Abstract

BackgroundLinezolid-resistant enterococci pose great challenges in clinical practice. The aim of this study is to study the mechanisms underlying the resistance and genetic environment of antimicrobial resistance gene of linezolid-resistant enterococci.ResultsThe linezolid MICs of 16 enterococci were 4 mg/L to 16 mg/L. Four strains belonged to multi-drug resistant (MDR) bacteria. The sequence types (STs) of 13 enterococci strains performed WGS were diverse: 3 ST476, 1 ST86, ST116, ST480, ST59, ST416, ST21, ST67, ST16, ST585 and ST18. None of them carried multi-drug resistance gene cfr. Only one strain had the G2658 T mutation of target 23S rRNA gene. Thirteen (13/16, 81.3%) strains harbored the novel oxazolidinone resistance gene optrA. WGS analysis showed that the optrA gene was flanked by sequence IS1216E insertion in 13 strains, and optrA was adjacent to transposons Tn558 in two strains and Tn554 in one strain. The optrA gene was identified to be co-localized with fexA, the resistance genes mediated florfenicol resistance in 13 strains, and ermA1, the resistance genes mediated erythromycin resistance in 9 strains, indicating that linezolid-resistant strains may be selected due to non-oxazolidinone antibiotics (i.e. macrolides and florfenicol) usage.ConclusionOur findings demonstrate the high diversity of optrA-carrying genetic platforms. The mobile genetic elements (MGEs) may play an important role in the dissemination of optrA into the enterococci isolates of human origin. The genetic evidence of transferable feature and co-selection of optrA should be gave more attention in clinical practice.

Highlights

  • Linezolid-resistant enterococci pose great challenges in clinical practice

  • Linezolid, which belongs to oxazolidinone, is the clinically last resort to treat vancomycin-resistant enterococci (VRE), methicillin-resistant Staphylococcus aureus (MRSA), and other multi-drug Gram-positive bacteria [1]

  • This study indicates that the transferable resistance gene optrA is very prevalent among linezolid-resistant enterococci strains isolated from human

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Summary

Introduction

Linezolid-resistant enterococci pose great challenges in clinical practice. The aim of this study is to study the mechanisms underlying the resistance and genetic environment of antimicrobial resistance gene of linezolid-resistant enterococci. Linezolid, which belongs to oxazolidinone, is the clinically last resort to treat vancomycin-resistant enterococci (VRE), methicillin-resistant Staphylococcus aureus (MRSA), and other multi-drug Gram-positive bacteria [1]. The resistance to linezolid by gram-positive bacteria can be achieved by target-modified 23S rRNA mutations [5], acquiring exogenous chloramphenicol-florfenicol resistance (cfr) [6], optrA [7] or poxtA [8]. The cfr gene encodes a methyltransferase that modifies the 23S rRNA at position A2503, which confers resistance to phenicols, lincosamide, oxazolidinones, pleuromutilin, and streptogramin A (PhLOPSA phenotype) [9]. The cfr gene has been identified in a variety of genera, including Staphylococcus [10], Bacillus [11], Enterococcus [12], Macrococcus [13], Chen et al BMC Microbiology (2019) 19:162

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