Vancomycin is a glycopeptide that inhibits cell wall peptidoglycan synthesis by blocking transpeptidation but by a mechanism different from that of the β-lactam drugs. Vancomycin binds directly to the D-alanyl-D-alanine portion of the pentapeptide, blocking transpeptidase binding. β-Lactam drugs bind to and inhibit the activity of the transpeptidase.
Vancomycin is a bactericidal agent effective against certain gram-positive bacteria. Its most important use is in the treatment of infections caused by S. aureus strains that are resistant to the penicillinase-resistant penicillins such as nafcillin and methicillin (e.g., MRSA). Since vancomycin is not a β-lactam drug, it is not degraded by β-lactamase.
Vancomycin is also used in the treatment of infections caused by Staphylococcus epidermidis, penicillin-resistant Streptococcus pneumoniae, and enterococci. Strains of S. aureus, S. epidermidis, and enterococci with partial or complete resistance to vancomycin have been recovered from patients.
Vancomycin can cause an infusion-related adverse effect where the patient develops a red flushing on the skin due to vasodilation induced by histamine release from mast cells and basophils. This is a direct effect of vancomycin on these cells and is not an IgE-mediated response.
Telavancin is a synthetic derivative of vancomycin that both inhibits peptidoglycan synthesis and disrupts bacterial cell membranes. It is used for the treatment of skin and soft tissue infections, especially those caused by MRSA. Oritavancin and dalbavancin are lipoglycopeptide derivatives of vancomycin and teicoplanin, respectively. These drugs inhibit the trans peptidases and transglycosylases required to synthesize the peptidoglycan of gram-positive bacteria. They are effective in the treatment of infections caused by S. aureus, including MRSA, and Enterococcus, including vancomycin-resistant enterococci (VRE).
