Concern about the appearance of glycopeptide resistance among staphylococci prompted us to examine 41 methicillin-resistant coagulase-negative staphylococcal clinical isolates recovered in a New York City hospital during a 5-month period between September 1995 and February 1996. Twenty-eight of 41 strains showed elevated teicoplanin MICs (8 to 32 µg/mL), and all 6 strains examined in more detail by population analysis profiles [1] also exhibited heteroresistance to vancomycin: Dense cultures contained bacteria with low frequencies (10^–5 to 10^–7) that could grow at 12 µg of the antibiotic per mL [2]. Pulsed-field gel electrophoresis showed that the 28 isolates represented unrelated strains (24 distinct patterns). Addition of teicoplanin to cultures of resistant bacteria caused inhibition of autolysis, formation of large cellular aggregates, and excretion of large amounts of extracellular material that had the appearance of cell walls. Such cultures could quantitatively remove teicoplanin from the medium during growth. All of these features are reminiscent of the properties of a recently described, highly vancomycin-resistant laboratory mutant of methicillin-resistant Staphylococcus aureus. This mutant did not cross-react with DNA probes for the enterococcal vancomycin-resistant genes but showed the unique ability to "capture" vancomycin molecules in biologically inactive cell-bound form [3].

Cultures of five of six coagulase-negative strains obtained from the preantibiotic era showed heterogeneous teicoplanin (but not vancomycin) phenotypes, suggesting that this property may be intrinsic to these species [2]. Under laboratory conditions, enrichment of cultures of the six coagulase negative strains for the more highly vancomycin-resistant subpopulations of bacteria was surprisingly easy. The extensive use of vancomycin in hospitals may also lead to the selection of such subpopulations, leading to the emergence of strains with substantially increased vancomycin MIC values that may then begin to jeopardize chemotherapy.

Our findings suggest that this novel type of glycopeptide resistance occurring through drug capture may already be widespread among hospital isolates of methicillin-resistant coagulase-negative staphylococcal isolates and may also find its way into clinical strains of methicillin-resistant S. aureus. Isolates of the latter that carry an as-yet-undefined resistance mechanism and cause clinical failure have been described recently in the United States [4] and Japan [5].