Poultry Diseases INDOVAX

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Ascites
Egg Drop Syndrome IBH – HHS (Leechi Disease)
Avian Encephalomyelitis
Fatty Liver Syndrome Infectious Coryza
Avian Infectious Bronchitis
Fowl Cholera Infectious Laryngotracheitis
Avian Influenza (HPAI)
Fowl Pox Lymphoid Leucosis
Avian Influenza (LPAI)
Fowl Typhoid Mareks Disease (MD)
Chicken Anaemia
Gout (Non infectious) Newcastle Disease (RD)
Collibacillosis
Gumboro Disease (IBD) Viral Arthritis
CRD
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Avian Encephalomyelitis

Avian encephalomyelitis is a disease of chickens marked by ataxia and tremor of

the head, neck and limbs.

Aetiology - Picorna virus.

Hosts
Affects chicken, quail, turkeys.

Transmission
Vertical transmission is a very important means of virus dissemination. Horizontal spread due to
direct or indirect contact with ailing birds. Virus is shed in droppings.

Susceptibility to chemical & physical agents

Formalin fumigation is effective.

Viral strains
Enterotropic strains, embryo-adapted strains.

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Avian Encephalomyelitis
Incubation period
1 to 7 days in embryo transmission
11 days by oral administration.

Symptoms
Chicks in first week of their life show unsteadiness, sitting on hocks, paresis and even complete inability to
move. The disease in adult birds is in apparent except for a transient drop in egg production.

Gross Pathology
In chicks – whitish areas on gizzard muscle .

Diagnosis
Based on history, signs and isolation of virus from brain tissue.

Material for Laboratory

Brain tissue from affected chick stored in 50% glycerine saline to be sent on ice.

Control
Control of AE is achieved by vaccination of breeder flock during the growing period to ensure that they do
not become infected after maturity.

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Chicken Anaemia

Chicken infectious anaemia is a disease of young chicken characterized by

aplastic anaemia and generalized lymphoid atrophy with concomittant
immunosuppression.

Aetiology
Virus classified as member of circoviridae – DNA virus.

Host
The chicken is the only known host for CIAV. All ages are susceptible but susceptibility to disease
rapidly decreases in immunologically intact chicks during first 3 weeks of life.

Transmission
Spreads horizontally and vertically. Horizontal infection occurs by direct or indirect contact with ailing
birds.

Resistance to chemical & physical agents

Extremely resistant to heat (56ºC to 70ºC for one hour). 1% glutarldehyde, 5% formalin, iodine,
hypochlorites are effective.

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Chicken Anaemia

Incubation period
Under field conditions vertically infected chicks show increased mortality beginning at 10 – 12 days of
age with peak at 17 – 24 days, second peak is at 30 – 34 days due to horizontal transmission.

Clinical symptoms
Poor growth, pale birds, sudden rise in mortality (usually 13 – 16 days of age). No clinical signs or
effect on egg production or fertility in parent flock during seroconversion.

Gross pathology
Pale bone marrow, atrophy of thymus and bursa,
discolored liver & kidney, gangrenous dermatitis.

Diagnosis
On basis of gross lesions, demonstration of ongoing
seroconversion is parent flock.
Virus may be isolated in specific cell line MDCC – MSB1.

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Chicken Anaemia

Material for Laboratory

Liver or spleen tissue or rectal contents from diseased chickens in early phase of the disease to be
sent on ice to the laboratory.

Control
In addition to bio-security measures vaccination of parents is an important strategy of control.
Current vaccine strategies are based on prevention of vertical transmission of virus by immunization
of breeder flock and have been successful in reducing the incidence of anaemia in chicks.

Both live and inactivated vaccines are reported to be useful.

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Viral Arthritis

Viral arthritis is a contagious disease of domestic fowl – particularly broiler breeds

– caused by REO virus.

Aetiology - REO virus.

Hosts
Primarily disease of domestic fowl.

Transmission
Vertical transmission through embryonated eggs. Horizontal spread occurs readily from bird to bird
mainly by ingestion of contaminated faeces. Infection can occur through respiratory route also.

Resistance to chemical & physical agents

REO virus is heat resistant. It can withstand 60ºC for 8 to 10 hours. In poultry sheds at 22ºC or so, it
can survive for a year.

Incubation period
Depends on virus pathotype. 9 to 13 days in contact exposure.

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Viral Arthritis

Symptoms
Lameness, low morbidity, poor growth, inflammation of hock, swelling of tendon sheaths, rapture of
gastrocnemius tendons.

Gross pathology
Swelling of tendon sheaths, swelling of footpad,
ulceration of articular cartilage, hemorrhage in tissues.

Diagnosis
Based on history, lesions.
Rising antibody titres, isolation of virus.

Material to be sent to laboratory

Affected joint in 50% glycerine saline to be sent on ice.

Control
In addition to bio-security measures, immunization of birds with live vaccine in growing stage followed
by inactivated vaccine when the birds come in lay.

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Egg Drop Syndrome

Egg drop syndrome is a contagious disease of poultry characterized by sudden drop

in production or a failure to achieve a normal peak in production.

Aetiology - Adenovirus subgroup III.

Hosts
Chickens of all ages are susceptible to EDS.

Transmission
Vertical transmission through eggs. Lateral spread of virus is slow and intermittent. In adult birds,
presence of virus in feces probably arises from contamination by oviduct exudates. Droppings contain the
virus in low titres and excretion of virus is intermittent.

Susceptibility to chemical & physical agents

Gets inactivated by 0.5% formaldehyde or 0.5% glutaraldehyde.

Clinical symptoms
Egg drop at peak or failure to peak. Egg drop may be 5 to 50% at least for 3 – 4 weeks. Rough, thin or
soft shelled, shell less eggs, loss of shell pigment. Except for egg drop or laying misshapen – shell less
eggs – there are no clinical symptoms.

