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A Simple Protocol for Platelet-mediated Clumping of Plasmodium falciparum-infected Erythrocytes in a Resource Poor Setting
Published on: May 16, 2013
Transient Pure Red Cell Aplasia in a Case of Plasmodium falciparum and Parvovirus B19 Coinfection
Christy Varghese John1, Ayan Basu1, Debdas Bose2
1Department of Infectious Diseases, Institute of Postgraduate Medical Education and Research, Kolkata, India.
Abstract:
Malaria predisposes to anemia in endemic areas, and this effect is compounded by other factors, such as malnutrition, HIV-1 infection, and intestinal helminth infestation. An association with human parvovirus B19 (B19V), with its high infectivity and seroprevalence, is also increasingly recognized. A 22-year-old gentleman, a native of West Bengal, India, was diagnosed with complicated falciparum malaria and treated with intravenous artesunate followed by artemether-lumefantrine. However, despite clearance of parasitemia, he developed a persistent hypoproliferative anemia with no evidence of hemolysis and positive antinuclear antibodies. Bone marrow examination showed markedly decreased erythroid cells with giant pronormoblasts typical of pure red cell aplasia, and B19V quantitative polymerase chain reaction testing showed 2.1 × 103 international units/mL. He recovered completely after treatment with intravenous immunoglobulin and a tapering course of prednisone. Similar coinfections are uncommon, and infection-related autoimmunity and dyserythropoiesis are features of both malaria and B19V infection. This case highlights that acute B19V coinfection should be considered in malaria patients with persistent anemia despite parasitological clearance.
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