Trace Element Deficiencies Flashcards

1
Q

What are “trace elements

A
  • we will need this in micrograms per day (so they are easy to miss and are poorly defined!)
  • trying to get farmers to feed on grass, should be the major constituent of the diet
  • Mg, Fe are also potential issues but these are the big 4
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2
Q

Challenges with Trace Elements

A
  • worry about how it integrates into nutrition
  • Every farm has a deficiency in calories (so you need to incorporate this deficiency into your plan)
  • production values will be more helpful to monitor changes than biochemistry
  • can still use but it really isnt that effective
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3
Q

TE Deficiency Occurrence

A
  • Up north, having an issue with Cobalt not being in the soil and plant that are inedble extracting it out?
  • some animals will show deficiency and struggle and some will not (animals can adapt to lower levels)
  • You can’t use reference ranges for these really, just a measure of returning to good performance
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4
Q
A
  • really a slow progression from one end to the other
  • before they get to the point where they are showing clinical signs, they are in marginal status where performance is lowering
  • may be coping with the deficiency and you can return them to performance with the slightest change
  • boluses - can be $$ and bring them to a slightly lower than ideal function (bring lab results up), concern is where they go down that curve towards clinical
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5
Q
A
  • Contamination of soil can be a good thing, but normally not (echo)
  • short plants will have different nutrition compared to a long/stemmed plant that is close to head
  • animals will want to eat the tasty part!
  • uneven distribution over field in type and growth stage
  • this can all lead to disease
  • you don’t need to figure this out, the animal already has so YOU test the animal!
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6
Q

Cobalt

(Co)

A
  • can supplement by throwing in soil, but is not recommended
  • really looking at the upland hills for this deficiency
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7
Q

Cobalt

(Clinical Features)

A
  • sheep are more prone than cattle in the TE deficicencies
  • roundworms will hinder the absorption of cobalt
  • poor group of animals that are doing as well as they should be basically
  • not growing well
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8
Q
A
  • open bones on some of the severe ones, can see anemia in some cases
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9
Q

Selenium/Vit E

A
  • if deficient–> immunosupressed
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10
Q

Selenium/Vitamin E

(clinical features)

A
  • rather dull/depressed
  • usually come across it post birth
    *
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11
Q
A
  • sit around, dont want to get up
  • GIve a dose of Sel/Vit E they jump up
  • echo
  • PME will show pale white muscle back
  • you will see a distinct change in muscle color from white to red (they do not work properly, cant stand)
  • As it gets more severe, diaphragm gets compromised
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12
Q
A
  • Sel/Vit E deficiency
  • slowed growth rates
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13
Q

Copper

(Cu)

A
  • wil get walking difficulties
  • coat color changes
  • gait abnormalitites
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14
Q

Copper

(Clinical Features)

A
  • Everything is going to cause poor thrift (pattern)
  • If Cu deficiency is in the ewe itself, you get this sway back disease
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15
Q

Appearance of Cu Deficiency

A
  • rings around the eyes (severish Cu def. -tyrosine kinase causing it?)
  • 15 mo old heifer with mates that are just not growing well
  • there are not many calories on that field! - this animal needs food- this cannot be fixed by just pumping in Cu to this animal
  • need to think about whole system
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16
Q
A
  • see in deer
  • changes in bone formation
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17
Q

Iodine

A
  • goitre- thyroid glands are trying to compensate for lack and therefore the glands swell
  • weak lambs that do not survive past a few days no matter how much effort or colostrum given
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18
Q

Common clinical pictures

A
  • if seeing more than one animal affected, definitely start thinking of this as an option!
  • If the farm has had a history or is in a known area of deficiency
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19
Q

Common clinical pictures:

Poor Growth of Young Animals

A
  • sheep usually get copper toxicity than deficiency as they pull it effectivey from the diet
  • If you are a young growing lamb, you need it more than an adult just trying to maintain itself
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20
Q

Common clinical pictures:

Gait abnormalities

A
  • much less common than your ill thrift
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21
Q
A
  • hypertrophy of glands to compensate for iodine deficiency
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22
Q