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• Signs
Egg Drop Syndrome

- Loss of pigmentation
- Thin, soft shelled and misshapen eggs

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Egg Drop Syndrome

Gross Pathology
No specific lesions.

Diagnosis
Abnormalities of egg production – High HI titres in affected birds which were not vaccinated with EDS
vaccine. Virus can be isolated in Duck embryo from the pouch shell gland of affected bird.

Material to be sent to laboratory

Serum samples, abnormal egg samples.

Control
An oil adjuvant inactivated vaccine is widely used and gives good protection against clinical EDS.
Birds should be vaccinated between 14 and 16 weeks.

Indovax offers an effective EDS inactivated vaccine for control of the disease.

Indovax can assist in determining seroconversion in vaccinated birds.

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Fowl Cholera

Fowl cholera is a serious, highly contagious disease caused by Pasteurella multocida.

Aetiology
Pasteurella multocida. Fowl cholera may be caused by any of 16 Heddlesson serotypes although certain
serotypes appear to be more often associated with disease.

Hosts
Affects poultry, turkeys, ducks and geese. Death losses usually occur in laying flocks.

Transmission
Chronically infected birds on the farm are major source of infection. Dissemination of Pasteurella
multocida with in a flock is primarily by excretions from mouth, nose. Diseased birds contaminate their
environment particularly feed & water. Disease could be mechanically transmitted by flies.

Incubation period
Incubation period is very short – 24 to 48 hrs.

Symptoms
Depression, ruffled feathers, loss of appetite, diarrhoea, coughing, swollen and cyanotic wattles (in chronic
cages), swollen joints (chronic cases), lameness, sudden death.

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Fowl Cholera
• Signs

Chronic - Swollen wattles, sinuses, leg or wing joints - Tracheal rales and dyspnoea

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Fowl Cholera
• Lesions

Liver - Swollen and usually contains multiple pin point foci

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Fowl Cholera
• Lesions

Ovary - Petechial and eccymotic haemorhhages

-General hyperemia is evident
-with haemorrhages on heart

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Fowl Cholera
• Lesions

Chronic cases - Oedematous lungs (Pneunomia)

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Fowl Cholera

Gross Pathology
Hemorrhages on myocardium – hemorrhages on duodenum, pericardial effusions, yolk peritonitis.

Diagnosis
Examine blood slides. Organisms can be isolated from heart blood.

Material to be sent to laboratory

Femur bone kept in charcoal to be sent on ice to laboratory.

Control
Bio-security measure, rodent control, control of flies and insects.
Protect all the birds with fowl cholera vaccine. Every bird needs a primary dose and a booster dose
set two weeks apart. The age of vaccination is decided on basis of the vulnerable age for this
infection as seen on farm. The booster dose should be given at least 15 days before the vulnerable
age – the age at which fowl cholera cases are seen on farm.

Vaccines
INDOVAX offers very effective vaccine for fowl cholera. The vaccines are designed on basis of
prevalent strain in locality and selection of strains is done on basis of cross protection tests in addition
to somatic/capsular typing.

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Infectious Coryza
Infectious coryza is an acute respiratory disease of chickens characterized by
nasal discharge, sneezing, swelling of face under the eyes.

Aetiology
Hemophilus paragallinarum – Serovars A and C.
Transmission
Chronic or healthy carrier birds on the farm. On farms where multiple age groups are brooded and
raised, spread of the diseases to successive age groups usually occurs with in 1 to 6 weeks after such
birds are moved from the brooder house to growing cage near older birds.
Susceptibility to chemical & physical agents
These are delicate organisms and get rapidly
inactivated outside the host.
Incubation period
24 – 72 hours.
Clinical symptoms
Facial swelling, purulent ocular and nasal discharge,swollen
wattles, sneezing, drop in egg production 10 – 40%, Inappetance.

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Infectious Coryza
• Signs

Seromucoid nasal and ocular discharge Sometimes swollen wattles

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Infectious Coryza
• Signs

Facial oedema and conjunctivitis

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Infectious Coryza

Gross pathology
Conjunctivitis, Tracheitis, Caseous material in sinuses.

Material for laboratory

Chopped off head to be stored on ice and sent to laboratory by air. It is better to send a live bird for
attempting isolation as the organism is very fragile and may get inactivated in transit.

Control
Bio-security. All in all out management. Vaccination of entire flock with coryza bacterin. Two doses are
necessary – primary and booster, set one fortnight apart. It is necessary to protect the birds at proper
age so that they complete the primary & booster applications at least 15 days before the chicks are
transferred in vicinity of older birds.
It is also necessary to confirm that birds receiving primary vaccination or booster are not already
suffering with coryza.
It may be necessary to press near the infraorbital sinus to confirm absence of nasal exudate.

Vaccines
INDOVAX offers H. paragallinarum vaccine containing local isolates belonging to group A and C. The
vaccine is presented in either aluminium hydroxide gel form or stable water in oil emulsion.

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Fowl Pox
Fowl pox is a slow – spreading viral infection of chickens and turkeys characterized
by proliferative lesions in the skin that progress to thick scabs and by lesions in the
upper GI and respiratory tracts (diphtheritic form).

Aetiology
Large DNA virus – an avian poxvirus – family poxviridae.

Hosts
Can infect birds of both sexes and all ages and breeds.

Incubation period
4 to 10 days.

Clinical signs
Warty, spreading eruptions on un-feathered part of body- particularly visible and comb, wattles. In
diphtheritic form caseous deposits are seen in buccal cavity, throat and some times in trachea. It is
relatively slow spreading viral disease.

Post mortem
The cutaneous form can be easily seen in life. In diphtheritic form of the disease caseous plaques can
be seen in mouth, pharynx, trachea and nasal cavities.

