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Animal Management Y2 > Ruminal Metabolism > Flashcards

Ruminal Metabolism Flashcards

1
Q

Describe the classification of lipids.

A

Glycerol based: neutral > triacylglycerol, and structural > glycolipids and phospholipids

Non-glycerol based: sphingomyelins, waxes, steroids, sterols, vitamins, prostaglandins/eicosanoids

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2
Q

What are the lipid recommendations of PUFA : SFA?

A

PUFA : SFA > 0.45 required to maintain healthy cell function and membrane fluidity (MUFA).

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3
Q

What are the lipid recommendations for omega-6:omega-3?

A

Omega-6 : Omega-3 < 4 balance of pro and anti-inflammatory (prostaglandins and eicosanoids)

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4
Q

Describe the oil content in the ruminant diet.

A

More oil decreases ability to digest fibre. Ruminants maximum 6% DM free oil = 5-6% fat in the diet

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5
Q

What does too much dietary fat in ruminants cause?

A
  • Impairs rumen fermentation
  • Reduces feed intake
  • Compromises production
  • Leads to milk fat depression
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6
Q

What is the effect of polyphenol oxidase in red clover in the ruminant diet?

A
  • Oxidises phenols to quinones in the presence of oxygen
  • Quinones are very reactive
  • Quinones bind to proteins to give protein-quinone complexes
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7
Q

What 2 types of feeding causes milk fat depression?

A

Highly polyunsaturated lipid in diet:
- Plant oils or cod liver oil – lower effect of tallow (SFA)
- Oil seeds or straight lipid

Low roughage and high concentrates:
- Low feeding frequency
- Finely ground roughage

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8
Q

What is milk fat depression?

A
  • Milk fat lowered by up to 50% with no change to lactose or protein.
  • Varies with feed fat level, feed frequency, stage of lactation and body condition score.
  • Trans 10, cis 12 C18:2 (intermediate of biohydrogenation) on high concentrate/oil diets
  • Decline greatest in de novo synthesis of fatty acids
  • Substantial increase in C18:1 fatty acids in milk
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9
Q

What conditions must be maintained to support microbial growth?

A
  • Temperature, moisture, pH buffered
  • Constant supply of nutrients
  • Continuous removal of products of digestion/fermentation – gases, including methane, used as H sink, VFA and ammonia
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10
Q

What is the content of acetate in metabolism?

A

50-75%

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11
Q

Describe acetate in rumen and metabolism.

A
  • Absorbed across rumen wall intact and converted to acetyl CoA in liver and enters Krebs citric cycle
  • High fibre diets favour acetate production
  • Lipogenic – stored as fat via acetyl-CoA
  • Milk fat precursor
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12
Q

What is the content of proprionate in metabolism?

A

15-40%

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13
Q

Describe proprionate in the rumen and metabolism.

A
  • High concentrate diets favour propionate production
  • 20% of propionate converted to lactate during absorption across rumen wall, enters gluconeogenic pathway in liver via phosphoenolpyruvate
  • The remaining propionate passes into liver and is converted into glucose via oxaloacetate and PEP intermediates
  • Gluconeogenic (glucose precursor supplies 50% of requirements). Stored as glycogen
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14
Q

What is the content of butyrate in metabolism?

A

10-15%

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15
Q

Describe butyrate in the rumen and metabolism.

A
  • Converted to beta hydroxybutyrate during absorption across rumen wall and then passed into liver and is converted into acetyl CoA.
  • Beta hydroxybutyrate may also be used as an energy source by heart and skeletal muscle
  • Less controlled by diet but slightly favoured on a high forage diet. Presence of protozoa will increase butyrate.
  • Butyrate is lipogenic, stored as fat via acetyl-CoA.
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16
Q

Describe methanogenesis.

A
  • Methanogenesis accounts for about 8% of gross energy
  • CH4 production is lower on concentrate diets/H2 sink
  • Methane suppressants, such as chloroform, bromoforms, 3-nitrooxypropanol, nitrate and monensin (inhibit archea)
  • Major issues in relation to carbon footprint of ruminants – 28 times higher GWP of CO2
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17
Q

How is rumen pH maintained?

A
  • VFA - must be removed – acidosis
  • Passively absorbed across rumen wall
  • Helps maintain pH at 6.7  0.5
  • Saliva also provides buffering capacity
  • Cattle = 180L per day – 70% water entering the rumen
  • Rich in buffer ions – Na, K, PO4 ad HCO3
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18
Q

Describe nitrogen ruminal metabolism.

A
  • Quality and quantity of dietary protein is different from that in the small intestine
  • Made up of Digestible Microbial True Protein (DMTP) and Digestible Undegraded Dietary Protein (UDP)
  • Rumen microbes
  • Some amino acids > organic acids, NH3 , CO2
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19
Q

Describe ammonia as a key intermediate in nitrogen ruminal metabolism.

