Jennings F W, Hunter C A, Kennedy P G, Murray M
Department of Veterinary Parasitology, University of Glasgow, UK.
Trans R Soc Trop Med Hyg. 1993 Mar-Apr;87(2):224-6. doi: 10.1016/0035-9203(93)90502-h.
The use of a rapid curative chemotherapeutic regimen for experimental infection of the central nervous system (CNS) of mice by Trypanosoma brucei has indicated that this 'aggressive' treatment does not precipitate the development of post-treatment meningo-encephalopathy. If meningoencephalitis is already established at the time of the treatment there is no exacerbation of the reaction and the CNS pathology rapidly returns to normal. Paralysis is not precipitated by the rapid curative treatment of either primary or relapse infections, in contrast to non-curative treatments. Mice showing this overt clinical paralysis in addition to histological meningoencephalitis soon regain mobility and the CNS pathology is rapidly resolved after curative chemotherapy. These experiments provide no support for the concept that the rapid release of trypanosome antigens in situ in the brain exacerbates the post-treatment encephalopathy. They do support the concept that it is viable trypanosomes remaining in the brain which are responsible.