Wj. Martone, SPREAD OF VANCOMYCIN-RESISTANT ENTEROCOCCI - WHY DID IT HAPPEN IN THEUNITED-STATES, Infection control and hospital epidemiology, 19(8), 1998, pp. 539-545
The question of why vancomycin-resistant enterococci (VRE) became epid
emic in the United States can be answered on at least three basic leve
ls: (1) molecular and genetic, (2) factors affecting host-microbe inte
ractions, and (3) epidemiological. This article will address the epide
miological 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 mid-
and late-1980s. Since that time, scientific reports of VRE have increa
sed over 20-fold. Among hospitals participating in the National Nosoco
mial Infection Surveillance System from 1989 to 1997, the percentage o
f 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-inte
nsive-care settings. Factors leading to the spread of VRE in US hospit
als include (1) antimicrobial pressure, (2) sub-optimal clinical labor
atory recognition and reporting, (3) unrecognized ''silent'' carriage
and prolonged fecal carriage, (4) environmental contamination and surv
ival, (5) intrahospital and interhospital transfer of colonized patien
ts, (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 Dise
ase Control and Prevention's Hospital Infection Control Practices Advi
sory Committee address each of these factors. The impact of these guid
elines on the spread of VRE within individual institutions has been va
riable, and the overall impact of the guidelines nationally is unknown
.