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Rickettsia typhi<\/jats:named-content>belongs to the typhus group (TG) of this family and is the causative agent of endemic typhus, a disease that can be fatal. In the present study, we analyzed the course of<jats:named-content content-type=\"genus-species\">R. typhi<\/jats:named-content>infection in C57BL\/6 RAG1<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Although these mice lack adaptive immunity, they developed only mild and temporary symptoms of disease and survived<jats:named-content content-type=\"genus-species\">R. typhi<\/jats:named-content>infection for a long period of time. To our surprise, 3 to 4 months after infection, C57BL\/6 RAG1<jats:sup>\u2212\/\u2212<\/jats:sup>mice suddenly developed lethal neurological disorders. Analysis of these mice at the time of death revealed high bacterial loads, predominantly in the brain. This was accompanied by a massive expansion of microglia and by neuronal cell death. Furthermore, high numbers of infiltrating CD11b<jats:sup>+<\/jats:sup>macrophages were detectable in the brain. In contrast to the microglia, these cells harbored<jats:named-content content-type=\"genus-species\">R. typhi<\/jats:named-content>and showed an inflammatory phenotype, as indicated by inducible nitric oxide synthase (iNOS) expression, which was not observed in the periphery. Having shown that<jats:named-content content-type=\"genus-species\">R. typhi<\/jats:named-content>persists in immunocompromised mice, we finally asked whether the bacteria are also able to persist in resistant C57BL\/6 and BALB\/c wild-type mice. Indeed,<jats:named-content content-type=\"genus-species\">R. typhi<\/jats:named-content>could be recultivated from lung, spleen, and brain tissues from both strains even up to 1 year after infection. 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