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Macrolide resistance and erythromycin resistance determinants among Belgian Streptococcus pyogenes and Streptococcus

P Descheemaeker1, S Chapelle, C Lammens

  • 1Department of Microbiology, University Hospital Antwerp, Universitaire Instelling Antwerpen, Universiteitsplein 1, B-2610 Wilrijk, Antwerp, Belgium.

The Journal of Antimicrobial Chemotherapy
|February 8, 2000
PubMed

Insights

Erythromycin resistance in streptococci is mainly due to target modification or efflux. Belgian Group A streptococci (GAS) showed high M-resistance, while Streptococcus pneumoniae displayed lower M-resistance. New macrolides and ketolides show promise against resistant strains.

Area of Science:

  • Microbiology
  • Antibiotic Resistance
  • Molecular Biology

Background:

  • Macrolide antibiotic resistance in streptococci arises from target-site modification or drug efflux mechanisms.
  • Target-site modification can manifest as inducible or constitutive resistance phenotypes.

Purpose of the Study:

  • To survey the prevalence of macrolide resistance phenotypes in Belgian Group A streptococci (GAS) and Streptococcus pneumoniae isolates.
  • To determine the minimum inhibitory concentrations (MICs) for seven antibiotics against resistant strains.
  • To explore the clonality of erythromycin-resistant streptococcal isolates.

Main Methods:

  • Phenotypic characterization of erythromycin resistance (M-resistance, constitutive, inducible).
  • Polymerase chain reaction (PCR) to detect mefA/E and ermB genes.
  • Pulsed-field gel electrophoresis (PFGE) for GAS genomic analysis and arbitrarily primed PCR for S. pneumoniae clonality assessment.
  • MIC determination for seven antibiotics.

Main Results:

  • Of 2014 GAS isolates, 6.5% were erythromycin-resistant, predominantly exhibiting M-resistance (84.0%). No inducible resistance was found in GAS.
  • Among 100 S. pneumoniae isolates, 33% were erythromycin-resistant, with only 9.1% showing M-resistance.
  • PCR confirmed mefA/E and ermB genes correlating with M-resistance and constitutive/inducible resistance, respectively.
  • PFGE revealed 54 distinct GAS clones, with an M6 clone comprising 16.0% of resistant strains.
  • S. pneumoniae isolates were largely polyclonal.
  • Miocamycin, rovamycin, clindamycin, and HMR 3647 demonstrated excellent activity against M-resistant GAS and S. pneumoniae.

Conclusions:

  • Belgian GAS isolates show a high prevalence of M-resistance, unlike S. pneumoniae which has lower M-resistance.
  • Specific resistance genes (mefA/E, ermB) and clonal structures were identified in resistant streptococci.
  • Novel macrolides and ketolides are effective against macrolide-resistant GAS and S. pneumoniae.

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