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ANS 319 Animal Nutrition > Chapter 9 Rumen Acidosis > Flashcards

Chapter 9 Rumen Acidosis Flashcards

1
Q

What’s the dilemma that is with feeding forages to high producing dairy cows?

A

They require increasing amounts of energy >30 Mcal/day
Feeding only forages cannot meet this energy requirement.
Concentrates are used to increase the energy density of the diet.
But theres a limit to how much grain can be fed due to rumen acidosis.

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2
Q

Propionate does it use carbon?

A

No, 3C

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3
Q

Does acetate use carbon?

A

Yes 1 carbon , so its (2C)

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4
Q

How does rumen acidosis occur?

A

1)Animals gorge on feed (large fluctuations in feed intake)
2)Fed too much concentrates
4)”empty” rumen
5)Heat stress *panting
6)In frequent feeding

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5
Q

In lactose synthesis, what two disaccharides are used?

A

Glucose + galactose, primary (CHO) in milk

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6
Q

What’s the lactose precursor?

A

Glucose

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7
Q

How much does it take of glucose to make 1kg of milk?

A

72g

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8
Q

What is the primary determinant of milk yield?

A

Lactose- Have the cow make lactose and then the more money you make.
Synthesis of lactose depends upon animals glucose status

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9
Q

Whats the precursor to glucose?

A

Propionate

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10
Q

Whats glucose made from?

A

Propionate

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11
Q

What is lactose made from?

A

Glucose

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12
Q

What is milk yield determined by?

A

The amount of synthesized lactose

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13
Q

What decreases the rumen pH?

A

-Eating and ruminating times are reduced, therefore decreased saliva production
-Rate and extent of acid production is greater
-Forages exert some buffering capacity (difficult to induce acidosis when the rumen is full of fibre
-More complete fermentation

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14
Q

Why do total VFA’s go up as you go from high forage to high conc diet?

A

VFA’S = acids. The pH rate of concentrates

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15
Q

Whats the monosaccharides in lactose?

A

gluocse and galactose

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16
Q

Precursor for lactose?

A

Galactose, VFA= (Propionate) makes more lactose, so we feed them a high concentrate diet if we want out animals to produce more lactose

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17
Q

Why does fermentation of conc reduce the pH

A

Glycolysis from glucose to pyruvate more hydrogen is being produced, you have more VFA’s being made , the rate in which there made= increased. Both of these drag the pH down. pH kills the bugs if they get too low.

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18
Q

explain what ruminations role is in rumen acidosis?

A

Concentrations (already a small particle, cow doesn’t have to spend energy making it smaller) less incentive for the cow to ruminate, to bring a cud back up to the mouth to chewing. Chewing = saliva production, saliva contains buffers(bicarbonate + phosphate) gets swallowed and goes back into rumen and the pH goes up. but if eating high con there isn’t a lot of chewing so less saliva production.

19
Q

On a high forage diet to high concentrate diet

A

They produce more VFA’s and its quicker. high forage diet favours bacteria that makes acetic.
high concentrate diet favours bacteria that makes propionate

20
Q

Rumen acidosis and the consequences

A

Rapidly fermented grain fed to cattle, acidosis(low rumen pH), gut lesions, Bacteria population increase, rumen wall abscesses inflammation and tissue death, bacteria travel to liver via blood, liver abscesses.

21
Q

Whats the dietary allowance of starch? and whats the type of grain and how do we store it? Whats important to know about processing starch?

A

Early April on forage diet- grass can contain high sugar levels may be carful animals don’t get rumen acidosis. 25-35% of DM as starch.
Type of grain-Barley or wheat (more more fermentable then processed corn) type of grain matters.
Storage- High moisture corn (much more fermentable than dry corn)
Biggest contributor about how digestible something is : How its processed:
* Degradability/fermentability increases with fineness of grind (surface area)
* Starch in steam flake corn is rapidly fermented that not steam flaked
* Starch in rolled corn silage degrades faster than if ”unrolled”

22
Q

What does rumen acidosis increase the production of? whats the pK of it?

A

-Lactic acid, its not absorbed from rumen as well as VFA’s
-Lactic acid = strong acid. pK: Lactic acid 3.08

23
Q

Whats the pK of Acetic, propionate, butyrate:

A

4.75-4.81

24
Q

What is the process of rumen acidosis :

A

Digestion in rumen goes down with acidosis. Non digestible feeds leave rumen undigested. Pancreatic amylase isnt being made in duodenum of ruminant because its not ment to make it to there. Now starch is arriving at illicial secal junction and then the same process that happens with people lactose intolerance happens with animals.