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Fowl Pox
• Signs - Vary depending on host susceptibility & virulence of the virus

Cutaneous - Nodular lesions on comb, wattle, eyelids & other unfeathered parts
of the body

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Fowl Pox
• Signs

Cutaneous - Nodular lesions on comb, wattle, eyelids & other unfeathered parts of
the body

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Fowl Pox
• Signs

Diptheritic - Yellowish lesions on mucous membrane of mouth, oesophagus or

trachea -- leading to respiratory distress

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Fowl Pox
Viral strains
A nucleoprotein precipitinogen is common to all poxviruses.

Transmission
By direct or indirect contact. The disease may be transmitted by a number of species of mosquitoes.

Resistance
Virus can survive in dried scabs for months or even years. It is resistant to 1% phenol and 0.1%
formalin. It gets inactivated by 1% caustic potash.

Diagnosis
It can be readily diagnosed on basis of flock history and presence of typical lesions.

Material for laboratory examination

Dry scabs stored in sterile vials, Diphtheritic lesions from throat stored in 50% Glycerin saline to be sent
on ice.

Control
Routine immunization of birds with pox vaccine is practical method of control. Indovax Fowl Pox vaccine
is available in 500 & 1000 dose vials along with a special diluent for the vaccine.

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Avian Infectious Bronchitis

Infectious bronchitis is an extremely contagious respiratory disease of chickens

characterized by coughing, sneezing, rales, egg drop and nephritis.

Aetiology
It is caused by a corona virus. Several sero types of corona virus have been recognized.

Host
All ages are susceptible but the disease is more severe in baby chicken. As age increases, chicken
become more resistant to the nephrogenic effects, oviduct lesions and mortality due to infection.

Incubation period
18 – 36 hours.

Clinical signs
Drop in egg production 20 – 50%, soft shell eggs, rough shells,
loss of internal egg quality, coughing and sneezing.

Gross pathology
Flaccid follicles, yolk in peritoneal cavity, caseous plugs found in
trachea of young chick, swollen pale kidneys with tubules & ureter distended with urates.

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Avian Infectious Bronchitis

• Clinical Signs (Layers / Adults)

- Decline in egg production in addition to respiratory signs

- Poor shell, shell less and mis-shapen eggs

- Severe decline in setting eggs and highly reduced hatchability

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Avian Infectious Bronchitis

• Clinical Signs (Layers / Adults)

- Inferior quality of eggs with watery albumin

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Avian Infectious Bronchitis

• Clinical Signs

- In broilers depression, ruffled feathers, wet droppings and nephrosis is seen

apart from respiratory signs

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Avian Infectious Bronchitis

Diagnosis
Isolation of virus in chick embryo. Several passages are necessary before the virus is isolated.
Rising Elisa titre in birds together with egg drop and or respiratory symptoms is indicative of active
infection.

Transmission
Highly contagious disease. When it occurs all susceptible birds on premises become infected. Air
borne disease can jump considerable distances during an active outbreak. It can be spread
mechanically by formites.

Resistance
Infectious bronchitis virus is considered to be sensitive to common disinfectants. The virus can
survive for about one fortnight in summer months and 56 days in winter months.

Material for virus isolation

Trachea, Kidneys, ileocaeccal tonsils duly preserved in 50% - glycerin saline should be sent on ice
to the laboratory.

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Avian Infectious Bronchitis

Control

Vaccination of birds with high passage Massachusetts strain of IB is a practical method of

control. Vaccination has to be repeated from time to time to ensure adequate protection.

Indovax offers following products for control of infectious bronchitis:

• Infectious bronchitis vaccine (live) Mass strain - Bronkichick

• Infectious bronchitis vaccine (Inactivated) for breeders. This vaccine has the advantage that
a prevalent strain of IB virus in a territory can be incorporated in inactivated vaccine.

• Newcastle disease + IB virus combined. Live vaccine available in the following combinations:
- Newcastle disease F. strain + IB virus for young chicks - Bronki-F
- Newcastle disease LaSota strain + IB virus for older birds - Bronki-L

• Infectious bronchitis vaccine inactivated alone or in combination with ND, IBD, EDS is
available for breeders.

Indovax can assist in sero monitoring of day old chicks, vaccinated birds.

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Gumboro Disease (IBD)

Infectious bursal disease is an acute, highly contagious viral disease of young

chickens. It is most often found in highly concentrated poultry producing areas. It
causes marked morbidity and mortality in affected flocks. Although the disease causes
severe losses, its affect on reducing the bird’s ability to develop immunity to other
diseases in the most serious effect produced by this disease.

Aetiology
Infectious bursal disease is caused by a birna virus. Serotype I variants of IBD virus have not been seen in
India so far.

Hosts
Chickens and turkeys are the natural hosts of the virus. The period of greatest susceptibility to clinical
disease is between 3 and 6 weeks of age. Susceptible chicken younger than 3 weeks do not exhibit clinical
signs but get sub clinical infection in which the bursa gets damaged resulting into immuno suppression.

Transmission
The spread of the disease can occur by direct contact, contaminated litter & feces, care taker, contaminated
air-equipment – feed, human traffic, insects and wild birds. It is extremely contagious.

Incubation period - 2 to 3 days.

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Gumboro Disease (IBD)

• Lesions

Haemorrhages in thigh and pectoral muscles

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Gumboro Disease (IBD)

• Lesions

Renal changes are prominent

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Gumboro Disease (IBD)

• Lesions

Bursa is enlarged, gelatinous &

sometimes even bloody

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Gumboro Disease (IBD)

• Lesions

Petechial or ecchymotic haemorrhages on mucosal surface, ocassionally

throughout the bursa

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Gumboro Disease (IBD)

Clinical signs
Depression, inappetance, unsteady gait, Huddling, Vent pecking, Diarrhoea with urates in mucus.

Post mortem lesions

Oedamatous bursa, may be hemorrhagic to start with followed by regression of bursa, hemorrhages in
skeletal muscles, swollen kidneys with urates.

