ABSTRACT
Binding of the antibiotics to cell wall peptides blocks continued formation of cross-linked peptidoglycan. It is this action on the bacterial cell that accounts for the antibacterial activity of these compounds. Cell-free experiments demonstrating effects of vancomycin on peptidoglycan biosynthesis confirmed the site of antibacterial action of this antibiotic. Vancomycin also affects the translocase reaction, but this effect requires higher concentrations than those needed to block transglycosylation. Experience with resistance in staphylococci has led to the suggestion that there may besubtle differences in the mode of action of vancomycin and teicoplanin. Although the target site of vancomycin is clearly present in Gram-negative bacteria, resistance is readily explained by the presence of the permeability barrier imposed by the outer membrane, which effectively blocks access to the target. Resistance is constitutively expressed and appears to be chromosomally mediated. This resistance can be clearly distinguished both genetically and phenotypically from the plasmid-mediated inducible resistance found in enterococci.
