CAL: Trace elements

Question 1

Describe Se levels in UK soil

Answer 1

Generally deficient (soil originated from granite and volcanic rocks)

Question 2

Why are most cases of Cu deficiency secondary diseases?

Answer 2

In the rumen, molybdenum, sulphur or iron can bind with copper making it unavailable to the animal.

Question 3

Why is Cu important to animals? 4

Answer 3

involved in enzymes associated with myelin formation, erythropoiesis, collagen synthesis and pigmentation

Question 4

Clinical signs - Cu deficiency

Answer 4

Swayback and hindlimb dysfunction (poor myelination of terminal spinal cord nerves)
Anaemia and lethargy (interrupted RBC formation)
Bone and CT abnormalities and spontaneous fractures (severe)
Unusual skin pigmentation, lightening of hair coat in dark coloured cattle
Poor thrift (young growing cattle)
Diarrhoea
Decreased milk yield in dairy (scant evidence)
Reduced fertility (cattle)

Question 5

How do you administer cobalt/vitamin B12 to sheep? 2

Answer 5

Oral drench - cobalt
SC or IM injection - vitamin B12
Intra-ruminal bolus - cobalt

Question 6

Clinical signs - Selenium/vitamin E deficiency - 4

Answer 6

White Muscle Diseases (WMD, classic sign, due to muscle cell necrosis, striated muscle cells are particularly susceptible to damage)
Neurological signs
Locomotor abnormalities (stiffness-recumbency)
Alimentary signs (indirect, inability to feed)
Poor growth rates (sheep and cattle, autumn)
Poor reproductive performance (sheep, possibly cattle, due to early embryonic loss)
Increased disease susceptibility and SCC levels (due to role in immune function, inconsistencies in evidence)

Question 7

What does Se/vit E normally do in an animal?

Answer 7

Antioxidant function - protect cells against free radicals and lipid peroxidases

Question 8

Which species/breeds are susceptible to copper deficiency?

Answer 8

Cattle and deer most commonly

Sheep rarely but breed variation (Scottish Blackface > Texel)

Question 9

Which species/breeds are susceptible to Se/Vit E deficiency?

Answer 9

All species are equally susceptible

Question 10

Which species/breeds are susceptible to cobalt deficiency?

Answer 10

Sheep most susceptible

Rare in cattle

Question 11

Which TE is most associated with poor thrift?

Answer 11

Cobalt deficiency. That said, poor thrift associated with TE deficiency is often multi-factorial and poor nutrition and/or parasitism are also important contributors

Question 12

Signs - cobalt deficiency

Answer 12

Poor thrift

Question 13

2 types of swayback = ?

Answer 13

Congenital - newborn lambs, recumbent, tremors, poor coordination

Delayed/ enzootic ataxia - 2-4 month old lambs, certain sheep breeds, well-defined geographic areas, presents as progressive weakness of hindlimbs

Question 14

When can WMD affect lambs?

Answer 14

Congenital - affected lambs are often stillborn or die soon after birth, typically it affects lambs at 2-6 weeks of age. Affected lambs have a sudden onset of stiffness progressing to recumbency

Question 15

Which TE(s) have been associated with lameness/gait abnormalities?

Answer 15

Copper (swayback)

Se/Vit E (WMD)

Question 16

Which TE(s) have been associated with possible reduced fertility?

Answer 16

Cu - weak evidence
Co - may not be a direct effect, rather poor ewe BCS
Se/VitE - early embryonic loss, evidence inconsistencies

Question 17

Which TE(s) have been associated with possible increased disease susceptibility?

Answer 17

Se/Vit E

Question 18

Which TE(s) have been associated with poor thrift?

Answer 18

Cu
Co - lambs, not adult cattle
Se/Vit E

Question 19

Which TE(s) have been associated with recumbency?

Answer 19

Cu - swayback

Se/Vit E - WMD

Question 20

How can the dietary status of sheep be assessed?

Answer 20

Compare the composition of forage/ration with somewhat arbitrary figure:
single figure ‘requirements’ (Co, Fe and Mn)
Expansive theoretical requirements (Cu, Se and Zn)

Question 21

Why do TE demands rise in small, out-wintered lambs by up to 30%

Answer 21

when ewes mobilise body fat to meet energy deficits, there is meagre TE release from adipose tissue

Question 22

Why don’t you test plants for TE levels and animals instead?

Answer 22

TE level vary markedly depending on:
plant type
part of plant
where in field it is growing
season
level of soil contamination

animal absorption of TE will vary
Requirements vary with age and physiological status

Question 23

How do you assess Se levels?

Answer 23

Small number (3) of blood samples
Blood or serum Se or glutathione peroxidase can be analysed
No body store
Little variation in animals grazing same pasture/forage

Question 24

How do you assess Cu levels?

Answer 24

Stored in liver
Much variation (especially if deficient)
Take as many liver samples as possible (can be difficult so testing blood samples may be valuable to confirm clinical deficiency. For economic reasons, usually limited to 5-7 samples.)
Adequate level (cattle) is >95 micromol/kg)

Question 25

How do you assess Vitamin B12/Co levels?

Answer 25

No real store so test blood

Moderate degree of variation so take 10 samples, can get expensive so people tend to test 6-7 to reduce cost.

Question 26

How do you interpret TE levels?

Answer 26

Not alone - in the light of history and clinical findings (especially poor thrift)

Also, even if an animal TE level falls into the marginal or low categories, it doesn’t mean there will be an economic response to supplementation.

Especially in cases of poor thrift, treatment/control trials are excellent in determining whether the TE levels are limiting impact on weight gain and response to supplementation Biologically sensible period of at least 8 weeks to allow any differences in weight gain to become apparent.

Question 27

Which TEs can cause death if given in an overdose?

Answer 27

Cu - toxicity more common than deficiency in sheep. Overdose causes RBC lysis and acute/sub-acute/chronic death.

Co/Vit B12 - no reported toxicity but not desirable to be overdosed

Se - very toxic with overdose and leads to rapid death.