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Systemic Veterinary Medicine-II

Ashir Azeem

Lectures by Sir Yaqoob

Congestive Heart Failure

The heart due to some intrinsic or extrinsic defects is unable to maintain circulatory equilibrium
even at rest, resulting in dilatation and congestion in the venous circuit, edema (lungs and/or
periphery) and cardiac enlargement.
Etiology:

• Mitral valve regurgitation.

• Dilated cardiomyopathy. Heart loses its contractility power.
• Hypertrophic cardiomyopathy. Heart layer increases so lumen becomes narrow.
Clinical Signs:
In case of left sided heart failure edema is in the lungs and it results in suffocation. While in case
of right sided heart failure edema is in the body periphery, ascites and limb edema occurs. In
complex both sides of the heart are effected.
Diagnosis:
History, clinical signs and lab tests
Treatment:

• Lower the pressure on heart by giving diuretics (Lasix)

• Avoid exercise and salt
• Vasodilators

Cardiac Cycle: The deoxygenated blood enters right atrium through vena cava and
oxygenated blood enters left atrium through pulmonary veins. This relaxed period of heart
chambers is called diastole. The muscles of atria contract and blood passes through tricupsid
and biscupsid valves into the ventricles. Then ventricles contract and blood is pumped into
pulmonary artery and aorta. This is systole.

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Malignant Edema

Synonyms: Clostridial myonecrosis, Gas gangrene

Definition:
It is an acute infectious fatal disease of animals which is characterized by fever, edematous and
emphysematous swelling around the wound.
Etiology:
The causative agent is Clostridium septicum. It is a gram positive, soil borne, rod shape, spore
forming pathogen which produce different types of toxins like α and β toxins.
Susceptible Host:
Sheep, goat and cattle. Horses are also affected. Older animals are more susceptible than young
ones.
Transmission:
It is a soil borne pathogen. Transmission is mainly through wound, surgical injury like castration,
docking, injection and vaccination. This pathogen also occurs in dormant state in GIT normally.
Through contaminated feed and water. Through spores.
Pathogenesis:
First of all pathogen enter into the body through above mentioned transmission routes and then
spores enter into blood stream and circulate then lodge in peripheral body tissue of the animals
like gravitational portion, belly and limbs when that portion is wounded or contusion with any
injury, anaerobic condition will be developed. Due to anaerobic condition, this pathogen spores
germinate or multiply and produce different types of toxins like exotoxin α and β. These toxins
damage or destroy the peripheral tissue and convert into gangrene, edematous and
emphysematous lesions. After accumulation of huge amount of gas, the swelling spread beneath
the skin under the fascia and finally bursts. These toxins enter into blood stream and cause death.
Clinical Signs:
Fever, edematous swelling around wound in belly or limbs, loss of appetite, lethargy and sudden
death.
Postmortem Lesions:
Gangrenous and gelatinous material in the swelling, blood tinged fluid accumulate in pericardial,
pleural and peritoneal sac.

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Diagnosis:
History → Ask about docking, castration, parturition and vaccination.
Clinical signs, lab tests and postmortem lesions
Differential Diagnosis:
Black leg and anthrax
Treatment:

• Heavy dose of penicillin repeat in 4-6 hours if it is treated in time. Local appliance of
antibiotic is also effective.
• Non-steroidal anti-inflammatory (NSAIDs) drugs
• Supportive therapy includes administration of vitamins and minerals
• Use of antitoxin (toxoids)
• Drainage of swelling by H2O2
Prevention and Control:

• Vaccination
• Separate the infected animals from healthy animals
• Proper wound dressing
• Avoid contaminated feed
• Disinfection of farm premises

Gram-negative bacteria are surrounded by a thin peptidoglycan cell wall, which itself is
surrounded by an outer membrane containing lipopolysaccharide. Gram-positive bacteria
lack an outer membrane but are surrounded by layers of peptidoglycan many times thicker
than is found in the Gram-negatives.

Tetanus

Synonyms: Lock jaw

Definition:
It is a non-contagious infectious disease of animal which is characterized by spasmodic
contraction of skeletal muscle, hyperesthesia, asphyxia and death.
Etiology:

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Clostridium tetani
It is gram positive, spore forming, anaerobic, rod shape and long cylinder
Susceptible Host:
Horses are more susceptible. Cattle, sheep, goat are also susceptible.
Transmission:
Mainly in horses due to hoof injury. In cattle laceration during parturition. In sheep and goat due
to tail docking and castration. Other reasons are accidents, injuries and deep wounds. Through
punctured wound during partition, tail docking and castration. Foot wound during grazing.
Through ingestion and wound in buccal cavity and intestine.
Pathogenesis:
First of all pathogen enters into the body and becomes localized until favorable conditions. When
the favorable condition develops the organism multiply or proliferate and germinate and produce
toxins like tetanospasmin and tetanolysin. This pathogen cannot produce toxin if the
environment is aerobic or through oxidation-reduction reactions. Tetanolysin destroy red blood
cells and necrosis of the peripheral tissue. Tatanospasmin are highly toxic fatal toxin and absorbs
by peripheral motor nerves which move retrograde in CSF and produce ascending tetanus. Due
to ascending tetanus, voluntary muscles are flaccid. If the amount of this toxin is very high and
absorb in blood stream or lymph and reach CNS which produce descending tetanus. Due to
descending tetanus voluntary and involuntary muscles constrict. By constriction of involuntary
muscles of heart, lungs, diaphragm asphyxiation will be developed and animal is destroyed.
Idiopathic tetanus is without wound or through the intestinal wound.
Clinical Signs:
Lock jaw (contraction of masseter muscles), stiffness of head and neck region. Inability to move
in the hind end. Muscles of mouth becomes extremely stiff. Animal is reluctant to move and
cannibalism. Difficult in turning, backing and eating. Death occurs in 80 % in unprotected animals.
Prolapse of 3rd eyelid. It is a pathognomonic sign. Erection of ear and retraction of eyelids.
Postmortem lesions:
Congestion in spinal cord, early rigor mortis, hemorrhages in skeletal muscles. Lungs remain
hyperemic due to asphyxia.
Diagnosis:
History, clinical signs, lab tests and postmortem lesions
Differential Diagnosis:

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Grass tetany, milk fever, rabies, strychnine poisoning

Treatment:

• Antibiotic like Procaine penicillin @ dose rate of 2000 IU IM BID

• Neutralize the toxin by antitoxins (toxoids) @ dose rate of 3000-15000 IU IM and repeat
after 12 hours
• Control the spasm by using tranquilizers such as chlorpromazine @ 1mg/kg IM or 0.4-0.8
mg/kg IV 3-4 times daily
• Provide the supportive treatment
• Provide palatable feed and water via stomach tube.
• Provide dark and wide place due to hyperesthesia
Prevention and Control:

• Disinfection of wound properly by antiseptic

• Use of sterilized equipment
• Induce toxoid to produce active immunity
• More use of passive immunity like antitoxin (anti-tetanus serum)
• First administer anti-toxin and then perform any surgical procedure

Toxoid: A bacterial toxin that has been weakened until it is no longer toxic but is strong
enough to induce the formation of antibodies and immunity to the specific disease caused by
the toxin.

Bacillary Hemoglobinuria

Synonym: Red water disease

Definition:
It is an acute highly fatal toxemic disease of cattle and sheep characterized by jaundice, fever and
hemoglobinuria.
Etiology:
The causative agent is Clostridium hemolyticum. It is gram positive. It is soil borne bacteria and
naturally found in GIT. Mostly this disease is associated with proliferation of bacteria due to other
liver diseases like Fasciolosis.
Transmission:
Through wound and feeding.
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Pathogenesis:
This bacteria mostly occur in the environment in spore forming and normally in the body in GIT.
Then spore penetrate the lining of the intestine and spread through blood stream in the liver. In
liver it remains in inactive form until favorable conditions due to other liver diseases like
Fasciolosis. After providing the favorable conditions or anaerobic conditions spores proliferate
and produce two types of toxins. First one destroy the adjacent tissues of liver which also produce
anaerobic condition. The other toxin circulate in the blood stream and destroy the red blood cells
and change the color of urine. So that is why it is called as ‘red water disease’. Due to destruction
of the red blood cells, the level of oxygen in body depletes. Due to this animal can be destroyed
or dead.
Clinical Signs:
Sometimes cattle may be found dead without premonitory signs. Severe depression, fever,
abdominal pain, dyspnea, dysentery, hemoglobinuria, anemia, jaundice, brisket edema
Incubation period is 12 hours to 4 days. Mortality in untreated animals is about 95 %.
Postmortem Lesions:
Trachea contains blood with hemorrhages in mucosa. Carcass is anemic, sub-cutaneous edema.
Bloody fluid in abdominal and thoracic cavity. Small and large intestines are hemorrhagic and
contain blood. Liver is congested and lighter in color. Kidney becomes dark and friable. Bladder
contains reddish urine. After death rigor mortis become quick.
Diagnosis:
History → Ask about feeding and check for wound and liver damage and flukes. See if the area is
marshy
Clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
Babesiosis, post-parturient hemoglobinuria, anaplasmosis, anthrax, bracken fern poisoning,
leptospirosis
Treatment:

• Penicillin @ 20,000 IU/kg

• You can use other broad spectrum antibiotic like Farmox LA @ 1ml/15-20 kg IM
Prevention:

• Vaccination (follow the vaccination schedule)

• Separate infected animals from healthy animals
• Monitor wound conditions/cases.

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• Avoid contaminated feed.

• Dispose marshy areas

Black Quarter

Soil borne disease. Mode of action is same. Ingestion of spores and enter into blood stream and
circulation and lodge into different sites including tissues and muscles. Their main predilection
site is heavy muscle. They lodge into them. And there they remain in dormant state. If the blood
supply become less or depletion of oxygen takes place at the lodge site then they start to
proliferate as it is anaerobic. Anaerobic condition develops due to injury to muscle. Blood loss
occurs. Or animal may have a respiratory problem and resultant decreased supply of oxygen to
muscle tissue and they start to proliferate. And toxins are produced. And they will damage the
connective tissue of muscles. Gangrenous and necrosis develops. And gas is produced. After
necrosis that muscle gives crystalline appearance and it becomes harden. And then on pressure
that muscle gives crepitation sound. It is the pathognomonic sign. If thigh muscle is effected and
walk of animal the crepitation sound is produced. It is highly fatal disease and it causes sudden
death. Vaccination of the disease is available.
Synonyms: Black Leg Disease
Definition:
It is an acute highly fatal infectious but not contagious disease of livestock which is characterized
by the development of focal gangrenous, emphysematous myositis, hemorrhages and swelling
of the heavy muscles like thigh muscles.
Etiology:
Clostridium chauvei
It is gram positive and soil borne bacteria.
Susceptible Host:
Cattle, sheep, goat are more prone than horse.
Transmission:
Through ingestion of contaminated feed, ingestion of spores. Through any wound like castration,
docking, shearing, lambing and tattooing.
Pathogenesis:

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First of all pathogen enter into body through the ingestion or wound. The spore enter into blood
stream and circulate in circulatory system and lodge in different organs or tissues including
muscles. Mostly predilection site of this bacteria is heavy muscles like thigh muscles. They remain
dormant until favorable condition develop when the oxygen level become decreased due to
deficiency of oxygen anaerobic condition will be developed. Due to anaerobic condition,
pathogen multiply and proliferate and produce toxins. These toxins damage/destroy peripheral
tissue of heavy muscles. Damaged portion become gangrenous, necrosis and emphysematous.
Clinical signs:
Sudden death, lameness, fever, swelling of the muscles, swelling spread and gas form under the
skin which produce crackling sound when pressed with hand and movement of the body.
Postmortem lesions:
Muscles of shoulders thigh and neck are usually affected. Lesions are also observed on the
tongue, diaphragm and myocardium. Blood stained discharge/fluid accumulate in pericardium.
Heart muscle remain blackish red. Liver, kidney, lungs and spleen are hemorrhagic. Rectal
prolapse can be detected. Bloody froth/fluid in later stage ooze from the natural orifice.
Diagnosis:
History → Wet dirty feed, castration and tattooing, and injury
Clinical signs, lab tests and postmortem lesions
10-15 % diseases can be diagnosed by history.
Lab tests 100 % sure.
Differential Diagnosis:
Anthrax, malignant edema (ME), bacillary hemoglobinuria (BHU)
Treatment:

• Penicillin is a drug of choice. (250000 IU/per kg)

• Broad spectrum Formox LA
Prevention and Control:

• Vaccination properly.
• Isolate effected animals from healthy animals.
• Dead animals should be disposed of properly.
• Avoid contaminated feed.

