MBIO 3010 Lecture Notes - Lecture 22: Bacitracin, Clindamycin, Telithromycin

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Beta-lactams: which structurally look like d-ala d-ala) disrupt cell wall synthesis by being binding irreversibly to pbp and this preventing transpeptidation (cross-linking) Beta lactams interacting with pbps resulting in inhibition of peptidoglycan synthesis which activates autolysis which read down existing peptidoglycan and lead to cell death. Glycopeptides - work by binding to the terminal d-ala d-ala residues this preventing cross- linking of the peptidoglycan. Bacitracin blocks the dephosphorylation of bactoprenol pyrophosphate. Very large molecule - bactericidal - narrow spectrum (staph, strep) Binda to d-ala d-ala - no crossing over occurs, cell rapidly dies. We can swap out last d-ala to a different amino acid to stop it from binding. Only staph and strep - bactericidal - binds to bactoprenol phosphate carrier and inhibits it. No resistance to bacitracin - cant give it orally because it will kill human cells (white/red blood cells, epithelial cells) Made up of 50s and 30s units. Made up of 60s and 40s subunits.

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