The incidence of enterococcal infections is increasing with the emergence of vancomycin-resistant strains. Enterococci are collectively the second most prevalent nosocomial isolate in the United States, representing more than 9 per cent. Enterococci were reported in 8 per cent of positive blood cultures taken because of suspected infection from a series of general and thoracic surgical patients, and represent an increasingly important cause of invasive burn wound infection.

Four enterococcal species can cause disease in humans. Enterococcus fecalis accounts for 85 per cent of isolates, whereas Enterococcus fecium accounts for 5 to 15 per cent of strains and Enterococcus casseliflavius and Enterococcus durans are rarely pathogens. Enterococcal infections may involve intra-abdominal or surgical wound foci, be complicated by bacteremia, or follow manipulation of the urinary tract, placement of intravascular catheters, or antibiotic therapy or prophylaxis with agents that are ineffective against enterococci (notably cephalosporin therapy).

The source of the enterococci in these infections is usually endogenous. Enterococci are part of the normal flora of colon, oropharynx, gallbladder, urethra, and the external female genitalia. The hospital environment may render endogenous flora more invasive. Antibiotic therapy may result in enterococcal overgrowth in fecal flora, with the potential for transmission by the fecal-oral route or by bacterial translocation.

However, there is evidence that extrinsically acquired strains of enterococci which may be resistant to aminoglycosides may cause disease, particularly in epidemic infections. Beta-lactamase production by gentamicin-resistant enterococci, the gene for which is in the same plasmid as that for gentamicin resistance, may make treatment of serious enterococcal infections with penicillins more difficult in the future.

Vancomycin resistance is troublesome. Approximately 15 per cent of enterococcal isolates in the United States are now resistant to vancomycin, with the vast majority being E. fecium. Alteration of the microbial ecology of the hospital by widespread use of vancomycin and third-generation cephalosporins has been implicated as an etiological factor. Patient-to-patient transfer by contaminated medical equipment has also been documented. Vancomycin-resistant strains are occasionally susceptible to ciprofloxacin or doxycycline, but the drugs are not bactericidal in clinically achievable concentrations in serum, and many strains now require chloramphenicol therapy. Vancomycin-resistant strains of enterococci are now widespread in hospitals, and are clearly present in the community in that they have been isolated from sewage and farm animals, including human foodstuffs.

Surgical drainage or removal of infected vascular catheters or prostheses is the cornerstone of therapy for enterococcal infections involving a discrete focus, such as an abscess. Empirical therapy for Enterococcus in intra-abdominal, non-biliary, or non-urinary infections does not appear necessary in good-risk patients, nor is therapy necessary if Enterococcus is isolated from a good-risk patient who is untreated but doing well. However, specific antibacterial therapy against enterococci is warranted in many of the circumstances typified by the seriously ill patient. If the patient has had enterococci cultured previously during hospitalization or if the infection is nosocomial, particularly with previous gastrointestinal or genitourinary surgery or previous antibiotic therapy, a drug effective against enterococci should be included in the regimen for both proved and presumptive abdominal or pelvic infections, or for burn or surgical wound infections. This is particularly true in patients with valvular heart disease or a prosthetic heart valve. Enterococcal bacteremia due to a sensitive strain requires parenteral antibiotic therapy with ampicillin, an acylureidopenicillin, or vancomycin (only for penicillin-allergic patients). As enterococcal bacteremia is often polymicrobial, appropriate therapy should be directed against all isolates. Appropriate therapy clearly reduces mortality. All patients must be monitored closely for the development of endocarditis.

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