Diagnosis of TE deficiency

A
  • dont just throw a multi trace bolus at them!
  • blood sample the animals - as they have decided what they are going to have on board in terms of what trace elements they are taking in
  • TEST THE ANIMAL
  • for copper deficiency, take a sample from liver often (either live, PME, slaughter)
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23
Q
A
  • No storage site for Co, Se? (echo)
  • If there is a very varied level of what is needed in the herd, then take more samples
  • few samples –> would be about 5
  • more–> would be about 12
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24
Q

Liver Collection

A
  • may not be the most effective way to determine it
  • suggest taking liver samples only when you can
  • can take it blindly if you know your anatomy well enough OR contact the abattoir (get the liver samples)
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25
Q

Diagnosis of TE deficiency

Treatment/control trial

(esp Co)

A
  • This will tell you what the animal holds in its system

-is there a deficiency?

  • cant really know, need to make an evidence based judgement
  • do a treamtent to control trial
  • how much improvement is that intervention actually making?
  • Take the data that is important ( lambs–> weight gain) - differences in weight gains between two groups and what is the actual difference (gives you extra pounds of meat per animal against the cost of the bolus)
  • about 6 or 7 gbp a bolus
  • echo
  • not all about changing the biochemistry values
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26
Q

Supplementation

A
  • If putting a supplementation programme in place, monitor effectiveness
  • usually want to make sure that every single animal is getting this supplementation
  • rain may wash this off the field if attempted to be given this way
  • even incorporating into the feed, there are some that will not come up to the trough
  • be aware of overdosing toxicities!
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27
Q

Ensuring sufficiency vs. diagnosing deficiency

A
  • could be monitoring weight gains
  • supplementation trial (animals unsupplemented/supplemented –> lamb percentages, slaughter weight)
  • can look at bloods, but keep in mind what the goal of the farm is!
  • you may need to work up to showing that the supplementation is what they need rather than just throwing it at them
  • also think geographically and known deficiencies!
28
Q

Use and abuse of TE analysis

A
  • make sure the economic response is there (at least 7 or 8 gbp per head back for the farmer)
  • make the investment worth it!!
29
Q

Summary Points

A
30
Q

Animal Requirements for Trace Elements

A
31
Q

Primary trace Element Deficiency

A
  • a lack of TE in the soil
32
Q

Secondary Trace Element Deficiency

A
  • soil levels of copper may be adequate but secondary interactions occur within the animal.
  • For example in the rumen, molybdenum, sulphur or iron can bind with copper making it unavailable to the animal
33
Q

Copper

A

Copper deficiency can be due to either a primary or secondary deficiency. The on-farm incidence can vary from year to year because copper availability to the animal is affected by:

  • Age of animal
  • Pasture composition and time of year (e.g. copper absorption is higher from summer pasture than autumn pasture, or from hay compared to silage)
  • Genetic influence – particularly in sheep due to the ability to absorb and store copper.
  • Molybdenum, sulphur and iron – bind to copper in the rumen making it unavailable to the animal.

Copper is an essential part of many enzyme systems in the body. For example it is involved in enzymes associated with myelin formation, erythropoiesis, collagen synthesis and pigmentation.

34
Q

Based on the body functions which copper-containing enzymes are involved in, list the body systems you would expect to be affected by copper deficiency.

(Also list some possible clinical signs)

A
  • Myelin formation - will affect the nervous system. Associated clinical signs might include nerve dysfunction. Indeed, “swayback” or hindlimb dysfunction is associated with copper deficiency because the nerves of the terminal spinal cord are inadequately myelinated.
  • Erythropoiesis – will affect the haematogenous system. Associated clinical signs could include anaemia and lethargy.
  • Collagen synthesis – will affect the locomotor system. Associated clinical signs could include abnormalities of bones and connective tissue. Indeed, spontaneous bone fractures are associated with severe copper deficiency.
  • Pigmentation – will affect the skin. Associated clinical signs could include unusual pigmentation. Indeed, lightening of the hair coat in dark coloured cattle is associated with copper deficiency (but can also occur in other conditions).
35
Q

