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The immune reaction in Trypanosoma lewzisi infection in the rat has been described as operating in two ways (Taliaferro, 1932). An antireproductive antibody, ablastin, is formed first. This antibody inhibits the reproduction of the parasites. A second antibody, the trypanocidal antibody, is then formed which destroys the parasites. The question of the existence, formation, nature and operation of ablastin has received a great deal of attention by many investigators. Taliaferro (1924, 1925, 1926, 1932) reported that ablastin was a protein in the euglobulin fraction of serum, that it was passively transferable, that it would not unite with trypanosomes in vitro, and that it neither killed the parasites nor affected their motility or vitality. Its only manifestation was that of in vivo suppression of the reproduction of the parasite. Becker and co-workers (1943, 1947) reported that pantothenic acid deficiency affected the antireproductive activity of ablastin so that reproduction continued and the infection became pathogenic. Becker and Gallagher (1947) found that treatment of infected rats with sodium salicylate had a similar effect on ablastic activity. Blood sugar studies by Schern (1928) and Poindexter (1933) indicated an inverse relation between the amount of blood sugar and the numbers of trypanosomes in pathogenic trypanosomiases. Tubangui and Yutuc (1931) found that hypoglycemia occurred only shortly before death. Linton (1929) found that in the non-pathogenic T. lewisi there was no change in blood sugar levels in the rat during the course of the infection. Minoru (1940) reported changes in blood sugar levels in rabbits as a result of sodium salicylate administration. In low amounts there was a hypoglycemia. In greater amounts there was a hyperglycemia. Brown (1915) and Taliaferro (1926) suggested that the difference between pathogenic and non-pathogenic trypanosomiases might be based on the absence or presence of antireproductive activity. In this study an attempt was made to examine the interrelationships among antireproductive activity, pathogenicity, blood glucose levels, blood pantothenic acid levels, blood protein levels, as associated with sodium salicylate treatment. This was done in order to learn something of the nature and operation of ablastin and the way in which salicylate interferes with ablastic activity.
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M.G. Lysenko (1951) studied this question.
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