Editorial Commentary: Vancomycin‐ResistantStaphylococcus aureusin the Clinic: Not Quite Armageddon

Abstract

In 1992, Noble et al. [1] reported that they could transfer the vancomycin-resistant genes vanA, vanH, vanX, and vanY from vancomycin-resistant enterococci to a strain of Staphylococcus aureus both in vitro and on the skin of an obese mouse. The world then waited for vancomycin resistance to be identified in a naturally occurring clinical isolate of methicillin-resistant S. aureus (MRSA). Dire warnings about the major clinical implications of multidrug-resistant MRSA and vancomycin-resistant S. aureus (VRSA) led to much speculation about untreatable staphylococcal infections. However, after waiting 10 years, some clinicians concluded that this was not going to happen on the basis of the observation that enterococci and staphylococci frequently occupy the same ecological niche and had been given every reasonable opportunity to exchange genes in multiple-patient microenvironments. Unfortunately, as was seen in the summer of 2002, two strains of vanA-producing MRSA were identified in the United States within 3 months of each other in unrelated patients in Michigan and Pennsylvania [2, 3].