Botulism
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Definition:
It is a toxemic, paralytic disease of animal characterized by fatigue, visual disturbance such as
double vision, difficulty in focusing the eyes, loss of ability of pupil to accommodate the light,
muscle weakness, dysphagia and poor muscular tone.
Etiology:
Clostridium botulinum. It is a spore forming, obligate anaerobic, soil borne bacteria which
produce different types of toxins from Type A-G.

Animals A B C D E F G
Horses ✓ ✓
Cattle ✓ ✓ ✓
Sheep ✓
Dog ✓ ✓

These toxins create flaccid paralysis in the body by binding the neuromuscular junction.
Susceptible Host:
Horses, cattle, sheep and dog
Transmission:
Through ingestion of contaminated feed with toxins, spores which are pathogenic. Through
wound and also occur naturally in the intestine. Through inhalation is also reported but animal
to animal is not documented.
Pathogenesis:
First of all pathogen/toxin/spore enter into the body then produces toxins. These toxins absorb
in blood stream and circulate. During circulation these toxins stop the release of
neurotransmitter like acetylcholine at the junction of muscles and nerves. Due to absence of
these neurotransmitter muscle becomes flaccid, weak and paralyzed. Due to weakness and
paralysis of muscles asphyxia develops. When cardiac or diaphragm muscles are involve the level
of oxygen deplete in body which causes death.
Clinical Signs:
Ataxia, recumbent, head turned into flank due to cranial never dysfunction. Ruminal stasis, atonic
bladder, loss of urination, dyspnea, muscle tremors, unable to retract the tongue, drenching
pneumonia, dysphagia, ptosis (inability to raise upper eyelid), mydriasis, constipation, urine
retention, death due to respiratory paralysis. Mortality rate is 90 % if it is not protected.

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Postmortem Lesions:
There are no characteristic lesions in the carcass.
Diagnosis:
History → Ask about feed
Clinical signs, lab tests → Animal inoculation test and antigen-antibody test
Differential Diagnosis:
Parturient paresis, ketosis, rabies, equine encephalomyelitis, scrapie, spinal cord trauma, three
day sickness/ephemeral fever, tick fever
Treatment:

• Antibiotic is not so effective. But you can use metronidazole @ 10-60 mg/kg of BW IM/IV
• Antitoxin @ 30,000-70,000 IU
• Supportive therapy include fluid therapy and catheterization of bladder if possible
Prevention and Control:

• Good husbandry practices

• Rodent control
• Proper carcass disposal
• Avoid poor quality silage
• Vaccination

Anthrax

Synonyms: Splenic fever, Wool sorter’s disease

Definition:
It is an acute septicemic disease of animals which is characterized by sudden death, absence of
rigor mortis, tary color blood from natural openings and widespread hemorrhage.
Etiology:
Bacillus anthracis
Susceptible Host:
Anthrax can occur in wild and domestic animals that graze such as cattle, sheep and goats.
Transmission:
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Through ingestion or inhalation of spores and vegetative forms of the organism or entry through
broken skin. Through gastrointestinal tract (rare).
Pathogenesis:
The infection occurs through ingestion or inhalation of spores/vegetative forms of the organism
or entry of the organism or entry of bacteria through broken skin. After entry the spores
germinate and localize for multiplication and spread by means of lymphatics to lymph nodes and
then in blood stream causing severe septicemia. The bacteria possesses both capsule and
exotoxin. Due to presence of capsule phagocytic cells become unable to destroy them. The
exotoxin is lethal in nature, it causes edema and tissue damage. The exotoxin is lethal in nature,
it causes edema and tissue damage. The exotoxin has 3 components: 1) Edema factor (EF) or
factor I is adenyl cyclase which causes increase in cellular c-AMP level that causes electrolyte and
fluid loss. 2) Protective antigen (PA) or factor II is a fragment of exotoxin and has anti-phagocytic
activity. 3) Lethal factor (LF) or factor III stimulates macrophages for production of oxidizing
radicals and cytokines. Mainly IL-1 and TNF-α which induce shock and death.
Clinical Signs:
High fever 105-107 ℉, hemorrhage from natural orifices, dyspnea, tary color blood. Sudden
mortality up to 90 %
Postmortem Lesions:
Discharge of blood from vagina, anus and mouth, tary color of blood, enlargement of spleen,
widespread hemorrhage on serous surfaces of visceral organs, subcutaneous edema, spleen
shows hemorrhage and accumulation of blood in red pulp, hemorrhage in lymph nodes, liver,
lungs and kidneys and degenerative and necrotic changes in kidneys and liver.
Post mortem examination of animals suspected for anthrax should not be conducted.
Diagnosis:
History, clinical signs and lab tests (Immunodiagnostic tests for demonstration of
antigen/antibody – Elisa, AGPT (Ascoli test)
Differential Diagnosis:
Clostridial infections, bloat, lightning strike, acute leptospirosis, bacillary hemoglobinuria,
anaplasmosis, braken fern poisoning and lead poisoning
Treatment:

• Antibiotics such as ciprofloxacin, levofloxacin, moxifloxacin or doxycycline PO for 7 to 10

days
• Valotrim® (monoclonal antibodies that bind anthrax toxins)
Prevention and Control:

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• Vaccination
• Preventive antibiotics and other drugs
• Quarantine
• Burning and burial of suspect and confirmed cases

Tuberculosis

Mycobacterium tuberculosis is the causative agent. It can affect any part of the body but mainly
affects the respiratory system. It is contagious. Two ways of entrance: digestion and inhalation
route. After as a first entry it enters through lesions → tubercle formation → defensive system
macrophages engulf them → multiply in them → chemotactic response and other macrophages
from blood stream accumulate there; primary tubercle → burst → pathogen into blood stream
and other organs involve in digestive system retropharyngeal or cecal tonsils are more prone. In
respiratory system → caudal alveoli, lungs alveoli and bronchioles → macrophages of alveoli
engulf them → multiply → chemotactic response. Mycobacterium → acid fast staining carbol
fuchsin and red color develops. The chemicals → macrophages → immune system destroy the
bacilli if not then these multiply → macrophages die → liquefaction starts → blood stream other
macrophages comes after some time → internal macrophages layer dies → calcification and
liquefaction of lymphocytes and macrophages layer → granuloma and tubercle formation. Thus
called pearl disease. In lungs shiny tubercles and they become harden. On bronchioles it develops
a layer and if it breaks then bacteria in lungs and blood and reach to the body → tubercle
formations → calcification and solidification of the tubercles. It is chronic in nature. It preserves
for month and month. It is hard to eliminate. Ingestion and inhalation are entrance routes.
Synonyms: Pearl disease
Definition:
It is a chronic contagious disease of animals which is characterized by development of tubercles
with resultant caseation and solidification or calcification.
Etiology:
Mycobacterium tuberculosis. It is gram positive, acid fast, non-motile, cylinder rod shape bacteria
which can persist for long time in cold environment, dark and moist condition. In cattle the
causative agent is Mycobacterium bovis.
Susceptible host:
Cattle, goat are highly susceptible. Sheep ad horses are less susceptible but in some text they are
resistant. Experimentally are susceptible.

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Transmission:

• Through ingestion and inhalation.

• Through cutaneous (if there is wound)
• Through genital route (through AI)
Pathogenesis:
First of all pathogen enter into respiratory system (with respect to) then reach into bronchioles
and alveoli then infect the bronchioles. Within 2-8 weeks pathogen reaches into alveoli and
ingested by alveolar macrophages then pathogen multiply in macrophages and produce
chemotactic response that bring additional macrophages. Most of surrounding macrophages are
not successfully destroy bacilli tubercles but release enzymes and cytokines that destroy, damage
and inflame the lungs. Then macrophage die and release bacilli tubercle and form caseous center
in the tubercle. Macrophages and lymphocytes come from the blood stream ad gather around
the caseous center and form granuloma or tubercle which keep the bacilli contained and under
control LTBI (latent tuberculosis infection). Animal with LTBI will have mycobacterium
tuberculosis in body abut do not have tuberculosis in the body and cannot spread infection to
other animals. Caseous center enlarge and form air filled cavity and burst the granuloma and
release bacilli which spread through the blood stream to other parts of the body.
Clinical Signs:
It develops over months may become dormant. In early stages may be asymptomatic. In late
stages progressive emaciation, fever, weakness, inappetence, weakness, moist cough, enlarged
lymph nodes, diarrhea, vomiting, blindness, retinal detachment and uveitis
Postmortem Lesions:
Tubercles which appear like yellow caseous calcified may resemble like abscess. These tubercles
can also be seen in lymph nodes and other organs of body.
Diagnosis:
History → Ask about if animal is emaciating or weakens and ask about AI
Clinical signs → moist coughing
Lab tests → Tuberculin test, biochemical tests, culturing
Differential Diagnosis:
Bovine pleuropneumonia, pasteurellosis, aspiration pneumonia, traumatic pericarditis and
caseous lymphadenitis
Treatment:

• Isoniazid @ dose of 5g/kg of BW for 45 days

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• Streptomycin@ dose of 5g daily for 6-12 moths

Prevention and Control:

• Test and slaughtering

• Test and segregation
• Cleaning and disinfection
• Prohibit supplement feeding
• Prevent the contact with other healthy animal

Listeriosis

It is a bacterial disease. Listeria monocytogenes is the causative agent. Through ingestion,

suckling, drinking and venereal it penetrates the mucosa. From buccal cavity to brain and comes
to blood. Two modes of action. In ruminants it causes meningioencephalitis. Due to inflammation
and dysfunction of the brain, coordination of muscles disturbs and circling movement occurs and
then it enters into blood stream and it causes enteritis, diarrhea, blindness and abortion. There
are two forms: encephalitic form and septicemic form.
Synonyms: Circling disease, Silage sickness, Silage disease
Definition:
It is a bacterial disease which is characterized by meningioencephalitis, loss of muscular
coordination, paralysis, fever, abortion and septicemia.
Etiology:
Listeria monocytogenes is the causative agent. It is a gram positive, non-spore forming, highly
resistant to environment, motile and coccobacilli bacteria.
Susceptible Host:
Domestic mammals like sheep and goat and birds are mostly affected.
Transmission:

• Transmission through the ingestion of contaminated feed

• Through inhalation
• Through drinking of contaminated water
• Through venereal route
• It is zoonotic unpasteurized milk for neonate and meat it may transmit
Pathogenesis:

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First of all pathogen enters then penetrate through mucosa and enters into the brain and cause
inflammation of the brain and meninges. By the inflammation of brain the encephalitis the
coordination of nerves and muscles become weak and loss which causes facial paralysis. The
other form of pathogenesis is when pathogen enters into blood stream then multiplication occurs
and then circulates into the body and causes infection in different part of body like reproductive
system, eyes and intestine which causes enteritis, diarrhea, blindness and abortion.
Clinical Signs:
There are two forms:
Encephalitic form and septicemic form
In encephalitic form there are certain signs and symptoms like depression, decreased appetite,
decreased milk production, neuro-muscular incoordination which causes circling movement,
seizures, facial never paralysis, lock jaw, impaired swallowing
In septicemic form diarrhea, abortion, blindness and death. This form is mostly found in
monogastric animals.
Diagnosis:
History, clinical signs, lab tests and postmortem
Differential Diagnosis:
Rabies, caprine arthritis, Gid (Coenurosis), encephalitis and pregnancy toxemia
Treatment:

• Based on diagnosis
• Penicillin and tetracycline orally @ dose of 25 mg/kg of BW for 1 week
• If brain involves i.e. encephalitis you can use IV sodium penicillin @ dose of 40,000 IU/kg
every 6 hours.
• Dexamethasone @ dose of 1-2 mg/kg IV
• Supportive therapy, electrolytes and fluids
Prevention and Control:

• Spoiled food and hay should be discarded properly

• Improved sanitation of the pens, water supply, pasture and housing
• Keep wild birds away from the farm or housing or herd
• Kids should be fed with pasteurized milk

ELISA stands for enzyme-linked immunoassay. It is a commonly used laboratory test to detect
antibodies in the blood. An antibody is a protein produced by the body's immune system when
it detects harmful substances, called antigens.

