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In vivo development of elevated linezolid resistance mediated by a deletion in ribosomal protein L3 in clinical Enterococcus faecium | Antimicrobial Agents and Chemotherapy
Linezolid (LZD) is an important clinical option for treating serious gram-positive infections, especially multidrug-resistant strains such as methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and multidrug-resistant Streptococcus pneumoniae (1, 2). It exerts its antibacterial effect by binding to the ribosomal peptidyl transferase center (PTC) of the 50S subunit, thereby inhibiting bacterial protein synthesis. However, shortly after its introduction into clinical use in 2000, LZD-resistant strains emerged from clinical Enterococcus faecium and Staphylococcus aureus (3, 4) and subsequently were reported in coagulase-negative staphylococci (5) and other species (6).