Abstract
To investigate the role of a plasmid bearing the erm(B) gene on the prevalence of the macrolide, lincosamide and group B streptogramin (MLS(B)) phenotype of group A streptococci (GAS) and to characterize the plasmid and determine the clonal relation between the erythromycin-resistant isolates. Two hundred and five erythromycin-resistant GAS isolates were collected from 1990 to 2006. Colony hybridization, PCR, plasmid curing and PFGE techniques were used to analyse the mechanisms behind the phenotypes. Among the 56 isolates with constitutive MLS(B) (cMLS(B)) resistance, 53 isolates harboured a plasmid, pA15, of 19 kb. erm(B) was on pA15 and it confered a cMLS(B) resistance phenotype. The prevalence rate of the pA15-containing isolates was 36.3% from 1993 to 1995, but the plasmid could not be detected from 2004 to 2006. To link the high-level resistance to pA15, clinical isolate A15 was selected and pA15 was cured by novobiocin. In the plasmid-cured strain SW503, the erythromycin MIC decreased from 256 to 0.032 mg/L. By electroporation, pA15 was re-introduced into the plasmid-cured erythromycin-susceptible strain, and the high-level erythromycin resistance was restored. Plasmid pA15 was also transferred to group B streptococci and group C streptococci by electroporation. In all the pA15-containing isolates, emm1 type was present and pulse type J was predominant (48 of 54 isolates). The plasmid pA15 mediated cMLS(B) resistance in the mid-1990s, but pA15 was not detected in the clinical isolates from 2004 onwards, which correlates with the absence of cMLS(B) resistance in this region.
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