Immunopathological aspects of trypanosomal meningoencephalitis in vervet monkeys after relapse following BerenilR treatment

Four quarantined vervet monkeys were treated with intramuscular BerenilR in patent CNS infection after experimental trypanosome inoculation with Trypanosoma brucei rhodesiense or T. brucei brucei. All four animals relapsed in the post-therapeutic survival time of 37 to 209 days when they had fully developed meningoencephalitis in histological sections with the presence of interstitial intracerebral trypanosomes, which were confirmed in two monkeys by electron microscopy. In both, sequential samples of the serum and cerebrospinal fluid were analysed for circulating immune complexes, immunoglobulins and albumin. From these results the intracerebral IgG synthesis and the impairment of the blood-brain-barrier were calculated, both being present in advanced infection. Circulating immune complexes were present in the serum, but could not be demonstrated in the cerebrospinal fluid. The monkey model therefore permits the study of various aspects of cerebral trypanosomiasis. BerenilR treatment is inefficient in patent CNS infection and leads to a protracted, less virulent disease course with terminal meningoencephalitis and intracerebral "persister” trypanosomes. This drug-induced trypanosome shift with meningoencephalitis could be used for chemotherapeutic purposes to test new compounds in late stage diseas

From the laboratory to the home of the patient infected with

If dosed correctly, amocarzine has onchocercacidal effects with acceptable clinical tolerability. Up to now over 1 900 patients were exposed to an initial amocarzine regimen and over 500 have been re-exposed to amocarzine 2 years after initial therapy. Amocarzine is a promising onchocercacidal drug and a potential candidate for onchocerciasis control programmes