Of all farm animals, sheep are the most susceptible to copper poisoning.
This essential trace mineral is important for the production and maintenance of tissues, including bone, iron absorption, enzymes and red blood cell formation.
Copper is essential for life, but the window between deficiency and toxicity is narrow. The element is problematic in Western Canada because of its association with copper deficiency in cattle.
Copper poisoning occurs in two ways:
- A single, high dose, which is usually in the form of an injected supplement, can cause the acute form.
- The chronic form results from long-term consumption of food and supplements that are high in copper.
Pastures fertilized with manure from poultry and hog farms can be a source of copper because the mineral can be added to their feed. Grain that was previously treated with copper-based antifungals can be another source.
However, the most common cause of chronic copper poisoning is from allowing sheep access to mineral licks intended for cattle, which have much higher levels of copper than those intended for sheep and goats.
Copper toxicity has also been reported from feeding high amounts of palm kernel oil.
Sheep that suffer from the acute form experience vomiting, diarrhea and sudden death. The most common clinical signs of long-term exposure include lethargy, pale mucous membranes, jaundice and red-brown urine. Ewes may abort and those that survive may have difficulty giving birth in subsequent pregnancies.
Consuming small, frequent doses leads to a gradual buildup of copper in the liver. There are no signs of illness while this is occurring, which can go on for months. The liver’s storage capacity is eventually overwhelmed and a hemolytic crisis occurs.
This involves the sudden death of liver cells, releasing massive amounts of copper from the liver. The copper enters the blood stream, where it causes red blood cells to burst. This in turn releases the oxygen transport molecules (hemoglobin), which subsequently turn tissues from white to yellow (jaundice) and produce red-brown urine. Death results from a lack of red blood cells for delivering oxygen to tissues and damage to the kidneys from excreting hemoglobin.
Precipitating factors of the hemolytic crisis include stressful events such as transportation, flock mixing, lactation and poor nutrition.
Treatment of affected animals is usually ineffective during the hemolytic crisis.
It’s possible to supplement with molybdate and sodium sulfate, which binds to copper and promotes excretion in the feces. Vitamin E, which is a potent antioxidant, can be injected to reduce the oxidative damage. Heroic treatments such as blood transfusions can be done for valuable animals.
Adding molybdenum to diets in areas known to have high copper content in forage can reduce the risk. High-protein diets can also be somewhat protective.
The toxic dose of copper varies with the concentration of other minerals, such as molybdenum, zinc and sulfate. The high number of variables that can affect toxicity makes it difficult to suggest an exact dose, but 20 parts per million for several months can cause chronic toxicity in sheep.
Horses appear the most resistant to copper poisoning, while cattle susceptibility falls in between those of horses and sheep.
Goats are considered to have similar susceptibility as sheep.
There are some remarkable breed variations in susceptibility, with Merino sheep being more resistant than the British breeds. This resistance likely reflects the natural copper levels of the areas where these breeds were developed.
Copper poisoning can be diagnosed after death by associating jaundice and kidney damage with elevated copper in the liver.
Diagnosis before death is more challenging. A liver biopsy is usually required because copper doesn’t increase in the blood until just before the hemolytic crisis. Certain liver enzymes become elevated in the blood before the hemolytic crisis. This simple blood test can be useful to monitor flocks.
Producers should ensure that they use trace mineral supplements that are specifically labelled for use in sheep and goats.
Dr. Jamie Rothenburger is a veterinary pathology resident at the Western College of Veterinary Medicine, University of Saskatchewan.