Abstract

The aim of this study was to map and investigate linezolid resistance mechanisms in linezolid-resistant enterococci in the Czech Republic from 2009 to 2019. Altogether, 1442 isolates of Enterococcus faecium and Enterococcus faecalis were examined in the National Reference Laboratory for Antibiotics. Among them, 8% of isolates (n = 115) were resistant to linezolid (E. faecium/n = 106, E. faecalis/n = 9). Only three strains of E. faecium were resistant to tigecycline, 72.6% of isolates were resistant to vancomycin. One isolate of E. faecium harbored the cfr gene. The majority (87%, n = 11) of E. faecium strains were resistant to linezolid because of the mutation G2576T in the domain V of the 23S rRNA. This mutation was detected also in two strains of E. faecalis. The presence of the optrA gene was the dominant mechanism of linezolid resistance in E. faecalis isolates. None of enterococci contained cfrB, poxtA genes, or any amino acid mutation in genes encoding ribosomal proteins. No mechanism of resistance was identified in 4 out of 106 E. faecium linezolid resistant isolates in this study. Seventeen sequence types (STs) including four novel STs were identified in this work. Clonal complex CC17 was found in all E. faecium isolates.

Highlights

  • Enterococci are Gram-positive bacteria, commensals of the gastrointestinal tract and opportunistic pathogens able to cause community-acquired and nosocomial infections

  • 115 strains (8%) were resistant to linezolid: 106 isolates (13.4%) of E. faecium and 9 strains (1.4%) of E. faecalis

  • Resistance to vancomycin was confirmed in 72.6% (n = 77) of E. faecium strains

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Summary

Introduction

Enterococci are Gram-positive bacteria, commensals of the gastrointestinal tract and opportunistic pathogens able to cause community-acquired and nosocomial infections. Linezolid is a bacteriostatic antibiotic efficient only against Gram-positive bacteria including methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin resistant enterococci [4]. It inhibits the accuracy of the protein translation by binding to the peptidyl transferase centrum (PTC) in the V domain of the 23S rRNA inside the 50S ribosomal subunit [5]. Mutations in genes (rplC, rplD, and rplV) encoding these proteins lead to the amino acid changes followed by disruption of translation This type of mechanism is predominantly linked with linezolid resistance in Staphylococcus epidermidis [10]

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