Guest,您好!  [ 退出系统 ]
 
 
本系统提供的服务仅限于教学、科研及个人学习的目的,请合理使用!
首页 - 文献检索 - 文献细览(期刊文献)
 
Clinical Microbiology Reviews
0893-8512 Vol.22, 04(2009)
p.-
Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat
Strahilevitz, Jacob; Jacoby, George A.; Hooper, David C.; Robicsek, Ari
 Abstract:Summary: Although plasmid-mediated quinolone resistance (PMQR) was thought not to exist before its discovery in 1998, the past decade has seen an explosion of research characterizing this phenomenon. The best-described form of PMQR is determined by the qnr group of genes. These genes, likely originating in aquatic organisms, code for pentapeptide repeat proteins. These proteins reduce susceptibility to quinolones by protecting the complex of DNA and DNA gyrase or topoisomerase IV enzymes from the inhibitory effect of quinolones. Two additional PMQR mechanisms were recently described. aac(6')-Ib-cr encodes a variant aminoglycoside acetyltransferase with two amino acid alterations allowing it to inactivate ciprofloxacin through the acetylation of its piperazinyl substituent. oqxAB and qepA encode efflux pumps that extrude quinolones. All of these genes determine relatively small increases in the MICs of quinolones, but these changes are sufficient to facilitate the selection of mutants with higher levels of resistance. The contribution of these genes to the emergence of quinolone resistance is being actively investigated. Several factors suggest their importance in this process, including their increasing ubiquity, their association with other resistance elements, and their emergence simultaneous with the expansion of clinical quinolone resistance. Of concern, these genes are not yet being taken into account in resistance screening by clinical microbiology laboratories.
下载题录  |  原文收割  |  参考译文  |  推荐[0]  |  分享到:
新浪微博 腾讯微博  

关于我们   |   联系我们   |   意见或建议   |   检索技巧   |   在线客服
古扬科技   渝公网备:500199095-00008   渝ICP备:10200524号
建议使用IE6以上版本,1024*768分辨率浏览本页面