Beta-lactam resistance in Staphylococcus aureus: the adaptive resistance of a plastic genome.
Staphylococci have two mechanisms for resistance to beta-lactam antibiotics. One is the production of beta-lactamases, enzymes that hydrolytically destroy beta-lactams. The other is the expression of penicillin-binding protein 2a (PBP 2a), which is not susceptible to inhibition by beta-lactam antibiotics. Strains of S. aureus exhibiting either beta-lactamase or PBP 2a-directed resistance (or both) have established a considerable ecological niche among human pathogens. The emergence and subsequent spread of bacterial strains designated as methicillin-resistant S. aureus (MRSA), from the 1960s to the present, has created clinical difficulties for nosocomial treatment on a global scale. The recent variants of MRSA that are resistant to glycopeptide antibiotics (such as vancomycin) have ushered in a new and disconcerting chapter in the evolution of this organism.
Fuda
C C S
CC
Department of Chemistry and Biochemistry, University of Notre Dame, Indiana, 46556-5670, USA.
Fisher
J F
JF
Mobashery
S
S
D000222:Adaptation, Physiological; D000900:Anti-Bacterial Agents / Q000378:metabolism / Q000494:pharmacology*; D016680:Genome, Bacterial / Q000187:drug effects* / Q000235:genetics; D006801:Humans; D016106:Methicillin Resistance / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D013211:Staphylococcus aureus / Q000187:drug effects* / Q000235:genetics / Q000472:pathogenicity*
D000900:Anti-Bacterial Agents