Experimental animal study demonstrates blood pyruvate changes in rats with hemoprotozoan infections, indicating potential host utilization of parasite-derived metabolic products.
Data on blood lactate levels of animals infected with trypanosomes are available in the literature (summary in von Brand, 1950), but only one brief reference concerning blood pyruvate levels (Grant and Fulton, 1956) has come to our attention. This is rather surprising since the main metabolic end product of the carbohydrate metabolism of the trypanosomes belonging to the brucei group is pyruvic acid (literature in von Brand, 1952). A more detailed investigation of blood pyruvate levels of trypanosome-infected animals appeared of interest primarily from the standpoint of determining the ability of the host to utilize this metabolic end product of the parasite's metabolism. Utilization by the host had been suggested by Harvey (1949) as a mechanism of salvaging energy originally stored in the glucose molecule and thus preventing parasite autointoxication and host intoxication from excessive pyruvate levels. In conjunction with these studies on extra-cellular parasites, an investigation of blood pyruvate levels of rats infected with an intra-cellular form, Plasmodium berghei, seemed of comparative interest and was included in our studies.
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Coleman et al. (1957) studied this question.
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