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Published on: December 7, 2021

Resistance determinants and clonal diversity in group A streptococci collected during a period of increasing

Stefania Cresti1, Maria Lattanzi, Alessandra Zanchi

  • 1Clinica delle Malattie Infettive, Sezione di Microbiologia, Dipartimento di Biologia Molecolare, Università degli Studi di Siena, I-53100 Siena, Italy.

Antimicrobial Agents and Chemotherapy
|May 23, 2002
PubMed

Insights

Macrolide resistance in Streptococcus pyogenes significantly increased from 1992 to 1997, driven by erm(B) gene spread. Clonal diversity and varied resistance mechanisms contributed to this trend.

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Molecular Epidemiology

Background:

  • Streptococcus pyogenes is a significant human pathogen.
  • Macrolide and lincosamide antibiotics are crucial for treating S. pyogenes infections.
  • Monitoring antibiotic resistance trends is essential for effective treatment strategies.

Purpose of the Study:

  • To investigate the trends in macrolide and lincosamide resistance in Streptococcus pyogenes clinical isolates.
  • To identify the genetic mechanisms and epidemiological factors contributing to macrolide resistance.
  • To analyze the clonal diversity of S. pyogenes and its relationship with resistance phenotypes.

Main Methods:

  • Collection and susceptibility testing of 299 S. pyogenes isolates over a 6-year period (1992-1997).
  • Detection of macrolide resistance genes, including erm(B), erm(TR), and mef(A).
  • Molecular typing (e.g., pulsed-field gel electrophoresis) to assess clonal diversity.

Main Results:

  • Macrolide resistance rates in S. pyogenes increased dramatically from 9% in 1992 to 53% in 1997.
  • The rise in resistance was primarily associated with the erm(B) gene, often linked to a macrolide-lincosamide-streptogramin B resistance phenotype.
  • Isolates carrying the mef(A) gene showed stable, low-level macrolide resistance (around 13%) without a significant trend.
  • Molecular typing revealed diverse S. pyogenes clones and varied genetic environments for resistance genes.
  • An 'epidemic' spread of genetic elements carrying erm(B) contributed significantly to the increasing resistance.

Conclusions:

  • Macrolide resistance in S. pyogenes is a growing public health concern, influenced by multiple resistance mechanisms.
  • The erm(B) gene, spread through epidemic mechanisms, is a major driver of increasing macrolide resistance.
  • Understanding the interplay of clonal diversity and genetic elements is crucial for predicting and controlling antibiotic resistance in S. pyogenes.

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