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Vancomycin, a glycopeptide, was discovered in the mid-1950s. The drug inhibits peptidoglycan synthesis. Vancomycin has been the mainstay of therapy for infection with gram-positive organisms, including methicillin-resistant Staphylococcus aureus, coagulase-negative staphylococci, penicillin-resistant Streptococcus pneumoniae, and enterococci. The two most important enterococcal species are Enterococcus faecalis and Enterococcus faecium, with the former accounting for 80% of clinical isolates. Among vancomycin-resistant enterococci (VRE), 90% of the isolates are E. faecium.
In the late 1980s, the first clinical isolate of VRE was identified first in Europe and then in the United States. From 1989 through 1993, the percentage of nosocomial VRE isolates reported to the surveillance system of the Centers for Disease Control increased from 0.3% to 7.9%. In patients in ICUs, the increase in VRE was more dramatic, with almost 14% of isolates being resistant. Rates of resistance of enterococci to vancomycin in the non-ICU setting have increased and are now similar to rates in the ICU. Most hospitals in the United States have encountered at least one strain of VRE. VRE in the community has not been a problem in the United States, but the risk exists for transmission of strains of VRE from colonized patients after they leave the hospital.
Resistance of vancomycin can be classified as three phenotypes. Strains with van A resistance show a high level of resistance to vancomycin [minimum inhibitory concentrations (MICs) ³64 µg/mL) and resistance to another glycopeptide, teicoplanin (MICs ³16 µg/mL). Van A resistance occurs in both E. faecalis and E. faecium. Isolates with van B resistance are resistant to vancomycin (MICs from 4 µg/mL to 1,000 µg/mL or higher) but remain susceptible to teicoplanin. Strains with van C resistance have a low level of resistance to vancomycin (MICs of 4 to 32 µg/mL) and are susceptible to teicoplanin. Van C resistance occurs in all isolates of Enterococcus gallinarum, an organism found in stool that does not appear to cause disease. VRE would not be such a serious problem if it were not for the fact that VRE are also resistant to ampicillin, oxacillin, cephalosporins, aminoglycosides, sulfa-trimethoprim, clindamycin, and the fluoroquinolones.
Enterococci, which are gram-positive cocci, are part of the normal gastrointestinal flora, and they are also found in small numbers in the mouth, vaginal secretions, and perineal skin. Enterococci rank second or third in frequency as causes of nosocomial infections in the United States. The sources of enterococci, which can either infect or colonize patients, are the patient’s own normal flora (endogenous) and the hands of hospital personnel (exogenous). Enterococci have also been isolated in the hospital environment from bed rails, blood pressure cuffs, electronic thermometers, telephone handsets, and the surfaces of stethoscopes. Cultures of the surface environment yielded VRE in 7% to 46% of samples. Use of the usual disinfectants should be adequate to eradicate VRE from environmental surfaces. However, one report found that 8% of cultures after terminal cleaning still showed VRE.
Risk factors for acquiring VRE include serious underlying illness, advanced age, immunosuppression, ICU residence, prior surgery, renal insufficiency, long hospital stay (7 days or more), presence of a urinary or vascular catheter, and use of antibiotics, especially third-generation cephalosporins, vancomycin, and drugs for anaerobes. Once colonized with VRE, patients may remain so for years. When patients are not taking antibiotics, VRE counts in the stool may decrease, resulting in false-negative stool cultures for VRE. Cultures may again become positive when the patient is again given an antibiotic.
Once a patient is identified as being either colonized or infected with VRE, contact precautions as recommended by the Hospital Infection Control Practices Advisory Committee (HICPAC) are instituted (Table 45-1).

Table 45-1. Precautions to prevent patient-to-patient transmission of vancomycin-resistant enterococci

Prudent use of vancomycin has been reported to decrease the risk for colonization and infection with VRE. Hospitals should adopt the guidelines recommended by HICPAC, which list the situations in which vancomycin use is appropriate and those in which its use should be discouraged (Table 45-2 and Table 45-3). In addition to the prudent use of vancomycin and institution of barrier precautions, a decreased use of cefotaxime, ceftazidime, and clindamycin was noted in one report to result in a marked decrease (from 47% to 15%) in stools positive for VRE. Contamination of the environment and equipment for patient care with VRE is a problem, especially when patients have diarrhea. Because many patients may have both VRE and Clostridium difficile, measures to reduce the incidence of C. difficile may decrease the environmental contamination with VRE.

