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This article has been peer reviewed. It is the authors' final version prior to publication in Journal of Clinical Apheresis Volume 25, Issue 6, September 2010, Pages 358-361. The published version is available at DOI: 10.1002/jca.20262. Copyright © John Wiley & Sons, Inc.


Transfusion-acquired babesiosis can be an asymptomatic or self-limited febrile hemolytic illness in a healthy host. A persistent, relapsing, and/or fulminant course with the development of life-threatening complications may be seen in immunocompromised or splenectomized patients. As in malaria, erythrocyte parasitemia is often associated with nonimmune hemolysis, and can be treated with erythrocytapheresis. Just as warm autoantibodies have been reported in malaria infection, the development of autoantibody-mediated immune hemolysis has been reported in babesiosis. We treated a previously healthy male with multiple injuries from a motor vehicle accident necessitating massive transfusion. Late in the hospitalization, his blood smear revealed Babesia microti, confirmed by PCR study and serology. This was eventually traced to a unit of blood from an asymptomatic blood donor that was transfused during his initial trauma care. Specific antibiotic therapy was begun, and severe hemolysis from a high parasite burden required red blood cell exchange which led to rapid abatement of the hemolysis. He had a positive DAT (IgG with a pan-reactive eluate) but no serum autoantibody. This persisted for 10 days following cessation of hemolysis, and became negative while still on antibiotics while his parasite burden became undetectable. Reports of autoimmunity associated with community acquired babesiosis often have severe hemolysis from their autoantibodies, but our case shows that autoantibodies may also follow transfusion-acquired babesiosis. The nature of the autoantigen is unknown.

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