ArticleThe Journal of antimicrobial chemotherapy2025
rpoB mutations and their association with rifampicin resistance in clinical Staphylococcus epidermidis.
Article in The Journal of antimicrobial chemotherapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Genomic features of mecA-harboring Staphylococcus epidermidis infecting an illegally traded rufous-bellied thrush (T. rufiventris).Veterinary research communications · 2026Article
- Antibiotic resistance and population structure of Staphylococcus epidermidis from prosthetic joint infections in Sweden and France.The Journal of antimicrobial chemotherapy · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundStaphylococcus 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.
objectivesTo investigate the prevalence of rpoB mutations and their association with phenotypic rifampicin resistance in clinical S. epidermidis isolates from Denmark, France, and Sweden.
methodsAll 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.
resultsA 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.
conclusionsThis 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.
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