Spread of vancomycin-resistant enterococci: why did it happen in the United States?

The question of why vancomycin-resistant enterococci (VRE) became epidemic in the United States can be answered on at least three basic levels: (1) molecular and genetic, (2) factors affecting host-microbe interactions, and (3) epidemiological. This article will address the epidemiological issues and seek to defend the assertion that, once VRE had evolved, its spread throughout hospitals in the United States was all but assured. Nosocomial VRE outbreaks were reported first in the midand late-1980s. Since that time, scientific reports of VRE have increased over 20-fold. Among hospitals participating in the National Nosocomial Infection Surveillance System from 1989 to 1997, the percentage of enterococci reported as resistant to vancomycin increased from 0.4% to 23.2% in intensive-care settings and from 0.3% to 15.4% in non-intensive-care settings. Factors leading to the spread of VRE in US hospitals include (1) antimicrobial pressure, (2) sub-optimal clinical laboratory recognition and reporting, (3) unrecognized "silent" carriage and prolonged fecal carriage, (4) environmental contamination and survival, (5) intrahospital and interhospital transfer of colonized patients, (6) introduction of unrecognized carriers from community settings such as nursing homes, and (7) inadequate compliance with hand washing and barrier precautions. Guidelines developed by the Centers for Disease Control and Prevention's Hospital Infection Control Practices Advisory Committee address each of these factors. The impact of these guidelines on the spread of VRE within individual institutions has been variable, and the overall impact of the guidelines nationally is unknown (Infect Control Hosp Epidemiol 1998;19:539-545) . An isolate of Streptococcus liquefaciens (Enterococcus faecalis) with a vancomycin minimum inhibitory concentration (MIC) >100 lig/mL was reported among a series of 382 enterococci isolated from 1966 to 1969 at the Boston City Hospital.1 The significance of this finding is unclear, and it was not until the late 1980s that the first thorough characterization of vancomycin-resistant enterococci (VRE) and the first nosocomial VRE outbreak were reported.2,3 Coincident with the emergence of VRE as a major nosocomial pathogen in the late 1980s, interest in and reporting of laboratory, clinical, and epidemiological studies of VRE have increased by more than 20-fold (Figure 1). The magnitude and impact of the VRE epidemic in the United States probably is demonstrated best by the Centers for Disease Control and Prevention (CDC)'s National Nosocomial Infection Surveillance System. In the period 1989 through 1997, the percentage of enterococci resistant to vancomycin that was isolated from nosocomial infections in intensive-care-unit (ICU) patients rose from 0.4% to 23.2%. Likewise, the percentage of VRE isolated from nonICU patients rose from 0.3% to 15.4% (Figure 2). Initially reported mainly from large hospitals, VRE now is found in hospitals of all sizes (Figure 3). It is within the context of this dramatic national outbreak of VRE that the question is asked: Why did it happen in the United States? The current national epidemic of VRE is comprised largely of Enterococcus faecium and Enterococcus faecalis species. These organisms have a mechanism of vancomycin resistance involving seven genes that comprise the vancomycin-resistance locus.4 Murray points out that de novo evolution of this type of glycopeptide resistance through genetic mutation, induced by glycopeptide exposure, is unlikely or impossible.5 Thus, a number of other factors must be invoked to explain the rapid dissemination of this organism among hospitalized patients in the United States (Table 1). ANTIMICROBIAL PRESSURE Because resistance due to vanA and vanB does not arise through genetic mutation (s) during vancomycin exposure, the role of antimicrobials in promoting the spread of VRE must be indirect and probably involves at From the National Foundation for Infectious Diseases, Bethesda, Maryland. Address reprint requests to William J. Martone, MD, Senior Executive Director, National Foundation for Infectious Diseases, 4733 Bethesda Ave, Suite 750, Bethesda, MD, 20814; e-mail, wjmartone@aol.com. The author thanks Robert Gaynes, MD, Chief Nosocomial Infection Surveillance Activity, Centers for Disease Control and Prevention, and the hospitals contributing data to the National Nosocomial Infection Surveillance System, for updated data shown in Figures 2 and 3. 98-RVC-070. Martone WJ. Spread of vancomycin-resistant enterococci: why did it happen in the United States? Infect Control Hosp Epidemiol 1998; 19:539-545. This content downloaded from 157.55.39.87 on Sat, 09 Jul 2016 05:06:41 UTC All use subject to http://about.jstor.org/terms 540 INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY August 1998