Cobalt

A
  • Cobalt is an essential component of Vitamin B12.
  • Vitamin B12 is an essential part of an enzyme involved in the propionate to glucose pathway.
  • In ruminants carbohydrates are converted to 3 different volatile fatty acids, of which propionate is one, by microbes in the rumen. Propionate is converted to methyl-malonate and then to succinate via Vitamin B12-dependant enzymes. Succinate can enter the TCA cycle and function as a source of glucose.
  • Propionate is the ONLY direct source of glucose available to ruminants so cobalt deficiency effectively results in starvation
  • rumen microbes synthesise Vitamin B12, incorporating cobalt into it as they do so. The Vitamin B12 then enters the circulation. Hence in ruminants the blood/tissue levels of Vitamin B12 are analysed rather than the levels of cobalt.
36
Q

When supplementing sheep with cobalt deficiency by the following methods of administration, would you supplement with cobalt or with Vitamin B12?

Intra-ruminal bolus?

oral drench?

SC or IM injection?

A
  • Intra-ruminal bolus → Cobalt
  • Oral drench → Cobalt
  • SC or IM injection → Vitamin B12

Rumen microbes incorporate cobalt into Vitamin B12 so if supplementation is via the oral/GI route then cobalt should be provided.

With an injectable supplement, because the supplement is going directly into the circulatory system Vitamin B12 must be given.

37
Q

Selenium/Vitamin E

A
  • Selenium/Vitamin E have antioxidant effects to help protect cells against free radicals and lipid peroxidases.
  • If unchecked these can damage cell membranes and cause tissue necrosis.
  • Striated muscle cells are particularly susceptible to damage.
  • White muscle disease (WMD) is the ‘classic’ clinical presentation of selenium/Vit E deficiency and is the result of muscle cell necrosis. A wide range of other production issues have been associated with sub-clinical selenium/Vit E deficiency.
38
Q

What clinical signs could be associated with white muscle disease (WMD)?

A
  • Death

Animals born with congenital WMD may be still-born, or die soon after birth from starvation. If the heart muscle is affected rapid death can occur.

  • Locomotor abnormalities

WMD results in damage to skeletal muscles which results in locomotor abnormalities ranging from stiffness to recumbency

  • Respiratory difficulty

In some cases of WMD the skeletal muscle of the diaphragm may be affected, which may result in respiratory difficulty (although this is uncommon).

  • A range of other functions of selenium/Vit E are also postulated such as contribution to immune function

The following clinical signs are not associated with white muscle disease (WMD):

  • Neurological signs

WMD affects muscle cells. The nervous system is not affected.

  • Alimentary signs

WMD affects striated muscles cells not the smooth muscle cells of the gut. However, often animals with WMD cannot feed due to their locomotor abnormalities.

39
Q

Thought to play an important role in immune function

TE?

A

Selenium/Vit E

40
Q

An essential part of an enzyme involved in metabolism

TE?

A

Cobalt

41
Q

An essential part of an enzyme involved in collagen synthesis

TE?

A
  • Copper
42
Q

An essential part of an enzyme involved in myelin formation

TE?

A
  • Copper
43
Q

Protects cells against free radicals and lipid peroxidases

TE?

A

Selenium/Vit E

44
Q

Clinical Cases with TE deficiencies

A
  • the clinical signs associated with TE deficiencies are often vague and similar to those caused by other diseases.
  • However it should also be noted that the risk factors for TE deficiencies are now well defined and clinical deficiency is uncommon – e.g. if the clinical scenario is suggestive consider TE deficiencies but do not restrict your investigation solely to these!
45
Q

Species predilections for TE deficiencies

(4)

A
  • Cattle and deer are the most susceptible species to copper deficiency. Deficiency in sheep is rare although there is a large breed variation in susceptibility e.g. Scottish Blackface are far more susceptible than Texel.
  • Sheep are the most susceptible species to cobalt deficiency; their cobalt requirements are higher than those of cattle.
  • Cobalt/vit B12 supplements are rarely required in cattle.
  • All species are equally susceptible to selenium/Vit E deficiency
46
Q