Diagnosis
A workable diagnosis can be made on basis of flock history and post mortem lesions. A laboratory
procedure of isolation of virus can be used to substantiate the diagnosis.

Material to be sent to laboratory

The affected bursa stored in 50% glycerin saline needs to be sent on ice to the laboratory.

Control
It is universally accepted that the control of the disease depends on – (1) Bio-security (2) Proper
vaccination.

Susceptibility to physical & clinical agents

IBD virus is very stable. The hardy nature of this virus is one reason for its persistent survival in poultry
house. Formalin and iodophore are considered as effective disinfectants.

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Gumboro Disease (IBD)

Vaccination strategies
It is important to choose correct age for priming the birds. This can be done by knowing the maternal
antibody pattern. In view of the variance in maternal antibody pattern of chick population, it may be
necessary to do repeated vaccination. It is also necessary to review the vaccination strategies from time
to time – particularly in commercial farms as the chick population originating from a breeder lot may
have different levels of Mab – depending on immune status of the breeder flock.

VACCINES

INDOVAX offers very effective vaccines of proven worth for control of IBD.
• Infectious Bursal Disease vaccine (live) Intermediate strain - GEORGIA – for layer and broiler chicks.
• Infectious Bursal Disease vaccine (live) - IV95 strain for layer chicks carrying higher maternal
antibodies and where the outbreaks are persistent.
• Infectious Bursal Disease vaccine (live) – Bursa B2K strain for broiler chicks. A single application of
the vaccine at 11 – 12 day age of the birds is usually effective.
• Infectious Bursal Disease vaccine Inactivated alone or in combination with ND, IB is available for
Breeders.

Indovax can assist in studying MAb profile and deciding vaccination schedules.

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Infectious Laryngotracheitis

Infectious laryngo tracheitis is an acute, highly contagious herpes virus infection of

chicken characterized by sever dyspnea, coughing and rales. It may manifest as
subcute disease characterized by lacrimation, tracheitis, conjunctivitis and mild rales.

Aetiology
Herpes virus strains appear to be homogenous antigenically.

Hosts
All ages of fowl are susceptible. Young chicks are more vulnerable.
Disease is usually seen in birds 3 to 9 months of age.

Transmission
Vertical transmission not recorded. In the flock the disease spreads due to direct or indirect contact with
ailing birds and fomites. Recovered birds or even vaccinated birds act as carrier.

Susceptibility to chemical & physical agents.

It has been shown that the virus survives in trachea exudates & chicken carcasses for a period of 10 – 100
days at ambient temperature of 13 – 23ºC. However the virus gets inactivated at 38ºC within 48 hrs. 3%
cresol or 1% lye will inactivate the virus in less than one minute.

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Infectious Laryngotracheitis
Clinical signs
Dyspnoea, coughing of mucous or blood drop in egg prodution, ocular discharge, and sinusitis.

Gross Pathology
Sever laryngo tracheitis often with blood in lumen, caseous plugs may be presence.

Diagnosis
The acute disease could be diagnosed on basis of spread, clinical syndrome and lesions in trachea.
Mild forms cannot be diagnosed on clinical symptoms alone. Isolation of virus, intra nuclear inclusion
bodies in trachea tissues and increase in titre between acute and convale scant sera are methods
available.

Material to be sent to laboratory

Affected trachea stored in 50% glycerin saline to be sent on ice to the laboratory.

Control
Vaccination should only be done when there is a confirmed diagnosis of ILT. Live modified ILT vaccine
is available and it can be used on chicks as well as adult birds as per immune response. Vaccinated
birds can act as carries of the disease and hence vaccination should not be done where it is not
indicated.

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Mareks Disease (MD)

Marek’s disease is a lymphoproliferalive and neuropathic disease of domestic

chicken caused by a highly contagious, cell associated oncogenic herpes virus.

Aetiology
Cell associated lymphotropic herpes virus.

Hosts
MDV infection in chickens is ubiquitous among poultry population through out the world. Clinical signs
can be seen usually after 4 weeks of age. The age group 12 week to 24 week is very vulnerable.

Transmission
Direct and indirect contact. The epithelial cells in keratinising layer of feather follicle replicate fully
infectious virus and serve as source of contamination to the neighboring environment.

Sero types
Sero type I includes all oncogenic and pathogenic viruses, sero type II consists of naturally occurring
avirulent strains of Marek’s virus (example SB1 strains) HVT is sero type III virus.

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Mareks Disease (MD)

Incubation period
Cytolytic changes occur in between 3 to 6 days, for classical disease with lameness 8 – 12 days.

Symptoms
Paralysis of wings, legs and neck, loss of weight, grey iris, skin around feather follicle raised and
roughened.

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Mareks Disease (MD)

• Lesions

Peripheral nerves - Loss of striations and thickening

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Mareks Disease (MD)

Gross Pathology
Grey – white foci of neoplastic tissue in liver, spleen, kidney, gonads, heart & skeletal muscles
thickening of nerve trunks and loss of striation.

Material to be sent to laboratory

Enlarged liver, spleen, kidney, heart, gonads nerves for histopathology, skin with feather follicles for
viral isolation.

Diagnosis
History, clinical signs, distribution of lesions, age affected, histopathology. It is necessary to
differentiate from lymphoid leucosis.

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Mareks Disease (MD)

Disinfection
The stability of cell associated MDV sero type I and II strain is completely dependent on the viability
of the cells. Cell free virus found in feather follicle and cellular debris can remain viable for 4 – 8
months at room temperature. The virus gets inactivated by commonly used disinfectants.

Vaccination
The vaccination strategy depends on type of virulence of Marek’s infection. The infections caused by
mild (mMDV) and virulent (vMDV) could be controlled by use of HVT cell free vaccine or HVT frozen
vaccine. In case of very virulent (vvMDV) bivalent vaccines. HVT + SB1 would be necessary. In case
of very virulent to (vv + MDV) infections use of sero type I vaccines is indicated.

