Systemic Veterinary Medicine-I

(MED-401)
Lectures by Sir Yaqoob

Foot and mouth disease

It is a highly contagious disease of cloven footed animals which is characterized by erosions
in the mucosa of mouth and hoof.
Etiology
Genus Apthovirus
Family Picornviridae
7 serotypes
A O C SAT- I & Asia- I
SAT- II
SAT- III
There are further 60 subtypes
Susceptible host
All cloven footed domestic animals:
Cattle, buffalo, sheep and goat
And wild animals:
Deer, water buffalo, elephant, giraffe
Equine:
Horse, donkey and zebra are resistant
Pathogenesis
Animals acquire virus usually by inhalation and oral route. After 24 hours virus replicate in
respiratory epithelium, lymphoid tissue, pharynx and dorsal soft palate.
Virus persists there for long time. After this blisters are developed at infected site. Area fills with
serous fluid and becomes a vesicle. These vesicles enlarge and join together. After enlargement
vesicles rupture and fluid leaks. The expelled material (fluid) contains high quantity of virus.
Virus are also excreted in milk and through expired air.
Pathognomonic sign: “Tiger heart” - In young calve focal necrosis of cardiac muscle
Clinical signs
Fever 103-106 ◦F
Depression, anorexia, loss of milk production, blisters in mouth, excessive ropy viscous
salivation, blisters rupture within 24 hours leaving raw painful ulcers
Mouth lesion usually heal in 10-14 days
Transmission
Aerosols
Ingestion/inhalation
Through secretions saliva, urine, feces, semen and milk
Vectors such as vehicles, equipment
Treatment
No treatment
Antipyretic
Vaccination
Prevention and control
Biosecurity measures should be adopted strictly
Strict import/export restrictions and quarantine measures
Herd testing system
Slaughter/cull all infected animals

Bovine viral diarrhea

Definition
It is a viral disease of animals which occurs in sub-acute and acute form. It is characterized
by high rise of temperature and erosions of mouth, esophagus, rumen, abomasum and
intestine. It also causes abortion in pregnant animals.
Etiology
Caused by a pestivirus or BVDv
Family Flaviviridae
Two Types:
BVDv-I and BVDv-II
Susceptible Host
Cattle is more susceptible
Deer, buffalo and wild ruminant are also affected
Pig and sheep can be affected
Transmission
Through fomites, through ingestion of contaminated feed
By infected saliva, nasal secretion, ocular discharge, urine and feces
Direct and indirect contact with infected animals
Pathogenesis
Virus enters and contact with epithelium of mucosa and enters in epithelial cells and replicate
there. Then virus enters in blood stream within 2-4 days. During this virus gains entry to other
predilection sites and lymphoid tissue and cause infection in that sites.
Signs and Symptoms
Fever, lethargy, anorexia, ocular discharge, nasal discharge, oral lesions, decrease milk
production, diarrhea, reproductive disorders, loss of fertilization, abortion, premature birth
and death.
In rare cases by complication of secondary bacterial infection pneumonia develops.
Diagnosis
History, clinical signs and lab tests
Differential diagnosis
MCF, rinderpest, Bovine viral rhinotracheitis, Johne’s disease, heavy parasitism
Treatment
No treatment
But can be treated as secondary infection
Antibiotics and rehydration
Prevention and control
Biosecurity measures should be adopted strictly
Vaccination is an essential part of both control and eradication
Test for and cull persistently infected heifers
Immediately separate effected and exposed animals from rest of the herd

Rinderpest
Rinderpest is known as “cattle plague”
It is tetra-D
 Depression
 Diarrhea
 Dehydration
 Death
Epiphora, excessive lacrimation, nasal discharge, frothy saliva
It is fatal
Definition
It is an acute or subacute, contagious viral disease of ruminants which is characterized by
high fever, lacrimal discharge, inflammation, hemorrhage, necrosis, erosions of epithelium
of mouth and digestive tract, profuse diarrhea and death.
Etiology
Morbilivirus family paramyxoviridae
Virus resembles to PPR, measles and CD virus
Susceptible Host
All cloven footed ruminants are susceptible (not all clinically some subclinically)
Cattle and buffalo clinically
Sheep and goat subclinically
Camels are asymptmatic
Transmission
Through direct contact with infected animals
Body fluids, respiratory and lacrimal secretion and feces
Through ingestion
Fomites
Tabanus fly – biological vector
Pathogenesis
Virus enters in body through ingestion and inhalation and replicate in upper respiratory tract and
cause infection. After this it goes into blood → viremia → systemically spread to other
predilection sites (lymphocytes and alimentary mucosa) and appearance of signs and lesions
Clinical signs
Fever 104 to 107 ◦F
Fever, depression, red patches with discharge around the eyes, nose and mouth
Frothy saliva, conjunctivitis, photophobia and epiphora, congested mucous membrane,
constipation followed by severe diarrhea, leukopenia, corneal opacity and death
Case definition: ocular and nasal discharge with any two of the additional signs:
Fever, erosions in the mouth, diarrhea, dehydration and death.
Postmortem lesions: “Zebra stripes” on intestine
Diagnosis
History, Clinical signs, PM lesions, lab tests
Differential Diagnosis
FMD, BVD, VS, BT, MCF, Paratuberculosis, mycotic stomatitis
Treatment
No treatment
Slaughter the effected animals
Prevention and control
Carpet vaccination; vaccination of suspected animals
Import restrictions on susceptible animals
Import restrictions uncooked meat products from infected countries
Biosecurity measures should be adopted strictly

