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Once infected, the host quickly mounts a species- and strain-specific immunologic response that typically limits parasite multiplication and moderates the clinical manifestations of dis-ease, without eliminating the infection—a phenomenon referred to as premunition. A pro-longed recovery period marked by recurrent exacerbations in both symptoms and number of erythrocytic parasites follows. With time, these recrudescences become less severe and less frequent, eventually stopping altogether.
The exact mechanisms involved in this recovery are uncertain. In simian and probably in human malaria, recovery is known to require the presence of both T and B lympho-cytes. It is probable that the T lymphocytes act partially through their helper effect on an-tibody production. Some authorities have suggested that they also play a direct role through lymphokine production by stimulating effector cells to release nonspecific factors capable of inhibiting intraerythrocytic multiplication. The B lymphocytes begin produc-tion of stage- and strain-specific antiplasmodial antibodies within the first 2 weeks of par-asitemia. With the achievement of high levels of antibodies, the number of circulating parasites decreases. The infrequency with which malaria occurs in young infants has been attributed to the transplacental passage of such antibodies. It is uncertain whether they are directly lethal, act as opsonizing agents, or block merozoite invasion of RBCs.
In simian malaria, the parasite can undergo antigenic variation and thereby escape the suppressive effect of the antibodies. This antigenic variation leads to cycles of recrudes-cent parasitemia but ultimately to production of specific antibodies to the variants, and cure. It seems probable that similar changes occur in humans, leading to the eventual dis-appearance of erythrocytic parasites. With P. falciparum and P. malariae, which have no persistent hepatic forms, this results in cure. With P. falciparum, the disease typically does not exceed 1 year, but with P. malariae the erythrocytic infection can be extremely persistent, lasting in one case up to 53 years. How erythrocytic parasites circulating in numbers too small to be detected on routine blood films escape immunologic destruction remains a puzzle. In a closely related simian malaria, splenectomy results in rapid cure, suggesting that suppressor T lymphocytes in the spleen may play a protective role. In in-fection with P. vivax and P. ovale, latent hepatic infection may result in the discharge of fresh merozoites into the bloodstream after the disappearance of erythrocytic forms. This phenomenon, known as relapse, is capable of maintaining infection for 3 to 5 years.
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