| Symptoms |
| The physical symptoms of infection with malaria parasites vary with a number of factors, the two most important being the species of parasite and the immune status of the host. As the parasites proliferate during the erythrocytic cycle, and the percentage of infected erythrocytes increases, patients typically experience headaches, chills, joint pains and, characteristically, fever. The chills and fever (known as a paroxysm) are typically periodic, recurring at intervals characteristic of the species of parasite. A paroxysm lasts for 4-12 hours, after which time there is typically a cessation of symptoms for a period, before another wave of paroxysm. These paroxysms are extremely stressful for patients, which begin with an intense feeling of cold, and which can last for up to an hour. After this, the body temperature begins to rise and can reach to between 39 and 41oC. Associated with this fever are feelings of nausea and sometimes convulsions. The paroxysms are associated with the rupture of infected erythrocytes and the release of merozoites into the blood stream, and the length of the inter-paroxysm period is defined by the parasite species, with P. vivax, P. falciparum and P. ovale cycling every 48 hours, and P. malariae every 60 hours.
The most severe manifestations of the disease such as cerebral malaria, severe anaemia, splenomegaly, hepatomegaly and nephritic syndromes are usually associated only with P. falciparum. Cerebral malaria is, at least in part, caused by sequestration of the parasites in the capillary vasculature in the brain. This is thought to occur due to parasitized erythrocytes binding to each other (rosetting) (Pongponratn et al., 1991), and to the endothelium of the capillaries themselves (Macpherson et al., 1985) resulting in hypoxia. Another factor contributing to the severity of cerebral malaria is the release by the host of large amounts of toxic cytokines (Clark and Schofield, 2000). This combination of hypoxia and elevated cytokine levels has been shown to increase levels of nitric oxide synthase which in turn generates large amounts of pathogenic nitrous oxide (Melillo et al., 1995). Severe anaemia is caused by the destruction of erythrocytes infected by the parasite, but there is also evidence that the presence of the parasite reduces the host’s capacity to produce more erythrocytes by suppressing the response of bone marrow to erythropoietin (Kurtzhals et al., 1997). |
 |
 |
| References
Pongponratn,E., Riganti,M., Punpoowong,B., and Aikawa,M. (1991). Microvascular Sequestration of Parasitized Erythrocytes in Human Falciparum-Malaria - A Pathological-Study. American Journal of Tropical Medicine and Hygiene, 44, 168-175. Macpherson,G.G., Warrell,M.J., White,N.J., Looareesuwan,S., and Warrell,D.A. (1985). Human Cerebral Malaria - A Quantitative Ultrastructural Analysis of Parasitized Erythrocyte Sequestration. American Journal of Pathology, 119, 385-401. Clark,I.A. and Schofield,L. (2000). Pathogenesis of malaria. Parasitology Today, 16, 451-454. Melillo,G., Musso,T., Sica,A., Taylor,L.S., Cox,G.W., and Varesio,L. (1995). A Hypoxia-Responsive Element Mediates A Novel Pathway of Activation of the Inducible Nitric-Oxide Synthase Promoter. Journal of Experimental Medicine, 182, 1683-1693. Kurtzhals,J.A.L., Rodrigues,O., Addae,M., Commey,J.O.O., Nkrumah,F.K., and Hviid,L. (1997). Reversible suppression of bone marrow response to erythropoietin in Plasmodium falciparum malaria. British Journal of Haematology, 97, 169-174. |
 |
 |
|
|