Mechanisms of immunity in typhus infection: some characteristics of intradermal Rickettsia mooseri infection in normal and immune guinea pigs.

Rickettsia mooseri infection in skin at sites of intradermal inoculation was studied in nonimmune and immune guinea pigs with respect to dynamics of infection, localization of rickettsiae within tissues, and gross and microscopic pathology. Intradermal inoculation of R. mooseri into nonimmune guinea pigs resulted in gross lesions which, in magnitude, were directly related to the number of rickettsiae inoculated. The lesions progressively enlarged through 3 or 4 days and remained enlarged through at least 7 days. Histological examination revealed an early acute inflammation which progressed to a predominantly monocyte-macrophage inflammation and subsequently condensed into lymphocyte-containing granulomatous foci. Rickettsiae in the skin at sites of inoculation increased in numbers from 6 h through 3 days, in parallel with the increasing diffuse monocyte-macrophage inflammatory response, and then declined markedly on days 4 or 5 as ganulomatous foci appeared. Some rickettsiae, however, persisted through at least day 7. Fluorescent-antibody studies suggested that R. mooseri infected only a subset of cells available, i.e., cells associated with the microvascular system. Dissemination of infection was demonstrated by the presence of rickettsiae in the skin at sites distant from the point of inoculation. Immune guinea pigs, made immune by intradermal infection with R. mooseri 12 days before intradermal challenge, displayed an accelerated response. The lesions were maximal by 24 to 48 h and subsequently regressed. The inflammatory response of immune guinea pigs was a greater magnitude than the response of similarly challenged nonimmune guinea pigs, and the respose from acute inflammation through the formation of granulomatous lesions was accelerated. The number of rickettsiae in the skin of immune guinea pigs declined steadily from the time of inoculation, until no rickettsiae were recovered on or after day 3. Furthermore, dissemination of rickettsiae to sites in skin distant from the site of inoculation was not demonstrable. The results are discussed in terms of pathogenesis and of immunity to typhus.