USMLE

Chloramphenicol

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Antibiotics / Antiparasitics
  1. Penicillin Overview
  2. Penicillinase-Sensitive vs. Penicillinase-Resistant Penicillins
  3. Anti-Pseudomonal Penicillins
  4. Cephalosporins Overview
  5. 1st Generation Cephalosporins
  6. 2nd Generation Cephalosporins
  7. 3rd Generation Cephalosporins
  8. 4th Generation Cephalosporins
  9. 5th Generation Cephalosporins
  10. Carbapenems
  11. Monobactams (Aztreonam)
  12. Vancomycin
  13. Aminoglycosides
  14. Tetracyclines
  15. Tigecycline
  16. Chloramphenicol
  17. Clindamycin
  18. Linezolid
  19. Macrolides
  20. Polymyxins
  21. Sulfonamides
  22. Dapsone
  23. Trimethoprim
  24. Fluoroquinolones
  25. Daptomycin
  26. Metronidazole
  27. Rifamycins (Rifampin, Rifabutin)
  28. Isoniazid
  29. Pyrazinamide
  30. Ethambutol
  31. Chloroquine

Summary

Chloramphenicol is an antibiotic that works by binding the 50S subunit of bacterial ribosomes to prevent bacterial protein synthesis. The drug is used as a second or third line therapy for bacterial meningitis and to treat rickettsial diseases. Adverse effects of chloramphenicol include gray baby syndrome, anemia which is dose-dependent, and aplastic anemia which is dose independent.

Key Points

  • Chloramphenicol
    • Mechanism
      • Reversibly binds 50S subunit of bacterial ribosomes
        • Blocks peptidyltransferase and inhibits bacterial protein synthesis
      • Bacteriostatic
    • Clinical Use
      • Meningitis
        • e.g. H. influenzae, N. meningitidis, S. pneumoniae
      • Rickettsial diseases
    • Adverse Effects
      • Anemia (dose-dependent)
        • Anemia, leukopenia, thrombocytopenia are all possible
        • Reversible by stopping medication
      • Aplastic anemia (dose-independent)
        • Thought to result from autoimmunity induced by drug
        • Usually severe and fatal without bone marrow transplantation
      • Gray-baby syndrome
        • Presents in babies as gray skin, vomiting, lethargy, and cardiorespiratory suppression
        • Premature infants lack liver UDP-glucuronosyltransferase and cannot metabolize the drug, leading to toxic accumulation
    • Resistance
      • Plasmid-encoded acetyltransferase inactivates the drug