1. Dr. T.O. Hussein
OSUN – ODUA FARMERS’ ACADEMY
LECTURE NOTE ON ANIMAL HEALTH
BY
DR. T.O. HUSSEIN
COURSE OUTLINE
1. Role of Government in Animal Health Scheme
2. Zoonotic Disease
3. Introduction to Poultry Disease
4. Bacterial Disease of Poultry
5. Viral disease of Poultry
6. Protozoan Disease of Poultry
7. Parasitic Disease of Poultry
8. Disease of Unknown Aetiology.
9. Neoplastic Disease of Poultry
10. Metabolic and Nutritional Disease of Poultry
11. Quail Farming
12. Feed Formulation
13. Introduction to Ruminant Disease
14. Test
15. Exam
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2. Dr. T.O. Hussein
POULTRY HEALTH
Definition of Terms
I. Bacteria: Bacteria are the microscopic form of life also called
microorganism which can be viewed under ordinary microscope.
II. Virus: Viruses are the smallest unicellular microorganism, can be viewed
only under electron microscope.
III. Protozoan: Protozoan is a Unicellular Eucaryote.
IV. Fungus: Fungus is a eukaryotic microorganism.
V. Antibiotic are substances which inhibit the growth or kills
microorganism e.g. Penicillin, Streptomycin, Tetracycline, Ampicillin,
Gentamycin.
VI. Antigen: An antigen is a substance when introduced into the vertebrate
host, stimulate the production of certain serum protein called antibodies.
VII. Antibody: Antibodies are a group of serum proteins produced in
immunological response to an antigen.
VIII. Active Immunity: This is the specific resistance to a disease acquired by
administering an antigen to individuals.
IX. Passive Immunity: Passive Immunity can be produced by transferring
antibodies from a resistant individual to a susceptible individual.
X. Acute Disease: A disease condition is term acute, when the onset of the
disease is sudden, and may result into immediate death e.g. infections
bursa disease.
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XI. Chronic Disease: Takes longer period for causing changes in tissues
gradual; the course of the disease will be progressive.
XII. Pathogens: Pathogens are the biological agents that causes diseases or
pathological changes in tissue.
XIII. Morbidity: Is the percentage of the exposed birds in a flock that become
affected or sick to a disease.
XIV. Mortality: Percentage of birds which died due to the disease among the
affected birds.
XV. Virulence: Refers to the disease producing ability of microorganism in a
susceptible host.
METHOD OF DISEASE TRANSMISSION
Transmission of an infectious disease mean spread of a causal agent of
the disease from one place to the other and from one animal to the other.
Different channels by which the organism can enter into the body of bird are:
I. Skin: Through wound on the skin, biting or sucking insect.
II. Respiratory Tract: Through inhalation of air contaminated with
microbes.
III. Digestive Tract: Through feed and water.
IV. Eyes: Through conjunctiva.
V. Uro-Genital Tract: During mating or handling of reproductive passage.
How Infectious disease spread from farm to farm
I. Through the introduction of disease birds or carrier birds.
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II. From the shoe and clothing of visitors.
III. From carcasses of dead birds, that have not been disposed of properly.
IV. Through contaminated feed, feedbag delivery tracks.
V. Contaminated premises through soil or old litters.
VI. Egg transmission.
BACTERIAL DISEASES
I. PULLORIUM DISEASE
Aetiology/Causative Organism
Salmonella Pullorum
Transmission
Contaminated utensils
Contaminated feed
Contaminated water
Diseased pullets
Dead embryos
Dead chicks
Infected eggs
Infected incubator and hatches
Symptoms
Huddling of chick near heat source
Chalky/whitish diarrhea.
Pasty vent
Morbidity and mortality are high.
Greatest losses usually occur during 2nd
week after hatching
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Gross Lesion
Chicks
Coppery bronze appearance of lives unabsorbed yolk or omphalitis
Diagnosis: Isolation and identification of s pollorum
Treatment
Ciprofloxacin
Enrofloxacin
II. COLIBACILLOSIS
Aetiology/Causative Organism
EScherchia coli
Transmission
Soil and water are main source of transmission.
Infected cage and incubator act as a constant source of infection.
Fecal contaminated of eggs is infection.
Considered the most important source of infect
Predisposing Factors
Stress
Change in season
Dusty litter
Gross Lesion
• Respiratory tract infection
• Panophythalmitis
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• Pericarditis
• Salpingitis and Egg peritonitis
• Synovitis: Joint infection
• Coligranuloma
• Enteritis: Intestine becomes dark red.
