Figure 531

Life cycle of malaria parasites and locations where specific drugs are effective. The life cycles are not identical for every species.

blood. These latter forms invade host erythrocytes, where they again grow and divide asexually (erythrocytic schizogony) and become red cell schizonts. Some of the parasites differentiate into sexual (male and female) forms, or gametocytes. If the diseased human is bitten by a mosquito at this time, the gametes will be taken up into the organism's gut to repeat the sexual cycle. The gametocytes and the exoerythrocytic liver forms of Plasmodium spp. are not associated with the appearance of clinical symptoms of malaria.

The asexual intraerythrocytic parasites, that is, those that do not differentiate into gametocytes, also multiply and grow until they rupture the cells in which they reside; these new merozoites are released into the bloodstream. This occurrence not only sets up the subsequent cyclical red blood cell stages of the cycle but also gives rise to the symptoms associated with malarial infections. The recurrent chills and fever are thought to be related to the lysis of erythrocytes and the accompanying release of lytic material and parasite toxins into the bloodstream. Although the appearance of a cyclic fever is useful for diagnosis, this symptom may not occur during the early stages of the infection.

In individuals infected with either P. vivax or P. ovale, the exoerythrocytic tissue (e.g., liver) forms can persist after a latent period and give rise to relapses. In P. falciparum and P. malariae malaria, however, there do not appear to be any persistent secondary liver forms. Thus, in both of these forms of malaria, the physician must contend only with the asexual erythrocytic forms and the gametes, not with the latent liver forms found in P. vivax and P. ovale.

Patients who have blood transfusion malaria are infected with the asexual erythrocytic parasites only; exo-erythrocytic tissue forms apparently do not develop. Plasmodium malariae has been known to produce an infection after transfusion, even when the blood was obtained from a person whose only contact with malaria was 40 years previous to the donation of blood.

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