The Society for Healthcare Epidemiology of America calls vancomycin-resistant enterococci (VRE) one of the "most out of control" resistant pathogens in U.S. hospitals. Myriad aspects play into the development of this kind of epidemic--genetic and molecular features, environmental and host-microbe interactions, and epidemiological factors.
Continued attention on hospital-acquired infections has brought significant mainstream media attention to infections like those caused by VRE and methicillin-resistant Staphylococcus aureus. The clinical laboratory's role is crucial in identifying, monitoring and controlling the spread of VRE through hospitals.
Nosocomial VRE outbreaks in U.S. hospitals were first reported in the mid- and late 1980s.1 Since then, infections have remained common in hospital environments largely because of the intrinsic resistance of enterococci to commonly used antibiotics and their ability to acquire resistance to new antibiotics.
For many years, vancomycin was used almost exclusively to treat enterococci infections; now, widespread resistance has led to an industry-wide war on VRE.
The microbiology or molecular laboratory is an essential component in a healthcare facility's strategy to minimize the occurrence of VRE infections. Detecting the bacteria as well as performing susceptibility tests to identify resistance puts the lab front and center of the VRE epidemic.
Colonization Vs. Infection
While infections with VRE are disturbingly common in hospitals and long-term care facilities across the country, perhaps even more unsettling is the frequency of colonization without infection. Patients who are colonized, but not infected, with VRE do not have clinical signs or symptoms of infection, but may still be spreading the bacteria.
The distinction between colonization and infection is important in screening for VRE. Colony counts in stool samples are similar in both groups of patients, but if screening is only performed on symptomatic patients and reporting those numbers, a facility may be underestimating the impact of VRE.
The goal of screening should be to identify colonized patients, not just infected patients, so that adequate infection control measures can be implemented to limit the number of infections.2
VRE infections are most common in the ICU or in patients with extended hospital stays; it is often patients who are already sick who develop infections. Mortality rates can be staggeringly high in these patients--up to 60-70 percent (although the proven cause of death in patients with other serious underlying diseases can be difficult to establish).3
HIDDEN THREAT: Many patients can be colonized but not infected with antibiotic-resistant pathogens, and still spread them throughout hospitals and communities. ADVANCE illustration
The spread of VRE in hospitals or long-term care facilities is exacerbated by the fact that the bacteria can survive for days on surfaces. VRE have been recovered more than 24 hours after experimental contamination of bedrails, telephones and stethoscopes, and on a tourniquet 4 days after the colonized patient was discharged from the hospital. The organism has also been found on the hands of healthcare workers; this is probably the most common mode of transmission.3
Laboratorians may feel as though their role in minimizing the spread of VRE is minimal because they are not in direct contact with patients and are not the caregivers who may be spreading it on their own hands. But the laboratory identification of colonization or infection at the facility alerts those caregivers to use extra caution and potentially isolate those patients most likely to transmit the bacteria to others.
The effect of biofilms on VRE is not entirely understood, although it is known that they provide a protected mode of growth for bacteria like enterococci. Biofilms are microbial accretions encased in a matrix and irreversibly attached on biological or non-biological surfaces that can protect cells from hostile environments.
Enterococcus faecalis and E. faecium, the two most common enterococci species causing nosocomial infections in the U.S., both are capable of producing biofilms.4 While some species of enterococci have low levels of instrinsic resistance to vancomycin (E. gallinarum and E. casseliflavus/E. flavescens), E. faecalis and E. faecium show signs of acquired resistance-likely with the help of biofilm formation and/or the acquisition of genetic information from another organism.2
John G. Thomas, PhD, MS, HCLD, is director of Microbiology and Virology, West Virginia University Hospitals, and professor for the Departments of Pathology and Periodontics, West Virginia University Schools of Medicine and Dentistry, Robert C. Byrd Health Sciences Center-North, Morgantown, WV. He pointed out that VRE and E. faecalis are also problematic in oral health as well--30-60 percent of failed or infected root canals are attributed to VRE or E. faecalis in mixed infections, and biofilms are present in many of these infections, compounding the treatment challenges.
The prevalence of biofilm production by enterococci varies worldwide, and even hospital-to-hospital in the U.S. Variations also exist among the different enterococci species, and studies have suggested certain environmental conditions promote more long-term biofilm formation and maintenance. Further, many genetic factors play a role in the formation of biofilms around enterococci.5
While progress has been made in understanding the genetic and environmental roles involved in biofilm formation, a more complete understanding of how biofilms are formed and maintained may lead to improved infection control measures.
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