Esfahani Sarvenaz, Ahmadrajabi Roya, Mollaei Hamidreza, Saffari Fereshteh
Department of Microbiology and Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Infect Drug Resist. 2020 Feb 18;13:553-559. doi: 10.2147/IDR.S237299. eCollection 2020.
is one of the most common pathogens in urinary tract infections (UTIs). Fluoroquinolones have been frequently used to treat UTIs, and the emergence of fluoroquinolone-resistant strains has recently been reported in several countries. This study aimed to elucidate the mechanisms involved in fluoroquinolone resistance in clinical isolates by analyzing mutations in quinolone- resistance-determining regions (QRDRs) of A and C and investigating the role of some efflux pumps.
In total, 70 clinical isolates collected from UTIs were identified by phenotypic and genotypic methods. Antimicrobial susceptibility testing was performed and multidrug-resistant (including ciprofloxacin resistant) isolates were studied for minimum inhibitory concentrations to ciprofloxacin, levofloxacin, and ofloxacin. In the following, mutations in QRDRs of A and C and expression of EfrA, EfrB, and EmeA efflux pumps were investigated in 20 high-level ciprofloxacin resistant and two ciprofloxacin susceptible isolates.
High-level resistance to ciprofloxacin was detected in 97.5% of isolates. Sequencing of QRDRs revealed that 65% and 75% of isolates carried mutations in A and C, respectively. The presence of efflux genes was detected in all studied isolates, but expression of A, A, and B was demonstrated in 50%, 40%, and 30% of resistant isolates, respectively. Neither QRDR mutation nor the expression of efflux genes showed any significant association with MIC.
Co-incidence of mutation and efflux gene expression in more than half of isolates (13/20) suggests that both mechanisms may play a role in fluoroquinolone resistance. The other unknown mechanisms including different efflux pumps and probably other QRDRs mutations may contribute to fluoroquinolone resistance in .
是尿路感染（UTIs）中最常见的病原体之一。氟喹诺酮类药物一直被频繁用于治疗UTIs，最近在几个国家报道了耐氟喹诺酮菌株的出现。本研究旨在通过分析A和C喹诺酮耐药决定区（QRDRs）的突变以及研究一些外排泵的作用，阐明临床分离株中氟喹诺酮耐药的机制。
总共通过表型和基因型方法鉴定了70株从UTIs中收集的临床分离株。进行了抗菌药物敏感性测试，并对多重耐药（包括对环丙沙星耐药）的分离株进行了对环丙沙星、左氧氟沙星和氧氟沙星的最低抑菌浓度研究。接下来，在20株高水平环丙沙星耐药和2株环丙沙星敏感的分离株中研究了A和C的QRDRs突变以及EfrA、EfrB和EmeA外排泵的表达。
在97.5%的分离株中检测到对环丙沙星的高水平耐药。QRDRs测序显示，分别有65%和75%的分离株在A和C中携带突变。在所有研究的分离株中都检测到了外排基因的存在，但分别在50%、40%和30%的耐药分离株中证实了A、A和B的表达。QRDR突变和外排基因的表达均与MIC无显著关联。
超过一半的分离株（13/20）中突变和外排基因表达的同时出现表明这两种机制可能在氟喹诺酮耐药中起作用。其他未知机制，包括不同的外排泵以及可能的其他QRDRs突变，可能导致中的氟喹诺酮耐药。
