Transductional analysis of resistance to lincomycin and erythromycin in Streptococcus pyogenes.

Abstract

From the group A streptococcal strain 56188, mutants were selected for resistance to lincomycin. Among these, two distinguishable classes occurred: whereas mutations assigned to the linA locus did not change the susceptibility to erythromycin and were transducible by phage A25, class B mutations conferred erythromycin cross-resistance and failed to be transducible under the conditions employed. Corresponding findings have previously been made concerning the properties of mutants selected for resistance to erythromycin. By two-point transduction crosses, the eryA and linA loci were placed in the same linkage group, as defined by cotransfer with phage A25. A common feature of mutants carrying both an eryA and a linA mutation was the slower growth compared to that of the parental strains bearing either mutation alone. This interaction among eryA and linA mutations proved to be strongest in certain combinations which were phenotypically unrecognizable because the resultant strains failed to develop colonies under the conditions used. On the other hand, the mutations of the established double mutants did not interact with respect to their effect on the resistance characteristics of the strains, which were the simple addition of the effects of the single mutations. Both the linkage relationships and the phenotypic properties of the eryA and linA mutations suggested that they might occur in genes coding for ribosomal proteins. Mutations carried out by the B classes of the erythromycin-resistant and lincomycin-resistant strains appeared to be located outside the eryAlinA linkage group in region(s), the function of which is unknown.