Vesicular stomatitis
Vesicular stomatitis is an important livestock zoonotic viral disease which is characterized
by vesicles, erosions and ulcers on mouth, feet and udder. Pain, anorexia and decrease
productivity.
Etiology
Genus vesiculovirus
Family Rhabdoviridae
Major serotypes
VSV – New Jersey
3 subtypes
 Indiana I (Fort lupton)
 Indiana II (Cocal virus)
 Indiana III (Alagoas virus)
VSV Indiana (most common)
Susceptible host
Horses, cattle, camelids and human are susceptible
Sheep and goats are less susceptible
Outbreak of this disease mostly occur in cattle and horses
Transmission
Biological vectors: Sandflies and black flies
Direct contact; infected animals
Contaminated objects
Aerosol
Pathogenesis
Virus enters initially replicate in epithelium after replication enter into blood stream (viremia).
Other predilection sites and develop vesicles on the lips, muzzle, tongue, teats and interdigital
clefts. And erosions on muzzle and coronary bands.
Clinical signs
Incubation period is 3 to 5 days
Fever and vesicles
Horses are severely affected
Oral lesions – drooling, mouth rubbing, salivation
Coronary band lesions and lameness
Recover within 2 weeks
Postmortem lesions
Gross lesions
- Erosive, ulcerative lesions, oral cavity, nostrils, teats and coronary bands
- Histopathology: Degeneration of epithelial cells
Diagnosis
History, clinical signs, lab tests (virus isolation from vesicular fluid or epithelium, viral antigen
detection, ELISA, complement fixation test, virus neutralization test)
Antibody tests (serum sample, ELISA, complement fixation test, virus neutralization test)
Differential Diagnosis
FMD, RP, IBR, BVD, MCF, contagious exanthema, foot rot, chemical and thermal burn
Treatment
 No specific treatment available
Prevention and control
 Do not buy from positive herds for 3 months post infection
 Avoid grazing at peak insect feeding hours
 Segregation and isolation of infected animals from herd
 Milking equipment should be clean and disinfected
 Insect control programs
 Vaccination

Malignant catarrhal fever

Gangrenous coryza
Bovine malignant catarrhea
Malignant head catarrhea
Malignant catarrhal fever (MCF) is an infectious viral disease of ruminants which is
characterized by high fever, profuse nasal discharge, severe hyperemia, diffuse necrosis of
oral and nasal mucosa, leucopenia, ophthalmia, corneal opacity and enlargement of lymph
nodes
Etiology
Herpes virus
Two types: Alcelaphine HV- I in wild animals
Ovine HV- I in sheep transfer to cattle
Susceptible Hosts
Cattle, buffalo – clinically
Sheep and goat not apparent
Deer
Transmission
 Nose to nose contact with sheep is the most efficient method of spread
 Most cases of MCF in cattle have had contact with other animals that are actively
shedding the virus
 Rabbit considered as a reservoir
 Insects
 Fomite transmission is well documented
MCF characteristics
 Cattle are “dead end” hosts for the ovine strain – no documented spread from infected
cattle to other cattle
 High mortality in symptomatic cases
 Low morbidity – typically very few animals become symptomatic
Pathogenesis
 Entrance
 Replication in lymphoid tissue (lymph node, Peyer patches and spleen)
 Generalized infections
 Necrotic and proliferative changes with erosive lesions on epithelium
 Cerebromeningeal tissue, keratoconjunctivitis
Incubation Period: 40-60 days
Clinical Signs
 Clinical signs are most common in animals of age 2 months – 2 years
 Disease course may range from peracute to chronic
 In deer this disease is in peracute form and sudden death
 High fever 106-107 ◦F
 Swollen lymph nodes
 Mucopurulent exudation
 affecting the upper respiratory, ocular and oral mucosa
 Skin lesion (erythema, exudation, crackling & crust formation)
There are basically four clinical forms:
 Peracute form
 The head ad eye form
 The intestinal form
 Mild form
Peracute form
Short course of 1-3 days
High fever, dyspnea and acute gastroenteritis
Head and eye form
Reddened eyelids
Bilateral corneal opacity
Crusty muzzle & nares
Nasal discharge
Erosions on tongue and oral mucosa
Intestinal form
Fever, diarrhea, nasal and ocular discharge, enlargement of lymph node, hemorrhagic diarrhea
and bloody urine
The infection causes a vasculitis and lympho-proliferative reaction in many organs including
CNS
Mild form
Occurs most commonly in experimental animals
Transient fever and mild erosions appear on the oral and nasal mucosae
A distinctive clinical feature in chronic MCF is persistent bilateral ocular leukomata.
Diagnosis
History, clinical signs, post mortem lesions, lab tests, diagnosis is based on history, clinical signs
Differential diagnosis
BVD mucosal disease, blue tongue, Rinderpest, FMD, vesicular stomatitis, Salmonellosis, Oral
exposure to caustic materials, mycotoxins, poisonous plants
Treatment
Survival is rare
100 % mortality
Supportive therapy, antibiotics for secondary bacterial infection
Prevention and Control
Avoid exposing cattle and deer during parturition
Separate infected and carrier animals
Biosecurity measure should be taken
Possible value is intranasal vaccines with interferon production

Pestes des Petits Ruminants (PPR)

