2.75 lb/head/d of whole oats. ... Address correspondence and reprint requests to Dr. Murray ... patches of acetabular and femoral head cartilage peeled.
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Osteochondrosis and epiphyseal bone abnormalities associated with copper deficiency in bison calves Murray R. Woodbury, Murray S. Feist, Edward G. Clark, Jeremy C. Haigh Abstract Two bison calves were submitted to the Western College of Veterinary Medicine to confirm suspected copper deficiency. In addition to clinical signs, there were pathologic changes in the cartilage and subchondral bone of several joints. Water analysis indicated high levels of sulfate in the drinking water, contributing to a secondary copper deficiency.
Resume Ostetochondrose et anormalites de l'os ephiphysaire associes a une deficience en cuivre chez des veaux de bison. Deux veaux de bison ont ete presentes au Western College of Veterinary Medicine pour confirmer une suspicion de deficience en cuivre. En plus des signes cliniques, on pouvait observer des alterations du cartilage et de l'os sous-chondral au niveau de plusieurs articulations. L'analyse de l'eau de boisson indiquait un haut niveau de sulfate, ce qui contribuait a une deficience secondaire en cuivre. (Traduit par docteur Andre Blouin) Can Vet J 1999; 40: 878-880
The affected animals were from a herd of 82 animals, I thirteen of which were yearling calves. Of these 13, most appeared normal, some showed mild ill thrift, and 2 were severely ill. The affected calves were born in May. The herd calving rate was 96% and no illness or abnormalities were noted in the cows or other animals from the herd. All calves were raised on a crested wheat (Agropyron pectiniforme) pasture with the main herd. In November, at approximately 6 mo of age, the calves were weaned and were moved to a drylot. The diet provided was free-choice oat and barley green feed, crested wheatgrass hay, lentil straw, and approximately 2.75 lb/head/d of whole oats. No mineral supplement was fed. Well water was given ad libitum. All animals were vaccinated with an unspecified 7-way clostridial vaccine at weaning. By 8 or 9 mo of age (January-February), the 2 most severely affected calves began to exhibit a stiff gait, loss of coat color, and progressive emaciation. Several animals, including the 2 described in this report, had chronic diarrhea. The producer gave injections of antibiotics and vitamins A, D, and E with selenium, but no Department of Herd Medicine and Theriogenology (Woodbury and Haigh) and Department of Veterinary Pathology (Clark), Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5B4; Saskatchewan Agriculture and Food, Extension Research Unit, College of Agriculture, University of Saskatchewan, Saskatoon, Saskatchewan S7K 2H6 (Feist). Address correspondence and reprint requests to Dr. Murray R. Woodbury. 878
improvement in condition was observed. Instead, there was progressive, shifting, mild to severe lameness, and paresis. One animal eventually became recumbent and unable to rise. The other was able to stand but was very lame and reluctant to move. Both continued to eat and drink thoughout the course of illness. In April, when the calves were 11 mo of age, the producer contacted the Department of Animal and Poultry Science (DAPS) and the Western College of Veterinary Medicine (WCVM) at the University of Saskatchewan. Routine feed and water analyses were conducted by the DAPS for mineral levels, including copper and molybdenum levels, in feed, and sulfate levels, in the water. The feed samples had adequate levels of copper, ranging from 6.33 to 10.3 mg/kg in hay and straw and 6.47 mg/kg in the oats. The molybdenum levels in the feed were considered normal, ranging from zero (oats) to 3.50 mg/kg. Water analysis revealed normal levels of total dissolved solids but high levels of sulfates, at 1006 mg/L. The bison were presented to WCVM in a trailer with a request for live and subsequent postmortem examination. Despite their weakened condition, a physical examination was considered unsafe. Visual inspection was made and their ability to move normally was assessed. One animal could not rise. The other was able to stand but was obviously lame with bilateral hind limb paresis and abnormal positioning. The hocks were touching, with extreme outward rotation of the stifles. Both animals were considerably undersized for their age and emaciated. They had poor, coarse, "wooly" haircoats that appeared lighter in color than normal. Can Vet J Volume 40, December 1999