TE Deficiency and Poor Thrift

A
  • Poor production or poor thrift is a common clinical scenario in livestock and can be due to a variety of causes.
  • Cobalt deficiency is the TE most frequently associated with poor thrift for the reasons outlined in the “Animal requirements for trace elements” section
  • Copper deficiency can result in poor thrift, particularly in young growing cattle. It is often associated with diarrhoea, and poor coat pigmentation in dark-coloured cattle. However, note that cattle can have poor thrift, diarrhoea and poor coat colour in association with other diseases as well, e.g. under-nutrition and parasitism!
  • Sub-clinical selenium deficiency can result in poor growth rates of sheep and cattle; this is most commonly seen in autumn.

Note – “poor thrift” associated with trace element deficiency is often multi-factorial and often poor nutrition and/or parasitism are also important contributors to the problem

47
Q

Locomotor abnormalities: “Swayback”

A
  • “Swayback” is seen either in newborn lambs (congenital swayback) or in lambs 2-4 months of age (delayed swayback a.k.a. enzootic ataxia) and is due to copper deficiency in the pregnant ewe or growing lamb.
  • It occurs in certain sheep breeds in well-defined geographic areas.
  • In the congenital form, lambs may be recumbent or have poor coordination and tremors.
  • The delayed form presents as a progressive weakness of the hindlimbs.
  • Adult deer can also develop swayback associated with copper deficiency
48
Q

Locomotor abnormalities: Copper

A
  • Copper is involved in collagen synthesis and bone fragility with spontaneous limb fractures has been reported in some countries associated with copper deficiency.
49
Q

Locomotor abnormalities:

White Muscle Disease

(WMD)

A
  • White muscle disease (WMD) due to selenium/Vit E deficiency results in necrosis of skeletal muscles and associated clinical signs.
  • In the UK it can present either as congenital WMD – affected lambs are often stillborn or die soon after birth – or more typically it affects 2-6 week-old lambs.
  • Affected lambs have a sudden onset of stiffness progressing to recumbency. WMD is rarely seen now in the UK due to knowledge of the risk factors and use of supplementation.
50
Q

Cu Deficiency –> Milk Yield/fertility

A
  • Copper deficiency – has been linked to decreased milk yield in dairy cows although the scientific evidence is scant.
  • It has also been linked to reduced fertility in cattle
51
Q

Selenium/Vit E Deficiency

(Reproductive Rates/Immunity)

A
  • has been associated with poor reproductive performance in sheep and possibly cattle due to early embryonic loss.
  • Se/Vit E are thought to play a role in immune function and has been linked to susceptibility to disease and somatic cell count levels. Some of the scientific evidence for these is inconsistent
52
Q

What TE would lead to:

lameness/gait abnormalites?

Possibly reduced fertility?

recumbency?

Possibly increased susceptibility to disease?

Poor thrift / poor weight gain?

A
53
Q
A
54
Q
A
55
Q
A
56
Q

When assessing the needs of sheep (or other grazing livestock) for trace elements, why is it preferable to test the levels in the animal rather than the levels within the plants fed to the sheep?

A
  • Trace element levels within plants can vary markedly depending on the type of plant, which part of the plant is tested, where in the field it is growing, the season and the level of soil contamination.
  • Also, the absorption of trace element by the animal will vary.
  • Finally, the actual requirements of the animal will vary according to physiological status and age. Thus the animals themselves should be tested
57
Q

Evaluating Iodine levels in grazing animals

A
  • Note that there are currently no reliable laboratory tests to evaluate iodine status in grazing animals
58
Q

Which samples would be most appropriate to collect to assess selenium levels?

A

There is no store of Se in the body and there is very little variation in levels between animals grazing the same pasture or forage. Hence a small number of blood samples are all that is required. Either blood or serum Se, or Glutathione peroxidise (GPx-1) can be analysed.

The correct answer is: 3 blood samples (rather than 10)

59
Q

Which samples would be most appropriate to collect to assess copper levels?

A

Copper is stored in the liver so this is the best sample to test, if possible.

