Plasmid-Mediated Quinolone Resistance
Plasmid-Mediated Quinolone Resistance
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DOI：
10.1128/microbiolspec.plas-0006.2013
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发表时间：
2014-10-01
影响因子：
3.7
通讯作者：
Hooper, David C.
中科院分区：
文献类型：
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作者：
Jacoby, George A.;Strahilevitz, Jacob;Hooper, David C.
自1998年以来，质粒介导的喹诺酮类耐药（PMQR）的三种机制已被发现。质粒基因qnrA、qnrB、qnrC、qnrD、qnrS和qnrVC编码保护DNA促旋酶和拓扑异构酶IV免受喹诺酮抑制的五肽重复家族的蛋白质。qnr基因似乎是从水生细菌的染色体基因中获得的，通常与质粒上的移动或转座元件相关，并且经常被并入sul 1型整合子中。第二种质粒介导的机制涉及通过常见的氨基糖苷乙酰转移酶AAC（6 '）-Ib的变体使喹诺酮类与适当的氨基氮靶标乙酰化。第三种机制是由泵QepAB和OqxAB的质粒基因产生的增强的外排。PMQR已在世界各地的临床和环境分离株中发现，并且似乎正在传播。质粒介导的机制仅提供低水平的耐药性，其本身不超过敏感性的临床断点，但仍然促进了较高水平耐药性的选择，并使含有PMQR的病原体的感染更难治疗。
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.