Oxazolidinone Resistance Mediated by optrA in Clinical Enterococcus faecalis Isolates in Upper Austria: First Report and Characterization by Whole Genome Sequencing

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The genetic mechanisms associated with acquisition of linezolid (LZD) resistance are diverse, including point mutations in the V domain of the 23S rRNA and the 50S ribosomal proteins as well as cfr , optr A, and/or poxt A genes, which may be plasmid- or chromosomally encoded. The aim of this study was to investigate through Whole Genome Sequencing (WGS)-based typing the presence and location of genes and point mutations associated with LZD resistance in two Enterococcus faecalis isolates from Upper Austrian patients. The isolates were retrieved during screening by LZD disk diffusion test of a total of 911 clinical E. faecalis isolates in 2017. The two E. faecalis isolates had LZD minimum inhibitory concentrations of 8 and 32 mg/L and were optr A-positive (ST476 and ST585). Bioinformatic analysis revealed the presence of optr A located in the chromosome of both isolates. One isolate carried the optr A gene in the transposon 6674, previously reported as chromosomally encoded, and the second isolate in fragments originating from the integrative plasmid pEF10748. Additional mechanisms of LZD resistance on the 23S rRNA and the 50S ribosomal proteins were detected. None of the patients reported travels to geographical areas with high LZD resistance or previous LZD treatments. This is the first report of optrA carrying E. faecalis , including characterization by WGS from Austria. LZD resistance in a low-prevalence setting is of concern and should be further monitored.

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