TABLE 1422 Characteristics of Malaria Causing Plasmodium Species

Malaria may also be transmitted by direct transfusion of infected blood or passed transplacental^ from mother to fetus. In these cases, an exoerythrocytic phase is absent.

Disease ensues after an incubation period ranging from 8 days in the nonimmune and unprotected host to several weeks or more. Both incomplete suppression by partially active chemoprophylaxis and incomplete immunity can markedly prolong the incubation period to months or even years. Only the asexual intraerythrocytic parasite is responsible for the symptoms and pathophysiologic consequences. The hallmark of malaria is the recurring febrile paroxysm that corresponds to hemolysis of infected erythrocytes and release of antigenic products with activation of macrophages and production of cytokines.

Hemolysis can be high with P. falciparum infection, since parasitemia can be overwhelming and erythrocytes of all ages are susceptible. Parasitized erythrocytes lose flexibility and are removed in the microcirculation, with resultant obstruction and tissue anoxia of the lungs, kidneys, brain, and other vital organs. Noncardiac pulmonary edema, renal failure, and cerebral malaria may result. Sequestration accounts for the paucity of observed mature parasites in the peripheral smear of patients infected with P. falciparum.

In addition to prolonged high fever, hemolysis, and, in the case of infection with P. falciparum, obstruction to capillary flow, immunologic sequelae may also occur, resulting in glomerulonephritis, nephrotic syndrome, thrombocytopenia, and polyclonal antibody stimulation. Lastly, hypersplenism with resultant pancytopenia may occur, especially in cases of prolonged, untreated malaria.

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