- Infectious bursal disease
Infectious bursal disease (IBD) is a highly contagious disease of young
chicken s caused by "infectious bursal disease virus" (IBDV),cite book |chapterurl=http://www.horizonpress.com/rnav|author=Caston et al|year=2008|chapter=Infectious Bursal Disease Virus (IBDV)|title=Segmented Double-stranded RNA Viruses: Structure and Molecular Biology|publisher=Caister Academic Press|id= [http://www.horizonpress.com/rnav ISBN 978-1-904455-21-9] ] characterized byimmunosuppression and mortality generally at 3 to 6 weeks of age. The disease was first discovered inGumboro, Delaware in1962 . It is economically important to the poultry industry worldwide due to increased susceptibility to other diseases and negative interference with effectivevaccination . In recent years, very virulent strains of IBDV (vvIBDV), causing severe mortality in chicken, have emerged inEurope ,Latin America ,South-East Asia ,Africa and theMiddle East .IBDV is a double stranded
RNA virus that has a bi-segmentedgenome and belongs to the genus "Avibirnavirus " of family "Birnaviridae ". There are two distinct serotypes of the virus, but only serotype 1 viruses cause disease in poultry. [cite web | title = Infectious Bursal Disease: Introduction | work = The Merck Veterinary Manual | date = 2006 | url = http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/203100.htm | accessdate = 2007-06-26 ] At least sixantigen ic subtypes of IBDV serotype 1 have been identified by "in vitro " cross-neutralization assay. Viruses belonging to one of these antigenic subtypes are commonly known as variants, which were reported to break through high levels of maternal antibodies in commercial flocks, causing up to 60 to 100 percent mortality rates in chickens. With the advent of highly sensitive molecular techniques, such asreverse transcription polymerase chain reaction (RT-PCR) andrestriction fragment length polymorphism (RFLP), it became possible to detect the vvIBDV, to differentiate IBDV strains, and to use such information in studying the molecular epidemiology of the virus.IBDV genome consists of two segments, A and B, which are enclosed within a nonenveloped icosahedral
capsid . [ICTVdB Management (2006). 00.009.0.02.001. Infectious bursal disease virus. In: ICTVdB - The Universal Virus Database, version 4. Büchen-Osmond, C. (Ed), Columbia University, New York, USA [http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/] ] The genome segment B (2.9 kb) encodes VP1, the putative viralRNA polymerase . The larger segment A (3.2 kb) encodes viral proteins VP2, VP3, VP4, and VP5. Among them, VP2 protein contains important neutralizing antigenic sites and elicits protective immune response and most of theamino acid (AA) changes between antigenically different IBDVs are clustered in the hypervariable region of VP2. Thus, this hypervariable region of VP2 is the obvious target for the molecular techniques applied for IBDV detection and strain variation studies.Viral structure
The IBDV capsid protein exhibits structural domains that show homology to those of the
capsid proteins of some positive-sense single-stranded RNA viruses, such as thenodavirus es andtetravirus es, as well as the T=13 capsid shell protein of the "Reoviridae ". The T=13 shell of the IBDV capsid is formed by trimers of VP2, a protein generated by removal of the C-terminal domain from its precursor, pVP2. The trimming of pVP2 is performed on immature particles as part of the maturation process. The other major structural protein, VP3, is a multifunctional component lying under the T=13 shell that influences the inherent structural polymorphism of pVP2. The virus-encoded RNA-dependentRNA polymerase , VP1, is incorporated into the capsid through its association with VP3. VP3 also interacts extensively with the viral dsRNA genome.cite book |chapterurl=http://www.horizonpress.com/rnav|author=Caston et al|year=2008|chapter=Infectious Bursal Disease Virus (IBDV)|title=Segmented Double-stranded RNA Viruses: Structure and Molecular Biology|publisher=Caister Academic Press|id= [http://www.horizonpress.com/rnav ISBN 978-1-904455-21-9] ]Pathogenesis
The virus is attracted to lymphoid cells and especially those of B-lyphocyte origins. Young birds at around two to eight weeks of age that have highly active Bursa of Fabricius are more succeptible to disease. Birds over eight weeks are resistant to challenge and will not show clinical sings unless infected by highy virulent strains.After ingestion, the virus destroys the lymphoid follicles in the Bursa of Fabricius as well as the circulating B-cells in the secondary lyphoid tissues such as GALT (gut-associated lymphoid tissue) CALT (conjuntiva) BALT (Bronchial) caecal tonsils Harderian gland etc. Acute disease and death is due to the necrotizing affect of these viruses on the host tissue. If the bird survives and recovers from thise phase of the disease, they remain immunocompromised which means they are more succeptible to other diseases and vaccination in the face of outbreak will not be effective.Passive immunity protects against disease, as does previous infection with avirulent strains. In broiler farms, breeder flocks are immunised against IBD so that they would confere protective antibodies to their progenies which would be slaughtered for consumption before their passive immunity wears out.
Clinical Signs
In the acute form birds are depressed, debilitated and dehydrated. They produce watery diarrhoea and have swollen, blood-stained vent. Mortality rates vary with virulence of the strain involved, the challenge dose as well as the flock's ability to mount an effective immune response. Infectioun with less virulent strains may not show overt clinical signs but the birds may have fibrotic or cystic Bursa of Fabricus that has atropied prematurely (before six months of age) and may die of infections by agents that would not usually cause disease in immunocompetent birds.
ee also
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Double-stranded RNA viruses
*Animal virology References
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