Vaccines
INDOVAX offers High PFU HVT vaccine cell free, freeze dried, HVT frozen vaccine and HVT + SB1
frozen vaccine.

It is necessary to keep the vaccinated chicks away from infected sheds at least for one month during
which time the chicks would have acquired the required immune status.

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Lymphoid Leucosis

Lymphoid leucosis is a disease of adult chicks characterized by lymphoid tumor

response in most of the organs (except nerves) and lymphoid leucosis
manifestation in bones, lymphatics and myeloid tissue.

Aetiology
Caused by Exogenous lymphoid leucosis (LL) retro virus belonging to subgroups A, B, C, D, E and J.

Transmission
The disease is transmitted in a variety of ways. The causative viral agent is passed out of the body of
infected birds via eggs and feces. The virus may be transmitted mechanically from infected birds to
susceptible birds by blood sucking parasites or by man in such procedures as fowl pox vaccination.

Incubation period
Depends on strain and dose of virus in field outbreaks, LL cases can occur anytime after 14 weeks of
age, however incidence is usually highest at about sexual maturity.

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Lymphoid Leucosis

Clinical signs
Visceral tumors can be found in liver, spleen, kidneys and bursa of birds that are in general older
than 25 weeks. The disease may manifest as osteopetrosis, erythroid and/or myeloid leukemia.
The new J virus produces tumors in adult birds on surface of bones – junction of ribs, sternum and
pelvis.

Diagnosis
Histopathology of affected organs.

Control
No vaccine is available.
The only method available for control is laboratory detection
of infected breeder and their elimination.

Breeding leucosis free offspring from Leucosis free breeders can

eventually lead to eradication of this disease.

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Newcastle Disease

Newcastle disease is a contagious viral infection causing respiratory, nervous

disorders in several species of fowl including chickens and turkeys.

Aetiology
Paramyxovirus - 1 (PMV – 1) only one serotype of ND is known.

Pathology of the virus

ND – velognic – viscerotropic (vvND) it is also called as Asiatic or exotic ND. It is highly virulent
for chickens.
ND Neurotropic velogenic – causes neurological and respiratory signs.
ND Mesogenic – these viruses are used as vaccines in previously immunized birds.
ND Lentogenic – may cause sub clinical mild infections. Can affect any age. Most of the vaccine
strains are Lentogenic strains.

Hosts
Birds of all age group are susceptible. The vulnerable age for the disease is first 6 weeks of the life or
birds in late stage of their lay.

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Newcastle Disease

Transmission
Direct contact with secretions, specially feces from infected birds. Contaminated feed, water,
implements, premises, human clothing etc. Disease spreads through Air to long distances.

Incubation period
2 to 15 days (average 5 – 6 days).

Clinical signs
Gasping, coughing, drooping – wings, dragging legs,
twisting of the head and neck, in appetance, partial or complete
cessation of egg production, greenish diarrhoea.

Morbidity and mortality depend on virulence of virus, degrees of vaccinate

immunity and condition of flock.

Gross Pathology
Hemorrhage in proventriculus Necrotic plaques in proventriculus, intestine, caecal tonsils, tracheitis.

Material to be sent to laboratory

Lungs & Trachea, spleen in 50% glycerin saline to be sent on ice.

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Newcastle Disease
• Gross Lesions

- Inflammation of trachea with haemorrhages

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• Gross Lesions
Newcastle Disease

- Necrotic button ulcers in the intestines

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Newcastle Disease
• Gross Lesions

Necrotic button ulcers in the intestines

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Newcastle Disease
• Gross Lesions

- Airsacs are inflammed, cloudy and congested

- Ovaries flaccid. Peritonitis & watery yolk material in abdominal cavity

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Newcastle Disease

Diagnosis
Presumptive diagnosis may be made on basis of clinical syndrome, P.M. lesions, rising titres in
serology.
Mere isolation of ND virus from the tissues is not enough to pronounce ND. The isolate has to be
studied in tests known as minimum death time, intracerebral pathogenic index, intravenous
pathogenic index in chickens.

Control
Systematic vaccination is the key of Newcastle disease control.
Two types of vaccines are available: -
- Newcastle disease live vaccine.
- Newcastle disease inactivated vaccine.
Live vaccine – The immune response to a vaccine increases as the pathogenicity of live vaccine
increases. Therefore to obtain the desired level of protection without serious reaction, vaccination
programmes are needed that involve sequential use of progressively more virulent viruses or live
virus followed by inactivated vaccine.
Newcastle disease live vaccine F.strain (ICPI 0.25) is used as primary dose in first few days (2 -
3 days) of the chick. It is a mild strain well tolerated by a young chick.

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Newcastle Disease
The subsequent live vaccines consist of NDV LaSota strain which are administered 12 –15 days, 20 – 25
days, 35 –40 days ( if necessary). The repetition of LaSota vaccine will depend on Mab profile of the chick
population.
Newcastle disease mesogenic vaccine (R2B strain ) is administered when the birds are 8 to 10 weeks of
age.
Newcastle disease inactivated vaccine Encivax(Titre of bulk >109 EID50) is administered at point of lay.
The HI titre of birds is routinely monitored. The layer birds should have HI titre of >26 HI in order to ensure
sustained production. It may be necessary to boost the layer immunity by administration of LaSota (usually
every 3 months) as per need.
There are special circumstances when judicious use of ND killed vaccines is found beneficial in farms
where there is persistent problem of ND and/or great variation in Mab titre of chicks, simultaneous
vaccination of live and inactivated ND vaccine is found beneficial. Similarly in case of broiler birds having
high maternal antibody – in many cases – simultaneous vaccination of live + inactivated ND vaccine is
found beneficial.
Indovax offers world class highly effective live vaccines prepared from CAV free SPF eggs – viz.
Newcastle disease live vaccine F strain >106 EID50 with special diluent.
Newcastle disease live vaccine LaSota strain >106 EID50 with special diluent.
Newcastle disease live vaccine R2B strain >105 EID50 with special diluent.
Newcastle disease inactivated vaccine Encivax(>109 EID50) stable water in oil emulsion – dose for adult
birds 0.5 ml dose for chicks less than 1 month of age 0.2 ml.
Indovax can assist in determining Mab titres for ND and assess sero conversion due to vaccination from
time to time.

