Among the malaria parasites of humans, cytoadherence is purportedly unique to P. falciparum, resulting in sequestration of all but early trophozoite stages in falciparum malaria. Cytoadherence is often implicated in malaria pathology and is mediated by the expression of variable var gene products (of the PfEMP-1 family) at the surface of infected host red blood cells with concomitant expression of post-capillary endothelial cell receptors [15, [30] [31] [32] . Although not easily quantifiable, partial sequestration was observed in this fatal case of knowlesi malaria as evidenced by an abundance of large pigment bearing parasites on the blood film obtained post-mortem and as accumulations in the microvasculature. We hypothesize that partial sequestration may be due to P. knowlesi infected cell agglutination mediated by variant surface antigens of P. knowlesi SICA var genes (orthologues of the PfEMP-1 family) [33, 34] . Importantly, in this fatal case of P. knowlesi, up-regulation of ICAM-1 was not detected, nor was there evidence for cytoadherence as parasitized cells were not marginalized and were interspersed with uninfected erythrocytes in smaller vessels.