ArticleAntimicrobial agents and chemotherapy1998
Characterization of mutations in the rpoB gene that confer rifampin resistance in Staphylococcus aureus.
Article in Antimicrobial agents and chemotherapy, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.
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Who cites it
98 citing papers in PubMed, 1 synthesis or guideline pooled it, 226 citations in OpenAlex.
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- Molecular Characteristics and Prevalence of Rifampin Resistance inAntibiotics (Basel, Switzerland) · 2023Article
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- Molecular Basis of Non-β-Lactam Antibiotics Resistance inAntibiotics (Basel, Switzerland) · 2022Review
- Antimicrobial Peptide Combination Can Hinder Resistance Evolution.Microbiology spectrum · 2022Article
- Molecular Mechanisms of Drug Resistance inInternational journal of molecular sciences · 2022Review
- Virulence Determinants inFrontiers in microbiology · 2022Article
38 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the rifampin resistance-determining (Rif) regions of the rpoB gene of Staphylococcus aureus mutants obtained during therapy or in vitro were analyzed by gene amplification and sequencing. Each of the resistant clinical isolates, including five nonrelated clones and two strains isolated from the same patient, and of the 10 in vitro mutants had a single base pair change that resulted in an amino acid substitution in the beta subunit of RNA polymerase. Eight mutational changes at seven positions were found in cluster I of the central Rif region. Certain substitutions (His481/Tyr and Asp471/Tyr [S. aureus coordinates]) were present in several mutants. Substitutions Gln468/Arg, His481/Tyr, and Arg484/His, which conferred high-level rifampin resistance, were identical or in the same codon as those described in other bacterial genera, whereas Asp550/Gly has not been reported previously. Substitutions at codon 477 conferred high- or low-level resistance, depending on the nature of the new amino acid. The levels of resistance of in vivo and one-step in vitro mutants carrying identical mutations were similar, suggesting that no other resistance mechanism was present in the clinical isolates. On the basis of these data and the population distribution of more than 4,000 clinical S. aureus isolates, we propose </=0.5 and >/=8 microg/ml as new breakpoints for the clinical categorization of this species relative to rifampin.
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