Polymicrobial endocarditis caused by methicillin-resistant Staphylococcus aureus and glycopeptide-resistant enterococci.
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In this study we have evaluated the in vitro activity of teicoplanin, a potent anti-staphylococcal and anti-enterococcal agent, in combination with rifampicin, netilmicin, amikacin, fosfomycin and imipenem. Drug interactions were assessed using a microtitre checkerboard dilution method and a time-kill test. With rifampicin, indifference or an additive effect was the prevalent outcome with both methods. With netilmicin and amikacin synergism was seen against half of the enterococcal strains, whereas indifference was more common with staphylococcal isolates. Synergism predominated when teicoplanin was combined with fosfomycin and imipenem. Under no circumstances and with no combination of drugs were we able to detect antagonistic effects.
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The potential of fluidised microsphere beds as sources of nosocomial Enterococcal infection was investigated with the help of pyrolysis mass spectrometry. Isolates from clinical specimens collected from two patients who were nursed sequentially on a fluidized microsphere bed were compared with similar isolates cultured from the microspheres before and after decontamination. Pyrolysis mass spectrometry confirmed that nosocomial spread had indeed occurred and that the existing decontamination process was inadequate. Recommendations for improvements to this decontamination process appear to have prevented further cases.
Cytoplasmic precursors of the peptidoglycan biosynthetic pathway were purified from vancomycin-treated, glycopeptide-sensitive and -resistant strains of Enterococcus faecium. Resistance was due to production of a modified precursor, UDP-MurNAc-L-Ala-D-Glu-L-Lys-D-Ala-D-lactate, where lactate was identified on the basis of mass of the precursor and on its ability to act as a substrate for D-lactate dehydrogenase after release from the precursor. The presence of the D-lactate residue instead of D-alanine in the terminal position would hinder formation of a vancomycin-precursor complex, without preventing incorporation of the precursor into mature peptidoglycan.
The hemolysin/bacteriocin produced by some strains of Enterococcus faecalis is active in the lysis of human, rabbit, and horse erythrocytes, but not those from sheep. In this study, we determined that 20% of clinical enterococcal isolates tested in the clinical microbiology laboratory produced hemolysin and that pathogenic human E. faecalis were more likely to be hemolysin-producing isolates. Among the organisms isolated from different anatomic sites, variability in the degree of hemolysin production existed. We used an isogenic pair of E. faecalis organisms to demonstrate that hemolysin production was due to a hemolysin/bacteriocin determinant transmissible by a plasmid and was not strain dependent. This determinant may be linked to antibiotic resistance genes in some instances. Also, the erythrocyte lysis occurred only when hemolysin was in the presence of E. faecalis organisms, suggesting a bacterial cell dependency for activity of the hemolysin.