Biochemical changes in the small intestine during development of naturally acquired wheat-sensitive enteropathy of Irish Setters were investigated. To distinguish primary biochemical abnormalities from secondary effects of intestinal damage, progeny of affected dogs reared on a normal wheat-containing diet were compared with their own littermates reared on a cereal-free diet and with age-matched clinically normal Irish Setters fed the same wheat-containing diet. Peroral jejunal biopsy specimens were sequentially obtained between weaning and 1 year of age; specific activity and reorientating sucrose density-gradient distribution of organelle marker enzymes were determined. Major primary biochemical abnormalities were not detected in affected progeny. In affected dogs fed wheat, there was a selective, but secondary, loss of the brush border alkaline phosphatase and aminopeptidase N activities. This loss was associated with the development of partial villus atrophy, but represented a specific effect of dietary wheat on the brush border, not merely a nonspecific effect of mucosal damage, because other brush border enzymes, including disaccharidases, were not similarly affected. Increased soluble activities of lysosomal and peroxisomal marker enzymes late in the disease process may represent alterations in these 2 organelles as a secondary consequence of mucosal damage.

The influence of variable zinc content (29.1, 250, 1,000 and 2,000 mg/kg of dry weight) in a basic diet containing 7.7 mg of copper/kg on the ability of weanling foals to maintain normal copper balance was investigated. Serum copper and zinc concentrations were monitored, and terminal hepatic copper and zinc contents were measured in 4 weanling foals fed the basic diet containing 29.1 mg of zinc/kg and in 2 foals each fed the higher-zinc diets. Foals fed the lower-zinc diets (29.1 and 250 mg/kg) maintained normal serum copper and zinc concentrations for 14 to 15 weeks, whereas those fed the 2 higher-zinc diets became hypocupremic within 5 to 6 weeks and were lame within 6 weeks, owing to cartilaginous disease characteristic of osteochondritis dissecans. Serum zinc concentration in the foals fed the 2 higher-zinc diets increased to > 2 microgram/ml within 2 weeks. Foals fed the high-zinc diets became lame after serum copper concentration had remained at 0.3 microgram/ml for > 1 week. Serum copper concentration in these arthritic foals was less than or equal to 0.2 microgram/ml at the end of the study. In lame foals, fractures of the cartilage of the articular and growth physes occurred through the zone of hypertrophic cells, and varied from bilateral to unilateral and from small to large. Free masses and flaps of cartilage attached to one side were numerous.

The protein requirement of Pointer pups fed practical diets was assessed in 3 experiments. Eight-week-old pups required 25.2% protein when fed a combination of corn gluten meal, soybean meal, and meat and bone meal for 2 weeks. However, when a poor-quality poultry by-product meal was substituted for some of the corn gluten meal and meat and bone meal, the requirement increased to 27.5%. This increased requirement was explained by decreased digestibility of the poultry by-product meal diet. Pups fed each of the diets required 18% digestible protein to maximize growth rate. Sixteen-week-old pups were more efficient at utilizing the experimental diets, requiring only 23% crude protein (17.2% digestible protein) to maximize growth rate.

Morphologic changes in the small intestine were investigated during development of naturally acquired wheat-sensitive enteropathy in Irish Setters. To distinguish underlying morphologic abnormalities from non-specific effects of intestinal damage, progeny of affected dogs reared on a normal wheat-containing diet were compared with their own littermates reared on a cereal-free diet and with age-matched clinically normal Irish Setters fed the same wheat-containing diet. Peroral jejunal biopsy specimens were taken sequentially between 4 months and 1 year of age. At 4 months of age, there were no differences in villus height, comparing the 3 groups, but increased numbers of intraepithelial lymphocytes and goblet cells were already present in biopsy specimens from the affected Irish Setters fed wheat. Dietary wheat resulted in a progressive reduction in virus height in the jejunum of affected Irish Setters from 6 months onward. Underlying morphologic abnormalities were not found, and the characteristic morphologic changes of this enteropathy were secondary to the presence of dietary wheat. However, development of partial villus atrophy was preceded by increased numbers of intraepithelial lymphocytes and goblet cells.

