Journal Article

Pneumococcal Resistance to Macrolides, Lincosamides, Ketolides, and Streptogramin B Agents: Molecular Mechanisms and Resistance Phenotypes

Paul H. Edelstein

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 38, issue Supplement_4, pages S322-S327
Published in print May 2004 | ISSN: 1058-4838
Published online May 2004 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/382687
Pneumococcal Resistance to Macrolides, Lincosamides, Ketolides, and Streptogramin B Agents: Molecular Mechanisms and Resistance Phenotypes

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The macrolides, lincosamides, ketolides, and streptogramin B agents (the MLKSB antimicrobial agents) have related chemical structures and share similar molecular targets on the 50S ribosomal subunit of Streptococcus pneumoniae. Mutations in rRNA or ribosomal proteins generate a variety of resistance phenotypes. The M phenotype of S. pneumoniae, which predominates in North America, affords low-level resistance to macrolides only (excluding macrolides with 16-member rings) by means of an efflux pump encoded by the mefA gene. The MLSB phenotype, which predominates in Europe, affords high-level resistance to macrolides, lincosamides, and streptogramin B agents and arises, in most cases, from dimethylation of adenine 2058 in the 23S rRNA of the 50S ribosomal subunit. Other, less common, phenotypes arise from other 23S rRNA modifications (ML and K phenotypes) or from amino acid substitution (MSB phenotype) or insertion (MKSB pheotype) into the 50S subunit ribosomal protein L4. In all cases, the decrease in susceptibility to ketolides (for example, telithromycin) is less than the decrease in susceptibility for other MLKSB agents.

Journal Article.  3047 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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