Williamson R, Al-Obeid S, Shlaes J H, Goldstein F W, Shlaes D M
Laboratoire de Microbiologie Médicale, Université de Paris VI, France.
J Infect Dis. 1989 Jun;159(6):1095-104. doi: 10.1093/infdis/159.6.1095.
Strain D366, a clinical isolate of Enterococcus faecium, is resistant (minimum inhibitory concentration [MIC] 32 mg/L) to vancomycin. When exponential-phase cultures were exposed to half the MIC of vancomycin, a lag of 3-4 h occurred before growth resumed. Cells preexposed to 1/2 MICs of vancomycin did not show any lag. Pregrowth of D366 with vancomycin caused resistance to all glycopeptides tested. Pregrowth in vancomycin resulted in synthesis of a 3.95-kDa cytoplasmic-membrane-associated protein. This protein was correlated with resistance in mutants with high-level resistance, in the presence of NaCl, which inhibited the activity of vancomycin, and when several glycopeptides with varying activities were tested. Vancomycin-grown cells appeared abnormal and lysed at a much slower rate than did normal cells. We conclude that (1) vancomycin resistance in D366 is inducible; (2) resistance is correlated with the synthesis of 39.5-kDa cytoplasmic membrane protein; and (3) this protein play an additional role in the inhibition of normal lytic functions.
屎肠球菌临床分离株D366对万古霉素耐药（最低抑菌浓度[MIC]为32 mg/L）。当对数生长期培养物暴露于万古霉素MIC的一半时，生长恢复前出现3 - 4小时的延迟期。预先暴露于万古霉素1/2 MIC的细胞未显示任何延迟期。用万古霉素对D366进行预培养导致对所有测试的糖肽产生耐药性。在万古霉素中预培养导致合成一种3.95 kDa的与细胞质膜相关的蛋白质。在存在抑制万古霉素活性的氯化钠时，以及在测试几种活性不同的糖肽时，这种蛋白质与具有高水平耐药性的突变体中的耐药性相关。用万古霉素培养的细胞显得异常，且裂解速度比正常细胞慢得多。我们得出结论：（1）D366中的万古霉素耐药性是可诱导的；（2）耐药性与39.5 kDa细胞质膜蛋白的合成相关；（3）这种蛋白质在抑制正常裂解功能中起额外作用。