Synonyms: KATA, Goat plague, contagious pustular stomatitis, pseudo-rinderpest
Definition
It is a viral disease of small ruminants characterized by fever, sores in mouth, diarrhea,
pneumonia, dyspnea and death.
Etiology
Family Paramyxoviridae
Genus Morbillivirus
Closely related to Rinderpest virus
Susceptible host
Sheep and goat are highly susceptible
Cattle and buffalo are seroconvert but do not develop or transmit disease
Wild ungulates can be affected
Transmission
Virus shed in nasal and ocular secretions, saliva, urine, and feces
Close contact, inhalation
Through fomites
Pathogenesis
Inhaled/ingested virus
Upper respiratory infection → Regional lymph nodes – multiplication – viremia – Target cells
(lymphocytes, alimentary and respiratory mucosae – epithelial cells) and appearance of signs and
lesions
Morbidity and mortality
Young animals are mostly affected – age 2 months to 2 years
Varies by species, immunity, breed
Clinical signs
2-10 days
Peracute and Acute form
High fever, serous nasal and ocular discharge becomes mucopurulent, hyperemic gums, necrotic
oral lesions, profuse diarrhea, rapid respiration, dyspnea, abortion
And skin nodules around muzzle
Postmortem lesions
Inflammatory and necrotic lesions on oral cavity and GIT
Emaciation
Erosive lesions “zebra stripes”
Bronchopneumonia and enlarged lymph nodes
Diagnosis
History, PM lesions, clinical signs, lab tests
Differential diagnosis
Rinderpest, bluetongue, contagious exanthema, FMD, coccidiosis, mineral poisoning, contagious
caprine pleuropneumonia, pasteurellosis
Treatment
No specific treatment
Supportive and symptomatic therapy
Prevention and control
Quarantine measures
Movement controls
Euthanasia of infected and exposed animals
Cleaning and disinfection of infected premises
Blue tongue
- Sheep more as compared to goat
- Non contagious
- Coronitis – inflammation of coronary bands
Synonyms: sore Muzzel, Pseudo Foot and mouth disease and muzzle disease
Definition:
It is an arthropod born viral disease of ruminants like sheep which is characterized by catarrhal
stomatitis, hemorrhages, enteritis, cyanosis of oral cavity, laminitis, edema of head and neck
and torticolis
Etiology:
Family Reoviridae
- Genus Orbivirus
24 serotypes worldwide
Non contagious, insect-borne viral disease
Susceptible host
Ruminants: Primary host is sheep
Cattle, goats and deer can be affected
Transmission
Biological vectors, biting midges
- Genus cullicoides
Ticks and sheep keds
And mechanically
Pathogenesis
Virus enters then replicate and localize into lymph nodes and viremia
Damage of endothelial cells
Necrosis, edema and hemorrhages develops
Morbidity and mortality
Morbidity is 100 % and mortality is 30 %
Incubation period is 5-10 days
Clinical signs
Oral erosions and ulcerations, tongue will be swollen, protruding, cyanotic ‘blue tongue’
Reproductive failure, coronitis (inflammation of coronary bands), lameness (painful hooves)
Erosive crusts around nose and teats
PM lesions
Face and ear edematous
Dry, crusty exudate on nostrils
Coronary band hyperemic, hydroencephalitis, cerebellar dysplasia
Diagnosis
Clinical signs
History
Lab test
Differential diagnosis
FMD, VS, PPR, MCF, BVD, contagious pustular dermatitis, IBR, sheep pox, foot rot,
actinobacillosis
Treatment
No specific treatment
Symptomatic and supportive therapy
Prevention and control
 Control of vectors, confine animals indoors when vectors are active
 Quarantine and movement controls
 Disinfection: cleaning the premises sodium hypochlorite (bleach) and 3 % sodium
hydroxide (lye)
 Insect control, use of pyrethroids and organophosphates
 Vaccination

Canine Distemper
Synonyms: Hard-pad disease, canine influenza
Enter into respiratory system, lymphatic tissue; regional lymph nodes and viremia occurs
And affect other systems, GIT system, urogenital system, nervous system; optic nerve
Destroys epithelial lining and cause enteritis, vomiting occurs
Reddened eyes, coughing, sneezing etc.
Definition
It is highly contagious viral disease of dog which is characterized by diphasic fever,
leukopenia, ocular and nasal discharge, frequent cutaneous eruption, bronchopneumonia,
gastroenteritis and neurological convulsions.
Etiology
Family: Paramyxoviridae
Morbilivirus
It is highly sensitive to lipophilic substances i.e. ether and ethanol
It is relatively unstable outside the body
Transmission
Through direct contact with infected animals
With contaminated materials like secretions of respiratory system, urine, feces
Through inhalation
Pathogenesis
Virus enters into body and replicate in lymphatic tissue of respiratory tract then viremia then
infect other systems like respiratory, GIT, urogenital tract, CNS and optic nerve. Then
disease is followed by replication of virus in the epithelium of these sites.
Gastroenteritis, vomiting and convulsions
Clinical signs
Sneezing, coughing, thick mucus discharge from eye and nose, fever, lethargic, vomiting,
diarrhea, depression, loss of appetite (anorexia), reddened eyes, conjunctivitis, uveitis, optic
neuritis, hyperkeratosis of footpad, incoordination, abdominal pain, increasing lung sound,
dyspnea, rhinitis (inflammation of nares lining) sudden onset
PM lesions
Thymus becomes small and gelatinous, consolidation of lungs due to interstitial pneumonia,
enteritis, mucopurulent discharge from nose and eyes, bronchopneumonia,
Skin pustules and hyperkeratosis of foot and nose
Diagnosis
History taking; if other animals are affected
Clinical signs, PM lesions and lab tests
Differential diagnosis
Canine infectious tracheobronchitis (kennel cough)
Parvovirus
Bacterial enteritis
ICH
Rabies
Protozoal infection
Treatment
No treatment
Symptomatic treatment
Antibiotic
Antipyretic (NSAIDs)
Fluid therapy
Antidiarrheal
Anticonvulsant; valium
Antiemetic
Bronchodilator
Rehydration
Prevention and control
Separate the infected animals from healthy animals
Confine the movement of healthy animals
Before purchasing or entering the new animal; test system should be adopted strictly
Vaccination
 Uvea: comprised of iris, ciliary body and choroid
PM: Postmortem
AM: Anti-mortem
Prognosis: Probable outcome of a disease
Three types; favorable, guarded and poor
Diagnosis: the identification of the nature of an illness or other problem by examination of
the symptoms.
Pleuropneumonia: Inflammation of pleura and lungs
Bronchopneumonia: Inflammation of bronchus and lungs
Tracheobronchitis: Inflammation of trachea and bronchus

