Abstract

The effects of chicken anemia virus (CAV) and infectious bursal disease virus (IBDV) coinfection in commercial layer-type and meat-type (broiler) chickens with specific maternal immunity were evaluated. In addition, the broiler progeny used had been vaccinated in ovo against IBDV. Layer chickens were inoculated intramuscularly on day 3 of age with CAV and orally on day 7 of age with an IBDV standard strain (APHIS). Broiler chickens were exposed to CAV and/or an IBDV variant strain (AL2) via the drinking water on days 3 and 14 of age. Following CAV and IBDV inoculation neither mortality nor overt clinical disease was observed in any layer or broiler group. In spite of maternal immunity against both IBDV and CAV, mean hematocrits of all layer groups inoculated with CAV (CAV, CAV + APHIS) were lower than uninfected chickens. IBDV APHIS alone or in combination with CAV did not affect the layer weight gain. However, on day 30 of age and concomitantly with maternal antibody decay, bursa lymphocyte depletion became evident in CAV + APHIS-infected layer chickens. These birds (CAV + APHIS) also seroconverted to IBDV on day 35 of age. CAV persisted at low levels in the layer chickens throughout the experimental period in CAV- and CAV+APHIS-infected chickens. Similarly, infected broiler chickens did not show changes in weight gain. Compared to CAV-infected or uninfected controls, CAV+AL2- and AL2-infected broiler chickens showed significant lymphocyte depletion in the bursa as assessed both by bursal indices and histomorphometry. Broilers also seroconverted to IBDV after day 30 of age confirming that bursal lymphocyte depletion was due to IBDV resuming replication. Thymus histomorphometry revealed significant lymphocyte depletion in all infected broiler groups at 30 days of age, but only in CAV+AL2-infected broiler chickens at 41 days of age, suggesting that IBDV infection delayed repopulation of the thymus.