CDC: Take VRE fight seriously before resistant staph fully emerges
The wimp’ that roared: A 5,000-fold increase in VRE since 1989
With vancomycin resistance now emerging in Staphylococcus strains, public health officials are trying to end infection control complacency about a less dangerous but increasingly endemic pathogen vancomycin-resistant enterococci (VRE).
Despite an estimated 5,000-fold increase in VRE since its emergence in hospitals in the eastern United States in 1989, there appears to be some apathy about the pathogen in the medical community because it doesn’t have the level of high virulence and increased patient mortality feared in resistant staph strains.
"We are seeing VRE become prevalent in hospitals throughout the country," says William Jarvis, MD, acting director of the Centers for Disease Control and Prevention hospital infections program. "Many practitioners are telling us that either their infection control personnel, hospital epidemiologists, or administrative staff really don’t want to take this very seriously because it is not causing a lot of deaths. Or the cost of doing so is just too much."
While the actual prevalence of VRE is unknown, data from sentinel hospitals in the CDC National Nosocomial Infections Surveillance (NNIS) system indicate the percentage of VRE-caused nosocomial infections increased from 0.3% in 1989 to 14.2% in 1996. Most of the upsurge has been ascribed to VRE in intensive care units, but more recent data suggest a roughly equal proportion of VRE infections is now occurring in non-ICU settings. Other CDC data and anecdotal reports also confirm the general perception that VRE began in the Eastern United States and progressed steadily westward.
"Several years ago, people on the West Coast were comfortable that they had no VRE and didn’t have to worry about it," Jarvis says. "We’ve seen it gradually move across the country and become endemic everywhere."
While the rate of patient mortality directly caused by VRE is uncertain, VRE infections can be fatal in severely ill patients. The CDC currently estimates a 30% to 40% case-fatality rate, and reminds that some infections are virtually untreatable. (See the CDC’s VRE fact sheet, p. 163.)
Nonfatal infections still increase costs of care and prolong hospitalizations. The CDC estimates that a VRE bloodstream infection currently translates to some $18,000 in direct medical costs. By preventing such expensive infections, the full regimen of CDC isolation measures and antibiotic controls can ultimately prove cost-effective even though they may require initial expenditure to implement.1 For example, a CDC study at New York Medical College in Valhalla showed $157,977 in annual savings by reducing VRE BSIs and decreasing lengths of stay associated with infections.2
Beyond the cost issues, there are troubling patient management questions, particularly in long-term care facilities and other non-acute care settings that must find creative ways to keep VRE-colonized residents from becoming "prisoners" in their rooms. (See story in Infection Control Consultant, September 1997, pp. 137-138.)
"I think it behooves us to reduce the prevalence of VRE to reduce those costs, and there are also considerations in terms of the patients," Jarvis tells Hospital Infection Control. "There are a lot of reasons even though this isn’t killing everybody to take this organism very seriously. The overall burden of antimicrobial resistance is a major concern. VRE is also an indication of the probable widespread misuse of antimicrobials in facilities."
Forestalling a feared foe
In particular, the CDC is urging that antibiotic control efforts for VRE be redoubled in light of the emergence of vancomycin intermediate-resistant Staphylococcus aureus (VISA) strains in the United States and Japan.3-5 The thinking is essentially that renewed efforts against VRE, while justified in their own right, could forestall the arrival of far more threatening pathogens: VISA, and fully resistant S. aureus.
"If people fully implemented the VRE recommendations, it would decrease the likelihood that we would see further emergence of vancomycin resistance," Jarvis says.
By the same token, the CDC is still concerned that widespread prevalence of VRE could eventually lead to genetic transfer of vancomycin resistance capabilities from enterococci to staph strains, which thus far has only occurred in lab experiments. That has long been feared as the mechanism of resistance that could spell widespread emergence of resistant staph. Instead, the first VISA cases appear to be caused by mutations in methicillin-resistant S. aureus (MRSA) strains after prolonged exposure to vancomycin. (See story in HIC, October 1997, pp. 145-152.)
While some clinicians have questioned whether genetic transfer between species will ever occur in a clinical setting, the fact that VRE and MRSA now widely co-exist in health care facilities may make the possibility more likely.
"In facilities where MRSA became endemic, and now they are having major problems with VRE, there are literally hundreds of patients who are co-colonized with VRE and MRSA," Jarvis says. "We have to be very concerned about that."
To re-emphasize the importance of the issue, the CDC recently held a national educational satellite broadcast program to remind clinicians to treat the existing VRE guidelines with a new sense of urgency before the pathogen becomes hopelessly entrenched in the health care system. In doing so, CDC officials and conference participants addressed the difficult question of VRE mortality, one of the perceived stumbling blocks to greater compliance with the recommendations.
"The mortality rate of VRE is difficult to determine because of the issue of severity of illness," Jarvis said at the conference. "Some case studies without comparison groups show that VRE patients have a high mortality rate as much as 73%. These studies include very few patients with VRE infection, or don’t account for the patients’ severe underlying disease, and can’t really determine the mortality attributable to VRE vs. other factors."
