Browsing by Author "Ngure, R.M."
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Item Effects of tea on survival rates and liver pathology of Trypanosoma hruce; bruce; infected mice(2011) Mbuthia, S.K.; Wachira, N.F.; Ngure, R.M.; Ouma, J.M.; Kagira, J.M.; Department of Biochemistry and Molecular Biology, Egerton University, P.O Box 536, Egerton, Kenya, Tea Research Foundation of Kenya (TRFK), P.O. Box 820, Kericho, Kenya, Department of Biochemistry and Molecular Biology, Egerton University, P.O Box 536, Egerton, Kenya, Trypanosomiasis Research Centre (TRC), P.O. Box 362-00902, Kikuyu, Kenya, Trypanosomiasis Research Centre (TRC), P.O. Box 362-00902, Kikuyu, Kenya, Institute of Primate Research, P.O. Box 24481, Karen, Nairobi, Kenya.The current study investigated the effects of different types of Kenyan Tea extracts on the pathogenesis of Trypanosoma brucei brucei in a Swiss White mice model. Following infection with trypanosomes, the mice were monitored for survival and liver pathology. Tea significantly (P<0.05) enhanced the survival rate of tea, treated mice. Additionally, in tea treated but infected mice, there was reduction in infiltration of inflammatory cells into the periportal and parenchymal regions as well as hepatocyte cell damage compared to the infected untreated animals. Green and white teas were superior in most of the above effects while black tea and oolong teas had the least effects. The tea extracts were more efficacious than dexamethasone in prolonging the life of infected animals. It is concluded tea can act as adjunct therapeutic agent in treatment of diseases having hepatic inflammation, including trypanosomiasisItem Total Protein and White Cell Changes in the Cerebrospinal Fluid of Vervet Monkeys Infected with Trypanosoma rhodesiense and the Post-treatment Reaction(The Research Centre for Protozoan Molecular Immunology, 1994) Ndungu, J.M.; Ngure, R.M.; Ngotho, J.M.; Sayer, P.D.; Omuse, J.K.; Kenya Trypanosomiasis Research Institute; Kenya Trypanosomiasis Research Institute, P. O. Box 362, Kikuyu, KenyaIn an attempt to elucidate the events leading to the development of post treatment reactve encephalopathy in human Africa trypanosomiasis (HAT),a group of vervet monkeys (ceropithecus aethiops)were experimentally indfected with Trypanosoma rhodesiense. When terminally sick on day 12, they were treated with either diminazene aceturate, suramin or melarsoprol. Trypanosomes appeared in the cerebrospinal fluid(CSF)by day 1 of infection and increased in numbers with progress of the disease. However, only marginal increases in CSF total protein and white cels ocured during the same period. Treatment with Berenil resulted in persistence and increase in numbers of CSF.Trypanosomes, a dramaric increase in proteins and white cells up to 8 weeks after treatment,calminating in clinical encephalitis. Suramin cleared CSF trypanosomes within 4 weeks with marginal increase in proteins and white cells up to 8 weeks after treatment, folowes thereafter by a grasual and prolonged fall to pre-infection levels, Melarsoprol eliminated trypanosomes from the CSF in less than a week but the white cell and protein levels increased for another 4 weeks before finally falling. The pos-treatment increased in white cell numbers and total protein was therefore dependent on the trypanocidal drug, and was highest and most prolonged when Berenil was used and lowest with Suramin. The present studies demonstrate tha trypanocidal treatment of infected animals is followed by a post-treatment reaction in the central nervous system, the severity of which is related to the drug used and the presence of trypanosomes in the CSF.The vervet monkey therefore appears to be a good model for studying the reaction in HAT.
