Macrolide resistance in staphylococci is based on the expression of a number of genes which specify four major resistance mechanisms: (i) target site modification by methylation of the ribosomal target site in the 23S rRNA, (ii) ribosome protection via ABC-F proteins, (iii) active efflux via Major Facilitator Superfamily (MFS) transporters, and (iv) enzymatic inactivation by phosphotransferases or esterases. So far, 14 different classes of erm genes, which code for 23S rRNA methylases, have been reported to occur in staphylococci from humans, animals and environmental sources. Inducible or constitutive expression of the erm genes depends on the presence and intactness of a regulatory region known as translational attenuator. The erm genes commonly confer resistance not only to macrolides, but also to lincosamides and streptogramin B compounds. In contrast, the msr(A) gene codes for an ABC-F protein which confers macrolide and streptogramin B resistance whereas the mef(A) gene codes for a Major Facilitator Superfamily protein that can export only macrolides. Enzymatic inactivation of macrolides may be due to the macrolide phosphotransferase gene mph(C) or the macrolide esterase genes ere(A) or ere(B). Many of these macrolide resistance genes are part of either plasmids, transposons, genomic islands or prophages and as such, can easily be transferred across strain, species and genus boundaries. The co-location of other antimicrobial or metal resistance genes on the same mobile genetic element facilitates co-selection and persistence of macrolide resistance genes under the selective pressure of metals or other antimicrobial agents.
Keywords: Insertion sequences; LA-MRSA; Plasmid; Recombination; Transposon; erm genes; mph(C) genes; msr(A) genes.
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