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P Sayer

Publications and source records attributed to P Sayer.

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Trypanosoma brucei rhodesiense infection in vervet monkeys. I. Parasitologic, hematologic, immunologic and histologic results.

Twenty vervet monkeys infected with T. rhodesiense (Eatro 1989) developed chronic disease with an average duration of 65 days (variation 35-107 days). With respect to the course of the disease, and to the hematologic, immunologic and histological findings, the disease faithfully mirrored human T. rhodesiense infection. In all animals, parasitization of the CSF occurred only a few weeks after infection, and was accompanied by an increase in the cell count and the appearance of IgM in the CSF. The main histopathological feature was severe pancarditis which was responsible for death in almost all animals. Chronic leptomeningitis resulted as histological substrate of the early parasitosis of the CSF. In most animals meningitis was accompanied by a mitigated encephalitic early reaction characterized by sparse lymphoplasmocytic infiltrates, exclusively of the cerebral vessels, with a predilection for the base of the brainstem and the neighbourhood of the ventricles. Autonomous meningoencephalitis with parasites in the brain tissue was found in only one animal (with the longest survival period of 107 days). In view of the regular parasitosis of the CSF, T. rhodesiense infection of the vervet monkey may be considered a suitable animal model for the assessment of the liquor "uptake" of trypanocidal drugs.

Animals

Trypanosoma brucei rhodesiense infection in vervet monkeys. II. Provocation of the encephalitic late phase by treatment of infected monkeys.

Four out of 8 monkeys infected with Trypanosoma rhodesiense and treated with trypanocidal drugs at various intervals after infection (days 55-58, days 62-65, day 68) developed encephalitis. In 2 of these animals, killed 2 weeks after treatment, the encephalitis presenting was incipient; the other 2 monkeys died as a result of severe encephalitis a little more than 2 and 3 months after treatment, respectively. At the time of treatment, the animals revealed a parasitization of the CSF, but there were no clinical or neurological signs of any involvement of the central nervous system. The observations confirm observations made in human trypanosomiasis, and in experiments on rodents, which indicate that the encephalitic late phase may result from inadequate treatment. These observations may indicate that the encephalitis of the late phase may be methodologically provoked by infection and subliminal treatment after parasitization of the CSF, and that this procedure may be more promising of success than the method of infection only, as a method for the production of an animal model of the encephalitic late phase.

Animals

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