ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2018
The use of high-throughput sequencing to investigate an outbreak of glycopeptide-resistant Enterococcus faecium with a novel quinupristin-dalfopristin resistance mechanism.
Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Comparison of Two Quinupristin-dalfopristin Susceptibility Testing Methods and Two Interpretive Criteria forAnnals of laboratory medicine · 2025Article
- Seasonal prevalence and antimicrobial resistance profiles inItalian journal of food safety · 2025Article
- Genomic insights into antibiotic-resistance and virulence genes ofMicrobial genomics · 2022Article
- Dissemination of Quinupristin-Dalfopristin and Linezolid resistance genes among hospital environmental and healthy volunteer fecal isolates of Enterococcus faecalis and Enterococcus faecium.Molecular biology reports · 2022Article
- Evidence of Linezolid Resistance and Virulence Factors inAntibiotics (Basel, Switzerland) · 2022Article
- Loss of microbial diversity and pathogen domination of the gut microbiota in critically ill patients.Microbial genomics · 2019Article
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Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
Abstract
High-throughput sequencing (HTS) has successfully identified novel resistance genes in enterococci and determined clonal relatedness in outbreak analysis. We report the use of HTS to investigate two concurrent outbreaks of glycopeptide-resistant Enterococcus faecium (GRE) with an uncharacterised resistance mechanism to quinupristin-dalfopristin (QD). Seven QD-resistant and five QD-susceptible GRE isolates from a two-centre outbreak were studied. HTS was performed to identify genes or predicted proteins that were associated with the QD-resistant phenotype. MLST and SNP typing on HTS data was used to determine clonal relatedness. Comparative genomic analysis confirmed this GRE outbreak involved two distinct clones (ST80 and ST192). HTS confirmed the absence of known QD resistance genes, suggesting a novel mechanism was conferring resistance. Genomic analysis identified two significant genetic determinants with explanatory power for the high level of QD resistance in the ST80 QD-resistant clone: an additional 56aa leader sequence at the N-terminus of the lsaE gene and a transposon containing seven genes encoding proteins with possible drug or drug-target modification activities. However, HTS was unable to conclusively determine the QD resistance mechanism and did not reveal any genetic basis for QD resistance in the ST192 clone. This study highlights the usefulness of HTS in deciphering the degree of relatedness in two concurrent GRE outbreaks. Although HTS was able to reveal some genetic candidates for uncharacterised QD resistance, this study demonstrates the limitations of HTS as a tool for identifying putative determinants of resistance to QD.
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