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Emergence of group A streptococcus strains with different mechanisms of macrolide resistance
Edouard Bingen1, Roland Leclercq, Frédéric Fitoussi
1Service de Microbiologie, Hôpital Robert Debré, Paris, France. edouard.bingen@rdb.ap-hop-paris.fr
Abstract:
The mechanisms of resistance to macrolides in seven group A streptococcal (Streptococcus pyogenes) isolates that were the cause of pharyngitis in children who were unsuccessfully treated with azithromycin (10 mg/kg of body weight/day for 3 days) were evaluated. All posttreatment strains were found to be genetically related to the pretreatment isolates by random amplified polymorphism DNA analysis and pulsed-field gel electrophoresis. Two isolates had acquired either a mef(A) or an erm(B) gene, responsible for macrolide efflux and ribosomal modification, respectively. Three isolates displayed mutations in the gene encoding the L4 ribosomal protein that is part of the exit tunnel within the 50S subunit of the bacterial ribosome. In the two remaining posttreatment strains, the mechanisms of macrolide resistance could not be elucidated.
Insights
Mechanisms of macrolide resistance in Streptococcus pyogenes isolates causing pharyngitis were studied. Resistance was linked to specific genes (mefA, ermB) or ribosomal protein mutations, though some cases remained unexplained.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Group A Streptococcus (Streptococcus pyogenes) is a common cause of childhood pharyngitis.
- Macrolide antibiotics like azithromycin are frequently used for treatment.
- Emergence of antibiotic resistance necessitates understanding resistance mechanisms.
Purpose of the Study:
- To investigate the genetic and molecular mechanisms of macrolide resistance in Streptococcus pyogenes isolates from pediatric pharyngitis cases.
- To identify specific genes or mutations conferring resistance after unsuccessful azithromycin treatment.
Main Methods:
- Analysis of seven Streptococcus pyogenes isolates from children with treatment-failure pharyngitis.
- Genetic relatedness confirmed using random amplified polymorphism DNA (RAPD) and pulsed-field gel electrophoresis (PFGE).
- Detection of macrolide resistance genes (mefA, ermB) and mutations in ribosomal protein L4 (rplD).
Main Results:
- All post-treatment isolates were genetically related to pre-treatment strains.
- Two isolates acquired mefA (efflux) or ermB (ribosomal modification) genes.
- Three isolates exhibited mutations in the L4 ribosomal protein gene.
- Mechanisms in two isolates could not be identified.
Conclusions:
- Macrolide resistance in Streptococcus pyogenes can arise from acquired genes (mefA, ermB) or target site mutations (L4 ribosomal protein).
- These mechanisms explain resistance in a majority of treatment-failure cases.
- Further research is needed to elucidate resistance mechanisms in remaining isolates.