasciolidae and Dicrocoelidae. The important species of these
families are :
(i) Fasciola gigantica (common liver fluke in India).
(ii) Fasciola lzepatica (common liver fluke).
(iii) Fascioloides magna (large liver fluke).
(iv) Dicrocoelium dendriticum (lancet fluke).
Fasciola hepatic a is noticed in the liver, bile ducts and
gall bladder in cattle and sheep and animals like, goat, horse,
dog, deer and pig etc., may also be parasitised. Ova are laid
by this parasite in the biliary passages and they reach the
intestine with the biliary secretions to be finally expelled with
the faeces. The micracidium emerges from these ova and the
cercariae (motile forms) escape after many developmental
stages of the miracidium in the body of snails. These cercariae
encyst on the tips or blades of the grasses as metacercariae
which on being grazed with grass or ingested by the suitable
hosts like cattle, reach mature stages finally in the biliary
passages of the liver.
Signs
The main signs of fascioliasis are:
(i) Weakness, oedema, anaemia (paleness of the mucous
membrane), icterus and emaciation.
(ii) Diarrhoea, constipation and oedema in the
intermandibular spaces (called bottle jaw in parasitic
diseases).
(ill) Abortion in the pregnant animals. In cattle, the faeces
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Treatment/Management
The same steps as given under amphistomiasis are
followed. Certain details about patent preparation or dosage
schedule of different diseases (including parasitic diseases
are given in table 37 and 39.
Amphistomiasis (Paramphistomiasis)
The trematodes of the family Paramphistomidae set up a
pathological state known as amphistomiasis (stomach fluke
disease) in domestic animals like cattle, sheep and goats etc.
Paramphistomes are found in the rumen, reticulum and
intestines of the ruminants and immature forms of these
trematodes are very pathogenic in many kinds of ruminants.
The trematodes of the family are also found in pigs, equidae
and human beings. Paramphistomum cen}i is a conical pear
shaped fluke and is red in colour. This fluke is found in cattle,
sheep, goats and buffalo etc., Cotylophoron cotylophorom is
noticed in the rumen and reticulum of sheep, goat and cattle.
Calicophron calicopllOrum is a parasite of sheep and cattle and
found in their rumen and reticulum. Gigantacohjle explal1atU11l
is noticed in the bile ducts, gall bladder and duodenum of
buffalo and cattle. The cattle are less commonly infected with
the flukes.
Pathology
Liberated micracidia from the eggs enter the bodies of
suitable snails in which they undergo different developmental
stages Le., formation of sporocysts and rediae inside the body
of the snails. The rediae release the cercariae inside the body
of the snails in which they remain for some time for the sake
of maturation. After they have undergone maturation inside
the snails, the mature cercariae which are dark brown are
released and the liberated cercariae are immature
amphistomes (highly pathogenic forms for animals). These
amphistomes undergo encystment on plants in the form of
metacercariae which are dark or black in colour. The
~
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examina tions.
The drugs used for this disease are :
(i) Carbon tetrachloride can be used to treat such cases.
One should be careful in avoiding its use in debilitated
animals.
(ii) Distodin tab., fasinex tab, Terramaffin tab. Talzone F.
etc., can be used.
(ill) Trodex inj. can be used si c in positive cases.
(iv) Fluid therapy 5 to 10% Dextrose liver extract. Some of
the drugs acting on the guts can be used.
(v) To improve the general debilitating conditions, calboral
or mifex can be used.
Oxyc1ozanide, hexachlorophene, nic10samide are also
used to treat the cases of amphistomiasis in domestic animals.
Ancylostomiasis (Hook Worm Disease)
Hookworms are parasites of cosmopolitan distribution
and produce this disease in man and animals. However,
horses do not suffer from hookworms. The important
hookworms are :
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Trichostrongylosis
Trichostrongyles infect the domestic animals like cattle
and sheep etc. Affected animals show anaemia, cachexia,
diarrhoea and debility. Lambs and calves die of this disease.
The important trichostrongyles are as follows :
Table 22. Parasites and their hosts
Parasites Hosts
Hael1wnchus contortus Sheep, ~at and cattle
OstertaRia ostertaqi -Do-
Trichostron)[lvlus axei -Do-
Cooperia spp. e.g. C. punctata and Sheep and cattle
C. spntulnta
Nematodirus spp. e.g. N. spat/liRer -Do-
Mecis tocirrus di)[itatu s Sheep, cattle, Roats and buffaloes
-~
"-
H. contortus ingests large qualities of blood in the host
body and lacerations in the mucosae and gastritis are
produced. The infective larvae of T. axei burrow into the
mucosa of the abomasum but other species of the genera
Trichostrongtjlus and Cooperia invade the mucosa of the small
intestine. Larvae of Ostertagia spp. penetrate into the
abomasal mucosa and burrow deeper to cause severe
damages to the gastric wall. These parasites develop in small
nodules and the adults may emerge from the nodules in the
mucosa.
Signs
Infection with Haemonchus contortus even causes death
from loss of blood. There are oedematous swellings under
the jaw and ventral abdomen. Mucoid degeneration takes
place in the body fat (e.g., fat in the coronary groove of heart
or subcutaneous tissue) to produce gelatinous tissue (serous
atrophy of fat). Affected animals become weak, show
staggering gait and become moribund and later die.
Diarrhoea with thin, foeted, dark coloured faces and anaemia
are important signs of infection with trichostrongyles.
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Pathology
In acute cases, dead animals are severely anaemic. The
mucous membranes are pale and the blood is thin and
watery. Oedematous swelling in the subcutis under the jaw
and abdomen and excessive amount of fluid in pericardial,
thoracic and peritoneal cavities are important pathological
changes. The body fat is highly gelatinized. The liver is friable,
light brown and may show fatty changes. Large number of
worms are present in the abomasum. Mucosa of the
abomasum may show ulcers or red bite marks by the worms.
Small round nodules are found in the abomasal mucosae
and local lymph nodes are swollen. There is myeloid
hyperplasia in the bone marrow and liver shows fatty
changes and mucoid atrophy of fat is seen in the body. The
term bottle jaw refers to submandibular oedematous tissues
because of gastro intestinal parasitism.
Diagnosis
It is based on the detection of ova in the faeces and
helminths in the abomasum and small intestine of animals.
Anaemia and gelatinisation of fat (serous atrophy of fat) etc.,
aid the diagnosis of trichostrongylosis.
Treatment/Management
The round worms include different species or nematodes
affecting various domestic animals. Diarrhoea, potbelly,
urithriftiness, bottle jaw and fits etc., are important signs of
disease in cattle and young calves.
The drugs for treating round worms infection are as
follows:
(i) Piperazin adipate, vermex liquid dewormer, Helmacid
and helatac, etc.
(ii) Broad spectrum antihelminthic drugs like ivermectins,
benzimidazoles and imidazothiazoles etc., can be used
to treat round worm infection. Other drugs such as
panacure, albomar, zodex, banminth forte, zenil and
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Schistosomiasis
The disease produced by sachistosomes in animals is
called schistosomiasis. These flukes inhabit the blood vessels
and the eggs laid by them circulate as emboli in the
circulation. On being lodged in the tissues, these eggs behave
like foreign irritants to them and invoke pathological changes
(mainly proliferative or of a granulomatous inflammatory
type). The important blood flukes found in India are as
follows:
Table 23. Schistosomes and their hosts
Species Hosts Anatomic sites
ScJzistisoma Cattle, sheep, goat, Mesenteric, portal and
indicum horse and camel. pelvic veins.
S.incognitus Dogs and pigs. Mesenteric and portal
veins.
S. nasalis Cattle, goats and Nasal veins.
horse.
S. spindale Cattle, sheep, goats Mesenteric and portal
antelopes and water veins.
buffaloes.
Pathology
The male and female blood flukes copulate within the
lumina of the blood vessels and move against the blood stream
to lay eggs inside the small venules in the different organs or
tissue of the hosts. The ova with the help of cytolytic fluid
produced by them penetrate into the walls of the capillaries
and move throughout the tissues to reach in the lumen of
the intestine or the urinary bladder etc. The ova then leave
the body of the host with the faeces. The ova which fail to be
excreted with urine or faeces etc., reach at unusual sites in
the body and provoke tissue reaction~ at such sites. A
miracidium escapes from the fertile mature ovum in proper
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Pathology
The main pathological changes are as follows :
(i) Depriving the final host of food and nutrients. The hosts
starve and undergo emaciation and debilities but the
parasites multiply and thrive well in hosts's body. One
may find ascariasis as a febrile state in the patients.
(ii) Peritonitis following perforation of the intestinal wall
by the round worms.
(iii) Injuries to mucosae owing to abrasions caused by the
worms. The animal patients suffer form diarrhoea.
(iv) Icterus due to worm obstruction in the bile ducts. The
worms may even enter the stomach or pancreatic ducts
from the small intestine.
(v) Presence of neutrophiles, eosinophiles and lymphocytes
etc., in the liver due to inflammatory reaction. Epithe-
lioid cells, eosinophiles, lymphocytes and neutrophiles
are seen around areas of caseous necrosis in the hepatic
tissue.
(vi) Haemorrhages due to damages caused by migrating lar-
vae in the pulmonary capillaries and inflammatory
changes in the lungs. Bronchopneumonic changes in the
lung parenchyma are noticed.
(vii) White spots in the liver due to fibrosis at the necrosed
sites caused by the migrating larvae. Severe form of
enzooting pneumonia of pigs and swine influenza are
noticed in the pigs affected with ascariasis.
(viii)Presence of congestion, enlargement and subcapsular
haemorrhages in the livers of the affected animals. Mi-
grating larvae leave behind necrotic tracts during their
movements in the liver parenchyma.
(ix) Oedema, subpleural haemorrhages and cyanosis are
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Diagnosis
Treatment/Management
1. A void exposure of young pigs and goats to infested
adults and contaminated soil.
2. There should be periodical treatment of young animals.
3. Rearing of pigs in concrete pans to avoid the ascarid
infestation.
4. Piperazine adipate, vermox liquid dewormer, helmacid,
belatac etc., can be used. Pyrental tantrate and
levamisole are found quite effective in worm infected
pigs. Pyrenta1250 mg/kg or levamisole 7.5 mg/ kg body
weight gives good results in the buffalo calves.
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Chapter 6
Deficiency Diseases
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Table 26 Deficiency Diseases of Animals, their Pathological Science and Treatment
Deficiency Diseases Pathological Signs Treatment
l.Hypovitaminosis A Vitamin AI The main signs are: 1. Night blindness (nyctalopia). Inability of Since the tissue changes are
(retinoI1) and vitamin A2 (retinoP) are the animal patients to see in the parbal darkness. The light reversible, the symptoms or
its two forms. Vitamin A occurs in the bleached rhodopsin (visual purple) is not restored to its previous lesions dIsappear with
form of carotene (a yellow pigment status due to its deficiency. Presence of dryness of the eye due to normal supply of vitamin A
with chlorophyll in green plants). deficient lacrimal secretion. Thickening and sqamous metaplasia at the dose rate given below.
in the lacrimal ducts lead to ductal blockage. Conjunctivibs and See table-26b
keratitis present in the cattle and horses and Opacity, mfection
and ulcers occur in the eyes of the patients. Loss of reproductive
efficiency. Deficiency signs usually appear in animals. Other
signs in animals include failure of growth in the young animals,
improper development of the bones and nervous system,
degenerativt:' changes in the various glands and kidneys. Sterility
may supervene in male and females affected with Its deficiency.
Atrophy, metaplasia and necrosis affect the respiratory and
digestive tract mucosae. Urinary obstruction is present in cattle,
sheep and goats suffering from vitamin A deficiency which also
precipitates urolithiasis (renal culculi or stones etc.). Presence of
the comified epithelium in the vaginal wall. Foetal
malformations may occur. Piglets are bom without eyes. In
hypovitaminosis A. Diets deficient in viahnin A or defective
absorption of this vitamin from the gut causes its deficiency. In
short, the main signs of vitamin A deficiency are as under: (
nyctolopia) 1. Night blindness due to interference with
regeneration of visual purple. Vitamin A is a must for preventing
dim-light vision. It is needed for proper function of both rods
and cons. 2. Comeal keratinisation, and dryness of eyes
(xerophthalmia) and atrophy of retina, defects in the hooves and
loss of weight.
Deficiency Diseases Pathological Signs Treatment
3. Infertility and congenital defects in offsprings of the deficient darns.
4. hlcreased suscepbbility to many infectious diseases. Depressed
immlme system. 5. An increase in cerebrospinal fluid pressure in calv es
causing syncope, incoordination and convulsions in them 6. Poor bone
growth. Normal position and activity of osteoblasts and osteocysts is
main tained by vitamin A. h1coordination of bone growth or defective
moulding of bones present. Presence of distortion in the animal bone,
constrrtion of optic nerve, ataxia and weakness are also seen. 7.
Atrophy of the epithelial tissues, Secretory epithelial cells fail to divide
and there is an excesslve presence of stratified keratinised epithelial
cells. Secretory epithelium is replaced by keratinized epithelium in the
salivary glands and placenta etc. 8. Defective embrycnal development.
Ccngential defects in pigs and rats are seen. Congenital
IV
0'\ hypovitaminosis is seen in calves. Weakness, incoordination and
U1 blindness with dilated pupils are the changes noticed. Retinal dysplasia
and constriction of the optic canal may also be present. 9. Focal necrotic
hepatitis, squamous metaplasia of the epithelium in interlobular ducts
of glands e.g., salivary glands is a marked feature of this defriency. 1he
pathogncmonr lesions of vitamin A de&iency include sqamous
metaplasia and hyperkeratosis of mucous glands opening into the
oesophagous and pharynx and nodule formations in their mucosae.
Hyperkeratinisation of the epithelium of prefuce, rumen and reticulum
are some other importan t changes. Defective formation of den tin and
enamel.
Deficiency Diseases Pathological Signs Treatment
2. Hypovitaminosis B. Vitamin B Diseases like avian curly toe-paralysis, canine pellagra and chromic See table. 26b
includes chemical compounds as arthritis are caused by vitamin B dehciency. Paralysis and myelin
given below: 1. Thiamin (vitamin Bl) degeneration are noticed in birds. Cyanosis of the distal portion of
2. Riboflavin (vitamin Bl). tongue, petechiae or haemorrhages in the digestive canal mucosae,
haemorrhagic gastritis and enteritis, ulcers in the mouth, myelin
degeneration, dianhoea and ulceration of the buccal mucosa are the
signs of canine pellagra (or blue tongue).
3. Nicotinic acid (Niacin) 4. Pigs suffer from chronic enteritis, (diarrhoea), anorexia, stunted
Pantothenic acid 5. Pyridoxine growth and necrotic patchy mucous colitis. Bovines do not suffer from
VItamin Bh 6. Vitamin B12 ItS deficiency because of its manufacture by ruminal bacteria. Horses
(cyanocobalamin) Vitamin B"Cobait do not suffer from its deficiency. In experimental cases of thiamin
is needed for bacterial synthesis of deficiency, pigs show focal necrosis of atrial myocardium with
vitamin Bu. VItamin Bl 2 requires an flabbiness and dilatation of the heart. Microbes in the presence of
intrinsic factor ( a protein produced by adequate amount of cobalt play a role in its synthesis in intestines of
the gastric parietal cells) for its herbIvores. Deficiency of vitamin Bl and B2 produce severe aliments
absorption in the gut. in birds. Adult ruminants and horses suffers fI'om thiamine deficiency
because of consumption of plants containing thiaminase.
3. Hypovitaminosis C. Man, monkey In animals, only monkeys or guinea pigs suffer from its defiaency. See table. 26b
and guinea pigs need vitamin C in Lesions like subperiosteal haemorrhages, failure of the proper
their diets. It is present in large ossification of long bones, defective dentin formation and
quantities in animal and pljUlt tissues. hyperkeratotic deITIlatitis are noticed in the animals. Ordinarily, the
Birds and several types of animals domestic animals do not suffer from its deficiency. Poultry does not
synthesize it in their livers. need vitamin C in its feeds.
4. HypovItaminosis D Its Important Leg weakness ID chickens. Rickets in the young animals.,decrease in See table. 26b
components are: 1. Vitamin 0, appetite, poor and bending of bones and enlargement of joints are
(cholecalciferol) It is produced by seen in vitamin D deficient animals. Bones become fI'agile and are
sunlight in the skin. Vitamin D~ is an prone to multiple fIactures. Vitamin D needed for mmeralization of
ergocalciferol. osteoid and eplphysel cartilage and its deficiency leads to resorption
of bones.
Deficie~ Diseases Patholo~cal Sig!1s Treatment
5. Hypovitaminosis E This This deficiency produces white muscle disease in lambs. White muscle disease is a See table 26b
Vitamin (alphatocophevrol) degenerative in nature causing appearance of white streaks in the muscles. A
occurs in the wheat germ oil. weakness of the limbs develops in patients. Retarded development or death of the
Tocopherols have antioxidant embryo in the rodents, necrotic changes in the seminiferous tubules,
activity and prevent aspemlatogenesis, Zenker's necrosis and degenerative changes in the muscles are the
autooxidation of unsaturated main findings in cases of experimental vitamin E deficiency in rodents. Yellow fat
fatty acids. called ceroid which stains red by acid fist technique, is noticed at the interstices of the
adipose tissue (cells) and in phagocytes and Kupffer cells of the liver etc. Such
pathological state develops in pigs feeding with fish offal and seems to be connected
with vitamin E deficiency.
6. Hypovitaminosis K Its two As this vitamin is produced by bacteria in the nomlal animals they do not suffer from See table 26b
fomls are vitamin K2 (active its deficiency. It is required for proper fomlation of prothobin and clotting factors VII,
form) and vitamin K3. Vitamin K IX and X Anorexia, weakness, marked decrease in prothrombin are signs of vitamin K
is required for normal blood DefiCiency. Vitamin K deficiency is associated with a haemorrhagic disease in pigs
cloting Excessive haemorrhages which fail to grow, become pale and also show subcutaneous haemorrhages. Vitamin
are seen in vitamin K deficiencv. K is a powerful anti dote to sweet clover poisoning in the aninlals.
7. Iron deficiency Iron is a There is a need of iron for proper fonnation ot haemoglobin and the body gets it by See table 26b
cofactor in cytochromes, catalase absorption through the intestine. Iron deficiency leads to anaemia and failure to
and ferredoxin and forms an thrive properly in the animals. In young pigs, diarrhoea, lack of hydrochloric acid
essential part of haemoglobin. (achlorhydria) and destruction of red cells lead to the state of anaemia. When it
combines with calcium phosphate in bone, the disease produced is called osteomalacia
or rickets. A little amount of copper and cobalt is required for nomlal haematopoiesis.
Suckling pigs (1 to 8 weeks of age) affected with piglet anaemia are pale, emaciated,
unthrifty anaemic and stunted in growtll. At autopsy, oedematous lungs, dilated
heart, enlarged liver, pericarditis, pnl'UmOIUa, haemorrhagic gastritis and enteritis are
noticed in bodies of the dead pigs. Diarrhoea is a common sign in piglet arJaemia.
Affected pigll'ts also show dyspnoea, letllargy, pale r.lucosae and pigs deficient in iron
show a high inCidence of still births. Mottling of liver, fatty infiltration and decrease in
the panetal cells are some other changes in the iron deficient persons.
Deficiency Diseases Pathological Signs Treatment
There is a fall in values of red cell count and haemoglobm percentage (1 to 2 gm. per See table 26b
100 ml of blood) in the affected piglets. In general, the pathologic changes in the
anaemia are as follows: 1) Fall in red cell count (less than a million per cubic
millimeter of blood), and presence of anasarca in the body. 2) Pale red cells due to
haemoglobin deficiency 3) Presence of anisosytes, poikilocytes, polychromasia.
reticuIocytes and nucleated red cells in the blood smear 4) Oedematous and
haemorrhagic mucous membrane. 5) Pale organs. 6) Haematopoiesis (regenerative
changes) in the bone narrow seen postmortem. Replacement of fatty marrow by red
marrow. 7) Punctate basophilia is present in chronic lead poisoning and anaemia of
toxic origin. 8) Presence of megaloblasts in man affected with pernicious anaema due
to deficiency of liver factor or anti-anaemic factor i.e., vitamin B12 (cyanocobalamin).
7. Copper deficiency Copper is a Most of the tissues contain copper, 20 to 30 mg of copper is present in one kg of the dry See table 26b
part of ceruplasmin and enzymes matter of the central nervous system. Its deficiency leads to anaemia and unthriftiness
like superoxide dismutase in the animals.For example, steely wool is noticed in the copper deficiency affecting
cytochrome, oxidase and the sheep. Enzootic ataxia (sway back) is an other disease seen in sheep due to copper
tyrosinase. deficiency. The lesions or signs noticed in the lambs i.e., in the patients of enzootic
ataxia are the following: 1) Demyelinization of the central nervous system in
neonates and necroSIS, softening and cavities in the cerebral white matter in the brain
containing translucent, greyish white material. 2) In coordination and weakness of
the posterior limbs, following lesions due to copper deficiency is noticed in cows
which fall and die all of a sudden. Diffuse fibrous scarring of heart, haemosiderosis of
the liver, spleen and kidneys. Unthriftiness and aneantia and osteoporosis are some
effects of copper deficiency.
