Cerebral malaria (Plasmodium falciparum) is distinguished pathologically by cytoadherence of parasitised RBCs to cerebral endothelium mediated by which parasite ligand?
- A Merozoite surface protein 1 (MSP-1) binding to erythrocyte Band 3 protein
- B Circumsporozoite protein (CSP) binding to heparan sulfate proteoglycans on endothelium
- C PfEMP1 (Plasmodium falciparum erythrocyte membrane protein 1) binding to ICAM-1 and CD36 ✓
- D Knob-forming histidine-rich protein 2 (HRP2) binding to cerebral endothelium
Explanation
Cytoadherence is the central mechanism of cerebral malaria pathogenesis. PfEMP1 (encoded by var genes) is expressed on the surface of knobs on parasitised erythrocytes and binds to host endothelial receptors including ICAM-1 (intercellular adhesion molecule-1), CD36, PECAM-1, and E-selectin, causing sequestration of parasitised RBCs in cerebral microvascular endothelium. This leads to mechanical obstruction, local hypoxia, endothelial activation, and breakdown of the blood-brain barrier. MSP-1 is involved in invasion; CSP mediates hepatocyte invasion; HRP2 is an antigen used diagnostically in RDTs but is not the cytoadherence ligand.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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