Alterations in the nitrogen excretion pattern of chicks infected with Salmonella pullorum.

Investigations in our laboratory have established that infection with SalmoneUa pulorum strain CDC 3522/51 results in a decrease in arginine, methionine, glycine and tryptophan in the blood and liver of 1to 3-day old White Leghorn cockerels (Ross et al., 1955a). Subsequent experiments revealed that the administration of arginine within 24 hr following infection produced a marked increase in survival time of the chicks (Ross et al., 1955b). The investigations reported here suggest that the protection afforded by arginine during infection is accomplished through the increased synthesis of urea via the ornithine-citrulline cycle. Urea synthesis represents the principal pathway of nitrogen excretion during the early stages of embryonic development, but in the hatched chick apparently accounts for only a small amount of all excreted nitrogen. Needham et al. (1935) established that urea production in the chick embryo parallels arginase content and, thus, is the end product of the ornithinecitrulline cycle proposed by Krebs and Henseleit (1932). Accordingly, urea reaches its maximum level on the ninth day of incubation but, with the rapid decline in arginase, falls progressively, and by the end of the incubation period attains the percentage level demonstrated in adult birds. Clementi (1914, 1946) reported arginase and, consequently, the ornithine-citrulline cycle to be absent in hatched chicks. Investigations into the synthesis of urea and metabolism of arginine and other urea cycle intermediates in mammalian tissue have been capably reviewed by Rattner (1954). Arginine synthesis is regarded as minute