FAC29-30: Trace Elements Flashcards Preview

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Flashcards in FAC29-30: Trace Elements Deck (33):

What are the major elements for ruminants?









What are the trace elements for ruminants?









What are the various levels of trace element deficiency?

  1. Depletion: reduction in body stores
  2. Deficiency: subnormal concentrations
  3. Disorder/Dysfunction: malfunction of body processes (sub-clinical)
  4. 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



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?

  1. Selenium status
  2. Supply of other dietary anti-oxidants (primarily VitE)
  3. Supply of dietary oxidants (Polyunsaturated Fatty Acids)
  4. Generation of oxidants


Is there a correlation between selenium levels in soil and pasture and clinical disease?


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


What are the direct methods of treating selenium deficiency?

Oral compounds

  • Oral sodium selenate
  • Intra-ruminal boluses

Injectable compounds

  • Short-term supplementation
  • Long-term supplementation

Inclusion in compound feeds

Free-access minerals

Mediation of water supply


What are the indirect methods of treating selenium deficiency?

Application of selenium fertilizers to pasture


Can selenium/VitE supplementation pass through the placenta?


Supplementation of the dam's diet with selenium and VitE in late pregnancy will help to ensure good supplies to the newborn cal/lamb


Why is iodine important in the diet?

Iodine is essential as a constituent of the thyroid hormons


What is the cause of primary iodine deficiency?

Low iodine content in the soil and is associated with high rainfall


What is the cause of secondary iodine deficiency?

Due to goitrogens which act by disrupting the metabolism of iodine.

Deficiencies of other trace elements: selenium is required for the conversion of T4 to active T3

Environmental factors that increase the basal metabolic rate > increase in thyroid hormone production


What are the two main types of goitrogens?

Thiocyanate: act my impairing iodine uptake in the thyroid via competitive inhibition

Thiouracil: act by disrupting the iodination of thyroid hormones and prevent the conversion of inactive T4 to active T3


What are the direct methods of treating iodine deficiency?

Oral compounds

  • Oral iodine salts - potassium iodide
  • Intra-ruminal boluses

Painting of 5% tincture of iodine on the flank skin-fold once a week in cattle


  • Long-term supplementation of iodised poppy-seed oil

Inclusion in compound feeds

Free-access minerals

Medication of water supply


What are the indirect methods of treating iodine deficiency?

Application of iodine fertilizers to pasture (inefficient due to poor uptake by herbage)

Minimising effects of goitrogens

  • Thiocyanate: overcome with additional iodine
  • Thiouracil: cannot be overcome with additional iodine

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