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一个用于证明β-内酰胺酶相关抗生素捕获可能是一种潜在耐药机制的模型系统。

A model system to demonstrate that beta-lactamase-associated antibiotic trapping could be a potential means of resistance.

作者信息

Gutmann L, Williamson R

出版信息

J Infect Dis. 1983 Aug;148(2):316-21. doi: 10.1093/infdis/148.2.316.

Abstract

Addition of beta-lactamase to cultures of antibiotic-sensitive Escherichia coli protected the bacteria against lysis induced by either a hydrolyzable (cephalothin) or relatively nonhydrolyzable (ceftriaxone) cephalosporin. The later addition of a nonhydrolyzable, non-lysis-inducing beta-lactam antibiotic (oxacillin), which had a higher affinity for the beta-lactamase than ceftriaxone, allowed the reversal of the protection and the onset of lysis. These results suggest that trapping of the antibiotic by the enzyme, without significant hydrolysis, is a reversible process that may play a role in the resistance of some gram-negative bacteria to third-generation cephalosporins.

摘要

向对抗生素敏感的大肠杆菌培养物中添加β-内酰胺酶,可保护细菌免受可水解(头孢噻吩)或相对不可水解(头孢曲松)的头孢菌素诱导的裂解。后来添加一种对β-内酰胺酶亲和力高于头孢曲松的不可水解、不诱导裂解的β-内酰胺抗生素(苯唑西林),可使保护作用逆转并开始裂解。这些结果表明,酶对抗生素的捕获在没有显著水解的情况下是一个可逆过程,可能在一些革兰氏阴性菌对第三代头孢菌素的耐药性中起作用。

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