Current Diagnosis & Treatment in Infectious Diseases

Section V - Bacterial Infections

49. Enterococci

Robin Patel MD

Essentials of Diagnosis

  • Gram stain shows gram-positive cocci that occur in singles, pairs, and short chains; recovery of microorganism from culture of blood or other sterile source.
  • Lancefield group D antigen.
  • Clinical isolates: Enterococcus faecalis, 74%; E faecium, 16%; other species, 10%.
  • Facultative anaerobes grow in 6.5% NaCl at pH 9.6 and at temperatures ranging from 10°C to 45°C, and grow in the presence of 40% bile salts and hydrolyze esculin and L-pyrrolidonyl-β-naphthylamide.
  • Infections typically of a gastrointestinal or genitourinary origin.
  • The most common infections are urinary tract infection, bacteremia, endocarditis, intra-abdominal and pelvic infection, and wound and soft tissue infection.

General Considerations

  • Epidemiology.Enterococci are able to grow and survive under harsh conditions and can be found in soil, food, water, and a wide variety of animals. The major habitat of these organisms is the gastrointestinal tract of humans and other animals, where they make up a significant portion of the normal gut flora. Most enterococci isolated from human stools are E faecalis, although E faecium are also commonly found in the human gastrointestinal tract. Small numbers of enterococci are occasionally found in oropharyngeal and vaginal secretions and on the skin, especially in the perineal area. Because enterococci are part of the normal gut flora of almost all humans, infections caused by these organisms may be endogenously acquired from the patient's own flora.

Enterococcal infections also occur in hospitalized patients or in patients undergoing peritoneal or hemodialysis, and the organisms causing such infections often appear to be exogenously acquired. There is clear-cut evidence for spread of strains of enterococci between patients and even for dissemination of such strains from one institution to another. Strains of enterococci causing nosocomial infections have been found on the hands of medical personnel and on environmental surfaces in hospitals and in nursing homes. Most likely, enterococci from patients or hospital personnel first colonize the gastrointestinal tract (or occasionally the skin and groin or other contiguous areas) before causing infections in other patients. Devices such as electronic rectal thermometers may also aid in the spread of enterococci, especially antibiotic-resistant enterococci.

Enterococci account for 12% of nosocomial bacterial infections. The most common nosocomial enterococcal infections involve the urinary tract (62% of cases) and are often associated with urinary tract instrumentation or structural abnormalities. Wound infections are the next most common presentation of nosocomial enterococcal infections, usually involving abdominal or pelvic sites (25% of cases). Bacteremia (10% of cases) is the third most commonly reported nosocomial enterococcal infection.

Risk factors for acquiring nosocomial enterococcal infection or colonization, especially those caused by vancomycin-resistant enterococci (VRE), include being critically ill; having severe underlying disease; being immunosuppressed (especially patients on oncology or transplant wards); having renal insufficiency; undergoing intra-abdominal or cardiothoracic surgical or other invasive procedures; having an indwelling urinary or central venous catheter; having a prolonged hospital or intensive care unit stay; intrahospital transfer between floors; multi-antimicrobial agent, third-generation cephalosporin, anti-anaerobic antimicrobial or vancomycin therapy; proximity to infected patients; care by colonized staff; and the receipt of selective bowel decontamination, sucralfate, or enteral feedings.

  • Microbiology.Enterococci are gram-positive cocci that occur in singles, pairs, and short chains. The genus Enterococcus contains over a dozen species. E faecalis isolates account for ~74% of organisms encountered in the clinical microbiology laboratory. E faecium accounts for 16% of such isolates. The other Enterococcus species, including E durans, E avium, E casseliflavus, E gallinarum, E raffinosus, and E hirae (among others), are encountered clinically in ~10% of cases. Enterococci are facultative anaerobes that are able to grow in 6.5% NaCl at pH 9.6 and at temperatures ranging from 10 to 45°C. They carry the Lancefield group D antigen and will grow in the presence of 40% bile salts. They hydrolyze esculin and L-pyrrolidonyl-β-naphthylamide.