Diarrhoea, emaciation, lameness and changes in the hair are some other signs of
copper deficiency in animals. Villous atrophy of the mucosae of the small intestines
causing diarrhoea in patierits is noticed. Flabby heart, pale colour, sudden death and
atrophied muscle fibres with replacement by fibrous tissue are seen in falling disease
noticed in animal suffering from copper deficiency.
Deficiency Diseases Pathological Signs Treatment
9. Cobalt deficiency Cobalt Cobalt is required for proper activity of the ruminal bacteria and nomlal production of See table 26b
present in the soil and herbage vitamin B12. Its deficiency in the feeds causes deficiency of Vitamin B12 Its deficiency
etc. and 4 percent of Vitamin B12 produces a cachectic syndrome (e.g. an enzootic marasmus) in sheep and cattle (bulls
is constituted by this substance. and calves) which show gradual loss of appetite, wasting away, deatll, anaemia and
haemosiderosis in the organs like kidneys, liver and spleen etc. Fatty changes are
present in livers of dead sheep and cattle. When the pasteur contains less than 0.0 + 7
mg/kg dry matter, cattle suffer from cobalt deficiency. Sheep consuming pastern' with
cobalt less tllan 0.07 mg/kg dry matter also show signs of cobalt deficiency and show
pallor of the mucosae. Animals are emaciated and easily fatigued. Growth, milk and
wool production are badly affected. Decreased lambing percentage, increased rate of
still births and increased neonatal mortality are noticed in the calves. Reduced
concentraction of immunoglobulins and lower vitamin BJ2level are found in the cobalt
deficient dams. Lambs of such dams are slow to start sucking. Excess of haemosiderin
in the spleen and liver with high levels of iron in the liver and spleen. Cobalt level is
low in the liver of the deficient ruminants (e.g., cobalt content less than 0.07 mg/kg
id!Ymatter of tlle liver}.
la. Manganese deficiency It is required in small amounts for proper functioning of the body tissues. Its See table 26b
defiCiency in the rats produce aspermatogenesis, retarded growth, weakness and
defective offsprings. Perosis (i.e., the condition of slipped tendon) occurs in chickens
and turkeys. In slipped tendon, there is a medial displacement of the gastrocnemius
tendon. Defomled chicks with globular heads, short and thick legs and wings hatch
from th~ eggs laid by tlle manganese deficient hens. Infertility, congenital and
acquired skeletal deformities are some effects of this deficiency. Infertility problem in
the animals (e.g., cattle) rise, in case, tlle soil contains less tllan 3 mg/kg of manganese.
Manganese occurs as a cofactor in enzymes like arginase and phosphotransferase in
aninlals bodies. It plays its role in bone matrix formation and also in synthesis of
chordroitin sulphate which maintains the rigidity of the connective tissue.
Deficiency Diseases Pathological Signs Treatment
10 Zinc deficiency: Zinc is a Zinc in small amounts is an essential requirement for animals like pigs, sheep, cattle See table 26b
component of the enzyme and goats etc. Thickening of the stratifIed squamous epithelium in the skin and
carbonic anhydrase. oesophagus is produced by its deficiency in animals body. Zinc deficiency results in
parakeratosis (i.e., retention of nuclei in stratum comium in the pigs). One notices
thickening in the stratum SpinOSunl as well as the cornified layer. Hairs become
sparse in the rats affected with experimental zinc deficiency. Alopecia, wool eating,
abnormal hoof growth, lameness and unthriftiness are some other signs of zinc
deficiency. Skin biopsy of the zinc deficient patients reveals a prominent increase in
the thickness of all the elements of epidermis.
11 Iodine deficiency: It occurs in Man and animals require iodine in small amounts. Its deficiency causes goiter (i.e., See table 26b
soil and water etc. enlargement of the thyroid gland) (Fig. 5; p. 200) Hyperplastic changes are noticed in
the thyroid glands of cretins. Goiters are seen in the animals like lambs, pigs, calves
and newly bom colts etc. Iodrne deficiency results in the birth of hairless pigs. If
animals are not treated in time, they succumb to its deficiency. In the endemic zones
of goiter, both the soil and water are deficient in iodine. An excessive intake of iodine
leads to the state of iodism marked by lacrimationa and exfoliation of the epidermal
scales like dandruff. Alopecia, enlarged thyroid and myxoedema are the common
changes seen in iodine deficiency in animals. Hypoplastic hair follicles, delayed
osseous maturation, absence of centres of ossifications, retarded foetal brain
development, lack of wool growth and delayed skeletal maturation are some other
signs of iodine deficiency.
Deficiency Diseases Pathological Signs Treatment
12. Phosphorus deficiency Inorganic phosphorus 4 to 8 mg per 100 ml of blood is found in the normal animals. Its See table 26b
(aphosphorosis) imbalance or deficiency with calcium and vitamin D mly lead to rickets or
osteornaJ.osia in animals (for example, cattle). A depraved or an abnormal appetite
called pica develops in cattle due to aphosphorosis. Dirt is eaten by the affected
animals. Phosphorus deficient cattle chew bones of dead animals (osteophagia).
Rickets in sheep is mostly produced by phosphorus deficiency. In short, pica, poor
growth, oestodystrophy and infertility are the main signs of phosphours deficiency.
Weight loss, rough hair cat, lameness, fractures in the vertebrae, pelvis, ribs and
porous, chalky white, soft and fragile bones are seen in the experimental cases of
phosphorus deficiency in cattle. Such defiClency in cattle produces retarded growth,
reduced fertility and low milk yield in cattle. Rise in cases of bGlulism in cattle due to
osteophagia is noticed. Pregnant cows become recumbent. Poor stature and perverted
appetite are present in phosphorus deficient sheep and ,horses. Some other
pathological changes in the phosphorus deficient animals are as follows. 1. Lighter
bones showing a low ratio of ash to organic matter as seen in oesteomalacia. 2.
Excessive deposits of osteoid in the adult bones of animals 3. Softer and large bone
shafts due to subperiosteal osteoid deposits, enlarged jOints, epiphyseal cartilage
thicker than usual and the ash to organic matter ratio as 1:2 to 1:3 are noticed in the
cases of rickets. In healtll, the ratio of ash to organic matter in bones is 3:2 in animals.
13. Sodium chloride deficiency Deprivation of common salt in the feeds of animals causes anorexia, loss in body See table 26b
weight. Dairy cattle on a sodium deficient diet show polydipsia, polyurea, salt hunger,
pica, drinking urine, licking dirt, a fall in milk production and loss of appetite and
weight. Salt in tlle diet at allevel of 0.5% is quite adequate for all farm animal species.
Consuming inadequate amount of common salt causes poor growth, rough coat and
unthriftiness in such animals. Men and horses loose sodium chloride tlrrough
sweating. A cow can eat conunon salt upto 2lbs. per day for an indefinite period
without much ill effects. Animals may collapse and die due to salt deficiency. Excess of
common salt in feeds causes salt poisoning in pigs and chickens.
Deficiency Diseases Pathological Signs Treatment
14. Magnesium deficiency: It is a Bovines contain about 2 mg of magnesium per 100 ml of blood. It plays an See table 26b
cofactor in phosphotransferases important role in the transmission of impulses at the neuromuscular junctions. An
and phosphohydrolases. Bones excessive formation of acetyl choline is favoured by low concentration of magnesiunl
of animals contain about 7% and the low ratio of magnesiunl to calcium.
magnesium. It is an activator of When the level of magnesium goes below 0.7 mg per 100 nu of blood,
the enzyme alkaline phosphatase hypomagnesemia is noticed causing grass tetany in animals. The main changes of
and many enzymes utilizing experimental hypomagnesemia in calves are as under: 1. Opisthotonus, muscle
adenosinetriphosphatase (ATP). tremor and reluctance to move, nervous hyper irritability and apprenhensiveness. 2.
Sudden convulsive seizures, scratching and kicking at the belly. light stimuli produce
twitching in the skin. Continual shifting of weight from limb to limb and
incoordination. 3. Agonal haemorrhages in the heart, intestinal and mesentric serosae.
Presence of thrombosis of the venules in the heart
4. Deposition of calcium in the intemallayer of heart and large blood vessels.
Hypocalcaemia and hypomagnesemia are noticed in cattle and sheep affected with
hypomagnesemia. Agonal haemorrhages or convulsive death may be seen in the
patients of hypomagnesemia. Deficiencies of copper cobalt, selenium, zmc, iodine and
magnaese constItute important trace elements deficiencies.
15. Slenium and / or Vitamin E Either selenium or vitamin E or both may cause or be associated with development See table 26b
deficiencies. It is an essential of many diseases in animals like pigs, sheep, cattle and horses etc. Role of selenium
element but highly toxic in large and vitamin E is interlinked in either causmg a disease in an animal or in the
doses. It exists in the soil and treatInent of certain ailments produced. When these nutrients are given to animals,
certain seleniferous plants. It is a they recover from the maladies. An inter-relationship between seleniunl, vitamin E
component of the peroxidase. and sulphur containing amino-acids has been marked in preventing many nutritional
Selenium requirement in the diet diseases in animals. The main diseases associated witll the deficiencies of either
for most species of animals is 0.1- selenium or vitamin E or both are given below in Table- 26a
0.3 ppm of diet (mg/Kg) Toxic
level of selenium varies from 2-
10 ppm in the feed.
Table 26A. Pathological signs and lesions in animals
Deficiency diseases Animals affected Pathological signs
1. Nutritional muscular dystrophy. Cattle, sheep, pigs and Grey or white localized focal areas in the skeletal
horses. muscle and diaphragm due to degenerativecllanges in
the patients of nutritional muscular dystrophy. The
affected muscle, looks like fish flesh. !iJme grayim
streaks may involve group of muocle fibers. The affected
muscles are oedematous, friable and calcified. Sub-
endocardial white areas of degeneration are noticed in
the heart of the affected sheep and cattle. An extension of
such lesicns may lead to cardiac hypertrophy,
pulmonary congestion and oedema, cakific ation of the
dystrophic tissues and coagulaticn necrosis and hyaline
degeneraticn in the affected musclefibers. Yellowish
brown fat deposits causing discolouration in the muscles
is noticed in older aninlals.
2. Retained foetal membranes. Cattle The role of selenium deficiency as a cause of retained
foetal membranes is doubtful The findings on the
inferior reproductive performance are also inconsistent.
There is need of further research work in this direction.
3.Hepa tosis diaetetica : N ote:- Resistence to Pigs The VESD syndrome (vitamin E and selenium
infectious diseases (e.g., mastitis) increases with deficiency) affects the growing pigs (3 weeks to 4 months
maintenance of normal level of vitamin E and of age). The patholOgical state of hepatosis dietetica
selenium in the diet of the animals. Animals fed arises from consuming a diet low in vitamin E and
with diet low in vitamin E and selenium show selenium In Scandinavian countries (Sweden or
the following phenomena: 1. Immune response Denmark), the disease occurs even naturally in pigs.
of animals is badly affected 2. Development of Degenerative and necrotic changes are noticed in the
immunosuppression 3. Increased susceptibility organs like liver, heart, skeletal muscle and blood vessels
to bacterial and viral infections 4. Poor antibody etc. TIlere is a degenerative myopath y of caniiac and
lE!oduction or poor humoral immune resp)l1ses skeletal muscles. Oedema, microangiopathy and
Deficiency Diseases Pathological Signs Treatment
5. Suppression of proliferation of T and B yellowish discolouration of adipose tissue are also seen
lymphocytes. One also finds cytodestruction of in this condition. The affected pigs die suddenly.
T lymphocytes and natural killer lymphocytes.
6. The performance of neutrophils is rendered
poor. In other words, phagocytic role of
neutrophiles markedly declines. Decrease in the
phagocytic function of neutrophils is also
noticed in the mammary glands. Administration
of vitamin E and selenium to the animals
maintained on deficient diets greatly improves
the condition of these animal patients.
Potassium (a part of sodium potassium pump Almost all domestic The main signs or changes are as follows 1. Dehydration,
for maintenance of proper cellular osmotic animals chronic diarrhoea, hyperadrenalism, loss of appetite,
pressure). rough hair coat, muscular weakness and paralysis in the
deficient animals 2. Development of cellular oedema (the
mildest and earliest degenerative change in
parenchymatous organs due to failure of sodium
ipotassium pump and poor milk yield by lactating cattle
Table: 26b. Curative and Preventive Doses used in Avitaminoses and Mineral Deficiencies
in Animals
Deficiency Diseases Minerals Treatment Prevention
1. Cobalt deficiency Cobalt Sheep : 1 mgjkg body weight per day infected orally Sheep :0.1 mgj day to a sheep in
Lambs: 300 mg per lamb at an interval of a month feed. Cattle: 0.3 to 1.0 mgj day
Cattle: 3 to 10 mg feed to each animal. individually in feed.
2 Copper deficiency Copper Calves: 4 gms per calf per week (2-6 months) Cattle Calves: 1.5 gms at weekly
: 8 to 10 gms per animal at one interval for 3 to 5 interval in (2-6 months) feed.
weeks. Cattle : 4 gms orally at weekly
interval in feeds.
3. Iodine deficiency Iodine Therapeutic doses not recommended owing to its Lactating and pregnant Cows:
toxicity with body. 0.8 to 1.0 mg per kg dry matter
of the feed. Dry cows & calves:
0.1 to 0.3 mgjkg dry matter of
the feed.
4. Iron deficiency Iron Elemental Iron: 0.5 to 1 gm one injection once each Ferrous sulphate: 1.8 per cent 4
week in large animals like horse,Yitamin 1312 ml daily given to animals.
(cyanocobalamin) 5000 ug per week in a single dose to
large animals like horse. It is better to follow the
manufacture's guide.
5. Sodium chloride deficiency Sodium Farm animals : 0.5 of sodium chloride in the feeds per
chloride day.
6. Magnesium deficiency Magnesium Pigs: 400-500 mgjkg of the total per day.
7. Zinc deficiency Zinc Goat : Zinc sulphate 250 mgjkg daily for Zinc sulphate: 50 mgjkg of
4 weeks in the feeds Sheep : Zinc Oxide 200 mg given feed daily for pigs.
ij m in olive oil Lambs: 50 mg given Ij M in olive oil
Pigs: Zinc Inj. 2 to 4 mgjkg body weight to be given
Iparentereally daily for 10 days.
Deficiency Diseases Minerals Treatment Prevention
8. Potassium deficiency Potassium Pigs, piglets and ruminants: 65 mgjkg body weight
to be given in the diet.
9. Vitamin E selenium Selenium Calves, goats & lambs: 3 mg selenium and 150 LU.
deficiency per ml of DL alpha tocopherol @ 2 ml/45 kg body
weight intramuscularly. Only one injection sufficient.
E-Care-Se. Horse, cattle and Dogs: 1 nu per 25 to 50
kg body weight 1 nu per 25 kg body weight by
intramuscular route.
10. Calcium deficiency Calcium Parenteral administration of calcium preparations like
calboral25%, calcium borogluconate (25%) are used.
H + C - 200 - 400 m by i/v and sic route to animals.
Calcium sandoz (10%) Dog : 25ml to be given by i/v
route. Note: Daily requirements in gms of calcium,
Phosphorus and vitamin D for cattle are given as
below: Growing cattle Calcium Phosphorus Vit-D
15-3012-23 500 i/v kg dry matter intake Pregnant and
17-34 13-26 - do - Lactating cows.
For each kg of milk, 2 to 3 gms of calcium and 1.7 to
2.4 gms of phosphorus are to be given as milk
production requirement over and above maintenance
rate. Ewes 0.3-0.5-2 0.28 - 0.37 250-300I.U. Lambs 0.40
0.27150 LU. Horse (adults) 0.3-0.8 0.20 - 0.516-8 LU.
Iper Kg body wt.
11. Hypovitaminosis A Calf: 440 IU/kg body wt. I/M in a quar solution The Calf: 40 I. U. per kg body
main daily requirement of Vitamin A for all species is weight daily IjM.
40 IU by parenteral route.
Deficiency Diseases Minerals Treatment Prevention
12 Hypovitaminosis B VitantinB For all spe cie s Thiamine hydrochloride @ 5 mg/kg For monogastric animals.
body wt. If needed, it may be repeated after 3 hours. Tltiamine hydrochlOride @ 30 to
Initial dose is given by I/V rou te followed by 1/ M 60 ug per kg body weight
injectIon for 2 to 4 days. Berin For large animals: 10 parenterally with additional
m! of Berm is given 1/ M fur 5 to 7 days on alternate supply of yeast, cereals and
days to treat Vitantin B deficiencies in all species, the grain etc.
following treatment rate is recommended 1. Vibelan
Injection: 10 m! to large aninuls 2 to 5 rnl to small
animals 2. Conciplex Inj. : 10m! to large artimals 2 to
5 m! to small annnals 3. Neuroxin B12 : 10 nu to large
animals 2 to 5 nu to small animals. All the above three
products are given on alternate days for 5 to 7 days.
Vilantin B12 (cyanocobalamin) is required at the dose
rate of 20 to 40 ug daily be calves and goats. For pigs
the dose is 10 to 50mg of
Vilantin K is required per tone of its feeds. In case of a
ruenUa, monogastric ani,mals at the dose rate of 2 ug
vitamin 812 parenterally.
13. Hypovitaminosis K VitantinK Treatment For all animals Dose: 3 mg/kg body
weight parenterally as a single irqection resbres
deficiency or prev ents coagulation defects etc. Asa
preventive dose, 25 mg/kg of feed is given to all
aniamls for 4 days 300-500 mg/vitamin K is given
subcutaneously every 4 to 6 hours as anti dose to
counter poisoning in horses.
Note: Different proportions of Vitamins andntinerals
are available in the market. It is better to follow the
inoculation details fur their use to avoid reactions and
comp Iications.
Chapter 7
Pathologic Changes and
Treatment of the Cases of
Poisoning in Animals
Pathology
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Pathologic Ozanges and Treatment of the Cases of Poisoning in Animals
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Advanced Patlwlogy and Treatment of Diseases of Domestic Animals
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Pathologic Changes and Treatment of the Cases of Poisoning in Animals
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Pathologic Changes and Treatment of the Cases of Poisoning in Animals
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Advanced PatllOlogv and Treatment of Diseases of Domestic Animals
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Pathologic Changes and Treatment of the Cases of Poisomng In Animals
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Advanced Pathology and Treatment of Diseases of Domestic Animals
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Pathalagic Changes and Treatment af the Cases af Paisoning in Animals
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Advanced Pathology and Treatment of Diseases of Domestic Animals
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Pathologic Changes and Treatment of the Cases of Poisoning in Animals
16. Salt: 1. 0.9% Nacl kills the baby chicks. In order to treat the
Salt poisoning is 2. Presence of hydrothorax and case of salt
seen in pigs and hydroperitoneum ill the chickens. poisoning, the toxic
poultry due to Nephritis is also found in them. feed and water
excessive ingestion of 3. Blindness, hyperirritability and must be removed
sodium chloride. convulsive seizures are seen in salt immediately
Cattle tolerate larger poisoning in the animals. Symptomatic
doses of salt,in 4. Oedema in the tissues and body treatment includes
case,the water is cavities. use of alnnentary
available in plenty to 5. Eosinophilic meningoencephatitis tract sedatives in
these animals. is quite pathognomonic for swines. gastro-enteritis, and
Accumulation of eosinophiles can be provision of
found in the perivascular spaces of isotonic fluids when
the brain. dehydration has
occurred. In case of
cerebral oedema,
diuretics or
hypertonic solution
are injected
parenterally. A
balanced ration
(0.5% sodium
chloride) should be
given to poultry
and the feeding of
old feed should be
immediately
replaced by fresh
balanced poultry
feed.
289
Chapter 8
Some Miscellaneous
Pathological Conditions/
Diseases
Pneumonia
Inflammation of the lungs in man and animals is called
pneumonia. There are several causes (e.g., viruses and
bacteria etc.) of pneumonia. An acute inflammatory state of
the lungs is called pneumonia whereas pneumonitis refers
to an inflammatory disease of the lungs characterised by a
chronic reaction in the form of proliferative changes in the
fibroblasts and lining cells of the alveoli. Reticuloendothelial
cells, epithelioid cells and septal cells take active proliferative
or defensive role in the lungs.
In short, pneumonia refers to acute infectious
inflammation of the lungs with exudative changes in the
alveoli. Two main kinds of pneumonia are:
(i) Lobar pneumonia (croupous pneumonia).
(ii) Bronchopneumonia (lobular pneumonia).