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Avian Influenza (HPAI)

Highly pathogenic avian influenza (HPAI) is a highly contagious disease of poultry
caused by influenza A virus subtypes H5 and H7 possessing a sequence at the
hemagglutinating cleavage site that codes for multiple basic amino acids.

Aetiology
Virus family orthromyxoviridae influenza A type virus subtype H5 and H7 possessing multiple basic
amino acid at cleavage site.

Hosts
It is primarily a disease of chicken. All age groups are affected.

Transmission
Direct contact with secretions from infected birds, especially faces. The virus concentration in
droppings is highest. Contaminated feed, water, equipment and clothing. Clinically normal water birds –
water fowl, sea birds may introduce the virus in flocks.

Resistance to Physical & Chemical action

Inactivation at temperature 56ºC / 3 hours, 60ºC/ 30 min.
PH Inactivated by acid pH
Disinfectant – Inactivated by formalin and iodine compounds
Survival - Remains viable for long periods in tissue faces and also in water.

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Avian Influenza (HPAI)

Incubation period 3 – 5 days.

Symptoms
Sever depression, inappetance, drastic decline in egg production, facial oedema,
cyanotic combs and wattles, petechial hemorrhages on internal mucous surfaces,
sudden deaths (mortality can reach 100%).

Gross Pathology
In case of sudden deaths – no lesions will be seen. Birds which survive the infection for a day or two
may show sever congestion of musculature, oedema of head and neck area. Conjunctivitis,
hemorrhagic tracheitis and mucous plugs in trachea, petechiae inside sternum and so, abdominal fat.
Haemorrhages on all mucous surfaces.

Diagnosis
This is very important. It depends on isolation of the virus, typing of H and N antigens, intravenous
pathogenic test in 6-week-old chicks, sequencing and presence of multiple basic amino acids at the
hemagglution cleavage site. This is a highly specialized work and very few laboratories are equipped
to do this work.
We are fortunate to have high security disease laboratory of IVRI at Bhopal who are authorized to do
this work.

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Avian Influenza (HPAI)

Samples for viral isolation

Lung, Trachea, spleen pools of organs and faeces in glycerin saline to be sent on ice.

NOTE - The post motem and collection of samples should be left to experienced vets properly protected
by sterile facemasks, gloves and apparel.

Zoonoses

World Health Organization, OIE and all the Governments of different countries of the world are
apprehensive that the H5N1 outbreaks in poultry may infect human beings. If the virus mutates and gets
capacity of human to human transfer – it may repeat the 1918 history of influenza pandemic that killed
millions of human beings.
H5N1 outbreaks are being recorded in the world since 2003 and in 2006 it affected almost entire ASIA,
EUROPE and part of Africa.
So far there is no evidence of human to human transfer.

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Avian Influenza (HPAI)

Control
Important steps in effective control are: -

• Quick diagnosis of indicator case.

• Culling of infected birds and their immediate vicinity of at least 3km. radius.

• Sanitary disposal of dead birds, animal products, cleaning disinfections of poultry houses.

• Restrictive measures on trade vaccination of birds for HPAI has been a debatable issue.
Vaccinated birds may remain as healthy carrier of the disease. However, looking to the wide
spread outbreaks, the quantum of culling operations and impeding all time danger several
countries like Russia, China, France, Netherlands etc have opted for vaccination.

In India HSADL Bhopal has already developed an effective vaccine for H5N1. It is, however,
necessary to monitor vaccinated population either through DIVA strategy or through sentinel
birds or any such method which can detect a infected bird from vaccinated bird.

The OIE has already given a protocol for production & testing of avian influenza vaccines.
Vaccination is now being considered an important tool of control by most of the international
forums.

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Avian Influenza (LPAI)

Low pathogenic avian influenza (LPAI) is a highly contagious disease of poultry caused by
influenza virus type A other than H5 and H7.

Aetiology
Virus family orthromyxoviridae genus influenza A subtypes other than H5 and H7. there are 15
recognized H subtypes and nine N subtypes.
Influenza type A H9N2 has been causing serious losses to poultry industry, all the world over in recent
past by way of mortality, egg drop, poor growth and performance.

Hosts
It affects chickens, turkeys. All age groups are susceptible.

Transmission
Direct contact with secretions from infected birds, especially faece contaminated feed, water,
equipment and clothing. Clinically normal waterfowl can transmit LPAI. The disease quickly spreads
through airborne particles in a large geographical area.

Incubation period
Depends on the dose of virus, the route of exposure & ability to detect clinical signs.

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Avian Influenza (LPAI)

Symptoms
LPAI viruses when tested under laboratory conditions for IVPI test done on 6 week old bird, are not
lethal.
But when LPAI viruses infect the farm birds, they cause sizeable mortality. In uncomplicated
infections of H9N2, the virus may cause serious drop in egg production, respiratory disease,
anorexia and depression sinusitis low but elevated mortality. When other organisms such as
pneumoviruses, Newcastle disease, E.coli, Pasteurella, Mycoplasma are present in population or
birds under any stress are on the farm, the mortality may rise to high as 60 – 70%. There is
considerable mortality in broiler chicks.
Gross Pathology
Facial swellings, egg peritonitis, mild preventricular haemorrhages, haemorrhatic tracheitis,
pancreatic, nephritis.
Material for laboratory investigation
Serum, eggs for estimation of HI antibodies lung/trachea/spleen in glycerin saline to be sent on ice
for virus isolation.
Diagnosis
Depends on isolation of virus and its subtyping in H and N antigens.
Control
In addition to bio-security measures systematic vaccination of the population with the inactivated oil
adjuvant vaccine is beneficial for control of the disease. The immunized birds perform well and
losses due to egg drop on incidental mortality excited by secondary pathogens is avoided.

