COPPER DEFICIENCY IN DEER
Jeff Fyffe BVSc MRCVS MACVSc
OVERVIEW
Copper is one of the most significant elements in body function being involved in at least 10 enzymes. These effect bone and connective tissue development, maintenance of nervous tissue, pigment, red and white cell development and overall growth. It is also implicated in reproductive performance.
Copper deficiency in ruminants may be primary or secondary.
Primary copper deficiency results from dietary inadequacy.
Secondary copper deficiency occurs in the face of apparently adequate dietary levels with a variety of conditioning factors. The most common conditioning factor is a dietary excess of molybdenum; however zinc, iron, lead and calcium carbonate are also considered to be conditioning agents. Dietary excess of molybdenum, sulphur and iron has been clearly identified as suppressants of copper uptake in ruminants.
The relationship between sulphur and molybdenum levels and the effect on copper absorption is complex and has been the basis for many livestock experiments. In certain instances, ruminants with excess dietary sulphur in the presence of low molybdenum intake, will have reduced copper absorption.
The complexity of ruminant copper-molybdenum-sulphur (Cu-Mo-S) metabolism with the example of secondary copper deficiency in sheep on elevated sulphate diets. In that species an increase in sulphate concentration from 0.1 to 0.4% can potentiate a molybdenum content as low as 2 mg/kg to reduce copper intake below normal levels.
The critical copper:molybdenum ratio in animal feeds is 2:1.
In beef cattle the sulphur requirement of feed is 1.0 g/kg.
The metabolism of copper in deer differs from other ruminants.
This is typified at least, by the marked variation in the onset of enzootic ataxia in deer compared with sheep. It is therefore difficult to extrapolate the known effects of Cu-Mo-S metabolism in other ruminants to deer.
The daily dietary copper requirements and many aspects of copper metabolism in deer are not known.
Secondary copper deficiency in deer can be induced by the wrong combinations of feed or incorrect feeding methods.
Lupin grain is high in Molybdenum while Lucerne is high in Sulphur. The combination can have a depressing effect on the absorption of Copper. In addition feeding on the ground rather than in troughs, will lead to the ingestion of soil and hence iron which will further depress copper absorption.
THE DISEASE IN DEER
Enzootic Ataxia
Arthritis
Steely Coats
Reduced Fertility
Reduced Velvet Production
The deer foetus is unlike any other ruminant foetus in that it can selectively remove Copper from it's mother for it's own benefit.
Consequently deer calves/fawns are born with high levels of liver copper.
Lambs, by comparison, cannot do this, and if their mothers have low copper levels, they will be born with low copper levels.
1. Enzootic Ataxia
This is a sporadic disease caused generally by PRIMARY copper deficiency in calves after birth.
Unlike sheep, the condition is not seen until deer are about 9 to 12 months of age.
The symptoms are typically an inco-ordination of the hind limbs which is due to disruption of the nerve cells in the spinal cord.
There is no cure.
2. Arthritis
Particularly of hip and hock joints.
Same age group affected but there is degeneration of the joints with enlargement of the hock joints particularly.
Principally a PRIMARY copper deficiency.
There is no cure.
3. Steely Coats
Seen particularly in winter when feed is in short supply and stock are feeding off the ground. This leads to excessive iron intake.
This is mostly a SECONDARY copper deficiency.
The coat is harsh and breaks off readily leaving bald areas that turn black.
Treatment is by supplementary copper administration.
4. Reduced Fertility
A very difficult condition to quantify but in AI programs, hinds that have been on copper treatment seem to cycle better than those that have not been supplemented.
5. Reduced Velvet Production
Another condition difficult to quantify.
Some reports from New Zealand indicate an improvement in velvet production after copper treatment.
I find stags that have been supplemented cast earlier and cut earlier than un-supplemented stags.
Diagnosis
The best diagnosis is based on the levels of copper in the liver. For practical purposes blood copper levels are used. It is necessary to test 10 deer from a herd before an accurate assessment can be made.
Prevention
Copper bullets, copper sulphate in the drinking water or pasture top-dressing.
