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 23–1 lists the microorganisms associated with the induction of hemolytic anemia. ++Table Graphic Jump LocationTABLE 23–1ORGANISMS THAT CAUSE HEMOLYTIC ANEMIAView Table||Download (.pdf) TABLE 23–1 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 cholerae Yersinia enterocolitica Source: Williams Hematology, 8th ed, Chap. 52, Table 52–1, p. 770. +++ MECHANISMS ++ Hemolysis may be caused by: — Direct invasion by infecting organisms (malaria). — Elaboration of hemolytic toxins (Clostridium perfringens). — Development of autoantibodies against red blood cell antigens (Mycoplasma pneumoniae). +++ MALARIA +++ Etiology and Pathogenesis ++ The world's most common cause of hemolytic anemia. Transmitted by bite of an infected female Anopheles mosquito. Parasites grow intracellularly and parasitized cells are destroyed in the spleen. Uninvaded cells are also destroyed (estimated at 10 × the number of infected cells). Erythropoietin low for degree of anemia secondary to release of inhibitory cytokines, especially in Plasmodium falciparum infection. Certain heterozygous mutations that interfere with invasion of red blood cells by parasites have developed in endemic areas (G-6-PD deficiency, thalassemia, other hemoglobinopathies, and hereditary elliptocytosis). +++ Clinical Features ++ Febrile paroxysms are characteristically cyclic: Plasmodium vivax every 48 hours, Plasmodium malariae every 72 hours, and P. falciparum daily. Rigors, headache, abdominal pain, nausea and vomiting, and extreme fatigue accompany the fever. Splenomegaly typically is present in chronic infection. Falciparum malaria is occasionally associated with very severe hemolysis and dark, almost black urine (blackwater fever). Cerebral malaria may result in delirium, other neurologic manifestations. Organ dysfunction (respiratory insufficiency and renal failure) may be present. +++ Laboratory Features ++ Signs of hemolytic anemia. Thrombocytopenia nearly always present. Diagnosis depends on demonstration of the parasites on the blood film (Fig. 23–1) or the appropriate DNA sequences in the blood. If greater than 5 percent of red cells parasitized or if two ring forms in a red cell, P. falciparum infection usually present. ++ FIGURE 23–1 A. Blood film from a patient with malaria caused by Plasmodium falciparum. Several red cells contain ring forms. Note red cell with double ring form in center of the field, characteristic of P. falciparum infection. Note the ring form with double dots at the left edge of figure, suggestive of P. falciparum infection. Note also high ... Your MyAccess profile is currently affiliated with '[InstitutionA]' and is in the process of switching affiliations to '[InstitutionB]'. Please click ‘Continue’ to continue the affiliation switch, otherwise click ‘Cancel’ to cancel signing in. 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 Username Error: Please enter User Name Password Error: Please enter Password Forgot Username? Forgot Password? Sign in via OpenAthens Sign in via Shibboleth