Vancomycin-resistant enterococci epidemiology and demographics
Vancomycin-resistant enterococci Microchapters |
Differentiating Vancomycin-Resistant Enterococci from other Diseases |
---|
Diagnosis |
Treatment |
Case Studies |
Vancomycin-resistant enterococci epidemiology and demographics On the Web |
American Roentgen Ray Society Images of Vancomycin-resistant enterococci epidemiology and demographics |
FDA onVancomycin-resistant enterococci epidemiology and demographics |
CDC on Vancomycin-resistant enterococci epidemiology and demographics |
on Vancomycin-resistant enterococci epidemiology and demographics |
Directions to Hospitals Treating Vancomycin-resistant enterococci |
Risk calculators and risk factors for Vancomycin-resistant enterococci epidemiology and demographics |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Please help WikiDoc by adding more content here. It's easy! Click here to learn about editing.
Epidemiology and Demographics
Developed Countries
In the United States, nosocomial transmission of VRE from patient to patient has been emphasized. Although VRE introduced into hospitals by colonized patients from VRE-endemic settings has been reported, it is unclear how VRE is first introduced into most U.S. hospitals.
Although no data so far support significant acquisition and transmission of VRE outside the health-care setting in the United States, a growing number of reports from Europe suggest that colonization with VRE frequently occurs in the community. Reports from Europe also have suggested that VRE exist elsewhere in the environment, including animal feces and human foods of animal origin. Additional evidence supports the transmission of VRE to persons in contact with these sources, resulting in an increased human reservoir of VRE colonization. If VRE is frequently introduced into health-care settings from community sources, its control will require community-based initiatives, unlike measures used to control nosocomial pathogens.
This review summarizes the existing evidence for community acquisition and transmission of VRE outside the health-care setting in Europe, relates these findings to the epidemiology of VRE in the United States, discusses steps to stem community transmission of VRE, and identifies research needs.
Nosocomial Infections
Enterococci account for approximately 110,000 urinary tract infections, 25,000 cases of bacteremia, 40,000 wound infections, and 1,100 cases of endocarditis annually in the United States. Most infections occur in hospitals. Although several studies have suggested an increase in nosocomial infection rates for enterococci in recent years, National Nosocomial Infections Surveillance system data show little change in the percentage of enterococcal bloodstream (12% vs. 7%), surgical site (15% vs. 11%), and urinary tract (14% vs. 14%) infections over the past 2 decades. Adequate surveillance data prior to 1980 are not available. Enterococcal infection deaths have also been difficult to ascertain because severe comorbid illnesses are common; however, enterococcal sepsis is implicated in 7% to 50% of fatal cases. Several case-control and historical cohort studies show that death risk associated with antibiotic-resistant enterococcal bacteremia is severalfold higher than death risk associated with susceptible enterococcal bacteremia. This trend will likely increase as multiple drug resistant (MDR) isolates become more prevalent.
Colonization
Colonization and infection with MDR enterococci occur worldwide. Early reports showed that in the United States, the percentage of nosocomial infections caused by VRE increased more than 20-fold (from 0.3% to 7.9%) between 1989 and 1993, indicating rapid dissemination. New database technologies, such as The Surveillance Network (TSN) Database-USA, now permit the assessment of resistance profiles according to species. TSN Database electronically collects and compiles data daily from more than 100 U.S. clinical laboratories, identifies potential laboratory testing errors, and detects emergence of resistance profiles and mechanisms that pose a public health threat (e.g., vancomycin-resistant staphylococci).
Resistance
Data collected by the TSN Database between 1995 and September 1, 1997 were analyzed to determine whether the earlier increase in vancomycin resistance was unique to vancomycin, whether it represented a continuing trend, and whether speciation is quantifiably important in analyzing this trend. E. faecalis resistance to ampicillin and vancomycin is uncommon; little change in resistance prevalence occurred from 1995 to 1997. In contrast, E. faecium vancomycin and ampicillin resistance increased alarmingly. In 1997, 771 (52%) of 1,482 of E. faecium isolates exhibited vancomycin resistance, and 1,220 (83%) of 1,474 isolates exhibited ampicillin resistance. E. faecium resistance notwithstanding, E. faecalis remained by far the most commonly encountered of the two enterococcal species in TSN Database. E. faecalis to E. faecium total isolates were approximately 4:1, blood isolates 3:1, and urine isolates 5:1. This observation underscores important differences in the survival strategies and likelihood of therapeutic success, critical factors usually obscured by lumping the organisms together as Enterococcus species or enterococci. Widespread emergence and dissemination of ampicillin and vancomycin resistance in E. faecalis would significantly confound the current therapeutic dilemma. There is little reason to suspect that vancomycin and ampicillin resistances only provide selective advantage for the species faecium and not faecalis. The relative absence of these resistances in E. faecalis may simply reflect a momentary lack of penetrance and equilibration of the traits. Because of these important differences between the two species, meaningful surveillance of enterococcal resistance must include species identification.
Vancomycin Use
Vancomycin use in U.S. hospitals has increased dramatically in the past 10 to 15 years because of a variety of factors, including increases in the incidence of methicillin-resistant staphylococci, prosthetic device-related infections, Clostridium difficile colitis, and inappropriate use of the drug. Although vancomycin and other glycopeptide use in European health-care settings has not been similarly documented, this marked increase in human glycopeptide use is thought to be primarily a U.S. phenomenon. Because the use of vancomycin and other antimicrobial drugs is an important risk factor for human VRE infection, if glycopeptides were prescribed in European hospitals at levels common in U.S. hospitals, there might be an even greater incidence of VRE infections in Europe. Likewise, given the suspected greater use of glycopeptides in U.S. hospitals, if community carriage of VRE were to increase in the United States, there might be an even greater incidence of VRE infections in U.S. hospitals.