Falciparum malaria in naturally infected humans. III. Platelet ultrastructural alterations during thrombocytopenia.

Abstract

Platelet ultrastructural alterations are described in thrombocytopenic Saudi patients with acute falciparum malaria (AFM) and compared with the appearances of platelets from same patients after successful antimalarial treatment. Some altered platelets lost their discoid form and showed concentration of organelles in the cell centers. Other platelets were devoid of the alpha- and dense granules usually seen in normal cells. The lack of these granules is known to be associated with bleeding symptoms. The bundle of microtubules known to maintain the discoid form of platelets, and the contractile fibrillar elements responsible for "platelet propulsive movement" were either dispersed or absent. The open canalicular system known to be the main endocytic and secretory pathway was either absent, or distended and obstructed by cytoplasmic extensions. Most of platelets developed surface pseudopodia and endocytic vacuoles that are characteristic features of phagocytic cells. Different mechanisms have been suggested as the cause of these alterations. This study indicates that AFM is associated with platelet structural alterations which could be an important cause of thrombocytopenia; the frequency of these alterations correlated with the degree of parasitaemia. Older patients presented with less marked parasitaemia than younger patients, possibly due to the less mature immune system in the latter. It is also possible that AFM may have independent effects on the structure of human platelets.