Editorial Open Access

Shizonts of P. falciparum malaria have knobs that can cytoadhere to vascular endothelium. The other human malaria species have no cytoadherance. In patients with severe falciparum malaria, parasitized red blood cells sequestering in microvasculature cause vital organ hypoxia and dysfunction. In microcirculation, rupturing shizonts release up to 32 merozoites causing an exponential rise in parasitemia [1,2]. A high shizont count is likely to precede a rise in parasitemia and may be an early marker of severe malaria diseases. Cut-off for hyperparasitemia of WHO Malaria Treatment Guidelines trended to decline since 2006 (2006 Guidelines: ≥ 5 % parasitemia in low-transmission areas and ≥ 10 % in a high transmission areas vs 2010 Guidelines:>2 % in low-transmission areas and>5 % in a high transmission areas) [3,4]. Tangpukdee et al. [4] showed cut-off of parasitemia ≥ 0.5 % was associated with severe malaria in Thailand where was a low transmission area [5]