The influence of thymic and bursal lymphoid systems in avian tuberculosis

Intact and immunologically deficient chickens inoculated with M avium were examined for structural changes in the spleen, the tuberculin reactions and antibody formation. Intravenous inoculation caused miliary tuberculosis of spleen and liver but not brain; intracerebral inoculation caused massive lymphocytic tuberculosis meningitis with later spread to spleen and liver. Neonatal bursectomy and thymectomy did not significantly alter the disease in terms of survival and lesion structure. Cortisone induced earlier development of lesions.In spleen, bacilli were first seen 5 days after inoculation in macrophages in the lymphoid sheath-particularly in capsules of germinal centers. Subsequent lesions were tubercles in the lymphoid sheath, hyperplasia of penicillar arteriolar sheaths, lymphoid atrophy and amyloid deposition. Tubercles were composed of infected macrophages located centrally and surrounded by lighter noninfected macrophages. Cell membranes were extensively interwined where these cells were in contact. Mycobacteria were present within dense, membrane-bound residual bodies.Antibody was first detected 8 days after inoculation in intact birds and persisted throughout the disease. Tuberculin reactions were mixtures of a perivascular monocytic response (delayed hypersensitivity) which developed early and was absent terminally, and a vasculonecrotic response which developed later and persisted to death of the bird. Both reactions occurred in the absence of detectable antibody in bursectomized birds.