• 15 July 1988
    • journal article
    • research article
    • Vol. 193  (2) , 215-221
Abstract
Four Thoroughbred foals were weaned from their dams when they were 1 day old and were fed a liquid milk-replacer diet containing approximately 1.7 .mu.g of coppler/g from plastic buckets for 4 to 7 months. They were kept in stalls with fiberglass walls and asphalt floors covered with rubber pads. Serum copper and zinc concentrations were determined 3 times/week by atomic absorption spectrophotometry, and liver copper and zinc concentrations were determined similarly after acid digestion of tissues taken at necropsy. The amount of soluble collagen in articular cartilage and aortic tissue was determined after necropsy. Clinical signs of illness, particularly evidence of lameness, were monitored daily. The foals were weighed weekly, and growth rate was monitored by measurement of height at the withers. Packed cell volumes and total and differential WBC counts were measured each time blood was drawn for copper and zinc concentration determinations. The foals were examined by necropsy at the end of the experiment, and the tissues were examined histologically. The foals developed intermittent, but nondebilitating, diarrhea with the onset of low serum copper concentrations. Considering the totally liquid diet, the foals grew well. Serum copper concentrations decreased to less than 0.1 .mu.g/ml in 13 to 16 weeks. Lameness was evident 2 to 6 weeks after serum copper concentrations decreased to their lowest value (< 0.1 .mu.g/ml). All foals developed stilted gaits and ultimately walked on the front of their hooves. Major hematologic changes and alterations of hair color were not evident. Soluble collagen of articular cartilage and aortic tissue increased from 340 to 600% greater than that of control foals. At necropsy, focal segments of articular cartilage were loose and broken in many joints throughout the skeleton. In some areas, there was intracartilaginous separation, and in others, there was complete breakage of fragments from the joint surface of form free cartilaginous bodies in the joint cavity. In the lesions formed early in the course of the experiment, a residual layer of cartilage remained over the underlying bone. Also, cartilage of the metaphyseal physis had broken. Hypoplastic and necrotic chondrocytes were scattered among normal-appearing columns of chondrocytes. The cartilaginous lesions were essentially the same as those described previously in clinically diagnosed copper deficiency of foals, in early cases of osteochondritis dissecans of unknown cause in horses, after long term administration of dexamethasone to foals, and in zinc toxicosis of foals.