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Molecular epidemiology of macrolides-lincosamides-streptogramin B resistance in Staphylococcus aureus and

Insights

Macrolides-lincosamides-streptogramin B (MLS) resistance is prevalent in Staphylococcus aureus and coagulase-negative staphylococci. The ermA and ermC genes, responsible for MLS resistance, are found on plasmids or integrated into the chromosome, with potential for interspecies spread.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Macrolides-lincosamides-streptogramin B (MLS) resistance is a significant clinical concern in Staphylococcus aureus and coagulase-negative staphylococci.
  • Prevalence rates of MLS resistance in these bacteria were observed at 22% and 45%, respectively, in isolates from New Jersey hospitals.

Purpose of the Study:

  • To investigate the molecular basis of MLS resistance in Staphylococcus aureus and coagulase-negative staphylococci.
  • To characterize the erm gene variants and their genetic location (plasmid or chromosome) in resistant isolates.

Main Methods:

  • Dot blot and Southern hybridization analyses were employed to detect and characterize the erm gene variants.
  • Restriction pattern analysis was used to determine the genomic location and organization of the erm genes, including transposon structures.

Main Results:

  • All examined Staphylococcus aureus isolates (35/35) and a majority of coagulase-negative isolates (39/42) harbored either the ermA or ermC gene variants.
  • ermC genes were found exclusively on plasmids, while ermA genes were located on the chromosome, often within the Tn554 transposon.
  • Multiple chromosomal inserts of Tn554 were observed in Staphylococcus aureus, and coagulase-negative staphylococci frequently displayed multiple, distinct ermA inserts.

Conclusions:

  • Coagulase-negative staphylococci serve as a substantial reservoir for ermA and ermC resistance determinants.
  • The genetic mobility and varied locations of these resistance genes suggest a significant potential for interspecies spread within staphylococcal populations.

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