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Hemorraghic Septicemia

Pasteurella multocida is the causative agent. It is gram negative bacterium. It is an opportunistic

organism. Enters by inhalation and localize in tonsils and until predisposing factors it remains
inactive and pulmonary defensive system is active. Due to long transportation, malnutrition,
climate change → active stage and leukocytes and macrophages damage and two kind of amines
are released histamine, prostaglandin and fibrinoblastic → clot the blood and prostaglandin
produce fever, pain and inflammation and lungs parenchyma inflammation blood clots and
consolidations of lungs → peri-subcutaneous tissue, muscles and neck inflammation and
hemorrhages → suffocation, asphyxia and hypoxia develops and leads to death.
Synonyms: Shipping fever, Bar borne disease, Pasteurellosis, Stock yard pneumonia, Stock yard
disease
Definition:
It is a bacterial disease of animals which is characterized by pneumonia, high temperature,
depression, pericarditis and high mortality.
Etiology:
Pasteurlla multocida is the causative agent. It is gram negative, cocci short rod filamentous which
can be destroyed by heat and light.
Pasteurella multocida have been typed:
Carter’s type A - E and Robert’s type I - IV
Robert’s type on the base of mice (based on virulence)
Carter’s type on the base of capsular antigen
Susceptible Host:
Cattle and buffalo are more susceptible at 6 month to 2 years.
Sheep and goat are also susceptible.
Horse maybe susceptible.
Rats and guinea pigs are resistant.
Transmission:
It is contagious. Through inhalation and suckling of milk.
Pathogenesis:

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First of all pathogen enters into the body. And it remains in dormant form at the site of bronchial
and alveoli and they remain in inactive form and cannot perform infectiveness due to pulmonary
defensive system and when some predisposing factors like long transportation, malnutrition and
climate change occur. These pathogens become active and damage the parenchyma cells of the
lungs and leukocytes and macrophages. By destroying the macrophages, amines are released like
histamine, prostaglandin and fibrinoblastic. By prostaglandin the inflammation and pain will be
developed. Due to fibrinoblastic, fibrin accumulates in the lungs. Due to accumulation and
clotting of blood the lungs become consolidated. Due to consolidation of the lungs and
inflammation of the neck respiration will be disturbed. Due to the disturbance of respiratory
system oxygen level will deplete and then hypoxia can occur. Due to hypoxia animal can be
destroyed.
Clinical Signs:
High rise of temperature 104-107 °F with shivering. Profuse salivation, lacrimation, nasal
discharge, conjunctivitis, reduced milk production, lungs become inaudible due to consolidation,
localization of the edematous swelling in head, neck and brisket region, swelling area is hard and
painful. Due to swelling on the neck region respiratory passage is blocked and dyspnea will occur.
Sometime abdominal pain and diarrhea and death occurs within 24 hours if it is in acute form.
Postmortem Lesions:
Edema and thickening of interlobular septa in the lungs. Accumulation of fluid in thoracic cavity
and pericardial sac. Edema on the peri-laryngeal and peri-tracheal regions. Petechial
hemorrhages on the thoracic membrane.
Diagnosis:
History: predisposing factors Ask about vaccination and climate change
Clinical Signs:
Lab tests → appropriate media
Postmortem lesions
Differential Diagnosis
Anthrax, black leg, leptospirosis, bovine respiratory complex
Treatment:

• Sulphonamide @ 150 mg/kg of body weight

• Oxytetracycline @ 5-10 mg / kg of body weight
• Corticosteroid: Dexamethasone @ 20 mg / large animal
• Treatment should be continue for 1-3 days consecutive; without this pattern it is useless
Prevention and Control:

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• Adequate management
• Avoid long transportation
• Vaccination 1 – 2 month before monsoon season
• Vaccinate all the organisms including organized farms (control sheds)

Fowl Cholera

Synonyms: Pasteurellosis, Avian cholera, Avian hemorrhagic septicemia

Definition:
It is an infectious bacterial disease of domestic and wild birds which is characterized by
septicemia and sudden death in acute form. And diarrhea, mucus and nasal discharge and
anorexia in chronic form.
Etiology:
Pasteurella multocida is the causative agent. It is gram negative bacterium.
Susceptible Host:
Chicken, turkeys, ducks
Transmission:

• Through direct contact

• Through ingestion of contaminated feed and contaminated water
• Through biological vectors mice, flies and rodents
Pathogenesis:
First of all pathogen enters into the body then create localize infection. After this enters in blood
stream and cause septicemia, due to septicemic condition sudden death occurs
Clinical Signs:
Effected birds are depressed and listless and decreased appetite.
In acute form mortality will be high septicemia, combs and wattles are bluish and swollen.
In chronic form mortality will be low. Wattle and combs are also swollen.
Postmortem Lesions
Vascular changes in the body through hemorrhages like liver, ovaries will be swollen and necrosis.
In chronic form facial edema, torticollis and meningitis occurs.

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Diagnosis
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis
Infectious coryza, salmonellosis, colibacillosis
Treatment:

• Antisulphonamide sulpha drugs

• Kanamycin tetracyclin
Prevention and Control:

• Hygienic measures
• Appetite forms
• Depraved appetite.

Allotriophagia: A morbid impulse to eat unnatural foodstuffs; such as, ice, dirt, paint
(including flaking paint), clay etc.

Infectious Bursal Disease

Susceptible host is poultry. It is viral disease. Pathogen enters through ingestion → digestive
system and intestine → localize into lymphoid and cause infection and migrate to liver → blood
stream (viremia) and circulate in the body and there are two predilection sites: bursa of fabricius
and kidney. Bursa of fabricius gets inflamed and atrophied and becomes reddish and in kidney it
causes nephritis.
Synonyms: Gumboro disease
Definition
It is an infectious acute viral disease of poultry which is characterized by inflammation of bursa
of fabricius, nephritis, immunosuppression, urate stained feather around the vent and watery
white diarrhea.
Etiology:
Birnaviridae: Birnavirus
Its strains can be divided into classical and variant strains. It is very stable and difficult to eradicate
from the infected farms.
Susceptible Host:

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Chicken and turkeys are natural hosts.

Transmission
It is a contagious and transmission from bird to bird through utensils clothing fomites but there
is no evidence for vertical transmission.
Pathogenesis:
First of all pathogen enters through oral and infect intestinal lymphoid. After 8-12 hours reach
into the liver then into the blood stream and cause viremia. And then enter into bursa of fabricius
and spleen then further multiplication occurs and cause inflammation in bursa of fabricius, spleen
and kidney. Within 5 days it reach to high concentration. After 3 days of post infection you can
detect antibodies.
Clinical Signs:
Mostly this disease occurs within 3-8 weeks of age. Birds are listless, hurdling, pale, watery white
diarrhea, due to immunosuppression the secondary infection like respiratory. High FCR and low
weight gain.
Postmortem Lesions:
Bursa of fabricius is enlarged, gelatinous and bloody, muscle hemorrhages, kidneys are pale. If
the case is chronic then bursa of fabricius is smaller than normal.
Diagnosis:
History, clinical signs, Post mortem lesions and lab tests
Differential Diagnosis:
Sulphonamide poisoning, aflatoxins, vitamin E deficiency
Treatment:
Treatment for secondary infection.
Prevention and Control:

• Vaccination of breeder flock

• Isolate the infected birds from healthy birds

Infectious Coryza

Definition:

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It is a bacterial disease of poultry which is characterized by nasal discharge, sneezing and swelling
of the eyes and face.
Etiology:
It is caused by Avibacterium paragallinarum.
The old name of this bacterium is haemophilus paragallinarum.
It is gram negative.
There are three common serotypes: A, B, C
Susceptible Host:
Chicken is a natural host for this bacterium in any time.
Transmission:

• From bird to bird and from flock to flock → horizontal transmission

• Through air borne vectors and dust particles and droplets
• Through drinking water
• Through contaminated equipment
• Through any other contaminated manure
Pathogenesis:
First of all pathogen enters into the body and cause rhinitis and then pathogen enters into blood
stream and then circulate into body and cause the infection in different organs like lungs and
cause pneumonia liver hepatitis, intestine enteritis, diarrhea and fatty changes in the heart.
Clinical Signs:
Acute inflammation around the eyes and upper respiratory tract, facial edema and conjunctivitis,
serous mucoid discharge from the nasal cavity. Feed and water intake deplete, loss of weight and
loss of production. Day old chicks from the infected breeder quality wise decrease, Morality rate
varies but generally low. This disease makes the complicated and worse develop associate with
other disease like Mycoplasmosis, MG, MS disease, ND, ILT, IB, CRD.
Incubation period is 1-3 days.
Postmortem Lesions:
Conjunctivits, tracheitis, air saculitis and bronchitis
Diagnosis:
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis:

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Mycoplasmosis, chronic respiratory disease (CRD), ILT, IBD, ND, Avian Influenza (AI), swollen head
syndrome
Treatment:
Erythromycin and tetracycline can be used common at @ 10 mg/kg body weight
Prevention and Control:

• Sound management
• Isolation of the infected birds
• Replacement of infected birds from contaminated shed to disinfected shed
• Vaccination

There are several types of vaccines, including:

• Inactivated vaccines
• Live-attenuated vaccines
• Messenger RNA (mRNA) vaccines
• Subunit, recombinant, polysaccharide, and conjugate vaccines
• Toxoid vaccines
• Viral vector vaccines

Lymphoid Leucosis

In lymphoid leucosis, cancer develops and sarcoma of lymphoblast is formed. Neurons are not
affected/damaged in lymphoid leucosis. It is a viral disease caused by retrovirus; a bursal
dependent virus. It multiplies in bursa of fabricius and it changes genetic makeup of lymphoblast
and as a result neoplastic growth develops and enters into blood and spread to other body organs
and sarcoma and neoplastic growth develops in the kidney, intestine and ovaries and heart and
in all visceral organs cancerous lymphoid granules and nodules formation. Liver and kidneys are
affected at 14-18 week as it intensify. Incubation period is 7 days to 12 or 14 weeks.
Synonyms: Big liver disease, Visceral leucosis
Definition:
It is a viral disease of poultry which is characterized by diffuse or focal neoplastic growth of
lymphoblast in viscera, gradually growing. Mortality is low.
Etiology:

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Lymphoid leucosis is caused by retrovius. Pathogen gene enters into DNA of host cell and DNA
changes. Effected DNA will produce protein → neoplastic growth
Susceptible Host:
Chicken are more susceptible.
Transmission:
Through horizontal and vertical. Ovary is affected thus egg is affected.
Pathogenesis:
It is a bursal dependent viral disease. After entering, it multiplies in the bursa of fabricius, bone
marrow and connective tissue then produce neoplastic cells after 4-8 week of post infection.
These neoplastic cells migrate through blood stream and produce metastatic foci and tumors in
other parts of body like viscera and reproductive tract. And produce visceral leucosis and
lymphoid leucosis.
Clinical Signs:
Visceral tumors like liver, spleen, kidney and bursa generally at the time 25 week old. Effected
layers tend to low egg production. Effected birds are listless and pale.
Postmortem Lesions:
Hepatomegaly, enlarged bursa, neoplastic nodules on bursa, tumors on the mesentery and
abdominal, tumors in the bone, neural involvement never seen
Diagnosis:
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
Marek’s disease
Treatment:
No treatment
Prevention and Control:

• Elimination of virus from the breeder hen

• Testing and slaughtering
• Restrict virus spread to progeny

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In poultry two diseases Marek’s disease and lymphoid leucosis develop cancer and sarcoma
lymphoblast formation. There is a small difference between them. Neurons are not
affected/damaged in lymphoid leucosis.
Percussion: Percussion is a method of tapping body parts with fingers, hands, or small
instruments as part of a physical examination. It is done to determine: The size, consistency,
and borders of body organs. The presence or absence of fluid in body areas.

