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1998 年以来喹诺酮类耐药的可转移机制。

Transferable Mechanisms of Quinolone Resistance from 1998 Onward.

机构信息

Universidad Continental, Lima, Peru

出版信息

Clin Microbiol Rev. 2019 Aug 14;32(4). doi: 10.1128/CMR.00007-19. Print 2019 Sep 18.

DOI:10.1128/CMR.00007-19
PMID:31413045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6730498/
Abstract

While the description of resistance to quinolones is almost as old as these antimicrobial agents themselves, transferable mechanisms of quinolone resistance (TMQR) remained absent from the scenario for more than 36 years, appearing first as sporadic events and afterward as epidemics. In 1998, the first TMQR was soundly described, that is, QnrA. The presence of QnrA was almost anecdotal for years, but in the middle of the first decade of the 21st century, there was an explosion of TMQR descriptions, which definitively changed the epidemiology of quinolone resistance. Currently, 3 different clinically relevant mechanisms of quinolone resistance are encoded within mobile elements: (i) target protection, which is mediated by 7 different families of Qnr (QnrA, QnrB, QnrC, QnrD, QnrE, QnrS, and QnrVC), which overall account for more than 100 recognized alleles; (ii) antibiotic efflux, which is mediated by 2 main transferable efflux pumps (QepA and OqxAB), which together account for more than 30 alleles, and a series of other efflux pumps (e.g., QacBIII), which at present have been sporadically described; and (iii) antibiotic modification, which is mediated by the enzymes AAC(6')Ib-cr, from which different alleles have been claimed, as well as CrpP, a newly described phosphorylase.

摘要

虽然对喹诺酮类药物的耐药性的描述几乎和这些抗菌药物本身一样古老,但可转移的喹诺酮类药物耐药机制(TMQR)在 36 年多的时间里一直没有出现,最初是零星出现的事件,后来又出现了流行。1998 年,首次对可转移的喹诺酮类药物耐药机制(TMQR)进行了详细描述,即 QnrA。多年来,QnrA 的存在几乎只是一个传闻,但在 21 世纪的第一个十年中期,TMQR 的描述呈爆炸式增长,这彻底改变了喹诺酮类药物耐药性的流行病学。目前,有 3 种不同的临床相关的喹诺酮类药物耐药机制是由移动元件编码的:(i)靶位保护,由 7 种不同的 Qnr 家族(QnrA、QnrB、QnrC、QnrD、QnrE、QnrS 和 QnrVC)介导,总共超过 100 个已知的等位基因;(ii)抗生素外排,由 2 种主要的可转移外排泵(QepA 和 OqxAB)介导,它们共同占超过 30 个等位基因,以及一系列其他外排泵(如 QacBIII),目前这些外排泵只是零星地被描述过;(iii)抗生素修饰,由酶 AAC(6')Ib-cr 介导,其中有不同的等位基因被报道,还有 CrpP,一种新描述的磷酸化酶。

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