A
  • Low dietary protein > decreased ammonia > slow microbial growth > decreased CHP breakdown
  • Rapid degeneration of dietary protein or insufficient FME > increased ammonia. If optimum ammonia is exceeded (85-300mg/l) > rumen amminia > blood > liver > urea
  • Urea to the rumen via saliva converted to ammonia by bacterial urease in nitrogen recycling and excreted in the urine
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20
Q

What is the optimal rumen ammonia?

A

Aim is to maintain 8 mMol to prevent excess or deficiency.

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21
Q

What factors affecting ruminal efficiency of microbial protein synthesis?

A
  • Form of nitrogen
  • Balance of supply of energy and nitrogen – improvements in the balance of supply of nitrogen and energy lead to improvements in the efficiency of microbial protein synthesis.
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22
Q

How can nitrogen utilisation in the rumen be manipulated to improve balance?

A

Increase levels of readily available energy

Decrease protein solubility of forage protein

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23
Q

What are the causes of twin lamb disease?

A
  • Poor rationing during late pregnancy/last 4 weeks of gestation – often related to poor ME silage, resulting in negative energy balance
  • Or outdoor sheep in poor weather conditions
  • Ketosis
  • More at risk with multiple foetuses
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24
Q

What are the signs of twin lamb disease?

A
  • Disclination to move (stupidity)
  • Ketone bodies formation
  • Disturbed vision
  • Constipated
  • Recumbency and death
25
Q

How is twin lamb diseases treated?

A
  • Dextrose (Bolus IV admin 500 Ml 50% dextrose)
  • Propylene glycol & glycerol drench
  • Glucocorticoids
26
Q

How is twin lamb disease prevented?

A
  • Ensure good quality nutrition in the last 8 weeks of pregnancy
  • Supplement rations with high quality hay/silage or concentrate
27
Q

What are the causes of hypomagnesaemia?

A
  • Fresh lush pasture is low in magnesium
  • Fertiliser, nitrogen or potassium can reduce uptake of magnesium into pasture, potassium locks magnesium in soil
  • First cut silage can be low in magnesium
  • Usually during lactation
28
Q

What are the signs of hypomagnesaemia?

A
  • Less than 0.8mmol/L in the blood is subclinical
  • Hyperexcitable frothing at the mouth
  • Muscle twitching, mainly around the neck area of the animal, and teeth grinding
  • Dead stock at pasture
29
Q

How is hypomagnesaemia treated?

A
  • Animal should not be stimulated
  • Magnesium sulphate can be given subcutaneous
  • Hay treated with 60g of magnesium oxide daily
30
Q

How is hypomagnesaemia prevented?

A
  • Requirements – 2.5g/kg dry matter of magnesium for lactating cows at pasture
  • Known you swards – calcined magnesite. Soil assessment regarding potassium and magnesium levels
  • Herbage may be dusted with powered magnesium oxide or sprayed with a 2% solution of magnesium sulphate
  • Mineral licks or slow release boluses on known trouble swards
31
Q

What are the causes of cerebrocortical necrosis/polioencephalomalacia?

A

Vitamin B1/thiamine deficiency. Typically caused by:
- Rapid change in plane of nutrition – poor to high quality – which leads to subclinical lactic acidosis and so an alternation in ruminal microflora, reducing production of B1.
- Destruction of B1 within the rumen/GI tract. Thiaminases > bracken fern or produced by gut flora

Sulphur excess

32
Q

What are the signs of cerebrocortical necrosis/polioencephalomalacia?

A
  • Nervous disease resulting in necrosis of the brain
  • Animal twists the head backwards
  • Circle
  • Blindness
  • Convulsions
  • Collapse
  • Leg-kicking
  • Die
33
Q

How is cerebrocortical necrosis/polioencephalomalacia treated?

A

Early administration of thiamine may be curative but if the lesion is more advanced, then surviving animals may remain partially blind and mentally dull.

34
Q

How is cerebrocortical necrosis/polioencephalomalacia prevented?

A
  • Duet formulation to ensure no SARA
  • Prophylactic administration of vitamins
  • Check bracken fern levels in fields
  • Check possible fonts of sulphur excess
35
Q

What are the causes of swayback?

A
  • Low ewe blood copper results in underdevelopment of the myelin sheath in lambs
  • Low copper uptake or usually poor absorption due to the formation of copper thiomolybdate
36
Q

Describe the relationship between Cu, S and Mo.

A

If we have either or all of these 3 elements in excess or in normal concentrations on the farm, then there is a lack of synergistically being able to bind out copper from the diet.

37
Q

How can swayback be prevented?

