Predictors of childhood severe malaria in a densely populated area: Douala, Cameroon

The physiopathology of malaria is complex. More understanding would be useful for a better management of the disease. This study was undertaken to describe clinical presentation and some biochemical parameters in childhood malaria in order to identify some factors of disease severity. Eighty six (86) children (0 to 15 years old) were recruited in Douala, clinical data recorded and blood sample collected. Thirty one (31) healthy children were also targeted to serve as control. Blood glucose, hemoglobin, transaminases and nitric oxide were determined by spectrophotometry. C reactive protein (CRP) was also investigated. The results confirmed that severe malaria significantly affects children under 5 years. Severe malaria was associated with hyperpyrexia and prostration. Coma, convulsions and unconsciousness were more indicative of cerebral malaria. Hemoglobin and blood glucose levels decreased significantly in severe malaria patients compared with uncomplicated malaria patients or controls (P < 0.001). On the contrary, blood transaminases and CRP levels increased significantly in malaria patients compared to controls (P < 0.001). From these results, it is clear that childhood severe malaria is associated with prostration, coma, unconsciousness, convulsions and hyperpyrexia. Low levels of haemoglobin and glycemia, as well as high levels of transaminases and CRP has been identified as predictor of malaria severity.Keywords: Childhood malaria, clinical presentation, physiopatholog

Circulating endothelial cell-derived extracellular vesicles mediate the acute phase response and sickness behaviour associated with CNS inflammation.

Brain injury elicits a systemic acute-phase response (APR), which is responsible for co-ordinating the peripheral immunological response to injury. To date, the mechanisms responsible for signalling the presence of injury or disease to selectively activate responses in distant organs were unclear. Circulating endogenous extracellular vesicles (EVs) are increased after brain injury and have the potential to carry targeted injury signals around the body. Here, we examined the potential of EVs, isolated from rats after focal inflammatory brain lesions using IL-1β, to activate a systemic APR in recipient naïve rats, as well as the behavioural consequences of EV transfer. Focal brain lesions increased EV release, and, following isolation and transfer, the EVs were sequestered by the liver where they initiated an APR. Transfer of blood-borne EVs from brain-injured animals was also enough to suppress exploratory behaviours in recipient naïve animals. EVs derived from brain endothelial cell cultures treated with IL-1β also activated an APR and altered behaviour in recipient animals. These experiments reveal that inflammation-induced circulating EVs derived from endothelial cells are able to initiate the APR to brain injury and are sufficient to generate the associated sickness behaviours, and are the first demonstration that EVs are capable of modifying behavioural responses