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SUMMARY
Hemolytic anemia is a prominent part of the clinical presentation of patients infected with certain organisms such as Plasmodium, Babesia, and Bartonella spp., which directly invade the erythrocyte. Malaria is the most common cause of hemolytic anemia worldwide, and much has been learned about how the parasite enters the erythrocyte and the mechanism of the development of anemia. Falciparum malaria, in particular, can cause severe and sometimes fatal hemolysis (blackwater fever). The zoonotic malaria parasite Falciparum knowlesi, prevalent in Southeast Asia, is also associated with severe hemolytic anemia. Other organisms cause hemolytic anemia by producing a hemolysin (eg, Clostridium perfringens), by stimulating an immune response (eg, Mycoplasma pneumoniae), by enhancing macrophage recognition and hemophagocytosis, or by as yet unknown mechanisms. The many different infections that have been associated with hemolytic anemia are tabulated and references to the relevant studies provided.
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Shortening of erythrocyte life span occurs commonly in the course of inflammatory and infectious diseases. This effect may occur particularly in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency (Chap. 16), splenomegaly (Chap. 25), and in the microvascular red cell fragmentation syndrome (Chap. 22). In some infections, however, rapid destruction of erythrocytes represents a prominent part of the overall clinical picture (Table 24-1).1-49 This chapter deals only with the latter states.
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Several distinct mechanisms may lead to hemolysis during infections.49 These include direct invasion of or injury to the erythrocytes by the infecting organism, as in malaria, babesiosis, and bartonellosis; elaboration of hemolytic toxins, as by Clostridium perfringens; and development of antibodies, either autoantibodies against red cell antigens or deposition of microbial antigens or immune complexes on erythrocytes, which result in hemolytic anemia.50
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