SPECIAL SECTION: ANTIMICROBIAL RESISTANCE

High-level aminoglycoside resistance in enterococci is mediated generally by aminoglycoside-modifying enzymes, which eliminate the synergistic bactericidal effect usually seen when a cell wall‐active agent is combined with an aminoglycoside. Clinical microbiology laboratories currently screen for aminoglycoside resistance in enterococci by testing gentamicin and streptomycin susceptibility. If the recently detected aminoglycoside resistance genes, aph(2 00 )Ib, aph(2 00 )-Ic, and aph(2 00 )-Id, become more prevalent among clinical isolates, the approach for detecting susceptibility to aminoglycoside synergism in enterococci will require modification. More potent aminoglycosides need to be developed that will be resistant to modification by a broad spectrum of aminoglycoside-modifying enzymes present in enterococci. Optimal antimicrobial therapy for serious enterococcal infections requires the use of synergistic combinations of a cell wall‐active agent, such as a penicillin or a glycopeptide, with an aminoglycoside, which results in bactericidal activity against this organism. Enterococci have acquired aminoglycoside resistance genes that mediate production of aminoglycoside-modifying enzymes, which eliminate this synergistic bactericidal effect. Detection of these enzymes has resulted in the traditional approach for predicting bactericidal synergism in enterococci. The discovery of several new aminoglycoside resistance genes in enterococci requires a reevaluation of how prediction of synergism in enterococci should be done. A different approach for predicting aminoglycoside synergism will need to be put in place should these newly discovered genes become more prevalent among clinical enterococcal isolates.