• Yolk sac infection.
Treatment
 Ciprofloxacin 15mg/kg body weight for 5days.
 Enrofloxacin
Prevention and Control
• Purchase the day old chicks from reliable hatchery
• Frequent collection and fumigation of egg.
• Proper vaccination programme
• Elimination of possible stress to chicks.
Chronic Respiratory Disease
Aetiology: Mycoplasma gallisepticum
Transmission: occur in three ways.
Aerosol
Contact
Vertical transmission through eggs.
Predisposing Factors
Change in season
Dusty or wet litter
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Overcrowding.
Symptoms
• The disease starts with sneezing, coughing, respiratory distress or gurgling
sound during respiration.
• The gurgling sound are more prominent during night hours.
• Eye show frothy exudate and conjunctivitis.
Post Mortem Lesion
• Air sac appear cloudy (Air saculitis).
• Pericarditis and perihepatitis
• Trachea and conjunctiva become congested and contain cheesy mass.
Treatment
Tylosine, Tylan 110mg/kg .
Terramyan L.A. @ 0.5ml/bird
Enrofloxacin @ 10mg/kg. for 5days
Ciprofloxacin @ 15mg/kg . for 5days
Prevention and Control
To prevent occurrence of the disease feeding method should be improved.
Use wood shaving not saw dust.
Maintain proper brooding temperature particularly during cold season.
Avoid feeding dusty feed to your bird.
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Infectious CORYZA
Aetiology: Haemophillus gallinarum
Transmission: Major source of infection is likely to be chronically infected
carrier birds; Rat and Flies.
Contaminated feed water and water.
Symptom
• The disease occur in bird of any age; but symptom are prominent in adult.
• The face and wattle may be swollen therefore the disease is also known as
swollen head.
• Mucoid nasal discharges.
• Facial edema
Treatment
• Terramycin L.A @ 0.5ml/bird
• Cosumix plus @ 1gm for 5days
• Esb3 @ 1gm/Liter of water for 5days.
Prevention and Control
• Isolation of carrier bird.
• Bird of different age group must be neared separately.
• Good management practices.
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FOWL CHOLERA
Aetiology: Pasteurella Multocida
Transmission
• Adult carrier birds
• Through contaminated food and water
• Contaminated crate, feedbags.
• Dissemination of the organism within a flock result from the excretion
through, nose, conjunctiva which contaminates the feed and water.
• Droppings of birds seldom contain the organism.
• Flies.
Symptom
Acute form is more common and chronic form as sporadic cases.
Acute Fowl Cholera
Characterize by fever, anorexia ruflfed features, mucus discharge from the
mouth, greenish diarrhea, loss of appetite, bluish of combs and wattles,
prostration, drooling of saliva; twisting of neck.
Chronic Fowl Cholera
Swelling of comb and wattles sinuses, leg or wing joint, foot pad, Torticolis
(Twisting of neck).
Post Mortem Lesion
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In acute form, petechial hemorrhage on heart, occationally on gizzard muscles,
proventiculus and serosa of intestines. Mesentry and abdominal fat are
common.
Venous congestion of internal organ, causing enlargement and dark
colouration of liver, kidney and spleen. Ova may be congested or ruptured.
Lungs may be congested.
Mahogany appearance of liver with pin point size spots all over the liver
parenchyma.
In chronic form, the affected wattles, combs and joints show yellowish, thick
pus or cheesy exudate.
Diagnosis
In acute form, high mortality. Blood smears should be stained and examined
for the presence of bipolar organism in large numbers.
Treatment
• Water source and storage should be clean regularly.
• Terramycin L.A. 0.5ml/bird s/c on 1st
day and 4th
day
• Consumix plus @ 1gm/Liter of water 3 to 5days.
• Esb3@ 1gm/Liter of water 3 to 5days.
• Robatran @ 1gm/Liter of water 3 – 5days.
Prevention
• Segregation of affected bird and treatment with terramycin
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• Rear the bird of different age group.
• Proper disposal of dead birds.
Control of Flies
Vaccination: Fowl cholera killed vaccine.
9th
week fowl cholera 0.5ml/bird 11th
week fowl cholera 0.5ml/bird 1/m
NECROTIC ENTERITIS Aetiology: Clostridium Perfringen
Type A and C
Predisposing Factor
 Direct damage to the intestinal lining by coccidian or other bacteria.
 Use of rancid fish meal, wheat maize, rice bran.
 Physical factors which damage the gut such as infection with Litter
material change in feed formula.
