Etiology and Transmission:

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

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. IBDV also may be isolated in cell cultures derived from the cloacal bursa and established cell lines, and some strains may be isolated in chicken-embryo fibroblasts. Cell-culture-adapted strains of IBDV produce a cytopathic effect, and such assays may be used for quantitative serological tests. Two serotypes of IBDV have been identified, and antigenic variation between strains within a serotype is considerable. Serotype 2 infects chickens and turkeys but does not cause significant clinical disease or immunosuppression.

“Variant” strains of IBDV, which have major antigenic differences from the “standard” strains, cause immunosuppression but not clinical disease in older chickens.

Clinical Findings:

Infectious bursal disease 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 normally subclinical. Chickens are most susceptible to clinical disease at 3-6 wk, but severe infections have occurred in Leghorn chickens up to 18 wk old.

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. Subclinical infections by the newer “variant” strains occur in immature birds, and severe long-term immunosuppression and bursal atrophy result from early infections.

In clinical infections, onset of the disease is sudden after an incubation of 3-4 days. Chickens exhibit severe prostration, incoordination, watery diarrhea, soiled vent feathers, vent picking, and inflammation of the cloaca. Losses range to >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.

Lesions:

At necropsy, the cloacal bursa is swollen, edematous, yellowish, and occasionally hemorrhagic, especially in birds that have died of the disease. Congestion and hemorrhage of the pectoral, thigh, and leg muscles is common. Chickens recovered from IBDV infections have small, atrophied, cloacal bursas due to the destruction and lack of regeneration of the bursal follicles.

Control:

There is no treatment. Depopulation and rigorous disinfection of contaminated farms have achieved limited success. Live vaccines of chick-embryo or cell-culture origin and of varying virulence can be administered by eye drop, drinking water, or SC routes at 1-21 days of age. The immune response can be altered by maternal antibody, and the more virulent vaccine strains can override higher levels of antibody.