Abstract
Intraruminal doses of tryptophan cause acute pulmonary edema and emphysema in cattle (ABPE), and the time course, clinical signs and pulmonary lesions are similar to those observed in naturally occurring ABPE which develops after an abrupt change in pasture conditions. Tryptophan is converted to indoleacetic acid by ruminal microorganisms and indoleacetic acid is decarboxylated to 3-methylindole (3MI) by a recently identified Lactobacillus organism. Three-methyl indole is the ruminal fermentation product of tryptophan which causes the characteristic pulmonary lesions in cattle. Metabolism of 3MI rapidly clears the blood and results in the urinary excretion of 10 metabolites, primarily oxindole derivatives. The formation of metabolites may be related to pulmonary toxicity of 3MI. It appears that high intake of lush, green forage could provide adequate amounts of tryptophan to cause ABPE under field conditions. Ruminal fermentation conditions can effect the conversion of tryptophan to 3MI and may influence the incidence and severity of ABPE. Antibiotics and inhibitors decrease the formation of 3MI from tryptophan and prevent the onset of experimentally-induced ABPE. Ruminal fluid and plasma of cows given access to lush, green pasture contain 3MI. The results support the hypothesis that 3MI, formed from tryptophan in the rumen, is associated with the development of ABPE.
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