Hypoglycaemia in human malaria is largely associated with Plasmodium falciparum infection. It is probably due to the direct effects of parasite products, although some workers feel it is cytokine mediated. The sickle cell gene confers protection against P. falciparum malaria whereas homozygosity for the Duffy negative gene confers total refractoriness to P. vivax infection. This association was not, however, confirmed by a study carried out by the same investigators in an East African population. Recently, it has been apparent that the patterns of malarial disease are undergoing temporal changes within regions.
Severe disease is seen extending into populations in previously less affected areas.
A probable factor contributing to these trends is in creasing resistance of the parasite to anti-malarial drugs, though other changes in the environment and in the human, parasite and vector populations may all be responsible. The diverse manifestations in a different individuals and in the same individual have been studied. It is an open question whether an all-encompassing theory to explain these, and for the pathogenesis may be found. However, the various factors involved and the threads linking them can be identified. Tumour necrosis factor and disease severity in children with falciparum malaria.