Marek’s Disease

Synonyms: Skin leucosis, Visceral leucosis, Paralysis, Neural lymphoma, Neurolymphomatosis

Definition:
It is a highly contagious viral disease of poultry which is characterized by tumor formation,
immunosuppression and neurologic disorders.
Etiology:
Alpha herpes virus.
Susceptible Host:
Chicken especially. But also quails, pheasants and turkey are also susceptible.
Transmission:
Horizontal transmission through indirect contact with infected premises. Mostly day old chick get
infection through respiration or inhalation from contamination of hatchery. Dander of infected
bird remain contaminated or remain carrier for 1 year.
Pathogenesis:
Virus enters into the non-lymphoid organs like lungs through inhalation. Then replication. After
replication lymphoid organs like thymus and bursa is effected and create cytolytic changes. Then
infected lymphocyte carries virus throughout body causing cell associated viremia and cause
cytolytic infection in feather follicles. Then proliferate whole body and cause cytolytic changes in
other visceral organs.
Clinical Signs:
Weight loss, paralysis, nerve involvement cause the death of the bird with showing one leg
forward and other leg backward (splayed leg posture), depression, mortality at age of 10-20
weeks old age. Mostly 50 % mortality in non-vaccinated farm or birds. If the eye involve then
irregular constriction, iris involvement due to ocular lymphomatosis.

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Postmortem Lesions:
Presence of tumors in whole visceral organs like spleen, kidney, lungs, skin, ovary and muscles. If
skin is involved tumors are seen in the feather follicles or in between follicles. If gizzard nerve is
involved then size of gizzard and intestine becomes small.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests.
Differential Diagnosis:
Lymphoid leucosis, ND and avian encephalomyelitis.
Prevention and Control:

• Good sanitary and hygienic measure for prevention from infection to early age chicks.
• Avoid farming with multiple age chicks.
• Vaccination → In ovo-injection at 18 day and day old chick

Aspergillosis

Synonyms: Brooder pneumonia, Fungal pneumonia, Mycotic pneumonia, Pneumomycosis

Definition:
It is a fungal disease of birds characterized by granulomatous lesions on lungs and skin.
Etiology:
Aspergillus fumigatus
Susceptible Host:
Young birds are more susceptible than older. Turkey, pheasants, quail and ducks are more
susceptible.
Transmission:
Through inhalation, fungus spores from contaminated environment, litter, contaminated feed
and contaminated hatchery.
Pathogenesis:
First of all fungal spores enter through inhalation. Then enter into upper respiratory tract. The
defensive system of upper respiratory tract tries to destroy these spores. If defensive system fails
then these spores enter into lower respiratory tract. Then alveolar defensive system activate and

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try to remove these spores. If these macrophages fail to destroy then spores become localized
germinate and form colonies. These colonies show as a granules on lungs and air sacs. When
these spores enter into blood stream and spread to other parts form localized infection like
granules on skin.
Clinical Signs:
Infected chicken are depressed, gasping, rapid breathing, dyspnea, inappetence, emaciation.
Mortality is 5-50 %.
Postmortem Lesions:
Primarily lungs and air sacs are effected. Yellow white pin head size lesions can be found on air
sacs. Sometimes all body cavities are filled with small yellow green granular fungal growth. Cream
color plague may be seen in ear passage.
Diagnosis:
History → Ask about litter and farm condition and see if this is brooding time
Clinical signs, postmortem lesions, lab tests
Differential Diagnosis:
IB, ND, ILT, dictylaria infection
Treatment:
Antifungals: Itraconzole or fluconazole or ketoconazole @ 10mg/kg of BW orally
Prevention and Control:

• Remove and destroy effected birds

• Strict hygienic conditions in breeder farm and hatchery
• Quality of litter should be fine
• Hatchery and breeder farm should be disinfected by anti-fungal
• Before commencing chicks fumigate the farm properly

Avian Influenza

Synonyms: Bird flu, Fowl plague

Definition:
It is a viral disease of poultry which is characterized by respiratory signs, depression, reduced
water and feed intake and reduced egg production

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Etiology:
Orthomyxovirus
On the base of pathogenicity strains are classified into HPAI (highly pathogenic avian influenza)
and LPAI (low pathogenic avian influenza). Currently there are some serotypes from H1-H16
(hemagglutinin) and N1-N9 (neuraminidase)
Susceptible Host:
Wild and domestic birds like chicken, turkey and ducks are more prone than other birds
Transmission:
Through aerosol route, direct and indirect contact with equipment. Through contaminated water
and feed. Through biological vectors
Pathogenesis:
First of all virus enters into the body and bind with sugar at epithelial cells of respiratory tract
and GIT. Then multiplication occurs and cause infection. Due to this infection general signs
appear like fever, respiratory problems, lethargy and depression.
Clinical Signs:
Clinical signs depend on the virulence of the strains like HPAI and LPAI and other risk factors.
According to LPAI mild to general signs appear like coughing, sneezing, wet eyes, nasal discharge,
depression, limited reduction of feed and water intake. Limited drop in egg production and low
mortality. According to HPAI increased mortality, bruising, depression, drop in egg production,
drop in feed and water intake. High mortality from 50-90 %.
Postmortem Lesions:
Hemorrhages and necrosis in GIT, respiratory tract and urogenital system.
Diagnosis:
History, clinical signs, lab tests and postmortem lesions
Differential Diagnosis:
Fowl cholera, ND and other respiratory diseases
Treatment:
No treatment. But antibiotics can be used as a secondary treatment.
Prevention and Control:

• Vaccination

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• Control of biological vectors

• Strict hygienic measures

Most of the influenza viruses circulating in birds are not zoonotic. However, some HPAI strains
have the ability to infect humans, posing a threat to public health. The main risk factor is the
direct or indirect exposure to infected animals or environments and surfaces contaminated
by feces.

Infectious Bronchitis

Definition:
It is an acute highly contagious viral disease of poultry which is characterized by respiratory signs
like gasping, coughing, sneezing, tracheal rales and nasal discharge.
Etiology:
Coronavirus
Several serotypes like Massachusetts contained different variants like IB4/91, QX, Arkansas,
Connectieut.
Susceptible Host:
Chicken is primary host. Quails and pheasants can also be affected.
Transmission:
Through contact from bird to bird through aerosol.
Pathogenesis:
First of all virus enter into the body, attach with glycoprotein receptors on respiratory epithelium.
Then replicate and cause infection. Due to this infection, loss of ciliary activity mucus
accumulation, necrosis, desquamation which cause respiratory distress, rawls and asphyxia. If
this virus enter into blood stream cause viremia and transfer to other parts of body mainly kidney
and reproductive system. In kidney it cause infection in the kidney epithelium, nephron tubules
cause kidney failure. Kidney become swollen, pale and ureter contains urates. In reproductive
system oviduct become infected which will lead to the sharp decline of egg production, shell less
eggs, fragile ruffled shell egg. If the lesion persists in oviduct for long time in age of puberty the
cyst can be developed in the oviduct and magnum gland can be affected. Due to the oviduct cyst,
the female bird becomes false layer.

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Clinical Signs:
In young chicken there are two forms: respiratory from and nephropathogenic form. In
respiratory form signs are gasping, sneezing, tracheal rales, nasal discharge, depression and
decreased feed consumption. Mortality is low. In nephropathogenic form initially there are
respiratory signs, depression, wet droppings, wet litter, increased water intake and increased
mortality. In adult laying birds mainly layer and breeder initially there are respiratory signs, drop
in egg production, loss in egg quality and false layer.
Incubation period is 1-3 days.
Postmortem Lesions:
In young chicks, yellow cheesy plugs in tracheal bifurcation. In case of nephropathogenic
infection pale and swollen kidney. Distended ureter with urates. In adult birds mucus and redness
of trachea and exudate in air sacs. There are various changes in oviduct. In false layer permanent
lesions in oviduct. Oviduct may block due to cyst.
Rudimentary oviduct is the one which is not completely developed.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
CRD, ND, IC and ILT
Treatment:
No treatment. Use of antibiotics as secondary treatment.
Prevention and Control:

• Isolate the infected animals

• Good sanitary and hygienic measures at farm
• Vaccination

Chronic Respiratory Disease

Definition:
It is a contagious disease of poultry which is characterized by persistent hacking cough, sneezing
and tracheal rales.
Etiology:

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Mycoplasam gallisepticum (MG+).

This condition is frequently triggered by other respiratory viruses ND, IB and subsequently by
other bacterial invasion and complex forms.
Susceptible Host:
Chicken and turkey are naturally susceptible. Pheasants, ducks and quails are occasionally.
Pigeon, peafowl, parrot infrequently.
Transmission:
There are two types of transmission: (1) Vertical through eggs. (2) Horizontally through bird to
bird, direct contact, indirect contact and air droplets.
Pathogenesis:
First of all pathogen enters. Initially there is no signs and ineffectiveness. But due to predisposing
factors like overcrowding, malnutrition, bad nutrition, bad hygiene, bad sanitation and infection
occurs. Mostly associated with other viral disease like ND, IB which form complication and infect/
inflamed entire respiratory system. Then infects other parts of body like pericardium, liver and
peritoneal cavity.
Clinical Signs:
Generally broiler and layer breeder show respiratory signs. Respiratory distress. Lack of appetite.
Drop in body weight, drop in egg production, increase FCR, sneezing and coughing, razor keel
bone. Ataxia and lameness accompanied by hock joint inflammation.
Incubation period is 4 days to 3 weeks.
Postmortem Lesions:
Reddish inflamed trachea. Frothy cheesy exudate in air sacs specially when complicated with
E.coli. Pericarditis, peritonitis and perihepatitis (layer of liver inflamed). In mild cases, slight
mucous in trachea and cloudy light froth in air sacs.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests.
Differential Diagnosis:
ND, IB, ILT and AI.
Treatment:

• Antibiotics: Tylosin tartarate @ 1g/liter.

• Lincomycin @ 1g/liter orally.

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Prevention and Control:

• Strict monitoring.
• Culling the infected bird.
• Seggregation
• Vaccination
• Good hygiene and sanitary measures.

Hydropericardium Syndrome

Synonyms: Litches diseases, Angara (1997, origin and mutation in Pakistan)

Definition:
It is a highly contagious viral disease of poultry characterized by sudden onset. Water
accumulation in pericardium and high mortality ranging from 20-70 %. Mostly occur in broiler at
age of 3-6 week.
Etiology:
Avian Adenovirus
Mostly occur with combination of other immunosuppressive disease like chick anemia virus
infectious bursal disease.
Susceptible Host:
Chicken, turkey, pheasants and other birds
Transmission:

• Vertical transmission through eggs

• Through horizontal from bird to bird
• Through direct contact through indirect contact
• Through contamination drop feces water, feeding, thorough vertical, through eggs the
bird immune virus cannot be detected from bird
Pathogenesis:
Virus enters into body through drinking or ingestion feeding in the intestine then go to heart and
infect the heart layer endothelia layer of heat heart layer dilate and increase permeability due to
increase the permeability of membrane the water contents ooze out from the capillaries or
vascular system to outside in the pericardial sac fluid accumulate in the pericardial sac due to
accumulation of water cannot contract proper the bird may be destroyed.

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Clinical Signs:
Depressed, lethargy, weight loss, hurdling with ruffled feather, yellow mucoid feathers, sudden
increase in mortality
Postmortem Lesions:
Hydropericardium yellow gelatinous type shining glistening fluid in the heart, excessive straw
color fluid distending the pericardium, enlarged pale, friable liver and kidney, congestion of
carcass, lungs edematous, Heart and liver disease these ascites and edema correlation, osmotic
pressure vessels dilate content of water ooze out
Diagnosis:
History → breeder hatchery, contagious (near flock)
Clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
Ascites, inclusion body hepatitis, nephritis, liver and heart diseases
Treatment:

• No treatment Liver tonic (Jetepar immune booster, Hepamerz)

• Prevention and control
• Avoid multistage farming
• Control predisposing factors
• Good sanitary hygenenic mesures by 0.1 – 2.5 % iodophore solution
• Vaccination (Formalin inactivated oil adjuvant)

Infectious Laryngeotracheitis

Definition:
It is a viral infection of poultry characterized by catarrhal hemorrhages and fibrinous
inflammation of respiratory epithelium/tract.
Etiology:
Herpes virus
Transmission:
Through inhalation. Through direct and indirect contact.

