Prevalence of erm gene
classes in erythromycin resistant Staphylococcs aureus strains isolated between 1959 and 1988.
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).The ribosomal methylation is responsible for cross-resistance to Macrolides, Lincosamides and Streptogramins B, called MLSb phenotype in staphylococci ermA and ermC.
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.
massiliense by hsp65 PCR and erm gene
sequencing (4) and 14-day susceptibility to clarithromycin (10).
(3,4) A common mechanism by which staphylococcal strains acquire resistance to MLSb antibiotics is the target site modification mediated by erm gene
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
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.
(5,6) Resistance to macrolides is associated with three mechanisms: i) target modification (mediated by erm genes
); ii) efflux pumps (mediated by msr genes); and iii) enzymatic modification (mediated by lun genes).
However, in some Staphylococci, those express erm genes
require an inducing agent to synthesise methylase for Clindamycin resistance.
Modification of the ribosomal target is encoded by the erm genes
and causes resistance to the macrolides, lincosamides, and type B streptogramins (MLSb resistance).
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.