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Animal nutrition > Animal nutrition - rumen acidosis, milk fever > Flashcards

Animal nutrition - rumen acidosis, milk fever Flashcards

1
Q

Main factors related to rumen acidosis (3)

A
  • Low fibre content and/or lack of effective fibre
    (mostly the lack of effective fiber)
  • High percentage of cereals/concentrates in ration DM
  • Low rumen buffering capacity
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2
Q

Pathogenesis of acidosis

A

ruminal atony

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3
Q

Clinical rumen acidosis is rare, but if it occurs the following happens: (5)

A

– fore-stomach contractions stop
– protozoa and cellulolytic bacteria die
– no digestion takes place (at least cellulose digestion stops)
– lactate is the main acid in the rumen
– treatment is hard and the disease often ends in death

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4
Q

Acidosis mostly occurs in what form

A

in the subclinical form (SARA), which is associated with many diseases and problems in the herd

Sub-acute ruminal acidosis (SARA)

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5
Q

Name 6 potential consequences of Sub-acute ruminal acidosis (SARA).

A

laminitis
low milk fat content
displaced abomasum
decreased fertility
ketosis
mastitis, metritis

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6
Q

Clinical acidosis appears when rumen pH is

A

< 5.0

– Predominant bacteria is Streptococcus bovis which produces lactic acid
– Bacteria that consume lactic acid disappear

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7
Q

In the case of subclinical acidosis, the rumen pH is mostly between

A

5.5- 5.6

– Subclinical acidosis is not necessarily caused by a high amount of lactic acid in the rumen -> the amount of total acids is more important.

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8
Q

At a pH of 6.0 in the rumen, the lactate isomers are equal to what percentage of total acids?

A

D-lactate, and L-lactate only 20%.

If the pH drops to 5.0 the proportion of produced lactate isomers equalise (50:50).

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9
Q

If the pH drops to 5.0, the proportion of produced lactate isomers do what?

A

equalise (50:50)

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10
Q

Previously was wrongly thought that main acidosis
causer is L-lactate, which absorbs heavily.

Today is known that both isomers, D and L lactates, do what?

A

Today it is known that both isomers absorb at equal rates, converted into BHB and are used in the peripheral tissue (incl. rumen epithelia cells) as energy source.

they metabolises in slightly different pathways but with the same efficiency

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11
Q

Surplus of lactic acid causes

A

subclinical acidosis,
more frequent shortly after calving when feeding is changed within a short period from silage-based to a cereal-based ration.

In this case there are more bacteria producing lactic acid than there are bacteria consuming it.

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12
Q

Recovery time of bacteria in the rumen varies:
– bacteria producing lactic acid, how long?
– bacteria consuming lactic acid, how long?

A

– bacteria producing lactic acid -> 2-3 weeks
– bacteria consuming lactic acid -> 4-5 weeks

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13
Q

Rumen papillae reach their maximum length at what point?

A

Rumen papillae reach their maximum length at 4 to 5 weeks after calving.

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14
Q

Rumen epithelial cells are not similarly protected as abomasum epithelial cells, and therefore

A

organic acids produced in the rumen injure them easily

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15
Q

Low rumen pH causes (4) morphological changes

A

rumenitis,
rumen parakeratosis,
erosion of the epithelial cells
and ulcers

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16
Q

In normal nutrition conditions the lactic acid
produced in the rumen will be used/consumed by what bacteria specifically (latin name)?
Whats their pH optimum?

A

the bacteria Megasphera elsdenii, whose pH optimum is 5.5- 6.0

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17
Q

If the acidity in the rumen increases and the
pH drops below 5.5, what type of bacteria prevail?
latin name?

A

lactic acid producing bacteria Streptococcus bovis start to prevail, whose pH optimum is 5.1- 5.3

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18
Q

name the species of lactic acid producing bacteria and the species of lactic acid consuming bacteria

A

lactic acid used by Megasphera elsdenii,
lactic acid producing bacteria Streptococcus bovis

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19
Q

At pH 5.1-5.3, what type of changes occur in the rumen and its microflora?