 Immunosuppression that reduce gut resistance and viral infection such as
IBD, mycotoxin and physical stress.
Sign
• Severe depression, loss of appetite, reluctant to move,
• Increase water intake
• Ruffled feather
• Shooting type of diarrhea shorting type of diarrhea leading to wet litter and
often blood tinged dark feces.
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Post Mortem
The intestines are distended, with gas severe necrosis of intestinal mucosa
cauliflower like diptheretic enteritis.
Diagnosis: on gross Lesion like cauliflower like intestinal mucosa.
Treatment
• Amopremix @ 125 to 150mg/kg body weight for 7day.
• Chlortetracycline @ 1gm/litter of water 5days.
Prevention
• Maintenance of dry litter with proper ventilation.
• Avoidance of overcrowding.
• Preventing coccidiosis
• Use of probiotic
• Reduction of stress factor.
• Proper biosecurity measure on the farm.
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VIRAL DISEASE OF POULTRY
Infectious Bursa Disease (IBD, Gumbro)
Aetiology: Birna virus
Transmission
In a fresh flock, the infection arises from the residual virus remained in
shed, or its surroundings or through personnel; trays, contaminated litter, food
and water, it short incubation period favors it rapid spread.
Symptoms
The disease is characterized by a spiking mortality i.e. it begins at 3
days, spikes at 5 – 7days and then starts declining.
Depression, disinclination to move and feed, low water intake, dehydration,
self-vent-picking, prostration and trembling before death sulfur colored
diarrhea
Post Mortem Lesion
• Dehydration of skin and muscle
• Kidney swollen and white due to accumulation of urate.
• Haemorrhage in thight muscle, proventriculus and it junction with
gizzard.
• The most prominent lesions are however in bursa of fabricius on 2nd
– 3rd
day of infection.
It is swollen and it outer surface is covered with a straw colored viscous
material.
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On cutting open the bursa, mucoid material is found contained in it.
It internal folds or plicae show swelling and echymotie haemorrhages. After 5th
day of infection, bursa starts its reduction in size and ultimately by 8th
day, it
is reduced to almost 1
/3
rd
of it normal size.
Diagnosis
Diagnosis of the disease is based upon the characteristic symptoms and
lesions, and by demonstration of antibody and/or virus in the bird.
Prevention and Control
• Sound biosecurity measure
• Isolation of breeder, broiler and commercial layers.
• All – in – all – out replacement programme.
• Thorough decontamination of houses between successive cycles.
Disinfection Protocol
After shifting the birds spray 5% Formalin on the Litter.
Leave it overnight, pack the entire litter in bag and throw away from farm
premises.
• Remove all Feeders, drinker etc. soak them in 5% formalin overnight,
wash and sundry
• Soak with caustic soda flakes at the rate of 10gm per liter of water
overnight.
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• Make shed air-tight and fumigate the shed with potassium
permanganate and formalin at the rate of 20gm kmno4 + 40ml formalin
for 100 cubic feet.
Vaccination
Commercial Layer
Vaccinated between days 12 to 14 days.
Infectious Bronchitis
Aetiology: coronavirus
Transmission
• The disease can occur in any season.
The respiratory form of IB may involve almost all the birds.
• Infection can be transmitted through eggs. I.B. affects only poultry. It
can produce disease in birds of any age.
• Nephrotic form of the disease is common among chicks.
Symptom
• Small chicks show sign of sneezing, coughing, respiratory races or even
dyspnea, eye may look wet.
• Bird become dull and tend to huddle towards the source of heat.
Diarrhea may be seen after a few days.
• Mortality is maximum within the first and second weeks after infection
and taper off by about the end of the third week.
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• Adult bird show sudden drop in egg production to as low as 25percent.
Egg production may return to normal after 1 to ½ month. Quality of eggs
may not be normal and hatchability may also decline.
• Some of the eggs may be thin shelled, rough shelled, deformed or
smaller than normal with watery albumen. Mortality varies from 10 to
100%.
Gross Lesions
• Nasal cavity and sinuses show the presence of cheesy exudate, grayish
and mottled.
Diagnosis
• The lesion in the respiratory tract, kidneys and oviduct help in
diagnosis.
• The isolation and identification of the virus and neutralization test
confirm the disease.
Prevention and Control
 1st
day IB live vaccine on arrival of chicks by beak dipping method.
 7th
day IB live vaccine on arrival of chick by drinking water
 14th
week IB live vaccine on arrival by drinking water.
