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青霉素诱导的屎肠球菌裂解与必需青霉素结合蛋白的饱和及脂磷壁酸释放的相关性

Correlation of penicillin-induced lysis of Enterococcus faecium with saturation of essential penicillin-binding proteins and release of lipoteichoic acid.

作者信息

al-Obeid S, Gutmann L, Williamson R

机构信息

Laboratoire de Microbiologie Médicale, Université Pierre et Marie Curie, France.

出版信息

Antimicrob Agents Chemother. 1990 Oct;34(10):1901-7. doi: 10.1128/AAC.34.10.1901.

Abstract

Clinical isolates of Enterococcus faecium that had a range of susceptibilities to penicillin were found to differ significantly in their responses to the antibiotic. In the penicillin-susceptible group (MIC, less than or equal to 4 micrograms/ml), the cessation of growth (bacteriostasis) at 10 x the MIC of penicillin appeared to correlate with the inhibition of penicillin-binding protein (PBP) 5*, whereas the onset of lysis (bactericidal effect) at higher antibiotic concentrations (100 x the MIC) was concomitant with the inhibition of the lower-affinity PBP 5. In contrast, in the resistant (MIC, greater than or equal to 8 micrograms/ml) group (in which most of the strains did not contain PBP 5*), the degree of saturation of PBP 5 seemed to determine the physiological response to the antibiotic: low levels of saturation caused growth inhibition, whereas almost complete saturation correlated with lysis. The penicillin-induced cell lysis of both penicillin-susceptible and -resistant strains was attributed, at least in part, to the extensive loss of acylated lipoteichoic acid into the growth medium.

摘要

已发现对青霉素具有不同敏感性的粪肠球菌临床分离株对抗生素的反应存在显著差异。在青霉素敏感组(最低抑菌浓度[MIC]小于或等于4微克/毫升)中,青霉素MIC的10倍浓度时生长停止(抑菌作用)似乎与青霉素结合蛋白(PBP)5的抑制相关,而在更高抗生素浓度(MIC的100倍)时裂解开始(杀菌作用)则与低亲和力PBP 5的抑制同时出现。相比之下,在耐药组(MIC大于或等于8微克/毫升)中(其中大多数菌株不含PBP 5),PBP 5的饱和程度似乎决定了对抗生素的生理反应:低饱和度水平导致生长抑制,而几乎完全饱和则与裂解相关。青霉素敏感和耐药菌株的青霉素诱导细胞裂解至少部分归因于酰化脂磷壁酸大量流失到生长培养基中。

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