The presence of trypanosomes situated in the brain parenchyma has been frequently documented in rodent models of HAT during both the chronic , ,  and more acute stages of the infection , . Furthermore, manipulation of the immunological microenvironment has been shown to alter the ability of the parasites to enter the neuropil and mice deficient in CXCL10 or IFN-γ show reduced parasite numbers in the parenchyma or fail to develop CNS-stage infections , . In this study, Taqman PCR was used to assess the number of trypanosome present within the brain. This technique is highly sensitive and showed that parasite DNA was present at low levels as early as 7-days after infection and found in rising quantities at 14, 21 and 28 days -post-infection. Taqman PCR does not provide details regarding the location of the parasites within the brain tissue. It is possible that small quantities of blood, remaining in the blood-vessels following perfusion, could be responsible for the low numbers of trypanosomes identified during the early stage of the infection. At later time-points a more substantial parasite burden was detected. However, since we have no information regarding the location of the parasites, it could be argued that they may not be present in the brain parenchyma but situated in the meninges, ventricles or other areas such as the circumventricular organs where the blood-vessel epithelium is fenestrated. In fact, recent investigations in a rat model of infection, using freeze fracture electron microscopy, suggested that trypanosomes do not reside in the neuropil of the brain, until the terminal stages of the infection, but persist between the cell layers in the pia mater where the population size is controlled by prostaglandin-D2 . The increasing brain parasite burden detected here argues against this scenario in this study; and since no cyclical fluctuations in the trypanosome population were apparent this would suggest that the parasites were not situated in the choroid plexus, or CSF , . The presence of high levels of residual DNA from dead or dying parasites also seems unlikely due to the high turnover of CSF in the brain , , .