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Hemolytic anemia is a prominent part of the clinical presentation of patients infected with organisms such as the malaria parasites, Babesia, and Bartonella, which directly invade the erythrocyte. Malaria is probably the most common cause of hemolytic anemia on a worldwide basis, and much has been learned about how the parasite enters the erythrocyte and the mechanism of anemia. Falciparum malaria, in particular, can cause severe and sometimes fatal hemolysis (blackwater fever). Other organisms cause hemolytic anemia by producing a hemolysin (e.g., Clostridium perfringens), by stimulating an immune response (e.g., 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 original studies provided.

Acronyms and Abbreviations

Acronyms and abbreviations that appear in this chapter include: CR1, complement receptor 1; EBA, erythrocyte-binding antigen; G-6-PD, glucose-6-phosphate dehydrogenase; ICAM, intercellular adhesion molecule; PfEMP, Plasmodium falciparum erythrocyte membrane protein; RSP-2, ring surface protein 2; VCAM, vascular cell adhesion molecule.

Shortening of erythrocyte life span occurs commonly in the course of inflammatory and infectious diseases. This may occur particularly in patients with glucose-6-phosphate dehydrogenase (G-6-PD) deficiency (see Chap. 46), splenomegaly (see Chap. 55), and in the microvascular fragmentation syndrome (see Chap. 50). In some infections, however, rapid destruction of erythrocytes represents a prominent part of the overall clinical picture (Table 52–1).1–49 This chapter deals only with the latter states.

Table 52–1. Organisms Causing Hemolytic Anemia

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 ...

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