Six primiparous Holstein cows were fed a Se-deficient diet, beginning at least 90 days before their first calving, and 6 other primiparous cows were given the same diet plus a supplement of 2 mg of Se/cow/d as sodium selenite. All cows were fed their diets for the duration of the experimental period. One uninfected quarter of each cow was injected with 25 microgram of Escherichia coli endotoxin at postpartum week 5. Leukocytes were isolated by centrifugation from milk collected at postinjection hour 16. Isolated cells were 92 +/- 3% neutrophils and were incubated with Staphylococcus aureus or E coli in a 1:300 ratio. Phagocytosis and intracellular killing by neutrophils were assessed after 0, 30, 60, and 90 minutes by a fluorochrome assay, using acridine orange. Viability of neutrophils was assessed by use of trypan blue. Superoxide anion production and hydrogen peroxide production by neutrophils also were determined. Cows fed Se-deficient diets had significantly (P < 0.05) lower blood Se concentration and blood glutathione peroxidase activity than cows fed Se-supplemented diets. Selenium status had no effect on the phagocytic capacity of neutrophils. Neutrophils obtained from cows fed Se-supplemented diets killed a significantly (P < 0.05) higher percentage of ingested bacteria than did neutrophils from cows fed the Se-deficient diet. Viability was significantly (P < 0.05) reduced by incubation with S aureus in neutrophils from both groups of cows, with neutrophils from Se-deficient cows having lower viability. Superoxide anion production did not differ significantly between neutrophils from the 2 groups, but extracellular hydrogen peroxide concentration was significantly (P < 0.05) higher in neutrophils harvested from milk of cows fed the Se-deficient diet.

Experiments were conducted to evaluate the effect of restricted feeding of a starter diet to suckling pigs (creep feeding) in a model of postweaning colibacillosis. The hypothesis that restricted creep feeding primes an intestinal allergic reaction to starter diet ingested after weaning was tested. Twenty-eight suckling pigs were fed a starter diet for 3 h/d on days 7, 8, and 9 after birth (creep-fed). Twenty-six suckling pigs were not fed the diet until 3 weeks of age (not creep-fed), when all pigs were weaned and given the starter diet. One day after weaning, 24 creep-fed and 22 not creep-fed pigs were inoculated with K88+ enterotoxigenic Escherichia coli, and 4 pigs in each group were kept as noninoculated controls. Among inoculated pigs (principals), 10 creep-fed and 12 not creep-fed pigs were found to be genetically resistant to K88+ E coli and remained healthy during the 6-day postinoculation period, as did the noninoculated controls. Eighteen (10 creep-fed and 8 not creep-fed) of the 24 genetically susceptible principals developed diarrhea after inoculation. There were no significant differences in the incidence and severity of diarrhea, amount of body weight loss, and mortality between creep-fed and not creep-fed susceptible principal pigs. Histologic examination of intestine from control pigs and principals that survived for 6 days after infection did not reveal any substantial morphologic difference between creep-fed and not creep-fed groups. In conclusion, creep feeding was not required for the production of diarrhea in this model. Creep feeding did not induce morphologic changes characteristic of an allergic reaction in the small intestine.

An experiment was conducted to determine whether balancing dietary crude protein for optimal rumen degradability would improve fertilization rate and quality of ova in lactating dairy cows. Thirty-eight Holstein cows in early lactation were fed 1 of 2 diets formulated to be isocaloric and isonitrogenous, containing 16% crude protein. Diet 1 contained 73% rumen degradable intake protein, whereas diet 2 contained 64% rumen degradable intake protein. The cows were induced to superovulate and were inseminated, and ova were recovered nonsurgically on postbreeding day 7. Ova were counted and classified as fertilized or unfertilized. Fertilized ova were scored as excellent, good, fair, poor, or degenerate. Unfertilized ova and poor and degenerate embryos were considered to be nontransferable ova and excellent, good, and fair embryos were considered to be transferable ova. There were no differences for mean number of fertilized, unfertilized, transferable, or nontransferable ova recovered from cows fed the 2 diets (P > 0.10). Mean percentage of fertilized ova recovered from cows was greater (P < 0.05) in those fed diet 2, compared with diet 1. Mean percentage of transferable ova recovered from cows tended to be greater (P = 0.06) in those fed diet 2, compared with diet 1. More cows failed to yield transferable ova (P < 0.05) when fed diet 1, compared with diet 2. Fertilization failure or early degeneration of embryos may occur in cows fed excess rumen degradable protein.