Sunday 15 July 2007
P. falciparum causes more severe disease than the other Plasmodium species do.
Several features of P. falciparum account for its greater pathogenicity:
P. falciparum is able to infect red blood cells of any age, leading to high parasite burdens and profound anemia. The other species infect only new or old red blood cells, which are a smaller fraction of the red blood cell pool.
P. falciparum causes infected red blood cells to clump together (rosetting) and to stick to endothelial cells lining small blood vessels (sequestration), which blocks blood flow. Several proteins, including P. falciparum erythrocyte membrane protein 1 (PfEMP1), form knobs on the surface of red blood cells. PfEMP1 binds to ligands on endothelial cells, including CD36, thrombospondin, VCAM-1, ICAM-1, and E-selectin. Ischemia due to poor perfusion causes the manifestations of cerebral malaria, which is the main cause of death due to malaria in children.
P. falciparum stimulates production of high levels of cytokines, including TNF, IFN-γ, and IL-1. GPI-linked proteins, including merozoite surface antigens, are released from infected red blood cells and induce cytokine production by host cells by a mechanism that is not yet understood. These cytokines suppress production of red blood cells, increase fever, induce nitric oxide production, leading to tissue damage, and induce expression of endothelial receptors for PfEMP1, increasing sequestration.
- Plasmodium vivax
- Plasmodium ovale
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