In contrast, a study by CDC investigators that included an assessment of severity of illness in a multivariate analysis showed no increase in mortality from VRE when underlying severity of patient illness was controlled for.6
"In other words, when patients with VRE infection were compared to other patients infected with vancomycin-sensitive enterococci [VSE], the increased mortality in the VRE group was attributable primarily to their increased severity of illness," Jarvis told participants at the conference. ". . . VRE tends to cause colonization and infection in very, very seriously ill patients. So when you are comparing the VRE-infected patients to the VSE patients, the severity of illness is much worse in the VRE patients, and as a result you don’t see a great impact of VRE as causing mortality."
Conference speaker Robert Weinstein, MD, director of the division of infectious diseases at Cook County Hospital in Chicago, said VRE is, indeed, a bit of a "wimpy" pathogen, but it still poses the risk of life-threatening infections to a subset of immunocompromised patients, such as transplant recipients.
"I think the presence of this bug is actually fortunate in that it is a call to attention to the emergence of potentially untreatable pathogens," he said. "It is fortunate that this first one is a little easier to deal with, at least from the clinical standpoint. It is alerting us and getting us ready for vancomycin-resistant Staph aureus, which will be a much more virulent pathogen and much more difficult to deal with. This is a kind of training exercise for us to get our systems up and going for antibiotic controls and better infection control."
VRE is a particularly troublesome nosocomial pathogen because it can cause prolonged contamination in the patient environment, and can survive for up to an hour on the hands of health care workers, Weinstein added. While commonly found in the gastrointestinal tract of colonized patients, VRE can also soil the skin and linger in the environment on bedside rails, medical equipment, bed linens, and gowns, he added.
"In essence, sources of VRE can include the patient’s gut flora, just like gram-negative bacilli; contamination of the patient’s skin, just like MRSA does; or contamination of the patient’s environment, just like C. diff. does," he said. "VRE represents a triple threat because it can originate through the patient’s gut, skin, and environment."
While it is hard to tell whether animate or inanimate reservoirs are more responsible for transient hand carriage by health care workers, proper hand washing continues to be the critical measure to prevent the spread of VRE, emphasized conference speaker Ava D. Lancaster, RN, BSN, CIC, director of infection control at St. Thomas Hospital in Nashville, TN.
"Wash with an antiseptic soap immediately after gloves are removed because gloves can leak and contaminate hands," she recommended. "Bland soap has been shown to be relatively ineffective in killing VRE on hands, although even these soaps will remove most superficial VRE."
In addition to infection control measures, antibiotic controls are critical because the only patient risk factor clinicians may be able to adjust for is receipt of vancomycin, Jarvis adds. In reviewing both outbreaks and endemic settings, Jarvis said the CDC is finding that receipt of vancomycin is one of the strongest risk factors for the acquisition of VRE, including both colonization and infection. The use of vancomycin is often associated with the presence of MRSA in the patient population.
"Infection control and pharmacy personnel should work together, identifying subspecialty groups using the most vancomycin and evaluating the appropriateness of that use," he said. "Educa tion and intervention programs for direct patient care staff could help curb improper use. A more drastic measure restriction policies may be implemented to enforce limits on vancomycin use."
If fully implemented, the CDC infection control measures and antibiotic controls can be effective, added Lancaster, immediate past president of the Association for Professionals in Infection Control and Epidemiology in Washington, DC.
"We have been able to control the transmission of VRE by using the recommendations of the CDC guidelines," she said. "I want to stress the importance of involving the entire facility to control this pathogen. You must collaborate among all disciplines if you are going to effectively deal with the many problems associated with VRE. This means aggressive infection control measures with strict compliance. Education is vital."
References
1. Centers for Disease Control and Prevention. Recommendations for preventing the spread of vancomycin resistance: recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC). MMWR 1995; 44:(No. RR-12)1-13.
2. Montecalvo MA, Uman J, Petrullo C, et al. The cost-benefit of enhanced infection control strategies to prevent transmission of vancomycin resistant enterococci. Abstract J-84. Toronto: Interscience Conference on Antimicrobial Agents and Chemotherapy; 1997.
3. Centers for Disease Control and Prevention. Reduced susceptibility of Staphylococcus aureus to vancomycin Japan, 1996. MMWR 1997; 46:624-626.
4. Centers for Disease Control and Prevention. Staphylococcus aureus with reduced susceptibility to vancomycin United States, 1997. MMWR 1997; 46:765-766.
5. Centers for Disease Control and Prevention. Update: Staphylococcus aureus with reduced susceptibility to vancomycin United States, 1997. MMWR 1997; 46:813-814.
6. Shay DK, Maloney SA, Montecalvo M, et al. Epidemiology and mortality risk of vancomycin-resistant enterococcal bloodstream infections. J Infect Dis 1995; 172:993-1000.
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