In man, lobar pneumonia is found and characterised
by inflammatory reaction at one point which spreads by
direct continuity to other parts of the lungs till the whole or
most of the lobes of lungs get involved in the extending
inflammatory reaction. In bronchopneumonia, the infection
spreads through the air passages i.e., there is an inflammation
of the bronchi or bronchioles (bronchiolitis). Croupous
pneumonia or lobar pneumonia occurs in the human beings
and is caused by a pneumococcus called Diplococcus
290
Some Miscellaneous Pathological Conditions/Diseases
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Advanced Pathology and Treatment of Diseases of Domestic Ammals
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Some Miscellaneous Pathological Conditions/Diseases
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Advanced Pathology and Treatment of Diseases of Domestic Animals
The colour of the lesions varies from red to pale or grey and
these may be solid to the touch and look more prominent
(i.e. raised) than the adjacent normal areas of the lungs. Large
areas of the lesions in the lobules are presented as confluent
bronchopneumonia which resembles lobular pneumonia.
The areas of the collapsed lungs are dark red, sunken in
appearance and are surrounded by small zones of the raised
emphysematous tissue. Such changes are observed in the
lungs of pneumonic cases.
Microscopic changes
Catarrhal inflammatory changes are found in the
smaller bronchial and associated air spaces. These
bronchioles show denudation of lining epithelium and may
be filled with catarrhal exudate which consists of red cells,
leucocytes and desquamated epithelium. A little fibrinous
material may be found in the exudate. Areas of collapse and
emphysema are found in the stained sections of the lungs. In
the collapsed areas, the alveolar walls are found
approximated (i.e., very close to each other) and the capillaries
are congested and more apparent. Ephysematous areas
bordering collapsed alveoli are marked by over distended
air spaces (alveoli) whose walls may be thin and look like
delicate strands of tissue. Ruptures in the alveolar walls of
such tissues can be noticed and ruptured alveoli
intercommunicate with each other.
When the exudate is removed by absorption or
expectoration, the lungs revert to the state normalcy.
Bronchopneumonia may pass on to chronic stage
characterised by fibrosis. Even suppurative or gangrenous
changes can occur in the lungs due to pyogenic or
saprophytic organisms in the dead and devitalised tissues.
The changes noticed in some types of pneumonia are
given in table 28.
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Some Miscellaneous Pathological Conditions/Diseases
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Advanced Pathology and Treatment of Diseases ofDomestzc Animals
Diagnosis
It is based on the symptoms, lesions and isolation of the
organisms from the diseased tissues in the affected animals.
Treatment/Management
After the diagnosis of pneumonia (bronchopneumonia)
has been confirmed in animals by clinical examination, a
systematic line of treatment is followed.
Pneumonia or pulmonary infections are caused different
kinds of bacteria, viruses, fungi and parasites etc. The
aetiology of pneumonia (i.e., viral or bacterial) should be first
established in making choices of drugs. When the aetilogy of
pneumonia gets established, a proper selection of drug can
be made for quick recovery. However, treatment can also be
done on the basis of presumptive diagnosis i.e., a diagnosis
without knowing exact cause of disease by means of
laboratory tests.
The steps of treatment are given below:
1. Administration of antibiotics and sulpha drugs such as
terramycin or gentamycin or ampicillin or Vesadin
(33.3%). Any of these can be used for 7 days.
2. Use of antipyretics or analgesics, such as Bolin inj. and
Novalgin inj. etc.
296
Some Miscellaneous Pathological ConditionsfDiseases
Infectious Hepatitis
It can be caused by various etilogical factors (i.e.,
bacterial and viral infections). Actinobacillus lignieresi and
Mycobacterium tuberculosis infections lead to hepatitis. In
pygonic infections (for example, strangles, abscesses, septic
metritis and ulcerative endocarditis etc.), the infectious or
septic emboli reach the livers through the blood vessels and
produce abscesses in their parenchyma. Pyaemic infections
can reach the liver by portal vein from the intestines. If there
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Advanced Pathology and Treatment of Diseases of Domestic Animals
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Some Miscellaneous Pathological ConditionsjDiseases
Gross Changes
The livers due to toxic effects are swollen or somewhat
smaller than normal, lighter in colour (pale or yellow) and
more red due to an increased amount of blood in the organ.
There is an accentuation of the lobular markings in the liver.
The centers of the liver lobules are congested (red) and the
peripheries of the lobules are more yellow or pale due to
degenerative changes like cellular swelling, fatty changes and
necrosis. The coagulated necrotic cells may form a pale part
at the centers of the lobules. In fascioliasis, the bile ducts are
enlarged and look like prominent macroscopic rigid tubes to
the naked eyes.
Coagulative necrosis is found in the cells of the liver
lobules. The hepatocytes show pyknosis and acidophilic
cytoplasm. Based on the position of necrosis, diffuse necrosis,
focal necrosis, peripheral necrosis, midzonal necrosis and
centrilobular necrosis and paracentral necrosis are certain
types of the necrosis found in livers. In paracentral necrosis,
the necrotic areas adjoining the central veins are found on
one side of the lobules.
The animals affected with acute toxic hepatitis may die
or the disease in them may pass on to chronic toxic hepatitis
(cirrhosis). The term cirrhosis is derived from the Greek,
Kirros, which means tawny or orange coloured. The main
characteristic change in the liver is formation of tissue growth
seen arising either from the portal connective tissue or from
that around the venous outflow or both.
In cirrhosis, the liver cells are injured or destroyed and
disappear from the lobules. It is followed by progressive
proliferative growth of fibrous tissue as a kind of replacement
299
Advanced Pathology and Treatment of Diseases of Domestic Animals
step. In short, it can be said that the toxins destroy the liver
cells and induce proliferative changes in the connective tissue
elements.
Cirrhosis can be classified into different types on the
basis of distribution of the connective tissue elements and
the main types are as follows:
(1) Multilobular Cirrhosis (older synonyms: atrophic
cirrhosis, postnecrotic cirrhosis and Laennec's cirrhosis).
In this cirrhosis, the newly formed connective tissue is
distributed along the interlobular branches of the portal vein.
In short, there is interlobular proliferation of the connective
tissue.
(2) Pericellular Cirrhosis
It is marked by arrangement of the penetrating
connective tissue elements around the individual liver cells.
In cirrhosis of the liver, the connective tissue elements
may be in the coarse and dense form or in more cellular or
fine form. The connective tissue elements may also be seen
encircling the bile ducts in the liver.
(3) Monolobular cirrhosis
In this, increased connective tissue elements are usually
seen around individuallobules.
Causes
The main causes are:
(1) Toxins of metabolic, bacterial or plant origin and chemi-
cal poisons like carbon tetrachloride and manganese
chloride etc. Toxins of plant origin also produce cirrho-
sis as caused by plants like lupin or ragwort in horses.
Toxins in moldy feed or toxins absorbed in gastritis and
entritis also lead to cirrhosis of the liver.
(2) Irritants in the biliary passages or concentrated bile can
act like an irritant.
300
Some Miscellaneous Pathological Conditions/Diseases
(3) Parasites
Liver flukes, migrating ascaris and ecchinoccus cysts
are known to produce parasitic cirrhosis in the liver.
The monolobular cirrhosis and pericellular cirrhosis are
associated with toxins of plant origin.
Gross Appearance
The liver is enlarged in the early stages of multilobular
cirrhosis. Later, it is reduced in size owning to contraction of
the connective tissue elements. The liver becomes firm in
consistency and is difficult to be cut into pieces with knife
and its surface bears a granular or nodulated appearance.
The liver possessing nodules is called hobnail liver. Such
cirrhosis causes reduction in size of the liver and is known
as atrophic cirrhosis. The mono lobular cirrhosis is
hypertrophic in nature because the liver is enlarged and bears
a fine granularity on its surface. Yellow brown colour due to
fatty changes or green colour due to bile staining of the tissues
can be seen in the liver parenchyma. Whole liver or only
parts of it can show cirrhosis and many newly formed bile
ducts in the portal spaces can be found in the stained sections.
Large bile ducts may be prominent, thickened and tortuous
in appearance.
Microscopic appearance
Course dense bands of fibrous tissue containing newly
formed bile ducts are noticed in the stained sections of liver
and these bands can encircle one to severallobules. The newly
formed connective tissue elements are found along the
interlobular branches of the portal veins. When these fibrous
bands contract, depressed areas are formed on the surface
of the liver. Degenerative changes like fatty changes and
necrosis are found in the liver cells. Hyperplasia of the liver
cells can be found with loss of normal architecture of the
liver lobules. The interalobular vein (central vein) may not
301
Advanced Pathology and Treatment of Diseases of Domestic Animals
Parasitic Cirrhosis
Now-a-days, the older terms are not in use and the
classification based on etiology, morphology and functional
state of the liver is quite satisfactory. The term cirrhosis can
be considered synonymous with chronic toxic hepatitis.
Under the heading cirrhosis, the types of cirrhosis like
parasitic cirrhosis, biliary cirrhosis, Glissonian cirrhosis and
central cirrhosis can be considered. A brief description of
these types is as follows:
Parasitic Cirrhosis
In fascioliasis, fibrous connective tissue elements are
found around the bile ducts. Such fibrous tissue can also be
noticed around one or more lobules of the liver. In the early
stages of fascioliasis, the liver lobules show hemorrhagic tracts
which are the paths followed by the migrating flukes. The
effects of cirrhosis in the individuals are jaundice, ascites,
chronic venous congestion and enlargement of the spleen.
Haemorrhages can be found in the veins in stomach and
intestines.
Porphyrinaemia and photosensitisation may be seen in
the patients of cirrhosis. Jaundice arises from biliary cirrhosis
in animals.
The migrating larvae of Stephanurus dentatus and Ascaris
lumbricoides cause necrotic changes in the hepatic lobules
where the latter show growth of fibrous tissue (cirrhosis).
302
Some Miscellaneous Pathological Conditions/Diseases
Biliary Cirrhosis
This is characterized by chronic inflammation of the
intrahepatic bile ducts. In animals, liver flukes produce just
an encircling fibrosis in the immediate vicinity of the invaded
bile ducts. In the sections of the affected liver, fibrous tissue
is found encircling the various bile ducts lodged with parasites
etc. (see Fig. 6; p. 200) Fibrosis spreads through the portal
areas and around the lobules and several newly formed
nonfunctional bile ducts are found in the biliary cirrhosis.
Infiltration of inflammatory cells, like lymphocytes and
monocytes can be noticed. Jaundice is almost always present
in this kind of cirrhosis. The liver is found enlarged with a
greenish hue and the surface of the liver is nearly smooth.
Glissonian Cirrhosis
In this, there is spread of the chronic fibrosing
inflammation of Glisson's capsule. The fibrosis extends over
a short distance beneath the capsule and is not considered
to be a cirrhosis.
Central Cirrhosis
In this, fibrosis occurs around the central veins due to
chronic valvular stenosis or incompetence. The fibrous tissue
around the central vein does not show extensive spreading
growth.
Treatment I Management
Hepatitis in domestic animals is caused by different
animate and inanimate factors like bacteria, viruses, parasites
and poisons etc. These factors can induce either acute or
chronic hepatitis. After the cause and the kind of hepatitis
have been diagnosed in animals, rational selection of drugs
can be made.
Hepatitis in animals can show changes like enlargement
of liver, chronic indigestion, dullness, clay coloured faeces,
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Acute Gastritis
It may be of catarrhal or haemorrhagic type.
Causes
The main causes are:
(1) Arsenic, phosphorus and carbontetrachloride in cat-
tle and sheep etc.
(2) Hot fluids, frosted foods and irritant vegetables.
(3) Bacteria, viruses and parasites.
Pasteurella multocida, rinderpest virus, Erysipelothrix
rhusiopathiae and trichostrongyles cause gastritis in the
animals.
Signs
Anorexia, vomiting and pain etc., are the main signs
of the gastritis.
PATHOLOGY
Gross Changes
The gastric mucosae may be swollen, reddened and
thrown into irregular folds. The mucosae can be found
covered with mucopurulent exudate. There can be reddening
and covering of the gastric mucosa with bloody exudate in
acute haemorrhagic gastritis. The presence of extravascular
blood on the gastric mucosa is an important sign of
haemorrhagic gastritis.
Microscopic changes
The mucosa of the stomach is found congested and also
shows numerous haemorrhages. The epithelium of the
abomasum or stomach may be found desquamated. Some
neutrophilic infiltration into mucosa and submucosa can be
found. Lymphoid hyperplasia in the mucosae may form some
nodules.
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Chronic Gastritis
Acute gastritis can be followed by chronic gastritis or it
may be chronic from the very outset. Parasites cause chronic
gastritis in animals.
The main parasites are:
Parasites Animals
1. Species of Ostertagia, Trichostrongylus and Cattle
Haemonchus
2. Gasterophilus and Trichostrongtjlus spp. Horse
3. Ascarides Puppies
Signs
Anorexia, vomiting, lethargy and anaemia are found in
the affected animals.
Pathology
The mucous membrane is prominently thickened near
the pylorus and elevation and folding of the mucosae can
arise from epithelial hyperplasia in the fundic region of the
stomach. Microscopically, the increase in the connective tissue
elements is noti~ed in the sections of the stomach.
Inflammatory cells are present in the lamina propria. The
mucosa of the stomach is covered with viscid, adherent and
mucopurulent material. The mucosa has reddish brown
colour due to haemorrhages and the surface of the mucosa
is irregular and granular in appearance. The surface
epithelium is desquamated and the glands may be atrophied
or cystic in appearance. In atrophic chronic gastritis, the
mucosa of the stomach is thinner and smooth but in the
hypertrophic form, the mucosa is thickened and prominent.
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Diagnosis
It is based on the symptoms, lesions and identification
of the etiological factors in the faeces. Bacteria like E. coli and
Salmonella spp. can be isolated from the faeces. Parasites can
be found in faecal matter. There is severe diarrohea, serous
atrophy of fat in the chronary grooves of the heart and bone
marrow and loss of weight with normal temprature in
oestertagiasis.
Treatment I Management
The condition of enteritis is recognised by diarrhoea (loose
motion) and dysentery (loose faecal matter mixed with blood).
There are diverse causes of enteritis and treatment of enteritis
can be successful if causes of enteritis like rinderpest, H,S
parasitic infection and Jhone's disease etc., are known.
Use of drugs acting selectively against the organisms or
parasite ensures success of treatment.
The specific treatment of enteritis has already been dealt
with under the heading of specific diseases.
However, the following general line of treatment can
be given to treat cases of enteritis in the absence of diagnosis
of causes.
(i) Use of Astringent powder such as Neblon powder,
Didisco powder - 50 gm BID for 5 days.
(ii) Sulpha drugs or antibiotics can be used such as sulpha
boulus or diadine bolus (3 boluses BID in large animals
for 5 days). Stec1in bolus or Terramycin tab. or Gastina
tab. 4-6 tab. twice daily for 3-5 days can be used.
(ill) In case of dehydration, fluid therapy should be given.
(iv) In case of enteritis with fever, antipyretics are recom-
mended.
If there is no recovery in the affected animals with
enteritis, it indicates turning of acute enteritis into chronic
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Gross Changes
In cattle, one or both kidney s are usuall y affected.
The main lesion s are :
(1) Enlarg ement of the kidney s.
(2) Thick capsul e adher ent to the under lying renal tissue.
(3) Mottle d surfac e of the kidney s (appea rance of greyis h
white patche s agains t the norma l reddis h brown col-
our ofthe kidney s).
(4) Absce sses and areas of haemo rrhage s.
(5) Dilata tion of the calices with dirty greyis h or brown ish
exuda te. The exuda te may be blood staine d, slimy or
muco id fluid contai ning pus, necrot ic mater ial and
conce retion s etc.
(6) Greyi sh white streak s owing to exten sion of the
suppu rative processess.
(7) Destru ction of the renal tissues borde ring the calices.
Pus can even replac e much of the renal parenc hyma.
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Microscopic Changes
In infectious of the kidneys, the uriniferous tubules are
found dilated and filled with desquamated epithelium,
leucocytes, cast and bacteria etc. A prominent leucocytic
infiltration is found around the tubules and glomeruli.
Necrotic changes are found in the renal tissues around the
renal pelvis. There is also presence of haemorrhages and
infarcts in the kidneys. There is a severe destruction of the
renal parenchyma and interstitial changes are seen in the
kidneys.
Pus, albumin, bacteria, blood and catarrhal cells are
found in the urine of such patients of pyelonephritis.
Perinephric Abscesses
In this condition, abscesses are found around the
kidneys. The suppurative processes may extend into kidneys.
It differs from pyonephrosis in which abscess is found in the
parenchyma of the kidneys.
Non-suppurative Nephritis
As the term implies, non-suppurative nephritis is caused
by different factors other than the pyogenic organisms or
non infectious agents and is commonly found in domestic
animals and its occurrence is not common in carnivores.
The details of the different kinds of non-suppurative
nephritis are as follows:
1. Acute Nephritis
In this, acute inflammatory changes are noticed in the
kidneys. Any injury to the glomeruli results into tubular
destruction as the blood supply to the tubules is dependent
upon the normal functioning of the associated glomeruli.
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Causes
The main causes are:
(1) Bacterial Toxins
Toxins are produced in pyaemia and strangles in the
body of animals.
(2) Chemical Poisons
Turpentine, cantharides and carbolic acid are examples
of such poisons.
(3) Harmful products of faulty metabolism.
(4) Extensive damage to the skin as seen in burns, mange
and eczema etc.
(5) Injuries or Cold
Nephritis can be caused by such aforesaid factors and
can assert itself in the exacerbated form with development
of acute inflammatory changes in the kidneys.
Pathology
Gross Changes
Little or no change can be seen in the kidneys. The
kidneys may be swollen and paler than normal. The kidneys
are soft to the feel or touch and the capsules are very much
distended and can be easily be striped off leaving behind a
smooth renal surface.
Small haemorrhages are found in the renal parenchyma
and the enlarged glomeruli are visible to the naked eyes.
Microscopic Changes
The histopathologic changes can be found in the
glomeruli, tubules and interstitial tissue and the conditions
produced are known as (1) glomerulonephritis, (2) tubular
nephritis and (3) interstitial nephritis respectively.
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317
Table30. Main Pathologic Changes in Some Types of Glomerulonephritis
Acute Proliferative Membrano Proliferative Chronic Focal Embolic Membranous
Glomerulonephritis Glomerulonephritis Glomerulonephritis Nephritis Glomerulonephritis
1. An important condition 1. It is seen as a na turally 1. Kidneys smaller than 1. it is noticed in 1. it is noticed in man and
noticed in children and occurring disease of nomlill with pitted surfaces the cases of arumals 2. Thickening,
some aninlills affected with animals. Increase of 2. Occlusion of the lumens bacterial splitting and reduplication
streptococcal mfections. 2. mesangial cells (a third of glomerular capillaries endocarditis in of the glomerular basement
Enlarged pale kidneys with kind of cells associated with and increased numbers of man, cattIe, swine membranE: 3. Loss of foot
petechiae and occluded tile endothelium and endothelial, mesangial and and dogs etc. 2. processes of tile podocytes
glomeruli 3. Enlarged epitIlelium of glomerular epithelial cells. 2. Abscesses and (i.e., the epithelial cells of
glomerular tufts due to tufts). 2. Thickened Proliferated epithelial cells petecluabon in the the glomeruli) 4. Irregular
proliferated endothelial and mesangial basement foffiling crescents in the kidneys 3. tluckening of the
mesangial cells of tile membrane and splitting of Bowman's capsules. 3. Proliferated glomerular basement
glomeruli 4. Neutrophiles tile basement membrane. 3. Bowman's capsules epitIlelial cells membrane and its humpy-
and monocytes infilterated Presence of obliterated or adherent to (bOtIl parietal and bumpy appearance.
into glomeruli and inununoglobulin deposits occluded glomerular tuft. 4. visceral) foffiling
compressed glomerular (humps) on the Degenerative changes in crescents in the
capillaries lacking red cells. subendothelial SIde of the the epithelium of Bowman's
5. Proliferated parietal basement membrane of the nephrons, ischaemia, capsules. 4.
epltIlelial cells (capsular glomeruli. 4. Humpy and tubular atrophy and Neutrophilic
epitIlelial cells of Bowman's bumpy appearance of the interstitial fibrosis. infiltration in the
capsules). Presence of fat in disrupted basement necrosed glomeruli
the swollen tubular membrane of the glomeruli and bacterial
epithelial cells of tile seen in stained sections of colonies lodged in
affected kidneys. tile kidneys by silver the glomeruh.
staining method.
Some Miscellaneous Pathological Conditions/Diseases
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Pathalogy
The kidneys are small, fibrous and pale in colour. The
renal surface may be rough or granular and the capsule may
be thickened and adherent to underlying renal tissue. The
stripped capsule shows fragments of the kidneys leaving
behind a rough surface. The cortex is very much narrow due
to destruction and can be seen as a mere rind i.e., hard skin
of the fruits. The medullary and boundary zones are wide
and show cysts due to dilatation of the tubules. In dogs,
proliferation of fibrous tissue is found in the medulla and
boundary zones. In a form of chronic nephritis of dogs, the
capsular adhesions are not the main changes and the medulla
and its boundary zone shows fibrous tissue proliferation. The
glomeruli can be found destroyed and there are crescents
showing hyaline changes or may be replaced by the fibrous
tissue in case of chronic nephritis. The increase of connective
tissue between the tubules is a conspicuous change. The
tubules may be dilated and form cysts like spaces due to
compression of the tubules by the growing fibrous tissue.
