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Microbiology · Parasitology: cerebral malaria pathogenesis
Sample itemA 5-year-old with Plasmodium falciparum malaria has deep coma, and the peripheral smear shows only ring forms, while trophozoites and schizonts are absent. Which mechanism best explains the cerebral involvement?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. PfEMP1-mediated cytoadherence of infected red cells to cerebral microvascular endothelium
P. falciparum inserts PfEMP1 into knobs on the red cell membrane. This binds endothelial receptors such as ICAM-1, CD36 and EPCR, so infected cells sequester in the microvasculature and obstruct flow, which is why later stages are absent from the peripheral blood. Cytokines add to the injury.
Option by option
A. PfEMP1-mediated cytoadherence of infected red cells to cerebral microvascular endothelium (correct)
Correct. Sequestration through PfEMP1 explains the absence of mature forms in the blood and the cerebral microvascular obstruction.
B. Rupture of hypnozoite-infected hepatocytes
Hypnozoites occur in vivax and ovale and are not a feature of falciparum malaria.
C. Direct invasion of neurons by merozoites
Merozoites invade red cells, not neurons.
D. Blockage of the portal vein by schizonts
Schizonts are sequestered in capillaries and are not found in a portal obstruction pattern.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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