Portal de Periódicos da CAPES

Induction of thiamine deficiency in sheep, with lesions similar to those of cerebrocortical necrosis

1975; Elsevier BV; Volume: 85; Issue: 2 Linguagem: Inglês

10.1016/0021-9975(75)90067-5

1532-3129

William C. Evans, I. Antice Evans, D. J. Humphreys, Benjamin Lewin, W.E. Davies, R. F. E. Axford,

Peroxisome Proliferator-Activated Receptors

Acute thiamine deficiency was induced in adult sheep by the inclusion of a potent source of thiaminase I in the form of low temperature dried, milled bracken rhizomes in the diet. Autoclaving the rhizome powder abolished its capacity to induce avitaminosis B1 and also inactivated the enzyme. The rhizome powder destroyed about 80 μg. thiamine per minute per gram, and the minimum quantity required was 15 to 25 per cent. by weight of the pelleted diet. When the plant source of thiaminase I formed 25 to 33 per cent. of the ration, symptoms took from 25 to 40 days to develop—roughly the time required in simple-stomached animals. Decreasing the concentration to 15 per cent. prolonged this time to 3 months, whilst a 5 per cent. level did not produce the disease. Thiaminase I activity was present in the contents from all parts of the alimentary tract and faeces of sheep fed the rhizome diets. Even when the enzyme concentration was insufficient to cause the clinical syndrome, animals did not thrive as well as sheep fed on similar diets in which the thiaminase I had been inactivated. Sheep made thiamine deficient in this way exhibited all the biochemical and clinical features characteristic of thiamine deficiency in homogastric animals; the response to thiamine therapy was dramatic in the early stages. The clinical features and histopathology resembled those of field cases of cerebrocortical necrosis in sheep. The results support the view that cerebrocortical necrosis is a “thiaminase disease” of ruminants.