Occurrence of an Infectious Bursal Syndrome Within an Australian Poultry Flock

Firth, G. A.

doi:10.1111/j.1751-0813.1974.tb05284.x

Cited by 41 publications

(14 citation statements)

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“…Infectious bursal disease, as it became known, was diagnosed in the UK in 1962 (Edwards, 1981). By the mid 1970s IBD was present in most countries with established poultry industries including Australia (Firth, 1974). New Zealand was free of the disease during the mid 1980s (Jones, 1986), but IBD was diagnosed in late 1993 and became endemic within months of the initial outbreak in Waikato (I?…”

Section: Introductionmentioning

confidence: 99%

Infectious bursal disease

Lasher¹,

Shane

1994

World's Poultry Science Journal

103

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Infectious bursal disease (IBD), caused by an avibirnavirus, has been an economically significant, widely distributed condition affecting immature chickens since 1960. The classical type 1 conventional strain is responsible for up to 5% mortality in susceptible flocks. As a result of immunosuppression, growth rate, liveability, and productivity may be adversely affected by subsequent exposure to a wide range of viral, bacterial, and protozoal agents. The emergence of highly pathogenic strains of IBD virus in 1988 caused heavy losses in broiler and replacement breeder and commercial egg pullets in Europe, and subsequently in Africa and Asia. The causal virus is extremely lymphocidal with an affinity for immature B cells resulting in bursal atrophy approximately four days after infection. IBD virus is resistant to environmental exposure and is transmitted laterally by direct and indirect contact between infected and susceptible flocks. Conventional IBD is controlled by immunization of parent stock followed by vaccination of progeny after maternal antibody levels have waned. Parent level stock is immunized by one or two successive doses of live, mild or intermediate strain, attenuated vaccine to prime the immune system, followed by inactivated oil emulsion vaccines at maturity and at the mid-point of the laying cycle to boost immunity and ensure transfer of protective maternal antibody to progeny. Highly pathogenic IBD is controlled by a number of alternative strategies, including administration of live vaccines of low attenuation or simultaneous doses of live intermediate strain attenuated vaccine with inactivated oil emulsion during the first week. All successful programmes require diligent care regarding handling and administration of vaccine. Serological monitoring using automated ELISA technology is an accepted method of confirming that flocks are adequately protected. In the future recombinant and subunit vaccines will be developed to control existing strains and the variants which will emerge in areas with a high density of poultry production. . (1988) Comparative studies on structural and antigenic properties of two serotypes of infectious bursal disease virus. Journal of General Virology 69: BENTON, W. J., COVER, M. S. and ROSENBERGER, J. K. (1967a) Studies on the transmission of the infectious bursal agent (IBA) of chickens. Avian Diseases 11: 430-438 BENTON, W. J., COVER, M. S., ROSENBERGER, J. K. and LAKE, R. S. (1967b) Physico-chemical properties of the infectious bursal agent (IBA) Avian Diseases 11: 438-445 BENGELSDORFF, H-J. and BERNHARDT, D. (1971) Serological examinations after vaccination of chicks with mouse-adapted infectious bursitis virus. Proceedings of the 19th World Veterinary Congress, Mexico City, Mexico 2: 786-787 BOX, P. (1988) Antibody profile of broiler breeders hens and their progeny immunized with bursalderived or embryo-origin killed infectious bursal disease vaccine.

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Section: Introductionmentioning

confidence: 99%

Infectious bursal disease

Lasher¹,

Shane

1994

World's Poultry Science Journal

103

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“…Two sources of IBD virus were used. The Australian isolate of IBD virus (002/73) used in all in vivo studies was originally described by Firth (1974) and identified serologically as type I IBD virus at the Central Veterinary Laboratory, Weybridge, U.K. Virus infectivity was titrated by inoculating 3-day-old SPF chickens intraocularly (i.o.)…”

Section: Methodsmentioning

confidence: 99%

Antibody to the 32K Structural Protein of Infectious Bursal Disease Virus Neutralizes Viral Infectivity in vitro and Confers Protection on Young Chickens

Fahey

O’Donnell

Bagust

1985

Journal of General Virology

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SUMMARYChicken sera containing IgG antibodies specific for the 32000 (32K) mol. wt. structural polypeptide of infectious bursal disease (IBD) virus, as assessed by Western blotting, neutralized the in vitro infectivity of tissue culture-adapted IBD virus. When injected into young chickens, the serum passively protected them from challenge with pathogenic IBD virus. Chickens immunized with the 32K structural polypeptide of IBD virus, prepared by electroelution from SDS-PAGE gels, produced antibody detectable by ELISA and the virus neutralization assay, while chickens immunized with the 37K or 41.5K viral polypeptides synthesized antibody detectable by ELISA, but only very low levels of virus-neutralizing antibody. The immunoglobulin fraction of sera obtained from chickens immunized with the 32K polypeptide, but not the 41.5K polypeptide, passively protected chickens from infection with IBD virus. It is concluded that the 32K polypeptide is a major protective immunogen of IBD virus.

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“…The Australian IBDV strains used included vaccine strains 002/73 and V877, 11 classical field strains (06/95, K-2, M-1, R-1, T-4, 01/96, N1/99, N2/99, A-1, SS-1, and Y5-3) and eight variant field strains (01/94, 02/95, 03/95, 04/95, 08/95, C-1, H-1, and 05-5) (Firth, 1974;Sapats & Ignjatovic, 2000;Ignjatovic & Sapats, unpublished results). Included also were three IBDV samples obtained from the same source as used in study of Jackwood & Sommer (1999) (Fort Dodge, Castle Hill, Australia).…”

Section: Virus Strainsmentioning

confidence: 99%

Restriction fragment length polymorphism analysis of the VP2 gene of Australian strains of infectious bursal disease virus

Sapats

Ignjatovic

2002

Avian Pathology

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Twenty-four Australian strains of infectious bursal disease virus (IBDV) were characterized by reverse transcription/polymerase chain reaction-restriction fragment length polymorphism and compared with previously published overseas strains. A primer pair designed to amplify a 743 base pair fragment of the VP2 gene was used and restriction fragment length polymorphism profiles were determined for each strain using three restriction enzymes, BstNI, MboI and SspI. Australian strains comprised 12 molecular groups that were unique and distinct from overseas IBDV strains. A specific SspI site that is used to predict a very virulent IBDV phenotype was absent from all Australian strains, contrary to a previous finding by Jackwood and Sommer (1999). One Australian strain (N1 /99 ) contained an SspI site; however, this was located at a different position than that found in very virulent IBDV strains. The results demonstrate that restriction fragment length polymorphism can be used to rapidly differentiate Australian IBDV strains from overseas strains. However, the existence of a large number of molecular groups might preclude its effectiveness for inter-strain differentiation.

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Occurrence of an Infectious Bursal Syndrome Within an Australian Poultry Flock

Cited by 41 publications

References 0 publications

Infectious bursal disease

Infectious bursal disease

Antibody to the 32K Structural Protein of Infectious Bursal Disease Virus Neutralizes Viral Infectivity in vitro and Confers Protection on Young Chickens

Restriction fragment length polymorphism analysis of the VP2 gene of Australian strains of infectious bursal disease virus

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