Enterococci are characterized by intrinsic resistance to many antibiotics (eg, oxacillin, clindamycin, cephalosporins, and aminoglycosides) and the capacity to acquire resistance to many others. The uniformly poor activity of β-lactams, particularly cephalosporins, against enterococci results from reduced affinity of the penicillin-binding proteins. Unlike most streptococci, enterococci are inhibited but not killed by apparently active penicillins (ampicillin, mezlocillin, penicillin, piperacillin), carbapenems (imipenem, meropenem), and glycopeptides (vancomycin or teicoplanin). Cephalosporins are not clinically useful against enterococci.

Enterococci are also naturally resistant to clinically achievable levels of aminoglycosides used alone. For treating serious enterococcal infections, combination therapy is recommended, generally penicillin, ampicillin, or vancomycin with an aminoglycoside, usually gentamicin or streptomycin. The rationale for this approach is to weaken the cell wall with the cell wall-active agent, thereby facilitating entry of the then bactericidal aminoglycoside. Such combinations have been shown to be synergistic, as long as the organism is susceptible to the cell wall-active agent and does not demonstrate high-level resistance to the aminoglycoside (gentamicin minimum inhibitory concentration < 500 µg/mL, streptomycin minimum inhibitory concentration < 2000 µg/mL).

Acquired resistance in enterococci can develop by genetic mutation or by acquiring altered DNA from a resistant organism. Enterococci have been reported to have acquired high-level resistance to aminoglycosides, cell wall-active agents (including penicillins and vancomycin), chloramphenicol, clindamycin, erythromycin, and the newer quinolones. E faecium isolates exhibit more antibiotic resistance than do other species.

Most enterococci with high-level resistance to aminoglycosides contain aminoglycoside-modifying enzymes. When high-level resistance to aminoglycosides is a concern, only gentamicin and streptomycin minimum inhibitory concentrations need to be tested in the clinical microbiology laboratory because the enzyme that neutralizes gentamicin also modifies tobramycin, amikacin, kanamycin, and netilmicin but not streptomycin. In addition to enzymatic resistance, ribosomal modification has been described as a second mechanism for high-level streptomycin resistance.

Acquired resistance to ampicillin and penicillin is generally caused by altered penicillin-binding proteins. This confers higher levels of resistance than the intrinsic resistance present in enterococci. This mechanism confers resistance to all β-lactams (including the carbapenems). β-lactamase production among enterococci is rare and has been reported in a few hospitals.

In the background of increasing resistance of enterococci to penicillins and aminoglycosides, vancomycin resistance emerged in the late 1980s. In vancomycin-resistant cells, an abnormal pentapeptide peptidoglycan precursor, with which vancomycin interacts minimally, is synthesized and incorporated into the cell wall of the organism. Resistance to the glycopeptide antibiotic vancomycin in enterococci, as understood to date, is phenotypically and genotypically heterogeneous. Three glycopeptide resistance phenotypes, VanA, VanB, and VanC, have been described in enterococci; they can be distinguished by the level and inducibility of resistance to vancomycin and teicoplanin. VanA-type glycopeptide resistance is characterized by acquired inducible resistance to both vancomycin and teicoplanin, and it is transferable. VanB-type glycopeptide resistance is characterized by acquired inducible resistance to various concentrations of vancomycin but not to teicoplanin, and it is also transferable. VanC-type glycopeptide resistance is characterized by low-level vancomycin resistance but teicoplanin susceptibility and has been described as an intrinsic property of most isolates of E gallinarum, E casseliflavus, and E flavescens. VanD-, VanE- and VanG- type glycopeptide resistance have been recently described and do not appear to be common.

