Macrolide and lincosamide resistance patterns in invasive and colonizing group B streptococcus isolated in Belgium

Increase of erythromycin and clindamycin resistance among group B Streptococcus (GBS) have been reported worldwilde. Therefore phenotypical and molecular surveillance of macrolides and lincosamides resistance patterns in Belgium has been conducted. Antimicrobial susceptilities to erythromycin and clindamycin were determined by Etest® (EUCAST interpretive criteria) on 275 clinical isolates (N1) obtained from the Belgian surveillance for invasive GBS disease in newborns and adults during 2008 to 2011 and on 53 recto-vaginal colonization in pregnant women (N2) in 2010. Inducible and constitutive resistance to clindamycin were assessed by a double-disk diffusion test. The presence of genes encoding RNA methylases (erm) and efflux pumps (mef) was confirmed by PCR. Of the 328 GBS isolates, 109 (33,2%) were resistant to erythromycin. Among these isolates, 102 (93,6%) exhibited the MLS phenotype (resistant to erythromycin and clindamycin); the M phenotype (resistant to erythromycin and susceptible to clindamycin) was expressed by 7 (6,4%) of the isolates; one isolate presented a L phenotype (susceptible to erythromycin and resistant to clindalycin). For cMLS, the most common genotype was ermB (65%) (P <0,05) followed by ermTR (30%) and ermB+ermTR (5%). All iMLS isolates harbored an ermTR gene except 3 (2 with ermB, 1 with both ermB and ermTR); and all M phenotypes were positive for mefA/B gene. In Belgium, by year 2010, prevalence of macrolide and lincosamide resistance in GBS exceed 30%, with a predominance of MLS phenotypes (target-site modification). Resistance surveillance is mandatory to guide prophylaxis and treatment of serious GBS infections but also to identify newly acquired resistance mechanisms such as the L phenotype.