Copper (Cu) Toxicity
What do you See?
- may not be apparent for some time that over consumption of copper is occurring
- sudden onset generally after a stressful event (transport, handling etc)
- signs include: rapid breathing, yellow tinge to skin and membranes; dark brown urine
- most affected sheep die
Cause/Transmission
- sheep are much more susceptible to copper toxicity than any other livestock species
- excessive intake of copper over a period of time causes a build up of copper in the liver
- liver reaches a maximum holding capacity (1-3 g of Cu/kg liver), may take 30-100 days
- as a result of stress, the liver suddenly releases stored copper resulting in the break down of red blood cells and jaundice
Treatment
- may not know until an animal dies; if diagnosed in post mortem as copper toxicity, treat flock to prevent more
- identify and remove the source of high Cu (cattle rations, high-Cu mineral mixes, licks, drenches, corroding Cu water pipes, Cu-contaminated pasture).
- add Cu-antagonists to the diet of the “at-risk groups” for 4-6 weeks. The best researched antagonists are Molybdenum (Mo), Sulfer (S), Zinc (Zn) and Iron (Fe) (veterinary prescription)
Prevention
- be aware of copper levels in supplements (don’t allow free access to supplements intended for other types of livestock)
- avoid using slurry from hog farms on fields used to produce feed for sheep (high in Cu)
- total Cu Intake by sheep should be no more than 8-15 mg Cu/kg feed dry matter basis; this can generally be supplied in the diet, without Cu added to a mineral supplement.
- have your feeds analyzed
- avoid using forages grown on fields fertilized with hog manure (often high Cu output). If this is unavoidable, have soil and feed tested for Cu
White Muscle Disease
What do you See?
- most often seen in newborn lambs, but may also occur in feeder lambs that have not grazed green forage for more than three months.
- depends on muscle groups affected may see: Stiff gait, difficulty getting up, unable to lift heads or suckle, rapid breathing, sudden death
- lambs are prone to starvation, pneumonia, diarrhoea
Cause/Transmission
- degenerative muscle disease
- deficiency of selenium (Se) interferes with the transport, storage, and usage of vitamin E in the body
- seen in areas that are deficient in Se in the soil and therefore in forage
Treatment
- injection of Se-tocopherol (Vit E)
- consult with veterinarian on specific product information
Prevention
- ensure ewes have sufficient Se in diet during pregnancy
- if soil is deficient (determine through feed analysis) provide commercial trace mineral mix with Se
- if ewes are not supplemented nutritionally, inject ewe and lamb after birth with Se/Vit E solution
Grass Tetany
What do you See?
- most often seen in ewes, 4-6 weeks after lambing
- relatively uncommon
- affects animals recently turned onto pasture
- animal is uncoordinated (staggers), muscle twitching, may have convulsions (legs remain rigid)
Cause/Transmission
- deficiency of magnesium (Mg), and possibly calcium (Ca), and high potassium (K) levels
- some areas are naturally low in Mg, therefore decreased in forages
- heavy applications of nitrogen also interferes with plant ability to take up Mg
- lush grass forage may also decrease Mg absorption by animal
- also considered a metabolic disorder
Treatment
- emergency treatment with Mg and Ca solutions (consult your vet)
- recovery occurs quickly if treated in time
Prevention
- if it is a problem test soil and forages for Mg content
- consider legume/grass combination for pastures (legumes convert nitrogen and provide higher mineral levels)
- soils with low Mg can be upgraded by application of limestone or supplement animal’s diet
- apply fertilizer at recommended levels
