Nutritional Management of the Calving and Lactating Cow Flashcards

1
Q

What are the risks of having a low body condition score (BCS) at calving in dairy herds?

A
  • Decreased dominant follicle diameter
  • Reduced insulin and IGF-1
  • Low LH pulse frequency

• Poor Fertility!

  • Plus increased risk of :
  • Retained placenta
  • anoestrous
  • metritis
  • Lameness
  • All of which contribute to further reductions in conception rate and increased days open (not in calf)
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2
Q

What are the risks of having a high BCS at calving in dairy herds?

A
  • Increased risk of:
  • Metritis • Ketosis
  • Milk fever
  • Cystic ovaries
  • All of which are likely to reduce conception rate and increase days open

• Poor fertility!

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3
Q

What is the recommended BCS for calving?

Avoid more than …. loss from partition to insemination

A
  • Calve in BCS 3 (on a scale of 1 to 5)
  • 5 on a scale of 1 to 9
  • Midrange
  • Avoid more than 0.5BCS loss from parturition to insemination/joining
  • Quality & quantity of DMI
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4
Q

High ….. can reduce progesterone [] and can lead to embryo loss

A

High DMI/energy

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5
Q

High ….. and high …. in diet around insemination reduces chances of conseption

A

high protein and high energy

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6
Q

How do we calculate the mineral requirement for a lactating cow?

A
  • Requirements calculated in similar way to energy and protein i.e. replace endogenous losses (faeces, urine skin)
  • Using factorial methods and balance studies
  • Recommended feeding values
  • Requirements are usually in gross amounts
  • Need to consider availability in feed
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7
Q

Ca and P in regards to lactation?

A
  • Net req. for lactation is amount deposited in milk
  • milk quality
  • High at peak lactation
  • may be difficult to obtain all from diet
  • Absorption highly variable
  • **Ratio important
  • MORE CA THAN P**
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8
Q

Where does most Ca loss occur?
How can we combat these losses through nutrition?

A
  • Renal losses small, but can be elevated with anionic feeds
  • Negatively charged feeds (salts)

• DCAD (Dietary Cation Anion Difference)

  • Prevent hypocalcaemia during transition
  • Most lost through faeces, colostrum and milk
  • PTH and 1,25-dihydroxycholecalciferol (calcitriol or 1,25- dihydroxyvitamin D3 ) and calcitonin key hormones
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9
Q

What is the process of hyPOcalcaemia (low)?

A
  • PTH synthesised by parathyroid gland
  • Stimulates Ca resorption from bone
  • PTH stimulates calcitriol synthesis in kidneys from precursor (25 hydroxyvitamin D3 )
  • Stimulates Ca transport proteins in gut to absorb more Ca, also stimulates Ca resorption
  • Requires vitamin D from diet or synthesis from cholesterol in skin on UV exposure
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10
Q

What is the process of hyPERcalcaemia (high)?

A

Calcitonin released from thyroid gland to promote bone mineralisation and reduce renal Ca reabsorption (increasing Ca excretion)

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11
Q

What are the direct economic costs of milk fever?

A
  • Treatment cost and reduced milk yield
  • 4-28% of cows relapse and may become ‘downer’ cows (20-67% of these die)
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12
Q

What are the indirect economic costs of milk fever?

A
  • Dystocia
  • poor appetite
  • uterine prolapse
  • retained placenta
  • Metritis (inflammation of uterine wall)
  • displaced abomasum
  • greater risk of developing ketosis and mastitis
  • All related to reduced muscle function
  • Low [Ca] also reduces insulin production
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13
Q

What are the dietary options for reducing milk fever?

A

Ca and vitamin D

• Manipulating dietary cation-anion difference (DCAD) by feeding anionic salts

  • Mobilise Ca from bones during transition
  • Replenishing Ca reserves
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14
Q

What are the non-diet risk factors associated with milk fever?

A

•Breed

  • Channel Island breeds most susceptible
  • Reduced concentration of intestinal receptors for calcitriol
  • *• Climate**
  • Incidence increases with evaporation rate
  • Greatest in cold, wet weather when big difference between max and min temperatures
  • Related to DMI and stress-induced adreno-cortical hyperactivity
  • Ca and Mg metabolism alter in cold-stressed sheep
  • Greater Ca excretion and lower plasma [Mg]
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15
Q

How can we manage milk fever?
-think age, BCS, genetics

A
  • Management
  • Greater in older cows
  • Reduced ability to mobilise bone Ca, reduced calcitriol production, reduced number of intestinal Ca receptors (ie less Ca absorbed)
  • Greater if BCS >3.5 and <2.5
  • Reduced DMI
  • Greater tissue catabolism
  • Increased milk protein (and therefore Ca secretion)
  • Greater in assisted cows
  • Less in induced cows and twin-bearers
  • More favourable physiological status
  • Genetics
  • More likely if already had Milk Fever
  • h2 estimates 0.09-0.13
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16
Q

Response to energy supplements

  1. efficiency of ME use for milk

How do acetate levels affect this?

A
  • Too low
  • Insufficient short to medium chain fatty acids synthesised required for milk synthesis
  • Too high
  • Insufficient propionate for gluconeogenesis
17
Q

Response to energy supplements

  1. Diet Substitution
A
  • Predicted increase in milk yield often not achieved due to substitution
  • Substituting forage for supplement vis. vis.
  • Greater for high quality forages
  • Greater at higher concentrate intake
  • Adjust stocking rate accordingly
18
Q

Response to energy supplements

  1. Milk yield and liveweight
A
  • Energy above maintenance partitioned between milk and liveweight gain/reduction in liveweight loss
  • Varies between genotypes
  • Proportion diverted to milk tends to decrease with increased energy intake
  • Affected by rumen VFA proportions
  • **Increase acetate = more milk
  • Increase propionate = more LWG**
  • Stage of lactation
  • Milk yield response greatest in early lactation
19
Q

response to energy supplements

  1. Milk components
A

• Increasing concentrates tend to suppress milk fat levels

  • Insufficient acetic acid
  • 22-24% ADF (32-36% NDF) commonly recommended