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
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).
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)
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
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
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
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
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
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
10
Q
What is the content of acetate in metabolism?
A
50-75%
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
12
Q
What is the content of proprionate in metabolism?
A
15-40%
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
14
Q
What is the content of butyrate in metabolism?
A
10-15%
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.
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
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
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
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
20
Q
What is the optimal rumen ammonia?
A
Aim is to maintain 8 mMol to prevent excess or deficiency.
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.
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
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
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
How is twin lamb diseases treated?
- Dextrose (Bolus IV admin 500 Ml 50% dextrose)
- Propylene glycol & glycerol drench
- Glucocorticoids
26
How is twin lamb disease prevented?
- Ensure good quality nutrition in the last 8 weeks of pregnancy
- Supplement rations with high quality hay/silage or concentrate
27
What are the causes of hypomagnesaemia?
- 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
What are the signs of hypomagnesaemia?
- 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
How is hypomagnesaemia treated?
- Animal should not be stimulated
- Magnesium sulphate can be given subcutaneous
- Hay treated with 60g of magnesium oxide daily
30
How is hypomagnesaemia prevented?
- 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
What are the causes of cerebrocortical necrosis/polioencephalomalacia?
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
What are the signs of cerebrocortical necrosis/polioencephalomalacia?
- Nervous disease resulting in necrosis of the brain
- Animal twists the head backwards
- Circle
- Blindness
- Convulsions
- Collapse
- Leg-kicking
- Die
33
How is cerebrocortical necrosis/polioencephalomalacia treated?
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
How is cerebrocortical necrosis/polioencephalomalacia prevented?
- Duet formulation to ensure no SARA
- Prophylactic administration of vitamins
- Check bracken fern levels in fields
- Check possible fonts of sulphur excess
35
What are the causes of swayback?
- 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
Describe the relationship between Cu, S and Mo.
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
How can swayback be prevented?
- 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
What are the causes of pine?
- 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
What are the signs of pine?
Loss of appetite
Unthrifty
Dull
Dry fleeces
Emaciation and death
40
How is pine treated?
Intramuscular injection of vitamin B12 and drenching with up to 1mg/kg bodyweight of cobalt salt
41
How is pine prevented?
- CoSeCure boluses or cobalt bullets
- Co status of the farm – swards and soil
42
What are the causes of white muscle disease?
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
Describe the role of selenium.
- 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
What are the signs of white muscle disease>
- Acute and rapid wasting of the skeletal muscles despite a good appetite
- Unable to stand
- Heart muscle damaged
- Death
45
How is white muscle disease treated?
Intramuscular or subcutaneous injection of young lambs with 0.75-1.5mg Se as potassium selenate and 24-86mg vitamin E
46
How is white muscle disease prevented?
- Supplementation of the dam’s ration during late gestation
- Injection of all new born lambs
- CoSeCure bolus or Sel-Plex (seleno-methianone)
47
What causes aphosphorosis?
Phosphorus deficiency due to poor diet or grazing arid soils low in phosphorus
48
What are the signs of aphosphorosis?
- 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
How is aphosphorosis treated?
- 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
How aphosphorosis prevented?
- Adequate diet rationing and P fertiliser of depleted soils
- Phosphorus concentration of 0.42% dry matter is adequate for high yielding dairy cows
51
What are the signs of vitamin A deficiency?
- Night blindness
- Impaired immunity
- Infertility
- Roughened coat and scaly skin
- Very weak/dead lambs
- Xerophthalmia
52
How is vitamin A deficiency treated?
Retinol injection plus a vitamin supplement in the feed
53
How is vitamin A deficiency prevented?
- Forage on the ration – carotene converted to retinol in intestine mucosa or liver
- 1-6mg/d in ruminants
54
What is goitre?
Enlarged thyroid gland
55
What are the causes of goitre?
- 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
What are the signs of goitre?
- Enlargement of thyroid gland – goitre
- Reproductive anomalies
- Weak hairless young or abortion
57
How is goitre treated?
- Oral dosing using potassium iodide
- Intraruminal boluses – iodine for 6 months
58
How is goitre prevented?
- Iodine is frequently added to concentrate rations for feeding to cattle, for example using seaweed preparations
- Rapeseed meals
