The following pathological features are associated with Plasmodium falciparum except-
Pathology Red cells infected with malaria are prone to haemolysis. This is most severe with P. falciparum, which invades red cells of all ages but especially young cells; P. vivax and P. ovale invade reticulocytes, and P. malariae normoblasts, so that infections remain lighter. Anaemia may be profound and is worsened by dyserythropoiesis, splenomegaly and depletion of folate stores. In P. falciparum malaria, red cells containing trophozoites adhere to vascular endothelium in post-capillary venules in brain, kidney, liver, lungs and gut by the formation of 'knob' proteins. They also form 'rosettes' and rouleaux with uninfected red cells. Vessel congestion results in organ damage, which is exacerbated by rupture of schizonts, liberating toxic and antigenic substances . P. falciparum has influenced human evolution, with the appearance of protective mutations such as sickle-cell , thalassaemia , glucose-6-phosphatedehydrogenase (G6PD) deficiency and HLA-B53. P. falciparum does not grow well in red cells that contain haemoglobin F, C or especially S. Haemoglobin S heterozygotes (AS) are protected against the lethal complications of malaria. P. vivax cannot enter red cells that lack the Duffy blood group; therefore many West Africans and African Americans are protected. Ref Harrison20th edition pg 1056
Cytoadherence
Sequestration
Rosetting
Tissue phase
Infection