2006
DOI: 10.1128/aac.50.2.817-818.2006
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Streptococcus pyogenes Isolates with High-Level Macrolide Resistance and Reduced Susceptibility to Telithromycin Associated with 23S rRNA Mutations

Abstract: Seven high-level macrolide-resistant Streptococcus pyogenes isolates had reduced activity to telithromycin but were negative for methylation and efflux genes. All were of the constitutive phenotype, were clonally related (emm type 12 and MLST type 36), and had identical dual mutations (A2058G and U2166C) in domain V of 23S rRNA.

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Cited by 15 publications
(8 citation statements)
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“…MLS B -ketolide resistance in Streptococcus pyogenes is mediated by either active efflux of the drug, inhibition of protein synthesis by methylation [mediated by either erm(B) or erm(A) subclass erm(TR)] or mutation at critical binding domains of the 23S rRNA target [33]. To date, telithromycin resistance in S. pyogenes has been mediated by either mutations in the erm(B) gene that result in a reduced inhibitory effect on both translation and 50S subunit synthesis [34] or by ribosomal mutations in the 23S rRNA alleles [35]. It will be interesting to investigate the mechanism responsible for telithromycin resistance in the 44 strains in this study as this information may provide clues to the ribosomal binding sites of CEM-101 that sustain activity.…”
Section: Resultsmentioning
confidence: 99%
“…MLS B -ketolide resistance in Streptococcus pyogenes is mediated by either active efflux of the drug, inhibition of protein synthesis by methylation [mediated by either erm(B) or erm(A) subclass erm(TR)] or mutation at critical binding domains of the 23S rRNA target [33]. To date, telithromycin resistance in S. pyogenes has been mediated by either mutations in the erm(B) gene that result in a reduced inhibitory effect on both translation and 50S subunit synthesis [34] or by ribosomal mutations in the 23S rRNA alleles [35]. It will be interesting to investigate the mechanism responsible for telithromycin resistance in the 44 strains in this study as this information may provide clues to the ribosomal binding sites of CEM-101 that sustain activity.…”
Section: Resultsmentioning
confidence: 99%
“…A possible explanation for the presence of erythromycin resistance besides mef A, erm B, and erm TR genes includes mutations of the 23S rRNA and the L4 ribosomal protein (not investigated). 25,26 …”
Section: Discussionmentioning
confidence: 99%
“…Here, the presence of 23S rRNA methylases (ermA, ermB, ermC, and ermF genes), a plasmid-mediated efflux pump (mefA/E genes), macrolide 2Ј-phosphotransferase (mphA gene), ERY esterases (ereA and ereB genes), and possible mutations in the mtrR gene/promoter and riboproteins L4 and L22 (rplD and rplV genes) were tested in all the isolates with ERY rs . Moreover, mutations in the 4 copies of the 23S rRNA genes identified in N. gonorrhoeae were analyzed, as well, using the strategy described by Farrell and colleagues (16,17). Briefly, a common primer inside the 4 copies of the 23S rRNA genes and specific external primers close to each of them were designed from the complete N. gonorrhoeae NCCP11945 genome (accession number NC_011035).…”
Section: Resultsmentioning
confidence: 99%