A

– the rumen papillae fall down/wither, epithelia damaged (rumenitis)

– bacteria named Fusobacterium necrophorum, reproduce quickly, which enter through injured rumen wall into the blood stream

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20
Q

Fusobacterium necrophorum are characterized as (what type of respiration)

A

facultative anaerobes

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21
Q

When Fusobacterium necrophorum enter the liver they

A

break up liver tissue,
feed on lactic acid produced during glycogenesis/glycogenolysis,
and encapsulate themselves in the liver’s serous membrane which results in liver abscesses.

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22
Q

incidence of liver abscesses in cattle fed high concentrate diets range from

A

10 to over 50%

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23
Q

why does epistaxis occur in SARA/ruminitis sometimes?

A

occurs secondarily to bacterial pneumonia or caudal vena cava
syndrome, both of which can be traced back to SARA induced rumenitis.

blood specifically originating from the lungs (not the nasal cavity)

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24
Q

Which cows are most vulnerable to rumen acidosis

A

Those in the post-calving period, when rumen microflora are not adapted to high amounts of concentrate .

(adaptation to ration includes microbial population, papillae development)

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25
Q

Cows with a high DM intake and/or who are fed a badly balanced ration are most susceptible to what

A

rumen acidosis

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26
Q

what makes it possible to sort concentrates from the total mixed ration?

A

dry or coarse-chopped forage makes it possible for the cows to sort concentrates from the rest

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27
Q

classic feed to induce rumen acidosis in the early post-partum period

A

excess of grain
(rapidly digestible starch, e.g. high moisture cereals)

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28
Q

Signs of subclinical rumen acidosis (4)

A
  • decreased and varying dry matter intake
  • Undigested grains and fibre parts in the faeces (high passage rate, the feed stays in the rumen only for a short time )
  • Milk fat content decreases
  • Limping, and cows with laminitis in the herd
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29
Q

Why does milk fat content sometimes decrease in cows with subacute ruminal acidosis (SARA)?

A

Due to reduced pH (below 6) in the rumen

– decreased amount of acetic acid produced
(previous theory)

– its been found that changes in the PUFA’s biohydrogenation pathways,
and the produced FA intermediates
(C18:2 t10, c12 (linoleic acid)) actually inhibit milk fat synthesis

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30
Q

Note, that if a high amount of a PUFA-rich feed
is fed the milk fat content does what

A

decreases, even when cows are not in acidosis!

so its the ration PUFA content that can inhibit milk fat synthesis and thus decrease its concentration

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31
Q

maximum amount of PUFAs per ration

A

should not exceed 25 g/kg DM

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32
Q

3 methods to Prevent acidosis in order of importance

A
  1. ration should contain adequate amounts of effective fiber
  2. regulate starch amount and pay attention to the starch sources (rate of digestibility etc.)
  3. Add sodium bicarbonate to the rations
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33
Q

effective fiber prevents acidosis how?

A

prickly rough roughage stimulates the ruman epithelium (aids rumination) and salivary production, thus increases the rumen’s buffer capacity and increases pH

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34
Q

grass silage % DM in a ration should be about 50%.

if grass and maize silage are fed together, what should be taken into account?

A

that maize silage also contains starch and sugars which must be adjusted for

260- 300g/kg DM mentioned in lecture but not sure exactly what - could be max. allowable starch content

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35
Q

which cereals are digested faster than others?

A

from fastest to slowest digestion =
barley > wheat/rye/triticale > oats > corn meal

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36
Q

what physical factor affects grain digestion speed?

A

from fastest to digest to slowest =
high moisture > ground/milled > cracked/crushed

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37
Q

NaHCO3 is useful for?

A

sodium bicarbonate buffer can prevent acidosis if added to the ration at an amount of ≥ 0.5 kg per day

to have any effect must be at minimum half a kg per ration

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38
Q

Feeding additional yeast cultures can help to..?
At what dose?

