Pathology of Experimentally Induced Chronic Selenosis (Alkali Disease) in Yearling Cattle

Abstract

Abstract. 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 highdose 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.

The Effect of Subclinical Selenium Toxicosis on Pregnant Beef Cattle

“…This calf had hepatic selenium levels of 9.68 ppm and myocardial lesions consistent with those described for selenium toxicosis. 8,19,26 Additional causes for myocardial necrosis, such as vitamin E deficiency, were not identified, and these animals did not have access to ionophores. Because hepatic selenium levels in this calf were Ͼ3 times the value reported to be indicative of perinatal selenium toxicosis (3.0 ppm), a case could be made that the clinical signs and lesions in this animal were associated with selenium toxicosis.…”

Bimodal actions of selenium essential for antioxidant and toxic pro-oxidant activities: The selenium paradox (Review)

“…However, a deficiency in selenium has been linked to many clinical symptoms including Kashin-Beck disease, which is characterized by bone and joint degeneration in children (6), and Keshan's disease that is known to cause cardiomyopathy in humans (1,7). Moreover, it is well known that an excessive intake of selenium results in toxic symptoms including alkaline disease and blind staggers in livestock (8,9). Selenium poisoning is thought to result from the generation of oxygen radicals that can lead to DNA damage, lipid peroxidation, and premature protein degradation inside the cell (10)(11)(12).…”

Selenium Poisoning of Wildlife and Western Agriculture: Cause and Effect

“…Research published in the veterinary literature suggests that blind staggers in cattle is not caused by selenium but by sulfate and other factors associated with high salt/alkaline soils (O'Toole and Raisbeck 1995). This research also shows that selenium causes sterility but is not teratogenic to livestock.…”