25
Q

Whats the problem with rumen acidosis (list them)

A
  • Decreased feed intake
  • Reduced microbial growth
  • Reduced cellulose digestion
  • Diarrhea
  • Bloat (especially in growing ruminants)
  • Milk fat depression (usually 4 but now could be 3)
  • Laminitis
  • Liver abscess
  • Death
26
Q

Explain to me why rumen acidosis causes liver absesses***

A
27
Q

Acute ruminal acidoses

A

less that 5.0-5.2 pH

28
Q

Subacute ruminal acidosis (SARA)

A

less that 5.6 pH

29
Q

Whats acute acidosis

A

this is when its recognised by farmer and nutritionist
* Most often recognized
* Diet transition period
* “Sudden Death Syndrome”
* Liver Abscesses
* Bloat
* Reduced feed intake
* Poor body condition and weight loss
* Unexplained diarrhea
* Temperature

30
Q

How would you recognises sub-acute acidosis

A
  • Occurs more frequently
  • Difficult to observe or identify
  • Major response = Reduced feed intake!
  • Pen feeding conditions
  • Individual reductions in feed intake
    masked by pen average
  • Erratic feed intake patterns
31
Q

If pH is high healthy what happens?

A
  • Good appetite
  • Good cellulose digestion
  • Good microbial growth.
32
Q

If pH is low what happens?

A
  • Poor appetite
  • Little cellulose digestion
  • Poor microbial growth.
    if it gets lower than 5:
    Acute Rumen Acidosis - Deep physiological changes -May cause death
33
Q

Whats the rate of VFA’s determined by?

A
  • Total rate of production and concentration
    of VFA are directly related to intake of
    fermentable organic matter
  • Rates of production and concentrations of
    individual VFA are affected by
    forage:concentrate ratio
34
Q

What type of bacteria does high pH favour?

A

Celluloytic bacteria

35
Q

What type of bacteria does low pH favour?

A

Amyloyltic bacteria

36
Q

Why does rumen acidosis cause diarrhoea

A

Ph goes down , digestibility of soluble nutrients goes down , starch gets to small intestine , no pancreatic amylase, starch passed to large intestine and now its like rocket fuel.
Acidosis in large intestine, damages the large intestine wall.

37
Q

Diarrhoea in Rumen and hind-gut fermenters:

A

Diarrhea:
Nutrients that are not absorbed in rumen or small intestine,
travel to large intestine and ferment
Extensive fermentation in the hind gut
Produces acids (VFAs) and other osmolites
Increased osmolarity pulls water into large intestine
Decreased pH damages gut wall
Mucin secreted
Mucin casts can be observed in feces
Produces gas (CH4 and CO2)
Gas bubbles in feces
Similar to the consequences of highly digestible nutrients
reaching the large intestine of a monogastric (e.g. lactose intolerance)

38
Q

Name the 3 problems with Acidosis:

A

-Laminitis (founder)
If rumen pH is chronically acidic
Epithelium releases metalloproteinases
Cause tissue degradation
If enter the blood stream causes inflammation
of laminae above the hoof
-Feedlot bloat
Starch fermenting bacteria secrete polysaccharides
Produce a foam
Gas trapped in foam
-Sudden death
If large amounts of starch escape the rumen
Overgrowth of Clostridium perfringens in the intestine
Produce enterotoxin that might cause death

39
Q

When are animals at highest risk for rumen acidosis?

A
  • Highest risk:
    – Last week before calving (if poorly managed transition
    diet)
    – The first few month after calving (high concentrate diet)
    – Heat Stress
40
Q

What are risk factors that aren’t as high as the last one?

A
  • Risk factors:
    – High concentrate diet (>55% diet DM)
  • Finely ground
    – High level of dry matter intake (i.e., high producing cows)
    – Lush Pasture (less salivation) and lots of soluble sugars
    – Method of feeding (TMR vs. separate ingredient)
    – Poor transition between dry cow diet and high producing
    cow diet (rumen papillae atrophy)
41
Q

What ferments quicker and slower in the rumen?

A

Quickest: Soluble Sugars
Middle: Starches
Slowest: Carbohydrates

42
Q

How do we manage acidosis:

A
  1. Allow time for adjustment to diets with grain
    Gradually increase grain in the diet
    Program “step up” rations
    Limit intake until adjusted
  2. Feed adequate roughage/forage
  3. Manage feed consumption
    Prevent gorging of high starch feeds
    one of the main issues with heat stress
    “Read bunks”
    System for knowing when to change
    amount of feed offered
  4. Feed ionophores
43
Q

In summary….

A
  • Highly digestible grains are necessary to allow cows to reach
    genetic potential for milk yield
    – Therefore this will continue to be a problem as annual milk yield continues
    to increase
  • Increased digestibility and too much grain can cause acidosis
  • Prevention strategies
    – Be careful with how much grain contributes to DM
    – Effective fiber (stimulate chewing and saliva production)
    – Dietary HCO3
  • Both concentrates and forages are essentially
    made up of repeating units of glucose
  • Microbes ferment these sugars into VFA
  • Processing of grains and forages alters their
    digestibility and fermentation pattern and
  • Waste products of fermentation are energy
    molecules for the ruminant animals
  • Gas production by microbes is a waste of money
    for the farmer

ANS 319 Animal Nutrition (17 decks)

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