Abstract
Pathological processes in malaria are the consequence of the erythrocytic cycle of the parasites. Merozoites invade erythrocytes, in which they develop through early trophozoites (ring forms) to late trophozoites and eventually to schizonts. During this process, development of knobs and cytoadherence or rosetting with the knobs play important roles for the falciparum malaria patient to be severely ill. Expression of variant surface neoantigens stimulates the reticuloendothelial system and can cause anemia, tissue hypoxia and cytokine production. Associated fever, paroxysms, headache and other pains are thought to result from cytokines such as interleukins, interferons and tumor necrosis factor released from macrophages or other cells at the time of schizont rupture. In the present paper, pathological and pathophysiological changes mainly in human falciparum malaria are reviewed, emphasizing the importance of basic research to “roll back” the emerging trends of malaria.