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Susceptible Host:
Chicken is primary host of this diseases. Pheasants are also affected.
Pathogenesis:
First of all virus enters into the body and respiratory system through inhalation. Then virus infect
epithelial cells and replicate. And then epithelial cells break down or killed and cause
inflammation. By inflammation and fibrinous exudate lumen becomes narrow and bird feel
difficulty in respiration.
Clinical Signs:
Nasal discharge, moist rales followed by gasping and marked respiratory distress. Expectoration
of blood stained mucous. Drop in egg production. Mortality rate is 5-70 % and incubation period
is 4-12 days. All these manifestation included by these two forms: (1) Laryngeotracheal form and
(2) Conjunctival form
Laryngeotracheal form: Suffocation, rales, cough. Bird head and neck are strongly extended
forward and upward during respiration.
Conjunctival form: Drop in egg production, ocular discharge from anterior canthus of eye.
Postmortem Lesions:
Lesions are found throughout respiratory tract. Most prominent on larynx and trachea.
Hemorrhages and congestion on trachea.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests.
Differential Diagnosis:
IB, ND, Influenza and CRD
Treatment:
No treatment.
Prevention and Control:

• Isolation of infected birds.

• Good sanitary measures.
• Daily wash equipment and utensils.
• Vaccination properly.

Femoral Head Necrosis

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Synonyms: Malabsorption syndrome, Runting stunting syndrome, Helicopter disease, Brittle

bone disease, Infectious proventriculitis, Pale bird syndrome
Definition:
It is characterized by enteritis with watery brown and foamy contents, undigested food particles
in intestine, mucosal and submucosal proventriculus lesions. Degenerative changes in pancreas,
osteoporosis, osteomyelitis and epiphysis of femur is usually soft.
Etiology:
This disease is developed due to complex of virus and bacteria like E.coli, streptococcus,
staphylococcus and enteric reovirus. Other predisposing factors are IBD, chick viremia which
affect digestive system of bird and create nutritional deficiency.
Susceptible Host:
Chicken and Turkey.
Transmission:
Horizontal and vertical.
Clinical Signs:
Mainly this disease is observed in broiler flock. Poor performance, increase FCR, retarded growth
with uneven flock, diarrhea, dropping with undigested food particles. Effected birds exhibit
malposition feather especially on wings, encephalomalacia, delayed growth and morality low
about 4 %.
Postmortem Lesions:
Enteritis (flappy, inflamed, blood, liquid) with watery brown foamy contents. Mucosal and
submucosal proventriculus lesions. Osteoporosis, osteomyelitis, epiphysis of femur usually soft.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests.
Treatment:
No treatment. But it can be treated according to signs and symptoms. Antibiotics, flushers and
appetized can be used.
Control and Prevention:

• Vaccination against reovirus in breeder farm.

• Strict hygienic and sanitary measures are helpful for reducing intensity of this disease.

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Avian Encephalomyelitis

Definition:
It is a viral disease of poultry which is characterized by variety of neurological signs like
incoordination, ataxia and tremor of head and neck.
Etiology:
Enterovirus belonging to Picornaviridae family.
Susceptible Host:
Chicken are susceptible. Turkey, pheasants are also susceptible.
Transmission:
Vertical transmission is major route of this disease.
Clinical Signs:
Tremors, drop in production and hatchability. In layer it can recover in 1-3 week. Mostly this
disease occurs in 1-3 week old age. Young favorable. Effected birds sit on hock joints and cannot
move.
Incubation period is 5-14 days.
Postmortem Lesions:
Lymphoid follicles in muscular tissue of gizzard, proventriculus, myocardium and pancreas.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests.
Differential Diagnosis:
Vitamin E deficiency (encephalomalacia/crazy chicken disease), vitamin B deficiency, ND,
encephalitis due to other bacteria and fungi and Marek’s disease.
Treatment:

• No treatment.
Prevention and Control:

• Vaccination of breeder and layer pullet.

• Breeder vaccination.

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Serotypes: Serotypes are groups within a single species of microorganisms, such as bacteria
or viruses, which share distinctive surface structures.
Phenotype and Genotype: The genotype is a set of genes in the DNA which are responsible
for the unique trait or characteristics. Whereas the phenotype is the physical appearance or
characteristic of the organism.

Actinobacillosis

Synonyms: Wooden tongue

Definition:
It is a chronic infectious disease of ruminants which is characterized by inflammation of soft tissue
especially tongue and less commonly pharyngeal lymph nodes, nares, esophagus and cheek
muscles.
It is a sporadic and self-limiting disease.
Etiology:
Actinobacillosis ligneresei. It is gram negative coccobacillus, pleomorphic, non-hemolytic on
blood agar and grows on blood agar.
Susceptible Host:
Cattle are more susceptible. Sheep is also susceptible. Horses are rarely susceptible.
Transmission:
Source of infection is pus, contaminated feed, laceration, abrasion or injury in mouth or buccal
cavity.
Pathogenesis:
First of all pathogen enter through the contaminated feed. After entrance, pathogen infect the
soft tissue by the abrasion, laceration or any injury and cause inflammation of soft tissue
especially tongue which become necrotic, suppurative and fibrotic. Tongue convert into hardness
which is called wooden tongue. Due to suppuration pus comes out which infect other soft tissues
like cheek, pharyngeal lymph nodes, external nares and face Due to these condition the animal
loss prehension, mastication and deglutition.
Clinical Signs:

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Incubation period is unknown. Morbidity and mortality is low. Course of the disease is very long.
Effected animal is unable to eat feed. By palpation, tongue feel like hard and inflamed or swollen.
Nodules on tongue can be palpated and felt. In later stages the inflammation becomes fibrotic,
tongue becomes shrink and immobile. In cutaneous form, granulomas occur on external nares,
cheeks, external face and sometimes on hind legs.
Postmortem Lesions:
Nodules, granulomas and granules on tongue and other soft tissues.
Diagnosis:
History, clinical signs, lab tests and postmortem lesions
Differential Diagnosis:
Actinomycosis, TB, abscess and tetanus
Treatment:

• KI2 @ 7-10 g/day orally. This treatment is continued until the iodism will be developed.
Lacrimation, coughing, anorexia and dandruff indicates maximum level of iodine has been
reached.
• Sodium iodide @ 1g/12kg of BW IV if soft tissue is involved. If bony tissue is involved then
recommend further two doses about 10-15 days interval.
• Sulphonamide, streptomycin or any other broad spectrum antibiotic @ 5g/day
Prevention and Control:

• Prevent pus to contaminate utensil by disinfection.

• Segregate the infected animals.
• Avoid spoiled or contaminated feed.
• Dressing the wound or injury properly.
• Try to minimize the predisposing factors as early as possible.

Pullet: A young hen, especially one less than one year old.
Benign and Malignant: A benign tumor has distinct, smooth, regular borders. A malignant
tumor has irregular borders and grows faster than a benign tumor. A malignant tumor can
also spread to other parts of your body. A benign tumor can become quite large, but it will
not invade nearby tissue or spread to other parts of your body.

Actinomycosis

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Synonyms: Lumpy jaw

Definition:
A chronic inflammatory debilitating disease of animals which is characterized by periostitis,
formation and bony cavities filled with pus particularly in mandible and maxilla.
Etiology:
Actinomycosis bovis
This bacteria is normally inhabitant in gums, oral cavity and GIT. It is coccoid, rod, branched
filamentous organism grows in blood agar. It is catalase negative bacteria.
Susceptible host:
Cattle is highly susceptible. Horses occasionally and goat are rarely susceptible.
Transmission:
Through pus which is transmitted by ingestion. Normally pathogen occur in gums, oral cavity and
GIT. Transmit via wound, abrasion or injury. It is mostly anaerobic.
Pathogenesis:
Entry is via ingestion of contaminated feed or present in gums normally due to predisposing
factors e.g. injury, wound which develop by foreign particle or object. Pathogen causes
inflammation of hard tissues e.g. mandible, maxilla and produce abscess/perostitis with honey
like pus. When abscess in increased and by rupturing the skin pus comes out and aspire. By
aspiration other organs e.g. esophagus, lungs, trachea, reticulum are also affected by developing
abscess. By inflammation of these organs other signs like bloat, diarrhea and dyspnea also
develop.
Clinical Signs:
Incubation period is unknown. Morbidity and mortality rates are low. Disease course is very long.
Bony inflammation is painful. Mastication and rumination disturb or stop e.g. reluctant to
masticate. Swelling is very hard, immovable when abscess enlarge, break the skin and pus comes
out which contain granules. Pus color is honey like, sticky in nature, impaired digestion, chronic
bloat sometimes diarrhea, undigested feed and particles in feces.
Postmortem Lesions:
Granulomatous lesions having pockets and pus in esophageal groove, lower esophagus, anterior
wall of reticulum and periostitis.
Diagnosis:

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History → See if there is no mastication, rumination, prehension and if there is glossitis and
gingivitis
Clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
Abscess of cheeks, muscles and throat, bony neoplasm, indigestion
Treatment:

• Debridement and dressing of effected area

• Streptomycin @ 20 mg/kg and penicillin @ 2000 IU for one month.
• Iodide e.g. NaI2 @ 7-10g/liter/animal daily
Prevention and Control:

• Isolation and segregation of effected animals.

• Dispose of carcass properly.
• Dressing of oral injury i.e. somogel
• Minimize the predisposing factors
• Isolate the animal from healthy animals
• Prevent pus to contaminate things.

Bovine Ephemeral Fever

Synonyms: Three day sickness, Three day stiff sickness, Bovine epizootic fever, Dragon boat
disease
Definition:
It is a noncontagious arthropod borne viral disease of cattle, buffalo which is characterized by
sudden onset of fever, depression, sickness, lameness and rapid recovery.
Etiology:
Family Rhabdoviridae
Genus: Bovine ephemeral fever
Rhabdo virus
Susceptible Host:
Cattle and buffalo

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Transmission:
Spread through biological vectors like insects and mosquitoes i.e. cullicodes there is no
documented report through direct contact.
Pathogenesis:
First of all virus enters through biological vector then enter into blood stream and cause viremia
and then multiplication which cause fever, inflammation vasculitis. And then localize in the
mesodermal tissue, especially in joints, lymph and muscle and cause dyspnea, lameness, arthritis,
and stiffness. During this condition, hypocalcemia also occurs which can be differentiated from
milk fever through some points like this condition occur in both male and female but in female
milk fever; it occurs preparturient.
Incubation period is 2-10 hours.
Clinical Signs:
Depressed, Biphasic fever 105-107 ℉. Serous ocular and nasal discharge anorexia, decreased milk
production, muscle stiffness, dragging of feet during walk. Animal can lie down during 3 days.
Morbidity is about 30 while mortality is very low. If death occur, it might be due other
complications like pneumonia, secondary infection. Muscle damage and pregnancy toxemia.
Postmortem Lesions:
Small amount of fibrin rich fluid in pleura, peritoneal, pericardial cavities and joint capsule. Lungs
may have patchy edema. Lung edema due to vasculitis epithelia pores widens and lymph adenitis
and necrosis of muscles.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
BT, milk fever, black leg and babesiosis
Treatment:

• Recovery with no treatment it is auto recover

• Broad spectrum antibiotics:
• Tetracycline @ 10-15 mg/kg
• Analgesic antipyretic antibiotic flunixin meglumine 2.2 mg/kg or
• NSAID Ketobrufen @ 3mg/kg
• Fluid therapy + Ca infusion
Prevention and Control:

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• Good sanitary measures

• Fly repellents
• Vaccine if available

Trypanosomiasis

Synonyms: Surra
Definition:
It is a protozoan disease of equine family which is characterized by fever, inflammation of lymph
nodes and brain spinal cord which lead to lethargic condition and death.
Etiology:
Trypanosoma evansi
Susceptible Host:
Horses, donkeys, mule camel, cattle, sheep, goat at also susceptible
Transmission:
Tsetse fly tabanus stomoxes
Biological vectors hematopota fly
Life Cycle and Pathogenesis:
First of all fly inject metacyclic trypanomestigote enter into blood stream and convert into blood
stream trypanomestigote which multiple by binary fission into blood fluid like blood, spinal fluid
or lymph. Trypanomestigote in blood can be ingested by tsetse fly goes into midgut and transfer
into procyclic trypanomestigotes. Leave midgut and transfer into epimestigote. Epimestigote
enter into salivary gland and multiply by fission and transfer into metacyclic trypanomestigote.
Then it is ready to infect other animals.
Clinical Signs:
Loss of appetite, weight loss, edematous swelling of lower art of abdomen, bilateral enlargement
of pre-scapular lymph nodes, intermittent fever, corneal opacity, excessive salivation,
lacrimation, anemia improper gait excessive salivation, lacrimation, anemia, ataxia, circling
movement due to nervous system problem. Abortion due to heavy parasitism.
Postmortem Lesions:
No postmortem lesions can be recognized.