Liquid feces were visible on the perineum and hind legs of both animals. The calves were sedated with a mixture of butorphanol (Torbugesic, Ayerst Laboratories, Montreal, Quebec), 0.1 mg/kg body weight (BW), and xylazine (Rompun, Haver-Lockhart, Mississauga, Ontario), 1.0 mg/kg BW, given intramuscularly to facilitate an intravenous injection of euthanasia solution (Euthanyl, MTC, Cambridge, Ontario). Physical examination of the sedated animals revealed no further abnormalities, except those associated with cachexia. Blood samples were taken for analysis and the calves were euthanized. Both animals were in poor body condition with marked depletion of body fat stores. Gross abnormalities were confined to the musculoskeletal system. There were remarkable degenerative lesions in all large joints but especially the hip, stifle, shoulder, and elbow joints. The articular cartilage was thinned and showed many small focal defects. Upon opening the hip joints, large patches of acetabular and femoral head cartilage peeled off the underlying bone (Figure 1). Subchondral bone in various joints showed multifocal necrosis and areas of possible collapse of bony architecture. Epiphyseal lines were multifocally cystic and irregularly thickened (Figure 2). One animal had severe damage to soft tissue joint structures in the pelvic limbs. There were multiple torn and ruptured joint ligaments, capsules, and tendons. Extensor tendons were ruptured and torn from the patellas, and flexor tendons had slipped from the tuber calcis in both limbs. Both patellas were fractured in this animal. Microscopic examination of major body organs found only myocardial lesions. There were randomly scattered foci of myocardial necrosis, fibrosis, lipidosis, and neovascularization in the left ventricle. No areas of inflammatory reaction or lesions of active necrosis were seen. Inspection of multiple decalcified sections of joint cartilage and epiphyseal lines found extensive linear fibrosis, especially below the growth plates of the upper metaphyseal regions. There was obvious defective osteochondral ossification, with absence of normal mineralization of cartilagenous columns, minimal or no osteoid production in the primary spongiosa, and minimal to no osteoblastic activity on bone spicules throughout metaphyseal trabecular bone regions. Irregular masses of persistent noncalcified cartilage and irregular foci of necrotic cartilage were common below and in the growth plates. Irregular masses of necrotic bone were also common. Fibrosis, microscopic fractures of bone spicules, hemorrhage, hemosiderosis, and irregular islands of nonossified cartilage were conspicuous features. These processes were also present in the growth plates and subcartilaginous regions of joint surfaces. There was minimal to no bone marrow activity in these sections of bone. These findings led to a diagnosis of osteochondrosis of multiple joint surfaces, and defects of endochondral ossification associated with cartilage and bone necrosis in subchondral and epiphyseal locations. Copper (Cu) deficiency was suspected as the cause of these lesions. Serum from antemortem blood samples and liver were submitted for toxicologic analysis. Serum copper levels were 5.6 ,umollL. Other blood analyses, such as Can Vet J Volume 40, December 1999
Figure 1. Femoral head with large patches of articular cartilage peeled off the underlying bone.
Figure 2. Longitudinal metaphyseal saw cut showing multifocally cystic (arrows) and irregularly thickened epiphyseal lines.