Infectious canine hepatitis

Definition
It is a highly contagious viral disease of dog which is characterized by high rise of
temperature, diarrhea, vomiting, icterus/jaundice and sometimes convulsion.
In this disease liver is mostly affected.
Etiology
CAV- I and CAV- II; canine adenovirus
This virus can remain stable for months in any ideal environment.
Susceptible host
Dogs of all ages are susceptible but puppies are more susceptible
Transmission
Through direct contact with infected animals and contaminated materials like saliva, secretions,
Feces, through inhalation, through biological vectors, ticks, fleas, mosquitoes, through carrier
animals. These animals can shed viruses after recovery up to 6 months or more
Pathogenesis
Virus enters into body then into primary predilection sites like peyer’s patches, tonsils, and
lymphatic tissue. After replication enter into blood stream and cause viremia and then disperse
into body and other predilection sites, liver, kidney, uvea and cause infection like hepatitis,
nephritis, uveitis, keratitis and cloudy eyes
The inflammation of cornea and uvea is called as blue eyes.
Clinical signs
The disease range is mild to severe. Nausea, vomiting, anorexia, jaundice, bleeding from nose
and gums, bloody vomiting and diarrhea, enlarged abdomen (ascites), seizures and coma.
Death occurs within five days
PM lesions
Enlarged liver - mottled, pale, inflamed liver and ascites, lymph nodes are swollen, enlarged and
hemorrhagic
Diagnosis
History – disease in periphery
Biological vectors involvement
Differential Diagnosis
Leptospirosis (liver and kidney effects)
Hemolytic anemia (RBC destroys)
Cirrhosis (fibrosis of liver)
Bile duct obstruction
Salmonellosis
Toxoplasmosis
Hepatic abscess
Hepatic neoplasia (tumors)
CD
Treatment
Symptomatic and supportive therapy
NSAIDs, antidiarrheal, fluid therapy
Prevention and control
Separate infected animals from healthy animals
Restrict movement of animals
Pest system should be adopted
Vaccination

Canine Parvovirus
Definition
It is highly contagious disease which is characterized by dehydration, severe vomiting,
hypovolemic shock and death
Etiology
Canine Parvovirus
CPV-I and CPV-II
Susceptible host
This virus is also stable outside body with ideal conditions for months. This virus prevails in
clothes, shoes and carpets
Dogs and canine family
Transmission
Through direct contamination with infected animals, urine, saliva, feces, unvaccinated animals
are more prone than the vaccinated animals.
Carrier animals are major threat
Pathogenesis
First of all virus enters into body. After entering localize into primary site and then enter into
blood stream and cause viremia. After this disperse into other sites and infect heart and
intestine and cause myocarditis & enteritis by the infection of myocardium and intestinal
crypts.
After infection of intestinal crypts villi become short and disrupt. Destruction of crypts and
villi leads to grey persistent foul smelling, diarrhea and hemorrhagic enteritis. By the
myocarditis, mostly sudden death occurs.
Clinical signs
Two forms:
Enteric form and myocardial form
Enteric form: sudden depression, loss of appetite (anorexia), fever, vomiting and diarrhea may
be hemorrhagic, rapid dehydration, shock and death, lethargic
Myocardial form: Sudden death occurs. Puppy looks normal but coloration of body, dyspnea,
coughing, ascites and malaise (discomfort due to illness)
In case of left side heart failure, edema in lungs and in case of right side heart failure edema in
periphery
Post-mortem findings
In enteric form lower and middle small intestine is dilated, intestinal contents are watery, bone
marrow is depleted.
In myocardial form lungs are heavy and edematous, congested, heart dilates and becomes pale,
pancreas becomes hemorrhagic, clear watery fluids in abdomen and thorax
In chronic cases, heart becomes fibrotic
Diagnosis
History, clinical signs and lab tests, HA and HI tests
Differential diagnosis
CD, ICH, Canine corona virus, canine herpes virus, salmonellosis, enterobacteriaceae, poisoning,
congenital heart anomalies
Treatment
No treatment, fluid therapy, antiemetic, antidiarrheal, antacid, antibiotic

Feline calcivirus
Upper respiratory system disease – larynx, upper trachea and oral cavity
Also affect ocular system and digestive system and if it prolongs then lower system can also be
affected and inflammation of joints also occurs (arthritis)
Ulcers of hard-pad and cheeks, lesions on tongue, rhinitis, ocular and nasal discharge; serous in
consistency becomes mucopurulent later on
Oro-nasal cavity entrance and replication there and infect the parts; if intensity is more than it
affects other systems
Definition
It is an upper respiratory disease of cat which is characterized by rhinitis, conjunctivitis,
lacrimation, salivation and oral ulceration
Etiology
Feline calcivirus
This virus occurs throughout the world, domestic and wild species of cat are mostly affected.
There are about forty different strains of this virus which are significantly antigenically
different.
Susceptible host
Cat
Transmission
Through aerosols, through fomites, through direct contact, unvaccinated cats are more
susceptible than vaccinated, through the contact with infected animal secretions.
Pathogenesis
Virus enters into body then cause pathogenicity in the upper part of the digestive, respiratory and
ocular systems which cause conjunctivitis, rhinitis, ulcers in tongue, ulceration of palate
Some strains of the virus have predilection sites other than the above mentioned sites like lungs
and joints. And cause arthritis and sometimes pneumonia
Clinical signs
Incubation period is 2-6 days
For upper respiratory system signs and symptoms are like sneezing, nasal congestion,
conjunctivitis, discharge from the nose, initially clear but with the passage of time it becomes
purulent
For the digestive system ulcers on tongue, hard palate and lips; due to these lesions cat
drool out excessive saliva
The other general signs which develop during disease, fever, anorexia, lethargic, enlargement of
lymph nodes
Diagnosis
History, PM lesions, lab tests
Differential diagnosis
Feline herpes virus, mycoplasma felis, Chlamydophila, Bordetella bronchiseptica
Treatment
No treatment
Prevention and control
Vaccination 8-10 week first shot and 2-3 week 2nd dose; booster dose
Vaccine is available in combined form

