I found out that the site, Saanendoah, is not being maintained anymore and some people can't even find the site in a Google search. The link above takes you directly to the page that talks about copper and its importance in goat health. I'm glad that I can still get to it, but the link may end up broken at some future date.
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.
Copper Deficiency: A Possible Cause of Polioencephalomalacia in Young Goats
Prairie Diagnostic Services - Canada
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.
If copper nutrition was as simple as determining the copper levels in the base diet and adding a highly available copper source/supplementation, copper deficiency would not be a problem. However, because copper absorption and metabolism can be affected by molybdenum, sulfur, calcium, zinc, iron, manganese, cobalt, lead, cadmium, and selenium, deciding how much supplemental copper is required is not always easy.
Early on (after we identified the problem) we tried via oral supplementation of different mineral mixes high in copper (up to 1100ppm) and feeding of other than goat specific feeds (horse pellets, horse minerals, etc.) to correct the problem, to date none of them has succeeded in bringing up the body stores of copper.
Absorption of copper can vary from zero to as high as 75% (Linder, 1991) depending on a number of factors. Copper availability in most feedstuffs fed to farm animals is between 1% and 15% (Hemken et al. 1993). Most minerals contain copper oxide in powder form, availability is poor when used in this form, the mineral passes through the gut with little absorption. (note: other areas of the US have had excellent results with just the addition of a mineral mix high in copper) in our area we have found copper boluses (copper oxide wire boluses) dosed to weight to be the most effective means of elevating the liver copper levels to within normal limits.
We had the first boluses brought into the US from New Zealand in the spring of 1994; since that time we have found a source of cattle copper boluses that we can downsize to goat doses. In this area 2000 to 2500+ goats have been on these boluses for nine years now (early '02).
Continuous laboratory work on bolused animals indicates we are achieving normal liver concentrations of copper. To this date (June 2006) we have not had a single case of copper toxicity, and only one elevated liver copper level. Liver concentrations remain in the low normal (30-80ppm) with only three animals testing above that range in the twelve years we've been using the boluses.
We've found that the boluses need to be administered at 5-6 month intervals to maintain adequate levels. After about 4 months, liver stores start to fall rapidly. In order to best protect the neonatal kids, we strive to use the boluses at times that will keep the does levels up during her entire pregnancy. Minnesota research with mice showed that perinatal brain development was affected by copper concentration in the mothers diet. Mice born to copper deficient dams had permanent brain disorders even when fed adequate copper after birth. Some breeders are routinely giving boluses (0.625 to 1.35 grams) to kids early on (2-4 weeks old) and it's proven to be very satisfactory (I've done this the last six years in my herd).
HOW THE COPPER BOLUSES WORK
References:
"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 | |
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When copper deficiency has been recognized, attempts to remedy it by provision of extra oral copper has proved unsatisfactory because of the unpredictable intake, rapid excretion, and variable effect. With an element such as copper, which is a cumulative poison, the risk of chronic copper poisoning from parenteral or oral copper treatment is positively correlated with its effectiveness in combating deficiency. Existing methods of treatment for copper deficiency have limitations. Mineral licks and supplements are unpredictable because of the individual refusal of some animals and over indulgence of others.
Copper sulfate (CuSo4) drenches are not only astringent (Cu sulphate drench, if it accidentally enters the lungs, can cause shock and death) but more than 90% of the copper is rapidly excreted from the body. Animals need to be drenched every 2-3 weeks. Boluses (glass) of copper that lodge in the rumen or reticulum can form unusable complexes with molybdenum, sulfur and iron. Compounding copper salts with concentrate rations can be effective (though it has not proven so with our animals).
Injectable copper (copper glycinate, CuCa-EDTA, copper methionates and Cu-oxyquin) can be acutely toxic (seen most often w/Cu EDTA which is no longer available), so inectable doses must be limited, the dose is often partly encapsulated at the injection site and thus prevented from achieving its objective. Side effects such as injection site abscesses (copper glycinate) and hepatic necrosis are potential problems with this method of treatment. Repeated injections are needed to maintain adequate protection. note: we only use copper glycinate (Molycu) injections in emergency situation, usually in young kids from unbolused dams.
Gelatin capsules containing copper oxide needles provide relatively long term protection against copper deficiency. The sustained activity after oral dosing with copper oxide needles as a means of alleviating hypocupremia in goats has been widely reported.
The gelatin capsules contain thousands of minute, blunt copper oxide rods. When give orally, the gelatin capsule dissolves in the rumen, releasing the copper oxide rods, which then pass into the abomasum where they lodge. There they release copper for the animal's immediate requirements and reserves. The rods dissolve completely over a period of time.
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.
Copper oxide needles are brittle rods (1 to 8 mm long , and 0.5+/- 0.1mm in diameter) made by oxidizing fine copper wire. They are nontoxic when given orally, and they can be given in doses sufficient to establish long-lasting reserves of copper in the liver. Their properties were discovered by Australian scientists, who found that a combination of small particle size and high specific gravity (2.0 and 7.0) caused them to become trapped in the folds of the abomasum. Copper oxide particles, released in the rumen pass through to the abomasum where they remain in the folds of the abomasum.
CSIRO (1978) and Judson et al., (1982) demonstrated that the particles remained for a period of at least 32 days. CSIRO (1978) showed that the excretion rate of copper from the copper oxide particles was about 0.2 grams by weight per day which allowed for the safe absorption of copper without toxicity being apparent. The accumulated hepatic stores of the absorbed copper can protect the animal against copper deficiency for periods of months (our lab work indicates 4.5-6 months).To be effective the Copper particles must be swallowed, administer by a conventional balling gun which delivers the capsule direct into the gullet. The gauge and weight of the copper particles is calculated so that they sink and lodge properly. Chewing rods/wires/particles will change both the gauge, weight, specific gravity, causing the particles to pass on through the animal in greater amounts than the dose is adjusted for.
(photo of Copasure bolus and stomach chart courtesy of Animax Limited) To get the most out of your copper supplementation program
Heavy worm burdens can affect copper uptake by altering the pH in the gut, making the copper less soluble. An effective worming program is therefore an important aspect of copper supplementation. Internal parasites can:
- 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.
While the use of cupric oxide rods has been shown to produce significant anthelmintic effects, their efficacy may be reduced by a heavy abomasal parasite burden. It is important that adequate selenium (Se) levels are also maintained. See: U.S. Geological Survey Selenium in Counties of the Conterminous States . Selenium testing: Whole blood (EDTA or heparin) is the best sample since most of the selenium is located on red blood cells. Serum selenium analysis is possible but does not reflect long-term status of the animal. In general, the Western states had lower mean serum copper concentrations compared to other regions.The mean serum copper concentration for operations in the Western regions was 0.63 ppm, while the Midwest and Southern regions recorded 0.70 ppm.
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. Copper can be toxic, it is important to stress again, that this is a local problem and solution, and though both primary and secondary Cu deficiency problems of different magnitudes may be found in other areas we do not recommend supplementation using these methods or doses without complete evaluation of your herd's copper status via laboratory work and veterinary consultation. Dose rates:
The animals are dosed to weight at the rate of 1 gram copper oxide in bolus form per 22 pounds at five to six month intervals, laboratory work has shown that liver and kidney concentrations start to fall rapidly after about four months.
