Antibiotics MOA and Selective Toxicity Exam 2 Flashcards
β-lactams MOA
- Inhibiting Cell Wall Synthesis
- Binding to CWT (irreversible)
Glycopeptides MOA
- Inhibiting Cell Wall Synthesis
- Targets peptide on peptidoglycans forming the wall (targeting the A-A)
- Lipoglycopeptide: Improved antimicrobial activity, dual mode of action involving both inhibition of cell wall synthesis and disruption of the bacterial cell membrane
Lipopeptides MOA
- Targeting the Cell Membrane
- Targets membrane phospholipids present in Gram+
- Binds to phospholipids that are specific for Gram +, create holes in the membrane
Polypeptide MOA
- Targeting the Cell Membrane
- Targets membrane lipopolysaccharides and LPS present in Gram-
- Act as “detergent” solubilizing the membrane, form pores in membranes
Oxazolidionones MOA
- Targeting Protein Synthesis
- Cross membrane to enter bacteria and bind to ribosome (cannot target gram-)
- binds subunit 50S on bacterial ribosome, inhibits binding of tRNA, inhibits protein synthesis
- no cross resistance with other classes
Streptrogramins MOA
- Targeting Protein Synthesis
- binds MLS(b) on bacterial ribosome 50S subunit
Lincosamides MOA
- Targeting Protein Synthesis
- binds MLS(b) on bacterial ribosome 50S subunit
Macrolides MOA
- Targeting Protein Synthesis
- binds MLS(b) on bacterial ribosome 50S subunit
Tetracyclines MOA
- Targeting Protein Synthesis
- Reversible binding to the 30S ribosomal subunit
Aminoglycosides MOA
- Targeting Protein Synthesis
- Irreversible Binding to 30S and to 50S to a lesser extent
Sulfonamides MOA
- Targeting Nucleic Acid Synthesis
- Targets synthesis of folic acid
Ansamycins MOA
- Targeting Nucleic Acid Synthesis
- Targets RNA polymerase
Quinolones / fluoroquinolones MOA
- Targeting Nucleic Acid Synthesis
- Irreversible binding to bacterial DNA gyrase, topoisimerase II or topoisomerase IV, which uncoil DNA
Nitromidazole MOA
- Targeting Nucleic Acid Synthesis
- Target DNA and causes DNA fragmentation
β-lactams Selective Toxicity
Bactericidal
Glycopeptides Selective Toxicity
Bactericidal
Lipopeptides Selective Toxicity
Bactericidal
Polypeptide Selective Toxicity
Bactericidal
Oxazolidionones Selective Toxicity
Bacteriostatic
Streptrogramins Selective Toxicity
Bacteriostatic
Lincosamides Selective Toxicity
Bacteriostatic
Macrolides Selective Toxicity
Bacteriostatic
Tetracyclines Selective Toxicity
Bacteriostatic
Aminoglycosides Selective Toxicity
- Bacteriostatic
- Bactericidal effect at high concentrations
Sulfonamides Selective Toxicity
Bacteriostatic
Ansamycins Selective Toxicity
Bacteriostatic
Quinolones / fluoroquinolones Selective Toxicity
Bacteriostatic
Nitromidazole Selective Toxicity
- Bacteriostatic
- Bactericidal activity on Gram + and Gram - anaerobes
What is the mechanism of resistance with beta lactams?
- beta lactamase
- altered CWT (G+)
- altered activity of bacterial influx / efflux transporters (G-)
What is the mechanism of resistance with oxazolidionones?
Modified binding site
What is the mechanism of resistance with streptrogramins, lincosamides, and macrolides?
- mutations in MLS(b)
- pumping out the drug
What is the mechanism of resistance with Ansamycins?
single amino acid change in the bacterial DNAdependent RNA polymerase
Mechanism of action for resistance against Quinolones / fluoroquinolones
mutations on binding sites or efflux pumps. These drugs enter the cells through porins by passive diffusion
Mechanism of action for resistance against Tetracycline
- Mutation of this binding site leads to resistant bacteria
- Horizontal gene transfer, production of a “ribosomal protective protein” or an efflux pump.
Mechanism of action for resistance against Aminoglycosides
Production of aminoglycoside modifying enzymes, mutations of binding site or influx pump
Mechanism of action for resistance against nitromidazoles
- ↘ Influx or ↗ Efflux
- ↘ Reduction or ↗ Oxidation
- ↗ Activity of DNA repair enzymes
