I wanted to make sure I always have the information handy so I decided to re-post it here. It is not my research, all the credit goes to Joyce Lazzaro who created, maintained, and researched this information for the site.
This post is quite long because this information is so important to me. Remember, I don't take any credit for finding or researching the information. I just want to preserve it.
During the spring of 1999, the Regina laboratory received submissions from a producer experiencing problems in pygmy kids between 1 1/2 - 2 months of age. The history presented for one kid included fever, depression, head pressing, circling and terminal opisthotonus. Another animal and several more at home exhibited generalized weakness and muscle tremors. Weakness was most pronounced in the hindquarters.
At necropsy, the kid with seizures had severe cerebral edema with laminar necrosis of the cerebral cortical gray matter (polioencephalomalacia). The spinal cord from the kid with generalized weakness displayed extensive hypomyelination with neuronal chromatolysis and necrosis. Both kids had decreased numbers of Purkinje neurons and cells within the granular layer of the cerebellum with chromatolysis of medullary neurons. Hepatic copper level from the kid with weakness was 2.4 ppm, a level considered very deficient (normal range 25-150 ppm). A CBC indicated marked nonregenerative anemia (hemoglobin 82 g/L; hematocrit 0.10). Both goats had mild to moderate thyroidhyperplasia. One animal had moderate coccidiosis.
The owner housed sheep with the goats. Both were receiving hay, barley, sheep supplement and cobalt/iodized salt. Drinking water sulphate and phosphorus levels were within normal ranges.
When sheep and goats are fed together, it is not uncommon to feed supplements designed for sheep. The practice predisposes goats to copper deficiency as their requirements at 10 - 20 ppm are much higher than those for sheep at 5 - 10 ppm. Although dietary copper levels were not calculated, a copper deficient diet with respect to goat requirements was strongly suspected. Genetic or breed predisposition and the interfering role of dietary molybdenum were not ruled out. Thyroid hyperplasia may have also been genetically related as dietary iodine levels appeared normal.
Copper deficiency in young goats typically appears as "enzootic ataxia" related to spinal chord and cerebellar changes. Cerebellar changes noted in this case were consistent with copper deficiency. Low copper levels were suspected as contributing to polioencephalomalacia. Similar lesions have been reported in young lambs from England. Other causes of polioencephalomalacia include: thiamine deficiency, high sulphates, water deprivation, hypoxia and any condition causing cerebral edema.
"Veterinary Drug Therapy" by Thomas Barragry '94.
"Cap With Confidence" Copacaps/Rhone Merieux Animal Health, New Zealand.
"Copper deficiency in sheep and cattle" Western Australia Dept of Agriculture
"A Comparison of the Efficacy of Proprietary Products in the Treatment of Molybdenum Induced Copper Deficienty - N.R. Kendall, C Middlemas, H. Maxwell, F Birch, D.V. Illingworth, D.W. Jackson & S. Telfer, Centre for Animal Sciences, Leeds Institute of Biotechnology and Agriculture, Schoo of Biology, Universitey of Lees, Leeds, LS@ 9JT, UK
NOTE: There is at least one study (Attempted Induction of Chronic Copper Poisoning in Boma Confined Impala. Research and Development, Kruger National Park, Skukuza, South Africa, '99) that indicates, via fecal copper concentrations, that a good portion of the of the copper oxide particles are excreated from the body. Dispite deliberate attempts to overdose the study Impalas with one time doses ranging between 125 mg/kg to 1000 mg/kg, less than 20% of the animals were found to have elevated liver copper levels after 52 and 105 days.
(photo of Copasure bolus and stomach chart courtesy of Animax Limited)
- Reduce the solubility of copper in the abomasum (fourth stomach), by up to 70 per cent.
- Reduce the subsequent uptake of dissolved copper by the liver by up to 50 per cent.
- Increase copper losses from the animal.
Almost half of Canadian feeds analysed at the Agricultural Soil and Feed Testing Laboratory (Canada) contain less than the estimated RDA of 10 ppm. Also, in the US 28.7% to 57.8% of pastures had molybdenum (Mo) and iron (Fe) levels high enough to cause copper malabsorption. To this can be added malbsorption through excessive sulfur intake.
NOTE: Alfalfa is notorious as a crop which is susceptible to copper deficiency. Wheat, barley and oats can also be deficient.
NOTE:: Molybdenum is common in alfalfa hays. Copper deficiency is likely if hay has less than four parts copper to each part molybdenum.
NOTE: Soil applied copper will generally have long-lasting residual effects. Beneficial effects from 1.3 to 2.7 pounds of copper per acre have persisted undiminished for up to 35 years (western Australia). Copper can be applied as organic compounds in the form of CuEDTA, copper ligninsulfonates, and copper polyflavonoids.