Takai S, Madarame H, Matsumoto C, Inoue M, Sasaki Y, Hasegawa Y, Tsubaki S, Nakane A
Department of Animal Hygiene, School of Veterinary Medicine and Animal Sciences, Kitasato University, Aomori, Japan.
FEMS Immunol Med Microbiol. 1995 Jun;11(3):181-90. doi: 10.1111/j.1574-695X.1995.tb00115.x.
Virulence of Rhocococcus equi ATCC 33701 and its plasmid-cured derivative ATCC 33701P- was compared in BALB/c and C3H/HeJ mice in terms of bacterial growth kinetics and histological changes in the liver, spleen and lungs, and humoral immune responses. Injection with a sublethal dose of 10(6) ATCC 33701 in mice resulted in microabscess formation after rapid multiplication in the liver and spleen by day 4, and then the bacteria were gradually eliminated with the formation of granuloma and the production of specific antibodies against 15- to 17-kDa antigens of the virulent bacteria. By contrast, ATCC 33701P- was avirulent as shown by early elimination of viable bacteria and no evidence of net multiplication in the organs. Histopathological changes consisted of only slight, transient infiltration of neutrophils and macrophages in the liver. Although live ATCC 33701P- did not evoke any humoral or histological responses in the mice, a large inoculum (10(8)) of killed ATCC 33701 and ATCC 33701P- resulted in the formation of granuloma in the liver and accelerated extramedullary hemopoiesis in the spleen. These results suggest that the pathogenesis of R. equi infection involves at least two important virulence determinants, both of which play critical roles in the disease: one is the virulence plasmid, which is required for R. equi to resist and grow within host cells; and the other is the granulomagenic activity that is related to the lipids and nature of the cell wall of the species, which induces the characteristic pathological changes.
在BALB/c和C3H/HeJ小鼠中，比较了马红球菌ATCC 33701及其质粒消除衍生物ATCC 33701P-在细菌生长动力学、肝脏、脾脏和肺部的组织学变化以及体液免疫反应方面的毒力。给小鼠注射亚致死剂量的10(6) ATCC 33701后，细菌在肝脏和脾脏中迅速繁殖，到第4天形成微脓肿，然后细菌逐渐被清除，同时形成肉芽肿并产生针对有毒力细菌15至17 kDa抗原的特异性抗体。相比之下，ATCC 33701P-无毒力，表现为活菌早期被清除，且器官中无净增殖迹象。组织病理学变化仅包括肝脏中中性粒细胞和巨噬细胞的轻微、短暂浸润。虽然活的ATCC 33701P-在小鼠中未引起任何体液或组织学反应，但大量接种（10(8)）的灭活ATCC 33701和ATCC 33701P-导致肝脏中形成肉芽肿，并加速脾脏中的髓外造血。这些结果表明，马红球菌感染的发病机制涉及至少两个重要的毒力决定因素，两者在疾病中都起关键作用：一个是毒力质粒，它是马红球菌在宿主细胞内抵抗和生长所必需的；另一个是与该菌种细胞壁的脂质和性质相关的致肉芽肿活性，它诱导特征性病理变化。
