PATHOLOGY OF EXPERIMENTALLY-INDUCED CHRONIC SELENOSIS (ALKALI DISEASE) IN YEARLING CATTLE

Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western U nited States is associated historically with 2 clinical syndromes: alk ali disease and ''blind staggers.'' The potential for Se-induced disea se in cattle and other species is considerable in areas with selenifer ous 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 yearlin g steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethion ine 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 g roup. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of whi ch had extensive separation of horn from lamellar and coronary epiderm is and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by isl ands of parakeratotic cellular debris, separated by more normal hoof m atrix. Two of the 5 steers also had hyperplasia, acanthosis, parakerat osis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These cha nges may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes pred ominate. In skin from the distal part of the tail of the animal that l ost 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. Aut ometallographic staining for catalytic Se bonds in various tissues, in cluding skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was po or. 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 (subclin ical) to severe (clinical) forms of alkali disease. No significant neu rological renal, or hepatic lesions developed, supporting the contenti on that blind staggers is caused by factors other than excessive dieta ry selenium.