By O'Toole, D. and Raisbeck, M. F., Journal of Veterinary Diagnostic Investigation, 1995
Description
Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western United States is associated historically with 2 clinical syndromes: alkali disease and "blind staggers." The potential for Se-induced disease in cattle and other species is considerable in areas with seleniferous shales, Se-accumulating plants, arid climates, and alkaline soils. These 2 Se-associated conditions were defined in the 1930s and 1940s, and the nosology of blind staggers is questionable. Seventeen yearling steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethionine or selenite for 120 days were euthanized and examined postmortem. Significant lesions were confined to 4 steers in the medium- and high-dose selenomethionine group and to 1 steer in the high-dose selenite group. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of which had extensive separation of horn from lamellar and coronary epidermis and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by islands of parakeratotic cellular debris, separated by more normal hoof matrix. Two of the 5 steers also had hyperplasia, acanthosis, parakeratosis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These changes may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes predominate. In skin from the distal part of the tail of the animal that lost its switch, most follicles were atrophic and devoid of hairshafts and displayed dyskeratosis and mild superficial follicular keratosis. No significant lesions developed in tissues other than integument. Autometallographic staining for catalytic Se bonds in various tissues, including skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was poor. These findings indicate that dietary exposure for 4 months to 0.28 and 0.8 mg Se/kg in the form of selenomethionine and to 0.8 mg Se/kg in the form of sodium selenite reproduces in some cattle mild (subclinical) to severe (clinical) forms of alkali disease. No significant neurological, renal, or hepatic lesions developed, supporting the contention that blind staggers is caused by factors other than excessive dietary selenium
Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western United States is associated historically with 2 clinical syndromes: alkali disease and "blind staggers." The potential for Se-induced disease in cattle and other species is considerable in areas with seleniferous shales, Se-accumulating plants, arid climates, and alkaline soils. These 2 Se-associated conditions were defined in the 1930s and 1940s, and the nosology of blind staggers is questionable. Seventeen yearling steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethionine or selenite for 120 days were euthanized and examined postmortem. Significant lesions were confined to 4 steers in the medium- and high-dose selenomethionine group and to 1 steer in the high-dose selenite group. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of which had extensive separation of horn from lamellar and coronary epidermis and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by islands of parakeratotic cellular debris, separated by more normal hoof matrix. Two of the 5 steers also had hyperplasia, acanthosis, parakeratosis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These changes may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes predominate. In skin from the distal part of the tail of the animal that lost its switch, most follicles were atrophic and devoid of hairshafts and displayed dyskeratosis and mild superficial follicular keratosis. No significant lesions developed in tissues other than integument. Autometallographic staining for catalytic Se bonds in various tissues, including skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was poor. These findings indicate that dietary exposure for 4 months to 0.28 and 0.8 mg Se/kg in the form of selenomethionine and to 0.8 mg Se/kg in the form of sodium selenite reproduces in some cattle mild (subclinical) to severe (clinical) forms of alkali disease. No significant neurological, renal, or hepatic lesions developed, supporting the contention that blind staggers is caused by factors other than excessive dietary selenium
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