New Castle Disease

Synonyms: Avian distemper, Avian pneumoencephalitis
Definition
It is a pneumoencephalitis, acute viral disease of poultry which is characterized by
sneezing, coughing, nervous behavior, tremors, circling, falling, twisting of head and neck
and paralysis.
Etiology
Family: Paramyxoviridae
Genus: Avulavirus
9 serotypes APMV-1 – 9
There are three types which are based on intensity;
1. Velogenic 2. Mesogenic 3.Lentogenic
These strains are neurotropic and viscerotropic
Velogenic are more virulent than mesogenic and lentogenic.
Mesogenic are more virulent than lentogenic and less virulent than velogenic
Lentogenic are less virulent than mesogenic and velogenic.
Velogenic strains produce nervous and respiratory signs and cause 90 % mortality.
Mesogneic strains produce coughing, sneezing and affect egg quality and production. And cause
10 % mortality.
Lentogenic produce negligible signs
Susceptible Host
Domestic birds; poultry, pigeon and peacock
Transmission
Direct contact with infected birds with secretion of infected birds, feed, water, equipment,
clothes
Unvaccinated birds are carrier for this virus
Through migratory birds
Pathogenesis:
Virus enters into body. Proliferate into primary site → viremia → affect other sites and
appearance of signs and symptoms
Clinical signs
Mortality is 90 % and morbidity is 100 %
Disease condition depends upon virulence of strains
Incubation period is 2-15 days; average is 5-6 days
Drop in egg production, numerous deaths within 24 to 48 hours, surviving birds may have
reproductive and neurological damages, edema of head especially around eyes, greenish
diarrhea, respiratory and neurological signs

PM lesions
Edema of head and neck, edematous hemorrhagic, necrosis and ulcerations of lymphoid tissues
Pathognomonic signs
Hemorrhages on tracheal mucosa, proventriculus and intestinal mucosa
Greenish fluid comes out from intestine
Diagnosis
History, clinical signs, PM lesions and lab tests
Differential Diagnosis
 Avian Influenza
 Fowl cholera
 Coryza
 Foul pox
 Psittacosis (viral disease of parrot)
 Mycoplasmosis
 Infectious bronchitis
Control and Prevention
 Management problem, poor ventilation; correction
 Disinfection of premises
 Delayed reintroduction of new birds for 30 days
 Control insects and mice
 Limit human traffic
 Proper destruction of old carcasses
 Use the detergents and ultraviolet lights and sunlight for disinfection
Inclusion Body Hepatitis
It is a viral disease; hepatocytes are affected
Enter epithelium of buccal cavity and intestinal epithelium, localize there and viremia, effects on
liver (mottled, pale, friable), skin; dermatitis, spleen atrophy and also of bursa of fabricius, and
relates to immunosuppressive diseases like IBD and infectious anemia
Spread through vertical transmission and horizontal transmission
Definition
It is a viral disease which is characterized by mottled liver, pale bone marrow, gangrenous
dermatitis. This disease is accompanied by other immunosuppressive diseases like IBD,
infectious anemia
Etiology
Avian adenovirus
There are 12 known serotypes which are known for the production of this disease
Susceptible Host
Chicken, turkeys and peasants
Transmission
Vertical transmission: from parents to offspring (through eggs)
Horizontal transmission: From bird to bird with contact with droppings
Once the bird becomes immune; the virus can no longer be isolated from droppings
Pathogenesis
First of all virus enters into body and then localize in epithelial cells of buccal cavity and
intestine then replication then disperse through blood to other organs like liver, kidney, bone
marrow, lymphoid tissue, respiratory tract, spleen and bursa of fabricius and cause infection and
appearance of signs and symptoms
Clinical Signs
Mostly birds are affected at age of 5 – 7 weeks, birds are listless with ruffled feathers.
Mortality is about 25 % and death occurs within 10 days
PM lesions
Mottled liver with pin point necrotic and hemorrhagic spots, pale bone marrow, gangrenous
dermatitis, kidneys are pale and swollen, spleen is usually quite small and atrophic, bursa of
fabricius is atrophic in case of presence of IBD in subclinical forms
Diagnosis
History; prevalence of disease in periphery
Lab tests, clinical signs, PM lesions
Differential Diagnosis
Chicken anemia, sulphonamide intoxification, infectious bursal disease, vibrionic hepatitis, fatty
liver syndrome, deficiency of vitamin B12
Treatment
No treatment; symptomatic and supportive therapy
Prevention and control
Separation
Knowledge about immunosuppressive diseases and time of vaccination
Vaccination

