Immunity and Prophylaxis

The average age of first infection with malaria is less than 1 year old for persons in most endemic areas. Estimates are that between 75,000 and 200,000 infant deaths each year are associated with malaria infection in pregnancy (78). Exposure does not induce lifelong immunity to further malaria infections. As children age, they acquire a functional immunity that provides fewer clinical attacks and lessened clinical symptoms. Adults can obtain sufficient immunity so that a substantial reduction in infection rates is observed. Asymp tomatic parasitemia may occur among persons who have been long-term residents of malaria-endemic areas. As a result, children have the highest levels of mortality and morbidity resulting from malaria. It had long been assumed that these data were the result of a high transmission rate of the parasite. New studies have indicated, however, that most endemic areas contain parasites with a high degree cf antigenic diversity (79). Each infection does in fact provide immunity to that particular strain; new infections are caused by parasites with different antigenic profiles. A calculation of transmission rates incorporating these considerations yields numbers an order of magnitude lower than previously estimated.

Pregnant women have a unique susceptibility to malaria, such that "maternal malaria," a distinct clinical entity, causes serious pregnancy-related complications in endemic areas. Increases in miscarriage, premature delivery, retardation of fetal growth, anemia, low birth weight, and mother and infant mortality rates are observed when the mother contracts malaria during pregnancy. Adult women acquire the same degree of immunity to the common strains of parasites as do adult men; however, after becoming pregnant, this acquired immunity diminishes markedly. With successive pregnancies, the loss of immunity is less pronounced. To explain the apparent loss of acquired immunity in pregnancy, researchers studied the binding of infected red blood cells to placental tissue (80). A subpopulation of P. falciparum parasites preferentially binds to placental tissue and multiplies there. The binding site in placenta normally binds chondroitin sulfate A (CSA). The severity of the infection must be caused by the initial appearance of placental tissue that harbors the infection. As the woman develops immunity to this subpopulation of parasites, the frequency and severity of malaria in a second or third pregnancy is lessened. With the rising incidence of HIV/AIDS in Africa and concern about maternal transmission of the virus, the problems of simultaneous multiple drug therapies emerge. For a review of the therapeutic and safety issues in the concurrent use of anti-HIV agents with antimalarial agents in pregnant patients, see Ref. 81.

Glucose-6-phosphatedehydrogenase(G6PD) deficiency is a genetic condition most prevalent among persons living in malaria-endemic areas. The most common African form of G6PD deficiency was associated with a 46-58% reduction in the risk of severe malaria (82). Parasites inflict oxidant damage to the erythrocytes that are infected and erythrocytes that are deficient in G6PD are especially susceptible to oxidant damage. In addition, it has been shown that phagocytosis of parasiticized G6PD-deficient erythrocytes occurs earlier than does phagocytosis of infected normal erythrocytes, perhaps accounting for the observed protective effect (83).

Other inherited red cell disorders contribute an immunity to malaria infections, at least partially as a result of sensitization to oxidant stress. These include the well-known example of heterozygous hemoglobin S (sickle cell trait) (84) as well as thalassemia (85), persistence of fetal hemoglobin, and hemoglobin E.

seems to increase susceptibility to malaria in early childhood and then offers immunity later in life (86). An explanation of the effect involving hemoglobin/ membrane interactions had been proposed (87). Southeast Asian ovalocytosis is another genetic disorder that confers marked protection against cerebral malaria (88). It is caused by a deletion in the gene for the erythrocyte membrane band 3. The band 3 protein is responsible to the cytoadherence of parasitized cells. The mutation occurs in high frequency in the western Pacific.

Non-immune travelers, with no prior exposure to malaria, are at greater risk cf acquiring serious infections. If the infection presents clinical symptoms only after return from a malarious area, there may be a delay in diagnosis by physicians unfamiliar with the disease. Travelers to endemic areas should seek advice about the use of chemoprophylactic regimens and stand-by treatment. Further protection is gained by preventing exposure to mosquitoes using insect repellents on clothes and skin and staying indoors at night. For reviews on malaria chemoprophylaxis, see Refs. 89, 90.

Chemoprophylaxis demands a nearly impossible level of safety, especially when used over long periods. Drugs are given to healthy individuals, most often to prevent a disease of low probability. The most successful agent to date has been chloroquine, with a 50-year safety record that is matchless among anti-infective agents. Malaria prophylactic regimens are generally highly efficacious and low in cost, especially when compared with the costs of treatment including hospitalization. Even so, compliance has remained an issue among U.S. travelers to malarious areas; only 21% of travelers used recommended malaria prophylaxis appropriate for their area of travel in 1997 (62). International travel recommendations are available from both the WHO (59, 91) and the CDC (92, 93).

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