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rpoB mutations and their association with rifampicin resistance in clinical Staphylococcus epidermidis
Department of Sequencing and Bioinformatics, Statens Serum Institut, Copenhagen, Denmark; European Society of Clinical Microbiology and Infectious Diseases (ESCMID) Study Group for Staphylococci and Staphylococcal Diseases (ESGS), Basel, Switzerland.
Department of Sequencing and Bioinformatics, Statens Serum Institut, Copenhagen, Denmark; European Society of Clinical Microbiology and Infectious Diseases (ESCMID) Study Group for Staphylococci and Staphylococcal Diseases (ESGS), Basel, Switzerland; Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark; Department of Immunology & Microbiology, University of Copenhagen, Copenhagen, Denmark.
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2025 (engelsk)Inngår i: Journal of Antimicrobial Chemotherapy, ISSN 0305-7453, E-ISSN 1460-2091, Vol. 80, nr 4, s. 1067-1071Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

BACKGROUND: Staphylococcus epidermidis is a ubiquitous member of the healthy skin and mucous microbiota but is also an opportunistic pathogen responsible for various infections, often treated with antibiotics like rifampicin. Resistance to rifampicin in S. epidermidis arises primarily through nonsynonymous mutations in the rpoB gene.

OBJECTIVES: To investigate the prevalence of rpoB mutations and their association with phenotypic rifampicin resistance in clinical S. epidermidis isolates from Denmark, France, and Sweden.

METHODS: All clinical isolates (N = 942) were whole-genome sequenced to identify mutations in rpoB and subsequently linked to phenotypic rifampicin resistance based on antimicrobial susceptibility testing.

RESULTS: A total of 64 (6.8%) isolates were resistant to rifampicin. They carried all mutational changes in the rifampicin resistance-determining region (RRDR). Among 12 identified nonsynonymous mutations, 11 were exclusively observed in resistant strains, including novel mutations not previously described in S. epidermidis.

CONCLUSIONS: This study highlights the diverse genetic variants of rpoB associated with rifampicin resistance in clinical S. epidermidis isolates, including novel mutations. The strong correlation between mutational changes in RRDR and phenotypic resistance reinforces the role of rpoB mutations as a primary mechanism of resistance in clinical isolates.

sted, utgiver, år, opplag, sider
Oxford University Press, 2025. Vol. 80, nr 4, s. 1067-1071
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URN: urn:nbn:se:oru:diva-119179DOI: 10.1093/jac/dkaf035ISI: 001414583300001PubMedID: 39913260Scopus ID: 2-s2.0-105001928349OAI: oai:DiVA.org:oru-119179DiVA, id: diva2:1935540
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Nyckelfonden, OLL-502241Tilgjengelig fra: 2025-02-07 Laget: 2025-02-07 Sist oppdatert: 2025-04-29bibliografisk kontrollert

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