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• W2101473785 abstract "Keywords. Enterococcus faecalis; infective endocarditis; high-level resistance; aminoglycosides.Since the first description of enterococ-cal infective endocarditis (IE) in 1899and the subsequent availability of antibi-otics for the treatment of this life-threat-ening infection, clinicians have facedimportant challenges in the manage-ment of this disease [1, 2]. Enterococciexhibit intrinsic antibiotic resistance (eg,to cephalosporins, clindamycin), are lesssusceptible to various antibiotics (eg, β-lactams) that are active against strepto-cocci and staphylococci, and are oftentolerant to compounds (penicillin) thatnormallyhaveabactericidaleffectagainstother susceptible bacteria. Indeed, thelack of bactericidal activity of penicillinagainst enterococci was recognized whenfailure rates using penicillin mono-therapy for the treatment of IE causedby enterococci were found to be higherthan when caused by staphylococci andstreptococci [3]. The lack of efficacy ofpenicillin for many cases of enterococcalIE sparked interest in possible alternativetherapies. Reports of clinical cure in pa-tients with enterococcal IE failing peni-cillin monotherapy when streptomycinwas added to penicillin resulted inseminal experiments in the 1950s thatshowed that the combination of penicil-lin plus an aminoglycoside was bacterici-dal in vitro [4, 5]. This combination wasused clinically with success and im-proved cure rates for enterococcal IE [6].However, after this regimen became thestandard of care, enterococcal strains ex-hibiting high-level resistance (HLR) tostreptomycin (mainly due to ribosomalmutations) and, eventually, gentamicin(due to acquisition of the bifunctionalenzyme AAC [6′]-Ie-APH[2′′]-Ia) weredescribed. More recently, the widespreaddissemination of antimicrobial resistancedeterminants in enterococci has furthercomplicated the clinical picture with theemergence and dissemination of strainsof Enterococcus faecium with HLR toampicillin, indicative of the hospital-associated clade of multidrug-resistantE. faecium causing nosocomial infec-tions worldwide [7, 8]. Modern-day clin-icalisolatesbelongingtothisgeneticcladeoften exhibit resistance to vancomycin(harboring the vanA gene cluster) andHLR to aminoglycosides, in addition toHLR to ampicillin (minimum inhibitoryconcentration >64 µg/mL), reducing an-tibiotic choices even further [9,10].Despitethehigh frequencyof ampicillin-resistant E. faecium, ampicillin-resistantE. faecalis is strikingly uncommon. Thepressing issue in the latter species is theincreasing frequency of HLR to all amino-glycosides, as the presence of HLR toaminoglycosides abolishes the synergis-tic, bactericidal effect of the penicillin-aminoglycoside combination againstenterococci. Additionally, toxicity of theaminoglycosidesisalimitingfactorfortheir use, even against E. faecalis isolateslacking HLR to aminoglycosides. Indeed,renal injury and ototoxicity are the 2 mostfeared complications of prolonged amino-glycoside therapy. An article entitled “Deafor Dead?” published in 1959 dramaticallyillustrates, albeit with neomycin, the poten-tial risks of using these drugs for E. faecalisIE [11]. Furthermore, the safety of amino-glycosides may be even more of an issuetoday, as patients who develop enterococcalIE in the modern-day era tend to be older,with a higher number of comorbidities andlikelyreceivingmorepotentiallynephrotox-ic agents than in previous decades, increas-ing the risk of aminoglycoside-related renaldysfunction.Theabove-mentionedlimitationsintheuseofaminoglycosideshavepromptedthestudy of alternative therapeutic strategies" @default.
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• W2101473785 date "2013-02-07" @default.
• W2101473785 modified "2023-10-02" @default.
• W2101473785 title "Editorial Commentary: Enterococcus faecalisInfective Endocarditis: Is It Time to Abandon Aminoglycosides?" @default.
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• W2101473785 doi "https://doi.org/10.1093/cid/cit050" @default.
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