Clindamycin resistant emm33 Streptococcus pyogenes emerged among invasive infections in Helsinki metropolitan area, Finland, 2012 to 2013.

In 2012, blood, skin and soft tissue infections caused by clindamycin resistant Streptococcus pyogenes (group A streptococcus; GAS) appeared to be increasing in the Helsinki metropolitan area. We compared monthly percentages of clindamycin resistant isolates in the area between 2012 and 2013, with those in 2010 and 2011. Resistance frequency in terms of patient age was also studied. We reviewed the medical records of bacteraemic cases in 2012 and 2013 and linked the data to emm types. To inform on the emm distribution among GAS isolated from skin and soft tissue infections during the epidemic, GAS isolates of one month (March 2013) were emm typed. For GAS blood, skin, and soft tissue isolates taken together, the proportions of clindamycin resistant isolates were significantly higher in 2012 and 2013 (23% and 17%, respectively) compared with the two previous years (3%, p<0,001). The erythromycin resistance percentages were almost equal to clindamycin (22% and 17%) in 2012 and 2013, respectively. Clindamycin resistance was most frequent in GAS isolates of 40 to 60 year-old patients (148/417; 36%). Among clindamycin resistant isolates, 12 of 14 blood isolates from 2012 to 2013, and 11 of 13 skin and soft tissue isolates from March 2013, were emm33. Emm33 GAS bacteraemia was associated with clindamycin and erythromycin resistance (odds ratio (OR): 7.0; 95% confidence interval (CI): 1.9-25.3). Infection focus was mainly the skin; either cellulitis (7/12) or necrotising fasciitis (3/12). All emm33 GAS isolates harboured the ermTR resistance gene with constitutive macrolides, lincosamides and streptogramines B (MLS(B)) phenotype. Emm33 GAS was responsible for the higher proportion of clindamycin resistance in skin, soft tissue, and blood isolates locally in 2012 and 2013.