There are two mechanisms, which can result in the resistance to this antibiotic, firstly the macrolide flux controlled by msrA and the second is the modification of the binding site in the ribosome, controlled by the erm gene (Erythromycin Ribosomal Methylase).
2010) study on the evaluation of the prevalence of erm genes inducible to Clindamycin in Staphylococcus aureus isolates from patients treated at the Clinical Hospital of Porto Alegre, it was shown that from 94 positive samples for S.
isolates analyzed, 77 had one or more erm gene
, the ermA, ermC, and ermB genes were found respectively at 49, 29, and three isolates and, the combination of these genes was found in four isolates, (13) data which differed from this study.
3,4) A common mechanism by which staphylococcal strains acquire resistance to MLSb antibiotics is the target site modification mediated by erm gene
massiliense by hsp65 PCR and erm gene
sequencing (4) and 14-day susceptibility to clarithromycin (10).
For isolates with positive results in the phenotypic test for inducible resistance to clindamycin, erm gene
PCR amplification was performed according to the multiplex PCR protocol developed by Khan et al.
Other investigators have also found that ermA is the dominant erm gene
The presence of more than one erm gene
was not detected in S.
Therefore, we hypothesized that either mutations in the erm gene
promoter region have upregulated methylase expression or that mutations in the coding region have changed the methylase specificity to include the additional binding sites of telithromycin.
permanently alter ribosomes causing an inability of the macrolides to bind, thus inhibiting the drug's action.
Macrolide resistance in Streptococcus pyogenes results primarily from modification of the drug target site by methyltransferases encoded by erm genes
, erm(A) and erm(B) or by active efflux mediated by a mef-encoded efflux pump.
These mechanisms include target site modification by methylases encoded by erm genes
, in particular erm(A), erm(B), and erm(C).