A simple mention of the word “copper” is likely to strike fear among most sheep raisers. It is true that sheep have a unique process of metabolizing copper which puts them at higher risk for copper toxicity compared to other species. However, the role of copper in sheep diets is too complex to let this fear drive the decision making. Copper is essential for many life functions making it a necessary component of sheep diets. This creates a narrow margin between under supplementation and over supplementation in which producers must manage their flock. The information below is provided to enhance the understanding of copper requirements in sheep and the circumstances in which copper affects animal health.
Do sheep need copper?
Copper is necessary for generation of cellular energy, proper bone formation, and production of proteins essential for the development of arteries, ligaments, and skin. Have you wondered what gives your black-faced sheep a black face? Aside from genetics, copper is responsible for producing the hair, wool, and skin pigment in livestock. Additionally, copper is involved in the development of the central nervous system and helps maintain proper immune function. These are just a few of the benefits of copper in the physiology of sheep and explains why this important mineral should be included in their diet.
How much copper do sheep need?
In general, it is recommended to supply sheep with at least 5 ppm copper on a dry matter basis. However, dietary requirements fluctuate based on the sex, weight, and production phase of the animal. Additionally, copper digestion not only depends on the amount of available copper in the diet but is also determined by the capacity of the animal to absorb that copper. To complicate matters further, copper absorption can also be affected by the amount of other minerals present in the feed. Therefore, it is always best to consult a ruminant nutritionist to establish the appropriate feeding practices for your flock.
Most sheep rations will contain enough elemental copper to meet the animal’s copper requirement. All feedstuffs (whether forage or supplements) have some level of elemental, or baseline, copper. This fraction of copper is intrinsic to the ingredients in the diet and is not a form of added copper. Therefore, it is possible for a copper specification to be listed on a supplemental feed tag, but that does not mean copper was intentionally added to the diet using an external source.
Can sheep become copper deficient?
Sheep can become copper deficient under two different scenarios. Primary deficiency occurs when available dietary copper is insufficient to meet the physiological requirements mentioned previously. Not following proper feeding directions and suggested feeding rates or feeding a ration that was not developed for the stage of life your livestock are in can all contribute to copper deficiency. Overly cautious producers may even inadvertently create a primary deficiency while trying to avoid copper toxicosis. Sheep grazing native pastures can also be affected by primary deficiencies if they are grazing copper-deficient areas. Secondary deficiency is characterized by a lack of copper absorption due to antagonistic mechanisms from other microminerals in the diet. Three such antagonistic minerals are molybdenum, sulfur, and iron. Each of these minerals has a high affinity for copper in the rumen and will form insoluble copper complexes. Under extreme circumstances, excessive amounts of dietary molybdenum, sulfur, or iron can bind most of the dietary copper increasing the risk of copper deficiency in sheep.
Swayback or enzootic ataxia are the most severe symptoms of copper deficiency. Both are disorders of the central nervous system in young lambs that cause incoordination, paralysis, and death. Lambs can be born with the condition (swayback) or develop it within the first six months of life (enzootic ataxia). Either way, the condition is almost always deadly. Potential onset of swayback and enzootic ataxia is ultimately determined by copper status during fetal development. Thus, treatment after birth is often not effective as the condition is “programmed” during gestation. The most successful prevention against these detrimental nervous system disorders in young lambs is to closely monitor copper requirements in their dams, especially during the last half of gestation.
Less fatal, but nevertheless important, symptoms of copper deficiency include loss of pigmentation, especially in black-wooled sheep, reduced wool quality, increased occurrences of long bone fractures, anemia, and general unthriftiness, to name a few. Unlike congenital defects, these symptoms present after an extended period of limited copper intake and/or absorption. If caught early enough, animals have the potential to recover from their symptoms through judicious use of dietary supplemental copper, oral copper drench, or copper injections. For grazing sheep, copper-containing fertilizer can be applied to pasture to fortify forage. Always consult a nutritionist or veterinarian before supplementing sheep or fortifying pastures with copper if you suspect copper deficiency within your flock. Although it is a required mineral, copper can easily become toxic if it is delivered incorrectly.
What causes copper toxicity in sheep?
Ruminants are less efficient at excreting excess copper than non-ruminant species, making them more susceptible to toxicity. Prolonged exposure to moderately high concentrations of copper can lead to an accumulation of copper in the liver. Once liver stores are full, stressful events, such as extreme weather or handling, can trigger the spontaneous release of copper from the liver, initiating a fatal series of events. The slow buildup of copper in the liver followed by a deadly release is characteristic of chronic copper toxicity and can occur over a period of several months to a year. Often, the only symptom is dead sheep, especially following a particularly stressful event. On the other hand, acute copper toxicity results in quick and sudden death in sheep consuming highly toxic levels of copper. This type of toxicity is often the result of feeding a ration not designed for sheep.
Recommendations for avoiding toxicity are to limit dietary copper to 15 to 20 ppm on a dry matter basis. This recommendation is dependent on dietary concentrations of other microminerals and assumes “normal” conditions with dietary molybdenum ranging from 1 to 2 ppm and sulfur ranging from 0.15 to 0.25%. Copper consumption exceeding 15 to 20 ppm is likely to result in high mortality rates within the flock. Death is the primary symptom of copper toxicosis, but clinical signs preceding death may include diarrhea, weakness, yellowing of the skin and eyes, and dark urine. Treatment options exist but may prove to be futile depending on the severity of toxicity. Even if treatment is successful in reducing death loss, affected animals may sustain lingering effects hindering future productivity. Therefore, it is important to continually monitor the flock’s copper status and take appropriate management steps to help prevent the onset of copper toxicosis. If you suspect a toxicity issue in your flock, contact a veterinarian immediately to discuss mitigation and treatment options.
The role of copper in sheep diets is much more complex than many realize. A single-minded approach to simply minimize copper as much as possible will not always be advantageous and can even be deadly in some situations. On the other hand, copper can very easily become toxic if feeding programs, including both the forage and supplemental fractions of the diet, are not carefully managed. A diligent review of feeding protocols should consider the many external factors affecting copper homeostasis, such as elemental copper in pasture forages, the presence of other microminerals relative to copper, and even breed of sheep (Texel breeds are known to be among the most susceptible of all sheep breeds). Although often grouped together under one umbrella, goats should be managed separately from sheep as they have different copper requirements and tend to not be as susceptible to copper toxicosis.