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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.
Abstract:
Resistance of streptococci to macrolide antibiotics is caused by target-site modification or drug efflux. The phenotypic expression of target-site modification can be inducible or constitutive. The prevalence of the three phenotypes among Belgian erythromycin-resistant Group A streptococci (GAS) and Streptococcus pneumoniae isolates was surveyed, their MICs for seven antibiotics were determined and the clonality of the isolates was explored. Of the 2014 GAS isolates tested 131(6.5%) were erythromycin resistant (MIC > 1 mg/L): 110 (84.0%) showed the M-resistance phenotype whereas the remaining 21 strains (16.0%) were constitutively resistant. No inducibly resistant strains were detected. Of 100 S. pneumoniae isolates, 33 were erythromycin resistant (MIC > 1 mg/L). In contrast to the GAS isolates, only 9.1% of the 33 erythromycin-resistant S. pneumoniae isolates showed the M-resistance phenotype. The presence of mefA/E and ermB genes in the M-resistant and constitutively and inducibly resistant strains, respectively, was confirmed by PCR analysis. Genomic analysis based on pulsed-field gel electrophoresis (PFGE) using the restriction enzyme SfiI, revealed 54 different PFGE patterns among the 131 erythromycin-resistant GAS isolates, of which an M6 clone represented 16.0% of the strains; all other clones, exhibiting different M-types, represented <7% of the strains. The S. pneumoniae isolates also appeared to be polyclonally based, as determined by arbitrarily primed PCR. The macrolides miocamycin and rovamycin, the lincosamide clindamycin and the ketolide HMR 3647 showed excellent activity against the M-resistant GAS and S. pneumoniae strains.
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.