  • This is particularly the case if animals are in the depletion/deficiency phase e.g. before disorder occurs.
  • However, obtaining liver can be difficult and testing blood samples may be of value to confirm clinical deficiency.
  • As there is large variation in copper levels of animals in the same group it is ideal to test as many as possible but economic considerations mean it is usually limited to 5-7 samples.

The correct answer is: 7 liver samples

60
Q

Variation in liver copper levels in a herd of grazing beef suckler cows

A
  • 7 cows out of a herd of 80 were liver biopsied and the liver analysed for copper levels. The group mean liver copper value was 91.6μmol/kg liver (reference range for adequate levels is >95 μmol/kg).
  • Individual cow liver copper levels were: 28.2, 38.0, 43.6, 51.4, 94.2, 103.0, 282.6.
  • If only 3 samples were collected and by chance the last cow in this sequence was included as one of the three, think how this would change the interpretation of the results.
61
Q

Which samples would be most appropriate to collect to assess Vitamin B12 (cobalt) levels?

A
  • There is no real store of Vitamin B12 in the body so it is most cost-effective to test the blood. As there is moderate variation in Vit B12 levels between animals it is best to sample 10 animals although this can get expensive! Some people only test 6-7 to reduce the cost.
  • The correct answer is: 10 blood samples
62
Q

Treatment and control trials for evaluating trace element deficiencies

A
  • It is important to recognise that published reference ranges for ‘low’, ‘marginal’ and ‘adequate’ levels of trace elements need to be interpreted with caution and ALWAYS in light of the history and clinical findings.
  • Particularly in the situation of poor thrift / poor weight gain, which is a vague and often multi-factorial condition, animal TE levels do not always give a good ‘feel’ for how much of a contributor the TE deficiency was. Further, even if animal TE levels fall into the ‘marginal’ or ‘low’ categories it does not mean there will be an economic response to supplementation.
  • Particularly in the case of poor thrift, treatment/control trials are an excellent option for determining whether the TE levels are limiting, how much of an impact they are having on weight gain and whether there is likely to be an economic response to supplementation.
63
Q

Imagine you have a sheep-farming client with 500 six-month-old wether lambs being finished for slaughter. Their growth rates have been sub-optimal and as part of your investigation you have established that the mean serum vitamin B12 levels fall in the ‘marginal’ range. The farmer is keen to know whether supplementation is going to be worthwhile and wants you to help her design a trial to test this. In the text box below briefly outline how you would design your trial.

A
  • Animals – Use all 500 lambs: 2 groups of 250 - one group will be treated and the other will not (control). Or could use a smaller number of lambs in the control group. Make sure the separate groups are clearly identified!
  • Trial period – it needs to run for a biologically sensible period of time to allow any differences in weight gain to become apparent. At least 8 weeks.
  • Supplementation – supplement the treatment group with a supplement that is known to increase Vitamin B12 levels – ensure animals are suitably supplemented for the entire trial period.
  • Data recording – weigh lambs on Day 0 and then at regular intervals for the trial period. Could individually ID lambs and record individual weights (time-consuming but ideal), or weigh all lambs without individual ID and compare mean weights.
  • Lamb management – need to graze the group together so no nutritional differences. Aim for good husbandry e.g. worm control. Any treatments given (apart for Vit B12 supplementation) must be the same for both groups!
64
Q

Which trace elements can cause rapid death if given in overdose?

A

Copper

  • Copper is very toxic in overdose and toxicity is a relatively common condition particularly in sheep. It is often stated that in the UK copper toxicity of sheep is a more commonly diagnosed condition than copper deficiency in sheep. Overdose results in lysis of red blood cells and acute, sub-acute or chronic death.

Selenium

  • Selenium is very toxic in overdose and overdose of selenium results in rapid death. A widely publicised case of this occurred in a group of polo ponies in the USA who were given a “performance enhancing” injection containing selenium shortly before a tournament – unfortunately the selenium levels had been mis-calculated.

There is no reported toxicity associated with overdose of cobalt/Vitamin B12 although clearly it is not desirable to overdose animals.

65
Q
A