期刊
MICROORGANISMS
卷 9, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/microorganisms9051023
关键词
antimicrobial resistance; linezolid; Staphylococcus epidermidis; whole genome sequencing; surveillance
类别
资金
- Bridge project Advanced Pathogen Detection in Blood Stream Infection [871243]
- Austrian Research Promotion Agency (FFG)
Whole genome sequencing is a useful tool for monitoring resistance mechanisms in bacteria. This retrospective study found that the major resistance mechanisms in linezolid-resistant Staphylococcus epidermidis (LRSE) were mutations in 23S rRNA and the presence of the cfr gene, with most LRSE isolates showing high resistance levels to linezolid. Linezolid usage was identified as the main factor contributing to the development of resistance, and monitoring of the cfr gene in LRSE and restriction of linezolid usage are potential key steps to reduce resistance and transmission.
Whole genome sequencing is a useful tool to monitor the spread of resistance mechanisms in bacteria. In this retrospective study, we investigated genetic resistance mechanisms, sequence types (ST) and respective phenotypes of linezolid-resistant Staphylococcus epidermidis (LRSE, n = 129) recovered from a cohort of patients receiving or not receiving linezolid within a tertiary hospital in Innsbruck, Austria. Hereby, the point mutation G2603U in the 23S rRNA (n = 91) was the major resistance mechanism followed by the presence of plasmid-derived cfr (n = 30). The majority of LRSE isolates were ST2 strains, followed by ST5. LRSE isolates expressed a high resistance level to linezolid with a minimal inhibitory concentration of >= 256 mg/L (n = 83) in most isolates, particularly in strains carrying the cfr gene (p < 0.001). Linezolid usage was the most prominent (but not the only) trigger for the development of linezolid resistance. However, administration of linezolid was not associated with a specific resistance mechanism. Restriction of linezolid usage and the monitoring of plasmid-derived cfr in LRSE are potential key steps to reduce linezolid resistance and its transmission to more pathogenic Gram-positive bacteria.
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