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See anemic carcass, emaciated carcass, anasarca, enlargement of lymph nodes, liver spleen and
corneal opacity.
Diagnosis:
History (Ask about fly population)
Clinical Signs, postmortem lesions and lab tests (PCR or staining)
Differrential Diagnosis:
Anasplasmosis, babesiosis, malnutrition, helminthosis and hemorrhagic septicemia
Treatment:

• Quinapyramine sulphate @ 3-5mg/kg S/C or

• Diminazine aceturate @ 3-5 mg/kg IM
• Dermal skin underskin in fascia we inject and subcut difference
• Routes of drug administration
Prevention and Control:

• Good husbandry measures

• Fly repellents
• Prophylactic measures antiprotozoan
• Prevail resistant breeds

Difference between Surra and Dourine: Dourine is a venereal disease.

Babesiosis

Synonyms: Piroplasmosis, Tick fever, Red water disease, Taxes fever

Definition:
It is a febrile tick borne disease of cattle characterized by extensive erythrocyte lysis which leads
to anorexia, icterus, hemoglobinuria and death.
Etiology:
Babesia bigemina, Babesia bovis, Genus of this agent is Babesia bigemina, babesia bovis genus of
this agent is babesia order piroplasma, phylum epicomplexa
Susceptible Host
Mostly cattles are most infested other ungulates are also affected dog is also susceptible.

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Transmission:
Through biological vectors like ticks boophilus annulatus and boophlius microplus
Life Cycle and Pathogenesis:
First of all protozoa enter into the body through inoculation by infected ticks like Boophilus which
form sporozoites. Sporozoites enter into the RBCs convert into tropozoites then tropozoites
enlarge and multiply in RBCs then become merozoites which is an infective stage of this
protozoan and infect and other RBC then new ticks take them during feeding theses merozoites
sexually multiply into gametes. These gametes fuse in salivary gland and ovary of the tick and
become into zygote. These zygotes which occur in the salivary gland inoculate or transmit other
host during feeding. The other zygote which are in ovary, transfer into new adult at nymph which
can also infect other new animals without prior infestation. During life cycle main pathogenicity
develop in the body like anemia, destruction of RBCs, pale mucosa, decrease erythrocyte,
hemoglobinuria and lack of oxygen.
Clinical Signs:
Dysbolism (abnormal metabolism), Ardent fever (severe), fever about 40-42 °C, TPR increases,
ruminal stasis, emaciation, jaundice, hemoglobinuria, decreased production and sometimes
abortion
Incubation period 10 – 14 days.
Postmortem Lesions:
Anemic carcass, pale mucosa, hemoglobinuria brownish urine in bladder hepatomegaly,
splenomegaly
Diagnosis:
History, clinical signs, postmortem lesions and lab tests (blood smear – giemsa stain seen within
RBCs)
Differential Diagnosis:
Bacillary hemoglobinuria, postparturient hemoglobinuria (phosphorus deficiency), anaplasmosis,
Trypanosomiasis, theleriosis, leptospirosis and poisoning
Treatment:

• Antiprotozoan inj. Diminazine @ 3-5 mg/kg IM

• Imidocarb @ 1-2 mg/kg SC
• Blood transfusion (risky no cross math) as supportive therapy
Prevention and Control:

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• Tick control by fumes because of its reservoir a lot fly repellents difficult to eradicate
• Proper sanitation
• Use of lime
• Vaccination

Compare babesiosis with postparturient hemoglobinuria and bacillary hemoglobinuria. In

Postparturient hemoglobinuria there is deficiency of phosphorus. In bacilliary
hemoglobinuria there is fever and red urine.

Theleriosis

Synonyms: East coast fever, Red water, Tick fever

Definition:
It is an acute disease of animal which is characterized by fever, swelling of lymph nodes, dyspnea
and death
Etiology:
Theileria parva, Theileria annulata and Theileria mutans
Theileria anulata is extensively distributed. The family of Theileria is Theileridae, order
Piroplasmida and genus Theileria
Susceptible Host:
Cattle are more susceptible than other animals.
Transmission:
Through biological vectors like Riphicephalus appendiculatus, Hyalomma ticks which inject the
protozoan into the body. The tick population mostly enhance in rainy season due to humid
climate. This season is more prone than other. This disease is also transmitted by mechanical
vectors like blood and other secretions like liver, spleen and lymph nodes.
Life Cycle and Pathogenesis:
First of all tick bites and inoculate the sporozite form of protozoan into the body which infect
lymphocytes and convert into tropozoites. By asexual multiplication shizonts may develop. Then
transfer into merozoites. It is infective stage and in this stage it is also called as piroplasma
because it can infect red blood cells. These engulf or feed by ticks which convert in gametocytes

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in salivary glands of ticks. These gametes fertilize into zygote which is also called kinete. Then this
kinete transfer into sporozoites. This is the infective stage for the host lymphocytes. Infection of
red blood cells is important for transmission. Infection of lymphocytes is important for pathology.
Clinical Signs:
Fever 40-41 ℃, enlargement of regional lymph nodes, restlessness, rough coat, anorexia, watery
lacrimation, corneal opacity, labored respiration, serous nasal discharge, depression, and
petechial hemorrhages on conjunctive (pathognomonic sign), anemia, urticarial type lesion on
skin, weakness, neurological disorders which is also called ‘Turning sickness’ and death with 8-30
days.
Diagnosis:
History, clinical signs, lab tests and postmortem lesions
Differentia Diagnosis:
Trypanosomiasis, anaplasmosis, babesiosis, MCF, BVD and RP
Treatment:

• Buparvaqon @ dose of 2-5 mg/kg IM

• Broad spectrum antibiotic such as oxytetracyclin
Prevention and Control:

• Use of ectoparasite killer

• Vaccination
• Prevail resistant animals
• Use of fly repellent and cypermethrin spray.
• Tick control program

Anaplasmosis

Synonyms: Gall sickness

Definition:
It is a rickettsial disease of ruminant which is characterized by pyrexia, anemia and emaciation.
Etiology:
Anaplasma marginalae and Anaplasma centralae

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It is obligate intracellular pathogen. Anaplasma centralae causes mild infestation in cattle.

Anaplasma ovis affects sheep which is mostly in sub-clinical form.
Susceptible Host:
Cattle, sheep, goat and buffalo
Transmission:
Through ticks like Ixodes (Ixodidae) flies like Tabanus and Stomoxys and mosquitoes. Through
iatrogenic route. Through transplacental.
Life Cycle:
First of all ticks bite and inject anaplasma into the host body which infect the red blood cells.
These infested red blood cells engulf or feed by another ticks then enter into the midgut and then
replicate. After midgut enter into salivary gland. After this tick is ready for injecting the other
animals. During this life cycle pathogenesis will be developed like red blood cells infestation, lysis
and phagocytosis by reticulo-endothelial system which cause anemia. During this inflammatory
reaction and fever also develop.
Clinical Signs:
Anemia, fever, weight loss, difficult breathing, uncoordinated movement, ataxia, abortion and
death
Diagnosis:
History → See for ticks and flies population and rainy season
Clinical signs and lab tests
Differential Diagnosis:
Babesia, theleria and leptospirosis
Treatment:

• Tetracycline or oxytetracycline @ dose of 10-15 mg/kg IM

• Animal once infested becomes carrier for lifetime if it is treated. Not 100 % recovery
occurs.
• Imidocarb hydrochloride @ dose of 5 mg/kg IM
• Estradiol cypionate @ dose of 14.3 mg/kg IM. It improves recovery by increasing
parasitemia during treatment.
Prevention and Control:

• Minimize transmission route/agents like ticks and flies by using fly repellents.

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• Strict hygienic measures for the control of insect population through acaricides and sparys
such as cypermethrin spray.
• Carrier animals should be isolated and disposed of.
• Screening test should be made at every farm for isolation of carrier animals.

Equine Influenza

Synonyms: Equine distemper, Typhoid fever, Pink eye, Influenza catarrh

Definition:
It is a highly contagious viral disease of equine which is characterized by general septicemia and
respiratory problems accompanied by severe persistent dry cough.
Etiology:
Strain/species influenza virus A Genus influenza virus and orthomyxoviridae family.
Susceptible Host:
Equines like horses, donkeys, mules and zebra. Young animals are more susceptible than adults.
Transmission:

• Through direct contact.

• Through inhalation.
• Through physical transmission by humans, equipment and fomites.
Pathogenesis:
First of all virus enter into the body then haemagglutinin glycoprotein spike attack with the
respiratory epithelium. Then virus enters into the cells through endocytosis. After endocytosis
virus replicate and multiply in the cell which cause breakdown of the cells. After breakdown of
cells, virus release into the periphery and infect the surrounding epithelial cells. By infection these
cells become necrosed and the desquamation occurs. Then protein rich fluid secrets in the
airways which clump the cilia. Due to clumping the cells drain out fluid and it stop and accumulate
which acts as predispose for the secondary infection. Due to secondary infections the complex
will be developed and animal will suffer from persistent dry cough.
Clinical Signs:
Deep dry hacking cough, labored breathing, nasal discharge which is initially watery than thick
cloudy. Sudden increase of temperature, depression, loss of appetite (anorexia), muscular pain
and stiffness.

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Postmortem Lesions:
Destruction of bronchial and tracheal epithelium and cilia destruction.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis:
Strangles, equine viral arteritis, equine viral pneumonia, equine adenovirus and equine
rhinovirus.
Treatment:
No treatment. Secondary treatment like antibiotics.
Prevention and Control:

• Good sanitary measures.

• Good ventilation.
• Quarantine measures should be adopted before entering new animals.
• Screening tests must be applied before purchasing the animals.
• Complete rest about 3-4 weeks.
• Accessories of stall/stud form should be cleaned timely.
• Vaccination.

Equine Viral Arteritis

Definition:
It is a global infectious disease of equine family which is characterized by pan vasculitis which
include edema, hemorrhages, pink or red conjunctivitis, enteritis and abortion in pregnant mare.
Etiology:
Arteribrius virus of Arteriviridae family (Togaviridae)
Susceptible Host:
All equine family like horses, donkey, zebra, mules and pony.
Transmission:

• Through venereal from infected mare to stallion or vice versa.

• Through inhalation.

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• Through fomites mechanical or physical.

Pathogenesis:
First of all virus enter through any transmission route like inhalation. Enter into respiratory
system binds with respiratory epithelium. Then infect pulmonary macrophages and inflamed
bronchial lymph nodes. Then enter into blood stream cause viremia. During this stage virus can
be detected in monocytes. In blood vessels virus damage endothelium necrosed and inflamed.
By damaging endothelial layers of vessels in different predilection sites like renal portal vessel
(artery), conjunctiva and reproductive system. In reproductive system cause necrotizing
myometritis, low level of blood flow in fetus. After the infection 28 days virus cannot be detected
in whole body except sex tissues. By the presence of virus in sex organs animal acts as carrier and
can transmit the disease to other animals through venereal transmission.
Clinical Signs:
Pneumonia, enteritis, depression, anorexia, edematous, swelling, serous ocular and nasal
discharge abortion and still birth in pregnant animals, decreased fertility of male animals,
decreased sperm quality due to increased scrotal temperature and edema and decrease libido.
Postmortem Lesions:
Edema, edematous swelling in body cavities, lungs, pneumonia, enteritis, endometrial
hemorrhages, fetus autolyzed partially
Diagnosis:
History, clinical signs, lab tests, postmortem lesions (virus isolation, PCR, antigen detection
VNT, CFT, ELISA)
Differential Diagnosis:
Equine Influenza, Purpura hemorragica, Equine infectious anemia, African horse sickness, Equine
adenovirus and equine herpes virus
Treatment:
No treatment.
Prevention and Control:

• Stop venereal transmission by management

• Separate pregnant mare from other horses
• Breed carrier stallion only to well vaccinated mare (seropositive) male precious
• Vaccination
• Carrier animals or stallion should be isolated
• Clean and disinfect the fomites

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• Screening tests must be applied for isolation or entering the new animals.

