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COPPER DEFICIENCY IN A HERD OF ANGORA GOATS
By: Darcy Dark (1994) |
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A 3-month old female Angora goat kid was admitted to Purdue University Large Animal Hospital because she was unable to stand on her rear legs. This kid came from a farm of approximately 25 does and two other kids at the farm were showing similar clinical signs. Upon presentation, the kid was bright and alert but emaciated and infested with lice. Feces were matted to the fleece on her rear legs but diarrhea was not clinically evident. The kid made several unsuccessful attempts to stand. She did not appear to be in pain and held herself in sternalrecumbency with her rear legs on either side of her body rather than with both legs folded to one side. Questioning of the owners revealed that there had been no additions to the herd, no goats showed any signs of swollen joints or arthritis and that there had been four kids born weak or dead, an unusually high number of perinatal deaths for that herd. The does had access to pasture and were fed a grain/protein supplement mix and trace mineral salt formulated for sheep. Despite the lack of clinical signs of Caprine Arthritis Encephalitis, or CAE, this was the primary differential diagnosis. Other differentials were spinal abscesses, trauma and copper deficiency. Blood samples were taken for serology for CAE and blood copper levels. By the third day in the clinic, after consuming high quality hay and a commercial goat ration (containing copper sulfate), the kid was able to stand without assistance and remain standing when downward pressure was applied to her hindquarters. Serology for CAE was negative. Blood copper levels were 0.20 ppm. (Deficient is 0.04-0.40 ppm.) The cause of ataxia in this particular kid was presumed to be copper deficienct because of deficient blood copper levels and rapid response to adequate copper in the diet. To hasten her recovery, we decided to supplement the copper already in the diet. No approved source of copper could be obtained from the pharmacy, so the goat was treated orally with copper sulfate crystals dissolved in water at a dose of 80 mg. copper per day for 7 days. By the end of the treatment period, the kid's blood copper level was 1.06 ppm. (Normal is >0.80 ppm.) The kid was also treated with VI-Sorbin(R) for a mild anemia and procaine penicillin for pneumonia, most likely due to her debilitated condition. The kid improved steadily throughout her hospital stay. Copper deficiency in this kid was thought to be a herd problem because of two similarly affected kids at the farm. Blood samples were taken from the two affected kids and a representative sample of unaffected kids and does. Of the ten animals tested, one doe had blood copper levels in the low marginal range (0.40-0.80ppm.) while the remaining nine animals were in the deficient range. The water was analyzed and no sulfates were found. Both the grass and grain samples had copper:molybdenum rations in the copper deficiency-causing, or toxic range, thus making this a case of secondary copper deficiency. The two affected kids were treated with copper sulfate solution orally, 80 mg. copper per day for 7 days. We also recommended that the rest of the herd be supplemented with copper by feeding a calf protein supplement for 6 weeks and that they use a free choice salt mix containing 0.2-0.25% copper sulfate. Other methods of supplementing copper in the diet are: Fertilize pasture with copper sulfate (only works in acidic soils) or giving a parenteral injection of copper glycinate or copper EDTA. We visited the herd about three months later to check the progress of the kids. No weakness or ataxia could be detected in any of the kids, even when they were driven around the pasture. The horns of the kids, which had previously been flattened, dry and flaky, showed a more normal appearance with the new growth. Since the goats were white, no pigmentation changes were seen, nor were any hair changes. |
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