Abstract
The aim of this study was to characterize fluoroquinolone (FQ)-resistant Escherichia coli isolates from bacteremia in Taiwan in 2001–2015. During the study period, 248 (21.2%) of 1171 isolates were identified as levofloxacin-resistant. The results of phylogenetic group analysis showed that 38.7% of the FQ-resistant isolates belonged to phylogenetic group B2, 23.4% to group B1, 22.6% to groupA, 14.9% to group D, and 0.4% belonged to group F. FQ-resistant isolates were highly susceptible to cefepime (91.5%), imipenem (96.0%), meropenem (98.8%), amikacin (98.0%), and fosfomycin (99.6%), as determined by the agar dilution method. β-lactamases, including blaTEM (66.1%), blaCMY-2 (16.5%), blaCTX-M (5.2%), blaDHA-1 (1.6%), and blaSHV-12 (1.6%), were found in FQ-resistant isolates. The results of PCR and direct sequencing showed that 37 isolates (14.9%) harbored plasmid-mediated quinolone resistance (PMQR) genes. qnrB2, qnrB4, qnrS1, coexistence of qnrB4 and qnrS1, oqxAB, and aac(6′)-Ib-cr were found in 1, 4, 4, 1, 15, and 14 isolates, respectively. PMQR genes were successfully transfered for 11 (29.7%) of the 37 PMQR-harboring isolates by conjugation to E. coli C600. These findings indicate that qnr genes remained rare in E. coli but demonstrate the potential spread of oqxAB and aac(6′)-Ib-c in Taiwan.
Highlights
The topoisomerase IV enzymes (ParC and ParE)[1]
FQ resistance can arise by a range of mechanisms, the greatest concern is placed on these bacteria harboring transferable plasmid-mediated quinolone resistance (PMQR) genes; for example qnr alleles, oqxAB, qepA, and aac(6′)Ib-cr[5,6,7,8]
We present the characteristics of 248 FQ-resistant bacteremia isolates of E. coli from Taiwan, 2001
Summary
The topoisomerase IV enzymes (ParC and ParE)[1]. despite prescribing guidelines that recommend reserving FQ use, over the last decade, worldwide spread of FQ-resistant organisms has reduced their therapeutic effectiveness and emerged as an important threat to global health[2]. Resistance can be conferred by upregulation of chromosomal multidrug efflux pumps (for example, AcrAB-TolC) (by mutations in regulatory proteins), increasing the capability of actively removing FQs and other drugs from the bacterial cell[4]. FQ resistance can arise by a range of mechanisms, the greatest concern is placed on these bacteria harboring transferable PMQR genes; for example qnr alleles, oqxAB, qepA, and aac(6′)Ib-cr[5,6,7,8]. The binding of the Qnr protein to the topoisomerase physically prevents the intercalation of the FQs with the target enzyme and causes drug resistance[5]. The aim of this study was to investigate the molecular epidemiology of FQ-resistant E. coli isolated from patients with bloodstream infections in Taiwan, 2001–2015
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