Influence of ascorbic acid on the adverse effect of feeding a diet containing excess tyrosine to chicks

1. The effects of dietary or parenteral administration of ascorbic acid on the adverse effects of excess dietary tyrosine were investigated with young male White Leghorn chicks in a 2‐week experiment.

2. Addition of 10 g ascorbic acid/kg to the control diet (without excess tyrosine) produced no beneficial effects on performance. Excess dietary tyrosine caused depressions in all measures of performance.

3. Adding 0.1, 1, 10 or 20 g ascorbic acid/kg to the diet containing excess tyrosine tended to improve performance.

4. Subcutaneous injection of 50 mg ascorbic acid/bird d to chicks receiving excess tyrosine brought about a significant improvement in body‐weight gain.

5. The elevation of plasma free tyrosine caused by excess dietary tyrosine decreased as dietary ascorbic acid increased.

6. Ascorbic acid can alleviate, though not completely counteract, the adverse effect of excess dietary tyrosine.     

Gastrointestinal colonization by salmonellae and pathogenic Escherichia coli in monoxenic and holoxenic chicks and poults

Chicks monocolonized by either salmonellae or pathogenic strains of Escherichia coli had persistent and undiminished colonization of all levels of the gastrointestinal tract and frequently had bacteremia during test periods ranging to 35 days. Poults monocolonized by salmonellae or Arizona hinshawii 7:"1,7,8 developed a similar pattern of colonization. Conventionally reared chicks and poults had rather variable colonization by these pathogens, and it was most persistent in the ceca. Groups treated with a native protective microflora were infrequently colonized. Differences in colonization are explainable by lack of competing bacteria in the monocolonized group and by various degrees of protection provided by microflora colonizing the other groups.     

Clinical and pathological studies in adult sheep and goats experimentally infected with Wesselsbron disease virus

The clinical symptoms and pathology in 33 adult sheep and 31 adult goats experimentally infected with Wesselsbron disease virus are described. There was moderate to severe hyperthermia in most animals, but no other clinical signs of disease or deaths were recorded. Eleven sheep and 6 goats were sacrificed for pathological studies at various stages during the febrile response. The macroscopic and microscopic lesions in these cases are described. Microscopic studies revealed that the liver was consistently affected and showed small foci of necrosis. These were sparsely distributed and associated with a marked localized Kupffer cell response ("retothelial nodules"). In addition, acidophilic bodies and small groups of necrotic hepatocytes were evident in some lobules. Apart from the hepatic lesions, mild to moderate pyknosis and karyorrhexis of lymphocytes were seen in the spleen and lymph nodes. This report also compares the microscopic lesions in the livers of adult sheep and goats with those of new-born lambs for Wesselsbron disease as well as with those reported for Rift Valley fever in adult sheep.     

Selenium deficiency, the drug metabolising enzymes and mycotoxicoses in sheep

An examination was made of the relationship in Romney sheep between selenium deficiency and (i) the state of the liver drug metabolising enzyme system, (ii) subclinical liver damage, (iii) susceptibility to facial eczema, and (iv) susceptibility to ryegrasss staggers. The microsomal electron transport detoxifying enzymes based on cytochrome P-450 were unaffected by Se deficiency, suggesting that these enzymes are uninduced on ryegrass/clover pastures. Selenium deficiency had no effect on sporidesmin-induced liver damage, which makes it unlikely that peroxidative events countered by Se-dependent glutathione peroxidase (E.C.1.11.10) have a major role in the mechanism of sporidesmin toxicity. Selenium deficiency did appear to suppress the development of photosensitisation. There was no major effect on ryegrass staggers and no deficiency-induced subclinical liver damage.