Infectious Bursal Disease - Pathogenesis

Pathogenesis

Clinical disease is associated to bird age with the greatest bursal mass, which occurs between 3 and 6 weeks of age. The greatest bursal mass is mostly a result of a large population of maturing IgM-bearing B-lymphocytes (lymphoblasts), the main target of infection. Young birds at around two to eight weeks of age that have highly active bursa of Fabricius are more susceptible to disease. Birds over eight weeks are resistant to challenge and will not show clinical signs unless infected by highly virulent strains.

Subclinical disease occurs in chickens infected before three weeks of age. At this age the B-lymphoblast population is smaller and the systemic effects are insufficient for generating clinical signs. However, the B-cell destruction is usually most severe in subclinically infected young, as virus will destroy a smaller population and most cells in one place (the bursa).

After ingestion, the virus destroys the lymphoid follicles in the bursa of Fabricius as well as the circulating B-cells in the secondary lymphoid 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 effect of these viruses on the host tissues. Kidney failure is a common cause of mortality. If the bird survives and recovers from this phase of the disease, it remains immunocompromised which means it is more susceptible to other diseases.