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Co-Incidence of Type II Topoisomerase Mutations and Efflux Expression in High Fluoroquinolone Resistant Enterococcus faecalis Isolated from Urinary Tract Infections

Authors Esfahani S, Ahmadrajabi R, Mollaei H, Saffari F

Received 4 November 2019

Accepted for publication 21 January 2020

Published 18 February 2020 Volume 2020:13 Pages 553—559


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Joachim Wink

Sarvenaz Esfahani, Roya Ahmadrajabi, Hamidreza Mollaei, Fereshteh Saffari

Department of Microbiology and Virology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran

Correspondence: Fereshteh Saffari

Introduction: Enterococcus faecalis is one of the most common pathogens in urinary tract infections (UTIs). Fluoroquinolones have been frequently used to treat E. faecalis UTIs, and the emergence of fluoroquinolone-resistant E. faecalis strains has recently been reported in several countries. This study aimed to elucidate the mechanisms involved in fluoroquinolone resistance in clinical E. faecalis isolates by analyzing mutations in quinolone- resistance-determining regions (QRDRs) of gyrA and parC and investigating the role of some efflux pumps.
Methods: In total, 70 clinical E. faecalis 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 gyrA and parC and expression of EfrA, EfrB, and EmeA efflux pumps were investigated in 20 high-level ciprofloxacin resistant and two ciprofloxacin susceptible isolates.
Results: 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 gyrA and parC, respectively. The presence of efflux genes was detected in all studied isolates, but expression of efrA, emeA, and efrB 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.
Conclusion: 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 E. faecalis.

Keywords: E. faecalis, UTI, gyrA, parC, efflux pump

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