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Role of efflux in macrolide resistance in {beta}-haemolytic streptococci of groups A, B, C and G collected in an Irish teaching hospital.

There has been an increase in macrolide resistance in b-haemolytic streptococci (BHS) reported worldwide. Macrolide resistance rates among group A streptococci (GAS) are variable, and range from 2 to 32 % in areas of the USA and Canada, from 5 to 29 % within Europe, and are as high as 63 % in Taiwan (Leclercq, 2002). Furthermore, a recent study in Spain found erythromycin resistance to be 26.1 % in GAS, 15.7 % in group B streptococci (GBS), 5.3 % in group C streptococci (GCS) and 33.3 % in group G streptococci (GGS) (Merino Dı́az et al., 2008). Mechanisms that confer resistance to macrolide, lincosamide and streptogramin B (MLSB) antibiotics in BHS include target site modification by methylation of the 23S rRNA binding site. This mechanism is mediated by the erm gene, which confers cross-resistance to all MLSB antibiotics. Resistance can be either inducible (iMLSB), where the methylase is produced in the presence of an inducer (such as erythromycin), or constitutive (cMLSB), where the methylase is produced constitutively. Drug efflux, which has been increasingly recognized, is mediated by the mefA/E gene, which encodes a 12membered transmembrane protein that pumps out 14and 15-membered ring macrolides only, with the isolate remaining susceptible to 16-membered MLSB antibiotics (M phenotype). The third resistance mechanism occurs as a result of antibiotic inactivation. Resistance is usually conferred to only one of the three classes (M, L or S). In Enterococcus faecium the linB gene encodes lincosamide nucleotidyltransferase, which inactivates lincosamides, conferring resistance to clindamycin only (L phenotype). The latter phenotype has been reported in clinical isolates of GBS (Gygax et al., 2006). The only Irish data published on the prevalence of erythromycin resistance and mechanisms of resistance in BHS reviewed GBS only (Kiely et al., 2010). Surveillance data in an Irish tertiary-care centre showed an increase in macrolide resistance among BHS groups A, B, C and G recently. Erythromycin resistance increased from 10 % in 2004 to 14 % in 2009, while clindamycin resistance rates remained steady over the same period, 6 % in 2004 and 5 % in 2009. The aims of this study were to determine the prevalence of erythromycin resistance in BHS groups A, B, C and G from clinical isolates in the largest hospital in Ireland (St James’s Hospital). Furthermore, resistance mechanisms to macrolides were determined by molecular methods.