Rickettsiae and hosts.

Abstract

Protective immunity to Rickettsia tsutsugamushi in a murine model is dependent upon the development of cell mediated immunity, as demonstrated by lymphocyte transfer, production of lymphokines and -interferon by thymus-derived lymphocytes, activation of macrophages by lymphokines and demonstration of delayed-type hypersensitivity response following exposure to these organisms. Infection of mice with small numbers of Rickettsia typhi inoculated by a peripheral route leads to a more complex pattern of immune development, with a distinction between resistance to local and systemic infection. Nevertheless, thymus-derived lymphocytes and activated macrophages play a major role in modulating pathogenesis of infection, and delayed-type hypersensitivity responses are evident. Spotted fever group rickettsiae also elicit a cell-mediated response in rodents, and protection against Rickettsia conorii infection has been achieved by adoptive transfer of thymus-derived lymphocytes from immune animals. Limited studies with Rickettsia akari suggest that activation of mouse macrophages is critical to host survival following infection with this organism.