Enterotoxemia
Effects intestine (damage intestine)
Causative agent: Clostridium perfringens (soil borne)
Highly concentrated diet or irregularity in feeding or excess feeding and heavy parasitism →
predisposing factors
Penetrate intestinal wall and proliferate there and produce toxins (necrotizing and neurotoxic)
Capillaries damage, nerves damage in brain, kidney damage (Pulpy kidney disease) cells
damage, water accumulation, ascites
Synonyms: Over eating disease, pulpy kidney disease for Clostridium perfringens Type D
Definition
It is a bacterial disease of animals which is characterized by diarrhea, paralysis,
convulsions and death
Etiology
Clostridium perfringens Type A necrotic enteritis in poultry and dog
Clostridium perfringens Type B Lamb dysentery
Clostridium perfringens Type C Goat enterotoxemia
Clostridium perfringens Type B & C Calf enterotoxemia
Clostridium perfringens Type D Pulpy kidney disease, over eating disease
Young animals (newborn) are more affected
Susceptible host
Sheep, goat, cattle
Pathogenesis
First of all pathogen enter into epithelium of small intestine. Predisposing factors:
 Ingestion of excessive amount of feed or milk by very young animals
 Highly concentrated diet
 Sudden change in feed
 Irregular feeding
 Heavy parasitism
 Indigestible food
 Lack of natural or acquired immunity
Due to these predisposing factors clostridium perfringens attack or penetrate epithelial cells of
intestine and proliferate and produce different types of toxins
Type A produces alpha and CPE toxin
Type B produces alpha, beta, epsilon and CPE
Type C produce alpha, beta and CPE
Type D produce alpha, epsilon and CPE
These toxins necrotize or damage the capillaries / epithelium and increase the permeability of
intestinal mucosa. These toxins also damage capillaries of other organs like kidney, lungs and
brain.
Due to damaging of epithelium of mucosa or capillaries extracellular type edema produce.
Due to this edematous swelling and other nervous signs will be produced.
Clinical Signs
Sudden death, anorexia, recumbency, coma, dull and depressed, frothy salivation, greenish
pasty diarrhea, staggering, opisthotonus, bloat, chumping of jaws, shallow respiration and
blindness
PM lesions
Hemorrhagic enteritis, ulceration of intestinal mucosa, excessive serous fluid in peritoneal
cavity, thick blood tinged fluid in small intestine, hemorrhages may be seen in thymus and heart
Diagnosis
History, clinical signs, PM lesions and lab tests
Differential Diagnosis
 Colibacillosis
 Salmonellosis
 Enteritis
 Listeriosis
 Rabies
 Ruminal impaction
 Pregnancy toxemia
 Enteritis (Enterobacteriaceae)
 Pasteurellosis
 Lead poisoning
Treatment
Sulphonamide / sulphadimidine - 50 mg/kg/orally
Oxytetracycline - 5-10 mg/kg of body weight IM or IV
Immunity boosters
Injection E-sel, Injection V-sel, Injection AD3-E: 15-25 ml / large animal
Toxin binders chelating agents like EDTA, DTPA
Hyper immune sera
Prevention and Control
Correction of managemental errors
Reduce the concentrate amount in feed
Vaccination containing toxoids
First dose at early age of animals and booster dose after 4 weeks and after 6 months repeat
Pregnant animals vaccination in 2 week intervals

Coccidiosis
Poultry disease
Protozoal disease
Bloody diarrhea
Sporulated oocyst → animal ingestion → intestine → it bursts 8 sporozoites → intestinal
epithelium penetration and convert into merozoites through schizogony (shizonts: nucleated cell)
→ macrogametocytes and microgametocytes, they penetrate and they produce microgamete and
macrogamete → zygote formation and cell wall maturation and cyst formation (such cyst
contains zygote; non-infective stage) and comes into intestine and comes out through excreta.
Zygote containing oocyst matures and convert into sporulated oocyst (infective)
Definition
Coccidiosis is protozoal disease of animals which is characterized by enteritis, loss of
production, morbidity and mortality.
Etiology
Phylum Apicomplexa
Genus Eimeria
There are many species like
 E. acervulina
 E. tenella
 E. mitis
 E. brunetti
 E. maxima
 E. praecox
 E. necatrix
E. maxima, E. tenella and E. necatrix → active in poultry
Susceptible Host
Poultry, sheep, goat and cattle
Dog, cat and horses are less susceptible
Transmission
Ingestion of contaminated feed and water
Pathogenesis
Life cycle: First of all eimeria enters into the intestine through ingestion in sporulated oocyst
form within the intestine. These sporulated oocysts release 8 sporozoites. These sporozoites
penetrate into intestinal wall or cells. These sporozoites convert into the merozoites through
shizogony.
The merozoites containing cells burst and each merozoite penetrate into other epithelial cell.
After penetrating these merozoites become the macrogametocytes and microgamtocytes which
produce microgametes and macrogametes. These microgametes enter into the other cell which
contain macrogametes. After penetration and fertilization of macrogametes and microgametes
zygotes will be developed. Zygote containing cells becomes oocyst by producing the cyst in
outer wall. Now the zygote containing oocyst (non-infective) comes into lumen of intestine and
pass out and converts into sporulated oocyst.
Clinical Signs
Loss of appetite, loss of weight, loss of production, diarrhea with blood, dehydration and death.
Red feces; blood tinged feces, bed will be wet due to droppings (predisposing factor for
colibacillosis)
PM lesions
Hemorrhages on lumen of intestine
Diagnosis
History, clinical signs, PM lesions, lab tests
Differential Diagnosis
Necrotic enteritis
ND
Treatment
Coccidiostats
Coccidiocidal
Amproleum 125 mg / liter of water / per kg of feed
Sulphonamide 125 mg / liter of water / per kg of feed
Vitamin K Capsule Zincovit K – coagulant
1 capsule in 40 liter of water
Prevention and Control
 Good management
 Good sanitation
 Feeding and watering devices should be cleaned properly
 Stress should be minimized
 Anti-coccidial drugs can be given
 Vaccination
Exanthema
A skin rash accompanying a disease or fever
Tenesmus
a continual or recurrent inclination to evacuate the bowels, caused by disorder of the rectum or
other illness.
Opisthotonus
spasm of the muscles causing backward arching of the head, neck, and spine, as in severe
tetanus, some kinds of meningitis, and strychnine poisoning.
Otitis
inflammation of the ear, usually distinguished as otitis externa (of the passage of the outer
ear), otitis media (of the middle ear), and otitis interna (of the inner ear; labyrinthitis)
Lymphangitis
inflammation of the walls of the lymphatic vessels.
Lymphadenitis
Inflammation of lymph nodes
Epiphora
excessive watering of the eye.
Antibiotics
 Penicillins
 Cephalosporins
 Macrolids
 Fluoroquinolones
 Sulphonamides
 Tetracyclines
 Aminoglycosides
Jhone’s Disease
Mycobacterium paratuberculosis is the causative agent.
Poison, heavy paratism or fascilosis, shoo
Shotting diarrhea, projectile diarrhea, windpipe
Bacterium very bad intracellular previail like tuberculosis no responsive to treatment by nature
slow progressive enteritis it causes , chronic condition enteritis diarrhea and after that severe
emaxiation, intesint clolnize adhere yo intestine infect it infection immune system phagocy ngulf
and proliferate inside cells autoimmune system effect it and cyst formation and thicken the
intestinal layer and there arises microscopic changes normal physture change and chronic
diarrhea and septimea in blood and other organs effect mostly effect reproductive system and
comes udder to milk and effect offspring prevail
3 4 points nonsrresponsive to treatment chronic dia sever ema projectile and windstem diarrhea
pathognomic signs

