Murphy J R, Wisseman C L, Fiset P
Infect Immun. 1978 Aug;21(2):417-24. doi: 10.1128/iai.21.2.417-424.1978.
Rickettsia mooseri infection has been studied in syngeneic guinea pigs inoculated intradermally with the objective of developing a model for the study of immune mechanisms. Characterization of infection included the following: a study of replication, dissemination, and clearance of rickettsiae; measurement of the antibody response with different rickettsial antigens and tests; and attempts to measure the cell-mediated immune response using the correlate of delayed-type hypersensitivity skin reactions. Following intradermal inoculation, rickettsiae replicate locally and then spread to the draining lymph nodes and subsequently cause systemic infection. Spread to draining lymph nodes occurred before the appearance of circulating antibody, whereas systemic infection occurred afterwards. Two distinct patterns of acquired resistance developed. The first was marked by a cessation of rickettsial growth within a given organ and the second by a clearance of rickettsiae. The duration of each of these phases differed markedly from one organ to another. Delayed-type hypersensitivity was not demonstrated by skin testing.
为了建立一个研究免疫机制的模型,已在同基因豚鼠身上进行了莫氏立克次体感染的研究,这些豚鼠通过皮内接种。感染的特征包括以下方面:对立克次体的复制、传播和清除进行研究;用不同的立克次体抗原和试验测量抗体反应;并尝试利用迟发型超敏皮肤反应的相关指标来测量细胞介导的免疫反应。皮内接种后,立克次体在局部复制,然后扩散到引流淋巴结,随后引起全身感染。在循环抗体出现之前,立克次体已扩散到引流淋巴结,而全身感染则在之后发生。出现了两种不同的获得性抗性模式。第一种模式的特点是在特定器官内立克次体生长停止,第二种模式的特点是立克次体被清除。这些阶段在不同器官中的持续时间差异显著。皮肤试验未显示迟发型超敏反应。