Pathogenesis of anemia in Trypanosoma brucei-infected mice.
The pathogenesis of anemia was studied in trypanosome-infected mice. A strain of Trypanosoma brucei, TREU 667, was used which first produces an acute phase marked by waves of parasitemia. Erythrocytes from infected animals were coated with immunoglobulin M during or just before the waves of anemia and parasitological crises. Erythrocytes from normal animals could be sensitized with "precrisis" sera presumably containing antigen and antibody. These data suggest that anemia during the acute phase is due to sensitization of erythrocytes with immunoglobulin M-antigen complexes. The anemia is partially compensated by a strong erythropoietic response. The acute phase is followed by a chronic phase marked by a constant high parasitemia and immunosuppression. The less marked anemia occurring during this latter phase is due to hemodilution and perhaps a low but significant immune response to the parasites, which causes continuing erythrocyte sensitization by immunoglobulin M-antigen complexes.
D000740:Anemia / Q000209:etiology*; D000818:Animals; D000906:Antibodies / Q000032:analysis; D001810:Blood Volume; D002417:Cattle; D004195:Disease Models, Animal; D006529:Hepatomegaly / Q000209:etiology; D007075:Immunoglobulin M / Q000032:analysis; D008206:Lymphatic Diseases / Q000209:etiology; D051379:Mice; D013163:Splenomegaly / Q000209:etiology; D013997:Time Factors; D014346:Trypanosoma brucei brucei; D014354:Trypanosomiasis, Bovine / Q000150:complications*
D000906:Antibodies; D007075:Immunoglobulin M