Increasing Antimicrobial Resistance: Therapeutic Implications for Enterococcal Infections

Enterococcus was designated a genus distinct from the streptococci in 1984. Enterococci cause a variety of monomicrobial and polymicrobial infections, mainly in compromised patients. These infections include bacteremia, urinary and biliary tract infections, intra-abdominal sepsis, and decubitus and diabetic foot ulcers. Enterococcal infections may be acquired from the patient's endogenous intestinal flora or exogenously from a fecally contaminated environment. Enterococci are inherently resistant to many antimicrobial agents and readily acquire additional resistances, which is likely the reason that enterococci have become prominent nosocomial pathogens. Only the combination of a cell wall-active antibiotic to which the Enterococcus is susceptible (ie, certain beta-lactams or vancomycin) plus an aminoglycoside (ie, gentamicin or streptomycin) is bactericidal, and is required for cure of endocarditis, meningitis and probably infection in neutropenic patients; bacteriostatic activity is sufficient to treat most other infections. Treatment of infections caused by strains resistant to beta-lactams, glycopeptides and aminoglycosides has become problematic due the limited number of therapeutic options. No medical therapy is reliably effective for endocarditis caused by strains resistant to all cell wall-active antibiotics and all aminoglycosides. New antimicrobial agents, such as linezolid and quinupristin/dalfopristin, have recently become available, but their activity against enterococci is mainly bacterostatic.