Histopathological studies in cerebral malaria have revealed microbleeds in brain parenchyma secondary to microangiopathy. Susceptibility weighted imaging, being exquisitely sensitive to microbleeds may provide additional information and improve the diagnostic accuracy of MRI in cerebral malaria.
Cerebral malaria claims the lives of over 600,000 African children every year.
CM isolates bind significantly more to CD36 than to ICAM-1, which was correlated with high transcription level of group B var genes, supporting their implication in malaria pathogenesis.
In the Plasmodium infected host, a balance between pro- and anti-inflammatory responses is required to clear the parasites without inducing major host pathology.
In a new study, Coban and colleagues provide new clues on the involvement of the olfactory bulb during experimental cerebral malaria in mice that open the way to testable hypotheses and potentially earlier intervention in humans.
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.