Copper toxicity and deficiency in sheep
Learn about dietary sources of copper and the signs of copper toxicosis and copper deficiency in sheep.
Overview
Excess copper can be toxic to humans and livestock, but sheep are particularly susceptible to copper toxicosis because their bodies can’t get rid of copper very well.
Excess copper is stored in the cells of the liver over the course of weeks, months or years, eventually reaching toxic levels, causing disease and death. Copper, however, is an essential mineral that animals, including sheep, require. Insufficient levels of copper intake can cause deficiency, resulting in negative impacts on health.
Dietary copper sources
Consider all potential sources of copper in the diet. Monitor levels of copper to prevent each copper deficiency and toxicosis in your flock.
In the case of disease, get the diagnosis confirmed by your flock veterinarian and diagnostic laboratory, then look for all obvious sources of copper.
Potential sources of copper include:
- forages or pasture
- grains and commodities
- vitamin/mineral premixes
- salt, trace-mineralized salt
- purchased feeds, supplements
- mixing errors in feed or mineral orders
- ingesting things not for consumption such as ingestion of copper sulfate footbaths
Copper can also accumulate in the liver due to a complex interaction of copper with other minerals such as:
- molybdenum
- sulphate
- iron and
- zinc
These minerals occur naturally in forages and on pasture and are also combined into commercial mineral mixes and feeds.
Molybdenum in particular binds copper and decreases its absorption, which can help prevent copper toxicosis or exacerbate deficiency. Molybdenum intake of less than 1 parts per million (ppm) is insufficient and may lead to excessive accumulation of copper in the liver
Copper toxicosis
Cause
Sheep are susceptible to copper toxicosis because their bodies don’t get rid of extra copper very well and the excess is stored within their liver. The liver can only store a limited amount of copper before there are negative health impacts on the animal which can include death.
Breed and age also play a role in the animal’s susceptibility for copper accumulation.
Lambs are most susceptible to copper toxicosis because they absorb copper more easily and have an immature excretion system, reducing their ability to eliminate excess copper.
When the liver’s capacity to store copper is exceeded or after the animal undergoes a stress event, copper is released from the liver into the bloodstream. This triggering stress event can be due to:
- weather (for example, heat stress)
- diseases
- poor nutrition
- transportation
- exertion
- handling
Once copper is in the blood stream at a sufficient concentration, it causes haemolysis, a breakdown of the red blood cells (RBCs). RBCs are required to transport oxygen throughout the body into tissue. Hemoglobin is also released into the bloodstream from the broken RBC, which is toxic to the kidneys.
Signs and diagnosis
The breakdown of RBC causes the animal to become anemic. A sheep with anemia initially has very pale mucous membranes and appears dull. Signs of disease progression include:
- weakness
- increased time spent lying down or inability to stand
- reduced appetite
- increased thirst
- difficulty breathing and death
The visible mucous membranes in the mouth and around the eye rapidly yellow as jaundice (icterus) sets in throughout the body. At postmortem examination, all tissues of the affected sheep appear pale to dark yellow, the kidneys are very dark and the urine is a bloody colour. If hemolysis is severe, sheep can die suddenly without showing any sign of jaundice.
The diagnosis of copper toxicosis is made based on:
- symptoms
- exposure history
- postmortem findings
- laboratory diagnostics
A diagnosis and response should be made in consultation with a veterinarian. Supportive treatment should be provided to clinically ill sheep, but the prognosis for recovery is poor. To reduce the impact of copper toxicosis in the rest of the group or flock, sheep may be supplemented with dietary ammonium molybdate as a molybdenum source, sodium thiosulfate or zinc.
Copper deficiency
While it is essential to control a sheep’s diet to prevent copper toxicosis, be careful not to cause copper deficiency. Copper is an essential mineral required by enzymes to support a sheep’s:
- growth
- immune function
- reproduction
- wool production
Copper deficiencies can be the result of low copper intake or from high concentrations of molybdenum, sulfur or iron in the diet. Sheep require copper in their overall diet at a minimum of 6 ppm and the copper to molybdenum ratio should be 5:1 to 10:13. Lambs require copper for proper growth and development and are particularly susceptible to copper deficiency.
Signs of copper deficiency include:
- anemia
- decreased milk production
- poor quality wool, including loss of pigment of black fleece, crimping and decreased tensile strength
- lambs with swayback, uncoordinated gaits, increased fractures, slow growth or lameness
- sudden death due to heart failure
- poor fertility
Work with your nutritionist and veterinarian if your sheep are showing signs of copper deficiency. They can facilitate getting a laboratory diagnosis, supplementary copper to the rest of the animals at risk and to help correct the cause of the deficiency. Like copper toxicity, routine feed analysis and trace mineral testing of the flock can help prevent the problem of copper deficiencies in your sheep.
Prevention
A mineral analysis should be performed on all elements of the sheep’s diet, including the water and mineral mix if fed, but especially forages. Results should be interpreted with the help of a veterinarian and a nutritionist. The maximum concentration of copper tolerated in feed is 15 ppm. Breed and age play a role in the animals’ susceptibility for copper accumulation which should be taken into consideration when planning a diet or analyzing rations.
Prevention strategies
To prevent copper toxicosis:
- work with a nutritionist
- check the copper and molybdenum levels regularly in your forages and pasture
- routinely test sheep that have died or have been harvested for their trace minerals to know your flock’s baseline levels
- feed sheep the label dose of free-choice mineral premixes to avoid over-supplementation
- label and store feed for other species away from sheep feed to prevent accidental feeding
References
- National Research Council of the National Academies (2007). Nutrient Requirements of Small Ruminants. Sheep, Goats, Cervids and New World Camelids. The National Academies Press
- Borobia, M.; Villanueva-Saz, S.; Ruiz de Arcaute, M.; Fernández, A.; Verde, M.T.; González, J.M.; Navarro, T.; Benito, A.A.; Arnal, J.L.; De las Heras, M.; et al. Copper Poisoning, a Deadly Hazard for Sheep. Animals 2022, 12, 2388.
- Pugh, D.G. and Baird, N.N. (2012) Sheep & Goat medicine-E-book. Elsevier Health Sciences.
Footnotes
- footnote[1] Back to paragraph 1. Menzies, P. I., Boermans, H., Hoff, B., Durzi, T., & Langs, L. (2003). Survey of the status of copper, interacting minerals, and vitamin E levels in the livers of sheep in Ontario. The Canadian veterinary journal = La revue veterinaire canadienne, 44(11), 898–906. Survey of the status of copper, interacting minerals, and vitamin E levels in the livers of sheep in Ontario - PMC