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拓扑异构酶突变的联合效应在大肠杆菌对氟喹诺酮耐药性中的作用

Contributions of the combined effects of topoisomerase mutations toward fluoroquinolone resistance in Escherichia coli.

作者信息

Morgan-Linnell Sonia K, Zechiedrich Lynn

机构信息

Department of Molecular Virology and Microbiology, Baylor College of Medicine, One Baylor Plaza, Mail-stop BCM-280, Houston, TX 77030-3411, USA.

出版信息

Antimicrob Agents Chemother. 2007 Nov;51(11):4205-8. doi: 10.1128/AAC.00647-07. Epub 2007 Aug 6.

DOI:10.1128/AAC.00647-07
PMID:17682104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2151436/
Abstract

In defined, isogenic strains, at least three mutations, two of which must be in gyrA, were required to exceed the CLSI breakpoint for fluoroquinolone resistance. Strains with double mutations in both gyrA and parC had even higher MICs of fluoroquinolones than strains with totals of three mutations.

摘要

在特定的同基因菌株中，至少需要三个突变（其中两个必须位于gyrA基因）才能超过氟喹诺酮耐药性的CLSI断点。gyrA和parC基因均发生双突变的菌株，其氟喹诺酮的最低抑菌浓度（MIC）甚至高于总共发生三个突变的菌株。

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本文引用的文献

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Segregation of New Lysogenic Types during Growth of a Doubly Lysogenic Strain Derived from Escherichia Coli K12.源于大肠杆菌K12的双重溶源菌株生长过程中新溶源类型的分离
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