Handwerger S, Kolokathis A
Department of Medicine, Beth Israel Medical Center, New York, NY 10003.
FEMS Microbiol Lett. 1990 Jul;58(2):167-70. doi: 10.1111/j.1574-6968.1990.tb13972.x.
Vancomycin resistance has recently been recognized among clinical isolates of enterococci. Resistance is inducible, and associated with production of a novel 39 kDa membrane protein. The mechanism by which exposure to vancomycin, which does not penetrate the cell membrane, induces resistance is unknown. In the vancomycin resistant strain Enterococcus faecium 228, resistance was also inducible by moenomycin, suggesting that inhibition of the transglycosylation step in peptidoglycan synthesis may be required for induction of resistance. Cytoplasmic pools of peptidoglycan precursors were increased after exposure to vancomycin or moenomycin, representing a potential means for regulation of induction.
最近在肠球菌临床分离株中发现了对万古霉素的耐药性。这种耐药性是可诱导的，并且与一种新的39 kDa膜蛋白的产生有关。万古霉素不能穿透细胞膜，但其暴露诱导耐药性的机制尚不清楚。在耐万古霉素的屎肠球菌228菌株中，莫能菌素也可诱导耐药性，这表明肽聚糖合成中糖基转移步骤的抑制可能是诱导耐药性所必需的。暴露于万古霉素或莫能菌素后，肽聚糖前体的细胞质池增加，这是调节诱导的一种潜在方式。
