Murphy J R, Wisseman C L, Fiset P
Infect Immun. 1978 Dec;22(3):810-20. doi: 10.1128/iai.22.3.810-820.1978.
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.
在非免疫和免疫豚鼠中，研究了莫氏立克次体在皮内接种部位皮肤的感染情况，涉及感染动态、立克次体在组织内的定位以及大体和微观病理学。将莫氏立克次体皮内接种到非免疫豚鼠体内会导致大体病变，其严重程度与接种的立克次体数量直接相关。病变在3或4天内逐渐扩大，并至少持续扩大7天。组织学检查显示早期为急性炎症，随后发展为以单核细胞 - 巨噬细胞为主的炎症，随后浓缩为含淋巴细胞的肉芽肿病灶。接种部位皮肤中的立克次体数量从6小时到3天不断增加，与弥漫性单核细胞 - 巨噬细胞炎症反应的增加平行，然后在第4或5天随着肉芽肿病灶的出现而显著下降。然而，一些立克次体至少持续到第7天。荧光抗体研究表明，莫氏立克次体仅感染了一部分可用细胞，即与微血管系统相关的细胞。在远离接种点的皮肤部位发现立克次体，证明了感染的传播。通过在皮内攻击前12天皮内感染莫氏立克次体而产生免疫的免疫豚鼠表现出加速反应。病变在24至48小时达到最大，随后消退。免疫豚鼠的炎症反应比同样受到攻击的非免疫豚鼠的反应更强烈，并且从急性炎症到肉芽肿病变形成的反应加速。免疫豚鼠皮肤中的立克次体数量从接种时开始稳步下降，直到第3天或之后未再检测到立克次体。此外，未证明立克次体传播到远离接种部位的皮肤部位。从发病机制和对斑疹伤寒的免疫方面对结果进行了讨论。
