RETRACTED CHAPTER: Pathogenesis of Plasmodium falciparum

Plasmodium falciparum causes malaria through a complex interaction of parasite-induced changes in red blood cell (RBC), including microcirculatory abnormalities, immunological reactions, and numerous clinical manifestations of variable severity and symptoms. Female Anopheles mosquito bites a person and delivers the parasite into the blood. Normally, the children under 5 and pregnant women are at most danger from malaria claiming the death toll up to 2.5 million people annually. P. falciparum is cause for vast severe illness, sequestration and accumulation of parasite-infected erythrocytes, involving brain, lung, and placenta. Infection from P. falciparum plays a critical role in the severe forms of malaria development. Adhesive interactions cause sequestration of proteins of Plasmodium infected tissues, exhibited symptom out of surface of infected red blood cells and a from diverse host biomolecules present on the epithelium surface of blood and lymph vessels, plasmocytes, and healthy RBCs. The Plasmodium has numerous proteins secreted from erythrocyte membrane, parasite itself, ligand, and antigens from membranes of red blood cells which all are encoded through an important multigene family allowing it to evade specific immune responses as the parasite has multiple and efficient immune evasion mechanisms. Targets for preventing or treating severe malaria may be uncovered through an anticipation of extremely complex RBCs—parasite relationships in the context of clinical illness and immunity levels.