a complete blood cell count or routine chemistry analysis, were not performed. Reliable normal values for bison serum Cu are not available, but in cattle, this level would be deficient. Liver Cu levels were 0.02 l±moUg, which is considerably below normal for cattle. Liver molybdenum (Mo) levels were found to be those that are normal for cattle. Copper deficiency is a well described nutritional problem in domestic ruminants (1-5) and Cervus spp. (6), but has not been previously described in farmed bison (Bison bison). Primary Cu deficiency occurs when dietary Cu levels are insufficient to meet metabolic demand. Secondary Cu deficiency occurs when dietary factors inhibit the absorption of Cu from the digestive tract, or if Cu metabolism is inadequate (1,2). For example, high levels of Mo in the diet can bind with Cu in the reticulo-rumen, creating an insoluble Cu molybdate complex. Similarly, in the presence of dietary sulfates, Cu binds to sulfur, forming a nonabsorbable Cu sulfate complex. This reduces Cu absorption, and if persistent, creates a secondary state of deficiency (3,4). Ingestion of water containing sulfate at a concentration of 600 mg/L has been reported to induce Cu deficiency in Saskatchewan beef cattle (5). 879
Although liver Mo levels were within normal limits, the excessive levels of sulfate in the well water, which was the only source of water for the calves, and the pathology findings suggest a diagnosis of secondary Cu deficiency. Absorption of dietary Cu in these cases was impaired by the formation of Cu sulfate through the interaction of Cu in the feed and sulfates in the drinking water. The adult animals on the farm had a similar diet but did not suffer a deficiency because they were free ranging and used snow as their water source. Under these normal conditions, an appropriate dietary intake of Cu could be assured by way of trace mineral supplementation to a level of 25 mg Cu per kg of feed (5). The clinical manifestations of Cu deficiency in ruminants include diarrhea, anemia, poor growth rate, poor body condition and changes in hair or coat color. Skeletal abnormalities and lameness are common, resulting from defects in articular cartilage and subchondral bone lesions (2). Collectively, these lesions are called osteochondrosis. Osteochondrosis is thought to develop from the trauma of weight bearing on rapidly growing but poorly formed cartilage and underlying bone. The result is necrosis and trauma to cartilage and associated joint tissues. The joint pathology associated with a Cu deficiency occurs because this trace mineral is essential for normal elastin and collagen production in cartilage, osteoid, ligaments, tendons, and blood vessel walls. Copper is an important constituent of the enzyme lysyl oxidase. Ineffective enzymatic processes resulting from Cu deficiency lead to deficient cross linking, ineffective maturation of collagen and elastin, and subsequent defects in normal production of bone and cartilage (3). The pathologic changes found in the myocardial tissue may have resulted from myocardial necrosis associated with Cu deficiency (7). Alternatively, in this case, they were perhaps due to the excessive catecholamine production associated with the chronic stress that the calves must have been experiencing. The pathology resulting from Cu deficiency in these bison is similar to that described in cattle. The clinical manifestations of osteochondrosis and growth plate abnormalities are also similar to those seen in cattle (2). The advanced progression of disease and severity of signs observed in these particular bison calves is more likely due to the lengthy period between onset of signs
and the request for assistance by the producer than from any increase in susceptibility to the effects of Cu deficiency in bison. However, Cu deficiency remains an important issue to the bison industry, because its effects on animal productivity are often much more subtle than those described in this report and because little is known about trace mineral requirements of bison (8). cvi
References 1. Underwood EJ. The Mineral Nutrition of Livestock. 2nd ed. Slough, England: Commonwealth Agricultural Bureau, 1981. 2. Maas J, Bradford PS. Copper deficiency in ruminants. In: Bradford PS. ed. Large Animal Internal Medicine. Toronto: Mosby, 1990: 832-836. 3. Gooneratne SR, Buckley WT, Christensen DA. Review of copper deficiency and metabolism in ruminants Can J Anim Sci 1989; 69: 819-845. 4. Henderson JA. Conditioned copper deficiency in Canadian cattle. Can J Comp Med 1957; 21: 332-336. 5. Smart ME. Factors influencing the plasma and liver copper and zinc concentrations in beef cattle (PhD dissertation). Saskatoon, Saskatchewan: University of Saskatchewan. 1984. 240 p. 6. Mackintosh CG, Orr MB, Turner K. Enzootic ataxia in wapiti. Proceedings of a deer course for veterinarians. N Z Vet Assoc Deer Branch. 1986; 3: 165-169. 7. Jones TC, Hunt RD, King NW. Veterinary Pathology. 6th ed. Baltimore: Williams and Wilkins, 1997: 805-807. 8. Feist MS. Evaluation and development of specialized livestock diets in Saskatchewan (MSc thesis). Saskatoon, Saskatchewan: University of Saskatchewan, 1998. 154 p.
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Can Vet J Volume 40, December 1999
