FAC29-30: Trace Elements Flashcards
What are the major elements for ruminants?
Calcium
Magnesium
Phosphorous
Potassium
Sodium
Chloride
Sulphur
What are the trace elements for ruminants?
Copper
Cobalt
Selenium
Iodine
Iron
Zinc
Manganese
What are the various levels of trace element deficiency?
- Depletion: reduction in body stores
- Deficiency: subnormal concentrations
- Disorder/Dysfunction: malfunction of body processes (sub-clinical)
- Disease: presence of clinical disease
Define primary trace element deficiency.
Define secondary.
Primary: Levels of mineral in the diet are inadequate
Secondary: levels of mineral in the diet are normal but absorption and uptake from the diet are indequate
What are the direct methods for correcting a trace element deficiency?
- Inclusion of element in compound feeds
- Free-access minerals
- Medication of water supply
- Oral compounds
- Injectable compounds
What are the indirect methods for correcting a trace element deficiency?
Application of fertilisers to pasture
Minimising antagonists
Genetic selection
What are the factors that influence the absorption of dietary copper?
Sulpher: sulphur is converted to sulphides in the rumen, which then reacts with copper to form insoluble copper sulphide (CuS)
Molybdenum: reacts with sulphur in the rumen to form thiomolybdate, which irreversibly binds copper and prevent its absorption
Iron: iron can form insoluble compounds with copper or combine with sulphides to for FeS, which then binds copper
Differences between feedstuffs
Intercurrent disease
Genetics
How is copper metabolised?
Liver is the major organ for storage
Caeruloplasmin is the major transport protein for copper
How do you treat sheep with copper deficiency?
Sheep are highly susceptible to copper poisoning. Therefore, supplementation should only be given to sheep if the clincial disease has been previously diagnosed, and hypocuprosis has been confirmed.
What oral compounds can be used to treat copper deficiency?
Oral copper sulphate: prior to lambing to prevent swayback
Copper oxide needles: lodges in abomasum to give slow-release copper 2-3 months
Intra-ruminal boluses: Slow release copper for 6 months
What are the direct methods of treating copper deficiency?
Oral compounds
Injectable compounds
Inclusion in compound feeds
Free-access mineral
Medication of water supply
What are the indirect methods of treating copper deficiency?
Application of mineral fertilizers to pasture
Minimising molybdenum and iron intakes
Genetic selection
How do you treat and prevent swayback in sheep?
- It may be worth treating mildly affected lambs to stop progression of the disease using very small doses of copper
- All remaining pregnant ewes should be given copper and all surviving lambs born out of pregnant ewes that have not been given copper should be dosed to prevent cases of delayed swayback
Prevention in subsequent years:
- House sheep during last 6-8 weeks of pregnancy
- Provision of supplementary feeding during late pregnancy
- Copper supplementation of sheep in early pregnancy (using one method only)
Why is cobalt important in the diet?
Cobalt is required for the manufacture of VitB12, which is required for:
Propionate metabolism: glucose metabolism and energy balance
One-carbon metabolism: building carbon chains
Why is cobalt deficiency not seen in suckling ruminants?
They have low requirements (since they rely on glucose as their main energy source)
VitB12 concentrations in milk are high and so deficiency does not tend to occur in suckling animals unless the mothers are deficient in cobalt
What are the direct methods of treating cobalt deficiency?
- Oral compounds: oral drenching with cobalt sulphate, intra-ruminal boluses
- Injectable compounds: short- and long-term supplementation
- Inclusion in compound feeds
- Free-access minerals
- Mediation of water supply
What are the indirect methods of treating cobalt deficiency?
Application of cobalt fertilizers to pasture
Why are selenium and VitE important in the diet?
They are antioxidants that help protect cells against damage by lipid peroxidases and free radicals. Failure leads to membrane damage and tissue necrosis.
What impacts the occurrence of clinical disease caused by anti-oxidant deficiencies?
- Selenium status
- Supply of other dietary anti-oxidants (primarily VitE)
- Supply of dietary oxidants (Polyunsaturated Fatty Acids)
- Generation of oxidants
Is there a correlation between selenium levels in soil and pasture and clinical disease?
Yes!
Low soil selenium, low pasture selenium, and clinical disease are well correlated
Where is VitE obtained in the diet?
VitE is synthesized by plants and levels are high in green pastures. However, levels decline rapidly during long-term storage, and it is destroyed by various treatment methods (addition of alkali)
What is another name for nutritional muscular dystrophy?
White muscle Disease
What biochemical indicators help diagnose white muscle disease?
Indicators of muscle damage: Creatine kinase (CK), AST
What is the standard biochemical test for selenium deficiency?
Glutathione peroxidase in blood - GSHPx is a selenium-containing enzyme and is the standard biochemical test for selenium deficiency.
Reflects long-term selenium status
