2022
DOI: 10.1007/s11033-022-07627-3
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Dissemination of Quinupristin-Dalfopristin and Linezolid resistance genes among hospital environmental and healthy volunteer fecal isolates of Enterococcus faecalis and Enterococcus faecium

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Cited by 4 publications
(4 citation statements)
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“…To the best of our knowledge, this is the first study performing Boodaghi Malidareh et al, 2022;Miller et al, 2014). Almost all sequenced E. faecium strains in this study, except strain E5-100, carried the msr(C) gene.…”
Section: Discussionmentioning
confidence: 89%
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“…To the best of our knowledge, this is the first study performing Boodaghi Malidareh et al, 2022;Miller et al, 2014). Almost all sequenced E. faecium strains in this study, except strain E5-100, carried the msr(C) gene.…”
Section: Discussionmentioning
confidence: 89%
“…Our results are also in accordance with the high resistance prevalence against quinupristin/dalfopristin in E. faecium from healthy food‐producing animals in Europe (de Jong et al, 2019 ). Quinupristin/dalfopristin resistance in E. faecium can be achieved through several different mechanisms, including the presence of acquired ARGs like vat (D), vat (E), vgb (A), vgb (B), and eat (A), as well as the presence of the intrinsic gene, msr (C) (Boodaghi Malidareh et al, 2022 ; Miller et al, 2014 ). Almost all sequenced E. faecium strains in this study, except strain E5‐100, carried the msr (C) gene.…”
Section: Discussionmentioning
confidence: 99%
“…E. faecalis shows a negative correlation with these antibiotics (p < 0.001), differing from that of E. faecium. This resistance pattern of E. faecalis is likely due to the lsa gene, which confers innate resistance to quinupristin/dalfopristin [5].…”
Section: Discussionmentioning
confidence: 99%
“…Enterococci inherently resist many antibiotics, including cephalosporins, aminoglycosides, trimethoprim-sulfamethoxazole, lincosamides, and quinolones. For instance, this intrinsic resistance to quinupristin/dalfopristin in E. faecalis is attributed to the lsa gene [5,6]. Furthermore, enterococci rapidly acquire resistance to antibiotics through mutations (various levels of resistance to aminoglycosides) or genetic transfers through plasmids, transposons, or integrons (resistance to glycopeptides, mainly vancomycin) [7].…”
Section: Introductionmentioning
confidence: 99%