Antimicrobial Drug Use and Macrolide-Resistant Streptococcus pyogenes, Belgium

摘要: Macrolide resistance in Streptococcus pyogenes results primarily from modification of the drug target site by methyltransferases encoded erm genes, erm(A) and erm(B) or active efflux mediated a mef-encoded pump. Of these, is inducibly expressed (1) generally confers low-level to macrolides, whereas lincosamides streptogramins B (MLSB), which share overlapping binding sites, remain against erm(A)-harboring S. (2). Conversely, can be constitutively high-level MLSB mef(A) also but low moderate 14- 15-membered macrolides susceptibility 16-membered (2). That macrolide use main driver streptococci has been well demonstrated at population individual levels (3,4). Because mef are cocarried with tet genes on mobile elements, tetracycline affects (4). In addition, acquisition often cost bacteria, magnitude parameter influencing rate development stability mechanisms and, conversely, would decrease under decreasing antimicrobial drugs (5). We investigated temporal changes molecular epidemiology macrolide-resistant during 1999–2009 relation strain fitness (i.e., ability bacteria survive reproduce) outpatient Belgium.