Immunity

Acquired and innate immunity are important factors in the epidemiology of malaria. Innate resistance has been recognized in some human populations. In parts of Central and West Africa, many individuals lack the Duffy blood group antigens Fya and Fyb and are thus resistant to P. vivax infection. Generally, in these areas, P. ovale replaces P. vivax as the prevailing cause of benign tertian malaria. In endemic P. falciparum areas of Africa, those individuals heterozygous for hemoglobin AS or sickle trait are more likely to survive malignant tertian ma laria than are hemoglobin A homozygotes. The persistence of sickle-cell disease (in hemoglobin SS homozygotes), with its unfortunate consequences, is balanced by the substantial advantage conferred by the AS condition, but only as long as P. falciparum remains endemic in the area. Several other hemoglobin variants have been thought to provide some protection against P. falciparum infection; it is known that persistent hemoglobin F (fetal Hb) delays development of falciparum parasites (Bruce-Chwatt 1987). Another genetic condition, deficiency of the red blood cell enzyme glucose 6-phosphate dehydrogenase (G6PD), also provides a degree of protection against falciparum infection.

Acquired immunity in malaria is species-specific and also specific to stage, that is, to the sporozoite, to the asexual forms in the blood, or to the sexual stages (Clyde 1987). In endemic areas, newborns may be protected for a few months by maternal antibodies that have crossed the placenta. After this phase of protection, however, infants and toddlers are especially vulnerable; most of the severe illnesses and deaths due to malaria in endemic regions occur in these early years. Older children and adults gradually acquire immunity with repeated exposure to infection. This partial immunity (premunition) is sustained in the presence of low densities of parasites in the blood. In premune individuals the spleen may remain enlarged; hence the spleen rate may be relatively high in an adult population despite a low parasite rate. With prolonged exposure and infection, however, as in a holoendemic area, eventual spleen scarring and shrinkage leads to a low adult spleen rate. Attenuated malaria certainly contributes to impaired resistance to other diseases; thus improved malaria control in endemic areas generally results in declines in morbidity and mortality from all causes (Bruce-Chwatt 1987).

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