首页> 外文期刊>Antimicrobial agents and chemotherapy. >Novel variants of the qnrB gene, qnrB22 and qnrB23, in Citrobacter werkmanii and Citrobacter freundii.
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Novel variants of the qnrB gene, qnrB22 and qnrB23, in Citrobacter werkmanii and Citrobacter freundii.

机译:在韦氏柠檬酸杆菌和弗氏柠檬酸杆菌中,qnrB基因的新变体qnrB22和qnrB23。

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摘要

Resistance to quinolones in Gram-negative bacteria is usually mediated by the following: (i) chromosomal mutations that alter the target enzymes, DNA gyrase and topoisomerase IV, in their quinolone resistance-determining regions (QRDR), (ii) changes in drug entry (loss of porin channels), and (iii) the presence of plasmid-mediated quinolone resistance (PMQR) determinants [qnrA, qnrB, qnrS, qnrC, and qnrD, coding for Qnr proteins that protect DNA gyrase from quinolone attack; aac(6')-Ib-cr, coding for a protein that acetylates quinolones; and qepA, coding for a quinolone efflux pump] (2, 12). The recent worldwide emergence of PMQR due to the qnr and aac(6')-Ib-cr genes is a concerning fact among human and animal Gram-negative pathogens (8).
机译:革兰氏阴性细菌对喹诺酮类药物的耐药性通常由以下因素介导:(i)改变其喹诺酮耐药性决定区域(QRDR)的靶酶,DNA促旋酶和拓扑异构酶IV的染色体突变,(ii)药物进入的变化(丧失孔蛋白通道),以及(iii)质粒介导的喹诺酮抗性(PMQR)决定簇[qnrA,qnrB,qnrS,qnrC和qnrD,它们编码保护DNA旋转酶免受喹诺酮攻击的Qnr蛋白; aac(6')-Ib-cr,编码使喹诺酮乙酰化的蛋白质;和qepA,编码喹诺酮外排泵](2,12)。由于qnr和aac(6')-Ib-cr基因引起的PMQR在全球范围内的出现是人类和动物革兰氏阴性病原体中令人关注的事实(8)。

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