Unusual inducible cross resistance to macrolides, lincosamides, and streptogramins B by methylase production in clinical isolates of Staphylococcus aureus.

Clinical strains of Staphylococcus aureus UCN7 and UCN8 were inducibly resistant to erythromycin, clindamycin, lincomycin, and quinupristin. This unusual inducible MLS(B) resistance was due to the presence of an erm(A) or an erm(B) gene, which both encode a ribosomal methylase, in S. aureus UCN8 and UCN7, respectively. The inducible cross resistance expressed by S. aureus UCN8 was associated with an 83-bp deletion in the attenuator of the erm(A) gene that removed the second of the two leader peptides and several inverted repeats. The presence of an inducible erm(B) gene in S. aureus UCN7 conferred a cross-resistance MLS(B) phenotype, similar to that usually observed in streptococci. Therefore, in S. aureus, besides the classical inducible MLS(B) phenotype characterized by inducible resistance to 14- to 15-membered ring macrolides, an additional type of inducible cross resistance to macrolides, lincosamides, and streptogramins B due to variants of erm(A) or erm(B) genes exist.