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Macrolide-resistance genes in clinical isolates of Streptococcus pyogenes

Carmela Cascone1, Maria Santagati, Silvana Noviello

  • 1Department of Microbiological Sciences, University of Catania, Italy.

Microbial Drug Resistance (Larchmont, N.Y.)
|July 18, 2002
PubMed

Insights

Macrolide resistance in Streptococcus pyogenes is often due to mef(A) or erm(B) genes, leading to distinct resistance phenotypes. These macrolide-resistant strains are polyclonal but form homogeneous groups based on their resistance patterns.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Streptococcus pyogenes is a common cause of pharyngotonsillitis in children.
  • Macrolide antibiotics are frequently used to treat S. pyogenes infections.
  • The emergence of macrolide resistance in S. pyogenes poses a significant public health concern.

Purpose of the Study:

  • To investigate the prevalence and types of macrolide-resistance genes in S. pyogenes strains isolated from children with pharyngotonsillitis.
  • To correlate the presence of specific resistance genes with observed macrolide resistance phenotypes.
  • To analyze the genetic relatedness of macrolide-resistant S. pyogenes isolates.

Main Methods:

  • Polymerase Chain Reaction (PCR) was used to detect macrolide-resistance genes (mef(A), erm(B), erm(TR)).
  • Macrolide resistance phenotypes (M and MLSB) were determined.
  • Pulsed-field gel electrophoresis (PFGE) was employed for macrorestriction fragment pattern analysis.

Main Results:

  • The mef(A) gene was detected in 46.6% of strains, associated with the M phenotype.
  • The erm(B) gene was found in 41.7% of strains, associated with the MLSB phenotype.
  • erm(TR) was present in 10 strains, often co-occurring with mef(A) or erm(B).
  • Inducible macrolide resistance was observed in 24/53 MLSB strains.
  • PFGE analysis indicated that erythromycin-resistant S. pyogenes strains are polyclonal but form distinct phenotypic groups.

Conclusions:

  • Macrolide resistance in S. pyogenes is primarily mediated by mef(A) and erm(B) genes, conferring distinct resistance profiles.
  • The genetic diversity of resistant strains suggests multiple origins or acquisition events.
  • Understanding these resistance mechanisms and genetic patterns is crucial for effective antibiotic treatment strategies.

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