Production Diseases: Microelements Flashcards

1
Q

When are mineral deficiencies likely to occur

A

Deficient soils

Antagonists:

  • Soil pH, moisture and other elements and chemicals
  • Plant
  • Ex. goitrogens

Performance animals at grass:

  • Growing lambs
  • NZ type dairy systems

Animals being fed unconventional diets or grazed in certain microenvironment

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2
Q

how do mineral toxicities occur

A

Soil

Reclaimed land from mining

Or land with spoil heaps/slag or ash

Certain plants can accumulate selenium/copper to toxic levels

Pig slurry (less common now)

Iatrogenic

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3
Q

how do you assess mineral adequacy

A

soil sampling

forage sampling

animal sampling

supplementation and measurement

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4
Q

why is soil sampling hard to interpret

A

Is it in the plants? Are the animals eating these plants? Are the minerals in the plants even available to the animal?

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5
Q

how is forage sampling interpreted

A

It is for sure in the plant but does the mineral get absorbed/available for the animal?

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6
Q

how are animal samples interpreted

A

Stores

Circulating pool

Function

One has to understand the at risk population and the variability within the population (sample size)

  • Lambs/calves

The half life of the measured parameter, does handling of the animal prior to sampling affect the result?

Whether we are measuring a storage or transport pool or the function associated with the nutrient, which homeostasis will strive to maintain within confines

  • Ex. Calcium vs cobalt

Most of all is the result interpretable?

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7
Q

what are the functions of cobalt

A

Vitamin B12 used in methyl transfer — so TCA cycle and purine and pyrimidine synthesis

Rumen microbes produce B12 from cobalt

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8
Q

what are the clinical signs of cobalt deficiency

A

Result in Vit B12 deficiency (pine)

Starvation with appetite suppression, ocular discharge, anemia and fatty liver

Lambs > adult sheep > cattle

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9
Q

how is cobalt deficiency diagnosed and treated

A

Vit B12 blood in sheep

Cattle:

  • Not in blood so liver, milk vit B12 or methylmalonic acid in serum (not practical at all)

Fertilizer/boluses/feed/injections (short or long acting) or mineral added to diet

  • Drenching every 2 weeks
  • Not good at storing water soluble vitamins
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10
Q

what is the funciton of selenium

A

Selenoproteins:

  • Glutathione peroxides responsible for controlling reactive oxygen species

Transforming thyroxine (T4) to triiodothyronine (T3)

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11
Q

what are the clinical signs of Se deficiency

A

Oxidative damage — white muscle disease

  • Fast growing animals on diets with high oxidative stress

Reduced growth, especially wool

Reduced immune function and fertility (not simple relationships)

Reduced ovine neonate survival due to less T3

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12
Q

how is Se deficiency diagnosed

A

serum glutathionine peroxidase

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13
Q

how is Se deficiency treated

A

Boluses/oral dose/injections (depot)/fertilizer/mineral addition to diet

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14
Q

what are the toxic effects of Se (3)

A

Direct inhibition of cellular oxidation/reduction reactions by depleting glutathione and S-adenosylmethionine reserves

Production of free radicals that cause oxidative tissue damage

Replacement of sulphur/sulphur-containing amino acids in the body with selenium/seleno-amino acids

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15
Q

what is chronic Se toxicity associated with

A

Chronic is associated with geographical sources — no treatment (but possibly try sulphates and copper)

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16
Q

what are the clinical signs of chronic Se toxicity

A

Non-specific

Dullness

Ill-thrift

Anemia

Rough coat

Brittle hooves (sloughing in extreme cases)

Joint pain — to the point of immobility

17
Q

what are the clinical signs of acute Se toxicity

A

Toxic damage to cardiovascular system

Dyspnea

Salivation

Recumbency

Diarrhea

Death

18
Q

what are the clinical signs of copper deficiency

A

Ataxia

  • Neonatal/delayed and atypical (stand transfixed with head quivering due to cerebral edema)

Steely wool-crimp loss

Depigmentation

Diarrhea

Anemia

Infertility and poor growth

Fractures in adults

19
Q

what are Cu functions and deficiency signs

A
20
Q

how is Cu deficiency diagnosed

A

liver store

serum - transport hemostasis

21
Q

how is Cu deficiency treated

A

Fertilizer

Drench/bolus/ruminal needles

Genetic selection

Need to be careful

Sheep accumulate Cu and it accumulates year on year

22
Q

what elements antagonize Cu

A

Remember molybdenum/iron and sulphur all antagonize copper absorption

23
Q
A
24
Q

what does Cu toxicity present as

A

Presents as acute hemolytic crisis disease but usually chronic with an acute crisis

25
Q

what are causes of Cu toxicity

A

Cattle feed to sheep

Red clover

Over supplementation

Grazing land with a history of pig slurry

Holstein vs Jersey (Jersey more susceptible?)

Distillers by-products

Can have high liver levels with no crisis, or have crisis and death with lower liver copper levels

26
Q

what is the function of iodine

A

Manage metabolic rate via T3

27
Q

what can iodine deficiency be categorized as

A

Primary

Secondary due to goitrogens

28
Q

how can secondary iodine deficiency due to goitrogens be subdiviced as

A

Plant chemicals (2 further subgroups)

  • Glucosinolates — produce HCN which is converted to thiocyanates which inhibits absorption of iodine (extra iodine is protective)
  • Thiouracil goitrogens prevent iodination of tyrosine in the thyroid (extra iodine is minimally protective)

Inorganic goitrogens — defined in humans but not animals

29
Q

what are the clinical signs of iodine deficiency

A

Goitre

Scant wool

Sometimes high mortality in absence of goitre due to starvation/hypothermia

30
Q

how is iodine def diagnosed

A

Can be difficult

PM

  • Measure ratio of thyroid weight:body weight (<0.4g thyroid:1kg BW)

Plasma inorganic iodine (PII)

  • Contemporary iodine intake
  • Good estimate of sufficiency
31
Q

how is iodine def tx

A

Intramuscular injection of iodized oil pre-mating

Oral dosing

  • 280mg KI 8 and 4 weeks before lambing

Sustained iodine ruminal boluses

  • I, Se, Co

Pour on (cattle)