肺炎克雷伯菌临床分离株中对替加环素耐药性降低与 ramR 突变有关。
ramR mutations in clinical isolates of Klebsiella pneumoniae with reduced susceptibility to tigecycline.
机构信息
Institute of Medical Microbiology, Virology and Hygiene, University Medical Centre Hamburg-Eppendorf,Martinistrasse, Hamburg, Germany.
出版信息
Antimicrob Agents Chemother. 2010 Jun;54(6):2720-3. doi: 10.1128/AAC.00085-10. Epub 2010 Mar 29.
Abstract
Five Klebsiella pneumoniae isolates with reduced susceptibility to tigecycline (MIC, 2 microg/ml) were analyzed. A gene homologous to ramR of Salmonella enterica was identified in Klebsiella pneumoniae. Sequencing of ramR in the nonsusceptible Klebsiella strains revealed deletions, insertions, and point mutations. Transformation of mutants with wild-type ramR genes, but not with mutant ramR genes, restored susceptibility to tigecycline and repressed overexpression of ramA and acrB. Thus, this study reveals a molecular mechanism for tigecycline resistance in Klebsiella pneumoniae.
摘要
对 5 株对替加环素（MIC，2μg/ml）敏感性降低的肺炎克雷伯菌进行了分析。鉴定出肺炎克雷伯菌中与沙门氏菌 ramR 同源的基因。对非敏感性肺炎克雷伯菌株中 ramR 的测序显示存在缺失、插入和点突变。用野生型 ramR 基因转化突变体而非突变型 ramR 基因可恢复对替加环素的敏感性，并抑制 ramA 和 acrB 的过度表达。因此，本研究揭示了肺炎克雷伯菌对替加环素耐药的分子机制。
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