Zefur IV Mechanism of Action

Pharmacotherapeutic group: Antibacterials for systemic use, Second-generation cephalosporins.
Pharmacology: Pharmacodynamics: Mechanism of action: Cefuroxime inhibits bacterial cell wall synthesis following attachment to penicillin binding proteins (PBPs). This results in the interruption of cell wall (peptidoglycan) biosynthesis, which leads to bacterial cell lysis and death.
Mechanism of resistance: Bacterial resistance to Cefuroxime may be due to one or more of the following mechanisms: hydrolysis by beta-lactamases including (but not limited to) extended-spectrum beta-lactamases (ESBLs), and Amp-C enzymes, that may be induced or stably derepressed in certain aerobic Gram-negative bacterial species; reduced affinity of penicillin-binding proteins for Cefuroxime; outer membrane impermeability, which restricts access of Cefuroxime to penicillin binding proteins in Gram-negative bacteria; bacterial efflux pumps.
Organisms that have acquired resistance to other injectable cephalosporins are expected to be resistant to Cefuroxime. Depending on the mechanism of resistance, organisms with acquired resistance to penicillins may demonstrate reduced susceptibility or resistance to Cefuroxime.
Pharmacokinetics: Cefuroxime is widely distributed in the body including pleural fluid, sputum, bone, synovial fluid, and aqueous humour, but only achieves therapeutic concentrations in the CSF when the meninges are inflamed. It crosses the placenta and has been detected in breast milk. It is excreted unchanged, by glomerular filtration and renal tubular secretion, and high concentrations are achieved in the urine. Following injection most of a dose of Cefuroxime is excreted within 24 hours, the majority within 6 hours. Probenecid competes for renal tubular secretion with Cefuroxime resulting in higher and more prolonged plasma concentrations of Cefuroxime. Small amounts of Cefuroxime are excreted in bile. Plasma concentrations are reduced by dialysis.