MRSA: Current Perspectives, Horizon Scientific Press September 2003, Chapter 8 (p.187-213)
Department of Bacteriology, Faculty of Medicine Juntendo University, 2-1-1 Hongo, Bunkyo-ku, 113-8421, Tokyo, Japan. longzhu@med.juntendo.ac.jp
The glycopeptide antibiotics, vancomycin and teicoplanin, were the only licensed antibacterial compounds, until recently, to which methicillin-resistant Staphylococcus aureus (S. aureus) clinical isolates have remained uniformly susceptible. However, the worldwide increase in the incidence of S. aureus clinical isolates with reduced susceptibility to vancomycin and teicoplanin raises the possibility that glycopeptide resistance in S. aureus is becoming an important clinical problem. S. aureus has evolved genetic and biochemical ways of resisting these antimicrobial actions. Genetic mechanisms include multistep mutations in bacteria chromosome without acquisition of new DNA. A review of available biochemical studies suggests that S. aureus does not resist glycopeptides by inactivating the drugs or altering the drug target, but reducing drug access to bacterial cell membrane by thickened cell wall and changed cell wall components. This article outlines the background to this developing issue with a focus on the mechanisms of resistance. The geographic prevalence, potential for continued spread, and proposed strategies for prevention and control are also discussed.