A prospective cohort study was undertaken in a farrow-to-farrow swine herd to describe patterns of pneumonia, and to identify host risk factors associated with the extent of pneumonic lesions in 2 weight groups of slaughter swine. The risk of coughing and pneumonic lesions increased with increasing age of pigs within the herd (P < 0.0001). The age-specific prevalence of pneumonic lesions was low (2.7%) in pigs < 16 weeks old at slaughter, but increased rapidly when pigs were between 16 and 22 weeks old (8.6 to 67.9%). After 22 weeks, the prevalence remained relatively constant at about 80%. Associations between possible risk factors and pneumonia were investigated by use of multiple-regression models. Age at weaning (< 24 days) and birth weight (< 1 kg) exerted small, but significant (P < 0.002), effects on the extent of pneumonic lesions in pigs slaughtered at 30 to 50 kg live weight. For pigs slaughtered at 90 to 110 kg, pneumonic lesions were more extensive (P = 0.007) in pigs sired by Yorkshire boars than pigs sired by non-Yorkshire sires (Duroc, Hampshire, Chester White, or American Spotted). Other host factor variables including weaning weight and clinical diseases (atrophic rhinitis, diarrhea, and arthritis) were not associated with pneumonia extent in either weight group. Higher pneumonia percentages were also associated with reduced growth rates in the grower/finisher phase. Pigs sired by Yorkshire boars grew significantly (P < 0.0001) more slowly from entry into shed 2 (mean, 38 kg) until about the time of exit (mean, 92 kg) than pigs sired by other breeds (747 g/d and 795 g/d, respectively).

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.

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire X Landrace X Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time. Treatment with T-2 toxin induced microcytic hypochromic anemia, increased numbers of circulating metarubricytes and decreased absolute numbers of lymphocytes. Hepatocellular lesions in barrows of the AF and the AF plus T-2 groups (2 and 4, respectively) were compatible with aflatoxicosis. When fed in combination, each toxin appeared to have a sparing action on certain effects of the other, and the responses elicited were either additive or less than additive.

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.

Two experiments were conducted to determine changes in body composition and various physiologic variables in feeder pigs under simulated marketing conditions. In the first experiment, pigs were assigned to 1 of 4 treatment groups for 48 hours: (1) no water and feed; (2) water ad libitum, no feed; (3) no water, feed ad libitum; or (4) water and feed ad libitum. During a 48-hour recovery period, all pigs were allowed feed and water ad libitum. Plasma triiodothyronine decreased (P < 0.01) within the first 24 hours in groups-1 and -2 pigs, but increased (P < 0.01) within the first 6 hours of the recovery period. The circadian rhythm of plasma cortisol was disrupted in groups-1 and -3 pigs and during recovery in group-1 pigs. Packed cell volume increased (P < 0.05) in groups-1 and -3 pigs and returned to initial values within the first 24 hours of the recovery period. In the second experiment, body composition was estimated by the 40K technique for fat-free body mass, percentage of nitrogen, and percentage of fat. Body composition was determined before and after pigs were allotted to 1 of 2 groups for 48 hours: group-1 pigs were given feed and water ad libitum and group-2 pigs were not given feed and water. Group-1 pigs gained 2.2 kg of body weight (P < 0.01), 0.6% fat (P < 0.01), 0.7 kg of fat-free body mass, and 0.02% nitrogen (P > 0.01). Group-2 pigs lost 2.3 kg of body weight (P < 0.01), 0.6% fat (P < 0.01), 2.0 kg of fat-free body mass (P < 0.01), and 0% nitrogen.

Newly hatched chickens were treated with the trichothecene mycotoxin, T-2 toxin, during the first day of life. Control chickens were treated with other agents known to cause immunosuppression-cyclosporine, cyclophosphamide, and aflatoxin. Chickens were infected on day 6 (5 days after treatment with T-2 toxin) by intraperitoneal inoculation with Salmonella typhimurium. Blood samples were collected from treated chickens (noninfected) and used to assess the responsiveness of blood lymphocytes to T-cell or B-cell mitogens, phytohemagglutinin, or lipopolysaccharide, respectively. The T-2 toxin had a profound negative effect on the ability of the chickens to resist salmonellosis, as measured by survival. However, the toxin effect in reducing phytohemagglutinin- and lipopolysaccharide-stimulated mitogenesis, though significant (P > 0.05), was not severe. Our data indicate a direct effect of T-2 toxin on native resistance to systemic salmonellosis, which was not accompanied by marked alteration in T- or B-cell responses to mitogenic stimulation.