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AM2 > Ruminant Protein and energy metabolism > Flashcards

Ruminant Protein and energy metabolism Flashcards

1
Q

What conditions are found within the rumen to support microbial growth?

A
  1. temperature, moisture and pH buffered
  2. constant supply of nutrients
  3. continuous removal of products of digestion and fermentation
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2
Q

What are the products of fermentation and digestion?

A

gases- including methane
VFAs
ammonia

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3
Q

What do the products of fermentation do?

A

Provide bulk of energy to the animal

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4
Q

What are the 5 starting products for digestion that produce glucose for fermentation?

A
  1. cellulose
  2. hemicellulose
  3. pectin
  4. fructans
  5. starch
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5
Q

What does glucose turn into?

A

Pyruvate

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6
Q

What are the three products of fermentation?

A
  1. Acetate
  2. Butyrate
  3. Propionate
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7
Q

How is Acetate absorbed?

A

Across the rumen wall, intact and converted to acetyl CoA in the liver where it enters the Krebs cycle.

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8
Q

What kind of diet favours acetate production?

A

High fibre diets, 70% of VFAs converted to acetate

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9
Q

What are the functions of acetate?

A

Lipogenic, can be stored as a fat

milk fat precursor

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10
Q

What kind of diets favour propionate?

A

high concentrate diets

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11
Q

how much of propionate is converted to lactate during absorption across the rumen wall?

A

20%

enters gluconeogenic pathway in liver via phosphoenolpyruvate

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12
Q

what happens to the remaining propionate?

A

passes to liver and is converted to glucose via oxaloacetate and PEP intermediates

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13
Q

what does PEP stand for?

A

PEP= phosphoenolpyruvate

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14
Q

how is propionate stored?

A

As glycogen

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15
Q

What is butyrate converted to during absorption across the rumen wall?

A

beta-hydroxybutyrate

energy source for heart and skeletal muscle

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16
Q

Butyrate production

A

less controlled by diet
slightly favoured on high forage diet
presence of protozoa

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17
Q

how is butyrate stored

A

its lipogenic so stored as fat

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18
Q

What is the main byproduct

A

methane

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19
Q

how is methane formed?

A
  • reduction of CO2 with H2 from acetate and butyrate formation
  • acetate decarboxylation
20
Q

How to maintain Rumen pH

A
  • VFA must be removed, acidosis occurs if they accumulate, they are passively absorbed across rumen wall
  • saliva= buffer
21
Q

pH impact on rumen bacteria activity

A
  • cellulolytic bacteria predominate in a high pH, high fibre diet
  • amylolytic bacteria, lower pH, increased concentrates, less fibre
22
Q

The process of Acute Ruminal lactic acidosis

A
  1. feed= rapidly fermentable carbohydrates, which means higher VFA
  2. amylolytic bacteria growth rate increases
  3. pH drops
  4. Lactate producing bacteria grow- detoxifying action of lactate-utilising bacteria
  5. growth rate of other bacteria decreases
  6. subacute acidosis, reduced enzymatic activities
  7. pH drops further, decrease in lactate utilising bacteria
  8. pH continues to drop, more D-lactate producers
  9. Acute acidosis
23
Q

What is Ketosis?

A

High energy demands, not enough carbs in the diet, use fat deposits

24
Q

SIgns of Ketosis

A
  • loss in body weight
  • dull and listless
  • ‘pear drops’ smell breath, urine and milk
  • decreased dry matter intake
25
Q

Treatment of Ketosis

A
  • dextrose Bolus
  • propylene glycol and glycerol drench
  • Glucocorticoids
  • dietary protocol
26
Q

Prevention of ketosis

A
  • balanced rations for all stages of the production cycle
  • maintain proper condition
  • prevent other diseases
  • manure observation
  • promote food cow comfort and welfare
27
Q

What is Hepatic lipidosis

A

fatty liver
due to excess energy intake during dry period and negative energy balance at calving
body fat mobilised more quickly that can can be used so taken up and stored by liver
often associated with ketosis

28
Q

Signs of hepatic liposis

A
  • no specific signs- increase in NEFA and beta butyrate

- occurs with metritis, mastitis, displaced abomasum and hypocalcaemia

29
Q

Treatment for hepatic liposis

A
  • similar to ketosis

- reverse negative energy balance as soon as possible

30
Q

Prevention of hepatic ketosis

A
  • monitor BCS during dry period
  • avoid excess BCS
  • minimise negative energy balance to decrease tissue metabolism
  • minimise stress
  • ration to animals’ needs
31
Q

What is displaced abomasum?

A

from normal orientation to the left or right side of abdomen, usually on ventral floor
80-90%= left displaced

32
Q

When does DA usually occur?

A

usually first 30 days post calving

33
Q

what are the causes of DA?

A
  • hypomotility of abomasum
  • decreased roughage and increased concentrate diets
  • decreased rumen fill implicated
  • other issues- hypocalcaemia, mastitis, metritis
34
Q

Signs of Left DA

A

anorexia, decreased milk production, hypomotility, gas production, decreased appetite, dehydration, alkalosis and hypochloraemia/hypokalaemia, and secondary ketosis.

35
Q

Signs of Right DA

A

more serious and has low recovery rate
same as LDA but rotation= impaired local circulation
ischemia, blood supply limited
necrosis

36
Q

treatment of DA

A
  • conservative or surgical
  • cast and roll cow
  • manipulation
  • treat other diseases
  • allow access to water and salt block for simple displacements
37
Q

Prevention of DA

A
  • promote DMI and rumen filling immediately post calving
  • feeding TMR
  • avoid rapid dietary changes
  • adequate roughage
  • avoid milk fever
  • treat ketosis
38
Q

What is retained placenta?

A

failure to expel foetal membranes within 24hours post calving
increased risk of diseases- such as metritis

39
Q

Causes of retained placenta?

A
  • nutritional imbalances
  • abortion
  • dystocia
  • twins
  • stillbirth
  • hypocalcaemia
  • heat stress
  • increased age/parity
  • previous history of RP
40
Q

treatment of RP

A
  • avoid manual removal
  • trimming of excess placenta
  • treat any signs of systemic illness
41
Q

prevention of RP

A
  • optimise Se supplement

- cull repeat offenders

42
Q

What is hypocalcaemia?

A

Milk fever
loss if control of plasma CA concentration at greatest demand when in lactation
normal = 85-100mg/l
hypo= 20-70 mg/l

43
Q

Causes of milk fever

A 
oversupply of CA during dry period 
poor mineral balance in dry diet 
inadequate vit D and mineral supply during dry period 
Inappropriate forages in dry cow diet 
C:P ratio too low post parturition 
breed
cows in lactations 2 and above
44
Q

signs of milk fever

A
  • depression in levels of CA in tissue fluid

- lactation tetany and eclamosia

45
Q

Incidence rate of Milk fever

A
  • 48 hours after birth
    75% 24 hours post parturition
    less than 5 % beyond 48hrs

AM2 (14 decks)

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