Mareks Disease
Synonyms: Range paralysis, Nara leucosis Neural Lymphomatosis.
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Cause
(1) Double stranded DNA virus of Herpesvirus group
(2) The virus exist in three serotype – 1, 2, 3
Serotype 1 is pathogenic and oncogenic
Serotype II is non-oncogenic
Serotype III is HVT non-oncogenic but giving immunity against
serotype I
Transmission
• Poultry litter may remain infected for up to serval weeks mode of up to
several weeks mode of infection is by respiratory route.
• The bird shed virus within 7days of infection and the peak in sheding it
reaches in the period of 4 to 6weeks in acute form and 12 to 14weeks in
classical type following the infection.
• The disease is spread through tips of the infected and desquamated
feather. Skin is always infected and virus is shed from infected tip in
the air virus particles from the air are inhaled and bird get infected.
• Saliva, nasal discharge and faeces.
• The litter is generally infected and the infection remains up to 15weeks.
Predisposing Factor
Stress
Symptom
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• Chicken of 12 to 24weeks are mostly affected and it does not generally
occur below 6weeks of age and older bird above 24weeks of age.
(i) Classical Form of Neural Form
• Bird of 16 to 20weeks of age usually suffer from the disease – mortality
rate is usually low and generally seen at the onset of sexual maturity i.e.
above 16weeks of age and the time of peak laying, paralysis of leg, wings,
swelling of nerves like sciatic of legs, brachial of wings, coelic of intestine
and vagus through neck.
Bird are unable to stand they remain in recumbent position.
• Leg and wings are stretched in opposite direction.
• The “split leg” stance is a usually posture.
• Ovaries look like regressed and cauliflower like Regressed bursa has
been a consistent feature.
• Greenish diarrhea
• In chronic condition one or two birds may die everyday over a
considerable period of time.
(ii) Acute or Visceral Form
Generally 3 to 4weeks bird usually suffer from this condition mortality
rate may go as high as 60%.
Birds may die all of a sudden without showing any remarkable sign.
(iii) Transitional Paralytic Form
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This occurs at the age of 5 to 18weeks of age and characterize by sudden
development of paralysis of the leg and wings and neck.
(iv) Occular Form: Blindness develops in the eyes showing white or grey or
pearly eyes.
(v) Skin or Cutaneous Form: Discrete white nodules will be seen on the
skin.
Post Mortem Lesion
• Affected nerve are thickened to more than 2 to 3 time than normal, there
is loss of glistening appearance and cross striations.
• Nodules on liver, spleen, heart, ovaries, testes muscles.
• Feather follicles and enlarged, skin contains nodules
• Proventricular wall thickened, white area in the iris.
• Nerves especially sciatic or brachial become thick and lusterless.
• Bursa become atrophied and porventiculus thickening.
Diagnosis
Symptom and Lesion
Control
• HVT (Freeze dried) Given at one day and again on 18th
day.
• Living HVT, FC 126 used in parents, grandparents and pure line
• Freeze dried FC 126 Day old commercial broiler and layer chicken in the
hatchery and also on 18 to 21days.
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FOWL POX
Synonym: Avian diphtheria
Cause: DNA virus belonging to pox virus group.
Transmission: The infected bird sheds the virus in environment through the
falling of the scabs or nodules when dried. The same virus may enter into the
blood, multiply and concentrate in unfeathered parts of the skin and produce
the Lesions.
• The virus may enter through the wounds in the skin and set up the
Lesions.
• Blood sucking or biting insects may also transmit the disease at times.
Symptoms
• If the skin alone is involved the Lesions are present on the skin and the
bird recovers after about a fortnight. Some drop in egg production may
occur – Dry pox.
• If the mucus membrane of mouth and respiratory tract are involved there
may be difficulty in respiration which may be showed by rapid and
shallow breathing neck extended up and keeping the mouth open and
may even die.
• Due to lesions in mouth, pharynx and oesophagus the bird may
consume less fed and become emaciated, egg production may drop and
the bird may die.
Lesions
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• Development of different stage as roseola, popular, vascular, pustular
or scab and nodular stage on unfeathered parts of the body as comb,
wattles around the beak or eye, shanks and feet.
• White membranous deposit on the mucus membrane of month, pharynx,
oesophagus, larynx or trachea, sometimes blocking these tabular
passages
Diagnosis
Symptom and lesions
Prevention and Control
• Sanitation and disinfection
• Vaccine
Vaccine
Fowl Pox Vaccine
 It is prepared by partially attenuated strain of fowl pox virus. This
vaccine is given by wing prick method with the help of a lancet.
