Malaria is a deadly infectious disease caused by parasites of the Plasmodium spp. that takes an estimated 435,000 lives each year, primarily among young African children. For most children, malaria is a febrile illness that resolves with time, but in ∼1% of cases, for reasons we do not understand, malaria becomes severe and life threatening. Cerebral malaria (CM) is the most common form of severe malaria, accounting for the vast majority of childhood deaths from malaria despite highly effective antiparasite chemotherapy.
Cerebral malaria (CM) accounts for nearly 400,000 deaths annually inAfrican children. Current dogma suggests that CM results from infected RBC (iRBC)sequestration in the brain microvasculature and resulting sequelae. Therapies targetingthese events have been unsuccessful; findings in experimental models suggest that CD8+ Tcells drive disease pathogenesis. However, these data have largely been ignored becausecorroborating evidence in humans is lacking. This work fills a critical gap in ourunderstanding of CM pathogenesis that is impeding development of therapeutics.
Acute seizures are common in pediatric cerebral malaria (CM), but usual care with phenobarbital risks respiratory suppression. We undertook studies of enteral levetiracetam (eLVT) to evaluate pharmacokinetics (PK), safety and efficacy including an open-label, randomized controlled trial (RCT) comparing eLVT to phenobarbital.
Cerebral malaria is a lethal complication of malaria infection characterized by central nervous system dysfunction and is often not effectively treated by antimalarial combination therapies. It has been shown that the sequestration of the parasite-infected red blood cells that interact with cerebral vessel endothelial cells and the damage of the blood-brain barrier (BBB) play critical roles in the pathogenesis.
Plasmodium vivax infection is rising in sub-Saharan Africa, where Plasmodium falciparum is responsible for more than 90% of malaria cases. While P. vivax is identified as a major cause of severe and cerebral malaria in South east Asia, the Pacific and South America, most of the severe and cerebral cases in Africa were attributed to P. falciparum. Cases of severe malaria due to P. vivax are emerging in Africa. A few severe P. vivax cases were reported in Eastern Sudan and they were underestimated due to the lack of accurate diagnosis, low parasitaemia and seldom use of rapid diagnostic tests (RDTs).
Breakdown of the blood brain barrier (BBB) is a feature of cerebral malaria (CM), a manifestation of infection with Plasmodium falciparum parasites that currently has a 20% fatality rate and disproportionately affects children under 5 years old.
Cerebral malaria (CM) is a major cause of death due to Plasmodium infection.
The deadliest complication of Plasmodium falciparum infection is cerebral malaria (CM), with a case fatality rate of 15 to 25% in African children despite effective antimalarial chemotherapy.
Severe brain swelling in paediatric CM was independent of tested blood pro-inflammatory and anti-inflammatory cytokines which are markers of systemic inflammation.
Sickness behaviors are a conserved set of stereotypic responses to inflammatory diseases.