A

help in the prevention of acidosis. the theory is that they suppress the lactic acid producers and promote the lactic acid utilizers

the yeast may be added at doses such as 50g/day into the mineral additive portion of the ration

e.g. Saccharamyces servicie

note: lecturer doesn’t believe this theory but he presented it nonetheless

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39
Q

Functions of saliva (5)

A
  • Helps to moisten feeds
  • Ensures body’s water balance
  • Avoids bloat
  • Ensures nitrogen recycling
  • Neutralises acids (is an endogenous buffer, pH > 8.1…8.9)
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40
Q

what percentage of water enters into the rumen via saliva

A

70%

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41
Q

how does saliva aid in avoiding bloat development?

A

saliva has antifoaming properties

42
Q

salivary pH is

A

8.1…8.9
an endogenous buffer so ruminant saliva neutralises acids

acids in the rumen are both produced there and gotten from acidic feeds (silage, e.g. 4.2-4.7 -> 6.0-6.5)

43
Q

Amount of saliva produced depends on

A

effective fiber & rumination activity

44
Q

cows can produce how many liters of saliva per kg of ration dry matter

A

10-32 litres

45
Q

saliva production can be how much higher when
the ration contains more roughages instead of
concentrates

A

about 5 times higher when the ration contains more roughages instead of concentrates

46
Q

rumen pH depends on

A

the amount of saliva

(and other factors but this is a big one)

47
Q

Correlation between ration NDF content and rumen pH is

A

weak

48
Q

describe Chemical fibre

A

– NDF (min 26%), ADF (min 19%), CF (min 14%)

– has low nutritional value;
is measured in the laboratory;
characterises plant cell wall substances

49
Q

Effective fibre (feed physical properties) ensures (5)

A

– normal ruminal digestion
– rumen acidity -> pH
– rumination activity
– saliva production
– sufficiently high milk fat content

50
Q

Possibilities of checking the amount/presence of effective fibre (3)

A

▪ Sifting of feed particles (if there is less than 7% long feed particles in the TMR there is a high risk of SARA)

▪ Count the ruminating cows -> at least 50% of laying cows and 40% of standing but not eating
cows should be ruminating

▪ Sensorally -> prepared TMR should prick your own hand

51
Q

What are you counting when Counting the ruminating cows

A

looking for signs of appropriate presence of effective fiber

at least 50% of laying cows and 40% of standing, but not eating, cows should be ruminating

52
Q

Biogenic amines are formed mainly by

A

decarboxylation of amino acids in feeds when other sources for producing ATP are in short supply

53
Q

Biogenic amines are produced in the

A

rumen or in the large intestine as a result of microbial fermentation, primarily when energy is deficient

54
Q

Amino acids that may be decarboxylated when microbes are deficient of other energy sources (5)

A

Arginine -> Putrescine + CO2
Glutamine -> γ – aminobutyrate + CO2
Histidine -> Histamine + CO2
Tryptophan -> Tryptamine + CO2
Tyrosine -> Tyramine + CO2

55
Q

Endotoxins, lipopolysaccharides, may be produced in the rumen and can play a role in the etiology of

A

laminitis

56
Q

especially what two species of gram negative rumen bacteria produce ruminal endootoxins

A

Megasphera elsdenii and
Selenomonas ruminantium

57
Q

Endotoxins reduce rumen (3)

A

motility,
promote rumenitis and
laminitis

58
Q

Laminitis is a

A

Multifactorial disease, related to low rumen pH and histamine concentration in rumen and blood.

Acidosis increases the blood flow.
Blood pressure increases due to endotoxins and histamine production

Histamine is a vasoactive amine which causes arterial constriction and permeability of the blood vessels.

Blood vessels break, bleed and bruise.

59
Q

Laminitis and histamine theory

A

multifactorial disease centering around histamine release

60
Q

Reasons related to feeding that cause laminitis (5)

A
  • High proportion of rumen fermentable concentrates in the ration
  • Lack of effective fibre
  • Lower saliva production
  • Deficiency of minerals
  • Deficiency of vitamins
61
Q

How to strengthen hooves? (4)

A
  • Check nutrients needed for the keratinisation
    process
  • Amino acids (especially those which contain sulfur such as cysteine and methionine)
  • Minerals
  • Vitamins
62
Q

amino acid with the most important role in the keratinisation process

A

cysteine with the sulphur contained in it

63
Q

most important minerals for hoof health (5)

A

calcium,
copper
manganese
selenium,
zinc

64
Q

most important vitamin for hoof health

A

biotin -> needs longer feeding (10-20 mg per day)

65
Q

Displaced abomasum is a disease caused by

A

low ration fibre content and low rumen fill

  • Reasons are
    – low amount of effective fibre

– large amount of easily digestible fibre in the pre-
and post calving rations (pectin, hemicellulose ->
distillers & brewer’s grains, soyabean hulls etc.)