Definition
It is a chronicm incurable bacuter disease mostly affect the lower part of the intestine of
ruminants which is charateriz by diarrheam, weight loss, severe emaciation\n, loss of production,
bottle jaw intermendibular edema , protein out from blood and minimum protein and edema
develops, good appetite*

Etiology
Parabacterium paratuberculosis

Susceptible Host
Almost all ruminants
Younger animals are more prone than older

Transmission
Thorugh ingestin of contamina feed and water.
Through intrauterine
Through the clostrum and milk

Pathogenesis
First of all organism enter tito thotygh ingestion or anyo thr transmit route in the wsmall
intestine. In the intestine they are engulfed by macrophages which are located in intestinal wall
after engulfing the bacteria multiply inside the cells (intrace ) by the autoimmunity or body
immnuit response the intracellular bacteria create the typical thickening and microscopic
distortion of intestinal wall. Epithelium starts to deteriorate and physiology alters. After this
diarrhaea and septicemia will be developed. In septicemic form bacteria prestn in blood and
lymh nodes which allow excess to the other part of body. Uterus and udder and comes in milk
Due to this organism can be isolated foemru terus uteruine wal placenta and colustrium and milk
of infected animal.
Atacia ribs are seen in this condtion
Emaciation, unresponsive to dewormer nad antibiotic
Appetite is normal but weight of the animal is decreased and death can occur.
Intermittent diarrhea, pipestem diarrhea, intermittent fever low grade fever, intermendibular
edema
Confuse with lumpy jaw , actinmycosis and fascilosis
Lethargic, depression, It is economically valuable disease because. Due to this severe loss of
produc, premature culling, loss of opportunity for sailing and export early control is highly
expensive or inexpensive. Cost is increased with the time.

Diagnosis
History CS, lab tests,
Differential Diagnosis
INtestin paratitsm, chronic malnutrition, caseous lymhadenitis, enviremental toxin and ?
Treatment
Non-responisve
If Isoniazid 6-8 mg orally KI NI can be
Prevention and Control
Strictly monitoring during the pursches of
pRevent the feeding of colustrom and milk to the new obrn from the infected animal
Monitor the recipient animal in ebmro transfer progaram which is major source of infection for
further progress
Prevent the grazing of animals on those pastruers which are contaminated with infected animal
manure
Clean and dry premises to prevent ingestion of manure by all animal particualry by young
animals.

Mostly effect digestive system

Colibacillosis next time

Brucellosis

Embryo transfer technique?

Actinomycosis , actinobascillosis, mycobact para tub or tuberculosis same make thick isoniazid
treatement dissolve. It is irresponsible. A
Colustrum

Salmonellosis

Non spore forming and rod shaped and gram negative ?

Family Enterobactericae
Found in water and Bar-B Qs Take care of it
Cause dehydaruion, enteritis, dehydration,
S. Typhmurium cause Typhoid S. Dubilin
Enteric form and septicemic form
After entering infective stage → sltiplication cause enteritis and penetrate to lamina propria it is
beneath the a connective layer residency there and proliferation and intestinal epithelial layer
beneath nd there prolifertation and later is damage layer and inflammation happens there
No absorbtion, no digestion and diarrhea
Phagocytic cells engulf and live in that cells and prevail there and body circulation and effect
other parts of body and infection
Brain – encephalitis, uterus abortion, bones osttitis and causes
Septicemic form

Definition
It is a bacterial disease of animal which is characterized by septicemia, acute en and chroic
enteritis
Etiology
This disease is cause by Salmonella
There are many species which infect different animals like in cattle S. Typhymurium, S. Dublin,
In sheep and goat S. Typhymurium, S. Dublin, S. anatum
In horses, S. Typhymirum and S. anatum
Salmonell Typhymurium is common mostly infect the animals.

Transmission
Though the ingestion of contaminated feed and water. Uncooked feed, unpasteurized milk,
thorught the eggs and meat from the infected birds. T vertical trasnission in poultry and also in
alge anim’

Pathogenesis
First of all bacteria enters into the body throught ingestion of contaminated feed or water then in
intestine and cause infection by mulktiplying. After multiplication pathogen enters into lamina
propria and damage the intestinal wall by causing the enteritis and diarrhea. Due to infection and
inflammation of intestine, the phagocytic cells engulf these bacteria These bacteria can survive
within the cell. Septicemic form followed by the infection of other organs like brain, menings
and uterus bones tip of ear tail and feet. By producing the signs like meningioencephaltis,
abortion, otitis and dry gangrenous on the tip of ear, tail and feet.

