Plasmid-Mediated Quinolone Resistance

质粒 DNA旋转酶 生物 拓扑异构酶 流出 遗传学 基因 喹诺酮类 微生物学 转座因子 大肠杆菌 抗生素 突变体
作者
George A. Jacoby,Jacob Strahilevitz,David C. Hooper
出处
期刊:Microbiology spectrum [American Society for Microbiology]
卷期号:2 (5) 被引量:451
标识
DOI:10.1128/microbiolspec.plas-0006-2013
摘要

Three mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998. Plasmid genes qnrA, qnrB, qnrC, qnrD, qnrS, and qnrVC code for proteins of the pentapeptide repeat family that protects DNA gyrase and topoisomerase IV from quinolone inhibition. The qnr genes appear to have been acquired from chromosomal genes in aquatic bacteria, are usually associated with mobilizing or transposable elements on plasmids, and are often incorporated into sul1-type integrons. The second plasmid-mediated mechanism involves acetylation of quinolones with an appropriate amino nitrogen target by a variant of the common aminoglycoside acetyltransferase AAC(6')-Ib. The third mechanism is enhanced efflux produced by plasmid genes for pumps QepAB and OqxAB. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. The plasmid-mediated mechanisms provide only low-level resistance that by itself does not exceed the clinical breakpoint for susceptibility but nonetheless facilitates selection of higher-level resistance and makes infection by pathogens containing PMQR harder to treat.
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