Singh K V, Qin X, Weinstock G M, Murray B E
Center for the Study of Emerging and Re-emerging Pathogens, University of Texas Medical School at Houston, USA.
J Infect Dis. 1998 Nov;178(5):1416-20. doi: 10.1086/314453.
A previously described mouse peritonitis model was used to study derivatives of Enterococcus faecalis strain OG1RF. The addition of sterile rat fecal extracts (SRFE) lowered the LD50 of OG1RF >10-fold. Hemolysin production caused a 35-fold lower LD50 and a much shorter survival, similar to previous results using a peritonitis model without SRFE. A purine (but not a pyrimidine) auxotroph was considerably less lethal than wild type; gelatinase mutants were also attenuated. A suicide vector was generated with an enterococcal selectable marker in order to disrupt a gene encoding an E. faecalis antigen; the resulting mutant was not attenuated despite a slower growth rate. In conclusion, this model allows attenuated mutants to be detected, corroborates prior reports that hemolysin is a virulence factor, and suggests a role for gelatinase in virulence of E. faecalis in mice; the attenuated purine auxotroph may provide a system for developing vectors for in vivo expression systems.
使用先前描述的小鼠腹膜炎模型来研究粪肠球菌OG1RF菌株的衍生物。添加无菌大鼠粪便提取物（SRFE）可使OG1RF的半数致死剂量（LD50）降低10倍以上。溶血素的产生导致LD50降低35倍，存活时间大大缩短，这与先前使用无SRFE的腹膜炎模型的结果相似。嘌呤（而非嘧啶）营养缺陷型的致死性远低于野生型；明胶酶突变体也减弱了毒性。构建了一个带有肠球菌选择标记的自杀载体，以破坏编码粪肠球菌抗原的基因；尽管生长速度较慢，但产生的突变体并未减弱毒性。总之，该模型能够检测出减毒突变体，证实了先前关于溶血素是一种毒力因子的报道，并表明明胶酶在粪肠球菌对小鼠的毒力中起作用；减毒的嘌呤营养缺陷型可能为开发体内表达系统的载体提供一个系统。