Table 45-2. Indications for vancomycin treatment

Table 45-3. Situations in which the use of vancomycin should be discouraged

Treatment of infections caused by VRE remains a major problem. Chloramphenicol shows activity in vitro against many strains and has been used with modest success. Oral chloramphenicol is not available; the drug must be given intravenously. Treatment with high doses of ampicillin-sulbactam (30 g/d) has also had some success. Also effective has been surgical debridement with drainage of an abscess, and removal of a Foley catheter or IV catheter without any specific antibiotic treatment. Dalfopristin-quinupristin, a streptogramin antibiotic, may be effective against some strains of E. faecium, but not E. faecalis. Experimental agents, which include linezolid and the ketolides as well as a semisynthetic glycopeptide designated as LY333328, may have a role in the management of VRE. (NMG)
Anderson RL, et al. Susceptibility of vancomycin-resistant enterococci to environmental disinfectants. Infect Control Hosp Epidemiol 1997;18:195–199.
No special disinfectants or procedures are needed to eradicate VRE from environmental surfaces.
Beezhold DW, et al. Skin colonization with vancomycin-resistant enterococci among hospitalized patients with bacteremia. Clin Infect Dis 1997;24:704–706.
Skin colonization (inguinal area and or antecubital fossa) was common (86%) among patients with bacteremia and may be the source of catheter-related sepsis.
Bonilla HF, et al. Colonization with vancomycin-resistant Enterococcus faecium: comparison of a long-term-care unit with an acute-care hospital. Infect Control Hosp Epidemiol 1997;18:333–339.
VRE was found frequently (13% to 41%) on the hands of health care workers.
Boyce JM. Vancomycin-resistant enterococcus. Detection, epidemiology, and control measures. Infect Dis Clin North Am 1997;11:367–384.
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 Morb Mortal Wkly Rep 1995; 44 (RR12):1–13.
Control of VRE will require (a) appropriate use of vancomycin, (b) staff education regarding VRE, (c) detection of VRE, and (d) implementation of infection control measures.
Edmond MB, et al. Vancomycin-resistant enterococcal bacteremia: natural history and attributable mortality. Clin Infect Dis 1996;23:1234–1239.
The mortality rate for patients with VRE bacteremia was 67%, which was twice that for matched controls.
Eliopoulos GM. Vancomycin-resistant enterococci. Mechanism and clinical relevance. Infect Dis Clin North Am 1997;11:851–865.
Evans ME, Kortas KJ. Vancomycin use in a university medical center: comparison with Hospital Infection Control Practices Advisory Committee guidelines. Infect Control Hosp Epidemiol 1996;17:356–359.
Only 35% of the vancomycin orders were consistent with HICPAC guidelines.
Joshi N, Milfred D, Caputo G. Vancomycin-resistant enterococci: a review. Infect Dis Clin Pract 1996;5:528–537.
Review. Risk factors for VRE infection include advanced age; severe underlying illness; immunosuppression; ICU residence; surgery; antibiotic exposure, especially with vancomycin and third-generation cephalosporins; and use of invasive devices.
Lai KK. Treatment of vancomycin-resistant Enterococcus faecium infections. Arch Intern Med 1996;156:2579–2584.
Removal of the IV catheter or Foley catheter and surgical debridement without antibiotics were effective in eradicating VRE.
Lai KK, et al. The epidemiology of fecal carriage of vancomycin-resistant enterococci. Infect Control Hosp Epidemiol 1997;18:762–765.
VRE carriage is often prolonged (19 to 303 days).
Montecalvo MA, et al. Natural history of colonization with vancomycin-resistant Enterococcus faecium. Infect Control Hosp Epidemiol 1995;16:680–685.
The rate of VRE colonization was 10 times the rate of infection among oncology patients and often persists for a year.
Montecalvo MA, et al. Bloodstream infections with vancomycin-resistant enterococci. Arch Intern Med 1996;156:1458–1462.
VRE bacteremia often persists in the immunocompromised patient.
Noskin GA, et al. Recovery of vancomycin-resistant enterococci on fingertips and environmental surfaces. Infect Control Hosp Epidemiol 1995;16:577–581.
Enterococcus faecalis survived for 5 days and Enterococcus faecium for 7 days on countertops.
Porwancher R, et al. Epidemiological study of hospital-acquired infection with vancomycin-resistant Enterococcus faecium: possible transmission by an electronic ear probe thermometer. Infect Control Hosp Epidemiol 1997;18:1771–1773.
VRE transmitted by an electronic ear probe.
Quale J, et al. Manipulation of a hospital antimicrobial formulary to control an outbreak of vancomycin-resistant enterococci. Clin Infect Dis 1996;23:1020–1025.
Decreased use of cefotaxime, ceftazidime, and clindamycin was associated with a decrease in stool colonization with VRE.
Rafferty ME, et al. Vancomycin-resistant enterococci in stool specimens submitted for Clostridium difficile cytotoxin assay. Infect Control Hosp Epidemiol 1997;18:342–344.
Seventeen percent of stools submitted for C. difficile testing were positive for VRE.
Saurina G, Landman D, Quale JM. Activity of disinfectants against vancomycinresistant Enterococcus faecium. Infect Control Hosp Epidemiol 1997;18:345–347.
Except for 3% hydrogen peroxide, phenolic and quaternary ammonium compounds were effective in eradicating VRE after a 10-minute exposure.
Slaughter S, et al. A comparison of the effect of universal use of gloves and gowns with that of glove use alone on acquisition of vancomycin-resistant enterococci in a medical intensive care unit. Ann Intern Med 1996;125:448–456.
Use of gloves and gowns was no better than gloves alone in preventing rectal colonization by VRE.
Stroud L, et al. Risk factors for mortality associated with enterococcal bloodstream infections. Infect Control Hosp Epidemiol 1996;17:576–580.
The mortality rate was 69% for patients with VRE bacteremia. The high mortality caused by bacteremia occurred in a cohort of severely ill patients.
Tornieporth NG, et al. Risk factors associated with vancomycin-resistant Enterococcus faecium infection or colonization in 145 matched case patients and control patients. Clin Infect Dis 1996;23:767–772.
Prolonged hospitalization (³ 7 days), intrahospital transfers, and use of vancomycin or third-generation cephalosporins were associated with an increased risk for VRE infection or colonization.
Tucci V, Haran MA, Isenberg HD. Epidemiology and control of vancomycin-resistant enterococci in an adult and children’s hospital. Am J Infect Control 1997;25:371–376.
The majority (83%) of cases of VRE were nosocomial.
Weber DJ, Rutala WA. Role of environmental contamination in the transmission of vancomycin-resistant enterococci. Infect Control Hosp Epidemiol 1997;18:306–309.
Environmental contamination in patients with VRE ranges from 7% to 46%.



  1. How long after treatment started before diarrhea ceases

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