The animals suffering from chronic nephritis ultimately
die.
Nephrosclerosis
In this, there is a renal fibrosis due to an arterial disease
(Le., an arterioselerotic condition). Hypertension is found in
man suffering from nephrosclerosis. Narrowing or
constriction renal of vessels causes necrosis and subsequent
fibrosis of the glomeruli. Necrosis follows obliteration of the
vessels. Tubules show degenerative changes. Atrophy, fibrosis
and necrosis are found alternating with areas showing little
change owing to existance of some normal glomeruli and
tubules. The kidneys present numerous infarcts in their
parenchyma. The depressions on the surface of the kidneys
are found due to contraction of fibrous tissue in the kidneys.
The nephrosclerosis may occur with or without hypertension
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Treatment I Management
Nephritis in animal is caused by different factors, like
bacteria, parasites and poisons etc. The signs of pain, dysuria,
albumin or blood in urine, oedema, and uraemia warrant
immediate attention of the clinician for the sake of treatment.
For treating nephritis, cultural examination of urine is done
to find out antibiotic sensitivity of organisms in question.
The treatment of nephritis is continued over a long
period, say 10 to 15 days, for eradicating infection. Antibiotics
such as streptomycin, gentamycin, nitrofuran and
ciprofloxacin etc., can be used. Leptospirosis causes nephritis
in dogs whereas pylonephritis (pyelitis and nephritis) are
caused by Conjnebacterium renale in cattle. These infections
in such animals respond well to treatment in time.
The other drugs used in nephritis are as follows:
(i) Use of diuretics: Diuretics should be used with caution
and also with object of eliminating toxic and waste metabolic
products from the body. The patients of nephritis are marked
by signs of ascites and oedema in their bodies. In cattle and
dogs, lasix can be used to treat the complications like ascites
or oedema.
Phenacetin in doses of 4 gm mixed with treacle can be
given twice to horse and cattle as diuretics.
(iii) Fluid therapy and antiemetics can be given to
animals (specially dogs) in case of vomiting and dehydration.
Oedema
It denotes the excessive accumulation of fluid in the
tissue spaces, body cavities and cells etc., due to disturbance
in the fluid interchange machanism between tissues spaces,
capillaries and lymphatic vessels.
The main types of oedema are:
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Pathology
Oedema in tissue spaces or serous cavities does not arise,
when the existing balance of pressure between the
hydrostatic pressure and the plasma osmotic pressure at the
venous end of capillaries permits the return of the fluid to
the capillaries from the tissue spaces. In other words, the
plasma osmotic pressure( inward attractive force) is greater
than capillary hydrostatic pressure( outward expulsive force)
at venous end of capillaries.
The main pathological conditions seen in animals are
as follows:
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perito mitis, pleuri tis (pleurisy) and perica rditis etc. In oedem a
due to hypop rotein aemia , one notices fall in the level of serum
protei ns.
Treatment I Management
The prima ry cause of oedem a is the guidin g princi ple of
treatin g the cases of oedem a.
1. Use cardia c tonics digito xin or digita lin to treat oedem a
in conge stive heart failure as seen in the cases of steno-
sis or incom petenc e of heart.
2. Oedem a due to parasi tic gastro entriti s is treate d by us-
ing anthel mintic s.
3. Oedem a due to hypro protei naemi a in anima ls needs the
admin istrati on plasm a substi tutes. Such anima ls may
be given diets rich in protie ns.
4. Water and salt intake s should be restric ted.
5. Restri ct the admin istrati on of diuret ics and aspira tion
of fluid. Dirure tics like laxis or diamo s may be used to
remov e oedem a fluid from the body.
6. Oedem atous fluid from the cavities should be aspira ted
slowly to avoid the periph eral circula tory failure or acute
dilata tion of splanc hnic vessels in the abdom inal cav-
ity. One-t hird of the fluid from a cavity (say, abdom inal
cavity) is to be remov ed by parace ntesis abdom inis.
7. As a suppo rtive treatm ent, liver extract, nervin e tonic
and vitam in B compl ex (oral) and iron prepar ation are
given to the anima l patien ts.
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Pathology
1. Marked hyperaemia and haemorrhages in tissues of cra-
nial part of body like tongue, nasal sinuses, lymph nodes
and proximal part of the oesophagus due to ruminal
tympany. Such changes are not apparent in the caudal
part of the body.
2. Distended abdomen and frothy contents seen at autopsy
conducted soon after death.
3. Compressed state of the lungs, pale liver due to expul-
sion of blood from the liver because of tympany.
Treatment I Management
Treatment measures depend upon the kind of tympary
and differ in both the frothy bloat or free gas bloat. The
trocar and canula is used for emergence or release of the
ruminal contents and gas in the bloat. H animal's life is not
threatened, the passage of the stomach tube is recommended
for immediate relief.
Viral Diarrhoea
Rota viruses, coronaviruses, toroviruses and
parvoviruses cause viral diarrhoea in new born farm animals
like lambs, kids, piglets, foals. Viral infections spreads to
healthy young animals by faeces. Specific antibody in
colostrum offers resistance to young suckling farm animals.
Bovine coronaviruses (being pneumonic tropic viruses) cause
respiratory diseases in young calves.
The main signs and age groups of different young farm
animals are as follows :
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Some Miscellaneous Pathological Conditions/Diseases
3. Parvoviruses
These have been associated in outbreak of postweaning
diarrhoea.
4. Toroviruses
These are also associated with diarrhoea in young calves.
Group A rotaviruses cause diarrhoea in foals.
Pathology
Calves, lambs, pigs and foals show similar viral
pathogenesis, infected epithelial cells become detatched and
epithelial regeneration is noticed within 4-6 days following
the onset of diarrhoea: Lactose malabsorption is noticed in
young patients of virus diarrhoea. Parvovirus infection causes
lymphopenia and damages the small intestinal crypt
epithelium with villous atrophy. The faeces are voluminous
mucoid and slimy, dark green or light brown in colour in
calves infected with coronaviral enteritis.
Diagnosis
It is based on symptoms, lesions and detection of virus
in faeces by electron microscopy. Immunofluorescence tests
using faecal smear and fluorescent antibody technique are
performed to confirm viral infection. ELISA test is done to
detect virus in the faecal matter.
The most marked pathological lesions of viral diarrhoea
are dehydration, fluid filled intestinal tract and distension of
abomasum. Villus fusion or atrophy is noticed in the intestinal
mucosae.
Treatmentl Management
The treatment procedure is the same as done in the causes
of undifferitiated diarrhoea of calves. The withholding of milk
for 24-48 hour is quite useful. Oral and parenteral fluid
therapy is quite essential in treating the diarrhoeic cases.
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Anaemia
Anaemia is a condition which is marked by either
deficiency of red cells or reduced haemoglobin content of
the blood. Red cells, incompletely charged with haemoglobin
may cause anaemia, despite the normal red cell count in the
patients. It can arise from defective blood formation or from
loss of blood (i.e. as a posthaemorrhagic phenomenon).
Excessive blood destruction causes haemolytic anaemia.
Babsia, anaplasma and bacterial haemolysins cause
haemolytic anaemia. Anaemia may be specific due to specific
causes. The main clinical signs of anaemia are pallor to
mucosae, thin and watery blood, petechial and ecchymotic
haemorrhages, haemoglobinuria and bleeding tendencies,
Postmortem findings are also specific to specific causes.
Decreased values of red cells, or PCV indicate anaemia.
Anaema may be classified as haemorrhagic or haemolytic
anaemia or anaemia due to decreased production of red cells.
In short, anaemia is marked by a decrease of red cells or of
haemoglobin or of both in the patients.
1. Haemorrhagic Anaemia
The causes of haemorrhagic anaemia are as follows :
1. Spontaneous rupture or traumatic injury to blood ves-
sels is seen in the cases of castration and dehorning.
2. Severe parasitic infestation e.g., Strongyles, hookworms,
Haemonchus spp. infestation, Fascicla hepatica and
coccidia cause severe loss of blood.
3. Clotting defects.
Anaemia is caused by coagulation defects as seen in
some acute haemolytic anaemia.
2. Haemolytic Anaemia
The causes of haemolytic anaemia are :
1. Babesiosis, anaplasmosis, trypanosomiasis and theiler-
iasis.
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Pathology
The main changes are:
1. Increase in number of immature red cells in the blood
and normal total protein in haemolyitc anaemia.
2. Presence of bilirubinemia and bilirubinuria and discol-
oured plasma. There is an increased red cell fragility
and a positive antiglobulin test in immune mediated
haemolytic anaemia.
3. Haemorrhages due to thrombocytopenia, thin watery
blood and contracted spleen, Icterus in haemolytic anae-
mia and decreased haemoglobin percentage.
4. Other changes affecting red cells are anisocytosis, (vari-
ations in sizes) poikilocytosis (variations in shapes), pres-
ence of nucleated red cells, reticulocytes and variations
in staining reaction (punctate basophilia)
5. Regeneration of red cells, replacement of the fatty mar-
row by red marrow and haemosiderosis in some organs.
Treatment/Management
The primary cause of anaemia determines the future
line of treatment in patients. Blood transfusion and
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Treatment/Management
Acute laminitis is an emergency disease which needs
immediate attention of surgeons or doctors.
The main steps of treatment of the horse are as follows:
1. Removal of causative agents.
2. Relief from pains.
3. Vasodilation of blood vessel in foot.
4. Prevention of formation of microthrombi in dermal cap-
illaries.
5. Avoiding the rotation of the pedal bone.
6. Promotion of keratinisation and hoof growth. Nor-
steroidal anti-inflammatory drugs (NSAIDS) are admin-
istered to sick horses. Phenyl betazone at doses of 2.2-4
mg/kg is given intravenously to horses. NSAID is also
administered to cattle suffering from laminitis.
Aspirin 0.3 grain/kg orally every 12 hours or phenyl
butazone 4.4 mg/kg orally every 48 hours is administered to
bovine cases of laminitis. Antibiotics are used to prevent
infection, Vasodilatory drugs are used to prevent infection.
These drugs are also used to retard progression of acute
laminitis in animals like solipeds and cattle. Anticoagulants
are used to prevent capillary microthrombi in the hoof of
the patients. -'
Diseases Caused by Zootoxins
Zootoxins introduced into the body of farm animals by
bites of snakes, stings of bees or tick bites etc., are very harmful
to these animals. Snake bites cause even death in large
animals. Fang marks are located or traced at the bitten sites.
Some details about diseases caused by zootoxins are as
follows:
Snake Bites
Snake bites inject venom in to the body of the victims
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Some Miscellaneous Pathological Conditions/Diseases
Treatment/Management
The principles behind treatment of snake bites in man
animals are almost identical.
A tourniquet is applied above the bitten site to restrict
the blood circulation. If possible, suction is soon carried to
remove the snake venom from the bite site. Tourniquet is
released at 20-minute intervals. The bitten site is incised to
reach the site of deposition of snake venom i.e., up, to a depth
of 0.5 cm. Excision at the bite site of snakes reduces local
tissue reaction. A firm pressure bandage is used in humans
to restrict distribution of snake venom by lymphatics. Snake
venom retained at bitten sites prevents systemic effects.
Application of firm pressure over the bitten areas delays
absorption of snake venom. A broad firm bandage around
the limbs above bitten areas occludes the superficial venous
and lymphatic outflow. Mechanical suction removes blood
or fluid from the bitten zones. A cross incision (about one
cm. long and 1/2 cm deep) over fang marks causes an escape
of blood or fluid containing the snake venom. The wound is
cleaned with sterile water or normal saline.
Antivenin, antibiotics and antitoxins are used Antivenin
contains antibodies against the venoms of all snakes in the
areas of snake bite incidence. The i/v route is preferred for
quick effects. One unit of antivenin is sufficient for animals
weighing 70 kg or more but smalIer animals of 9-18 kg b.w
require about 5 units of antivenin. Broad spectrum antibiotics
are administered into the victims to control the local infection.
Sedatives may be given to control pain and excitement.
ACTH, cortisone and antihistaminics are used to protect the
victims from anaphylaxis.
Bee Stings/Stings of Scorpions and Wasps
Severe local swellings (up to 6 cm. diameter) are caused
by multiple stings of bees. The swellings in lips, eyelids, tongue
and in vulva are painful. Diarrhoea, haemoglobinuria
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Some Miscellaneous Pathological Conditions/Diseases
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Some Miscellaneous Pathological Conditions/Diseases
1. Hypovolaemic Failure
It arises from reduction in circulationg blood volume
due to blood or fluid loss.
2. Vasogenic Failure
It is caused by peripheral vasodilatation, pooling of
blood in vessels and lack of blood into tissues.
3. Septic or toxic shock
Toxic or septic factors cause vasogenic failure because
of loss of vascular integrity or increased vascular permeability.
Impairment of oxygen uptake, anaerobic metabolism in tissues
and widespread cellular dysfunction cause shock to pass into
an irreversible shock or death.
Severe burn injuries, extensive surgery, prolapse of
uterus, sudden reduction of pressure in body (for example,
quick withdrawl of ascitic fluid), severe pain (as seen in colic)
and trauma with local sequestration of blood and fluid can
induce shock in animals. Potent endotoxins of Gram negative
organisms cause toxic (septic) shock in animals. Shock is seen
in animals affected with septicaemic diseases or Gram-
negative bacterial infections and toxic infections (e.g., acute
gangrenous mastitis, acute mastitis and paracute coliform
mastitis). An absorption of toxin from intestines and infarction
in intestines induce septic or toxic shock in animals.
Endotoxins or other bacterial toxins damage the endothelial
cells of the capillaries which turn into leaky vessels.
The main clinical findings are depression, weakness and
restlessness with a fall in body temperature.
Pathology
There are no specific autopsy findings in the cases of
shock. Congestion in the capillaries and small vessels of the
splanchnic area and pulmonary oedema are noticed in toxic
shock. Traumatic injury is noticed in the animals died of
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Some Miscellaneous Pathological Omditions/Diseases
351
Chapter 9
Some Metabolic Disorders
and Others
Milk Fever
The term milk fever is a misnomer as there is no fever or
no milk in this disease of animals. It does not indicate what
its term implies. and occurs in the dairy cows and some times
also in sheep. Hypocalcaemia and defects in the parathyroid
glands (poor level of parathormone) cause this condition in
the animals. It is characterized by hypocalcaemia (calcium
level may be as low as 3.0 mg per 100 ml of blood).
Hyposphosphatemia and slight hypermagnesemia are also
present. Certain information as regards the diseases in bovines
marked by recumbency are given in table 34.
Table 34. Pathological Signs and Lesions in the Diseases
of Animals (bovines) Marked by Recumbency
Diseases Diagnosed Common Pathologic SignsfFeatures Expected
Signs or
Lesions
(1) (2) (3)
1. Milk fever Recumbency Mature cows usually affected within 48
(parturient paresis) hours of calving. Early excitement and tetany
characterized by no followed by coma, hypothermia, flaccidity,
fever and no milk. dilated pupil, absence of ruminal
An example of movements, soft heart sounds and
metabolic disease impalpable pulse. Presence of hypocalcaemia
often noticed in (calcium less than 5 mg/ dl (l.25m moljL).
cows. High level of magneSium in serum (over 3
mg/ dl) 1.25 m moljL). inorganic phosphate
low i.e. less than 3 mg/ dl (0.9 m moljL).
Quick response follOWing injection of soluble
calcium salt. Absence of gross and
microscopic lesions in fatal cases.
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Some Metabolic Disorders and Others
Signs
The main signs of the disease are :
(i) Recumbency, somnolence. Often cows are found in
comatose condition. The sick animals are seen lying on
their sternum with their heads turned towards their
flanks.
(ii) Inability to stand on their feet and death within a day
or two due to lack of treatment.
353
Advanced Pathology and Treatment of Diseases of Domestic Anzmals
Pathology
There are no significant gross and microscopic lesions
in milk fever in the sick animals.
Downer Cow Syndrome
It refers to those cases of milk fever in cows which do
not respond to calcium therapy and patients fail to stand on
their feet. This syndrome incorporates complicated lingering
cases of milk fever. The animal may be alert with usual
appetite but attempts to stand on their legs are unsuccessful.
Treatment/Management
Since milk fever is a disease developing due to low blood
calcium level, treatment is directed towards correcting the
level of calcium in the body after detection of symptoms in
the animals.
The following drugs can be used:
1. Calcium borogluconate preparation is a drug of choice
and can be given in the doses of 400 - 500 m1 of a 20%
solution. Calcium borogluconate is given slowly by if v
route. It is better to warm the bottle equal to body tem-
perature and if v injection should be interrupted for 20
- 30 seconds twice during administration. The adminis-
tration may be completed within 20 - 30 minutes and
there should be auscultation of heart during if v admin-
istration of the drug. If there is any irregularity in heart-
beats, its administration is stopped immediately.
2. Antihistaminic drugs or cortisone can be given.
3. Mifex may also be used in place of calcium
boroglucona te.
4. In order to maintain blood calcium, drugs like Caldi -
12 in dose rate of 15 - 20 m1 if m daily for 3 days is
advocated.
Supportive treatment should also be given in the form
354
Some Metabolic Disorders and Others
355
Advanced Pathology and Treatment of Diseases o/Domestic Ammals
356
Some Metabolic Disorders and Others
357
Advanced Pathology and Treatment of Diseases of Domestic Ammals
358
Some Metabolic Disorders and Others
Magnesium Deficiency
Magnesium is an important intracellular bivalent cation
in the body of an individuaL It is involved in many enzymic
reactions or biologic activities. The different kinds of reactions
in which the magnesium is involved are as follows:
(i) Membrane transport.
(ii) Activation of aminoacid, acetate or succinate.
(ill) Synthesis of protein, nucleic acid, fat or co-enzymes.
(iv) Generation and transmission of nerve impulses and con-
traction of muscles.
(v) Oxidative phosphorylation.
(vi) Activatior of alkaline phosphatase and adenosine tri-
phosphatase (ATP) Normal level of magnesium in blood
is 2.0 mg/l00 ml.
Dietary deficiency causes low level of magnesium.
The main signs of magnesium deficiency are as follows:
There is a nervous hyperirritability. But high levels of
magnesium cause depression, coma and death.
Grass tetany of adult cattle and hypomagnaesema of
calves are its important clinical syndrowes.
359
Advanced Pathology and Treatment of Diseases of Domestic Animals
Hypomagesemia in Calves
A diet low in magnesium (like milk) causes this condition
in calves. The level of magnesium is 0.7 mg/lOO ml of blood
and magnesium falls to one third of its normal value.
Signs
There are hyperirritability, tetany, scratching, fixed
depression of the ears and opisthotonos, kis::king of the belly,
salivation and exophthalmos and tonic and clonic
convulsions.
Pathology
Necrosis of myocardial fibres takes place. Later,
calcification occurs at such sites. Metastatic calcification is
seen in calves maintained on a diet low of magnesium.
Calcification can also occur in the kidneys and muscles as
well. Due to hypomagnesemia, calcification in the internal
layer of heart and large blood vessels is noticed. Grossly, these
lesions occur as slightly raised, light coloured plaques on the
internal surfaces of heart etc. Renal tubules show toxic
degenerative changes. Agonal haemorrhages are noticed in
heart, intestinal and mesenteric serosae in calves.
Grass Tetany
Affected animals like cattle, sheep and rarely horses
show tetanic convulsive seizures and incoordination of limbs.
Asphyxia and agonal haemorrhages occur in the affected
animals.
In winter tetany in cows, hypocalcaemia and
hypomagnesemia are noticed. Nutritional deficiency of
magnesium causes hypomagnesemia. A ration deficient in
magnesium also produces metastatic calcification in foals.
Treatment/Management
Lactation tetany or hypomagnesemia arises from
360
Some Metabolic Disorders and Others
361
Advanced Pathology and Treatment of Diseases of Domes tic Animals
362
Some Metabolic Disorders and Others
pigments (myoglobins).
Diagnosis
It is based on the symptoms and lesions in the affected
muscles and presence of myoglobin in the urine of the
patients.
Treatment/Management
This disease affects the horses with characteristic
degenerative change in muscles and kidneys etc. The
treatment is directed as ameliorative measures. The measures
are as follows:
(i) The horses should be given complete rest and they
should never be put to exercise.
(ii) Give chloral hydrate 30 gm as a drench.
(ill) Alternatively inject largactil 5 % som. in dose of 4 to 6
m1 (ifm).
(iv) Thiamine hydrochloride can be given in dose of 500 mg
by if m or if m route.
