Clinical resistance to erythromycin and clindamycin in cutaneous propionibacteria isolated from acne patients is associated with mutations in 23S rRNA

Antimicrob Agents Chemother. 1997 May;41(5):1162-5. doi: 10.1128/AAC.41.5.1162.

Abstract

The genetic basis of erythromycin resistance in cutaneous propionibacteria was determined by comparing the nucleotide sequences of the peptidyl transferase region in the 23S rRNAs from 9 susceptible and 26 resistant clinical isolates as well as 4 laboratory-selected erythromycin-resistant mutants of a susceptible strain. In 13 isolates and the 4 laboratory mutants, cross-resistance to macrolides, lincosamides, and B-type streptogramins was associated with an A-->G transition at a position cognate with Escherichia coli 23S rRNA base 2058. These strains were resistant to > or = 512 microg of erythromycin per ml. Two other mutations were identified, an A-->G transition at base 2059 in seven strains, associated with high-level resistance to all macrolides, and a G-->A transition at base 2057 in six strains, associated with low-level resistance to erythromycin. These mutations correspond to three of four phenotypic classes previously identified by using MIC determinations.

Publication types

  • Comparative Study

MeSH terms

  • Acne Vulgaris / microbiology*
  • Anti-Bacterial Agents / pharmacology*
  • Clindamycin / pharmacology*
  • Drug Resistance, Microbial / genetics*
  • Erythromycin / pharmacology*
  • Humans
  • Microbial Sensitivity Tests
  • Mutation / genetics
  • Peptidyl Transferases / genetics
  • Phenotype
  • Propionibacterium / classification
  • Propionibacterium / drug effects
  • Propionibacterium / genetics*
  • Propionibacterium / isolation & purification
  • RNA, Bacterial / genetics*
  • RNA, Ribosomal, 23S / genetics*
  • Skin / microbiology

Substances

  • Anti-Bacterial Agents
  • RNA, Bacterial
  • RNA, Ribosomal, 23S
  • Clindamycin
  • Erythromycin
  • Peptidyl Transferases