In a previous commentary, we made the case that the fear of methicillin resistant Stnpl~yZc~occus QZLY~US (MRSA) in their burn units caused some clinicians to use vancomycin, inappropriately, as a first line antibiotic to treat patients with clinical signs of sepsis in the absence of microbiological evidence that the patient was, indeed, infected with MRSA [l]. Our concern was that vancomycin resistance information could be transferred MRSA from vancomycin resistant enterococci (VRE), which are becoming more prevalent in acute care treatment facilities, and that inappropriate use of this antibiotic would select for a vancomycin resistant MRSA. This bacterium, now resistant to vancomycin, the only antibiotic to which it was uniformly susceptible, heretofore, would be a ‘superbug’ causing infections exceedingly difficult to treat. We believe that inappropriate use of vancomycin in burn units because of inordinate fear of MRSA hastens the scenario described above. Therefore, lwe underscored the use of some well accepted guidelines [2,3], for vancomycin use in the treatment of burn infections. Another aspect of the inappropriate use of vancomycin, however, was not addressed previously: the generation and selection of VRE, per se. Enterococci associated with cultures obtained from burn patients have been on the increase, worldwide, over the past decade. In 1990, enterococci were the most prevalent bacterial isolate in a Swiss burn unit [4] and the third most prevalent isolate in a Norwegian burn center [5]. A report from an Italian burn unit which surveyed infections between the years 1976 and 1988 stated ‘The most striking finding was the increase in antibiotic resistant enterococci.’ [6] In the US, one burn center reported an increase in isolation of enterococci from 5 per cent in 1984 to 19 per cent in 1988 [7], and another unit reported that in a 3-year study period (1989-91), enterococci were responsible for 11-13 per cent of all infections in their patients [8]. Concomitant to their increased associations with burned patients, enterococcal infections rose in the general hospital environment and are now among the four most common nosocomial pathogens in the US and have been called the ‘nosocomial pathogens of the 1990s’ [9]. While there are a number of species in the genus Enterococcus, two species, E. faecalis and E. faecdium are associated with the largest numbers of nosocomial infections with the other species playing more minor roles [lo-131. Three types of antimicrobial resistance are associated with enterococci [lo]: Intrinsic this is defined as intrinsic resistance to several classes of antimicrobials that are normally active against (other types of streptococci (low level aminoglycosides, azthreonam, cephalosporins, clindamycin, imipenem [JZ. faecium], penicillin, trimethoprim-sulfamethoxazole). Tolerance (cell-wall active agents) where the minimal bactericidal concentration of antibiotic is far in excess of the minimum inhibitory concentration. Thus, concentrations of cell-wall active agents which will inhibit the growth of enterococci will not kill them. This becomes of considerable significance in infections, such as, endocarditis, osteomyelitis and memngitis, where bactericidal activity of antibiotics are essential for achieving acceptable cure rates [9]; Acquired the past two decades have seen the acquisition of resistance determinants to virtually every act.& antimicrobial agent [lo], including vancomycin [10,13-151, the ‘last, best hope’ for the treatment 0: enterococcal infections, and the subject of this commentary. Three phenotypes of VRE. Van A, Van B and Van C have been known for sometime [13] with a fourth phenotype, Van D, having been described recently [16j (Table 1). The various phenotypes are associated more or less with specific species of enterococci and these phenotypes vary in their susceptibility to another glycopeptide antibiotic, teicoplanin: Van A and Van B phenotypes exhibit clinically relevant inducible levels of vancomycin resistance, plus resistance to multiple other antibiotics. Their resistances are genetically transferable and they occur in enterococcal species most commonly involved in serious infections. They can be distinguished from each other by the fact that Van A strains are resistant to teicoplanin as well as vancornycin, while Van B strains are not. While not a !ot is