(v) Antihistaminics like Avil or Zeet in doses of 10 to 20 m1
can be given if m.
(vi) Vitamin E can be given interamuscularly.
(vii) Fluid therapy (5% or 10% Dextrose solution) can also
be given.
363
Advanced Pathology and Treatment of Diseases of Domestic Animals
Signs
1. Appearance of symptoms in the period 2-4 weeks after
calving. Sudden onset of haemoglobinuria, inappetence
and weakness in the calved animals
2. Fall in milk yield and discolouration of urine. Develop-
ment of dehydration, pale mucous membrane,
augumented pulse, rise of temperature upto 103.5F,
dry and firm faeces are noticed in the affected dams.
3. Other signs include dyspnoea, weakness, staggering and
recumbency, ketosis and sloughing of the tail.
4. Inorganic phosphorus level in the affected animal may
be as low as 0.4-1.5 mg/ dl (0.13-0,400 m moljL).
Marked fall in the red cell count and haemoglobin value
are noticed.
5. The urine in the affected animals is dark brown or black
in colour.
Pathology
The main changes are :
1. Jaundiced carcass due to haemolytic icterus.
2. Thin and watery blood. Red cell count less than 2 mil-
lion per cubic millimeter of blood (i.e., presence of
severe anaemia).
3. Swollen liver with fatty changes (fatty degeneration and
fatty infiltration) Centrilobular necrosis and midzonal
fatty changes are noticed. In short, there is a presence
of acute toxic hepatitis.
Diagnosis
It is based on the symptoms and changes in the blood
and urine etc. Occurrence of haemolytic anaemia within 4
weeks of calving is a characteristic indication of
postparturient haemoglobinuria. Haemolytic jaundice,
haemoglobinuria, and acute toxic hepatitis marked by
phosphataemia help diagnosis of postparturient
364
Some Metabolic Disorders and Others
haemoglobinuria.
Treatment/Management
The steps are as given below :
1. Transfuse 5 litres of blood to severely affected cows. If
required, transfusion may be repeated after 48 hours.
2. Fluid therapy (i.e., 5% dextrose) is also adopted to com-
pensate the fluid loss.
3. Administer sodium acid phosphate (60 gms in 300 m1
of distilled water by ilv route. The same dose in dis-
tilled water is also to be given to the patients by sic
route at the interval of 12 hours. A similar dose of so-
dium acid phosphate is also given orally.
Photosensitisation
It denotes the condition characterised by sentisisation
of the skin (Le., the superficial layers of lightly pigmented
skin), mucosa and cornea following exposure to sunlight in
animals like cattle and sheep. Photosensitivity in the skin
arises from the presence of photodynamic substances in
sufficient concentration in the skin. Porphyrins of both the
animal and plant origin are known to originate from the
decomposition of the pigments like haemoglobin and
chlorophyll. These substances are sensitive to light. Presence
of porphyrins in the blood is called porphyrinemia. If these
are present in the urine, the condition is called porphyrinuria.
Skin sensitisation to light arises from porphyrinemia.
The photodynamic substances may be exogenous or
endogenous in nature.
Types of photosensitisation
These are:
(i) Congenital porphyria or pink tooth.
(ii) Primary photosensitisation.
(iii) Secondary photosensitization.
365
Advanced Pathology and Treatment of Diseases of Domes tic Animals
I
The condition of pink tooth occurs in cattle whose
.
bones
and teeth possess reddish or brown colour due to deposition
of porphyrins in these tissues. Such pigments can also be
found in some internal organs. Porphyrinuria is also noticed
in the lead poisoning in dogs.
Aetiopatholgy
The causes and pathological changes are given in the
table 35:
Table 35. Types Causes and Pathological Changes in
Different types of Photosensitisation
Types of Causes Pathological Changes
Photosensitisation
(1) (2) (3)
1. Congenital 1. Porphyrins formed in 1. Presence of porphyrins in
porphyria excess due to aberrant the urine, bones and teeth.
pigment synthesis. 2. Reddish or brown colour of
the teeth etc.
2. Primary 1. Ingestion of exogenous 1. Presence of dermatitis in
photosensitisation photodynamic agents unpigmented skin. Animal
present in certain plants. The patients are very much
plants and the pigments are sensitive to light and prefer
as under. sheds. The liberated
Plants PhotodynaIDlc agents histamine from the damaged
HypericulIl Hypericin skin due to sun light leads to
perforatum tissue oedema and cell death.
Polygollllln
Loss of skin is noticed.
esculelltllm
Subcutaneous oedema and
Fagopyrum Fagopyrin enlargement of local lymph
eSCll/elltllm nodes are found.
2. Chemicals e.g.,
phenothiazine and sulfoxide
acridine dyes. The metabolic
product phenothiazine
sulfoxide is a photodynamic
substance in calves.
3. Hepatogenous 1. Phylloerythrin. It is an end The damaged liver fails to
photosensitisation product of chlorophyl remove phylloerythrine from
metabolism in the body and the portal blood and this
is excreted in the bile. pigment is carried to the skin
Hepatitis or biliary by circulating blood. When
obstruction causes the poorly pigmented skin is
accumulation in the skin exposed to sun light,
366
Some Metabolic Disorders and Others
Diagnosis
It is based on the followings :
1. Skin lesions on the unpigmented areas.
367
Advanced Pathology and Treatment of Diseases of Domestic Animals
Treatment/Management
Some steps of treatment are as follows :
1. Remove the animals from direct sunlight.
2. Prevent the animals, from taking the toxic water, soaked
hay or grass contaminated with fungi.
3. Administer laxatives to remove toxic materials from the
gut.
4. The animals are given anti-histaminics immediately in
adequate doses.
5. Use antibiotics to check the development of septicae-
mia in animal patients.
6. Administer 5% Dextrose as fluid therapy to dilute and
eliminate the absorbed toxins.
7. Calcium borogluconate (25%) at the dose rate of 250 m1
intravenously and the same dose by subcutaneous route
should also be given.
8. Liver extract (e.g., livogen, Belamyl) at the rate of 10 m1
intramuscularly is given on the altemate days.
External application of drugs on skin lesions include use
of Himax and Herbex.
Equine Colic
It is a disease of horses recognized by the presence of
abdominal pain. Colic arises from distension of the stomach
or intestines due to accumulation of ingesta, gas and fluid.
Transient distension also occurs due to spasm or increased
peristalsis in the intestine.
The chief causes of colic in horses are the following :
1. Low grade roughage, lush green feed, exhaustion, ex-
cessive perspiration and. retained meconium etc. Dis-
tension results from accumulation of ingesta as noticed
368
Some Metabolic Disorders and Others
369
Advanced Pathology and Treatment a/Diseases of Domestic Animals
Pathology
Rupture of the stomach or intestine can lead to death of
the horse. Large .quantities of toxic ingesta or faecal contents
in the peritoneal cavity can cause choking or death within a
few hours. The animals get exhausted due to pain or
autointoxication. There is a marked degenerative change in
the mucosae and this change is more evident in the
obstructive colic. The damage is more marked in the intestine.
Distension of the intestine is seen in cases of colic due to
peritonitis and verminous measenteric arteritis. Verminous
arteritis causes an infarction of the gut wall.
Diagnosis
It is based on the symptoms like severe pain, absence of
gut sounds and defaecation (acute obstruction of the small
intestine), recurrent attacks of pain (verminous mesenteric
arteritis), fever and toxaemia (infected verminous arteritis),
flank watching and lying down frequently (as seen in
subacute or chronic obstruction) Rupture of the gut or
deposits of faecal contents in the peritoneal cavity can be
seen postmortem.
Treatment
In cases of flatulent colic, gases from the stomach should
be removed by passing stomach tube. A funnel can be
attached to stomach tube and the following drugs can be
used
Oil terebinth 20 m1
Acid carbolic 20 m1
Oil line 300 m1
Timpol100 m1 is given as drench with lukewarm water.
Anti-allergic drug lke Avil-5 to 10 ml can be given by
intramuscular route.
In colic due to impaction of large intestine, the following
drug can be used
370
Some Metabolic Disorders and Others
Aloes barb IS gm
Aqua ferv (warm water) A.S.
01. Terebinth 60ml
Chlonal Hydras 30 gm
Ol.lini SOOml
RI
Mft. haust. sig. Dissolve aloes and chloral hydras in hot
water and shake well with oil of Turpentine and linseed oil.
Administrator as a dresh slowly.
Preparation to Treat Spasmodic Colic.
RI
Choloral Hydras 30 gm
01. Terebinth 30ml
01. Lini 500ml
Mft. Haust. sig. Administrater
by stomach tube or
inj. Novalgin (Hoechst)
inj. Beralgan (Hoechst) 15 - 20 ml intramuscularly
371
Table36. Physiological Values of Domestic Animals
373
Table 37. Some information about Chemotherapeutic agents
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs)
Administratio
Sp ecialities
n
Antibiotics Longacllhn, All Species of i. 4000-10000 In case of Parenter al Anthrax, B.Q.
1. BenzaUune 6,12,2448 lakh animals. uruts per kg. Benzyl (I/M) tetanus.
Penicillin and units mjectlon body weight penlCllhn 6-12 mahgna nt
derivatives 11. Pronape n 20 or hours and for oedema, baCillary
lakh Units 5mg/kg .bwt procaine haemogl obmuna ,
Iil. Pronape m-40 every week. penlCllhn 24 braxy, F.MD.,
lakh uruts hourly. entero toxaemia,
IV. Bestripen-40 Young F.M.D., foot rot,
lakh uruts arumals and Joint III or na vel
ProCllhn- vet. small ammals
20 and 40 lakh
ill.
are given
units higher doses.
VI. Frobfed
Procame peruclllln Dogs/Ca ts 2-4 Lakh
(inJ). umts.
2. Cloxa::illin & !.Indox SOOmg. All SpeCIes i. Large animals 12 hourly
ampicill in r/M Anthrax,B.Q.,H.S.
1000mg . and 4-7mg/ kg ,
2000 mg.mJectlOn Body weight tetan us, braxy etc.
11. Bmocm-1000 & 11. Small ammals
2000 mg. injection 4-10 mg/kg
Ill. Catloxln J.
iv. Betalactm InJ. -do- 1I1.5mg/kg.b.
wt.
Chemotherapeutic Pharmaceutical Species Dose rate Repetition Route of Indications
Agents products (drugs) Administrati
specialities on
3. Ampicillin i. Marcocillin inj. All species. 2-7mg/kg 12-24 I/M Respiratory, urinary,
ii. Albercillin inj. Body weight. hourly and genital tract
iii Conampi inj. 3-5days. infections. Anthrax,
iv. Eskycillin inj. B.Q., & tetanus etc.
v. Dynacil-Vet.inj.
vi. Catcillin inj.
vii. Vetampin inj.
viii. StancilIin inj.
4. Streptomycin i. Combiotic Large and liorse/foal/cow 10mg/kg 24 hourly I/M Urinary, respiratory,
and penicillin smaII vial inj. /calf Body weight gastrointestinal, tract
ii. Munomycin forte inj. /sheep/ goats/ infections. T.B.,
iii. Dicrysticin-s 10-20mg/kg Johne's disease,
Large vial Dogs and cats Body weight actinomycosis and
iv. Vetopeninj. O.5gm/SOkg bwt actinobacillosis etc.
0.5 gm, 1.0 gm, 25 Large animals 0.25mg/5kg bwt
gm SmaII animals
5. Kanamycin Kanacin inj. 1 gm All species 7-10 mg/kg Body 12 hourly I/M Urinary tract
weight infection. mastitis,
respiratory tract
infection, metritis
cervicitis etc.
6. Gentamycin i. Gentamycin inj. All species 12 hourly, Respiratory tract,
sulphate lP. ii. Genticin inj. SmaII animals 2-4 mg/kg bwt. for 7-9 days I/M urinary tract, geni tal
iii. Gentim inj. Large anintals 1-2 mg/kg bwt. tract infections,
mastitis etc.
Chemotherapeutic Phamtaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administratio
Specialities n
1 2 3 4 5 6 7
vi.Catlogenta Do Do Do Do Do
7. Amoxycillin I. Moxel inj. All species. 5-10mg/kg. 24 hourly I/M Respiratory
+ 2000mg. Body weight. problem, HS
Cloxacillin urinary tract
infection etc.
8.Oxytetracyc1in i. Terramycin inj. All species 5-10mg/kg 24 hourly I/M H.S., B.Q.,tetanus,
ii. Tetra inj. Body weight. respiratory,
..
ill. Oxy. Stec1in ID). urinary and
iv.Terramycin-LA genital tract
v.Oxyvet-LA 10-20 IDg./kg. At 72 hrs. infections
vi. Telon-LA Do Body weight. interval etc.actinomycosis,
vii. Veterinary anaplasmosis,
oxytetracyclin inj. Cattle/Horses/ 5-10 mg./kg. Do leptospirosis etc.
Buffaloes. bwt.
9. Tetracyclin Hostacyclin water Horse, cattle, 5 to 20 gm. or 24 hourly Oral use Pasteurellosis,
hydrochloride soluble powder sheep and pig 25 mg/30 kg restricted vibriosis,
Tetracycline bwt. depending / intra-uterine. anaplasmosis,
hydrochloride bolus on weight of the 24 hourly feline in fluenza
Steclin bolus. C/H/S/G pigs anin1.al 4-6 /48 hourly. Do and goat
boluses daily. Do Do pneumonia etc.
Do Do Do
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents products (drugs) Administratio
specialities n
10. Chlortetracyc1in Aureomycin Small animals 20-25mg/kg 12 hourly in Orally Mastitis,
hydrochlor bwt. hvo divided strangles,
doses. pasteurellosis
anthrax,
leptospirosis,
listeriosis,
glanders,
samonelia
infection.
1 2 3 4 5 6 7
Do Do Large animals 7-1Omg/kg bwt. 12 hourly Do Do
11. Chloramphenicol Neochlor inj. Large animals 2-4 mg/kg. bwt 24 hourly I/M Calf diphtheria,
pasteurellosis,
S/G/P/F/Calv 4-10mg/kg. footrot, virus
es Body weight pneumonia,
coliform or
Do -do- salmonella
Do infection. metritis,
kennel cough,
mastitis,
infectious bovine
keratitis, otitis,
eye infections etc.
12 Norfloxacin Neonox-200 C/B 1-2 tab in 4Bhourly Intraterine All bacterial
Dispersible tab. D/cats distilled water 24 hourly Orally after infections.
1 tab in distilled meals
water
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
13. Cephalosporins Keflong inj. All species 10-20mg/kg 24 hourly I/M Pneumonia, H.S.,
(0.5 gm., 19m.) Body weight metritis, nephritis,
cystitis, septicaemia
and otitis.
-do-
23. B.complex i. Uverjet inj. Large animals 5-10 ml daily Anorexia, liver
with liver ii. Livogen inj. disorder, hepatitis,
extract inj. iii. Belamyl inj. Jaundice. debility and
+ exhaustion, to
iv. Bivinal forte Small animals 1-2mldaily I/M maintain normal
inj. 24 hourly erythropoiesis and
v. Pepsid inj. check anaemia.
vi. Vibelan inj.
24.B.complex inj. i. Polybion inj. Large animals. 5-10 ml daily. 24 hourly or I/M Neurological disorder
ii.M.V.! alternate day. and paralysis
iii. Conciplex
24 hourly or
alternate day Do
B1B6B12 iv. Neurobion Small animals 2-3 ml daily. I/M
and other water soluble inj.
vitamins v. Vibelon inj. Large animals
vi. Triradisol. Do 5-10ml
inj. H-500 Do Do
vii. Triradisol Do Do
inj. H-lOOO C/B/H Do
viii. Neuroxin Dog 5-10ml Do Do
-B12Inj. 2-3ml Do Do
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
25. Anti allergiq Allergic reaction
anti histaminics allergic pulmonary
emphysema, asthma
Pheniramine uticaria, insect bite,
maleate i. Avilinj. All species 24 hourly. I/M taileczema, demlatitis.
Chlorphenriamine Large animals 5-10 ml daily ruminanl atony.
maleate ii. Zeet inj. Small animals. 1/2-1 nu daily. tympany and bloat in
ill. Cadistin inj. ruminants, acute
Promethazine Hcl iv. Catlan septicmetritis,
Promethazine Hcl v. Promethazine pregnancy toxaemia,
Anti-inflamnlatory / anti- inj. shock etc.
anaphylactic shock/ Anti Phenergan inj.
toxic.
Dexamethasone All species Ketosis, inflammation
Sodium Cattle/Buffaloe 4-20 mg daily 24 hourly I/M of respiratory tract,
phosphate i. Dexona inj. s/Horses 2-4mg daily in severe urogenital tract, local
Calves/Pigs/S 0.5to2mg. conditions it inflammatory
heep/ daily maybe condition arthritis,
Goat/ Dogs 8-20 mg daily repeated in 12 surgica shocks,
and Cats hour. anaphylactic shock,
ii. Dexavet inj. C/H/B traumatic shock
ill. Curadex inj. 2-4mgdaily pregnancy toxaemia,
iv. Cadex inj. 4-6n1l pneumonic
S/G/Calves 0.25-1 nu. pasteurellosiS, HS etc.
C/B/H
Betamethasone v. Dexanlethasone inj. Dog/Cat
Chemotherapeutic Phannaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
As given above
vi. Betanesol inj
vii. Betaeotril inj. All species
Prednisolone viii. Hostacortin- H Do
Do
50-200 mg daily
25-30 mg daily
Cattle/horses 10-30 daily.
Calves/Pigs
Dogs/Cats
26. Antiemetics/ Anti- All species I/Mor
convulsants Small animals 2.5 mg/kg.bwt. I/V Vomiting &
Chlorpromazine Hcl I/M restlessness.
Trifluopromazine Hel. i. Largactil
Trimeprazine tart
Prochlorperazine ii. Siquil Dog, Cattle, 1-2 mg/lb.bwt. 120r
mesylate Horse 10 mg/100Ib 24 hours
Metoclopramide Hcl iii.Vallergan bwt. Do I/M
iv. Stemitil inj. 10-15 mg/100 Do
Ibs do I/Mor
v. Perinonn inj. Small animals Body weight Do IjV
(Dog & cats). 1 amp.daily or Do I/M
twice daily
depending upon Do
the condition.
Chemotherapeutic Pharmaceutical Species OoseRate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
27. i. Pethidine Horse/cattle l50mgto Repitition I/M Painful condition,
Antispasmodic Hydrochloride Pigs, 200mg/SOkg depends upon I/M colic, difficult
Dogs, bwt. condition I/M parturition etc.
Cats 3-5 mg/kg.B.wt. Orally
10 mg/kg.B. wt. -00- SIC, I/V -do-
Large animals 25 mg/kg.B.wt. -00-
ii. Polygesic inj. D/C 5-10 SIC/or -do-
Foal/Calf mg/kg.B.wt. I/M
Large animals 20-60ml -00- I/M
ill. Ridalpin inj. Small animals l-2ml -do-
Calf/foal 5-l5ml Repeated after -do-
20-60ml 3 to 4 weeks
iv. Trigan-D inj. Large animals. 2-4ml -do-
"
2-l5ml -Do-
10ml
28. Anti trematodal i.Corbon Cattle, 5ml Repeated after Orally Liver flukes,
(Fluke remedies) tetrachloride Sheep and lml 2 weeks paramphistomiasis
goats Repeated after etc.
"
ii. Distodin (1 gm) Tab. Adult animals 1 gm tab/lOO
"
Distodin 100 mg. tab kg.b.wt. 2-3 weeks
Small animals 100 mg tab(1-2 Orally -do-
ill. Trodex inj., tab.)
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
Nitroxyl OxycIozanide Large animals As desired by SIC -do-
Oxyclozanide Cattle 10 nu. physician.
3. Tolzan-F susp. 10 ml/kg.b.wt.
4.Amfanide Cattle & Orally
Rafoxanide buffaloes 033 ml/kg.b.wt.
Sheep & goats. 7.5 mg/kg b.wt.
Orally
Oxyclozanide S.Hexanide C/B 10 mg/kgbwt. As desired by Orally Do
Oxyclozanide 6. Nilzan Swines 0.33 nu/bwt. kg. physician. Do do
do
+ Cattle + sheep do (60-90 ml) as Do Flukes.& Gl.tract
total dose do Do nematodes.
Tetramisole hel 7. Fasinex C/B/S/G 1-4 tablets. Do Do
Lithium Anthiomaline inj. Adult Cattle 20ml. Repeat twice a I/M Nasal Granuloma
antimony week deep (NG)
thiomalate MaximumS
Inj.
Sodium antimony Tartarematic Do 1 nu (4%) / 40 Do I/V Do
tartrate kg
b.wt. or 20 ml.
