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The response of host cells L929 infected with causative agent of spotted fever group (SFG) rickettsiosis in Japan, the Katayama strain, was studied by electron microscopy. The rickettsiae penetrated the cytoplasm and multiplied here and after prolonged incubation progressed into the dilated cisternae of rough endoplasmic reticulum (rER), the perinuclear space, the deep invaginated nuclear membrane, and then the nucleoplasm of the host cells. The intranuclear rickettsiae showed different states: one type was enclosed by the double membrane of the host cell and the other type was free in the nucleoplasm. In addition to these double membrane‐bound and membrane‐free intranuclear rickettsiae, various membrane structures, including rER‐like structures, were also found in the nucleus. The cells infected with the rickettsiae underwent distinctive morphological alterations which occurred mainly within intracellular membranes of the host cells. These findings indicate the possibility that the intracellular membranes are characteristic cytopathological sites in rickettsia‐host cell interaction, and that these alterations may be related to a possible route of rickettsial penetration into the nucleus: passage through vesicles formed from invaginations in the nuclear membrane.

Since 1984, it has been known that spotted fever group rickettsiosis exists in Japan. We isolated three strains of the causative rickettsiae, designated Katayama, Misaka, and Abe, from patients with the disease and studied the characteristics of the isolates. Nude mice and cyclophosphamide-treated mice died after infection with the isolates. However, infected normal mice recovered and acquired immunity. Infected adult male guinea pigs had fever, a scrotal reaction, and seroconversion. The isolates propagated well in tissue-cultured Vero cells. Analysis by the cross-immunofluorescence antibody method showed that these isolates were closely related serologically. To reveal their immunological properties in detail, we produced 21 anti-Katayama monoclonal antibodies. Seven of these antibodies reacted with all representative strains of spotted fever group rickettsiae used in this study, and five others reacted only with the homologous strain, revealing that the Katayama strain has a strain-specific antigen(s) different from those of other spotted fever group rickettsiae. Moreover, these strain-specific antibodies also reacted with the Misaka and Abe strains. These results demonstrate that the causative agent of spotted fever group rickettsiosis in Japan is a new serotype of spotted fever group rickettsiae.