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Macrolide Resistance in Streptococcus pneumoniae
Max R Schroeder1, David S Stephens2
1Departments of Medicine, Emory University Atlanta, GA, USA.
Abstract:
Streptococcus pneumoniae is a common commensal and an opportunistic pathogen. Suspected pneumococcal upper respiratory infections and pneumonia are often treated with macrolide antibiotics. Macrolides are bacteriostatic antibiotics and inhibit protein synthesis by binding to the 50S ribosomal subunit. The widespread use of macrolides is associated with increased macrolide resistance in S. pneumoniae, and the treatment of pneumococcal infections with macrolides may be associated with clinical failures. In S. pneumoniae, macrolide resistance is due to ribosomal dimethylation by an enzyme encoded by erm(B), efflux by a two-component efflux pump encoded by mef (E)/mel(msr(D)) and, less commonly, mutations of the ribosomal target site of macrolides. A wide array of genetic elements have emerged that facilitate macrolide resistance in S. pneumoniae; for example erm(B) is found on Tn917, while the mef (E)/mel operon is carried on the 5.4- or 5.5-kb Mega element. The macrolide resistance determinants, erm(B) and mef (E)/mel, are also found on large composite Tn916-like elements most notably Tn6002, Tn2009, and Tn2010. Introductions of 7-valent and 13-valent pneumococcal conjugate vaccines (PCV-7 and PCV-13) have decreased the incidence of macrolide-resistant invasive pneumococcal disease, but serotype replacement and emergence of macrolide resistance remain an important concern.
Insights
Macrolide antibiotics are crucial for treating Streptococcus pneumoniae infections, but resistance is increasing due to genetic elements like erm(B) and mef(E). This resistance can lead to treatment failures and remains a concern despite vaccination efforts.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- Streptococcus pneumoniae is a common bacterium causing respiratory infections.
- Macrolide antibiotics are frequently used to treat these infections.
- Increasing macrolide resistance in S. pneumoniae is a significant public health concern.
Purpose of the Study:
- To review the mechanisms and genetic elements contributing to macrolide resistance in S. pneumoniae.
- To discuss the impact of macrolide resistance on treatment outcomes.
- To highlight the ongoing challenge of macrolide resistance in the context of pneumococcal conjugate vaccines.
Main Methods:
- Review of existing literature on macrolide resistance mechanisms in S. pneumoniae.
- Analysis of genetic elements, such as Tn917, Mega, and Tn916-like elements, that carry resistance genes.
- Examination of epidemiological data regarding the prevalence of macrolide resistance and the impact of vaccination.
Main Results:
- Macrolide resistance in S. pneumoniae is primarily mediated by ribosomal dimethylation (erm(B)), efflux pumps (mef(E)/mel), and target site mutations.
- Specific genetic elements like Tn917, Mega, Tn6002, Tn2009, and Tn2010 facilitate the spread of these resistance determinants.
- While pneumococcal conjugate vaccines (PCV-7, PCV-13) have reduced invasive macrolide-resistant disease, serotype replacement and emerging resistance remain critical issues.
Conclusions:
- The genetic diversity of macrolide resistance determinants in S. pneumoniae poses a continuous challenge to antibiotic therapy.
- Understanding the mobile genetic elements involved is crucial for developing strategies to combat resistance.
- Ongoing surveillance and vaccine development are necessary to mitigate the impact of macrolide-resistant pneumococcal infections.
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