The pathophysiology of ovine trypanosomiasis caused by Trypanosoma congolense

This thesis concerns the pathophysiology of ovine trypanosomiasis caused by Trypanosoma congolense, and includes a review of relevant literature and description of a series of experiments conducted to investigate various aspects of this subject area, including pathogenesis, genetic and nutritional influences of susceptibility, and TNFalpha receptor expression on peripheral blood leucocytes. Chapter 1 comprises an introduction and review of previously published work on the subject of African animal trypanosomiasis with particular reference to pathogenesis of, and genetic resistance/host susceptibility to animal trypanosomiasis. In Chapter 2, general materials and analytical techniques used in experimental work are described. Chapter 3 describes the haematological and blood biochemical changes in Scottish Blackface sheep infected experimentally with T. congolense. In the following study (Chapter 4), the underlying causes of the anaemia observed in infected animals were investigated after 11 weeks of infection. Chapter 5 describes a study of comparative susceptibility of Scottish Blackface and Finn Dorset sheep to experimental infection with T. congolense. A comparative study of the pathogenicity of three clones of T. congolense (GRVPS 57/6, GRVPS 3/2 and GRVPS 92/3) is described in Chapter 6. Nutritional influences of the pathophysiology of T. congolense infection in sheep were evaluated in experiments described in Chapters 7 and 8. In Chapter 9, the expression of tumor necrosis factor alpha (TNFalpha) receptors on peripheral blood leucocytes of sheep infected with T. congolense and allowed either a high or a low energy intake was investigated. This was conducted by using labelled recombinant human tumor necrosis factor alpha and cytofluorimetric methods. It was found that tumor necrosis factor-alpha receptor expression changed throughout a course of trypanosome infection. The greatest increases in the percentage of cells expressing these receptors were observed in the granulocyte populations of infected animals, and these changes appeared to fluctuate with development of waves of parasitaemia. The monocytes of infected animals displayed a relative decrease in expression of tumor necrosis factor-alpha receptors compared to their uninfected controls while little variation in receptor activity was found in the lymphocytes. It was further observed that infected animals on high energy intake showed greater tumor necrosis factor-alpha receptor activity, and this was associated with greater resistance of these animals to the disease, as judged by lower intensity of parasitaemia, less severe anaemia and better weight gains, than the animals on low energy intake. These observations indicate that adequate energy intake may enhance the ability of trypanosome-infected animals to mobilise effective non-specific defence mechanisms against the parasite. (Abstract shortened by ProQuest.)