Cerebral malaria , development

Togbe, D., Schofield, L., Grau, G. E., Schnyder, B., Boissay, V., Charron, S., Rose, S., Beutler, B., Quesniaux, V. F., and Ryffel, B. (2007). Murine cerebral malaria development is independent of toll-like receptor signaling. Am.. Pathol. 170,1640-1648. 

Soumita Ghosh is a postdoctoral researcher in the Diabetes section in National Institute on Aging, Baltimore. She is involved in developing targeted proteomics technique for cannabinoid proteins. During her PhD., she worked in field of NMR metabolomics of murine cerebral malaria. She obtained her doctoral degree from Tata Institute of Fundamental Research in 2013. She obtained her MSc from IIT Kharagpur in 2008 and BSc from Calcutta university in 2006. 

CO prevents the development of experimental cerebral malaria in mice [21],... 

A 7-year-old Indian boy was diagnosed as having cerebral malaria and received quinine followed by mefloquine (dose not given) (500). He developed hallucinations and removed his clothes and danced. His symptoms resolved within 24 hours of stopping mefloquine. This case highlights the fact that mefloquine should not be given after quinine in cases of severe malaria. 

Chloroquine and desethylchloroquine concentrations have been studied in 109 Kenyan children during the first 24 hours of admission to hospital with cerebral malaria (10). Of the 109 children 100 had received chloroquine before admission. Blood chloroquine and desethylchloroquine concentrations were no higher in children who had seizures than in those who did not, suggesting that chloroquine does not play an important role in the development of seizures in malaria. 

Alongside the well-known development of resistance by P. falciparum to chloroquine, the emergence of chloroquine-resistant Plasmodium vivax is now clear (SEDA-13, 801). An increased frequency of cerebral malaria appears to coincide with the growing emergence of the chloroquine-resistant strains in Francophone Africa. 

Neutrophil depletion prevents development of cerebral malaria caused by P berghei ANKA and decreases sequestration of monocytes and microhemorrhage in the brain [87]. This is associated with downregulated levels of IFN-7, TNF-a, IL-2, and IL-12 p40 in the brain, with no corresponding Th2 cytokine increases. Peritoneal exudate neutrophils, obtained after intraperitoneal injection of P berghei ANKA-parasitized red blood cells, contain IL-12 p40 mRNA, but it is not clear whether this represents parasite-induced or preformed IL-12 message [88]. Likewise, the PMN were found also to express mRNA for IL-18, IL-10, IFN-7 and TNF-a, and the Thl chemoattractants MIG, MIP-la, and IP-10. 

Campanella, G.S., Tager, A,M El Khoury, J.K, Thomas, S.Y., Ahrazinski, T,A Manice, L.A., Colvin, R.A and Luster, A.D. (2008) Chemokine receptor CXCR3 and its ligands CXCL9 and CXCLIO are required for the development of murine cerebral malaria. Proceedings of the National Academy of Sciences of the United States of America, 105, 4814-4819. 

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