Lincosamides (clindamycin), oxazolidinones (linezolid, tedizolid), and streptogramins (dalfopristin [streptogramin A] and quinupristin [streptogramin B]) are structurally different but are grouped together because they have a similar mode of antibacterial action and similar antibacterial spectra. Macrolides (except for fidaxomicin) and chloramphenicol may be included with this group for similar reasons. All inhibit protein synthesis by binding to the 50S ribosomal subunit. Fidaxomicin has a completely different mode of action than other macrolides; it inhibits RNA polymerase by binding to the DNA template–RNA polymerase complex.
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Certain methyl-transferase enzymes can mediate resistance to multiple members of the above classes. The erythromycin resistance methylase (erm) gene commonly mediates resistance to macrolides, clindamycin, and quinupristin but not the oxazolidinones or dalfopristin. The chloramphenicol-florfenicol resistance (cfr) gene mediates resistance to chloramphenicol, dalfopristin, clindamycin, and oxazolidinones, but tedizolid may retain susceptibility in some strains. Certain multidrug efflux pumps can also produce cross-resistance between some of these classes as well.