ABSTRACT
Infections constitute a significant challenge during the management of chronic lym-
phocytic leukemia (CLL). Indeed, more than 50% of patients with CLL suffer recurrent
infections, and infection accounts for up to 60% to 80% of deaths from CLL (1-7). This
increased risk for infectious complications is the result of the interplay between the
immune defects inherent in CLL and the therapies given to control it. The introduction of
purine analogs (fludarabine, cladribine, and pentostatin) (8) and monoclonal antibodies
such as alemtuzumab (9) has led to significant progress in the treatment of CLL. Purine
analogs interfere with DNA synthesis through inhibition of DNA polymerases and
ribonucleotide reductase, leading to programmed cell death of malignant lymphoid cells,
but with a similar effect on the normal resting lymphocytes (10). This results in prolonged
lymphopenia, especially in the CD4 subset of T cells, which predisposes to opportunistic
infections (1-3,6,7).
