Overview of Infectious Bursal Disease in Poultry

IBD is caused by a birnavirus (infectious bursal disease virus; IBDV) that is most readily isolated from the bursa of Fabricius but may be isolated from other organs. It is shed in the feces and transferred from house to house by fomites. It is very stable and difficult to eradicate from premises.

Two serotypes of IBDV have been identified. The serotype 1 viruses cause disease in chickens and, within them, antigenic variation can exist between strains. Antigenic drift is largely responsible for this antigenic variation, but antigenic differences can also occur through genome homologous recombination. Serotype 2 strains of the virus infect chickens and turkeys but have not caused clinical disease or immunosuppression in these hosts. IBDVs have been identified in other avian species, including penguins, and antibodies to IBDV have been seen in several wild avian species. The contribution of IBDV to disease in these wild birds is unknown.

IBD is highly contagious; results of infection depend on age and breed of chicken and virulence of the virus. Infections may be subclinical or clinical. Infections before 3 wk of age are usually subclinical. Chickens are most susceptible to clinical disease at 3–6 wk 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 wk of age.

Early subclinical infections are the most important form of the disease because of economic losses. They cause severe, 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 immunosuppressed by early IBDV infections do not respond well to vaccination and are predisposed to infections with normally nonpathogenic viruses and bacteria. Common diseases are usually exacerbated by IBDV infections. Some strains of IBDV can cause subclinical infections in older birds (3–6 wk old), which leads to losses from poor feed efficiency and longer times to market. In these cases, the immunosuppression is usually transient, and convalescent birds may recover most or all of their humoral immune function. However, secondary infections that occur during the transient immunosuppression can cause significant economic losses.

In clinical infections, onset of the disease occurs after an incubation of 3–4 days. 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%. Recovery occurs in <1 wk, and broiler weight gain is delayed by 3–5 days. The presence of maternal antibody will modify the clinical course of the disease.

Virulence of field strains of the virus varies considerably. Viruses that range from naturally attenuated to very virulent (vv) have been observed. The vvIBDV strains that can cause high mortality (>20%) were first detected in Europe. They spread throughout the Middle East, Asia, and Africa, were detected in South and Central America in 1999, and in the USA in 2009.

Molecular diagnostic assays are most often used to identify IBDV in diagnostic samples. They use reverse-transcriptase PCR to identify the viral genome in bursa tissue. 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. IBDV may be isolated in 8- to 11-day-old, antibody-free chicken embryos with inocula from birds in the early stages of disease. The chorioallantoic membrane is more sensitive to inoculation than is the allantoic sac. 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.

There is no treatment. Rigorous disinfection of contaminated farms after depopulation has achieved limited success. 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 live-attenuated viruses bound to antibodies (immune-complex vaccines) are also available for in ovo or at hatch administration.

High levels of maternal antibody during early brooding of chicks in broiler flocks (and in some commercial layer operations) can minimize early infection, subsequent immunosuppression, or both. Breeder flocks should be vaccinated one or more times during the growing period, first with a live vaccine and again just before egg production with an oil-adjuvanted, inactivated vaccine. Inactivated vaccines of chicken embryo, bursa, or cell-culture origin are available. The latter vaccines induce higher, more uniform, and more persistent levels of antibody than do live vaccines. The immune status of breeder flocks should be monitored periodically with a quantitative serologic test such as virus neutralization or ELISA. If antibody levels decrease, hens should be revaccinated to maintain adequate immunity in the progeny.

The goal of any vaccination program for IBD should be to use vaccines that most closely match the antigenic profile of the field viruses. Diagnostic testing for the genomic sequences of field strains can be used to select the most appropriate vaccination program.