ENTERO COCCAL DISEASE : CLINICAL ASPECTS
Enterococci cause opportunistic urinary tract infections (UTIs) and occasionally wound and soft tissue infections, in much the same fashion as members of the Enterobacteriaceae.
Infections are often associated with urinary tract manipulations, malignancies, biliary tract disease, and gastrointestinal disorders. Vascular or peritoneal catheters are often points of entry. Respiratory tract infections are rare. There is sometimes an associated bacteremia, which can result in the development of endocarditis on previously damaged cardiac valves.
The outstanding feature of the enterococci is their high and increasing levels of resistance to antimicrobial agents. Inherently relatively resistant toβ-lactams and aminoglycosides, enterococci also have particularly efficient means of acquiring plasmid and transposon re-sistance genes from themselves and other species. All enterococci require 4 to 16 μg/mL of penicillin for inhibition due to decreased affinity of their penicillin-binding proteins for all β-lactams. Higher levels of resistance have been increasing, including the emergence of -lactamase-producing strains, particularly in E. faecalis. The -lactamase genes are identical to those in Staphylococcus aureus. Fortunately β-lactamase – producing strains have not yet become widely disseminated. Ampicillin remains the most consistently ac-tive agent against enterococci.
Enterococci share with streptococci a relative resistance to aminoglycosides based on failure of the antimicrobic to be actively transported into the cell. Despite this, many strains of enterococci are inhibited and rapidly killed by combinations of low concentra-tions of penicillin and aminoglycosides. Under these conditions, the action of penicillin on the cell wall allows the aminoglycoside to enter the cell and act at its ribosomal site. Some strains show high level resistance to aminoglycosides based on mutations at the ri-bosomal binding site or the presence of aminoglycoside-inactivating enzymes. These strains do not demonstrate synergistic effects with penicillin.
Recently, resistance to vancomycin, the antibiotic most used for penicillin-resistant strains has emerged. Vancomycin resistance is due to a subtle change in peptidoglycan precursors, which are generated by ligases that modify the terminal amino acids of cross-linking acid side chains at the point at which β-lactams bind. The modifications decrease the binding affinity for penicillins 1000-fold without a detectable loss in peptidoglycan strength. Although hospitals vary, the average rate of resistance in ente-rococci isolated from intensive care units is around 20%. Enterococci are consistently resistant to sulfonamides and often resistant to tetracyclines, erythromycin, and cephalosporins.
Penicillin or ampicillin remain the agents of choice for most UTIs and minor soft tis-sue infections. More severe infections, particularly endocarditis, are usually treated with combinations of a penicillin and aminoglycoside. If the strain fails to demonstrate penicillin – aminoglycoside synergism and/or is vancomycin resistant, some other combi-nation guided by susceptibility testing must be selected.
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