2-3 % as total
dose
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
29. 1. Vemlex Cattle & 15-30 m1/30 kg. Repeat after 3 Orally Round worms of
Antinematodal 2. Piperazine buffaloes B.wt. weeks poultry, cattle,
(Round worm remedies). Adipate 44.4 % Horses/ swines 15 m1/30 kg. buffaloes horses,
Piperazine 3. Helmacid B.wt. swine, dogs, cats etc.
salt liquid Calves/ Foals
4. Peperazine Dogs & Cats 15m1/25 kg.
45 % liquid B.wt.
2.5 mlll0 kg.
Fenbendazole B.wt.
5. Panacur Do Orally
bolus (2.5mg) Cattle,
6. Panacur tab. buffaloes
(l5Omg) /horse
Sheep/ Goats/ 5-10mg/kg
Pigs. B.wt.
Dog & cats
5 mg/kg B.wt.
15-25
mg./kg.bwt
Mebendazole 7. Wormin 500mg. C/B 5-10
bolus mg/kg.b.wt.upt
Fenbendazole 8. Curaminth C/H 0 Orally All round womlS i.e.,
9. Zodex do Do Round worms,
Calves/ sheep/ 5-10 WhipwomlS,
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
Morental citrate pigs/goats mg/kg.b.wt. hookworms etc.
10. Banminth Il 4-8 boluses For 3 days Orally Do
forte (lgm. All species 2-4 boluses continuously
Levamisole hel bolus) Tablet
11. Kalmisole 1 bolus/2oo kg Do Do Do
Albendazole vet tablet Livestock b.wt. Round wmms &
12. Albomar 1 tablet/20 kg Do Orally Flukes
suspension Do but.
/powder Tapeworm infestation
13. Analog One tablet/ 20 Do Repitition Orally
30. Anticestodal suspension C/B/H/S/G/P kgb.wt.
drug 14. Dicestal
Ivermectin Large animals 0.33ml/kg or 5- After 2-3 weeks All endo and ecto
15. (a) Ivomec Horses D/C/S 7.5 mg/kg b.wt. After weekly parasitic infections
inj. All species inetervals 2-3 SIC
(b) Mectin inj. C/H/D/S/ 1 mlf5 kg.fbwt. inj. Babesiosis +
31. Anti-haemo- theileriosis etc.
protozoal After 48 to 72 Do
4, 4' -diamidino-
0.5gm/4kg/bwt hours. I/Mdeep
i. Berenil All species
ii. Pronil-H. (cattle) 0.5
Small animals gm/3kg/bwt.
1 ml/50
kg/bwt.
orO.2mg/kg
bwt.
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
0.8 to 1.6
gm/lOO kg. B.W
3to4mg/kg
bwt
diazoaminobenzne
diaceturate
Sodium ill. Tartaremitic Horse/Cattle/ lmI4%/40kg Twice week for I/V Surra
antimony tartarate Camels bwt.or 20 ml. (2- 2 weeks
Quinapyramine sulphate iv. Trypnil inj. 3%501) After 3 months SIC Surra
and Q.P.chloride v. Triqininj. Horse/ Cattle 3mg./kg body
vi. Tribexine inj Camels wt.
32 Bupravaquone or 0.025 ml/kg Within 48-72
vii. Butalex Bwt.or (10-12 nu
hours of the l./M Theileriasis
Cattle as total douse)initial injection
33. Antianemic Twice weekly Anaemia,DegnaIa
drugs Do I/M disease and
i. Acetylarsan I ml/20kg.body Thrice daily debilitating conditions
(23.6%) Large animals wt. Twice daily I/M
ii. Cal-D rubra Dogs and Cats Thrice daily Orally Do
ill.Sharcopherol Small animals Alternate day Orally Do
iv.Neuroxin- Large animals Orally Do
B12 Small animals 5 to 10 ml Alternate day I/M Do
v. Imferon Inj. lt02ml daily Do
Large animals 10ml I/M Do
vi. Fesol cap. Small animals 50ml Orally
Dogs and Cats 5-l0ml
10ml
Chemotherapeutic Phannaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
It02ml
1 cap.
34. Intramammary i. Pendistrin-SH Large animals 1 tube every 12 5-7 days I/mamm Mastitis(acute and
infusions hrs. ary chronic)
Pencillin ii. Vetclox plus Cattle and Do Do
Streptomycin + buffaloes after milking Do
Hydrocortisone
Ampicillin + iii. Penicur-D 3-5 days Do
Cloxacillin + iv. Alciclox 1 tube every 12 Do
"
Dexamethasone v.Campidex (Acute mastitis) hours after
vi. Vetmas
" "
milking.
Chronic Do
M~tis.
35. Antiectoparasites 1. Ascabiol -do- Apply on Sarcoptic man-
(emulsion) Dogs affected surface Apply on
"Topical ge,parasitic
with a soft alternate day applicatio otitis,removal of lice.
2. Malathion brush n Ectoparasites of
3. Lorexane All species Spray or apply livestock poultry and
cream All species 0.5-1 % on the dogs. pets. Ectoparasites
suspension Applied as a -do- Effective at gainsticks,
4. Butox spray & pow- mites, lice and rues,
All species der should be Used as
5. Pestoban 1 % solution and sprinkled on spray as
0.6% dust. body. topingup
2ml/litre of May be repea- These drugs stimulate,
water for spray ted after 2 increase and maintain
or dip. weeks. milk~eld in the
Chemotherapeutic Phannaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
36. Galactogauge Leptaden tab. 3ml/litre of Twice daily for animals.
Large animals water for toping 2 to3 weeks or Do
ii. Dudhdan tabs up. more Orally
Cattle Buffaloes Twice daily for -do-
ill. Galog tabs. Goat and ewes 10 tabs. 2 Orally -do-
Large animals Weeks Orally
iv. Calsus Plus liquid. 3-5 tabs. Do -do-
Cattle / Buffalo 1 tab
37. Rumenotoric l.Bovirum bolus Do -do-
drugs 2.Rumenton 5-10 ml For a week -do-
3.Bio-spur bolus -do- -do-
3-4 boluses per
day -do-
-do-
2-4 boluses
38. Anti-convu- i. Mysoline tab. Small aninlals 250 Total dose Orally Epilepsy, epileptic
lsants(chorea) mg/5kg.B.wt. divided in to 2 form of convulsions,
parts given at and hysteria
intervals of 12 Nervous disorders
ii. Gardenal tab. Dog hours. Do convulsion,
and 30-300mg 30mg. tab- Oo cholrea.eclampsia,teta
Cats according to Thrice daily nty, poisoning by
bwt. strychnine and
cocaine.
ill. Lardopa Dogs Do
I(500mg) tab. once daily
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Administ
Specialities ration
iv. Pacitane Dogs 1/2 tablet followed Do
(2mg) Twice daily
v. Amantrel Dogs 1 tab. Thrice daily
(l00ntg) tab.
1 tab. Thrice daily
Cattle/Buffalo
Chemotherapeutic Pharmaceutical Species Dose Rate Repetition Route of Indications
~gents Products (drugs) Adminis
Specialities tration
40. Fluid therapy i. 5% Dextrose All species 25 ml to 50 12 or 24 hours IjV 1. In cases of
nu/kg Body wt. depending dehydration, from
upon severity vomiting, diarrhoea &
ii.5 to 10% Dextrose Do Do ofdeydration Do enteritis.
saline or (DNS) Depending 2. Jaundice, hepatitis,
upon the ketosis loss of appetite
severity of the and impaired
iii. Rintose disease (e.g., Do digestion etc.
solution C/B/H 500-1oooml jaundice) Do
iv. Ringer's S/G 1oo-2ooml Do
lactate Do Do 24 hrly.3 to 4 Do Do
v. Dextrose days
(5%,10%) Large animals 450 ml. 1000 ml. Do Do Do
(20%,25%) Sheep and goat 100-150 ml
vi. Electrovet Small animals 25 to 50 ml. Do Do
vii. Lecrivet C/B/H 500-2000 nu. Do Do
Large animals 450ml Do
Do Do
Do
Chemotherapeutic Phannaceutical Species Dose Rate Repetition Route of Indications
Agents Products (drugs) Adminis
Specialities tration ).
41. AntihaemoIT- i. Styptobion Dogs/Cats 1-2 ml. Twice daily Do Epistaxis, haemorrage
etc.
~
~
hagic ii. Styptochrome Large animals 10ml. Twice daily I/M
drugs (inj.) I/M Do
ill. Revice (inj.)
;;p
iv. Styptocid Do Do Do Do ~
Do
0'
v. Chromostat Do Do Do Do
vi. Kalpin (inj.) Do Do Do Do
42 Antibloat
[
i. Bloatosil Cattle 100ml. asa Repeated after Do Do ::;l
buffaloes drench 6-12 hrs or 24 Orally Do !l:
UJ
:f
horse
donkey
hours if needed Tympany, frothy bloat
f
....c
sheep & goat
ii. Blotinox Do Do
Cattle & Do
buffaloes 100ml.
Horse & Do Do ~
Donkey
50-100ml. Do
Orally
Do ~
Sheep & Goat Do
It
).
Do Do Do ;:!
For cattle, buffaloes and horses 27. Astringent mixture for enteritis, diarrhoea and dysentery
Anise powder -15 gm.
Ajwan powder -8gm. Rx
Camphoor powder -15 gm. (1) Adult cattle Calf.
Extract belladona -3gm. Pulv. Creta 30 gm. 10 gm.
Potassium chloride -I2gm. Pulv. Kaolin 30~ 10 gm.
Treacle -Q.5. Pulv. Catechu 30 gm. 10 gm.
Prepare electuary and feed thrice daily
2. Inj. Novalgin (Hoecht)
25. Tonics-
3. hlj. Polygesic (Hoecht) Large animals 20-60 ml.
For cattle, buffaloes and horses Calves/Foals 5-15 ml.
Rx Sheep/Goat 2-8 ml.
Cobalt sulphate -50mg. Dog/Cat 1-2 ml I/M
Copper sulphate -l00mg.
FelTous sulphate - 5 gm. 4. Trigan- D
Gentian powder -6gm.
Nuxvom powder -6gm.
Treacle -Q.5.
Such one dose thrice daily.
32 Triple Carb (Gastric sedative for dogs) 36. Diuretic for Dogs.
Rx. Rx.
Mag. Carbo Lev. Sod. Salicylas 0.5 gms.
Bismath Carbo Pot. Aceats 0.5 gms.
Sodi Bicarb aa 20 gm, Spt. Anun-Arom- 1-2mI.
Mft. Pulv 6. Sig. Give 4 hourly Syrup SmI.
Aqua ad1Snu.
33. Mistura alba (Laxative mixture for dogs) Mft. Haust SigT.D.
S-lOml SIC
2. Black Quarter Black quarter vaccine Cattle and buffaloes 1-2mIS/C 1 year Do before
(a) Monovalent sheep and goats Do 1 year monsoon.
(b) Polyvalent Do 1 year
-
Brucella vaccine 2-S year
3. Brucellosis (Strain- 19) Cattle 6 to 9 months and the 2-Syear Do
adult except pregnant anintals.
406
Table 39. PATENT PREPARATIONS USED IN ANIMALS
ANTIBIOTICS
Name Presentation Dose Manufacturer
AMIKACIN
Inj Akacin Inj. 2rnl amp (l00mg) 10mg/kgTID Morvel
Inj Vetacin Inj. 2rnl, 10ml, 30ml vial (25Omg/ml) !BC
FORTIFIED PROCAINE
PENICILLIN INJ
Fortified Procaine Penicillin inj Inj. 20 lac vial (procaine penicillin G 15 lac, Cattle, horse, sheep, goat, pig: Alembic
20 lac Ipenicillin G Sodium 5 Lac)/ vial 4000-10,000 IV/Kg BW
Fortified Procaine Penicillin inj Inj. 40 lac vial (Procaine penicillin G 30 lac, Dog: 10,OOO-20,OOOIU/Kg BW Alembic
40 lac Ipenicillin G Sodium 10 Lac)/vial
Fortified Procaine Penicillin 20 Inj. 20 lac vial (Procaine penicillin 15 lac, Benzyl IBC
lac Penicillin Sodium 5 Lac)/vial
Fortified Procaine Penicillin 40 Inj. 40 lac vial (Procaine penicillin 30 lac, Penicillin IBC
lac G Sodium 10 Lac)/vial
Fortified Procaine Penicillin 20 Inj. 20 lac vial (Procaine penicillin 15 lac, Benzyl Sarabhai
lac Penicillin Sodium 5 Lac)/vial Zydus
Fortified Procaine Penicillin 40 Inj. 40 lac vial (procaine penicillin 30 lac, Penicillin Sarabhai
lac G Sodium 10 Lac)/vial Zydus
AMPICILLIN
Ampilin Vet Inj. 2gm & 25gm vial Cattle, Sheep, Goat, horse, Pig: Lyka
Bacipen Inj. 2& 2.5 gmvial 5-10mg/kg BWQID Alembic
Catcillin inj. vet Inj. 25gm vial Dog, Cat 2Omg/kg BW QID Cattle
orally; lOmg/kg BW QID remedies
Conampi Inj. 19m, 2gm & 25gm vials parentraily Concept
Name Presentation Dose Manufacturer
Dynacil vet Inj. 19m & 2.5gm vial HAL
Roscillin Inj. 250, 500 mg& 19m vials Ranbaxy ~
Tab 125mg & 250mg
Syrup 12Smg/Sml & 25Omg/Sml ~
@
Stancillin Inj. 2gm vial Sarabhai ~
zydus ;p
Vetampin Inj. 2gm vial Wockhardt ~
RC forte
Inj. 2gm vial
Comoxyl powderSOOm!5g 100gm; SOOgm Cattle, horse: 20g for 3 days; Concept
sheep, goat, calf: 5gm for 3-
5days
Hipen Tab: 125 mg & 250 mg; inj. 250mg and 500 mg vial 10 mgjkg BW BID (LA); 10-20 Cadila Health
mgjkg BW (SA) Care
AMOXYCILIN + CLAVULANATE POTASSIUM
Augmentin Dry syrup 30ml (Amoxycilin 200mg + Clavulanic Dog & cat 12.5-25 mg/Kg BW Smith Kline
acid28.75mg)j 5ml BID Beecham
Augmentin lOOODUO Tab lOOOmg (Amoxycilin 875mg + Clavulanic -do- Smith Kline
acidl25mg) . Beecham
Temobax Dry susp 6.6gm (30 ml) -do- Ranbaxy
AMOXYCILIN + CLOXACILLIN
Amc10x Inj. 2g (Amoxycillin sodium 19 and cloxacillin Novartis
sodium1gm)jvial
Centamox Inj. 2g (Amoxycillin sodium 19 and cloxacillin Century
sodium1gm)jvial
inj. SOOmg (Amoxycillin sodium 250mg and
cloxacillin sodium 25Omg}/vial
Comaxvet Inj. 500mg & 2gm vial Vetindia
Conmox Inj. 2gm vial Concept
Name Presentation Dose Manufacturer
Crilmox inj. vet Inj. 2gm vial Cattle
Remedies
Hipenox Inj. 19m & 2 gm vial Sarabhai
zydus
Inimox Inj. 500mg, 2gm & 4 gm vial Indian
ImmunoJogica
Is
Intamox Ini. 500mg, 2gm, 2.5gm & 4 gm vial Intas
-
Klomivet Ini. 2gm vial Lyka
Megamycin Ini. 2gm vial Pfizer
Megamycin forte Ini. 3gm vial Pfizer
Moxel Ini. 500mg, 2gm & 3 gm vial Alembic
Moxyclox Ini. 3gm vial Wockhardt
CEPHALOSPORINS
CEPHALEXIN
Sporidex Drops: lOO mg/ ml, 10 ml Small animals Ranbaxy
Granules: 125 mg/5ml, 30 ml 10-25 mg/kg BW/ 8-12 h PO
Granules: 250 mg/5ml, 30 ml
DT-tab; 125 & 250 mg, ID's
Cap: 250& 500 mg, ID's
Name Presentation Dose Manufacturer
Alcephin Tab: 125 mg, 10's -do- Alembic
Syrup: 125mg/SmJ., 40 ml
Phexin Drops: 100 mg/ml, 10 ml -do- Glaxo pharma
Syrup: 2S0 mg/Sml, 30 ml
DT-tab; 125 mg, 10' s
Cap: 250& 500 mg, 10' s
Sepexin Kid-Tab 125mg, 10's Lyka
Disp-Tab 25Omg, lO's
Syrup: 125 mg/Sml, 30 ml
CEFIRlOXONE
Cefaxone Inj. 25Omg, SOOmg, 1 g vial IS-SO mg/kg BW/ day Lupin
Monotax Inj. 125mg, 250mg, sOOmg, 1 g vial -do- Biochem
Zefone Inj. 250mg, 1 g vial -do- Cadila
healthcare
CEFOTAXIME
Biotax Inj. 125mg, 250mg, SOOmg, 1 g vial Dog; 10-SO mg/kg BW/ 6-8h Biochem
Taxim 1nl. 125mg, 250mg, sOOmg, 1 g vial Goat SO mg/kg BW/ 12 h Alkem
Britax Inj. 250mg, SOOmg, 1 g vials Brihans
Lyfovet Inj. 2gm vial Oriental
Name Presentation Dose Manufacturer
CEFADROXIL
Cefadrox Kid-Tab 125mg, lO's Dog, Cat 10-30mg/kg BW TID Aristo
Syrup: 125 mg/Sml, 30 ml
Droxibid Kid-Tab 2S0mg, 4's HAL
Tab SOOmg, 4's
Droxyl Kid-Tab 250mg, 4'8 Torrent
Tab SOOmg, 4's
Susp 250mg/ Sml, 30ml
Lydroxil Dis-Tab 250mg, 4's Lyka
Syrup 125mg/Sml, 40ml
STREPTOMYCIN
Ambistryn-S Inj. 1 gm vial All animals: 10 mg / kg BW Sarabhai
KANAMYCIN
Kancin inj Inj. SOO mg & 19 vial Cattle: S-10 mg / Kg BW IM, N Alembic
Kanamycin Inj. 500 mg & 19 vial Dog, Cat S mg / Kg BW IM, N Biochem
Indomycin Inj. 2gm vial IBC
GENTAMICIN (40 mg in each ml)
Catlogenta Inj Vet Inj. lOml & 30ml vials Cattle, Sheep, Goat, Pig, Dog, Cattle
Cat: 4mg/kg BW BID remedies
Poultry: 3-Smg/kg BW
Name Presentation Dose M'lnufacturer
G-Cin Inj. 30mI & 90ml vials Indian
Inununologica
Is
Gentamicin Inj. 30mI & 100ml vials Alembic, IBC
TIK, Vetcare,
Wockhardt,
Ranbaxy
Gentamicin Inj. 10ml & 30ml vials Vetindia
Marcogenta Inj. 2m!, Sml, 10 mI vial& 30ml vials Marc
Gentiminj. Inj. 10 & 30 mI vial Merind
ERYTHROMYCIN
Althrocin Tab Tab 250 mg, SOO mg Cattle, sheep, goat, horse: 2.2-4.4 Alembic
Liq25mg/mI mg/kgBW
Anithrocin FS Powder 20mg/ g Pig: 2.2-6mg/kg BW IBC
Anithrocin SP Powder sOmg/ g Dog 10-40 Mg/kg BW IBC
CHLORAMPHENICOL
Chloramphenicol sodium Inj.1 gm vial LA- 2-4 mg /kg I/V 20-30 mg KAPL
Succinate I/M
Chloramphenicol sodium !nj. 19m & 2gm vials Lyka
Succinate
Chlorophen Ini. 30 ml vial (100 mg/ml) Vetindia
Chlorovet 30 ml vial (100 mg/mI) LA-4mg/kg G. Loucatos
SA-S-1S mg/kg
Neochlor Inj. 10 & 30 ml vials (each ml contains 100mg) 4-11 mg/ kg I/m Vet care
Name Presentation Dose Manufacturer
Neochlor forte powder 20% 50gmpack 19m/Lt of water on day 1; Vet care
w/w 19m/lO Lt. of water for next 3-5
dilY~.
Lykacetin Inj. 19m, 2gm, 3gm vials Lvka
Vetnicol bolus Bolus 500 mg(4's) Vets farma
CIPROFLOXAON
C-Flox Inj. 40mg/ nu (SOnu vial) Dog, Cat: 5-15mg/kg BW Intas
Ciprovet Inj. 10ml, 30nu vial Cattle, sheep 4-5 mg/kg BW Vet India
Ciplox Tab 250mg (lO's) Cipla
INF IV 2Omg/lOml Q.OOml).
