Donor-derived Plasmodium vivax infection following volunteer unrelated bone marrow transplantation

Abstract

Summary:achieving haematological but not cytogenetic remission. She had no HLA-identical siblings. In March 1996, she developed bone pain, increasing hepatosplenomegaly, and A 14-year-old girl from the UK underwent volunteer unrelated donor bone marrow transplant (VUD BMT) a rising white cell count. Her peripheral blood film showed 10% blasts, although cytogenetic analysis remained for accelerated phase chronic myeloid leukaemia. On day +40 she became febrile, and peripheral blood unchanged. She was treated with 'DAT 3+10', and underwent splenectomy, followed by allogeneic bone marsmears demonstrated a 1% Plasmodium vivax parasitaemia. Although she had never been outside the UK, her row transplantation from a fully matched volunteer unrelated donor in September 1996. Conditioning was with male donor had documented Plasmodium vivax infection during a vacation in Papua New Guinea. Following cyclophosphamide (120 mg/kg), etoposide (50 mg/kg), and fractionated total body irradiation (1440 cGy) with lung appropriate treatment, he had been asymptomatic for 11 months before marrow harvesting. This is the first shielding. GVHD prophylaxis was with cyclosporin A and methotrexate. In addition she received Campath 1H case report of malarial transmission by VUD BMT, and illustrates the potential problem of recrudescence of lat-(5 mg/day) from day −5 to day +5. The unrelated donor was a German male, and the total cell dose received was ent, dormant forms of Plasmodium vivax infection following transplantation into an immuno-compromised 5.2 × 10 8 /kg. Her post-transplant course was complicated by marked recipient. Even after appropriate therapy, malarial infection should be included in the differential diagnosis mucositis, confluent oesphagitis necessitating total parenteral nutrition, and mild graft-versus-host disease of gut for all post-transplant febrile episodes.

Evidence and Implications of Mortality Associated with Acute Plasmodium vivax Malaria

“…Viable asexual trophozoites of P. vivax in infected reticulocytes (or erythroblasts) have indeed been observed in the bone marrow (95,(166)(167)(168)(169)(170)(171) and spleen (172). In one case, a subpatent parasitemia confirmed by PCR contrasted with a ruptured spleen very heavily laden with P. vivax-infected reticulocytes (175).…”

Transmission of donor illness by stem cell transplantation: should screening be different in older donors?

“…22 Transfusion-transmitted malaria has been reported previously and represents a potential problem in blood transfusions and HCT. 23,24 Malaria as a complication in HCT is extremely unusual. One case of Plasmodium falciparum transmission after sibling allogeneic HCT and two of Plasmodium vivax, one after unrelated HCT and one recrudescence after autologous HCT, have been reported.…”

“…One case of Plasmodium falciparum transmission after sibling allogeneic HCT and two of Plasmodium vivax, one after unrelated HCT and one recrudescence after autologous HCT, have been reported. [24][25][26] The risk is likely to be dependent on the geographical location of both patient and donor. In malaria nonendemic areas such as the United States, the estimated incidence of malaria transmission by blood transfusion is one per one million units.…”

Changes in bone marrow in malaria-a prospective study of 47 cases

“…4 In addition, two case studies reported P. vivax infections after autologous bone marrow transplantation and a third one documented an accidental P. vivax infection due to bone marrow transplantation between a malaria infected donor and a malaria free recipient. [5][6][7] In Brazil, one patient with persistent thrombocytopenia and an enlarged spleen was diagnosed with chronic P. vivax malaria after the finding of schizonts in the bone marrow aspirate. 8 The hematological changes seen in patients with malaria include anemia, neutropenia, reactive lymphocytosis, monocytosis, eosinopenia , neutrophil leukocytosis and thrombocytopenia.…”