On a global scale, malaria still represents a major problem of public health, principally because of its two major complications, cerebral malaria (CM) and severe malarial anemia. The disease manifestations apparent during that stage of the malaria parasite lifecycle when it is circulating within host erythrocytes are a result of complex host–parasite interactions. In man, most of the pathology is due to Plasmodium falciparum. In the case of CM, the microcirculation, and in particular the endothelium, appears to be pivotal in the interplay between infected erythrocytes (IEs), host immune cells, and host tissues.

We focus here on the cerebral syndrome, but the endothelium also has a central role in other aspects of malarial pathology; these have been reviewed recently elsewhere (1). For example, severe malaria may be complicated by pulmonary edema, the cause of which is still unknown. It shares many features with the adult acute respiratory distress syndrome (ARDS). Rehydration may predispose patients with severe malaria to develop pulmonary edema, although it is by no means a prerequisite. Indeed, evidence suggests that an increase in the lung capillary permeability – as distinct from simple intravascular volume overload – may be at the origin of this complication. Acute or chronic renal insufficiency is another common complication of severe malaria, and is often lethal. It occurs in adults and older children. The mechanisms leading to the acute tubular necrosis are not fully understood. A cytoadherence of IEs in glomerular capillaries sometimes can be observed, but is never as prominent as in the brain. Renal pathology in malaria often presents as a more chronic pathology, most notably with glomerulonephritis associated with deposits of immune complexes (2–5).