The GVR 35 T.b.brucei mouse model is well established and characterised. In this model administration of trypanocidal drugs used to treat stage-1 infections, such as diminazene aceturate or suramin, will successfully cure the disease when they are given prior to day 21 post-infection. If chemotherapy is delayed beyond this point, only drugs tailored to cure stage-2 infections such as melarsoprol will prove effective . Melarsoprol, unlike the stage-1 drugs, can cross the BBB to reach therapeutic concentrations within the brain. This information allows us to deduce that mice, infected with T.b.brucei GVR35, have entered stage-2 disease, with parasites established within the brain, by 21 days following initial infection , , . The results of the present study indicate the development of statistically significant neuroinflammatory reactions, parasite burden and BBB dysfunction in animals at 14 days -post-infection, prior to the onset of established CNS-stage disease. All of the criteria investigated increased as the infection progressed through to the CNS-stage and demonstrated significantly greater levels on day 28 post-infection compared with day 14 post-infection.