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Inclusion body hepatitis – Hydropericardium syndrome (Leechi/Angara disease)

Inclusion body hepatitis – hydro pericardium syndrome (Angara disease) is a

contagious disease of poultry birds – particularly broiler birds characterized by high
mortality due to hepatitis accompanied with hydro pericardium.

Aetiology
Fowl adeno virus sero type 4. F. adv. 4.

Hosts
The layer chicks can be infected experimentally. But the disease
in nature is usually seen only in broilers. Disease is seen in
all age groups of commercial broilers.

Transmission
Vertical transmission. Horizontal spread due to direct or indirect
contact with ailing birds or its excretions.

Incubation period - Incubation period is short – 24 to 48 hrs.

Symptoms
Depression, ruffled feather, respiratory distress inappetance. Death after a short sickness.

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Inclusion body hepatitis – Hydropericardium syndrome (Leechi/Angara disease)

• Lesions
Pericardium filled with fluid (Leechi appearance)
Heart - petechial haemorrhages

Liver - Enlarged and congested

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Inclusion body hepatitis – Hydropericardium syndrome (Leechi/Angara disease)

Gross Pathology
Liver is congested to start with in advance stages the liver is pale yellow. There is spectacular
hydropericardiiuum. The heart is completely immersed in yellowish pericardial fluid.

Diagnosis
The liver tissue gives a positive AGPT test against known positive serum. Virus can be isolated by yolk
sac inoculation.

Material for diagnosis

Liver in glycerin saline to be sent on ice.

Control
In addition to bio-security measures vaccination of the commercial broilers is highly beneficial. Inclusion
body hepatitis – hydro pericardium syndrome inactivated vaccine gives solid protection to vaccinates.
Usually one vaccine dose is sufficient. In such flocks where the virus load is more, two doses may have to
be given. Vaccination age is to be decided on basis of vulnerable age.
If the disease appears in chicks less than 10 days of age, it is advisable to immunize broiler breeders so
that the chicks have sufficient maternal antibody.
Indovax offers a very effective vaccine for control of inclusion body hepatitis hydropericardium syndrome,
both for commercial broilers as well as broiler breeders. The dose for commercial broiler is 0.2 ml. and
dose for broiler breeders is 0.5 ml.

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Fowl Typhoid
Fowl typhoid is an acute or chronic, septicaemic disease of poultry characterized by
dullness, loss of appetite, fever and yellowish diarrhoea.

Aetiology
Salmonella gallinarum

Hosts
Primarily affects chickens & turkeys. Guinea fowls, quails, pheasants and ducks are also susceptible.
Broilers are more susceptible to disease.

Transmission
Spreads by both vertical and horizontal transmission. Horizontal transmission is through infected hen,
egg, incubators and contaminated premises. Mechanical transmission also occurs. Infected and
carrier birds shed the organisms in their droppings.

Susceptibility to chemical & physical agents

Organism died within 10 min. at 60ºC and within a few minutes by direct exposure to sunlight. Gets
inactivated by Phenol, dichloride of mercury, Potassium permagnate, formalin.

Incubation period
Usually 4 – 6 days.

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Fowl Typhoid
Symptoms
Signs include sudden or sporadic mortality, listlessness, loss of appetite, yellow diarrhoea
accompanied with pasting of vent feathers. Respiratory distress with rapid breathing can also occur.
Mortality may range from 10 to 90%. In chronic cases shrunken, pale combs and wattles are seen.

Gross Pathology
Enlarged & mottled spleen, enlarged friable liver colored dark red or greenish brown and surface has a
distinctive coppery bronze sheen after exposure to air for a short period is a consistent finding on post
mortem. Catarrhal enteritis & dark brown bone marrow is also seen.
Pericarditis with turbid yellow fluid pericardial sac & fibrin attached to surface of heart is a feature of
chronic fowl typhoid. In laying birds, there may be retained yolks.

Diagnosis
Based on gross lesions, isolation & identification of organism.

Material for laboratory examination

Affected internal organs to be sent on ice. Heart blood to be sent on ice.

Control
Strict hygiene measures. Chicks to be obtained from breeder flock known & tested to be free from
disease. Routine disinfection of incubators and eggs.

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Chronic Respiratory Disease (CRD)

It is a chronic respiratory disease of poultry characterized by respiratory rales, coughing,
nasal discharge and conjunctivitis and frequently in turkeys, infraorbital sinusitis.

Aetiology
Mycoplasma gallisepticum

Host
Affects 4 –10 weeks old birds especially the broilers & turkeys. Quail, duck, geese, pheasants are also
susceptible.

Transmission
Spreads by both horizontal and vertical transmission. Horizontal transmission occurs readily by direct or
indirect contact with infected birds or through droplet infection. Vertical transmission occurs through inovo
transovarian route. Additional transmission may occur via fomites.

Susceptibility to physical & chemical agents

Commonly employed chemical disinfectants are effective. Gets inactivated by phenol, formalin,  propiolactone
and merthiolate. Organism is inactivated at 50ºC.

Incubation period 6 –10 days.

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Chronic Respiratory Disease (CRD)

Clinical symptoms
Most characteristic signs are tracheas rales, nasal discharge and coughing, loss of appetite and birds
lose weight. Turkeys are more susceptible than chickens and develop more severe clinical signs
including infra orbital Sinusitis. Ataxia, lameness may also be seen in affected cases. There may be
reduction in egg production to as much as 50% in layer flock.

