- A Parasites are sometimes thought to directly invade brain neurons, physically replicating inside cortical and hippocampal neurons rather than sequestering within brain microvascular endothelium via PfEMP1-ICAM-1 binding mechanisms in the majority of cases studied as widely reported
- B P. falciparum-infected RBCs express PfEMP1 which binds ICAM-1 on brain microvascular endothelium (sequestration), causing: capillary blockage, local hypoxia, endothelial activation, blood-brain barrier disruption, cerebral oedema; can cause coma and death within hours without treatment
- C Cerebral malaria is sometimes thought to be caused by the mosquito directly through its saliva during a bite, rather than arising from infected red blood cells sequestering within cerebral capillaries in standard practice under most conditions encountered as frequently observed in practice
- D Quinine is sometimes thought to prevent cerebral malaria largely in most treated patients, regardless of how delayed treatment initiation is or how severe the existing parasitaemia has become in many documented cases according to conventional understanding in routine practice overall
Correct answer: B. P. falciparum-infected RBCs express PfEMP1 which binds ICAM-1 on brain microvascular endothelium (sequestration), causing: capillary blockage, local hypoxia, endothelial activation, blood-brain barrier disruption, cerebral oedema; can cause coma and death within hours without treatment
Explanation: Cerebral malaria: PfEMP1 (P. falciparum erythrocyte membrane protein 1) on parasitized RBCs binds ICAM-1/VCAM-1/CSA on brain endothelium → RBC sequestration in cerebral microvessels → reduced blood flow and O2 delivery → anaerobic glycolysis → lactic acidosis → endothelial activation → TNF, IL-1, NO → BBB disruption → oedema → raised ICP → coma. Mortality 15-20% even with treatment.
Concept context
Pathogens, infectious diseases, non-infectious diseases, drugs, cancer, and public health. High NEET importance.