  • Pathogenesis.Little is known about specific pathogenesis and virulence factors of enterococci. Enterococcal bacteremia has, however, been associated with high mortality rates (42–68%). In many cases, enterococci cause infections in severely debilitated hosts and are part of a polymicrobial infection. Thus their independent contribution to mortality and morbidity is difficult to assess. The intrinsic and acquired resistance of enterococci to many antimicrobial agents, as discussed previously, is an important factor that allows these organisms to survive and proliferate in patients receiving antimicrobial therapy. In addition, enterococci are able to adhere to heart valves and renal epithelial cells, properties that likely contribute to their ability to cause endocarditis and urinary tract infections, respectively.

Although enterococci are found in one-fifth of intra-abdominal infections, their exact role in polymicrobial infection is controversial. In cases of intra-abdominal infections, selective therapy against Escherichia coli and Bacteroides fragilis, which has minimal in vitro activity against enterococci, has been found to be sufficient to reduce enterococcal counts. Nevertheless, in animal models of experimental polymicrobial intra-abdominal infection, enterococci have been found to enhance abscess formation, weight loss, and mortality. Similarly, clinical reports have indicated the emergence of enterococcal abscesses and bacteremia after treatment of intra-abdominal sepsis with antimicrobial agents that lack significant in vitro enterococcal activity. A recent multicenter study of intra-abdominal infection has found that the presence of enterococci in the initial cultures, in addition to serious underlying disease, independently predicts treatment failure with broad-spectrum antimicrobial regimens that lack specific enterococcal activity.

 

CLINICAL SYNDROMES

URINARY TRACT INFECTION

Urinary tract infections, including uncomplicated cystitis, pyelonephritis, prostatitis, and perinephric abscess, are the most common type of clinical infections produced by enterococci (Box 49-1). Most enterococcal urinary tract infections are nosocomial and are associated with urinary catheterization or instrumentation.

BACTEREMIA & ENDOCARDITIS

Nosocomial enterococcal bacteremias are commonly polymicrobial. Portals of entry for enterococcal bacteremia include the urinary tract, intra-abdominal or pelvic sources, wounds (especially burns, decubitus ulcers, and diabetic foot infections), intravascular catheters, and the biliary tree. Metastatic infections other than endocarditis are rare in enterococcal bacteremia.

Enterococci account for ~5–10% of all cases of infective endocarditis (see Chapter 11). Most cases are caused by E faecalis, but E faecium, E casseliflavus, E durans, E gallinarum, and E raffinosus have also been isolated from patients with endocarditis. Only ~2% of cases of enterococcal bacteremia are associated with endocarditis, and this is much more common in patients whose bacteremia is community acquired versus those with nosocomial enterococcal bacteremia. Enterococcal endocarditis is a disease of older patients, with males outnumbering females in most series. Most cases occur in patients with underlying valvular heart disease or prosthetic valves, although enterococci are capable of causing infections of anatomically normal valves. An association between enterococcal endocarditis and urinary tract infection or urinary instrumentation in older men and abortion or childbirth in younger women has been suggested. Enterococci usually produce left-sided endocarditis with more frequent involvement of the mitral than the aortic valve. The typical clinical course of enterococcal endocarditis is that of subacute bacterial endocarditis. There is a suggestion that the relapse rate is higher in patients who have had symptoms of endocarditis for ≥ 3 months before treatment, which has implications for length of therapy (see below).

BOX 49-1 Enterococcal Infections

More Common

· Urinary tract infection

· Bacteremia

· Endocarditis

· Wound and soft tissue infection

· Intra-abdominal and pelvic infection

Less Common

· Meningitis

· Neonatal sepsis

INTRA-ABDOMINAL & PELVIC INFECTION

Enterococci are frequently found as part of mixed aerobic and anaerobic flora in intra-abdominal and pelvic infections. As discussed above, the exact role of enterococci in these mixed aerobic and anaerobic intra-abdominal and pelvic infections is unclear. Enterococci can cause spontaneous peritonitis in patients with nephrotic syndrome or cirrhosis and can cause peritonitis in patients undergoing chronic ambulatory peritoneal dialysis. Monomicrobial enterococcal peritonitis is also occasionally seen as a complication of abdominal surgery or trauma. Enterococci can produce abscesses and bacteremia as a complication of endometritis, Cesarean section, and acute salpingitis.

