Lipid metabolism of the parasite is associated with alterations in fatty acids and cholesterol in the erythrocyte plasma membrane, which in turn are responsible for changes in permeability and fragility. The augmentation of all the membrane systems of the infected erythrocyte causes the lipid content to rise rapidly, but the parasite lipid composition differs from that of the erythrocyte in many respects. Phospholipid metabolism has been identified as an ideal target for novel anti-malarial chemotherapy due to its vital importance to the parasite. This paper attempts to review the underlying lipid metabolic pathways in the malaria parasite and their potential benefit as likely targets for novel anti-malarial chemotherapy.

Lipid trafficking pathways in malaria-infected erythrocytes are complex because the malaria parasite is separated from the serum by the erythrocyte and parasitophorous vacuolar membrane (PVM). The PVM lipids in malaria-infected erythrocytes are derived from host cells. Lipid rafts which are cholesterol and sphingolipid enriched membrane domains appear to be involved in malaria infection. Thus, perturbation of lipid raft specific lipids in the host erythrocyte membrane can influence the cell's ability to be infected. This paper attempts to discuss novel approaches in the treatment of malaria infection by targeting and manipulating host cell lipids based on recent discoveries on the role of lipid rafts in malaria pathogenesis.

Malaria infection is characterized by periodic fevers. These fevers, in Plasmodium falciparum and Plasmodium malariae (the tertian and quartan malaria respectively), arise through the synchronous release of parasite derived "toxins" during the 48 or 72-hour blood stage development. These in turn cause the release of endogenous pyrogens such as tumour necrosis factor (TNF) and interleukin-1 (IL-1) which mediate the febrile response by acting upon the hypothalamus. There is evidence suggestive of a role for TNF in wider spectrum of malaria associated disease, including severe clinical malaria, various malarial pathologies and even death. A case control study has shown a strong correlation between TNF and IL-1 levels in