The Journal of Infectious Diseases · 2006 · 449 citations · 37 references
Life SciencesInfectious DiseasesMicrobiologyAntimicrobial ResistanceMedical MicrobiologyMicrobial PathogenesisBacterial InfectionsBacterial PathogenesisBacterial ToxinsBacterial Virulence FactorsToxin ProductionToxin-mediated PathogenesisBacterial Toxin ProductionRegulation Of Toxin ExpressionToxic Shock SyndromeToxin Gene RegulationToxin GenesToxin-encoding GenesVirulence Factor Toxinsβ-Lactam Antibiotics
Extracellular protein toxins contribute to the pathogenesis of a wide variety of Staphylococcus aureus infections. The present study investigated the effects that cell-wall active antibiotics and protein-synthesis inhibitors have on transcription and translation of genes for Panton-Valentine leukocidin, alpha-hemolysin, and toxic-shock syndrome toxin 1, in both methicillin-sensitive and methicillin-resistant S. aureus. Subinhibitory concentrations of nafcillin induced and prolonged mRNA for Panton-Valentine leukocidin, alpha-toxin, and toxic-shock syndrome toxin 1 and increased toxin production. In contrast, clindamycin and linezolid markedly suppressed translation, but not transcription, of toxin genes. These results suggest (1) that protein-synthesis inhibition is an important consideration in the selection of antimicrobial agents to treat serious infections caused by toxin-producing gram-positive pathogens and (2) that, by inducing and enhancing toxin production, inadvertent use of beta-lactam antibiotics to treat methicillin-resistant S. aureus infections may contribute to worse outcomes.
37
Loren G. Miller, Françoise Perdreau‐Remington, Günter Rieg et al. · New England Journal of Medicine · 2005 · 1.1K citations · Full text