Beta-lactam antibiotics (penicillins, cephalosporins, carbapenems, and related agents) inhibit bacterial cell wall synthesis by binding penicillin-binding proteins that normally catalyze transpeptidase cross-linking of peptidoglycan, causing autocatalytic breakdown of the wall. Bacterial resistance arises primarily through beta-lactamase enzymes that degrade the beta-lactam ring, through structural alteration of penicillin-binding proteins (e.g., methicillin resistance), or through changes in outer membrane porin structure that block drug penetration (e.g., Pseudomonas); these mechanisms are countered pharmacologically by beta-lactamase inhibitors. This is a pharmacology topic within antimicrobial chemotherapy, organizing agents by structural class and spectrum of gram-positive versus gram-negative activity, alongside non-beta-lactam cell wall inhibitors such as vancomycin, bacitracin, and daptomycin that act via distinct mechanisms.
Beta-lactam antibiotics (penicillins, cephalosporins, carbapenems, and related agents) inhibit bacterial cell wall synthesis by binding penicillin-binding proteins that normally catalyze transpeptida…