Ciprobid Tab 250mg (10' s) Zydus Cadila
Inj. IV 2mg/ml (5Onu & 100 ml)
CiJlrowin Tab 250 mg & SOD mg (10' s) Alembic
CIPROFLOXACIN COMBINATIONS
AV-Floxin 2000 Powder (Ciprofloxacin 20g, Norfloxacin 20 g)/kg: Broilers: 500nlg/M ton of feed AVR
500 gm pack Layers, breeders: 1000mg/M
ton of feed
C-Flox-TZ Tab (Ciprofloxacin HO 250mg, Tinidazole 300mg): Large animal: 1-2 boll OD for 3- Intas
10's 5 days
Bolus: (Ciprofloxacin HO lSOOmg, Tinidazole Small animals: ltab/15-25 Kg
1800mg): 2' s BW
ENROFLOXACIN
Conflox-vet inj 5"11. Inj. 30ml (50mg/ ml) Concept
Conflox Vet Oral Solution 10% Soln 100ml & 500ml Poultry lOmg/kg BW Concept
Soln.J100mglml)
Enrocare Ini- 20ml vial (lOOmg/ ml) Vetcare
Name Presentation Dose Manufacturer
Enrodn Inj.15ml,5Oml, looml vials Ranbaxy
Enrodac-l0 Ini. l5ml vial Sarabhai
zydus
Enrofloxacin Ini. l5ml vial Vetindia
Enrox (10% wJv) Ini. l5ml & looml vial Alembic
Floxidin Oral Soln. (5% w Iv) 100ml & 250ml Poultry 1Omg/kg SW Intervet
Oral Soln. (10% w Iv) 100ml & 250ml 5% soln. 2ml/Lt. of water
Ini. (10% w Iv) 15ml & 50ml vial 10% soln. lml/Lt. of water
Meriquin TabSOmg (lO's) Poultry 1ml/10kg SW Wockhardt
Ini. (100mg/ml): lnu & 50ml vial
Uq (100mg/ml): 100ml & 500ml
QuinIntas Inj. (lOOmg/ml): l5ml, 3Om1 & 15ml vial Poultry Intas
Uq (100mg/ml): lOOml & lLt Prophylactic: lml/4-8 Lt. of
water
Curative: lml/2-4 Lt. of water
Roflox Inj. (10%): l5ml & lOOml Novartis
O~CYCLINES
AlcycIin-O Ini. 3Om1 vial (5Omg/ml) Cattle, sheep, goat, swine, horse: Alembic
Intamycin Inj.3Om1 & lOOml vial (5Omg/ml) 5-lOmg/kg SW/day Intas
Intamycin LA IInj. 3Om1 & lOOml vial (200mg/ml) Dog & Cat lO-2Omg/kg Intas
Oxy-l00 lni.3Om1 & lOOml vial (lOOmg/ml) BW/day Vetindia
Oxytetracycline lni.3Om1, 50ml & lOOml (SOmg/ml) Alembic, IBC
Oxytetracycline Ini. 3Om1 & lOOml vial (50mg/nu) Concept,
Indian
hnmunologica
Is
Name Presentation Dose Manufacturer
Oxytetracycline Inj. 3Oml, 50ml & looml (50mg/ nu) Vetindia
BolusSOOmg
Oxytetra-LA Ini. 30ml (200mg/ n1l). Vetindia
Oxyvet Inj. 3Onu, 50ml & lOOnu (SOnlg/ nu) Sarabhai
zydus
Oxyvet-LA Inj. 3OnlI. (200mg/ n1l) Sarabhai
zydus
Terramycin Inj. 30ml & lOOnU vial (50mg/nlI.) Pfizer
Tab 500mg (4's)
Soln 60 nlI. (5Onlg/nu)
Terramycin-LA Inj. 30ml & 50nu vial (200nlg/ nu) Pfizer
WolicycIine Inj. 30ml (50mg/n1l) Wockhardt
Wolicycline DS Inj. 30nll. (lOOmg/nu) Wockhardt
WolicycIine LA Ini. 30nu (2oomg/ nu) Wockhardt
TETRACYCLINE
Neocyclin bolus 500mg (4's) Intas
LINCOMYCIN (300 mg/mI)
AIincomycin - vet Inj. 5n1l vials Bovine:lOmg/kg BW Alved
Lincocin inj. Inj. 2nU vials Dog: 15-25mg/kg BW BID Max
Pig: llmg/kg BW BID
STREPTOMYCIN + PENICILLIN
Dicrysticin inj. Inj. 2.5 gm vial(procaine penicillin G 15Lac, Large Animal: 2nu/50kg BW Sarabhai
Penicillin G sodium 5 Lac, streptomycin sulphate Small Aninlal; ln1l/5kg BW Zydus
2.5 gm)/vial
Name Presentation Dose Manufacturer
Munomycin forte inj. Inj. 2.Sgm vial Large animal: 1-2 vials daily Glaxo
Smithkline
Vetopen inj. Inj. O.S,l.O, 2.5 gm vial HAL
Bistrepen-V Inj. 2.Sgm vial Alembic
SULPHONAMIDES
Sulphadimidine
Aldine BolusSgm All animals: loomgjkg BW oral, Alembic
Diadin BolusSgm IV Pfizer
Pabadine bolus Bolus Sgm (4' s) Intas
Sulfam Inj. lOOml vial (lgmj3m1) Pranav
Sulfamin Bolus Sgm(4's) Indian
Inj. lOOm!. & 4SOm1 (333mgj nu) Immunologica
Is
Sulpha BolusSgm Sarabhai
zydus
SULPHONAMIDES and TRIMETHOPRIM COMBINATION
Atrima bolus Bolus 1.2gm (Sulphadiazine 1gm, trimethoprim Large animals: lS-3Omgjkg BW Prima Vet
0.2gm) Dog: lSmgjkg BW Care
Bolus 2Agm (Sulphadiazine 2gm, trimethoprim
OAgm)
Name Presentation Dose Manufacturer
Bactridox Inj. 30 ml vial (sulphadoxine 20mg, -do- Alved
trimethoprim4mg) / mI
Bactrisol bolus Bolus 1.2gm(Sulphadiazine 1gm, trimethoprim -do- Alved
0.2gm)
BactrisolInj Inj 30 ml vial (Sulphadiazine 400 mg, trimethoprim Alved
80mg)ml
BiotrimIM Inj. 10 & 30 mI vial (Sulphadiazine 400 mg, Ranbaxy
trimethoprim 80mg)mI ,
BiotrimIV Inj. 30 ml vial(Sulphadiazine 200 mg, trimethoprim Ranbaxy
40mg)mI
Biotrim DS Bolus 2.4 gm (Sulphadiazine 2gm, trim~oprim Ranbaxy
0.4gm)
Cotrimal bolus Bolus (sulphamethoxazole 1.25gm, trimethoprim Alembic
O.25gm)
Cotrimal DS bolus Bolus (sulphamethoxazole 2.5 gm, trimethoprim Alembic
O.5gm)
Intrim Bolus (sulphamethoxazole 2 gm, trimethoprim 400 Indian
mg) Immunologica
Is
Intrim bolus Bolus (sulphamethoxazole 1.25 gm, trimethoprim Intas
250mg)
Name Presentation Dose Manufacturer
Intrim Forte Bolus Bolus (sulphamethoxazole 2 gm, trimethoprim 400 Intas
mg)
Oriprim Bolus Bolus (sulphamethoxazole 2 gm, trimethoprim 400 Sarabhai
mg) zydus
OriprimIM Inj.5mlamp Sarabhai
~dus
OriprimV Inj. 30ml vial Sarabhai
zydus
Sulcoprim Bolus (Sulphadiazine 2gm, trimethoprim 200mg) Concept
Sulprim-24 Inj. 30ml vial (Sulphadiazine 200mg, trimethoprim Unichem
4Omg)/ml
Oriprim powder Powder 100gm (Sulphamethoxazole SOOmg, Animals: 2g/40kg BW BID Sarabhai
trimethoprim 10Omg)/g Poultry: zydus
Upto 6 weeks:
2gm/100birds
6-12 weeks: 4gm/1oobirds
12-18 weeks: 8gm/1oo
birds
Biotrim oral Uq. Liq. 100ml (Sulphadiazine 200 mg, trimethoprim Poultry: 1ml in 2-4 Lt. Of Ranbaxy
4Omg)ml drinking water
Bactrisol Dispersible powder Powder 1OOgm, SOOgm & 1kg Chicks: 19m/ 2Lt of water Alved
Adults: 19m/ Lt of water
Name Presentation Dose Manufacturer
NORFLOXACIN
Anquin Tab 400mg (4's) Dog, Cat 22mg/kg BW BID Lyka
Negaflox Tab 400ng (8' s) Cadila Health
Care
Norflox Distab lOOmg, 200mg, 400mg (10's) Cipla
Uroflox Tab 400mg (10' s) Torrent
METRONIDAZOLE
Anarobin Inj. 50ml vial (5mg/ml) Dog: Unichem
Flagyl Tab 200mg, 400mg (10' s) 25-50mg/kg BW/ day in divided Rhone-
doses, Oral Poulenc
FlagylI.V Inj. lOOml (loomg/ml) 2Omg/kg BW / day in divided Rhone-
doses, IV Poulenc
Metrogyl Tab 2oomg, 400mg (lO's) Cattle: Unique
Susp 30ml, 60ml (200mg/5ml) 2Omg/kg BW/ day in divided
doses, IV
Inj. LV looml (500mg) .
Metronidazole Iitj. looml (5mg/ml) Prima Vetcare
Unimezol Tab 200mg (10's) Unichem
METRONIDAZOLE COMBINATIONS
Amedol-F Susp. 60ml; (MetrOnidazole lOOmg, Diloxanide Small animals 3-5 ml Vetchem
furoate l25mg, Furazolidone 5Omg)/5ml
Name Presentation Dose Manufacturer
Centrogyl LM Bolus (Metronidazole 19m, Furazolidone sOOmg, Large animals 4-6 boli / day Century
Loperamide hydrochloride 7Smg) Small animals 1-2 boli / day
DependalM Tab (Metronidazole 300mg, Furazolidone 100mg) Dog, Cat : 1 tab TID Smithkline
Beecham
Diamet Bolus (Metronidazole 19,Furazolidone 2oomg) Animals: 1 bolus/SOkg BW BID Novartis
Dirolin Bolus (Metronidazole 19, Furazolidone 200mg) Animals: 1 bolus/SOkg BW BID Vetindia
Fazole Bolus (Metronidazole 19, Furazolidone 200mg) Animals: 1 bolus/SO~ BW BID Unichem
Metrofural Bolus (Metronidazole 1gm, Furazolidone sOOmg, Large animals 4-6 boli / day Alembic
Loperamide hydrochloride 7Smg) Small animals 1-2 boli / day
PEFLOXACIN
Pelwin inj. 100 ml bottle 100 m.l/ 200 kg Wockhardt
I(Infusion)
Antidiarrhoeals
Name of Drug Presentation Dosage Firm
Diphenoxylate
Lomotil Tab 2.5mg (10'sO Dogs: 2-5mg (total dose) RPG
Cats: 0.5mg/k~BW
Loperamide
Lopamide Tab 2mg (lO's) Dogs, cats: 100nl&!K/i BW Torrent
Indigenous Preparations
Becknor Bolus Bolus Large Animals: 1bolus BID PO Naturalremetues
Small animals: 1/2 bolus BID
Catorrhoea Powder 100gm, 1 kg Cattle buffalo: 25-50 g BID/3-4 Tabs TID Cattle remedies
Tab 8X 6's Horse, mule: 20-30 g BID/2-3 Tabs TID
Sheep, Goat: 10-20 ~ BID/1-2 Tabs TID
Diamukt Dry susp. 15 gm (add water upto Dogs oral: (upto 10kg): Srnl TID Dabur
the mark on label) (more than 10 kg): 10-15 ml TID
DiarexVet Bolus Large animals: 2 boll BID PO Hirnalaya
Small animals: if2 -1 bolus BID PO
Diaroak Dry susp. 30gm, 400gm, 1kg, 2.5 kg Large animals: 30gm Dabur
Small animals 10-15gm
Poultry (mixing rate): 2.5 kg/ ton of feed
Neblon Powder Powder 100 gm & 1 kg pack Large animals:30-50gmBID / QID Indian herbs
Small animals: 6-10gm BID/QID
Dogs, piglets: 2-3 gm BID/QID
HEPATOBILIARY DRUGS
Name of Drug Presentation Dosage Firm
Beekom-L Inj. 30 mI vial Large Animals 5-10 mI, IM Wockhardt
Small Animals 0.5-2 ml , IM
Beekom-L Inj. 30 mI vial Large Animals 5-10 mI, IM Wockhardt
Small Animals 0.5-2 mI, IM
Belamyl Inj. Inj. 10 mI, 30ml & 50ml vials Large Animals 5-10 mI , IM Srabhai Zydus
Small Animals O.25-O.5mI, IM
Bivinal Forte Inj. 10 mI, 30mI vials Large Animals 5-10 mI, IM Alembic
Small Animals 0.5-2 mI , IM
Bovoplex-CC Inj. 10 mI, 30ml vials Large Animals 5-10 mI, IM Indian Inununologicals
Small Animals 0.5-2 nu , IM
Brotone Liq 120mI & 500mI Cattle: 4Om1 OD for 3 days Glaxo
Dog5mI BID
Poultry:
Broliers: 5-10mI/100 birds
Growers & lClYers: 20mI/100 birds
Hepaplex Inj. 10 mI, 30mI vials Large Animals 2.5-5 mI, IM Unichem
Small Animals 0.5-1 mI , IM
Livamyl Inj. Vet Inj. 10 mI, 30nu vials Large Animals 4ml , IM Cattle Remedies
Small Animals 0.25-O.5nu, IM
Name of DruJ( Presentation Dosage Firm
Livaplex Inj. 30ml Vial Large Animals 5-10 ml, IM Pranav
Small Animals 0.5-2 ml, IM
Liverjet Inj. 10 ml, 30mI vials Large Animals 5-10 ml, IM Cadila Pharma
Small Animals 0.5-2 ml , IM
Livogen Inj. 10 ml, 30ml vials Large Animals 5-10 ml, IM Glaxo
Small Animals 0.5-2 ml , IM
Nutriliv injection Inj. 10 ml, 30ml vials Large Animals 5-10 ml, IM Vetcare
Small Animals 0.5-2 nu , IM
Nutriliv forte Liq 500ml, 5Lt., 30 Lt. Broilers: 5-10mI!100 birds PO Vetcare
Layers: 20nll.!100 birds
Pepsid Inj. 10 ml, 30mI vials Large Animals 3-5 ml, IM Concept
Small Animals 0.5-1 nu, IM
Stronic Inj. 10 ml, 30nll. vials Large Animals 5-10 ml, IM Ranbaxy
Small Animals 0.5-2 ml , IM
Enliv Powder 1kg, 5kg pack Chicks: 3ml!1000 chicks! day Alembic
Liq.: 1Lt, 5 Lt Growers: 7ml!12000 birds! day
Layers!brolers: 10nll.!1000 birds! day
Liv 52 vet Powder 109, 100g, 1kg, 5kg Himalaya
UQ.: lloml, 1Lt., 5Lt
Liver Up Powder1kg Large animals: 5gm BID PO Sarabhai Zydus
Small animals: 2gm BID PO
Name of Drug Presentation Dosage Firm
Livol Powder lOOg & lkg Cow, Buffalo: 4O-6Ogm OD/BID PO Indian Herbs
Calf, heifer, colt, pig: 15-20g OD/BID PO
Sheep, Goat 8-12 gm OD/BID PO
Dog, Piglet: 3-5 gm OD/BID PO
Yakrifit Bolus Cow, buffalo, horse: 50ml or 2 bolus BID Dabur
Uq. 125ml, 250ml & 500ml Sheep, Goat: 15-20 mlor V2 bolus BID
Advanced Pathology and Treatment of Diseases of Domes tic Animals
Albendazole 7.5 5 5 - -
Fenbendazole 7.5 5 5-10 5 100
Tric1abendazole 12 10 - -
Dosage:
Species
Name of the
Ah~helmintic Cattle Sheep Pigs Dogs Poultry
(mlYkg) (mlYkg) (mlYkg) (mlYkg) (mlYkg)
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Appendix
Niclosamide - - 150 PO
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428
Postmortem
Examination
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430
Appendix
Destruction
The dead animals after autopsy must be either burnt or
suitably buried between layers of lime sufficiently deep (about
6 feet in depth) in the ditches dug for such purposes.
Care of the Instruments
These must be sharp and properly sterilized to protect
the autopsists during postmortem examination. The
autopsists must be properly dressed i.e., there shuuld be
utilization of aprons, white coats, gumboots during autopsy.
Recording the Lesions
Postmortem findings must be recorded immediately after
autopsy in the postmortem hall by another person. There is
usually a need of three persons (including the autopsist) for
postmortem work.
A uniform and careful method should be followed for
opening the dead body and examining the organs of the
cadaver. To maintain anatomical continuity of the organs of
a system during postmortem examination is very helpful to
make conclusions about the cause of death. This helps in an
easy detection of an obstruction (e.g., stone or calculus) in
the tubal structures (say, bile lluct, urethera and parts of the
gut etc.).
Postmortem protocol refers to a detailed written
description of the postmortem findings. The protocol includes
all information in history of the case or in relation to
preautospy data (e.g., antemortem changes, age, breed, etc.),
findings of external and internal examination along with
pathoanatomical diagnosis and epicrisis.
Postmortem report refers to a brief report of the protocol
and usually consists of pathoanatomical diagnoses as cause
of death. A vetromedical report must be brief to prevent
confusion in the court.
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Advanced Pathology and Treatment of Diseases o/Domestic Animals
(3) .................................................................... ..
The said animal has got the following injuries on its body
(4) .................................................................... ..
I am of opinon ........................................................ .
Place: Signature
Qualification
Designation
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Autopsy of Horse
The autopsy technique is much the same as in the cattle
and buffalo except for the abdominal organs. The body is
placed on its back and inclined towards its r~ght.
Evisceration of the abdominal and thoracic cavities
should be performed from the right side.
Inspect the contents of the abdominal cavity. The
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442
Appendix
Autopsy of Carnivores
On the whole, the autopsy technique for these species
follows the description described above but with the following
differences.
Examination and removal of the abdominal organs.
The incision along the linea alba should not extend
farther forwards than the xiphoid cartilage, otherwise, the
diaphragm can easily be damaged. The omentum with the
spleen is lifted up and folded over the thoracic wall so that
position of the abdominal organs can be inspected.
The intestinal tract is removed. Divide the rectum in the
pelvis, after ligatation, if necessary, and then work forwards
by cutting along the mesenteric attachments. Continue until
the tip of the duodenal branch of the pancreas is reached.
This represents the junction between the duodenum and
jejunum. Ligate the small intestine at this point and divide
it.
The omentum and spleen are removed along the
insertion of the omentum, taking care to avoid the splenic
branch of the pancreas.
The liver stomach pancreas and duodenum are removed
together.
Begin by freeing the pancreas from the root of the
mesentery and the dorsal abdominal wall. The ligaments of
the liver are, then, freed to avoid damaging the diaphragm.
Follow the contour of the liver very closely. The stomach is,
then, cut free through the cardiac region, the incision should
not be made too far otherwise the plieural cavities will be
opened. Then, cut through the vena cava to free the liver
completely. After breaking down or cutting through any
remaining ligaments, the organs can be removed in one piece.
The autopsy is, then, continued as for the cattle with
the exception that the sternum is removed by cutting through
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Advanced Pathologlf and Treatment of Diseases of Domes tic Animals
444
Appendix
Precautions
When a case of a dead animal is presented for
postmortem examination, there are certain extremely
important precautions to be remembered and followed
during autopsy work. Postmortem work done in a haphazard
manner will lead one to no conclusion with waste of the
material and time.
The precautions are as follows:
1. Consideration of a postmortem case should be made as
a serious bit of research work and anamnesis (history)
of the case should be read carefully. If necessary more
information about the dead animal can be obtained from
either the attending veterinarian or owner of the ani-
mal.
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Advanced Pathology and Treatment of Diseases of Domestic Animals
. . Weight of organ
Relative weIght = x 100
Weight of the body
446
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Appendix
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Advanced Pathology and Treatment of Diseases of Domestic Animals
1. Serum
It is prepared by allowing the blood to clot by keeping
the glass tubes in slanting positions at a cool place. Separated
serum can be preserved on ice or one drop of 1 % merthiolate
(Aq. Sol.) is added to 10 m1 of the serum as a preservative. 1
m1 of 5 per cent solution of phenol can be mixed with 10 m1
of serum for preservation.
1. Blood
It is collected from the patients for investigational
purposes and can be preserved with suitable anticoagulants.
Anticoagulants for hematological studies.
There are different kinds of anticoagulants used for this
purpose and some of these are as under:
1. EDATA: 1 % (1m1 for 10 m1 of blood)
2. 4% Sodium citrate (1 m1 for 10 m1 of blood)
3. 1 m1 of 10% solution of potassium oxalate for 3 oz of
blood is used for chemical analysis. No oxalated blood
is used for determination of calcum, magnesium or
acetone iP.. the blood.
4. Mixture of 6 parts (say, gms) of ammonium oxalate and
and 4 parts of potassium oxalate in 100 m1 of distilled
water is prepared and kept in a reagent bottle. 0.3 m1 of
this solution is taken in small specimen bottles and kept
in the incubator overnight to allow the evaporation of
water. The sedimented salt is sufficient for 5 m1 of blood.
