Plasmid-Mediated Quinolone Resistance

被引:9
|
作者
Jacoby, George A. [1 ]
Strahilevitz, Jacob [2 ]
Hooper, David C. [3 ]
机构
[1] Lahey Hosp & Med Ctr, Burlington, MA 01805 USA
[2] Hadassah Hebrew Univ, IL-91120 Jerusalem, Israel
[3] Massachusetts Gen Hosp, Boston, MA 02114 USA
来源
MICROBIOLOGY SPECTRUM | 2014年 / 2卷 / 05期
基金
美国国家卫生研究院;
关键词
D O I
10.1128/microbiolspec.PLAS-0006.2013
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
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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页数:24
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