TAILIEUCHUNG - Chapter 127. Treatment and Prophylaxis of Bacterial Infections (Part 5)

Vancomycin Clinically important resistance to vancomycin was first described among enterococci in France in 1988. Vancomycin-resistant enterococci (VRE) have subsequently become disseminated worldwide. The genes encoding resistance are carried on plasmids that can transfer themselves from cell to cell and on transposons that can jump from plasmids to chromosomes. Resistance is mediated by enzymes that substitute D-lactate for D-alanine on the peptidoglycan stem peptide so that there is no longer an appropriate target for vancomycin binding. This alteration does not appear to affect cell-wall integrity, however. This type of acquired vancomycin resistance was confined for 14 years to enterococci—more specifically,. | Chapter 127. Treatment and Prophylaxis of Bacterial Infections Part 5 Vancomycin Clinically important resistance to vancomycin was first described among enterococci in France in 1988. Vancomycin-resistant enterococci VRE have subsequently become disseminated worldwide. The genes encoding resistance are carried on plasmids that can transfer themselves from cell to cell and on transposons that can jump from plasmids to chromosomes. Resistance is mediated by enzymes that substitute D-lactate for D-alanine on the peptidoglycan stem peptide so that there is no longer an appropriate target for vancomycin binding. This alteration does not appear to affect cell-wall integrity however. This type of acquired vancomycin resistance was confined for 14 years to enterococci more specifically to Enterococcus faecium rather than the more common pathogen E. faecalis. However since 2002 S. aureus isolates that are highly resistant to vancomycin have been recovered from four patients in the United States. All of the isolates contain vanA the gene that mediates vancomycin resistance in enterococci. In addition since 1996 a few isolates of both S. aureus and Staphylococcus epidermidis that display a four- to eightfold reduction in susceptibility to vancomycin have been found worldwide and many more isolates may contain subpopulations with reduced vancomycin susceptibility. These isolates have not acquired the genes that mediate vancomycin resistance in enterococci but are mutant bacteria with markedly thickened cell walls. These mutants were apparently selected in patients who were undergoing prolonged vancomycin therapy. The failure of vancomycin therapy in some patients infected with S. aureus or S. epidermidis strains exhibiting only intermediate susceptibility to this drug is thought to have resulted from this resistance. Aminoglycosides The most common aminoglycoside resistance mechanism is inactivation of the antibiotic. Aminoglycoside-modifying enzymes usually encoded on .

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