Abstract
Enterococcus faecalis is one of the major causes of urinary tract infection, showing acquired resistance to various classes of antimicrobials. The objective of this study was to determine the prevalence of drug resistance and its genetic determinants for E. faecalis clinical isolates in north-central Bangladesh. Among a total of 210 E. faecalis isolates, isolated from urine, the resistance rates to erythromycin, levofloxacin, and gentamicin (high level) were 85.2, 45.7, and 11.4%, respectively, while no isolates were resistant to ampicillin, vancomycin and teicoplanin. The most prevalent resistance gene was erm(B) (97%), and any of the four genes encoding aminoglycoside modifying enzyme (AME) were detected in 99 isolates (47%). The AME gene aac(6′)-Ie-aph(2”)-Ia was detected in 46 isolates (21.9%) and was diverse in terms of IS256-flanking patterns, which were associated with resistance level to gentamicin. Tetracycline resistance was ascribable to tet(M) (61%) and tet(L) (38%), and mutations in the quinolone resistance-determining region of both GyrA and ParC were identified in 44% of isolates. Five isolates (2.4%) exhibited non-susceptibility to linezolide (MIC, 4 μg/mL), and harbored the oxazolidinone resistance gene optrA, which was located in a novel genetic cluster containing the phenicol exporter gene fexA. The optrA-positive isolates belonged to ST59, ST902, and ST917 (CC59), while common lineages of other multiple drug-resistant isolates were ST6, ST28, CC16, and CC116. The present study first revealed the prevalence of drug resistance determinants of E. faecalis and their genetic profiles in Bangladesh.
Highlights
Enterococcus is ubiquitously distributed in the environment and constitutes the normal flora of the intestinal tract in humans and animals
During the past decade, resistance to oxazolidinones and daptomycin has been reported in many parts of the world, posing a concern for a serious limitation in the treatment of human infections caused by vancomycin-resistant enterococci (VRE) and methicillin-resistant S. aureus (MRSA) [5,6,7]
We investigated the prevalence of resistance to clinically important antimicrobials and genetic mechanisms of the resistance for E. faecalis clinical isolates, to delineate the comprehensively drug resistant traits of this species in Bangladesh
Summary
Enterococcus is ubiquitously distributed in the environment and constitutes the normal flora of the intestinal tract in humans and animals. Among this genus, Enterococcus faecalis and Enterococcus faecium have been recognized as the common opportunistic pathogens implicated in urinary tract infections, wound/surgical site infections, and catheter-associated infections of the bloodstream [1]. Resistance to penicillin, aminoglycoside (high-level), glycopeptide has been the major issue of clinical practice in the treatment of enterococcal infections. For such drug-resistant E. faecalis strains, represented by those with vancomycin resistance, newer compounds including linezolid, daptomycin, and tigecyclines have been used recently. Daptomycin resistance is associated with increased cell wall thickening and other structural alterations of the cell wall caused by mutations in various genes responsible for call wall biosynthesis [5,6]
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