Enterococci, formerly called group D streptococci, come well equipped with a variety of intrinsic (ie, naturally occurring) antibiotic resistances; they are also capable of acquiring new resistance genes and/or mutations. The combination of high-level resistance to ampicillin, vancomycin, and aminoglycosides is now fairly common among hospital-acquired Enterococcus faecium in the United States and has a major impact on therapeutic options. (See "Epidemiology, prevention and control of vancomycin-resistant enterococci".)
Problems in the treatment of enterococcal infections were noticed as early as the 1950s with the observation that enterococcal endocarditis was not cured nearly as often as streptococcal endocarditis with penicillin . The reason for the poorer response appears to be that penicillin is not as bactericidal against enterococci as it is (or was in the 1950s) against most viridans streptococci. This phenomenon, which has been commonly described as tolerance, is characteristic of many enterococcal strains and, even in those that do not initially display tolerance, can be rapidly elicited by pulsed (intermittent) penicillin exposure. The latter observation has led to some support for the use of continuous infusion penicillin or ampicillin in an attempt to avoid eliciting tolerance .
GENETICS OF RESISTANCE IN ENTEROCOCCI
Despite the many intrinsic resistances of enterococci, most enterococcal infections, until recently, could be treated with penicillin, ampicillin, or vancomycin with or without an aminoglycoside. Unfortunately, enterococci have now acquired resistance to these and many other agents as a result of mutations (eg, causing high-level resistance to streptomycin or to fluoroquinolones) or the acquisition of new gene(s).
With respect to the acquisition of new genes, enterococci have several different ways of transferring DNA by conjugation (bacterial mating):
●One mechanism, involving pheromone-responsive plasmids, causes plasmid transfer between E. faecalis isolates at a very high frequency .