 It cannot be given to chicks below 6weeks of age or in laying bird
because it reduces the egg production.
In Layer flock it is given twice during the growing stage, the first at about
7th
to 8th
week and the other at 15th
to 16th
week.
New Castle Disease
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The new castle disease is a highly contagious disease in many species of
domestic exotic and wild birds.
Depending on the strain of virus and its tissue tropism, the post-mortem
findings are very variable. Petechial haemorrhage are seen on heart, abdominal
(at, trachea, mucosa and air sacculitis may be seen with some pneumotropic
strain of the virus).
Proventiculus
Proventricular haemorrhages are usually seen on the surface of papillae
and can be distributed in a ring near the junction with the gizzard.
Haemorrhagic lesion may also be found in the intestine, particularly on the
surface of the caecal tonsil.
Prevention and Control
• Pressure cleaning
• Chemical treatment
• Heat treatment
• White wash of the shed.
• Fumigation (40gm of pottasum permagnate and 80ml of formalin).
• Rigid biosecurity
• Restricting movement of men and materials.
• Restricting entry of vehicles
• All in all out system.
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• Sparrow proffing of shed.
This is carry out to prevent entry of sparrow and wild birds in shed.
Control by vaccination.
Suggested Vaccination Practice
Age Commercial Layers
5 – 7days Lasota - 1
/0 or 1
/N and ND killed 0.2ml s/c
21st
day Lasota (for Broiler only) Booster (D/W)
30th
day Lasola Booster (D/W)
7th
week lasota Booster (D/W)
10th
week R2B live 0.5ml (1
/m)
17 – 18th
week ND (k) 0.5ml s/c
Inclusion Body Hepatitis
Aetiology: Adenovirus
Transmission
• The disease occur with very short incubation period
• It is self-limiting up to 10 – 14days
• Virus can be transmitted horizontally up to 14th
week of age.
• Aerosol spread may occur but for short distance. Virus replicate in
intestinal tract, hence feces are highly infectious.
Symptoms
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• The disease occur in acute and per acute forms.
• In per acute form, birds die suddenly without any specific lesions.
• In acute form depression, hiding and ruffled feather seen before death.
Lesion
• Presence of straw coloured or translucent transudate in pericardial sac.
This give an appearance of Leechi fruit to the heart and hence the local
name Leechi Heart Disease.
• Bursa enlargement or atrophy can be observed.
• Motting of liver and spleen is also seen.
• Pale or dehydrated breast muscle with splashes of haemorrages can be
observed with anemia.
Prevention and Control
• To prevent high morbidity and mortality vaccination is the only way.
• Parent flock are vaccinated before start lay. This will help to transfer
material antibodies in progeny chicks.
• Vaccination with MD and IBD is essential to reduce the impact of
immunosuppression.
Vaccination Schedule
For chicks up to 4week of age use 0.2ml dose by subcutaneous route, for
parent bird.
Avian Influenza
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Aetiology: Avian Influenza Virus
Source of Infection
• Domestic and wild bird
• Mixing pig 5 and birds on the same premises may lead to serious
problem.
• Poor status of biosecurity. Increase risk of introduction of A.I. virus.
Clinical Sign
• Decline in water and feed consumption, sudden mortality in flock, ruffled
feathers.
• Sudden and sharp drop in egg production.
• Shell – less or soft shelled, misshapen egg, depression and dropines
cyanosis (purplish blue coloring) of wattle and combs.
• Edema and swelling of head, eye-lid, combs, wattles and hocks,
subcutaneous hemorrhage of the shank region, diarrhea.
• Acute onset of respiratory rales
• Blood tinged discharge from the nostrils.
Incoordination including loss of ability to walk and stand.
• A.I. may be confuse with infections bronchitis, infections
Laryngotrachitis, fowl cholera and Ranikhet Disease.
Post Mortem Lesion
• Pin point hemorrhage in the muscle
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• On the serous surface of viscera and within the mucosa of the
proventriculus.
• Diffuse hemorrhage in pancrease.
• Hemorrhage beneath the lining of the gizzard – Trachitis with
hemorrhage clear straw colored fluid in the subcutaneous tissue
In mature bird, there is cessation of ovarian function. Ovules and yolk
materials may be present in the body cavity.
• Young broiler may show signs of severe dehydration with other lesion.
Prevention and Control
• Preventive measure include preventing introduction of A.I. virus in
domestic poultry population.
• Early detection of A.I is the key to control it spread.
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