WOUND & SOFT TISSUE INFECTION

Enterococci may be isolated from mixed cultures with gram-negative bacilli and anaerobes in surgical wound infections, decubitus ulcers, and diabetic foot infections; the significance of enterococci in these settings is difficult to assess. Enterococcal wound colonization and sepsis have been described in burn patients whose wounds have been covered with porcine xenografts presumably contaminated with enterococci. Enterococci occasionally cause chronic osteomyelitis.

MENINGITIS

Enterococci rarely cause meningitis. Most cases occur in patients who have anatomic defects of the central nervous system or who have had previous neurosurgery or head trauma. Rarely, however, meningitis may be a complication of high-grade bacteremia such as that seen in patients with enterococcal endocarditis. Meningitis may also be seen in association with enterococcal bacteremia in patients with human immunodeficiency virus infection and acute leukemia and in neonates and transplant recipients.

NEONATAL SEPSIS

Enterococci may cause neonatal sepsis characterized by fever, lethargy, and respiratory difficulty accompanied by bacteremia, meningitis, or both. Early onset bacteremia in otherwise normal neonates may be seen, as well as nosocomial bacteremia, meningitis, or both, which has been described in premature or low-birth-weight neonates who have nasogastric tubes and intravascular devices.

Diagnosis

The diagnosis of enterococcal infection is made by isolating enterococci from typically sterile sites (eg, urine, blood, intra-abdominal or pelvic fluid, or spinal fluid). As discussed above, community acquisition of enterococcal bacteremia suggests the possible presence of endocarditis. The diagnosis of endocarditis, in the appropriate clinical context (see Chapter 11), may be further confirmed by the presence of clinical findings consistent with endocarditis as well as by the use of echocardiography. The diagnosis of intra-abdominal and pelvic infections, in the appropriate clinical context, can be assisted by the use of ultrasound or computed tomographic imaging with drainage, Gram stain, and culture of any fluid collection(s) present.

The diagnosis of enterococcal meningitis can be confirmed by the isolation of enterococci from the spinal fluid. Typically, enterococcal meningitis is associated with a low cerebrospinal fluid leukocyte count (< 200/mL), although this is not always the case.

The isolation of enterococci from respiratory secretions is of questionable significance, although there are very rare well-documented cases of enterococcal pneumonia and even lung abscesses in patients with severe and debilitating diseases.

Treatment

Penicillin or ampicillin remains the antibiotic of choice for treating enterococcal infections such as urinary tract infections, peritonitis, and wound infections (ie, infections that do not require bactericidal treatment) (Box 49-2). Vancomycin is the alternative agent for patients allergic to penicillin or for organisms with high-level penicillin resistance that are β-lactamase negative and vancomycin susceptible.

Combination therapy with a cell wall-active agent such as penicillin, ampicillin, or vancomycin, along with an aminoglycoside, is essential for the treatment of enterococcal endocarditis and probably for enterococcal meningitis as well. The situation is not as clear-cut for enterococcal bacteremia alone; there is no consensus as to whether combination therapy is required in this setting.

For the treatment of enterococcal endocarditis, combinations of cell wall-active agents such as penicillin, ampicillin, or vancomycin with aminoglycosides (usually streptomycin or gentamicin) are required (see Chapter 11 for specific treatment recommendations). In most cases, 4 weeks of combination therapy appear to be adequate, with a 6-week regimen reserved for patients who have had symptoms for > 3 months before starting treatment, for patients with prosthetic valves, or for patients who have relapsed after previous shorter courses of therapy.

Most strains of enterococci are susceptible to nitrofurantoin, and this agent has been successfully used to treat uncomplicated enterococcal infections limited to the urinary tract. The quinolones such as ciprofloxacin, ofloxacin, levofloxacin, gatifloxacin, enoxacin, and norfloxacin have in vitro activity against enterococci and may be useful for treating some enterococcal urinary tract infections, but their effectiveness for enterococcal infections in general has not been convincingly demonstrated, and increasing resistance has been demonstrated. Tetracyclines and chloramphenicol may exhibit in vitro activity against some strains of enterococci, but they are only bacteriostatic against enterococci, and clinical failures of chloramphenicol and tetracyclines have been reported.

