African trypanosomiasis: haematogenic brain parasitism early in experimental infection through bypassing the blood-brain barrier, with considerations on brain trypanosomiasis in man.

A hematogenic invasion of the brain in suckling NMRI mice infected with Trypanosoma brucei rhodesiense was initiated by means of a mechanical damage of the blood-brain barrier. The brain was punctured after development of a blood infection. Brain infection was found in 31 out of 32 animals examined. Trypanosomes are initially capable of rapid multiplication. The number of parasites was highest during the 1st week. From the middle of the 2nd week the number of parasites decreased continuously, alongside increasing atrophy. In the 3rd and 4th week only rare degenerating or ghost trypanosomes were present. No reactions were detected in the glial and mesenchymal cells. It is presumed that the short phase of trypanosome multiplication is due to the temporary collateral oedema of the brain tissue. The decrease in parasites from the 2nd week onwards is mainly attributed to natural death due to particular anatomical features of the brain tissue. These are also responsible for the absence of defensive inflammatory reactions, based on the hypothesis that contact between trypanosomes and the cells of the brain blood vessels is prevented.