December 2nd, 2020
Malaria is a mosquito-borne protozoan infection caused by Plasmodium spp transmitted to humans via the species of the Anopheles mosquito. Malaria is most prevalent in Africa, Asia, and Latin America.
Patients with malaria classically present paroxysms consisting of several hours of fever and chills every 48-72 hours depending on the species. These episodes are caused by the cyclic rupture of mature schizonts in the blood and the resulting activation of cytokines.
Patients with cerebral malaria (CM) due to P. falciparum can develop confusion, drowsiness, convulsions, and coma due to cerebral tissue hypoxia from microvascular obstruction and endothelial activation, with pro-inflammatory cytokines likely playing a role. P. falciparum erythrocyte membrane protein 1 (PfEMP1) is expressed on the surface membrane of RBCs, leading to cytoadherence with points of attachment on the endothelium, resulting in blood vessel blockage.
The incubation period for P. falciparum ranges from 9 days to 14-30 days, 12-17 for P. vivax, and up to 40 days for P. malarie.
Patients with uncomplicated malaria may present with non-specific flu-like symptoms, such as headache, cough, myalgia, abdominal pain, and diarrhea due to release of proinflammatory mediators.
Complicated malaria can present with CM, acute respiratory distress syndrome (ARDS), and jaundice. In children, severe malaria can present with CM, anemia, and acidosis. This is caused by infected erythrocytes binding to the endothelium of blood vessels, leading to microvascular obstruction, blood-brain barrier (BBB) permeability, the release of proinflammatory mediators, and cerebral edema.