Sheep are highly susceptible to copper toxicity due to their low dietary requirements and inability to manage levels in excess of those requirements. Certain species of sheep are more susceptible than others. Finn sheep are more tolerant to toxicity while Texel sheep are more sensitive.
Unlike other minerals, copper is not absorbed based on an animal’s daily requirements but in proportion to the concentration in their diet. The extra copper gets stored in the liver and is only slowly eliminated via the kidneys. Copper absorption is also affected by the presence of interacting minerals in the diet. Molybdenum exhibits the strongest interaction with low dietary levels of Mo associated with increased absorption of Cu. Other interacting minerals include zinc, sulphur and iron.
Depending on the amount of copper in the diet, it could take months or years for the copper to accumulate to a toxic level (chronic copper toxicity) or it can occur within days (acute copper toxicity). However, most clinical disease is acute in onset. Once a certain threshold is reached in the liver cells, they can no longer cope and start to die – releasing large amounts of copper into the circulation. Stressful events, such as lambing, severe weather changes, poor nutrition, transportation or shearing, may precipitate this event.
Rapid release of large amounts of copper into the blood causes hemolysis of the red blood cells and the sheep rapidly become anaemic. A blood sample drawn during a crisis will not clot. Other signs include acute onset of depression, dehydration, grinding teeth from abdominal pain (likely associated with the liver damage) and jaundice. Urine is a dark, rusty colour due to breakdown products of red blood cells, i.e. methaemoglobin and haemoglobin. During an acute crisis, serum copper levels will be elevated – although normal in non-clinical copper-loaded sheep. Liver enzymes will also be greatly elevated. In cases where there is a prolonged exposure to a small excess of copper, the sheep may go through periods of poor health then recover until an excessively high amount of copper has accumulated in their liver. If liver damage is more chronic, the animal may show neurological signs due to high blood ammonia levels, i.e. hepatic encephalopathy.
At post-mortem, the sheep carcass often is jaundiced (yellow), the liver is swollen and jaundiced and the kidneys are swollen and black due to accumulated red blood cell breakdown products. If the case is prolonged, jaundice may be absent but there will be gross and histological evidence of liver and kidney damage. Case fatality rate is very high – close to 100% even with treatment. Diagnosis is confirmed by analyzing liver and kidney for copper levels. If the animal survives the initial disease incident, liver copper may be normal but kidney copper will be high.
There are many sources where sheep can obtain an excessive amount of copper. Water is only rarely the source. The copper levels in Ontario’s natural water supply (well water) are relatively low in most agricultural areas but presence of copper piping (usually associated with research facilities) has been associated with outbreaks of copper toxicity. Farms located in mining areas should have well water tested for presence of all heavy metals, including copper.
Feed is the most common source of excessive copper. Some feeds are naturally high in copper, e.g. soybean meal – commonly used as a protein supplement in sheep. Producers may incorrectly purchase feeds with added copper. The most common mistake made by new producers is to feed their sheep mineral supplements intended for cattle. This includes loose mineral and salt/mineral blocks. Occasionally, a sheep producer may purchase a feed supplement labelled for cattle – not understanding that this feed contains toxic levels of copper. However, accidental exposure to elevated copper levels is likely the most common reason for outbreaks of copper toxicosis in sheep. Feed mixed or pelleted at a feed mill, even when specifically formulated for sheep, may be inadvertently contaminated with feed intended for other livestock species (e.g. cattle, swine, poultry) all of which contain higher levels of copper. Proper sequencing of the feed through the mixer or pelleter can lower risk. If a high copper feed has been processed prior to sheep feed, then the pelleter or mixer should be cleaned out first. All components of the feed (e.g. minerals, soybean protein supplements) should be sampled and tested for copper levels prior to mixing. Each batch of feed should have a “hold-back” sample, i.e. a representative sample that is kept for analysis if a problem arises after the batch is fed.
The copper content present in forages, such as hay, is dependent on the copper levels of the soil where the plant grows, the plant species and growing conditions. Ontario’s soil does not naturally contain an excessive amount of copper but certain management practices can affect the mineral levels of soil such as the application of fertilizer or manure. Livestock feeds such as swine and poultry have a high copper content; therefore manure from these species also contains a high level of copper. Forages from fields on which these nutrients have been spread may contain toxic levels of copper. Certain pesticides and other chemical solutions applied to crops can also contain a significant amount of copper. Sheep farmers must be careful when purchasing hay from an external source. It is prudent to test each batch of hay prior to purchase for its nutritional value including copper levels.
As previously mentioned, copper absorption is affected by the level of interacting minerals in the diet, with molybdenum being the most important. When Mo levels are low (< 1 ppm), even “safe” diets may be risky. A goal is to keep Cu:Mo ratios approximately 6:1. Conversely, addition of these minerals to the diet may help protect sheep being fed diets with higher levels of copper. These minerals make the copper less readily available for absorption by forming Cu-MoO4 complexes, increasing the amount of copper excreted.
Once a sheep is in a copper toxicosis crisis, it is very difficult to save its life. Preventing exposure of the sheep to excessive copper levels is the recommended approach to this condition.
|
Diet |
Liver |
Kidney |
Serum |
Muscle |
Deficient |
0.5-3.0 |
0.5-4.0 |
3.0-4.0 |
0.10-1.00 |
|
Marginal |
3.0-4.5 |
5.0-20.0 |
4.0-5.0 |
0.40-1.00 |
0.9-1.2 |
Adequate |
5.0-10.0 |
25-100 |
4.0-5.5 |
0.70-2.00 |
1.0-1.3 |
High |
10-20 |
100-500 |
4.0-10 |
1.00-5.00 |
1.1-1.6 |
Toxic |
>20 |
250-1000 |
18-260 |
3.30-20.0 |
|
|
ppm |
ppm wet weight |
ppm wet weight |
|
Brain |
Lung |
Wool |
Spleen |
Pancreas |
Milk |
Fetal-Liver |
Deficient |
1.4-4.5 |
|
0.5-2.5 |
|
|
|
1.0-10 |
Marginal |
3.5-7.0 |
|
2.0-4.0 |
|
|
0.04 |
10-14 |
Adequate |
5.0-14 |
2.4-2.7 |
2.8-10 |
0.9-1.5 |
0.7-2.0 |
0.2-1.5 |
16-54 |
High-toxic |
17-18 |
|
|
20-60 |
1.0-5.0 |
|
|
|
ppm dry weight |
ppm wet weight |