Inducible clindamycin resistance in β-hemolytic streptococci and Streptococcus pneumoniae.

Resistance to macrolides in beta-hemolytic streptococci and Streptococcus pneumoniae arises primarily due to Erm(B) or Mef(A). Erm(B) typically confers high level resistance to macrolides, lincosamides and streptogramin B (MLSB phenotype), whereas Mef(A) confers low level resistance to macrolides only (M phenotype). To investigate the incidence of macrolide resistance mechanisms in isolates of beta-hemolytic streptococci and pneumococci in Israel, with particular emphasis on inducible MLSB phenotype. We collected 316 clinical isolates of streptococci during May-August 2010. Erythromycin resistance mechanism was determined by the erythromycin-clindamycin double disk diffusion method. Erythromycin and clindamycin resistance rates were 19.4% and 13.4% for S. pneumoniae, 4.7% and 1.6% for group A Streptococcus (GAS), 17% and 17% for group B Streptococcus (GBS), and 38.8% and 27.8% for group G Streptococcus (GGS) respectively. The most common resistance mechanism for all streptococci was constitutive MLSB (cMLSB). Inducible MLSs (iMLSB) mechanism was found in 3% of all strains and represented 25% of resistance mechanisms. The prevalence of macrolide resistance and the distribution of resistance mechanisms differ among beta-hemolytic streptococci and S. pneumoniae, with GBS, GGS and S. pneumoniae showing the highest resistance rate. Macrolide or lincosamide cannot be empirically used for severe streptococcal infections before strains are proved to be susceptible. Continuous surveillance of erythromycin and clindamycin resistance patterns among streptococci is needed.