An Immunological model of Trypanosoma (Trypanozoon) Brucei Brucei in the vervet Monkey (Cercopithecus aethiops). Volume 2.
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Dallas, A, B. 1982, An Immunological model of Trypanosoma (Trypanozoon) Brucei in the vervet Monkey. PhD thesis.University of Nairobi.
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The African trypanosomiases constitute a multifaceted medical-veterinary-economic problem of vector-borne human and livestock diseases (157, 416) which pose a great menace to human life and needs. Over 500 million ac r es of fertile but tsetseinfested land for settlement, agriculture, livestock, (except poul try ke epd ng ) and economic development denied to man by trypanosomiases could have supported 114-125 million cattle (416). The total effect has been reduced protein production, malnutrition, increased death rate, shortened life expectation, chronic ill-health and reduced power source for tilling the land and for ferrying goods (388). Today, almost a century since the discovery of African trypanosomiases, very little is known about every aspect of the human and animal diseases. Similarly no ideal model for the human disease has been developed. Since the purpose of, this thesis was to set-up an immunological model of Trypanosoma brucei infection in a non-human primate,Ce'rcopithecus aethiops (the vervet monkey) so as to mimick the human disease, literature review will centre on the human and animal diseases caused by T.gambf.e ns e , T. rhodesiense and T. brucei and on the animal models , Human sleeping Sickness is a very complex disease involving the causative paraSites T. gambiense and T. rhodesiense, the African-confined Glossina tsetse-fly vector, wild and domestic mammalian-reservoir hosts and the associated ecosystems of lakes, rivers and savannah woodlandS either rich or poor in game. Trypanosoma rhodesiense and T. gambiense classically and, respectively, cause the acute Rhodesian and chronic Gambian sleeping sickness (153) characterised by parasi taemia, polyadenitis, late meningo-encephalitis and death if untreated Sleeping sickness is distributed over a wide Sub-Saharan African area between 12 Nand 20 S of the equator while African trypanosomiases occur in over 36 tropical countries. The causative parasites are distinctly distributed though patients with may occur where prevails. Clinically the disease types are not easily separable thereby making their distinguishing characteristics such as, virulence, vectors or drug responses only relatively valuable (29, 153). An intermediate type between the classical forms of sleeping sickness occurs in the Zambezi basin and Botswana. Parasites Trypanosomiasis is caused by flagellated protozoa of the genus (137), family Trypanomastidae, order Kinetoplastida, phylum Protozoa. The genus is divided into 2 main sections, the Stercoraria and the Salivaria (154). All important African'trypanosomes belong to the Salivaria and include nse, T. equiperduT. evansiidentical and closely related important African mammalian trypanoso of the subgenus (153, 215). The first two are important to man but all are pathogens of his domestic animals. The Salivaria also include the pathogenic (Nannomonas) congolTrypanosoma (Duttonella) vivaxtogether w?ith they cause nagana, the animal disease. Exam and are digenetic parasites, distributed in Africa like their tsetse vectors. Their life cycles alternate between the tsetse's gut and vertebrate host's blood (and/or tissues) wherein flagellates develop, and live,respectively. In the mammal ian 'blood the on are pleomorphic. The r s etee+ borne and show all the 3 stumpy, intermediate, and slender forms (constant pleomorphism) while T and lack the stumpy forms (inconstant pleomorphism) and are transmitted directly and mechanically between hosts by flies or by contact including coitus. The slender forms occur in all the 5 subspecies. Tryposomabrminor and lowly pathogenic veterinary parasite of livestock. It (154). bruceiTrypanosoma bcanines subacute in sheep and goats and lowly pathogenic in pigs Cattle are relatively resistant and self-cure. However, it is highly pathogenic and can be lethal within days to all laboratory rodents, for virulence increases with passages. Although, pleomorphic it becomes monomorph'ic (slender) after prolonged pas