3. IBD OR GUMBORO
It is also known as Gumboro disease,Infectious bursitis,Infectious avian nephrosis.
The first report of a specific disease affecting the bursa of Fabricius in chickens was
made by Cosgrove in 1962.
The first cases were observed in the area of Gumboro, in Delaware (United States of
America), which is the origin of the name, although the terms 'IBD' or 'infectious
bursitis' are more accurate descriptions
Infectious bursal disease is a viral infection, affecting the immune system of poultry.
The disease is highly contagious, affects young chickens, and is characterized by the
destruction of the lymphoid organs, and in particular the bursa of Fabricius, where B
lymphocytes mature and differentiate.
It is the disease of great economic importance due to heavy mortality in chickens and
Immunosupression which can leads to vaccination failure and secondary infections like
E.coli infection , gangrenous dermititis, inclusion body hepatitis-anaemia syndrome.
4. ETIOLOGY
Infectious bursal disease virus is a birnavirus.
It is highly stable and resistant to many physical and chemical agents.
It is highly contagious and is be spread by contaminated feces, water and feed.
It can also be carried by vectors such as darkling beetles (feed on decaying
plant and animal matter ) and rats.
RNA viruses is Positive-sense/ plus sense double –stranded RNA genome
Monopartite (single NA molecule protected in shell of protein or lipid),
Birnavirus virions are nonenveloped, approximately 65 nm in diameter, and hexagonal with a single
shell having icosahedral symmetry .
There are two serotypes of IBDV, serotype I and serotype II.However, chickens only develop IBD after
the infection by serotype I IBDV strains, serotype 2 also occurs in turkeys and ducks.
The genome consists of two unrelated molecules of linear double-stranded RNA, designated A and B
(Fig.). Segment A ranges from 3.1 to 3.6 kbp in size and contains at least two open reading frames, the
largest of which encodes a polyprotein that is processed to form the structural proteins, VP2 and VP3,
and a viral protease (designated as VP4 or NS, depending on the virus) that autocatalytically cleaves
the polyprotein.
The virus loose viability at temperature 70ºC for 30 minutes, by exposure to 0.5% formalin, and 0.5%
chloroquine for 10 minutes destroys the infectious agent.
5.
6. GENOME
Segment A contains two
overlapping open reading frames,
the larger of which encodes viral
proteins VP2, VP3 (both
structural capsid proteins), and
VP4 (a viral protease).
The smaller open reading frame
encodes the nonstructural protein
VP5.
Segment B encodes VP1 which is
a multifunctional polymerase.
7. PATHOGENESIS
After infection,virus present in macrophages and lymphoid cells in caeca, lateron in small
intestine.
Then virus first reaches the liver,enters the blood and distributed to other tissues,
including bursa.
The bursa is infected through the blood and many cells in organ contain the virus.
The viremia occurs in other organs including spleen ,Harderian gland (lymphoid organ
near eye), and thymus.
The kidney are swollen due to urate deposition.
The cause of hemorrhages in muscle is unknown.
Depletion of B-lymphocytes result in extremely poor immune response.
Infections before 3 week of age are usually subclinical.
Chickens are most susceptible to clinical disease at 3–6 week of age when immature B
cells populate the bursa and maternal immunity has waned, but severe infections have
occurred in Leghorn chickens up to 18 week of age.
8. CLINICAL SIGNS
Elevated body temperature, (111ºF/44ºC), watery urate diarrhoea, anorexia, depression,
ruffle feathers, head trembles, sleepiness and lameness can occur.
Poor immune response.
Kidney are swollen and contain urate deposits.
long-lasting immunosuppression due to destruction of immature lymphocytes in the bursa
of Fabricius, thymus, and spleen. The humoral (B cell) immune response is most severely
affected; the cell-mediated (T cell) immune response is affected to a lesser extent.
Chickens may exhibit severe prostration, incoordination, watery diarrhea, soiled vent
feathers, vent picking, and inflammation of the cloaca.
Flock morbidity is typically 100%, and mortality can range from 5%–20%.
The presence of maternal antibody will modify the clinical course of the disease.
11. POST MORTEM FINDINGS
Dead birds are in debilitated condition.
IBDV strains that cause subclinical disease (sometimes referred to as variant strains) cause
atrophy of the cloacal bursa without inflammation.
Chickens that have recovered from IBDV infections have small, atrophied, cloacal bursas due
to the destruction and lack of regeneration of the bursal follicles. In period of 3-8 days the
bursal organ losses physiological function and becomes smaller in size.
Bursa is double of its normal size, with necrotic foci and cheasy mass within its lumen. For
strains that cause a clinical disease, the cloacal bursa is swollen, edematous, yellowish, and
occasionally hemorrhagic, especially in birds that died of the disease. Bursa is edematous and
inflamed.
Dehydrated carcass,haemorrhages in brest and thigh muscle. Patechial hemorrhages in thigh
and legs are seenalso in liver and mucosa of intestine.
Kidney swollen and white in appearance due to dilatation of tubules of urates.
Enlarged spleen ,severe changes in caecal toncil,spleen,thymus and bone marrow. At
necropsy, the lesions seen will depend on the strain of IBDV. Caecal tonsils contains
hemorrhage and thick caseated mass.
12. DIAGNOSTICS
The bursa is most commonly used tissue for isolation of virus
ELISA is most common serological test for evaluation of virus antibodies.
Cell culture
Some strains of IBDV may also be isolated in cell cultures that include chicken embryo
fibroblasts, cells from the cloacal bursa, and established avian and mammalian cell lines.
Cell culture–adapted strains of IBDV produce a cytopathic effect and may be used for
quantitative titration of the virus and virus-neutralization assays.
13. DIAGNOSIS
Real-time PCR based Diagnostics:
Molecular diagnostic assays are most often used to identify IBDV in diagnostic samples.
They use reverse-transcriptase PCR. It has been proven as a valuable diagnostic tool for
rapid and sensitive detections of evolving pathogens in the environments to identify the viral
genome in bursa tissue.
Fluorescence probe based real-time PCR have been developed and are used in diagnostic
laboratory, i.e., for the detection and differentiation IBDV subtypes
Sequence analysis of the VP2 coding region has been used to further characterize the viruses.
Samples for molecular diagnostic testing are typically collected after maternal antibodies have
waned.
The other more commonly used advanced techniques include immuno-histochemistry (IHC),
in situ hybridization (ISH), and tissue microarrays.
The results from these techniques provide different information regarding the infectious
agents in the organ systems they involve .
14. CONTROL
The Managemental practice like all in ,all out can reduce the virus.
Formaldehyde and Iodophore shown to be effective disinfectant.
Vaccination is main method of control. Especially brooder flocks in order to provide maternal
Antibodies to their progeny for 1-3 weeks and booster with killed vaccine can be extended to
4-5 weeks.
Live vaccines of chicken embryo or cell-culture origin and of varying low pathogenicity can be
administered by eye drop, drinking water, or SC routes at 1–21 days of age.
Replication of these vaccines and thus the immune response can be altered by maternal
antibody, although the more virulent vaccine strains can override higher levels of maternal
antibody.
Vectored vaccines that express the IBDV VP2 protein in herpesvirus of turkeys (HVT) can be
used in ovo or at hatch.
These HVT-IBD vaccines are not affected by maternal antibodies. Vaccines that use
liveattenuated viruses bound to antibodies (immune-complex vaccines) are also available for in
ovo or at hatch administration.
