Goat Minerals
Minerals are perhaps the single most important nutritional component to ensure health and vigor. Let’s... View more
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Copper
Copper
Post all data, research, questions and information related to the mineral copper here.
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This discussion was modified 7 months, 1 week ago by
Rachel.
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This discussion was modified 7 months, 1 week ago by
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Effects of copper levels on goat carcass traits and meat quality
“In conclusion, high Cu levels are recommended in the goat diet to enhance meat quality without affecting slaughter variables.”
https://www.sciencedirect.com/science/article/pii/S0921448821001681
Effects of Daily Oral Administration of Copper to Goats
“Three goats were dosed orally with a 0.2 % aqueous copper sulphate solution. The dosing was 20 mg copper sulphate/kg body weight twice a day for 56 to 113 days. One of the goats accumulated substantial amounts of copper in the liver and developed two haemolytic crises. The two other goats showed only increased liver copper concentrations before they were killed. The results indicate that the goats were susceptible in varying degrees to repeated oral copper dosing, and that two of the goats were significantly less susceptible to copper than sheep. The goat that turned into a haemolytic crisis showed changes similar to those seen in sheep as far as blood and plasma parameters are concerned. The gross and histological lesions were also mainly of the same type as described in sheep. The hepatic lesions found in the goat differed to some degree from those found in sheep as the necroses were more distinctly located to the centrilobular area, and as the iron pigments were mainly located in phagocytes in the hepatic sinusóides.”
https://actavetscand.biomedcentral.com/articles/10.1186/BF03547595
Effect of Copper Methionine Supplementation on Growth Rate and Nutrient Utilization in Male Goat Kids
Twenty male goat kids (10.94±0.35 kg body weight; 4–5 months age) were divided into four equal groups and offered a standard diet comprising of concentrate mixture and wheat straw in the ratio of 60: 40. Animals of control group (T1) were not fed additional Cu, while the animals of treatment groups were provided additional 7 ppm Cu (as CuSO4) in T2, 7 ppm Cu (as Cu methionine) in T3 and 3.5 ppm Cu (as Cu methionine) in T4 group diets. Experimental feeding was done for 120 days. The intake and digestibility of DM, OM, CP, ether extract, neutral detergent fibre, acid detergent fibre, cellulose and hemicelluloses were similar (P>0.05) among the four groups. Supplementation of Cu as CuSO4 and Cu-methionine also had no significant (P>0.05) effect on balance of nitrogen, calcium and phosphorus; feed: gain ratio and intake of digestible nutrients. However, copper balance was significantly (P<0.05) higher in T3 than T1, T2 and T4. The growth rate (g/d) of the goat kids in all the three mineral supplemented groups was not different. Supplementation of 7 ppm Cu (as CuSO4 or Cumethionine) and 3.5 ppm Cu (as Cu-methionine) had no beneficial effect on the growth rate and nutrient utilization in the goat kids.
https://indianjournals.com/ijor.aspx?target=ijor:ijan&volume=31&issue=1&article=008
Laryngeal Neuropathy in Adult Goats With Copper Deficiency
Emphasis mine in the abstract below. Clinical symptoms of copper deficiency.
Abstract
The aim of this study was to elucidate the cause of a neurological syndrome characterized by stridor in adult goats with clinical signs of copper deficiency. The main clinical signs consisted of apathy, emaciation, pale mucous membranes, mucous nasal discharge, dyspnea, severe achromotrichia, diffuse alopecia, torpor, ataxia, and stridor. When the goats were forced to move, the stridor increased. In a herd of 194 Toggenburg goats, 10 adult goats with clinical signs of copper deficiency were removed from the herd and divided into 2 groups: group 1, which consisted of 4 nannies and 1 buck with stridor, and group 2, which consisted of 4 nannies and 1 buck without stridor. Group 3, used as a control, consisted of 5 adult goats from another flock without any clinical signs of disease. The mean serum copper concentrations were 1.3 ± 0.3 μmol/L in group 1, 8.1 ± 1.1 μmol/L in group 2, and 11.3 ± 2.2 μmol/L in group 3. The mean serum iron concentrations were 42.3 ± 14.2 μmol/L in group 1, 39.1 ± 8.2 μmol/L in group 2, and 20.6 ± 6.1 μmol/L in group 3. The main histological lesions in goats from group 1 were axonal degeneration of the recurrent laryngeal nerves and atrophy of the muscles of vocal folds and of the dorsal cricoarytenoid and right and left cricothyroid muscles. Goats with ataxia had neuronal degeneration and necrosis of cerebellar Purkinje cells and of the cranial cervical ganglion. We concluded that the stridor was caused by axonal degeneration of the recurrent laryngeal nerves due to the severe copper deficiency.