--------------------------------------------------------------------------------
http://www.diaa.org/copper.htm
Jeff Fyffe BVSc MRCVS MACVSc
OVERVIEW
Copper is one of the most significant elements in body function being involved in at least 10 enzymes. These effect bone and connective tissue development, maintenance of nervous tissue, pigment, red and white cell development and overall growth. It is also implicated in reproductive performance.
Copper deficiency in ruminants may be primary or secondary.
Primary copper deficiency results from dietary inadequacy.
Secondary copper deficiency occurs in the face of apparently adequate dietary levels with a variety of conditioning factors. The most common conditioning factor is a dietary excess of molybdenum; however zinc, iron, lead and calcium carbonate are also considered to be conditioning agents. Dietary excess of molybdenum, sulphur and iron has been clearly identified as suppressants of copper uptake in ruminants.
The relationship between sulphur and molybdenum levels and the effect on copper absorption is complex and has been the basis for many livestock experiments. In certain instances, ruminants with excess dietary sulphur in the presence of low molybdenum intake, will have reduced copper absorption.
The complexity of ruminant copper-molybdenum-sulphur (Cu-Mo-S) metabolism with the example of secondary copper deficiency in sheep on elevated sulphate diets. In that species an increase in sulphate concentration from 0.1 to 0.4% can potentiate a molybdenum content as low as 2 mg/kg to reduce copper intake below normal levels.
The critical copper:molybdenum ratio in animal feeds is 2:1.
In beef cattle the sulphur requirement of feed is 1.0 g/kg.
The metabolism of copper in deer differs from other ruminants.
This is typified at least, by the marked variation in the onset of enzootic ataxia in deer compared with sheep. It is therefore difficult to extrapolate the known effects of Cu-Mo-S metabolism in other ruminants to deer.
The daily dietary copper requirements and many aspects of copper metabolism in deer are not known.
Secondary copper deficiency in deer can be induced by the wrong combinations of feed or incorrect feeding methods.
Lupin grain is high in Molybdenum while Lucerne is high in Sulphur. The combination can have a depressing effect on the absorption of Copper. In addition feeding on the ground rather than in troughs, will lead to the ingestion of soil and hence iron which will further depress copper absorption.
THE DISEASE IN DEER
Enzootic Ataxia
Arthritis
Steely Coats
Reduced Fertility
Reduced Velvet Production
The deer foetus is unlike any other ruminant foetus in that it can selectively remove Copper from it's mother for it's own benefit.
Consequently deer calves/fawns are born with high levels of liver copper.
Lambs, by comparison, cannot do this, and if their mothers have low copper levels, they will be born with low copper levels.
1. Enzootic Ataxia
This is a sporadic disease caused generally by PRIMARY copper deficiency in calves after birth.
Unlike sheep, the condition is not seen until deer are about 9 to 12 months of age.
The symptoms are typically an inco-ordination of the hind limbs which is due to disruption of the nerve cells in the spinal cord.
There is no cure.
2. Arthritis
Particularly of hip and hock joints.
Same age group affected but there is degeneration of the joints with enlargement of the hock joints particularly.
Principally a PRIMARY copper deficiency.
There is no cure.
3. Steely Coats
Seen particularly in winter when feed is in short supply and stock are feeding off the ground. This leads to excessive iron intake.
This is mostly a SECONDARY copper deficiency.
The coat is harsh and breaks off readily leaving bald areas that turn black.
Treatment is by supplementary copper administration.
4. Reduced Fertility
A very difficult condition to quantify but in AI programs, hinds that have been on copper treatment seem to cycle better than those that have not been supplemented.
5. Reduced Velvet Production
Another condition difficult to quantify.
Some reports from New Zealand indicate an improvement in velvet production after copper treatment.
I find stags that have been supplemented cast earlier and cut earlier than un-supplemented stags.
Diagnosis
The best diagnosis is based on the levels of copper in the liver. For practical purposes blood copper levels are used. It is necessary to test 10 deer from a herd before an accurate assessment can be made.
Prevention
Copper bullets, copper sulphate in the drinking water or pasture top-dressing.
--------------------------------------------------------------------------------
http://www.diaa.org/copper.htm