Gross pathology
Most important pathological lesion is cloudy appearance of air sacs and air sacculitis. There is
catarrhal inflammation of trachea, nasal passages, sinuses and bronchi. Pericarditis and perihepatitis
is seen in cases complicated with E.coli. Trachea and conjunctive may be congested. Occasionally
arthritis and tenosynovitis is observed in chickens.

Diagnosis
Post mortem examination. Blood testing by rapid serum agglutination test and Elisa. Isolation of
organism from trachea or air sacs of affected birds.

Material for laboratory - Serum samples to be sent on ice.

Control
Control strategy is based on maintaining Mycoplasma free breeding stock. High level of bio-security is
pivotal. All in all out production system and routine serological monitoring are helpful.

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Collibacillosis

Collibacillosis is the commonest disease of poultry characterized by dullness,

listlessness, ruffled feathers, diarrhoea, respiratory signs and septicemia.

Aetiology - Escherichia coli organisms.

Hosts
Chickens, turkeys, ducks and pheasants all are affected but disease is most commonly seen in young
chickens.

Transmission
E.coli is present in intestinal tract as normal inhabitant and shed in the faeces. Infection is transmitted by
oral or inhalation route due to direct or indirect contact with ailing birds.

Susceptibility to chemical & physical agents

Inactivated by most of disinfectants and temperature of 70 –80ºC.

Incubation period
3 – 5 days.

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Collibacillosis
Symptoms
The symptoms vary with the different types of infections. In acute septicemic form, mortality may begin
rapidly and progress rapidly. However, in most cases, symptoms are listlessness with ruffled feathers,
loss of appetite, dyspnoea, sneezing. Diarrhoea may be evident. Past like faeces soil the vent feathers.
Omphalitis and naval infection is seen in young chickens.

Gross pathology
Lesions vary from acute to chronic in the various forms of disease. Characteristic gross lesions are
airsacculitis, peritonitis, perihepatitis and pericarditis. Fibrinous pericarditis and perihepatitis are most
striking gross lesions. Liver, kidney and spleen are congested in septicemic cases. Omphalitis,
salpingitis may be seen in young birds.

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Collibacillosis

Diagnosis
On basis of gross lesions. Isolation and identification of organism from heart blood using growth media
like EMB, MacConkey’s Agar.

Material to be sent to laboratory

Heart blood with anticoagulant to be sent on ice, dead bird as such can be sent on ice.

Control
Maintain highest standards of flock management. Good hygiene in handling of hatching eggs. Control
of predisposing factors and infections.

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Ascites

Ascites is a disease of broiler chickens characterized by accumulation of

non-inflammatory transudate in abdominal cavity.

AETIOLOGY
Right ventricular failure or hepatic fibrosis or lung damage. Also associated with inadequate
supplies of oxygen, poor ventilation and physiology.

Hosts
Affects all species of poultry.

Clinical symptoms
There are sudden deaths in rapidly developing birds.
Progressive weakness and abdominal distension,
which is followed by recumbency.
Clinically affected birds show signs of dyspnoea and cyanosis.

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Ascites

Gross Pathology
On post mortem, enlarged heart, enlarged and thickened right ventricle, fluid in body cavities and
heart sac is observed. Lungs and intestines are congested. Liver is enlarged, congested and have
clotted protein adherent to its surface. There is general venous congestion.

Diagnosis
Gross lesions are characteristic.

Material to be sent to laboratory

Dead bird as such can be sent to lab. on ice for diagnosis.

Control
Ascites caused by pulmonary hypertension is controlled by reducing birds oxygen requirement,
giving good ventilation and reducing ammonia in the shed. Ascites caused by lung damage or
avoiding etiologic agents involved can control liver damage. Avoid predisposition of birds to other
respiratory diseases.

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Gout (Non-infectious)
Gout is a metabolic disease of poultry characterized by depression, low feed intake
and growth and swelling of joints.

Aetiology
Excess protein or reduced water intake in diet, nephropathy, and deficiency of Vitamin A, high – calcium
laying feed in layers.

Hosts - All poultry species are susceptible.

Symptoms
Affected birds are dull, depressed and stunted.
There is loss of appetite.
There may be signs of lameness in cases of articular gout.

Gross Pathology
Chalky white deposits/urates are seen on pericardium, liver, air sacs and peritoneum. Kidney is swollen
and greyish in colour. Ureter is dilated with white pasty material. Similar deposits may be seen in joints.

Diagnosis - Based on gross lesions.

Material to be sent to laboratory -Dead bird as such can be sent on ice.

Control - Balanced diet with adequate supply of vitamin A should be given, ample supply of water.

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Fatty Liver Syndrome

Fatty liver syndrome is a non-infectious metabolic disease of layers

characterized by enlarged fatty liver and excessive abdominal fat deposits.

Aetiology
Excessive caloric intake/ faulty diet.

Hosts
- Affects chickens primarily cage layers.

Clinical symptoms
Affected birds appear overweight with heavy abdominal fat.

Egg production is decreased. Birds died due to liver rupture have pale combs & wattles.

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Fatty Liver Syndrome

Gross pathology
Primary gross lesion is an enlarged, yellowish, friable liver. Liver may show rupture with internal
hemorrhage. Blood clots are found in abdominal cavity. Abdominal wall and subcutaneous tissues
are generally full of fat.

Diagnosis - Based on gross lesions.

Material for laboratory - Dead hen as such can be sent on ice.

Control - Balanced ration containing adequate level of proteins and vitamins should be given.
High energy diets should not be fed.

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For more information, please contact :

INDOVAX
Corporate Heights, SCO-24, Sector – 14
Gurgaon 122 001 – Haryana (INDIA)

Ph: 0091-124-231 5044 to 46, Fax: 0091-124-231 4680

E-mail: mail@indovax.com Website : www.indovax.com