Sections View Full Chapter Figures Tables Videos Annotate Full Chapter Figures Tables Videos Supplementary Content +++ INTRODUCTION ++ Hemolysis represents a prominent part of the overall clinical picture in many infections. Table 21–1 lists the microorganisms associated with the induction of hemolytic anemia. ++Table Graphic Jump LocationTABLE 21–1ORGANISMS THAT CAUSE HEMOLYTIC ANEMIAView Table||Download (.pdf) TABLE 21–1 ORGANISMS THAT CAUSE HEMOLYTIC ANEMIA Aspergillus Babesia microti and Babesia divergens Bartonella bacilliformis Campylobacter jejuni Clostridium welchii Coxsackie virus Cytomegalovirus Diplococcus pneumoniae Epstein-Barr virus Escherichia coli Haemophilus influenzae Hepatitis A Hepatitis B Herpes simplex virus Human immunodeficiency virus Influenza A virus Leishmania donovani Leptospira ballum and/or butembo Mumps virus Mycobacterium tuberculosis Mycoplasma pneumoniae Neisseria intracellularis (meningococci) Parvovirus B19 Plasmodium falciparum Plasmodium malariae Plasmodium vivax Rubella virus Rubeola virus Salmonella Shigella Streptococcus Toxoplasma Trypanosoma brucei Varicella virus Vibrio cholera Yersinia enterocolitica Source: Williams Hematology, 9th ed, Chap. 53, Table 53–1. +++ MECHANISMS ++ Hemolysis may be caused by: — Direct invasion of red cell by infecting organisms (Plasmodium sp) — Elaboration of hemolytic toxins (Clostridium perfringens) — Development of autoantibodies against red blood cell antigens (Mycoplasma pneumoniae) +++ MALARIA +++ Plasmodium Species and Severity of Anemia ++ Five species of the genus Plasmodium cause human malaria: Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae, Plasmodium ovale, and Plasmodium knowlesi. P falciparum and P vivax cause the most cases worldwide and are principally associated with hemolytic anemia. P vivax invades only young red cells. P falciparum attacks both young and old cells, and anemia tends to be more severe with this form of malaria and is the most deadly type. +++ Etiology and Pathogenesis ++ Malaria is the world’s most common cause of hemolytic anemia. The disease is transmitted by the bite of an infected female Anopheles mosquito. Parasites grow intracellularly, and parasitized red cells are destroyed in the spleen. Uninvaded red cells are also destroyed. Erythropoietin is low for degree of anemia secondary to release of inhibitory cytokines, especially in P falciparum infection. Prevalence of certain heterozygous mutations that interfere with invasion of red blood cells by parasites has evolved in endemic areas (eg, glucose-6-phosphate dehydrogenase [G6PD] deficiency, thalassemia, sickle cell trait, other hemoglobinopathies, and hereditary elliptocytosis). +++ Hemolytic Mechanisms ++ Destruction of parasitized red cells occurs largely in the spleen. Splenomegaly typically is present in chronic malarial infection. “Pitting” of parasites from infected erythrocytes may occur in the spleen. Degree of red cell parasitemia, in part, determines the destruction of infected erythrocytes. Low rates of parasitemia may not contribute to the development of anemia; high rates (eg, 10%) may have very significant effects. The degree to which anemia develops is disproportionate to the number of cells infected with the parasite. For each infected red cell, ten times the number of uninfected red cells are removed, magnifying the hemolytic rate. Hemin ... Your Access profile is currently affiliated with [InstitutionA] and is in the process of switching affiliations to [InstitutionB]. Please select how you would like to proceed. Keep the current affiliation with [InstitutionA] and continue with the Access profile sign in process Switch affiliation to [InstitutionB] and continue with the Access profile sign in process Get Free Access Through Your Institution Learn how to see if your library subscribes to McGraw Hill Medical products. Subscribe: Institutional or Individual Sign In Error: Incorrect UserName or Password Username Error: Please enter User Name Password Error: Please enter Password Sign in Forgot Password? Forgot Username? Download the Access App: iOS | Android Sign in via OpenAthens Sign in via Shibboleth You already have access! Please proceed to your institution's subscription. Create a free profile for additional features.