– large amount of rumen fermentable concentrates

66
Q

Displaced abomasum Usually appears

A

in the first month after calving

67
Q

Milk fever is a

A

calcium metabolism-related disease, which occurs most frequently in high yielding dairy cows up to 48 hours after calving, less often before calving

68
Q

In milk fever, the cow’s body cannot mobilize what?

A

calcium from either bones (resorption) nor from feed (absorption)

69
Q

What hormones may be inactive during milk fever?

A

parathyroid hormone (PTH) but also,

enzyme 1α-hydroxylase (catalyzes the synthesis of the active form of vitamin D),

and the vitamin D metabolite [1,25(OH)2D3] are inactive

70
Q

What receptors may be insufficient in number during milk fever?

A

insufficient number of Ca-mobilizing hormone receptors in target tissues (bones, intestine)

71
Q

In the dry period, the cow’s calcium requirement is very low – about

A

20g /day

72
Q

grass-legume mixture silages canccontain Ca in excess of

A

10g/kg DM

73
Q

due to calcium oversupply what happens?

A

calcitonin is active and the excess calcium is excreted
via faeces

74
Q

1 kg of colostrum contains how much Ca+?

A

2.5g of calcium per kg of colostrum

75
Q

For colostrum production, calcium is removed from where?

A

body fluids
and from peripheral tissues into milk

76
Q

clinical signs of milk fever (2)

A

the animal is unable to rise, and
the rear of the body becomes insensitive

muscles cease contracting and nerve impulses
are no longer transmitted

77
Q

Feeding strategy to reduce hypocalcaemia (milk fever)

A

The idea of the strategy is to activate „wake up“ parathyroid hormone (PTH) at calving time.

In the dry period the Ca requirement is low and PTH is inactive.

  • Strategy must increase Ca availability either from feeds or from bones.
  • Two possibilities:
    – feed low Ca-containing ration to activate PTH or
    – induce metabolic acidosis
78
Q

Two possibilities for activating PTH

A

– feed low Ca-containing ration to activate PTH or
– induce metabolic acidosis

79
Q

(CAB)

A

(dietary )Cation-anion balance

Body’s acid-base balance can be influenced by positively charged ions [cations -> potassium (K+) and sodium (Na+)], and by negatively charged ions [anions -> chlorine (Cl-) and sulphur (S2-)]

potassium
sodium
chloride
sulphur

are used to calculate this dietary balance

80
Q

Metabolic acidosis can be induced when

A

anionic salts are fed to cows.

This induces a shift in the cation-anion balance which can stimulate PTH to “wake up”.

81
Q

Negative Cation-anion balance in the ration results in (4)

A

– increases Ca mobilizaton from the bones
– activates Ca absorption mechanisms

– reduces hypocalcaemia
– prevents milk fever

82
Q

It is Mostly recommended that the prepartum ration Cation-anion balance should be from

A

-100 to -250 mEg/kg DM

– no clear agreement between researchers

83
Q

If the CAB is < 250 mEq/kg we can use

A

Anionic salts to shift this balance and thus increase the Sensitivity of PTH receptors

84
Q

if the CAB is > 250 mEq/kg we can administer

A

feed with Low ration Ca content < 20 g/day,
Vitamin D analogues
(increase Calciotropic hormones)

or

Ca gels,
pastes,
rumen boluses (Passive absorption)

85
Q

describe using anionic salts as a Feeding strategy to avoid
hypocalcaemia

A

Anionic salts -> feed only 2-3 weeks before calving.