A
  • CoSeCure boluses – copper, selenium and cobalt
  • Great care with sheep – supplementation with copper oxide (following guidelines and record Cu intake in diet)
  • Sheep are unique in that they accumulate copper in the liver more readily than other farm animals so can have excess in the liver.
  • Cu toxicity: Sheep require ~5 mg/kg DM in the total diet. Toxicity can occur exceeding 25 mg/kg DM
  • Assess Cu, Mo and S levels of sward and soil
  • Higher Mo levels found in legumes – required for root nodule N-fixation
38
Q

What are the causes of pine?

A
  • Lack of Co and inability to manufacture vitamin B12 in the rumen due to lack of cobalt
  • Vitamin B12 -250-500 pg/mL blood
  • May be exasperated in parasitic gastroenteritis
39
Q

What are the signs of pine?

A

Loss of appetite
Unthrifty
Dull
Dry fleeces
Emaciation and death

40
Q

How is pine treated?

A

Intramuscular injection of vitamin B12 and drenching with up to 1mg/kg bodyweight of cobalt salt

41
Q

How is pine prevented?

A
  • CoSeCure boluses or cobalt bullets
  • Co status of the farm – swards and soil
42
Q

What are the causes of white muscle disease?

A

Nutritional muscular dystrophy:

  • Selenium and vitamin E deficiency – cellular antioxidants
  • Bioavailability of inorganic selenium is poor
  • Sulphur levels influence the incorporation of selenium into organic form on pasture
43
Q

Describe the role of selenium.

A
  • Se is a trace element essential for normal cellular function
  • Cofactor for reduction of antioxidants enzymes such as glutathione peroxidase
  • Cofactor for thyroid hormones deiodinases
  • Removes reactive oxygen species and controls metabolic rate
44
Q

What are the signs of white muscle disease>

A
  • Acute and rapid wasting of the skeletal muscles despite a good appetite
  • Unable to stand
  • Heart muscle damaged
  • Death
45
Q

How is white muscle disease treated?

A

Intramuscular or subcutaneous injection of young lambs with 0.75-1.5mg Se as potassium selenate and 24-86mg vitamin E

46
Q

How is white muscle disease prevented?

A
  • Supplementation of the dam’s ration during late gestation
  • Injection of all new born lambs
  • CoSeCure bolus or Sel-Plex (seleno-methianone)
47
Q

What causes aphosphorosis?

A

Phosphorus deficiency due to poor diet or grazing arid soils low in phosphorus

48
Q

What are the signs of aphosphorosis?

A
  • Animal down or like ‘crawler cow’
  • Most common around calving
  • Deficiency causes rickets/osteomalacia
  • Stiff joints, muscular weakness
  • Slow growth
  • Poor fertility – ovary function
  • Reduced milk yield
  • Pica – not necessarily carnivory, but pica
49
Q

How is aphosphorosis treated?

A
  • Mild to moderate phosphorus – oral Pi supplement or solutions of sodium phosphate salts
  • Oral Pi administration rapidly increases plasma Pi concentration. Not for vomiting and diarrhetic animals
  • Cattle – oral sodium phosphate salts increase the plasma Pi concentration within 3-4 hours and effect within 12 hours
50
Q

How aphosphorosis prevented?

A
  • Adequate diet rationing and P fertiliser of depleted soils
  • Phosphorus concentration of 0.42% dry matter is adequate for high yielding dairy cows
51
Q

What are the signs of vitamin A deficiency?

A
  • Night blindness
  • Impaired immunity
  • Infertility
  • Roughened coat and scaly skin
  • Very weak/dead lambs
  • Xerophthalmia
52
Q

How is vitamin A deficiency treated?

A

Retinol injection plus a vitamin supplement in the feed

53
Q

How is vitamin A deficiency prevented?

A
  • Forage on the ration – carotene converted to retinol in intestine mucosa or liver
  • 1-6mg/d in ruminants
54
Q

What is goitre?

A

Enlarged thyroid gland

55
Q

What are the causes of goitre?

A
  • Iodine deficiency causes thyroxine and triiodothyronine production declines
  • Goitrogens in brassicas: kale, cabbage, rape, soya. Reduce production or release of triiodothyronine T3 and/or thyroxine T4 even with sufficient Iodine
56
Q

What are the signs of goitre?

A
  • Enlargement of thyroid gland – goitre
  • Reproductive anomalies
  • Weak hairless young or abortion
57
Q

How is goitre treated?

A
  • Oral dosing using potassium iodide
  • Intraruminal boluses – iodine for 6 months
58
Q

How is goitre prevented?

A
  • Iodine is frequently added to concentrate rations for feeding to cattle, for example using seaweed preparations
  • Rapeseed meals

Animal Management Y2 (16 decks)

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