Visceral leishmaniasis after alemtuzumab in a patient with chronic lymphocytic leukaemia

Abstract

A 64-year-old, human immunodeficiency virus-negative, man was diagnosed in 2009 as Rai stage IV chronic lymphocytic leukaemia with unmutated IGHV genes and del 17p13.1. He was treated with six courses of intravenous fludarabine, cyclophosphamide and rituximab, attaining a partial remission that lasted only 28 weeks. Overt progression was then managed with subcutaneous alemtuzumab at 30 mg three times a week for 12 weeks. After this treatment, the enlarged lymph nodes disappeared, while the CD4-positive T-lymphocyte count decreased, from 0·09 × 109/l to 0·003 × 109/l (normal range: 0·5–1·0 × 109/l). Four weeks after completion of alemtuzumab therapy, the patient developed fever (39°C) and was readmitted to our hospital. The blood count showed pancytopenia (haemoglobin concentration 70 g/l, white cell count 1·8 × 109/l and platelet count 22 × 109/l). Computed tomography of the chest, abdomen and pelvis showed massive splenomegaly. Bone marrow films showed no signs of a lymphoproliferative disease but, to our surprise, numerous amastigotes of leishmania species were seen (top, right and left); furthermore, leishmania parasites were also demonstrated in May-Grünwald-Giemsa stained peripheral blood films (bottom, right and left). The patient was treated with liposomal amphotericin B and no leishmania amastigotes were detectable in bone marrow films at the end of treatment. Severe immunodeficiency characterized by a marked lymphopenia is a well-known risk factor for opportunistic parasitic infections. Clinicians should be alert to the possibility of leishmaniasis not only in endemic areas but also when there is the possibility of a latent infection that may become clinically apparent when a patient becomes profoundly immunosuppressed.