Emergence of group A streptococcus strains with different mechanisms of macrolide resistance

Abstract

The mechanisms of resistance to macrolides in seven group A streptococcal (Streptococcus pyogenes) isolates that were the cause of pharyngitis in children who were unsuccessfully treated with azithromycin (10 mg/kg of body weight/day for 3 days) were evaluated. All posttreatment strains were found to be genetically related to the pretreatment isolates by random amplified polymorphism DNA analysis and pulsed-field gel electrophoresis. Two isolates had acquired either a mef(A) or an erm(B) gene, responsible for macrolide efflux and ribosomal modification, respectively. Three isolates displayed mutations in the gene encoding the L4 ribosomal protein that is part of the exit tunnel within the 50S subunit of the bacterial ribosome. In the two remaining posttreatment strains, the mechanisms of macrolide resistance could not be elucidated.

FIG. 1.

(A) PFGE patterns of the pre- and posttreatment GAS isolates digested with SmaI. Lane 1, isolate 11 V1; lane 2, isolate 11 V2; lane 3, isolate 124 V1; lane 4, isolate 124 V2; lane 5, isolate 390 V1; lane 6, isolate 390 V2; lane 7, isolate 286 V1; lane 8, isolate 286 V2; lane 9, isolate 133 V1; lane 10, isolate 133 V2; lane 11, isolate 323 V1; lane 12, isolate 323 V2. (B) Southern blot of the gel with an erm(B) probe. Lane 8, isolate 286 V2 shows a signal with the probe. The molecular sizes of the standards (in kilobases) are shown to the right of the gels.

FIG. 2.

PFGE patterns of the pre- and posttreatment GAS isolates digested with SfiI. Lane 1, isolate 11 V1; lane 2, isolate 11 V2; lane 3, isolate 124 V1; lane 4, isolate 124 V2; lane 5, isolate 390 V1; lane 6, isolate 390 V2; lane 7, isolate 286 V1; lane 8, isolate 286 V2; lane 9, isolate 133 V1; lane 10, isolate 133 V2; lane 11, isolate 323 V1; lane 12, isolate 323 V2; lane 13, isolate 508 V1; lane 14, isolate 508 V2.