Could a Phosphotransferase System Provide the Means to Control Outbreaks of Enterococcus faecium Infection?

The epidemiology of enterococcal infections has changed dramatically over the past 100 years [1]. Until relatively recently, the vast majority were caused by Enterococcus faecalis and were acquired in the community; then, during the 1970s– 1980s, the percentage of nosocomial infections due to E. faecalis tripled [2,3],an increase temporally associated with increasing use of third-generation cephalosporins. In the United States, an increase in the proportion of nosocomial infections caused by Enterococcus faecium was observed in the 1980s [4, 5], and by 2006–2007, a Centers for Disease Control survey of healthcare-associated infections found that approximately 38% of clinical enterococcal isolates identified to the species level were E. faecium [6]. This increase was blamed on the acquisition of vancomycin resistance by E. faecium (which seldom occurred in E. faecalis) and the increasing use of vancomycin in hospitalized patients. However, the epidemiology of vancomycin-resistant E. faecium (VREfm) presented a quandary: at the time, VREfm was alreadyacommon cause of US healthcare-associated infections, such organisms were not found in the community [7].Yet, concurrently, VREfm was rare as a cause of infection in the European Union but were commonly found in feces of food animals in Europe, in products derived from these animals, in feces of individuals handling them, and even in feces of