Equine Infectious Anemia

Synonyms: Swamp fever, Coggin’s disease

Definition:
It is a viral disease of equine family which is characterized by anemia, intermittent fever, weight
loss and anemia. It is also called swamp fever due to requirement of swampy or moist
environment.
Etiology:
It is caused by retrovirus (lentivirus). This virus is closely related to HIV.
Susceptible Host:
Equine family is more susceptible for this disease. Some animals show clinical signs like horses
and mules. Some animal are asymptomatic or carrier like donkey.
Transmission:
Through insect bite. Like bot fly, stable fly, deer fly. Through mechanical and iatrogenic through
knives, syringes and surgical instruments. Through blood transfusion.
Pathogenesis:
First of all virus enter into the body through biting fly during feeding. After entrance virus infect
the tissue macrophages especially spleen. Then cause viremia and destruct macrophages then
release viruses and other components. By the production of antibodies, antigen-antibody
complex will be developed which induce fever, anemia, thrombocytopenia, glomerulitis,
nephritis and hemolysis which activate reticuloendothelial system.
Clinical Signs:
Generally following signs are developed like anemia, fever, lethargy, emaciation, edematous
swelling of ventral abdomen and legs and jaundice. These signs present in 3 phases:
In acute phase fever, anemia, anorexia and death.
In chronic phase weight loss, anemia and edema.
In unapparent phase no clinical signs but animal is positive for this virus.
Postmortem Lesions:

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Enlargement of lymph nodes, liver, spleen, pale mucous membrane, emaciation, edema,
petechial hemorrhages (thrombocytopenia).
Diagnosis:
History, clinical signs, lab tests and postmortem lesions.
Differential Diagnosis:
Coggin’s test (agar gel immunodiffusion) is mostly used for the diagnosis.
Leptospirosis, fasciolosis, babesiosis, strongylosis, autoimmune hemolytic anemia, equine viral
arteritis, purpura hemorrhagica
Treatment:
No treatment.
Prevention and Control:

• Vaccination
• Health condition can be improved by improving management through following
guidelines:
• Use disposable syringes, needles and sterilized instruments.
• Use sterile instruments for tooth rasping.
• Coggin’s test should be applied annually.
• New purchased animal must be tested before entering in the herd. Newly purchased
animal must be kept in quarantined for 45 days before entering in the herd.
• Tested horses/animals should be brought in horse races, fare and market.
• Fly repellent should be applied in surroundings.
• Good pasture management.

Equine Encephalitis

Definition:
It is an infectious disease of equine characterized by sudden death and central nervous system
disturbance.
Etiology:
Alphavirus genus of family Togaviridae.
Susceptible Host:

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Horses, asses, donkey, mule and zebra.

Transmission:
Through mosquito (Culex and Aedes)
It is of three types: Eastern equine encephalomyelitis, Western equine encephalomyelitis and
Venezuelan encephalomyelitis
Pathogenesis:
First of all pathogen enter into the body by biting of mosquito which effect nervous system by
three stages or pattern. (1) Neurotropism in which the ability of virus infect neural cells. (2)
Neuroinvasiness enter into CNS. (3) Neurovirulence after entrance produce disease in the CNS.
Clinical Signs:
Depression, loss of appetite, decrease weight, blindness, excitability, lack of coordination, lack of
chewing movement, convulsion, paddling, irritability, aggressiveness, abnormal sensitivity to
light.
Mortality is 70%.
Diagnosis:
History, clinical signs, lab tests, isolation and identification of virus by blood tests.
Differential Diagnosis:
Rabies, tetanus, African horse sickness, bacterial meningitis and toxic poisoning.
Control:

• Isolation of infected animals from healthy animals.

• Good cleanliness.
• Vaccination.
• Control mosquitoes by fly repellents.

Equine Viral Rhinotracheitis

Definition:
It is a viral disease of equine which is characterized by respiratory infection in young animals,
abortion in mare, septicemic and viremic condition in foal neonatal and nervous signs in adult.
Etiology:

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Herpes virus. There are four types: EHV-1, EHV-2, EHV-3 and EHV-4. EHV-1 and EHV-4 are more
common infection in equine family. EHV-1 is more prone than other cause abortion and
respiratory distress.
Transmission:
Through inhalation, ingestion and contact with carrier animals discharge like ocular and nasal
discharge.
Pathogenesis:
First of all pathogen enter which causes infection in URT and cause rhinitis. Then viremia then
other parts of body like lungs, pneumonia, brain encephalitis, reproductive tract fetal infection,
placentitis and abortion.
Clinical Signs:
Rhinitis, conjunctivitis, coughing, nasal discharge, enlargement of submandibular lymph node.
Edematous swelling, abortion, nervous signs like paralysis, ataxia, recumbency and death.
Differential Diagnosis:
Strangles, catarrhal rhinitis, equine viral arteritis, equine influenza, purpura hemorrhagica
Treatment:
No effective treatment.
Prevention and Control:

• No venereal.
• Isolation of infected animals.
• Aborted fetus should be disposed of properly.
• Testing system and sanitary measures.
• Vaccination if available.

African Horse Sickness

Definition:
It is a highly infectious non contagious viral disease of all species of equidae family which is
characterized by pulmonary and cardiac signs.
Etiology:

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Orbivirus. It has 9 serotypes.

Susceptible Host:
Donkey, mule, zebra, horse and dog. Sheep, goat and cattle are also recorded by the presence
of antibodies in Egypt.
Transmission:
Through biological vectors like flies, mosquitoes, insects. Through means. Through ingestion of
contaminated meat of horse reported in dogs.
Pathogenesis:
First of all virus enters into the body and then viremia occurs and virus goes into endothelium
and multiply there and after this goes into the predilection site like heart and pulmonary region
and multiply there and infection occurs.
Clinical Signs:
There are four forms.
Per Acute Form: It is also called pulmonary/dinkop/thin head form. It involves acute fever, severe
respiratory distress. Infected animal stand with abducted forelimbs with stretched head and
dilated forelimbs. Tachypnea, forced expiration, perfuse sweating, spasmodic cough, frothy
serofibrinous nasal exudate and dyspnea progress rapidly and animal die within few hours.
Subacute Form: It is also called edematous/cardiac/dikkop/swollen head form. Fever loss within
3-6 days. Edematous swelling in supra orbital fossa and eyelids. This swelling spread into regional
sites like cheek, lips, tongue, intermandibular space, neck, shoulder and chest. Severe depression.
Echymotic lesions under tongue. Petechial hemorrhages under conjunctiva. Mostly death occurs
in this form.
Acute or Mixed Form: In this form above mentioned forms or mixed may occur.
Horse Sickness Fever: Clinical signs are mild. Fever loss in 3-8 days. Mild anorexia and depression.
Mild edema on supraorbital fossa. Congested mucosal membrane. Heart rate is increased.
Diagnosis:
History → Inquire about vector
Clinical signs and lab tests
Differential Diagnosis:
Pluropneumonia, equine viral arteritis, strangles, equine infectious anemia, purpura
hemorrahgica and endocarditis

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Treatment:
Unresponsive.
Prevention and Control:

• Strict monitoring during the purchase of animal.

• Prevent the colostrum to the offspring to the infected dam.
• During embryo transfer technique avoid the infected animal.
• Prevent the grazing of animals in that feed which have infected animal manure.
• Clean and dry the premises to prevent the ingestion of manure contaminated feed or
things.

Epizootic Lymphangitis

Synonyms: Equine blastomycosis, Equine histoplasmosis, Pseudo-glanders, African glanders

Definition:
It is a pyogranulomatous contagious chronic disease of equine family characterized by ulcerative
dermatitis, suppurative dermatitis, lymphangitis and pneumonia or ulcerative conjunctivits.
Etiology:
Histoplasma capsulatum (old name). Histoplasma farcinosum (new name).
It is a yeast like dimorphic double walled capsule ovoid lemon shape fungus. It replicates by
budding.
Susceptible Host:
Donkey, mules and horses are more susceptible. Camel, dog and cattle are also susceptible.
Transmission:
Main source is skin lesion. Skin wound. Soil. Ocular and nasal discharge. Transfer through flies
‘Musca’ and ‘Stomoscus’. These flies transmit this from one lesion to another. If flies transmit in
ocular lesion then create ocular form. If fungus invaded by flies in skin lesions then skin form.
Pathogenesis and Clinical Signs:
The disease is characterized by freely movable cutaneous nodules, which originate from
infected superficial lymph vessels and nodes and tend to ulcerate and undergo alternating
periods of discharge and closure. Affected lymph nodes are enlarged and hard. The skin
covering the nodules may become thick, indurated, and fused to the underlying tissues. Lesions

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also may be present in the lungs, conjunctiva, cornea, nasal mucosa, and other organs. The
nodules are pyogranulomas with a thick, fibrous capsule and contain thick, creamy exudate and
the causative organisms.
Treatment:
No completely satisfactory treatment is known. Surgical excision of lesions combined with
antifungal drugs (amphotericin B) could be used.

Strangles

Synonyms: Distemper
Definition:
It is an acute infectious disease of horses caused by streptococci and characterized by abscess in
pharyngeal and maxillary lymph nodes, pericarditis, pleurisy, suppurative pneumonia, presence
of abscess on liver, kidneys and spleen.
Etiology:
Streptococcus equi
Transmission:
Through inhalation. Through fomites.
Pathogenesis:
The bacteria reaches on pharyngeal and nasal mucosa and causes acute pharyngitis and
rhinitis. Drainage to lymph nodes leads to formation of abscess. Guttural pouches are filled with
pus. Then infection spreads in other organs and causes suppuration in kidneys, brain, liver,
spleen, tendon sheath and joints. After an attack, strangles has subsided and purpura
hemorrhagica may develop due to the development of sensitivity to streptococcal proteins.
Clinical Signs:
Fever (104-107 °F), abscess in throat region, dyspnea, mucoid to mucopurulent nasal discharge
and suppurative pneumonia
Postmortem Lesions:
Abscess in pharyngeal and sub maxillary lymph nodes. Abscess in liver, kidneys and spleen.
Diagnosis:

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History, clinical signs, lab tests and postmortem lesions

Differential Diagnosis:
Equine infectious anemia, parasitism, inadequate nutrition and neoplasia
Treatment:

• Antimicrobial therapy
• NSAIDs can be administered to reduce pain and fever
• Tracheotomy may be required in horses with retropharyngeal abscessation and
pharyngeal compression
Prevention and Control:

• Clinically affected horses should be physically separated from the herd.

• Clean the farm premises.