Also in the paper above about laryngeal neuropathy, a therapeutic injection of three copper types:
“Therapeutics
After the initial visit, goats in the herd were subcutaneously injected with a commercially available copper solution (5.5 mg copper lactobionate + 3.1 mg copper gluconate + 980 mg copper octadecanoate) at a dose of 0.1 ml/kg of body weight. This treatment was repeated after 30, 60, 90, and 120 days.”
This treatment resolved copper deficiency in most goats but the worst affected did not recover and “died between 6 and 8 months after the onset of clinical signs.”
A CASE OF FATAL COPPER SULFATE TOXICITY
I spoke with Cherrie earlier today to clarify her experience with fatal copper toxicity and got permission to share her story:
“When I was running goats at the Badger Army Ammunition Plant in Sauk County, WI about 10 years ago, I was trying the Pat Coleby mineral offerings (separate copper, dolomite, kelp, sulfur). I made the mistake of using open containers. We had a huge rain and the containers filled with water, so it basically made a very concentrated copper sulfate water. Apparently, there is not enough post-ingestive feedback that occurs quickly enough when an animal is drinking water to tell them that the other things in the water are worse for their body than walking 20 feet to the tank of water that had no unusual minerals in it. They drank, laid down in the brush near the water and died shortly afterwards of hemolytic anemia from copper toxicity. Many looked like it happened so fast that they died in their sleep, as they were in a normal sleeping position when I got there the next morning, but they were dead. No paddling marks were visible, no other signs of thrashing or prolonged death.
You’re welcome to quote me, and this is one very important reason that trace minerals shouldn’t be available to livestock in bulk concentrated forms. Diluted with a carrier allows animals to consume what sticks to one tongue dip without getting too much. A small mistake with a concentrated trace mineral can mean death. I can’t remember exact numbers of dead but it was somewhere around 10, out of probably around 40 that I had in that paddock at the time.”
This is one of many such examples I’ve seen over the years and part of why I am a. emphatically opposed to feeding undiluted copper sulfate and b. okay–with a bit of grumbling–about the dilution rates of FCE’s copper, because the stakes are high when we feed minerals that have the potential for fatal toxicity. You can read more of my own thoughts on Pat Coleby style minerals here: https://littleavalonfarm.com/pat-coleby-minerals/.
littleavalonfarm.com
Pat Coleby Minerals: Feeding Undiluted Minerals for Goats – Little Avalon Farm
Pat Coleby Minerals: Feeding Undiluted Minerals for Goats – Little Avalon Farm
Kathy Winters’ experience a few years ago had a profound impact on me and how I view minerals in goats. Despite feeding “goat formulated” minerals, she began having significant losses–fatalities–in her Nigerian Dwarf goat herd due to copper toxicosis. This experience was one of the big reasons I moved to mineral buffet. I mention her frequently and have linked to her posts in my other work. Here, in the archival spirit, I am adding complete screen captures of her posts so that they are preserved in their entirety. You can read the full post here: https://www.facebook.com/RedHorseValley/posts/pfbid02fGZYQuk87HeDZcFwAjqbnroLE43j4ghBf2wy1CVF1dotjN3rSWPdCE6AD1XH7LiPl
In this post, Kathy details improvement in what many might consider symptoms of mites when the goat in the photo began treatment for copper toxicity.
facebook.com
Some of us like to see a response to treatment to also help us validate the diagnosis. It isn’t always clear cut, but here is a dramatic example for you. Ten days after starting antidote treatment...
More from Kathy Winters. Here is a goat displaying scaled skin and fish tail. In Internetland, just about everyone will tell you that:
-fish tail absolutely means copper deficiency
-hair loss and scales is ALWAYS either mites or zinc deficiencyYet this herd is copper toxic. We simply cannot ever know mineral status based on appearances. Period. Full, hard stop. I can’t stress this enough.
See the full post here: https://www.facebook.com/RedHorseValley/posts/pfbid0jFm5HBRAu5ryxyP8yeUXgVzJ1ft7tcQVj9R7G3BALq2iB46o1nxNYsiZ55QmqRral
facebook.com
Some claim that “fish tails” or balding tail tips are indicative of copper deficiency. Please learn that it can be a sign of mineral imbalance, as my herd is thoroughly documented as having excess...
