The few reports detailing the neuropathological features in post-mortem samples from fatal cases of HAT describe the development of a diffuse meningoencephalitis, with the inflammatory infiltrate comprised of macrophages, lymphocytes and plasma cells , , . Astrocyte and microglial cell activation was also noted. The neuroinflammatory changes were most apparent in the white matter of the cerebral hemispheres but also occurred in the circumventricular areas. The neuroinflammatory picture has also been described in rodent , , , , , , , ,  and primate , , ,  models of trypanosome infection. Although these studies reported a similar response to that described in human cases the development of a meningoencephalitis, with inflammatory cells infiltrating the brain parenchyma, was only seen on a few occasions and was more commonly associated with treatment failures , , . In the T.b.brucei murine model used in this study only mild to moderate neuroinflammation, with inflammatory cells present in the meninges and infiltrating the perivascular space in the later stages of the infection, was found corresponding with the reaction previously reported in the alternative animal models.