Response to Salmonella enteritidis Infection by the Immunocompromised Avian Host

To develop knowledge of the avian immune response and improve the ability of chickens to resist infection by Salmonella enteritidis (SE), the role of the different components of the immune response against SE infection was examined. Birds were given treatments with cyclophosphamide, cyclosporine A, or testosterone propionate to induce immunological deficiency, and experiments were performed to determine the effects of each on the immune response. Each treatment reduced hatch rate, survival rate, and rate of weight gain. As measured by flow cytometry, treatments with cyclophosphamide and testosterone propionate decreased the percentages of B cells to background levels and increased the percentages of CT8 cells significantly above controls. The intestinal shed rate of SE increased after treatment with testosterone propionate and cyclophosphamide, but dissemination to the spleen of infected birds was not different from controls for any treatment. The SE infection was also immunosuppressive as measured by the proliferative response to mitogenic stimulation. Maximum lymphocyte proliferation occurred 1 wk after infection in response to .5 micrograms concanavalin A per 10(6) cells. By the 2nd wk, proliferation dropped 10-fold to almost no response. Results showed that immunocompetence relied on interdependent functions of multiple components of the immune response, i.e., aspects of both humoral and cell-mediated immunity.