Mode of action of antibiotics

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  1. Cell wall
  2. Protein synthesis (70S)
  3. DNA/RNA synthesis
  4. Other targets

1.CELL WALL

a. Cytoplasmic  phase

Fosfomycin– MurA analog, blocks muramyl-pentopeptide

b. Membrane associated phase

Bacitracin– blocks lipid carrier

c. Extra-cytoplasmic phase:

B-lactam (penicillin, cephalosporins, carbapanems, monobactams)- blocks transpeptidase ( penicillin binding protein), effects cross-linkage

Glycopeptide (vancomycin, avoparcin)-  avoids transpeptidase formation, cause cross-linkage (D-ala D-ala termini)

Polymyxin (colistin)- effects peptidoglycan layer, increases permeability

2. PROTEIN SYNTHESIS

a. 50S (31 protein+ 23S RNA+ 5S RNA)

Macrolide, linozalid, streptogramin (MLS), chloramphenicol, clindamycin– Peptide bond formation.

B. 30S (21 protein + 16S RNA)

Tetracycline– blocks binding tRNA

Aminoglycoside– impair proofreading

 

3.DNA/RNA SYNTHESIS

      Quinolone- a. DNA gyrase (topoisomerase II)- Beginning at the replication fork in gram negatives; GyrA* and GyrB / b.Topoisomerase IV- later at claving stage in gram positives; parC* and parE . (* where mutations usually occur)

Rifomycin– inhibits transcription (DNA –> mRNA)

4. OTHER

      Trimethoprim- It  is a folic acid inhibitor.  It binds to dihydrofolate reductase and inhibits the synthesis of tetrahydrofolic acid which plays an essential role in thymidine synthesis consequently inhibits DNA synthesis.

     Sulfonamides- competitor for the enzyme dihydropteroate synthetas which blocks PABA joining folic acide molecule, so prevent folic acide synthesis which are essential for bacteria.

 

Note to myself: I will improve this section later.