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Ribosomal mutations in Streptococcus pneumoniae clinical isolates.
Marja Pihlajamäki1, Janne Kataja, Helena Seppälä
1Antimicrobial Research Laboratory, National Public Health Institute, Turku, Finland. mapihla@utu.fi
Antimicrobial Agents and Chemotherapy
|February 19, 2002
Summary
Unusual macrolide resistance in Streptococcus pneumoniae was linked to specific genetic mutations. These findings in Finnish clinical isolates highlight novel resistance mechanisms in this bacterium.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Streptococcus pneumoniae is a leading cause of bacterial infections worldwide.
- Macrolide antibiotics are crucial for treating pneumococcal infections.
- Emergence of antibiotic resistance in S. pneumoniae poses a significant public health threat.
Purpose of the Study:
- To investigate the molecular basis of an unusual macrolide resistance phenotype in clinical isolates of Streptococcus pneumoniae.
- To identify the genetic mechanisms underlying resistance to macrolides and streptogramin B, while maintaining susceptibility to lincosamides.
Main Methods:
- Phenotypic characterization of macrolide, lincosamide, and streptogramin B resistance in eleven clinical isolates.
- Molecular analysis to detect known acquired macrolide resistance genes.
- Sequencing of domain V of the 23S rRNA gene and ribosomal protein L4 gene to identify mutations.
Main Results:
- Eleven clinical isolates of Streptococcus pneumoniae exhibited resistance to macrolides and streptogramin B, with varying susceptibility to lincosamides.
- No acquired macrolide resistance genes (e.g., erm, mef) were detected in these isolates.
- Mutations in domain V of the 23S rRNA gene (A2059C, A2059G, C2611G) or ribosomal protein L4 (69GTG71-to-69TPS71 substitution) were identified as the cause of the observed resistance phenotype.
Conclusions:
- The unusual macrolide resistance phenotype in these Streptococcus pneumoniae isolates is attributed to target site modifications (mutations in 23S rRNA or ribosomal protein L4) rather than acquired resistance genes.
- These findings expand our understanding of macrolide resistance mechanisms in S. pneumoniae and have implications for antimicrobial stewardship and treatment strategies.