Infectious bursal disease

Abstract

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.

Extensive antigenic changes in an atypical isolate of very virulent infectious bursal disease virus and experimental clinical control of this virus with an antigenically classical live vaccine

“…Although both live and inactivated vaccines have been developed to control IBD in intensively grown poultry, difficulties may occur in implementing these vaccines in combination with efficient sanitary measures under field conditions. Such difficulties may explain why IBD-induced immunosuppression is still frequently encountered and represents a major threat to the control by vaccination of other infectious diseases affecting intensively grown poultry (Lasher & Shane, 1994).…”

“…Serotype 1 IBDV replicates in and induces lysis of the IgM-bearing B lymphocytes (Hirai et al, 1981), mainly in the bursa of Fabricius, thus causing a major fatal or immunosuppressive condition in young chickens. The disease has been recognized worldwide since the mid-1970s (Cosgrove, 1962; for a review, see Lasher & Shane, 1994). Although both live and inactivated vaccines have been developed to control IBD in intensively grown poultry, difficulties may occur in implementing these vaccines in combination with efficient sanitary measures under field conditions.…”

Sequence Comparison of the VP2 Variable Region of Infectious Bursal Disease Virus Isolates from Vietnam.

“…A phylogenetic tree was prepared by the neighbor-joining method. Deduced amino acid sequences used for comparison were obtained from the following accession numbers: 002-73, accession X03993 [12]; 52/70, accession Infectious bursal disease (IBD), caused by infectious bursal disease virus (IBDV), is a highly contagious disease of young chickens that results in significant losses to the poultry industry worldwide [19]. The disease primarily affects the bursa of Fabricius of chickens between 3 and 6 weeks of age, resulting in reduced feed efficiency, reduced weight gain, increased mortality, and immunosuppression [11,24].…”

Effect of dietary supplementation of trace elements on blood chemistry and selected immunological indices depending on the age of broiler chickens

“…The titres of infectious bursal disease virus (IBDV) antibodies significantly increased in the blood serum of broilers at the day 21 in comparison to the day 35, although we did not vaccinate the birds against this disease. Our explanation is based on the transovarial transfer of maternal antibodies into egg yolk (Lasher and Shane 1994), as a result of routine vaccination of Results are presented as mean ± S.D., n = 15 Significant differences at the day 21 vs. day 36, and the day 36 vs. day 42 (*P < 0.05; **P < 0.01; ***P < 0.001) At the day 21, the activity of blood glutathione peroxidase (GSH-Px) was found to be significantly higher in chickens supplemented with Na 2 SeO 3 compared to selenized yeast, thereafter no differences due to the form of Se administered were found, indicating that the GSH-Px activity reaches a plateau in all groups of broilers (Fig. 1).…”