The emergence of multiply resistant enterococci now greatly complicates therapeutic choices. For patients who have endocarditis caused by enterococci with high-level gentamicin resistance, it is useful to test for high-level streptomycin resistance because some highly gentamicin-resistant strains are synergistically killed by cell wall-active agents plus streptomycin. For endocarditis due to strains with both high-level streptomycin and gentamicin resistance, no combination will consistently produce synergism. These patients may be treated with prolonged courses (8–12 weeks) of intravenous ampicillin given by continuous infusion, although this approach should be considered experimental at this time. Surgical excision of infected valves may be required in such cases.

Infections caused by enterococci with high-level penicillin resistance and β-lactamase negativity should be treated with vancomycin. β-lactamase–producing, penicillin- and ampicillin-resistant enterococci remain susceptible to β-lactam–β-lactamase inhibitor combinations such as ampicillin-sulbactam and amoxicillin-clavulanate. VRE that remain susceptible to penicillin or ampicillin may be treated with penicillin or ampicillin. Infections caused by organisms with both high-level penicillin resistance and vancomycin resistance should be treated with either quinupristin-dalfopristin or linezolid. Notably, E faecium is more susceptible to quinupristin-dalfopristin than is E faecalis. Neither quinupristin-dalfopristin nor linezolid have bactericidal activity against VRE resulting in enormous challenges in the management of VRE endocarditis.

Prevention & Control

Prophylaxis for Infective Endocarditis. Antimicrobial prophylaxis for enterococcal endocarditis is recommended for patients with certain cardiac lesions predisposing to endocarditis who undergo invasive procedures with an increased risk of enterococcal bacteremia. Details of patients, procedures, and regimens are outlined in Chapter 11.

BOX 49-2 Treatment of Enterococcal Infectionsg1

 

Uncomplicated Urinary Tract Infection

Bacteremia, Intraabdominal or Pelvic Infection, Wound or Soft Tissue Infection, and Neonatal Sepsis

First Choice

· Amoxicillin, 250–500 mg orally every 8h
OR

· Ampicillin, 250–500 mg orally every 6 h

· Aqueous crystalline penicillin G, 18–30 million U/24 h IV either continuously or in 6 equally divided doses with or without gentamicin2 (1 mg/kg IV/IM every 8h)
OR

· Amipicillin sodium 12 g/24 h IV in 6 equally divided doses with or without gentamicin2 (1 mg/kg IM/IV every 8 h)

Second Choice

· Nitrofurantoin, 50–100 mg orally every 6 h
OR

· Ofloxacin, 200 mg orally every 12 h
OR

· Ciprofloxacin, 250–500 mg orally every 12 h
OR

· Levofloxacin, 250 mg orally every d
OR

· Norfloxacin, 400 mg orally every 12 h
OR

· Enoxacin, 200–400 mg orally every 12 h
OR

· Gatifloxacin, 200–400 mg orally every d

· Vancomycin, 30 mg/kg/24 h IV in 2 doses, not to exceed 2 g/24 h unless serum levels are monitored with or without gentamicin2 (1 mg/kg IV/IM every 8 h)

Pediatric Considerations

· Amoxicillin, 25–50 mg/kg/d in divided doses every 8 h

· Penicillin G, 100,000–250,000 U/kg/24 h IV/IM in divided doses every 4 h with or without gentamicin2 (1 mg/kg IM/IV every 6 h)
OR

· Ampicillin, 100–200 mg/kg/24 h IM/IV in 4–6 divided doses with or without gentamicin2 (1 mg/kg IV/IM every 6 h)