– the most advanced and simplest way to avoid hypocalcaemia; can be easily used in the composition of TMR

86
Q

in order to avoid hypocalcemia, keep K

A

as low as possible (<1.2%),

+ narrow ratio of Ca:P (1.3 : 1)

87
Q

in order to avoid hypocalcemia, Add anionic minerals into the ration but also reduce

A

amount of cationic feeds in the ration

88
Q

Adding anionic minerals into the ration (but also
reducing the amount of cationic feeds in the ration)
– decreases what?

A

decreases metabolic alkalosis and shifts the organisms
acid-base balance towards metabolic acidosis

– this helps after calving to increase the availability of Ca
from bones and Ca absorption from small intestine

89
Q

describe Oral administration of CaCl2
give a pro and a con

A

Calcium chloride is an inorganic compound used to avoid hypocalcemia and consequent milk fever.

administer 2…3 times if a water solution, before and after calving; is effective, but vary labour intensive

as a paste/gel administer 2…3 times -> during calving, 12h and 24h after calving

Pro: both decrease blood pH, which stimulates Ca-releasing
hormones

Con: both have corrosive effects and can, in excess, induce
metabolic acidosis, which reduces feed intake

90
Q

describe Oral administration of Ca-propionate paste/gel
give a pro and a con

A

has slower effect than CaCl2

Pro: blood acidifier effect is missing and propionate is a glucose precursor in gluconeogenesis

Con: contains a smaller amount of Ca and therefore the administration amount should be large than CaCl2

91
Q

How does calving affect the immune system

A

Ability of the immune system declines with respect to calving

– the ability of neutrophils to destroy invasive bacteria in the body decreases about 40%

– the ability of lymphocytes to produce antibodies decreases by about 30%

92
Q

Effect of hypocalcaemia and milk fever on immunity

A

As a result of Ca deficiency

– increased cortisol secretion, which in turn can cause retained placenta

– decreases muscular tone
(cortisol = flabby smooth muscles), as a result:
▪ a flabby teat sphincter can allow bacterial invasion resulting inmastitis

▪ flabby uterus muscle -> retained placenta ->
bacterial invasion -> metritis

93
Q

Possibilities to strengthen the immune system (2-3)

A
  • Ensure the necessary metabolisable protein level (glutamine!)
  • Ensure requirements for the following are met (on DM basis in kg):
    – vitamins A (7500 IU) and E (60 IU)
    – Copper (15mg) , zinc (60mg), selenium (0.3mg)
    – check iron content
94
Q

high iron cotent can compete with what other mineral

A

can impede assimilability of copper

Also note,
* Free iron ion generates free radicals in the tissues, which cause “oxidative stress„
* Free iron ions required by bacteria

= too much iron bad

95
Q

Iron content should be
– in the ration ? mg per kg DM
– in drinking water ? mg per litre

A

– in the ration ‹ 750 mg per kg DM
– in drinking water < 0.4 mg per litre

  • Free iron ion generates free radicals in the tissues, which cause “oxidative stress„
  • Free iron ions required by bacteria
96
Q

How much time is needed to recover the population of lactic acid consuming bacteria?

A

B. 4-5 weeks

97
Q

What is the most important nutritional tool to avoid subclinical SARA?

A. Adding high moisture barley
B. Using buffers
C. Increase amount of effective fibre
D. Using yeast cultures

A

C. Increase amount of effective fibre

98
Q

What kind of relationship is between ration fibre (NDF) content and rumen pH ?

A. Weak
B. Medium
C. Strong

A

A. Weak

99
Q

Which minerals we should look when we form close-up dairy cow ration?

A. Ca, P, K, Na and Mg
B. Ca, P, Cl, S and Mg
C. Ca, P, K, Na, Mg, Cl and S

A

C. Ca, P, K, Na, Mg, Cl and S

100
Q

What is the most effective nutritional tool to prevent milk fever?

A. Use of Ca pastes and gels
B. Use of anionic salts and/or minimise Ca and
K amount in the ration
C. Inject calciotropic hormones

A

B. Use of anionic salts and/or minimise Ca and
K amount in the ration

101
Q

What can probably indicate more, that we have hypocalcaemia in the herd?

A. Low milk fat content
B. Reduced dry matter intake
C. Increased incidences of mastitis and metritis

A

C. Increased incidences of mastitis and metritis

Animal nutrition (19 decks)

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