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ANTIBIOTICS INHIBITORS OF CELL WALL SYNTHESIS (Peptidoglycan)

ANTIBIOTICS INHIBITORS OF CELL WALL SYNTHESIS (Peptidoglycan) NAM SYNTHESIS: D-cycloserine mimics D-Alanine, prevents synthesis. SHUTTLE: Bacitracin interferes with C55 lipid shuttle by binding it. TRANSGLYCOSYLATION: Glycopeptides (e.g. Vancomycin) prevents it.

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ANTIBIOTICS INHIBITORS OF CELL WALL SYNTHESIS (Peptidoglycan)

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  1. ANTIBIOTICS • INHIBITORS OF CELL WALL SYNTHESIS (Peptidoglycan) • NAM SYNTHESIS: D-cycloserine mimics D-Alanine, prevents synthesis. • SHUTTLE: Bacitracin interferes with C55 lipid shuttle by binding it. • TRANSGLYCOSYLATION: Glycopeptides (e.g. Vancomycin) prevents it. • CROSSLINKAGE: b- lactams mimic D-ALA-D-ALA of NAM and interfere with the enzymes that do the crosslinking. • Penicillins • Cephalosporins • Monobactams • CELL MEMBRANE TARGETS Lipopeptides are amphiphilic, contain D-amino acids, disrupt CM, are potent but not selective; for “compassionate use” • Polymyxins • Gramicidins • INHIBITORS OF mRNA SYNTHESIS • Rifamycins: Bind to DNA-dependent RNA polymerase β subunit, prohibits mRNA transcription. • Rifampin • INHIBITORS OF PROTEIN SYNTHESIS (TRANSLATION) the concentration of these antibiotics can become toxic to us. • BACTERIOSTATIC (are reversible) • Tetracyclines (Target 30S ribosome) • Amphenicols (Target 50S ribosome) • Macrolides (Target 50S ribosome) • Erythromycin • Azithromycin • Clindramycin • BACTERIOCIDAL (are irreversible) • Aminoglycosides: All bind on 50S. These are strong, but not very selective. They can cause kidney and inner ear damage. • Gentamicin (made by microsporin fungus) • Streptomycin (made by streptomyces fungus) • Kanamycin (“ “ “) • Tobramycin (“ “ “) • Amikacin • INHIBITORS OF DNA SYNTHESIS (Target is ENZYMES that control DNA) • Quinolones: Target and block DNA gyrase • Ciprofloxacin, Levofloxacin, Norfloxacin, • Metronidazole (“Flagyl”): Used against ANAEROBIC bacteria. Generates toxic O2 metabolites • ANTIMETABOLITES (Inhibits Folate Synthesis) We need Folic acid from our normal flora in GI tract. These abs can cause a lack of folic acid in us. • Sulfonamides mimic PABA (Sulfamethoxasole) • Trimethoprim targets DHF reductase • Cotrimoxazole (Bactrim): combination of above two antibiotics. This is a synergistic use of antibiotics; They target different sites. • ANTIMYCOLATES: Inhibit trans Δ24 desaturase, required to go from lipid  mycolipid. Lysosomes can now stick to phagosome and lyse the bacteria. • Isoniazid • Ethambutol • P. Aminosalicylic Acid

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