Glanders

Synonyms: Farcy
Definition:
It is an infectious disease of equines characterized by ulcers in nasal passage, miliary nodules in
lungs, edema of lymph nodes, lymphangitis and lymphadenitis.
Etiology:
Burkholderia mallei
Transmission:
Through ingestion of contaminated feed and water. Through inhalation. Through farm premises.
Pathogenesis:
The organism invades the intestinal wall and causes septicemia (acute form) or bacteremia
(chronic form). The organism may invade the regional lymph nodes by pharyngeal lymph nodes
and proliferate there. The respiratory mucosa and lungs are most commonly affected but
disseminated lesions may occur. Nasal involvement is indicated by a copious and persistent nasal
discharge. In cutaneous form there is development of lesions along the lymphatics resulting in
lymphangitis and lymphadenitis.
Clinical Signs:

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Fever (103-105 °F), dyspnea, discharge of pus from lymph vessels and lymph nodes and ulcer in
nasal passage and thick, mucopurulent, yellowish nasal discharge
Postmortem Lesions:
Abscess in superficial lymph nodes and discharge of oily pus from lymph vessels in hind legs.
Abscess in lungs and liver
Diagnosis:
History, clinical signs, lab test and postmortem lesions
Lab test is Mallein test
Differential Diagnosis:
Any infectious disease causing fever, headache, muscle pain with pneumonia, abscesses, or skin
involvement
Treatment:
Sulfadiazine and sulfadimidine for 20 days
Prevention and Control:

• Detection and elimination of confirmed cases

• Cull of infected animals
• There is no vaccine for glanders

Rabies

Definition:
It is a fatal viral disease of animals which is characterized by certain manifestations such as biting
without provocation, eating abnormal things, running without reason, voice change and
excessive salivation.
Etiology:
Lyssavirus (RNA virus) of Rhabdoviridae.
Susceptible Host:
Through biting, inhalation, ingestion and transplantation is also documented.
Pathogenesis:

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Virus enters into body. Then replicate. After replication enter into peripheral nerves. Through
nerve fluid virus move towards CNS, centripetal force. Then enter into CNS further replication.
Then centrifugally virus move towards other organs salivary gland, kidney and lungs (respiratory
arrest).
Clinical Manifestations According to Life Cycle/Stages:
The life cycle of this disease contain main two stages: (1) Prodermal stage (2) Encephalitic stage
Generally these two stages consist of four phases (i) Prodromal (ii) Encephalitic (iii) Coma (iv)
Death
Prodromal phase contains signs like behavioral changes, personality changes, aggressiveness,
biting and avoiding light.
Encephalitic phase consists of two phases: furious phase (mad dog syndrome) and dumb phase
(paralytic form)
According to furious phase there is manifestation of certain signs and symptoms like sensitivity
to noise, anxiety, facial muscle spasm, lips drawn, ingestion of foreign object, hyperesthesia,
hydrophobia, aerophobia, hyperactivity.
In paralytic form there is paralysis of larynx, pharynx and other body parts like limb. Due to
pharyngeal paralysis animal cannot swallow or eat, excessive drooling of saliva, reluctant to
move, dropping jaw and coughing.
General Signs:
Fever, seizures, hydrophobia, drop lips and jaw, inability to swallow, barking tone change,
roaring. Excessive excitability, excessive salivation and pica condition develops.
Diagnosis:
History → ask about biting, eye swelling and aggressive behavior
Clinical signs, lab tests → negri bodies
Differential Diagnosis:
Polioencphalomyelitis, encephalomyelitis, landry/Guillan barre syndrome (muscle weakness, low
immunity and effect on nervous system)
Treatment:
No
Prevention and Control:

• Pre-exposure 0, 7, 21 or 28 days active immunization

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• Post-exposure
• Washing with detergent.
• Stop bleeding.
• 0, 3, 7, 14, 21 or 28 day booster dose
• Passive immunization HIRG (human immuno rabies) 20 IU IM

Bovine Spongiform Encephalopathy

Synonyms: Mad cow disease

Definition:
It is characterized by mental disorders, behavioral changes, incoordination and death.
Etiology:
Prion
Transmission:
Through ingestion of contaminated feed or wrong composite feed from infected animals.
Clinical Signs:
Nervousness, aggressiveness, changed temperament, abnormal posture, lack of coordination,
loss of weight and death.
Diagnosis:
History, clinical signs and lab test → brain stem sample
Differential Diagnosis:
Ketosis, hypomagnesemia, listeriosis, rabies, brain tumor, lead poisoning and spinal cord trauma
Prevention and Control:

• Prevent feed from contamination.

• Avoid used for feed as infected animal byproduct.
• Test any animal showing abnormal behavior
• Follow all SOPs of farm.
• Good management, sanitation and hygiene at farm.

Ovine Spongiform Encephalopathy

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Synonyms: Scrapie
Definition:
It is a fatal degenerative disease of sheep and goat which affects nervous system characterized
by lack of coordination, rub against wall or tree.
Etiology
Prion
Susceptible Host:
Sheep and goat
Transmission:
Through ingestion. Through contact with placental materials, contaminated urine. Direct contact
at place of races or market.
Clinical Signs:
Effected animal apart from rest animals. Trembling, convulsions, scraping body with walls,
blindness, drinking small quantity of water often.
Diagnosis:
Clinical signs and lab tests
Differential Diagnosis:
Pseudorabies, listeriosis, hypocalcemia, hypomagnesemia, mange, pregnancy toxemia and other
toxins
Treatment:
No effective treatment.
Prevention and Control:

• Treat effected animals separately.

• Do not mix foreign breed with native without test.
• Use scrapie resistant breed for herd.
• Cull the effected animals.

Contagious Bovine Pleuropneumonia

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Synonyms: Lung plague, Lung sickness

Definition:
It is an infectious disease of cattle characterized by cuprous pneumonia, pleurisy and dilation of
lymph vessels.
Etiology:
Mycoplasma mycoides
Transmission:
Through inhalation and direct contact
Pathogenesis:
The infection spreads through inhalation of droplets from infected animals. The recovered
animals act as source of infection at least for a period of 3 years. After entering through
respiratory tract the organism reaches to bronchioles. It may remain in retropharyngeal gland
from where it may spread in whole body. The organism from bronchioles enters into interlobular
septa and causes inflammation followed by edema which causes dilation and subsequent
thrombosis of lymph and blood vessels prior to development of pneumonic lesions. Death
occurs due to anoxia and toxemia.
The incubation period varies, but most cases occur 3–8 weeks after exposure. In some localities,
susceptible herds may show up to 70% morbidity.
Clinical Signs:
Fever (104-106 °F), dyspnea, nasal discharge, signs of pneumonia and pleuritis.
Diagnosis:
History, clinical signs, lab tests and postmortem lesions
Postmortem Lesions:
Congestion and consolidation of lungs, serofibrinous exudate in thoracic cavity and serofibrinous
pericarditis
Differential Diagnosis:
East Coast fever, bovine pasteurellosis and bronchopneumonia
Treatment:

• Tylosin @ 10 mg/kg, IM, every 12 hours, for six injections

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• Danofloxacin @ 2.5 mg/kg/day for 3 consecutive days

Prevention and Control:

• Quarantine measures
• Culling of effected animals
• Vaccination

Canine Ehrlichiosis

Synonyms: Canine typhus, Canine hemorrhagic fever

Definition:
It is a tick borne disease of dog characterized by fever, lethargy, lameness and bleeding tendency.
Etiology:
Ehrlichia canis
Transmission:
Through brown dog ticks.
Clinical Signs:
Thrombocytopenia, fever, depression, anorexia, hemorrhage, nephritis, splenomegaly, renal
failure, cerebral ataxia, staggering, incoordination and hyperesthesia.
Diagnosis:
Clinical signs and lab tests
Treatment:

• Tetracycline @ 22 mg/kg PO bid in acute case but in chronic case @ 20-30 mg/kg PO for
20-30 days.
• Doxycycline @ 5-10 mg/kg for 10 days.
• Imidocarb @ 5-7 mg/kg IM.
Prevention and Control:

• Prophylactically tetracycline @ 6.6 mg/kg PO daily.

• Control of ticks.

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Purpura Hemorrhagica

Definition:
It is a condition of hemorrhages and edema which is triggered by allergic type reaction associated
with bacterial disease equine streptococcus (strangles). It is also consequence of hypersensitivity
in horse due to vaccination.
Etiology:
Actual cause unknown but can be thought due to sensitivity reaction, when Ag-Ab complex
adhere and damage capillaries.
Pathogenesis:
First of all pathogen enter then antibodies produce. Then Ag-Ab complex. Then high amount
antibodies penetrate vessels and activate strong immune response. Then WBCs accumulate
release enzymes and damage blood vessels. Damage blood vessels leak. Blood contents leak out
and accumulate in peripheral tissue showing hemorrhages and edema.
Clinical Signs:
Two forms:
In mild form there is muscle stiffness, inability to move neck, urticarial lesions on skin, slight
edema of legs and abdomen. Petechial hemorrhages on mucus membrane, increased body
temperature and respiratory distress.
In severe case effected skin sloughed off and serum ooze out of skin.
Diagnosis:
History, clinical signs and lab tests.
Differential Diagnosis:
Laminitis, chronic arthritis, viral arthritis and equine infectious anemia (EIA)
Treatment:

• Penicillin is a drug of choice.

• Corticosteroids @ 0.04-0.1 mg/kg IV/IM
Prevention and Control:

• Fresh water and feed availability.

• Leg may be bandaged with cotton wool.
• Full attention during illness.

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Infectious Bovine Rhinotracheitis

Definition:
It is a viral disease of cattle characterized by severe loss of production, abortion and death.
Etiology:
Herpes virus.
There are 3 genotypes:
BHV-1, BHV-2 and BHV-3
BHV-1 cause infectious bovine rhinotracheitis. BHV-2 causes IPV (infectious pustular-vaginitis).
Also cause IBP (infectious balanoposthitis). BHV-3 causes neurological signs.
Transmission:
Through aerosol, inhalation, through venereal. Through carrier animal. Through secretions like
nasal discharge. Ocular discharge.
Pathogenesis:
First of all pathogen enter into body. Initially infect upper respiratory tract like nasal cavity,
pharynx, larynx and cause inflammation. Then cause viremia. After this virus disseminate
systemically to other organs like brain, eye and reproductive tract cause encephalitis, ocular
discharge, conjunctivitis, placentitis, fetal infections associated with abortion.
Clinical Signs:
Coughing, nasal discharge, conjunctivitis, lacrimation, abortion, high fever, inflammation of
nostrils also called red nose. Erosion of nasal mucosa. Drop in milk production.
Mortality is about 10% in severe cases.
Postmortem lesions:
Swelling and congestion of respiratory surface mucus. If secondary bacterial infection then
mucopurulent discharge in respiratory tract. Inflammation of cervical lymph nodes.
Conjunctivitis, clear ocular discharge then mucopurulent discharge.
Diagnosis:
History, clinical signs, postmortem lesions and lab tests
Differential Diagnosis:

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All respiratory diseases like pneumonia, pastuerullosis, pleuropneumonia and rhinitis

Prevention and Control:

• Infected animal should be isolated.

• Testing procedure must be opted before entering new animal in herd.
• Mating and copulation with tested animal.
• Sanitary measure should be adopted properly.
• Quarantine measures before entering animal.
• Testing system for segregation of healthy from infected animals.

Borna Disease

Synonyms: Lyme disease

Definition:
It is a tick borne zoonotic bacterial disease of dog and cat which is characterized by fever, rashes
and inflammation of joints.
Etiology:
Borrelia burgdogeri
Transmission:
Through ticks (ixodes).
Clinical Signs:
Fever and arthritis.
Diagnosis:
Blood culture for the spirochete.
Differential Diagnosis:
Canine arthritis.
Treatment:
Combination of ampicillin and tetracycline @ 20mg/kg PO.

Bovine Farcy

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Definition:
Bovine farcy is an uncommon cause of chronic lymphangitis, lymphadenitis and cutaneous
nodules.
Etiology:
This particular manifestation of bovine nocardiosis is usually limited to the topics. Bovine farcy
is caused by former Nocardia farcinica. Occasionally, Mycobacterium farcinogenes and
Mycobacterium senegalense are also identified in similar lesions.
Pathogenesis:
Initially, the lesions consist of cutaneous nodules, particularly in the leg and neck regions. These
nodules may slowly enlarge and coalesce to lesions of up to 10 cm in diameter, which rarely
ulcerate. The lymphatic vessels appear cord-like.
Diagnosis:
Tuberculin test is for diagnosis.

Mallee

Definition:
It is a disease of camel characterized by enlargement of lymph nodes.
Etiology:
Unknown
Clinical Signs:
Difficulty in breathing and increased temperature. Onset is rapid.
Treatment:
Sulpha and penicillin drug in massive amount.

Kaupali

Definition:

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It is a disease of camel characterized by pus formation in frontal and maxillary sinus.

Etiology:
Exact unknown but may be due to hit of stick by owner over frontal region.
Clinical Signs:
Mucopurulent discharge from one or both nostrils, animal hold its heed high then normal with
straightening neck and muzzle pointed. Increased temperature, decreased appetite, suspension
of rumination and constipation. Percussion of sinus show dull sound due to presence of pus.
Treatment:
Cavities should be washed with KMnO4 solution. Sulpha and penicillin drugs can be used.

Vail

Definition:
It is commonly found in female camel characterized by loss of control over hind legs due to
nervous disturbance.
Etiology:
Exact unknown
Clinical signs:
Difficulty in standing and sitting, staggering and trembling thigh muscle. Animal becomes
incapable of feeding and become emaciated. Mostly occur in adult or old female.
Treatment:
Nervine tonic (neurobion)

Kumree

Definition:
This disease is characterized by trembling and tightening of muscles of hind quarter when
camel at rest.
Etiology:

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Exact unknown.
Signs:
Animal cannot sit easily. Very less recovery. Symptoms become worse and worse. Animal
becomes emaciated.
Treatment:
Not satisfactory. High attention and investigation is required.

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