The data appears consistent with the methaemoglobin/haem hypothesis in malaria and sepsis pathogenesis.
In animal models of experimental cerebral malaria (ECM), neuropathology is associated with an overwhelming inflammatory response and sequestration of leukocytes and parasite-infected RBCs in the brain.
During experimental cerebral malaria (ECM) mice develop a lethal neuropathological syndrome associated with microcirculatory dysfunction and intravascular leukocyte sequestration.
Systemic inflammation and sequestration of parasitized erythrocytes are central processes in the pathophysiology of severe Plasmodium falciparum childhood malaria.
This study demonstrates that protection for ECM depends on the numbers of the parasites, S. japonicum and P. berghei, during co-infection. Alterations in the regulatory response appear to play a key role in this adaptation.
In patients with cerebral malaria (CM), higher levels of cell-specific microparticles (MP) correlate with the presence of neurological symptoms.
If you care for patients with cerebral malaria or know someone who does, then we would appreciate your help in distributing this short survey.
Please use the following link to complete the survey: Cerebral Malaria Diagnosis Survey
I am an ophthalmologist with a background in malaria biology, and I am leading a survey study to understand how clinicians diagnose cerebral malaria.
Cerebral malaria (CM) is associated with a high mortality rate, and long-term neurocognitive impairment in approximately one third of survivors.
This study reaffirms the importance of context specific intervention planning.
In summary, the current study provided further evidence that CM affects key brain areas related to cognition process.