Groves M G, Kelly D J
Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
Infect Immun. 1989 May;57(5):1476-82. doi: 10.1128/iai.57.5.1476-1482.1989.
Pathogenicity of Rickettsia tsutsugamushi for laboratory mice is known to be influenced by at least three factors: (i) route of inoculation, (ii) antigenic strain, and (iii) natural resistance of the host. By using Karp, Gilliam, and Kato strains of R. tsutsugamushi, we examined the effect of these three pathogenicity factors on the kinetics of infection and the development of immunity in BALB/cDub and C3H/HeDub mice. The appearance of rickettsemia in the pathogenic infections generally preceded infections of reduced pathogenicity by 1 to 2 days in both magnitude and time of onset. Mice infected by the subcutaneous route with normally pathogenic rickettsiae, i.e., Gilliam-infected C3H/HeDub mice and Karp-infected BALB/cDub mice, consistently maintained a detectable rickettsemia over a 1-year period. Rickettsiae were recovered from the spleens of 95% (19 of 20) of these mice 52 weeks postinfection. In contrast, mice with infections of reduced pathogenicity, i.e., BALB/cDub mice infected by intraperitoneal and subcutaneous inoculation with Gilliam, did not have detectable rickettsemia from week 20 through week 52 postinfection except for a single mouse on week 44 postinfection. Rickettsiae were detected in the spleens of only 40% (8 of 20) of these mice after 1 year. In both Gilliam-infected mouse strains, protection against heterologous challenge with Karp or Kato rickettsial strains was incomplete up to 7 days postimmunization. Infections of reduced pathogenicity did not result from an enhanced systemic immune response by the host. The onset of the humoral response was not different for the pathogenic and reduced-pathogenicity infections. Pathogenicity differences seemed to result from the more rapid growth of the rickettsiae in the pathogenic infections.
（i）接种途径，（ii）抗原菌株，以及（iii）宿主的天然抵抗力。通过使用恙虫病立克次氏体的Karp、Gilliam和Kato菌株，我们研究了这三个致病性因素对BALB/cDub和C3H/HeDub小鼠感染动力学和免疫发展的影响。在致病性感染中，立克次体血症的出现通常在致病性降低的感染之前，在数量和发病时间上提前1至2天。通过皮下途径感染正常致病性立克次体的小鼠，即感染Gilliam的C3H/HeDub小鼠和感染Karp的BALB/cDub小鼠，在1年时间内始终保持可检测到的立克次体血症。感染后52周，从这些小鼠的脾脏中回收了95%（20只中的19只）的立克次体。相比之下，致病性降低的感染小鼠，即通过腹腔内和皮下接种Gilliam感染的BALB/cDub小鼠，除了感染后第44周的一只小鼠外，在感染后第20周至第52周没有可检测到的立克次体血症。1年后，这些小鼠中只有40%（20只中的8只）的脾脏中检测到立克次体。在两种感染Gilliam的小鼠品系中，在免疫后7天内，对用Karp或Kato立克次体菌株进行的异源攻击的保护都是不完全的。致病性降低的感染并非由宿主增强的全身免疫反应所致。致病性感染和致病性降低的感染的体液反应开始时间没有差异。致病性差异似乎是由于立克次体在致病性感染中生长更快所致。
