Chloramphenicol was introduced into medical practice in 1949. At therapeutic concentrations of 10 to 20 micrograms drug per ml, the drug inhibits bacterial ribosomal and, to a lesser extent, mammalian mitochondrial protein synthesis but concentrations above 60 micrograms drug per ml induce progressive reduction of oxygen-dependent cellular metabolism. Some adverse reactions (e.g. bone marrow suppression and the "gray baby syndrome") reflect these effects. The pathogenesis of chloramphenicol-induced aplastic anemia remains unclear. Chloramphenicol is most bioavailable after oral administration and has a remarkable ability to diffuse into body fluids and tissues. However, there are wide interindividual variations in its metabolism and elimination, particularly in newborns. Chloramphenicol is indicated for invasive ampicillin-resistant H. influenzae infections; for patients allergic to penicillin with pneumococcal, meningococcal or H. influenzae meningitis; in patients under 8 years of age with Rocky Mountain spotted fever; and for the treatment of brain abscess and other severe anaerobic infections (excluding endocarditis) due to B. fragilis. Other indications include selected patients with Salmonella meningitis or carditis, rickettsioses and intraocular infections. Unravelling the pathogenesis of chloramphenicol-induced aplastic anemia is critical to more widespread application of this remarkable antimicrobial.