5. Heparin 1 % solution - Rinse the vial or syringe with 0.1-
2 m1 solution for 10 m1 of blood for glucose estimation.
2. Faeces
It is collected directly from the rectum at the time of
defaecation. 4- 10% of formalin is used for collecting faeces
to detect heminthic eggs. Postassium dichromate is a suitable
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Appendix
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Appendix
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Advanced Pathology and Treatment of Diseases of Domestic Animals
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Appendix
457
Advance d Pathology and Treatment ofOlseases of Domestic Animals
select only those cases with typica l sympt oms of the diseas e
for labora tory invest igation . These sick cases are sent throug h
courie r with prope r precau tion to preve nt spread of the
outbre ak to health y anima ls during transp oratio n from place
of occurr ence of the diseas e to the labora tory.
Mater ials can be sent to the labor atory for
histop atholo gical exami nation and to Forens ic Labor atory
for identi fying the chemi cals etc. used to kill the anima L
The metho ds follow ed are as under :
1. Despa tch of the materi als for histop atholo gical exami na-
tion.
2. Despa tch of the materi als for chemi cal exami nation in a
Forens ic Labor atory.
458
Appendix
460
preservative. The blood or muscle can be sent on ice in suitable
containers. The weights of the organs and stomach contents
etc., to be preserved for chemical analysis in large animals
are as under :
Liver 1/2 kg.
Kidney 1/2 kg.
Ruminal contents 1/2 kg.
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Ad,'ance d PatllOloglf and Treatme nt of Diseases of Domesti c Animals
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464
Appendix
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466
Appendix
Level
- -- 2 hours
at - -- + L
evei at one h our
2
2
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Requirements
1. Saturated solution of basic fuchsin in acetone free me-
thyl alcohol.
2. Saturated solution of methylene blue in acetone free
methyl alcohol.
3. Working solution.
Methylene blue (in methyl alcohol) 2 parts
Basic fuchsin (in methyl alcohol) 1 part
Mix the two solutions for immediate use.
Procedure
1. Make impression smears from the hippocampus major
in the brain of the suspected case. Moist films are used
without fixation over flame.
468
Appendix
2. Put the mixture of the stain over the film just for a few
seconds (2-3 seconds.)
3. Wash the smear in running water. A properly stained
film will show a violet colour. In case, the staining solu-
tion is not properly balanced, a trial should be made by
adjusting the proportions of basic fuchin and methyl-
ene blue solution in order to obtain the violet colouration
of the film.
Results
Negri bodies are stained bright red or cherry red with a
halo around them and other structures are stained blue. The
presence of Negri bodies is pathognomic for diagnosis of
rabies. Staining of distemper inclusions is done with Shorr
s3 differential stain. Lyssa bodies are small granular bodies
in the neurons of animals infected with the fixed virus.
Staining of Acid Fast Organisms by Ziehl Neelsen's Method
Req u i rements
1. Ziehl-Neelsen carbol fachsin
Basic fuchsin 19m
Absolute alcohol 10 cc
Aqueous solution of 100 cc
Carbolic acid (Phenol 1 to 20)
Dissolve the stain in alcohol and add aqueous phenol
solution to it.
2. Acid alcohol (1 to 2%)
Concentrated hydrochloric acid -2 cc
Absolute alcohol: 98 cc
3. 1% aqueous methylene blue solution make a working
dilute solution of the stock solution by adding 1 cc of
1 % metheylene blue to 9 m1 of distilled water for using
as a counter stain.
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Advanced Pathology and Treatment of Diseases of Domestic Antmals
Procedure
1. Fix the smear above the flame of the sprit lamp or gas
burner.
2. Pour Z.N. carbol fuchsin on the smear and warm the
slide till the stain steams. Maintain the temperature and
let it cool slowly for 3 to 5 minutes.
3. Wash it in running water.
4. Decolourise the smear with acid alcohol (2%) till the
thickest part remains a faint pink.
5. Wash in water to remove traces of acid alcohol.
6. Counterstin the film with working aqueous solution of
methylene blue for 1/2 to 1 minute. Non acid fast bacte-
ria are stained blue with methylene blue.
7. Wash with water, dry it and examine under oil immer-
sion objective after putting a drop of cedar wood oil
over the smear. Acid fast bacteria stain red with carbol-
fuchsin.
470
Appendix
and only once from the starting point for a uniform film.
Dry the smear in the air. Make atleast three such smears and
save the slides from house flies which destroy the film by
licking.
Leishman's stain
Leishman's powder 0.15 gm
Acetone free, methyl alcohol 100 ml.
Procedure
1. Cover the blood film with Leishman's stain for 1 minute.
2. Apply double quantity of freshly prepared distilled
water (or buffer sol, pH 6.6 ) and mix by blowing with a
pipette.
3. Leave the stain for 10 minutes on the film. This time
limit may vary according to the quality of the stain.
Overstaining is to be avoided for smooth counting of
the leucocytes.
4. Wash the smear with fresh or neutral distilled water.
Dry and examine under the oil immersion objective af-
ter placing a drop of cedar wood oil over the stained
film. Acidic water is not used for washing the blook
smears to avoid red colouration of the blood films.
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Advanced Pathologtf and Treatment of Diseases of Domestic AllImals
Procedure
1. Fix the smear by passing glass slide (quite above) over
the flame of the spirit lamp or gas burner for a few times.
Avoid the burning of the smear. The opposite surface of
the slide should be just tolerably hot to the touch.
2. Cover the slide for a half minute with 1 % solution of
crystal violet solution.
3. Pour off the stain and put Gram's iodine over it and
allow it to remain for 1 to 2 minutes.
4. Wash it with alcohol (95 %) till purple colour ceases to
come off.
5. Wash in water and counterstain with 1 % dilute carbol
fuchsin (1 to 10) for 1/2 minute.
6. Wash in water, dry an examine under oil immersion
objective after placing a drop of cedar wood oil over the
smear.
Preparation of Stained Tissue Sections
It includes the steps like fixing, embedding, section
cutting, staining and mounting of the stained sections. A
short description of the different processing steps are given
below:
1. Fixing
It is done to stop the tissue autolysis and also to obtain
the hardening of the pieces of the organs. Pieces of the tissues
(not more than 0.5 to 1 mm thick) are immersed for the sake
of preservation in the following reagents:
(a) 10% formalin (i.e., 40% formaldehyde gas in solu-
tion). Tissues are preserved in aqueous solution of
formalin (10%) for 12 to 24 hours.
(b) Absolute alcohol or methylated spirit.
The solid tissues can be preserved in absolute alcohol.
To strain the glycogen in tissues, the tissues are preserved in
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Solution Timin2
1. 80% Alcohol 1 to 2 hours
2.80% Alcohol 1 to 2 hours
3.95% Alcohol 1 to 2 hours
4.95% Alcohol 1 to 2 hours
5. Absolute alcohol or Acetone 2 to 3 hours
6. Absolute alcohol or Acetone 1 to 2 hours
7 Absolute alcohol or Acetone 1 to 2 hours
8. Benzene or chloroform 1 to 2 hours
9. Benzene or chloroform 1 to 2 hours
3. Processing in paraffin
The pieces of the tissues are given 3 changes of one hour
duration each in the melted paraffin (m.p.52c) and finally
the tissues are placed in the melted paraffin at 58c overnight.
Embed the tissues in the molten paraffin in moulds and
cool rapidly. When set, cut and trim the paraffin blocks.
4. Section Cutting
Paraffin sections (5 to 6 microns thick) are cut with th
microtome. Float the sections on to the slides smeared with
egg albumin and the sections are, then, left in the incubator
for 1 to 2 hours for attaching the sections to the glass surfaces.
5. Processing of the Paraffin Sections for Staining
Paraffin sections are treated with two changes of xylol
to remove the paraffin from the sections for 1 to 2 minutes.
Two changes for 1 to 2 minutes in absolute alcohol are given
to the sections to remove the xylol. The sections are passed
through all descending grades of alcohol (say, 95% and 70%
alcohol) and are then washed in water to remove the alcohol.
The washed tissue sections are, thus, ready for staining.
6. Staining
The different types of the staining solutions are used for
staining cells, fungi,bacteria and spirochaetes etc. The tissues
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Appendix
Requirements
1. 10% KOH solution.
2. Slides.
Procedure
1. Scrap the epidermis from the outer edge of the lesions
with a sterile scalpel. Scraping must have a few hairs
from the margin of the lesions and heat it for a few min-
utes in 10% KOH solution in a test tube and examine it
after taking a loopful on a clean slide after putting a
cover slip over it under low and high power objectives.
Micrometery
In order to measure a microscopic object (say, a
bacterium), the process adopted is called micrometery which
envisages the use of a stage micrometer, an occular
micrometer and a microscope. The one hundredth division
of the scale measures 1/100 (or 0.01 mm). A micron is equal
to 1/1000 mm (or 0.001 mm). One small division of the stage
micrometer measures lOll or microns (Le., 1/ .001 x 0.01=
1000 x 1/100= lOll). The objective, eye piece and "the tube
length of the microscope influence the millimeter value of a
division of the ocular micrometer (i.e., the eye piece scale).
The value of a division of the occular micrometer is
determined separately for the different objectives, eye piece
and tube lengths. The tube length is kept constant to avoid
errors. The scale of the occular micrometer (0.1 mm in length)
is divided into small divisions. The geometric relation between
a division of stage and occular micrometer is 1 to 10.
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Proce dure
(1) Insert an occula r micro meter inside the eye-pi ece of the
micro scope keepin g its tube length (usual ly 160 mm.)
consta nt.
(2) Place a stage micro meter on the micros copic stage.
(3) Find out the numb er divisio ns of the occula r microm -
eter which are in compl ete coinci dence or just coveri ng
the divisio ns of the microm eter scale.
Standardisation With 90 x Objective
50 divisio ns of the occula r micro meter = 5 divisio ns of
the stage micro meter
1 divisio n of the occula r micro meter = 5/50 = 5/50 x 10
= 1 !J. (micron)
!J.
(4) A staine d film of a bacter ial cultur e is moun ted on the
stage of the microscope. The divisio ns on the stage of
the micro meter coveri ng a bacter Ium are noted and, say,
two divisio ns are in exact coinci dence with the length
of an organi sm. So with the given objective, eye piece
and tube length , the bacter ium in questi on measu res 2
!J. (microns).
Note: With other two objectives (8 x or 40 x), the value
of the ocular micro meter divisio n is to be standa rdised , while
keepin g the tube length consta nt.
Estim ation of Age of Anim als
An autops ist's task is to estima te the age of the anima ls
during postm ortem exami nation . Determ inatio n of the age
of an anima l is of great impor tance in vetero legal cases.
All the teeth in the mouth of the anima ls erupt at
differe nt times which rough ly guide to estima te the ages of
animals. Wear of the teeth also guides in determ ining the
age of the anima ls.
Longe vity of cattle and buffal o is 20 years and 15 years
respec tively but these anima ls can live up to 28 years.
478
Appendix
480
Appendix
P3 2.1/2 to 3 years
Mi 5 to 6 months
M2 1 to 1.1/2 years
M3 2 to 2.1/2 years
Table 44. Appearance of Teeth at Various Ages
At birth All the temporary incisors cut through the jaws.
Atl month The temporary incisors are prominent and well
defined
Atl month The temporary molars are in wear.
At6month The 4th molar will cut through the gums. No over
lappinSI of the teeth.
At 1 Year The temporary incisors are in wear.
Atl Year The fifth molar will cut through the jaw.
Atl Year 3 The fifth molar is well up and in wear. The incisors
months show more signs of wear.
Atl Year 9 Eruption of the first pair of permanent incisors. The
months sixth molar will cut through the gums.
At two Years The first and 2nd permanent molars cut through the
gums. The first pair of permanent incisors are well up
and in full wear.
At 2.1/2 Years All the four permanent incisors are well up and in full
wear.
At3 years All the six permanent incisors are in full wear. The
molars~esent a uniform ridge.
At 3.1/2years All the eight permanent incisors are well up in Wear.
At 3.1/2 years The corners are obviously younger and less worn
than the others.
At 4 to 5 years The teeth are slightly worn along their cutting edges.
At6 years The surface of the wear reaches half way across the
upper surface of the teeth. A portion of the root is
exposed.
At 10 years The greater part of the crown is lost from the teeth. A
'portion of the root is exposed.
At 10 to 14 years Only stumps of the teeth remain. The teeth are widely
separated from each other.
At 16 years The teeth become close together again.
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Di 1 1 to4 weeks
Di 2 6 to 12 weeks
Di 3 before birth
DC before birth
DP 1 5 to 7 weeks
DP 2 5 to 7 weeks
DP 3 1 to4 weeks
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Advanced Pathology and Treatment of Diseases of Domestic Animals
Teething
Deciduous Horse Dog
Di 1 day -1 weeks 3-5 weeks
Di2 4-6 weeks 4-5 weeks
Di3 6-9 weeks 5-6 weeks
DC - 3-4 weeks
DP1 day-2 weeks 4-6 weeks
DP2 day-2 weeks 4-6 weeks
DP3 day-2 weeks 6-8 weeks
Permanent Horse D02
1 1 2.1/2 years 2-5 months
1 2 2.1/2 years 2-5 months
1 3 4.1/2 years 4-5 months
1 4 - -
C 3.1/2-5 xears 5-6 months
p 1 5-6 months 4-5 months
p 2 2.1/2 years 5-6 months
p 3 3 years 5-6 months
p 4 4 years 4-5 months
M 1 9-12 months 5-6 months
M 2 2 years 6-7 months
M 3 3.1/2-4 years 6-7 months
Horse
7 Years 11 Infundiblum
6 Years 13 (Upper) 7 year hook
6 Years 12 Infundiblum disappears
9 Years 13 -do- -do-
10 Years 13(upper) -do- Galvayne's groove appears
15 Years 13 ~do- -do- Y2 way down
21 Years 13 -do- -do- reaches tip
21 Years 13 -do- -do- gradually grows out
484
Table 45. Normal Physiological Value s and Some Reagents
Normal Range of Blood Value s:
Cow SheEp Goat Horse Pig Dog Poultry. Human
R.B.C (million~ 5.4-9 8.5-13.5 12.5-22.0 6.5-9.4 5.0-9.4 6.4-8.0 4-6
W.B.C 4.5-13.0 4.0-12.0 5-13 5-11 8.6-20 6-20 20-40 5-10
(thousa nds)
Neutro philes 3015-55 4020-50 36 5650-65 3930-50 6960-75 3120-40 55-70
i(percent)
Eosinophiles 81-15 60-15 3.5 41-5 4.51-10 5.2-10 62-10 1-4
i(percent)
Basophiles 0.5 0-1 0.2 0-2 0 0.5 0-1 11-4 0.5 0-2 2.51-4 0-1
(p_ercent)
Lymph ocytes 5240-70 5240-70 58 3020-40 5240-60 2010-30 7855-96
I(percen t)
25-70
Monocytes 93-15 41-12 2 82-12 31-10 62-12 10-3 3-7
'(percent)
Haemo globin 8.0-14.5 9.0-14.5 9.4-14.0 9.0-14 9.0-16.8 12.0-17.8 8.0-13.0 13-17
(gms/l 00ml)
Sedime ntation 0(30 0 0 2-12 (10 1-6 (30 0-6 (30 Men (3- Wome n
rate (E.s.R) mm min) min) min) min) 7mm/h r.) (0-15m m/hr)
Coagu lation 6 ---- ---- 11 3 4 ---- ----
time(min)
Advanced Pathology and Treatment o/Diseases o/Domestic Animals
486
Appendix
3. Leishman's stain
Dissolve 0.15 gm of Leishman's powder in 100 mI of
absolute (acetone free) methyl alcohoL Take 0.15 gm of
Leishman's stain in a glass mortar. Add 10 ml of methyl
alcohol (acetone free). Triturate with the pestle and decant
it into a glass bottle. Repeat it till the complete dissolution of
the stain in the mixture. Coloured bottle protect the stain
during storage. The volume of the stain is made up to 100 mI
in a coloured bottle by taking more methyl alcohoL
4. Glemsa Stain
Dissolve 0.85 gm of the Giemsa stain in 100 mI of a
mixture of equal parts of glycerol and acetone free methyl
alcohol by shaking and keep for 4 or 5 days.
5. Seller'S Stain
Stock solution
1. Methylene blue: 10 gm
Acetone free, methyl alcohol to make 1000 mI.
ll. Basic fuchsin: 5 gm
Acetone free methyl alcohol to make 500 mI keep the
stock solutions in blue ground glass stoppered bottles in a
refrigerator.
Staining solution is made at the time of staining the fresh
impression smears. Smears are made from hippocampus
major of the brain in dog or cerebellum in cattle. Methylene
blue solution 2 parts and basic fuchsin solution 1 part are
mixed well in a test tube before use to stain Negri bodies.
6. Benedict's Qualitative Reagent for Sugar
Copper sulphate 17.3 gm
Sodium .:itrate 173.0 gm
Sodium carbonate 100 mg
487
Advanced Pathology and Treatment of Diseases of Domestic Animals
488
Appendix
Chloform 30 ml
Clear
The proforma for postmortem report is given below:
Postmortem No-............................ .
Species ....................................... .
Colour ......................................... Breed ....-~........ .
Owner ........................................Sex ................. .
Residence ...................................... Age ................ .
Weight ............ .
By whom sent for examination and reasons if any
Date and hour of death / sacrifice Autopsy findings
Date and hour of postmortem examination 1.
History 2.
Cadaverous changes 3.
Rigor mortis
External appearance on removal of
skin (describe contusions and wounds etc.)
Mouth and pharynx
Nasal cavities
Larynx and trachea
Oesophagus
Pleural cavity and lungs
Pericardium and heart (absolute wt ....... relative wt .......... %
Peritoneum
Liver (absolute wt ........ relative wt. ............................. %
Gall bladder
489
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490
Appendix
492
Appendix
493
Advanced Pathology and Treatment of Diseases of Domes tic Animals
494
Appendix
495
Advanced Pathology and Treatment of Diseases of Domestic Animals
REFERENCES
Jones, T.e. and Hunt, R.D. (1983). Veterinary Pathology,
Lea and Febiger, Philadelphia.
Murphy, F.A; Gibbs, E.P.J; Horzinek, M.C and Studdert, M.J.
(1999). Veterinary Virology,3 rd ed, Academic Press, New
York.
Radostitis, Otto M; Gay, Clive C; Blood, Douglas, C and
Hinchc1iff, Kenneth, W. (2000). Veterinary Medicine,
ninth ed, W.B. Saunders Comapny, Ltd, New York.
Singh, V.K. (Head Department of Nephrology, P.M.CH.
Patna) and Gupta, V.K. (Medical Officer, Health De-
partment of Government of Bihar, Patna: Personal Com-
munication.
Singh, CD.N. and Lakra, P. (1972). Pathologic changes in
Naturally Occurring COhJlophoron Cotylophororum infec-
tion in Cattle, Am. J. Vet. Res. 2: 659-663.
497
Index
Abortion 88 Brucellosis 94
Acid fast staining technique Canine distemper 165
(Ziehl-Neelsen's method) 469 Canine parvovirus infection 160
Actinobacillosis 62 Carbon tetra chloride toxicity 265
Actinomycosis 59 Chlorinated hydro carbons
African horse sickness 143 toxicity 281
Amphistomiasis 237 Cirrhosis 299
Anaemia 333 Coccidiosis 219
Anaplasmosis 217 Coenurus cerebralis (Multiceps
Ancylostomisis 239 multiceps) infection 259
Antemortem wounds 434 Collection of materials in
Anticoagulants 450 differnt diseases 453
Anthrax 10 Colibacillosis 21
Aphtha, epizootic (foot -and- Common diagnostic tests 461
mouth disease) 120 Chemotherapeutic agents
Ascariasis 247 used in the veterinary
Aspiration pneumonia 295 practice 374
AUjeszky's disease 171 Curative and preventive
doses of vitamins
Autopsy technique of birds 444
and minerals 275
Autopsy of carnivores 443
Creepers (Aphosphorosis) 271
Autopsy technique in large
Crescents in nephritis 319
ruminants 437
Cretinism (Myxoedema) 270
Azoturia 361
Babesiosis 203
Cyanides poisoning 285
Dermatitis, contagious
Bacteraemia 02
pustular 142
Bang's disease (Brucellosis) 94
Despatch of materials to
Barbone (Haemorrhagic pathological laboratory 457
septicaemia) 15
Despatch of materials in medico
Bee sting 339 legal cases 459
Black- leg (Black -quarter) 76 Dropsy (Oedema) 322
Blue tongue 148 Dyctyocaulosis (parasitic
Botulism 83 pneumonia or lung worm
Bovine ephemeral fever 135 disease) 260
Bronchopneumonia (Lobular Echinococcus granulosus infection
pneumonia) 292 (Hydatid disease) 258
498
Index
499
Advanced Pathology and Treatment of Diseases of Domestic Animals
500