1. ANTIBIOTICS
They are divided into four categories based on their bacteriostatic or bactericidal effect(mode of action) on various structures and macromolecules in the bacterial cells:
A- Inhibition of cell wall synthesis
B- Injury to cell membrane
C- Inhibition of nucleic acid synthesis
D- Inhibition of protein synthesis

3. B- Binding with 50S ribosome:
1- Chloramphenicol: It inhibits bacterial protein synthesis selectively, because it binds to the catalytic site of the transferase in the 50s, blocks peptide bond formation & preventing elongation.
Characters:
1- Bacteriostatic against certain organisms, such as Salmonella typhi, but has bactericidal activity against Haemophilus influenzae.
2- broad spectrum 3-orally effective 4- It causes bone marrow toxicity,WHY?

5. 2- Macrolides:
1- Block the translocation step by preventing the transfer of the tRNA bound at the A site to the P site. 2- Blocking Peptidyl transferase.
Example: Erythromycin
Two recently macrolides, azithromycin & clarithromycin, are effective against a broader range of organisms and have a longer half-life. they can be taken only once or twice a day.
N.B: chloramphenicol is not a macrolide.
3- Clindamycin: Inhibits ribosomal translocation in a similar way to macrolides. It prevents elongation  blocks peptide bond formation.
Active against gm positive and anaerobes - useful in the treatment of osteomyelitis and gingivitis. Orally taken
Used in the treatment of acne ?-

6. 4- Fusidic acid:
It acts with elongation factor - blocks translocation
Produced by the fungus Fusidium -Active against beta-lactamase staphylococci

7. Bactericidal or Bacteriostatic
Antibiotic
Ribosomal Subunit
Mode of Action
Bactericidal or Bacteriostatic
Aminoglycosides
30S
Blocks functioning of initiation complex and causes misreading of mRNA
Bactericidal
Tetracyclines
Blocks tRNA binding to ribosome
Bacteriostatic
Chloramphenicol
50S
Blocks peptidyl transferase
Both
Erythromycin
Blocks translocation
Primarily bacteriostatic
Clindamycin
Blocks peptide bond formation

8. IV-NHIBITION OF NUCLEIC ACID SYNTHESIS
A. Inhibition of Precursor Synthesis: Sulfonamides & Trimethoprim.
B. Inhibition of DNA Synthesis: Quinolones, Nalidixic acid &Flucytosine
C. Inhibition of mRNA Synthesis: Rifampin
A. Inhibition of Precursor Synthesis
1-Sulfonamides : Mechanism f action: It is acompetitive inhibitor for p-aminobenzoicacid(PABA).There is some competition between the two substrate for the active site of dihydroptreroate synthase enzyme.
Are useful in urinary tract infections& otitis media
Why Sulfonamides have aselective action on bacteria?

10. Types of sulfonamides:
a-Rapidly absorbed and rapidly excreted sulfonamides e.g. Sulfadiazine and Sulfaisoxazole.
Sulfadiazine is the best sulfonamide for treating meningitis, why?
b- Rapidly absorbed slowly excreted sulfonamides e.g. Sulfamethoxazole.
c- Non-absorbable sulfonamides e.g. Succinyl and phthalylsulfathiazole
d- For special uses e.g. sulfacetamide. It is not used systemically. It is widely used in the form of eye drops and eye ointment. Why?

11. 2-Trimethoprim :it inhibits the enzyme dihydrofolate reductase
2-Trimethoprim :it inhibits the enzyme dihydrofolate reductase. It has specific activity for bacteria.
  Trimethoprim is used most frequently together with sulfamethoxazole
The advantages of the combination are:
1- Bacterial mutants resistant to one drug will be inhibited by the other and the two drugs can act synergistically.
 2-Trimethoprim-sulfamethoxazole is clinically useful in the treatment of urinary tract infections, and shigellosis

13. Prepared by Dr. Lina Jamil