Effects of treatment of growing swine with aflatoxin and T-2 toxin

Roger B. Harvey From the USDA, Agricultural Research Service, Veterinary Toxicology and Entomology Research Laboratory, College Station, TX 77840 (Harvey, Kubena, Huff, Corrier), the College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 (Rottinghaus), and the Department of Veterinary Public Health, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Phillips).

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Leon F. Kubena From the USDA, Agricultural Research Service, Veterinary Toxicology and Entomology Research Laboratory, College Station, TX 77840 (Harvey, Kubena, Huff, Corrier), the College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 (Rottinghaus), and the Department of Veterinary Public Health, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Phillips).

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William E. Huff From the USDA, Agricultural Research Service, Veterinary Toxicology and Entomology Research Laboratory, College Station, TX 77840 (Harvey, Kubena, Huff, Corrier), the College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 (Rottinghaus), and the Department of Veterinary Public Health, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Phillips).

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Donald E. Corrier From the USDA, Agricultural Research Service, Veterinary Toxicology and Entomology Research Laboratory, College Station, TX 77840 (Harvey, Kubena, Huff, Corrier), the College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 (Rottinghaus), and the Department of Veterinary Public Health, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Phillips).

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George E. Rottinghaus From the USDA, Agricultural Research Service, Veterinary Toxicology and Entomology Research Laboratory, College Station, TX 77840 (Harvey, Kubena, Huff, Corrier), the College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 (Rottinghaus), and the Department of Veterinary Public Health, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Phillips).

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Timothy D. Phillips From the USDA, Agricultural Research Service, Veterinary Toxicology and Entomology Research Laboratory, College Station, TX 77840 (Harvey, Kubena, Huff, Corrier), the College of Veterinary Medicine, University of Missouri, Columbia, MO 65211 (Rottinghaus), and the Department of Veterinary Public Health, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Phillips).

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SUMMARY

Effects of dietary aflatoxin (af) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire × Landrace × 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 γ-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.

SUMMARY

Effects of dietary aflatoxin (af) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire × Landrace × 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 γ-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.

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