Drug Classification: Antibiotic

Dapsone

Indications:

  • Antimicrobial: Leprosy; prophylaxis of malaria, pneumocystis
  • Disease-modifying drug in cutaneous vasculitis and some other skin conditions.

Mechanism of Action:

Dapsone is an antibiotic most commonly used for the treatment of Mycobacterium leprae infections (leprosy). Dapsone can also be used to treat dermatitis herpetiformis and other skin conditions. Dapsone is thought to act by depleting the body’s stores of para-aminobenzoic acid (PABA).

Lecture and CAL materials: (under review)

Fusidic acid

Indications:

  • Severe/chronic staphylococcal or streptococcal infections, usually as adjunct to other antimicrobials.
  • Sometimes topically for eye or skin infections caused by sensitive organisms.

Mechanism of Action:

Acts by interfering with bacterial protein synthesis, specifically by preventing the translocation of the elongation factor G (EF-G) from the ribosome.

Lecture and CAL materials: (under review)

Chloramphenicol

UNDER REVIEW (April 2017)

Mechanism of Action:

Inhibits protein synthesis in bacteria. Chloramphenicol stops bacterial growth by inhibiting the enzyme peptidyl transferase, which inhibits ribosomal activity and protein synthesis by preventing the binding of amino acyl-tRNA to the A site on the 50S subunit. Resistance to chloramphenicol is conferred by the cat-gene. This gene codes for an enzyme called “chloramphenicol acetyltransferase” which inactivates chloramphenicol by covalently linking one or two acetyl groups, derived from acetyl-S-coenzyme A, to the hydroxyl groups on the chloramphenicol molecule. The acetylation prevents chloramphenicol from binding to the ribosome.

Lecture and CAL materials:

Amoxicillin

UNDER REVIEW (April 2017)

Mechanism of Action:

Amoxicillin is an antibiotic derived from the earlier ampicillin. While having similar antibacterial spectrum to ampicillin it has much better oral absorption. Both are bactericidal antibiotics based on a betalactam ring and act by inhibiting the synthesis of bacterial cell walls. It inhibits cross-linkage between the linear peptidoglycan polymer chains that make up a major component of the cell wall of Gram-positive bacteria. They bind to the transpeptidase enzyme (‘also referred to as penicillin binding proteins’) involved in the final cross-linking phase of peptidoglycan synthesis. Penicillins affects only dividing cells, which swell and rupture because of the cell wall damage. Some bacteria produce beta-lactamases that breakdown pencillins and make them resistant to amoxicillin.

Lecture and CAL materials:

Clarithromycin

Mechanism of Action:

A semi-synthetic macrolide antibiotic chemically related to erythromycin. Macrolides prevent bacteria from growing by interfering with their protein synthesis. They bind to the subunit 50S of the bacterial ribosome, and thus inhibit the translocation of peptides during protein synthesis. Macrolides are concentrated within phagocytes and transported to the site of infection rapidly where large amounts of the drug is released during active phagocytosis. Clarithromycin is as active as and is metabolized to a compound twice as active as erythromycin against Haemophilus influenzae. It is more acid stable and therefore has fewer GI symptoms, a major problem with erythromycin.

Lecture and CAL materials: