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Studies in animal trypanosomiases. I. Nitrogen and mineral metabolic disturbances induced by Trypanosoma congolense and Trypanosoma brucei. II. Disturbances produced in the plasma proteins by Trypanosoma congolense and Trypanosoma brucei. III. The effects of Trypanosoma congolense and Trypanosoma brucei on blood urea



Studies in animal trypanosomiases. I. Nitrogen and mineral metabolic disturbances induced by Trypanosoma congolense and Trypanosoma brucei. II. Disturbances produced in the plasma proteins by Trypanosoma congolense and Trypanosoma brucei. III. The effects of Trypanosoma congolense and Trypanosoma brucei on blood urea



Jour Comp Path And Therap 51(1): 23-35, 36-41, 42-45



I. Both trypanosomes, although of markedly different pathogenicity, cause an increased excretion of N. body bases, chlorides and phosphates during their infection of cattle and sheep. Trypanosome infections lead to production of lactic acid and a lowering of the alkali reserve. which lead to the excretion of body bases in an attempt to get rid of the acidosis. Once a sufficiency of minerals in the ration is provided, any increased supply cannot alter the course of the infection.[long dash]II. Marked disturbances occurred in the plasma protein proportional distribution during infection of cattle, sheep, donkeys and guinea pigs with these organisms. The total plasma protein content did not vary in any constant manner. The non-protein N showed an increase at crisis or near death and following injections of antimosan. The proportional amt. of fibrinogen was not influenced. The relative proportions of the albumin fraction decrease and the proportional amts. of total globulin increase during infection, which latter is due to the great increase in relative proportions of euglobulin. Plasma protein changes are greater in T. b. than in T. c. infections and also in acute cases.[long dash]III. There is no alteration of the blood urea content as a result of infection of cattle and sheep by T. c. and T. b. except at the end of the disease when the animal is moribund. This terminal increase is considered to be due to the increased protein catabolism of the general autolysis of body tissue and not specifically to the infection.

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