Chloramphenicol produces two types of toxic effect in bone marrow: The first, a common, dose-related, reversible lesion occurs concurrently with chloramphenicol therapy and is characterized by a normally cellular marrow, maturation arrest, vacuolization in erythroid and myeloid cells, reticulocytopenia, and ferrokinetic changes indicative of suppressed erythropoiesis.1 The second is a rare, but devastating complication characterized by a late clinical onset (three to six weeks after last drug dose), lack of dose-effect relationship, bone marrow hypoplasia or aplasia, pancytopenia, and usually a fatal outcome, from hemorrhage or infection. There is no apparent relationship between these two types of toxic effect.
A great deal of progress has been made recently in elucidating the mechanism of reversible bone marrow suppression from chloramphenicol. The clinical and hematologic features of this lesion strongly suggest a direct metabolic effect of the drug on bone marrow cells. Although the mammalian cell has generally been found resistant