Incidence of mefA and mefE Genes in Viridans Group Streptococci

Viridans group streptococci form the major part of the commensal flora of the human upper respiratory tract. However, these organisms are also the leading cause of infective endocarditis and an increasing source of bacteremia in neutropenic patients (1). Beta-lactam agents are the treatment of choice for these infections, but macrolides and related drugs are recommended for prophylaxis and alternative treatment in allergic patients (1). The two presently recognized mechanisms of resistance to macrolide antibiotics in streptococci are (i) target site modification mediated by erythromycin resistance methylases (Erm), which confer cross-resistance to macrolides, lincosamides, and streptogramin B components (MLS phenotype), and (ii) active-drug efflux pumps, encoded either by the mefAE genes or by the mreA gene (3, 4, 11). The efflux systems encoded by the mef genes cause resistance to 14- and 15-membered macrolide compounds only, and this phenotype is designated M (10). Phenotype M is widespread among beta-hemolytic streptococci and Streptococcus pneumoniae in a number of countries (6, 7, 10). During a survey of antimicrobial resistance in viridans streptococci, strains with the M phenotype were investigated.