D. Otoole et Mf. Raisbeck, PATHOLOGY OF EXPERIMENTALLY-INDUCED CHRONIC SELENOSIS (ALKALI DISEASE) IN YEARLING CATTLE, Journal of veterinary diagnostic investigation, 7(3), 1995, pp. 364-373
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.