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Structure and distribution of an unusual chimeric genetic element encoding macrolide resistance in phylogenetically

David J Banks1, Stephen F Porcella, Kent D Barbian

  • 1Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, National Institutes of Health, Hamilton, Montana 59840, USA.

The Journal of Infectious Diseases
|December 16, 2003
PubMed

Insights

Macrolide antibiotic resistance in Group A Streptococcus (GAS) is a global issue. A novel chimeric genetic element carrying the mefA gene, responsible for resistance, was identified and found in diverse GAS strains across the US.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • Macrolide antibiotic resistance in Group A Streptococcus (GAS) presents a significant global health challenge.
  • Understanding the genetic basis of this resistance is crucial for effective treatment strategies.

Purpose of the Study:

  • To investigate the genomic structure of the genetic element responsible for macrolide resistance in a specific GAS clone.
  • To determine the prevalence and dissemination of this resistance element in GAS strains.

Main Methods:

  • Preliminary whole-genome sequencing of an erythromycin-resistant GAS clone.
  • Analysis of the genetic element containing the mefA gene.
  • Detection of the mefA element in diverse GAS isolates.

Main Results:

  • Identified a 58.8-kb chimeric genetic element comprising a transposon within a prophage, carrying the mefA gene.
  • The element also encodes a putative extracellular protein with a cell-wall anchoring motif.
  • The mefA element was detected in phylogenetically diverse GAS strains nationwide.
  • Extracellular DNA containing the mefA element was found in a resistant GAS strain.

Conclusions:

  • The mefA gene, encoding a macrolide efflux protein, is part of a complex genetic element facilitating its spread.
  • This element contributes to the molecular basis of macrolide resistance and its dissemination in GAS.
  • The findings provide critical insights into the mechanisms driving antibiotic resistance in GAS.

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