Novel mechanism of macrolide resistance in Streptococcus pneumoniae

Diagn Microbiol Infect Dis. 1996 Oct;26(2):73-8. doi: 10.1016/s0732-8893(96)00183-6.

Abstract

The mechanism of macrolide resistance was examined in 73 clinical isolates of Streptococcus pneumoniae. Two distinct resistance phenotypes were observed: high-level macrolides-lincosamides-streptogramin B (MLS) resistance and low-level macrolide resistance with lincosamide susceptibility. High-level MLS resistance was associated with the presence of ermAM. Strains with the low-level resistant phenotype (novel) were negative for ermA, ermC, ermAM, ereA, ereB and msrA by polymerase chain reaction (PCR) amplification with gene-specific primers. Ribosomes isolated from novel strains bound the same amount of [14C]-erythromycin as ribosomes from sensitive strains. These novel strains also did not inactivate the macrolide. The novel mechanism was found in 41% of the erythromycin resistant S. pneumoniae examined.

MeSH terms

  • Anti-Bacterial Agents / pharmacology*
  • Bacterial Proteins
  • Biological Assay
  • Carboxylic Ester Hydrolases / genetics
  • Clindamycin / pharmacology
  • DNA Primers
  • Drug Resistance, Microbial / genetics*
  • Erythromycin / antagonists & inhibitors
  • Erythromycin / pharmacology
  • Genes, Bacterial
  • Membrane Transport Proteins*
  • Microbial Sensitivity Tests
  • Polymerase Chain Reaction
  • Ribosomes / drug effects
  • Ribosomes / metabolism
  • Streptococcus pneumoniae / drug effects*
  • tRNA Methyltransferases / genetics

Substances

  • Anti-Bacterial Agents
  • Bacterial Proteins
  • DNA Primers
  • Membrane Transport Proteins
  • msrA protein, Staphylococcus epidermidis
  • Clindamycin
  • Erythromycin
  • tRNA Methyltransferases
  • Carboxylic Ester Hydrolases
  • erythromycin esterase