Penicillin Allergic/ High-Level Penicillin Resistance, β-Lactamase-Negative

· Nitrofurantoin, 50–100 mg orally every 6 h
OR

· Ofloxacin, 200 mg orally every 12 h
OR

· Ciprofloxacin, 250–500 mg orally every 12 h
OR

· Levofloxacin, 250 mg orally every d
OR

· Norfloxacin, 400 mg orally every 12 h
OR

· Enoxacin, 200–400 mg orally every 12 h
OR

· Gatifloxacin, 200–400 mg orally every d

· Vancomycin, 30 mg/kg/24 h IV in 2 doses, not to exceed 2 g/24 h unless serum levels are monitored with or without gentamicin2 (1 mg/kg IV/IM every 8 h)

Vancomycin and Penicillin Resistance

· Nitrofurantoin, 50–100 mg orally every 6 h

· Quinupristin/Dalfopristin, 7.5 mg/kg IV every 8 h

· Linezolid, 600 mg IV orally every 12 h

1Doses provided are for patients with normal renal function (creatinine clearance >70 mL/min). Abbreviations: IV, intravenously; IM, intramuscularly.
2For isolates without high-level gentamicin resistance.

Prevention of Vancomycin Resistance. From 1989 to 1993, the percentage of nosocomial enterococcal infections reported to the Centers for Disease Control and Prevention's National Nosocomial Infection Surveillance System that were caused by VRE increased from 0.3 to 7.9%. This overall increase primarily reflected the 34-fold increase in the percentage of VRE infections in patients in intensive care units (ie, from 0.4 to 13.6%), although a trend toward an increased percentage of VRE infections in non-intensive care patients was also noted.

Laboratory experiments have achieved the transfer of high-level vancomycin resistance from enterococci to Staphylococcus aureus, and reduced susceptibility of S aureus to vancomycin has recently been described in clinical S aureus isolates, although the mechanism of the latter resistance differs from that in enterococci. Vancomycin resistance has also been transferred by conjugation or transformation from enterococci to Streptococcus sanguis, Lactococcus lactis, Streptococcus pyogenes, and Listeria monocytogenes. The vanA gene has been found in vancomycin-resistant clinical isolates of Oerskovia turbata and Arcanobacterium haemolyticum (typically these organisms are vancomycin susceptible) isolated from the stools of two patients during an outbreak of VRE infection in London. The vanA gene has been identified in a Bacillus circulans clinical isolate. The vanB gene has recently been found in a vancomycin-resistant isolate of Streptococcus bovis isolated from a stool swab collected from a patient on admission as surveillance for VRE. The potential for emergence of vancomycin resistance in clinical isolates of Staphylococcus epidermidis, Streptococcus pneumoniae, viridans streptococci, and Corynebacterium spp. as a result of transfer of vancomycin resistance genes from enterococci is also a public health concern.

Table 49-1. Recommendations for preventing the spread of vancomycin resistance: prudent vancomycin use.

Situations in Which the Use of Vancomycin Is

Acceptable

Discouraged

· For treatment of serious infections caused by β-lactam-resistant gram-positive microorganisms

· For treatment of infections caused by gram-positive microorganisms in patients who have serious allergies to β-lactam antimicrobial agents

· When antibiotic-associated colitis fails to respond to metronidazole therapy or is severe and potentially life-threatening

· For prophylaxis as recommended by the American Heart Association for endocarditis following certain procedures in patients at high risk for endocarditis (see Chapter 11)

· Prophylaxis for major surgical procedures involving implantation of prosthetic materials or devices (eg, cardiac and vascular procedures and total hip replacement) at institutions that have a high rate of infections caused by methicillin-resistant Staphylococcus aureus or methicillin-resistant S epidermidis. (A single dose of vancomycin administered immediately before surgery is sufficient unless the procedure lasts more than 6 h, in which case the dose should be repeated. Prophylaxis should be discontinued after a maximum of two doses)

· Routine prophylaxis other than in a patient who has a life-threatening allergy to β-lactam antibiotics

