Pongponratn E, Riganti M, Harinasuta T, Bunnag D
Southeast Asian J Trop Med Public Health. 1985 Jun;16(2):219-27.
Ultrastructure of erythrocytes infected with Plasmodium falciparum in human brain, obtained 3 hours post mortem revealed gross distortion of host red cells with abnormality of the red cell surface. The superficial alterations of the parasitized cells as knob-like protrusion appear to be the sites of attachment to vascular endothelium. There was evidence of platelets sticking to the injured endothelium. The endothelial vesicular membrane is in close adhesion to the parasitized red cell, and also to the platelets involved in this mechanism. Thus, explaining the sequestration of parasitized red cell and obstruction in cerebral microcirculation, cerebral oedema and low peripheral platelet count. The was no evidence of inflammation, fibrin or thrombus formation observed in our studies.
在人死后3小时获取的感染恶性疟原虫的人脑红细胞超微结构显示，宿主红细胞严重变形，红细胞表面异常。被寄生细胞的表面改变如瘤状突起似乎是与血管内皮细胞附着的部位。有证据表明血小板黏附于受损的内皮细胞。内皮细胞的囊泡膜与被寄生的红细胞紧密黏附，也与参与这一机制的血小板紧密黏附。因此，解释了被寄生红细胞的滞留以及脑微循环阻塞、脑水肿和外周血小板计数降低的原因。在我们的研究中未观察到炎症、纤维蛋白或血栓形成的证据。
