INFECTIOUS BURSAL DISEASES Introduction Classification Virus Morphology • Serotypes • Resistance Cultivation Pathogenesis Symptoms Lesions Diagnosis Differential diagnosis Treatment and control
Zoonotic Importance
INTRODUCTION •
Highly contagious disease of young chickens
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Caused by infectious bursal disease virus (IBDV)
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Characterized by immunosuppression and mortality generally at 3 to 6 weeks of age.
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Characterised by the destruction of the lymphoid organs, in particular the bursa of Fabricius
CLASSIFICATION Family Birnaviridae
Genus Type
Species
Aquabirnavirus Avibirnavirus Entomobirnavirus
infectious pancreatic necrosis virus infectious bursal disease virus Drosophila X virus
Acronym IPNV IBDV DXV
VIRUS MORPHOLOGY •
IBDV is a double stranded RNA virus that has a bi-segmented genome
• The virions are non enveloped. • Capsid is composed of single layer and appear hexagonal Icosahedral symmetry.
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IBDV genome consists of two segments, A and B.
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The genome segment B encodes VP1, the putative viral RNA polymerase.
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The larger segment A encodes viral proteins VP2, VP3, VP4, and VP5.
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VP2 protein contains important neutralizing antigenic sites and elicits protective immune response.
SEROTYPES
• Two distinct serotypes 1 and 2. • Serotype 1 cause clinical diseases in chickens younger than ten weeks.Serotype 1 has been further divided into six distinct groups. • Serotype 2 does not cause any clinical diseases in chickens. RESISTANCE • The virus has no HA property •
Stable in acid environment of pH 3-7 and stable in alkaline environment of pH 7-9.
• Virions are not sensitive to treatment with heat (60 c , 1 hour) or ether.
CULTIVATION •
The virus is easily cultivable in chickens, ECE and chicken embryo fibroblasts.
1. CHICKENS •
Not recommended due to animal welfare concerns.
• The virus is inoculated as eye drop. • The virus kills the chickens 72-80 hours after inoculation. • The bursae if chickens infected with virulent serotype 1 IBDV appear yellowish (sometimes haemorrhagic) and turgid, with prominent striations. • Peribursal oedema. • The plicae are petechiated. •
The bursae of chickens infected with serotype 2 IBDV do not exhibit any gross lesions.
2. EMBRYONATED CHICKEN EGGS: •
Inoculated via yolk sac of five 6-8day old specific antibody negative (SAN) chicken embryos and on to the chorioallantoic membrane of five 9-11 day old SAN chicken embryos.
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Serotype 1 IBD produces dwarfing of the embryo, subcutaneous oedema, congestion and subcutaneous or intracranial haemorrhages.
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Serotype 2IBDV does not induce subcutaneous oedema or haemorrhages in the infected embryos
• Kidney, liver and spleen are enlarged.
3. CELL CULTURE Chicken embryo fibroblasts are normally used for cultivation.
EPIDEMIOLOGY • Infection which is usually acquired by the oral route • Spread to other poultry units byfomites occurs. •
Neither a carrier state nor vertical transmission has been demonstrated.
PATHOGENESIS Host: Chicken, turkey and ducks Route of transmission: Water, feed , droppings from infected birds Carrier : Meal worm and Aedes vexan (Mosquito) Morbidity and Mortality: Morbidity rates are high upto 100 percent. Mortality rates are variable and may go up to 25 % in broilers and 60% in layers.
Incubation period : 2-3 days. Ingestion ↓
Virus in macrophages and lymphoid cells in the Caeca, duodenum and jejunum ↓ Reach the liver via portal circulation ↓ Spread to bursa of fabricius ↓ Replication in cytoplasm ↓ Target cell – B lymphocytes ↓ Destroys lymphoid follicles in the bursa of fabricius
SYMPTOMS • Self vent pecking • Anorexia • Depression • Trembling • Watery and whitish diarrhea • Prostration and finally death.
LESIONS The following lesion are observed in dead birds: a. Enlarged cloacal bursa which is swollen and haemorrhagic in dead birds and is atrophied in recovered birds. b. Dehydrated carcass c. Dark skeletal muscles with haemorrhages. d. Opaque thymus with thickened gelatinous capsule e. Fatty bone marrow f. Swollen liver and kidneys
g. Intestines with increased mucus h. Changes in bursa 1. Inflammatory of the bursa and apoptosis of B lymphocytes. 2. Complete depletion of cells in the follicular cortex. 3. The bursa will reach five times its normal size during acute infections before atrophy begins. 4. At necropsy an atrophied, grey bursa is seen with no B lymphocytes in the bursal follicles or in other lymphoid tissues.
DIAGNOSIS: 1. Clinical symptoms and lesions. 2.
Isolation and identification: a. Clinical materials: 1. Fresh bursa and spleen for virus isolation. 2. Samples of bursa, spleen, intestines, liver and kidney in neutral buffered formalin for histopathology. 3. Blood samples for serology.
3.Serological tests 1. AGID 2. Quantitative AGID test. 3. Virus neutralization test 4. ELISA 5.FAT
4. Strain differentiation: IBDV serotypes are differentiated by cross neutralization, virus neutralization tests or by serological tests using serotypes specific monoclonal antibodies.
DIFFERENTIAL DIAGNOSIS IBD should be differentiated from Marek’s diseases, Mycotoxicosis, coccidiosis, Haemorrhagic syndrome, Avian adenovirus infection and Infectious bronchitis.
TREATMENT: Not effective IMMUNITY 1. VACCINES: IBD vaccines are made with serotype 1 IBDV only.
a. Live vaccines:
i. Live IBD vaccines are produced from fully of partially attenuated strains of virus known as mild, intermediate or intermediate plus respectively.
ii. Application is by means of intramuscular injection, spray or in the drinking water, usually at 8 weeks of age.
iii.Only healthy birds should be vaccinated.
b.
Inactivated vaccines:
1. It is used to produce high, long lasting and uniform levels of antibodies in breeding hens. 2. Only healthy birds known to be sensitised by previous exposure to IBDV should be vaccinated.
ERADICATION: • Recovered and vaccinated can carry and shed virus for long periods. •
Control of the disease implies 1. depopulation and rigorous disinfection of contaminated premises. 2. Disposal of litter, dead birds, used gunny bags, curtains by incineration or deep burial with slaked lime.
ZOONOTIC IMPORTANCE: No human infection has been reported with IBDV.