Clinical Signs
Mainly clinical signs are in two forms:
Septicemic form and enteric form
In septicemic form fever about 105 to 107 F, depression, fever, acute illness, death within 24
hours. Nerovus signs and pneumonia can occur. Mortaility about 100 %.
In enteric form divided in to 3 forms acute form subacute and chronic form
In acute form mostly occurs in first of age, fever 105 – 107 F severe watery diarrhea, dysentery,
tenesmus milk decline in production. Abdominal pain is common and severe in horses. In dogs
and cats acute diarrhea and pneumonia and abortion. Conjunctivitis is seen in cats.
In subacute form, mild fever 103 to 104, inapetance, dehydration, abortion and death. High
mortaility.
In chronic form, persistent diarrhea, severe dehydration, intermittent fever, poor response to
treatment. In this form, feces are some normal some time mucoid and sometime bloodish.

Diagnosis
History, clinical sings, lab tests
Differential Diagnosis
Diarrh, dystenrt ,coccidiosis, BVD, IBR, arsenic poisoning, copper deficiency (molybdenossi),
paratuberculosis, colibacillosis, septocemam, ostertagiasis

Treatment
Antibacgeria
Trimehtprim sulphonamide 15-60 I V
Inj Sulprim 10 -15 ml per large animal
1 -2 ml small animal
Ampicillin 5-10 mg/kg iv im sc
Cephalosporin (ceftiofer 1.1 mg/kg IM)
Nasaid flunix meglumin 1-2 mg/kg iv im po
Fluid Theray
Surgnist and antagonis becarful

Prevention and control

Don’t eat raw or uncooked feed.
Don’t prepare the food from the infected animals.
Wash the hand and other uteniils which are used.
Wash the hand after the contac infected animla feces
Avoid the direct/indirect contact between reptiles and infants.

Menings? A delicate sheet on the brain

Tenesmus
Subacute
Peracute
Acute
Reptiles ? vertebrate

Feline Panleukopenia

Feline Pan means deficiency of leukocytes means WBCs

A viral disease of cat and we see overall decrease in WBCs
Main Git involves other system are reproduce and cns , vominting, diarrhea, depression
And regarding CNS, ataxia whenever there is hypoplasia cerebellum remains
Incoordination and ataxia and if reproductive system involves abortion and stillbirth results.
Feline Panleukopenia virus same as of parvo virus, resistant and can survive in the envireoment
for years and years. Disinfectant we use normally alcohol, chloroform etc does not work but
bleack act on it. 56 C for 30 minutes. Pasteurization keep in mind. There is a set temperature.
There is fixed set point. If you grow a bacteria, keep optimum and limited point maybe threshold
point at which it can grows. Virus enters and oropharynx local tonisls localize there and replicate
there and cause infection. And then enters into blood stream and affect the organs of the system.
In reproductive system it will affect uterus brain cerebellum and git intestine and signs and
symptom shows

Sysnonyms
Felin Panleukopenia is also called feline infectious enteritis, feline distemper, feline ataxia, cat
plague

Defintion
It is a highly contagious viral disease of falidae family which is characterized by fever,
inappetance, vomiting, depression, dehydration, leukopenia, and high mortality.
If the other systems involve then the virus creats infect in the uterus and cause abortion, stillbirth,
neonatal death. Cereberllar hypoplasia, ataxia, at the age of 2 – 3 week mostly kittens are more
affected.

Etiology
This disease is caused by Panleukopenia virus. This virus is stable like Parvovirus and can
survive the external environment from motns to years with favorable enviroement. This virus can
resist the disfectant like ether, alcohol, formalin and heat about 56 C for 30 minutes. Chroxax
bleanc is eefective for destruction of this virus.
Susceptible Host
Falidae family like cat, raccoon,
Mustalidae family mink and ferret (wild animals like cat)
According to the age, the young animlas are more prone than the older animals.
Mainly due to the lack of immunity

Transmission
As it is highky contagnous through direct with infected animals.
Through the contact with contaminated fomites. Through the ingestion of material contaminated
food, secretin like saliva, urine ,feces, After recovery some animals become carrier and they are
big source of transmission of this virus. These Ticks are consider biological vector of this
disease.
Unvaccinated are more prone than the vaccinated animals.

Pathogenesis
First of all virus enters into the body and then localize in oropharynx lymphoid tissue like tonsils
after infection or replication and then virus enters into the blood and cause viremia. In viremic
condition, the virus disterse into whole body and the other predilections sites like rapidly
dividing in the chest like thymus and cerebellum, uterus and intestine and cause the infection in
these sites. Then the symptoms related to these sites occur like diarrhea, vomiting, hypoplasia,
still birth, abortion.

Clinical Signs
Following clinical sings appear due this disease are vomiting, depression, diarrhea within 1 to 2
days. Death within 12 to 24 hours, Fever, abdominal pain (cat cry in this disease). Within the
infected animals the mortality rate can become 90 % but if it is treated vigorously the mortality
can be decreased up to 30 %.

Postmortem lesions
Enteritis, pale color and weak carcass,

Diagnosis
History, clinical signs, PM lesions, and lab tests
Differential Diagnosis
Acute septicemia, gastroenteritis, acute toxoplasmniss, feline leukopenia

Treatment
No treatment but you have to treat according to sign and sypmtoms
In good prescriprion only 3 to 4 medine should be included.
Vomiting and diarrhea, dehydration is encounteted. Note that! Rehyrdation is of vital
importance.
Hypovolemic shock or brain becomes dead.
CRT test is simple. Rehydrate and secondary infection prevention , antibiotic
Antiemtic and antidaiirham antipyretic.

Prevention and control

Infected animals should be segrate tform healthy animals.
Qurantine measures adotion
Disinfect and clean the premises
Vaccination is of vial imporatance. Afer 8 week vaccine it 2 oe 4 week booster and then 3 rd
booser dose and then repeat it annually.

Ataxia
Atacia
What is immunity against foreign body
Mechanism of immunity
Fomites?

Stillbirth?