Copper deficiency reduces iron absorption and biological half-life in male rats
Abstract
Dietary copper deficiency (CuD) in rats leads to iron (Fe) deficiency anemia. Is this because CuD reduces Fe absorption? Fe absorption in CuD rats was determined by feeding diets labeled with (59)Fe and using whole-body counting (WBC) to assess the amount retained over time. Two groups, each with 45 male weanling rats, were fed an AIN-93G diet low in Cu (<0.3 mg/kg; CuD) or one containing adequate Cu (5.0 mg/kg; CuA). At intervals over the next 42 d, 5 rats per group were killed and blood was drawn to determine hematocrit, hemoglobin, and other indicators of Fe status. At d 7 and 25, 5 rats per group were fed 1.0 g of their respective diets that had been labeled with (59)Fe. Retained (59)Fe was monitored for 10 d by WBC; then rats were killed and (59)Fe was measured in various organs. Signs of Fe deficiency, such as low hemoglobin, hematocrit, and RBC count, were evident in CuD rats by d 14. At d 7, CuD rats absorbed 90% as much Fe as CuA rats (P > 0.20), but at d 25, CuD rats absorbed only 50% as much as CuA rats (P < 0.001). In the study beginning at d 7, the biological half-life (BHL) of (59)Fe in CuD rats was less (P < 0.02) than that in CuA rats [geometric mean (-SEM, +SEM); 75(62,91) d vs. 175(156,195) d]. In the study beginning at d 25, the BHL was again less (P < 0.02) in the CuD rats than in the CuA rats [33(23,49) d for CuD and 157(148,166) d for CuA]. Apparently, the route of Fe loss in the CuD rats was through the gut. At d 16 and 34, CuD rats lost 4 to 5 times more (P < 0.01) (59)Fe in the feces in a 24-h period than the CuA rats. Also, (59)Fe in the duodenal mucosa of CuD rats was approximately 100% higher (P < 0.01) than in CuA rats. These findings suggest that Fe deficiency anemia in CuD male rats is caused at least in part by reductions in Fe absorption and retention.
https://pubmed.ncbi.nlm.nih.gov/15284382/
pubmed.ncbi.nlm.nih.gov
Copper deficiency reduces iron absorption and biological half-life in male rats - PubMed
Dietary copper deficiency (CuD) in rats leads to iron (Fe) deficiency anemia. Is this because CuD reduces Fe absorption? Fe absorption in CuD rats was determined by feeding diets labeled with (59)Fe and using whole-body counting (WBC) to assess the … Continue reading
Copper Supplementation, A Challenge in Cattle
Abstract
Ensuring adequate copper supplementation in ruminants is a challenging task due to the complexity of copper metabolism in these animals. The three-way interaction between copper, molybdenum and sulphur (Cu-Mo-S) in the rumen makes ruminants, particularly cattle, very susceptible to suffering from secondary copper deficiency. Paradoxically, excessive copper storage in the liver to prevent deficiency becomes a hazard when ruminants are fed copper-supplemented diets even slightly above requirements. While cattle were traditionally thought to be relatively tolerant of copper accumulation, and reports of copper poisoning were until recently somewhat rare, in recent years an increased number of episodes/outbreaks of copper toxicity in cattle, particularly in dairy cattle, have been reported worldwide. The growing number of lethal cases reported seems to indicate that copper intoxication is spreading silently in dairy herds, urging the development of strategies to monitor herd copper status and improve farmers’ awareness of copper toxicity. In fact, monitoring studies carried out on numerous samples collected from culled animals in slaughterhouses and/or diagnostic laboratories have demonstrated that large numbers of animals have hepatic copper concentrations well above adequate levels in many different countries. These trends are undoubtedly due to copper supplementation aimed at preventing copper deficiency, as dietary copper intake from pasture alone is unlikely to cause such high levels of accumulation in liver tissue. The reasons behind the copper overfeeding in cattle are related both to a poor understanding of copper metabolism and the theory of “if adding a little produces a response, then adding a lot will produce a better response”. Contrary to most trace elements, copper in ruminants has narrow margins of safety, which must also be formulated considering the concentrations of copper antagonists in the diet. This review paper aims to provide nutritionists/veterinary practitioners with the key points about copper metabolism in cattle to guarantee an adequate copper supply while preventing excessive hepatic copper loading, which requires à la carte copper supplementation for each herd.
Some key points I’m adding from the paper:
“For example, when sulphur and molybdenum are present at quite high levels in the diet, the copper requirement in sheep is 10 mg Cu/kg of diet. However, if molybdenum concentrations in the diet are low, dietary supplementation at 10 mg Cu/kg can lead to toxicity in some breeds [5].”
“Inorganic and organic sulphur compounds are metabolized by microbes in the rumen, thus producing sulphide. Furthermore, sulphur and molybdenum react to form thiomolybdates (mono-, di-, tri- and tetrathiomolybdates). These compounds bind strongly to copper (tri- and tetrathiomolybdates bind copper irreversibly) to form copper thiomolybdates. The bound copper is insoluble, and is therefore not absorbed in the intestine. If there is no copper available in the rumen, the thiomolybdates will either be quickly absorbed through the rumen wall or will be absorbed more slowly via the small intestine and after that pass to bloodstream and can bind to copper in biological compounds.”
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