Macrolide resistance and erythromycin resistance determinants among Belgian Streptococcus pyogenes and Streptococcus pneumoniae isolates

Resistance of streptococci to macrolide antibiotics is caused by target-sit e modification or drug efflux. The phenotypic expression of target-site mod ification can be inducible or constitutive. The prevalence of the three phe notypes among Belgian erythromycin-resistant Group A streptococci (GAS) and Streptococcus pneumoniae isolates was surveyed, their MICs for seven antib iotics were determined and the clonality of the isolates was explored. Of t he 2014 GAS isolates tested 131(6.5%) were erythromycin resistant (MIC > 1 mg/L): 110 (84.0%) showed the M-resistance phenotype whereas the remaining 21 strains (16.0%) were constitutively resistant. No inducibly resistant st rains were detected. Of 100 S. pneumoniae isolates, 33 were erythromycin re sistant (MIC > 1 mg/L). In contrast to the GAS isolates, only 9.1% of the 3 3 erythromycin-resistant S. pneumoniae isolates showed the M-resistance pho notype. The presence of mefA/E and ermB genes in the M-resistant and consti tutively and inducibly resistant strains, respectively, was confirmed by PC R analysis. Genomic analysis based on pulsed-field gel electrophoresis (PFG E) using the restriction enzyme Sfil, revealed 54 different PFGE patterns a mong the 131 erythromycin-resistant GAS isolates, of which an M6 clone repr esented 16.0% of the strains; all other clones, exhibiting different M-type s, represented <7% of the strains. The S. pneumoniae isolates also appeared to be polyclonally based, as determined by arbitrarily primed PCR. The mac rolides miocamycin and rovamycin, the lincosamide clindamycin and the ketol ide HMR 3647 showed excellent activity against the M-resistant GAS and S. p neumoniae strains.