Abstract
It was demonstrated that spiramycin (SP)-resistance could be related to the decrease in binding of ribosomes to SP and that the SP-binding to ribosomes was related with inhibition of polypeptide synthesis by SP in a cell-free system in staphylococcal strains. These facts were also observed in Mac (macrolide)-inducible strains, in which resistance to Mac antibiotics is enhanced by prior treatment with subinhibitory concentrations of erythromycin. From these results, it was concluded that the mechanism of resistance to Mac antibiotics is accounted for by alteration of ribosomes in staphylococcal strains and that this alteration of ribosomes is caused not only by mutation but also by induction.
