Numerous neurological conditions, of both infectious and non-infectious aetiology, can initiate various degrees of BBB impairment , , . However, the impact of trypanosome infection on BBB function remains controversial , , , . Rhodamine dye, injected into the jugular vein of rats during the advanced stages of T.b.brucei infection, has been found permeating the brain cortical white and grey matter, indicating the presence of BBB dysfunction in these animals . In a similar rat model, Mulenga et al.  detected increasing numbers of parasites in the brain parenchyma as the infection progressed, though no changes were seen in the staining patterns of the tight junction proteins occludin and zonula occludens 1, or the penetration of fibrinogen or IgG. In this instance, the findings suggest that trypanosome infection and transmigration into the CNS does not result in loss of BBB integrity. The application of an in vitro BBB model utilising human brain microvascular endothelial cells has provided further evidence suggesting that trypanosomes do not cause lasting damage to the BBB . This study showed that T.b.rhodesiense induced only a transient reduction in transendothelial electrical resistance (TEER), which was most pronounced around 3 h following introduction of the parasites .