· Empiric antimicrobial therapy for a febrile, neutropenic patient unless initial evidence indicates that the patient has an infection caused by gram-positive microorganisms (eg, an inflamed exit site of a Hickman catheter) and the prevalence of infections caused by methicillin-resistant S. aureusin the hosipital is substantial

· Treatment in response to a single blood culture positive for coagulase-negative Staphylococcusspp. if other blood cultures taken during the same time frame are negative (ie, if contamination of the blood culture is likely) (Because contamination of blood cultures with skin flora (eg, S epidermidis) could result in inappropriate administration of vancomycin, phlebotomists and other personnel who obtain blood cultures should be trained to minimize microbial contamination of specimens)

· Continued empiric use for presumed infections in patients whose cultures are negative for β-lactam-resistant, gram-positive microorganisms

· Systemic or local (eg, “antibiotic lock”) prophylaxis for infection or colonization of indwelling central or peripheral intravascular catheters

· Selective decontamination of the digestive tract

· Eradication of methicillin-resistant S aureus colonization

· Primary treatment of antibiotic-associated colitis

· Routine prophylaxis of very-low-birth-weight infants (ie, infants who weigh less than 1,500 g)

· Routine prophylaxis for patients on continuous ambulatory peritoneal dialysis

· Treatment chosen for dosing convenience of infections caused by β-lactam sensitive, gram-positive microorganisms in patients who have renal failure

· Use of vancomycin solution for topical application or irrigation

In November 1994, the Hospital Infection Control Practices Advisory Committee of the Centers for Disease Control and Prevention issued the following recommendations for preventing and controlling the spread of vancomycin resistance with a special focus on VRE. It was recommended that each hospital through collaboration of its quality improvement and infection control programs; pharmacy and therapeutics committee; microbiology laboratory; clinical departments; and nursing, administrative, and housekeeping services, develop a comprehensive institution-specific strategic plan to detect, prevent, and control infection and colonization with VRE. The first aspect of this plan incorporated prudent vancomycin use. (Vancomycin has been reported as a risk factor for infection and colonization with VRE.) (Table 49-1.)

BOX 49-3 Prevention of VRE Transmission

· All patients harboring VRE should be placed in private rooms or the same room as other patients who have VRE.

· Clean, nonsterile gloves should be worn when entering the room of a VRE-infected or-colonized patient.

· When caring for such a patient, a change of gloves is necessary after contact with material that could contain high concentrations of VRE (eg, stool).

· A gown should be worn when entering the room of a VRE patient if (a) substantial contact with the patient or with environmental surfaces in the patient's room is anticipated; (b) the patient is in-continent; or (c) the patient has had an ileostomy or colostomy, has diarrhea, or has a wound drainage not contained by the dressing.

· Gloves and gowns should be removed before leaving the patient's room, and the health care worker's hands should be washed with antiseptic soap or waterless antiseptic agent.

· Dedicated noncritical items such as stethoscopes, sphygmomanometers, and rectal thermometers should be assigned to a single patient or cohort of patients infected or colonized with VRE.

· If such devices are to be used on other patients, they should be adequately cleaned and disinfected first.

In addition, education programs concerning the epidemiology of VRE and the potential impact of this pathogen on the cost and outcome of patient care were recommended for hospital staff including attending and consulting physicians; medical residents and students; pharmacy, nursing, and laboratory personnel; and other direct patient care providers. Specific recommendations were also issued for the microbiology laboratory regarding the detection, reporting, and control of VRE. In addition, recommendations were given regarding how to proceed when VRE are isolated from a clinical specimen, how to screen for detection of VRE, and how to prevent transmission of VRE once identified (Box 49-3). Recommendations for screening for roommates found to be infected or colonized with VRE were also issued.

REFERENCES

Centers for Disease Control and Infection: Nosocomial enterococci resistant to vancomycin—United States, 1989–1993. Morbid Mortal Weekly Rep 1993; 42: 597–99.

Hospital Infection Control Practices Committee. 1995 Recommendations for preventing the spread of vancomycin resistance. J Infect Control Hosp Epidemiol 1995;6: 105–13.