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Y4 Farm - Production diseases > Monitoring nutrition on farm > Flashcards

Monitoring nutrition on farm Flashcards

1
Q

Which diseases are we trying to avoid?

A
  • ketosis and NEB
  • hypocalcaemia
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2
Q

NEB - when are cows at risk?

A
  • just after calving
  • at peak lactation
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3
Q

Effects of subclinical ketosis/NEB

A
  • reduced milk quality
  • decreased fertility
  • impaired immune function (-> metritis/RFM, mastitis)
  • role in other dz (e.g. LDA)
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4
Q

BCS - key targets

A
  • no change over dry period
  • max decrease of 0.5 between calving and peak lactation
  • aim for 2.5-3 at calving, esp avoid >3
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5
Q

Metabolic profiles

A
  • Blood sampling a random selection of cows at specific stages
  • Usually “transition” cows (e.g. 21-7d pre-calving) and fresh calvers (e.g. 10-25 days in milk)

How many samples?
- Varies a bit with size of group (e.g. number of dry cows)
- 8-12 samples/group often appropriate

Interpreting results
- Target prevalence of high BHB or NEFA <10-20%
- Usually means any abnormal results suggest a problem
- >=3/12 abnormal results taken to indicate herd problem

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6
Q

Key indicators of energy balance

A

BHB (beta-hydroxy butyrate)
– Ketone body
– Current energy supply/demand
– Esp useful in fresh calvers

NEFA (non-esterified fatty acids)
– Transport form of fat
– Indicator of fat mobilisation
– Esp useful for transition

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7
Q

Using milk parameters

A
  • Many approaches – BF:Pr ratio (FPR) most common
  • None have good research evidence for UK situation, but common in practice
  • 1.4 is the cut off for normal BF:Pr for what is thought of as abnormal - may have NEB.
  • Easy “first step”, then investigate further with BCS/bloods?
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8
Q

How does NEB affect BF:Pr ratio?

A
  • milk protein tends to be lower, and butterfat tends to go up (more circulating fat, some tends to leak into the milk)
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9
Q

How does increased yield affect BF:Pr ratio?

A
  • will dilute the constituents out more so have lower protein and butterfat
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10
Q

How does increased fibre affect BF:Pr ratio?

A
  • same protein, increased butterfat
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11
Q

Ration analysis

A
  • Assess feed intake (“DMI”)
  • Calculate ration energy density and therefore daily energy intake
  • Compare to cow requirements
  • Specialist software available
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12
Q

NEB - effect on transition/calving

A
  • poor DMI
  • excess BCS/overfeeding
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13
Q

NEB - effect on early/peak lactation

A
  • poor DMI
  • low ration energy density
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14
Q

Rough target DMI for transition (late dry period) cow

A

> 12kg/d

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15
Q

Rough target DMI for high yielding cow

A

> 23kg/d

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16
Q

Measuring DMI

A
  • DMI = (kg fed per head – kg leftover refusals per head) * DM% of ration
  • or compared to what the ration sheet (“recipe”) says
17
Q

Improving dry matter intake

A
  • Minimise (impact of) group changes
  • Easy access, trough space per cow
  • Avoid over-conditioned cows (especially at calving)
  • Maximise ration palatability
  • Manage environment appropriately (temp, humidity, comfort)
  • Especially important around calving – “natural” drop in DMI
18
Q

Ration formulation (& why it can go wrong)

A
  • Diet usually carefully formulated by nutritionist
  • Almost always using software which flags “problems”

Why might it go wrong?
- Something “wrong” with calculated ration?
- Not being mixed or fed correctly?
- An element of the diet has changed
– e.g. silage changes in quality as the clamp is fed

19
Q

Why can’t we just increase the diet energy density?

A
  • Energy densities of ingredients don’t vary all that much
  • Need to maintain fibre intake to keep rumen healthy
20
Q

Additives/”treatments” to ration formulation

A
  • Propylene glycol
  • Protected methionine
    – Improves fat export from liver
  • Linoleic acid
    – Fatty acid with less tendency to accumulate in liver
  • Monensin
    – Antibiotic, changes rumen flora to aid energy balance - bolus for “at risk” cows
    – Most herds shouldn’t need to use Monensin
21
Q

Hypocalcaemia: Aetiology

A
  • Calcium in milk&raquo_space;> circulating calcium pool
  • Sudden increase in demand at calving (lactation)
  • If stores (mainly bone) not mobilised quickly enough:
    – Circulating [Ca] falls
    – Clinical or subclinical “milk fever”
22
Q

Hypocalcaemia: Pathophysiology

A

decreased plasma calcium concentration -> decreased muscle activity

effect on skeletal muscle:
- clinical signs of milk fever (recumbency etc)

effect on smooth muscle:
- subclinical effects
- uterus -> increased uterine infection
- GIT -> increased abomasal dz, decreased DMI

23
Q

Hypocalcaemia: Diagnosis

A

Clinical milk fever:
- Characteristic clinical signs
- Blood sample shows low plasma Ca

Subclinical milk fever:
- More difficult
- Control restored within 2-3d of calving
- Can monitor
– Clinical case rate
– Using blood samples within 24-48hrs of calving
– Urine macrominerals

24
Q

Hypocalcaemia target rate

A

<5 cases/ 100 cows/ year is a common target

25
Q

Hypocalcaemia prevention

A
  • Feeding in the final 2-3 weeks before calving is key to preventing hypocalcaemia
26
Q

DCAB

A
  • Difference between concentrations of major cations (Na+, K+) and major anions (Cl-, S2-) in the diet
    – i.e. it’s just a chemical property of a feedstuff or diet
  • DCAB = ([Na+] + [K+]) – ([Cl+] + [S2-]) (all in mEq/kg DM)
  • Diets with low DCAB (<0 mEq/kg DM) induce mild metabolic acidosis
  • metabolic acidosis means:
    – Enhanced uptake of Ca from the GI tract
    – Ca mobilisation from bone
    – Higher rate of vitamin D3 activation per unit PTH
    – Increased target tissue sensitivity to PTH and activated vit D3
    – So the cow is able to mobilise Ca from body reserves more quickly
27
Q

DCAB manipulation - “True” or “Full” DCAB

A
  • Aim for diet DCAB around -100 mEq/kg DM
  • Likely to require use of anionic salts (e.g. MgCl2, MgSO4)
    – anionic salts don’t taste nice so large use will decrease DMI
  • Usually needs Ca supplementation too
  • Effective but more involved/ expensive
28
Q

DCAB manipulation - “Partial” DCAB

A
  • Aim for diet DCAB around 0 to -50 mEq/kg DM
  • Often just by choosing lower DCAB feeds, may also use salts
  • Usually doesn’t require Ca supplementation
  • More common in lower yielding herds
29
Q

DCAB of grass silage

A
  • can vary substantially, and may be >500mEq/kg DM
30
Q

Other methods of hypocalcaemia prevention

A

Ca restriction
- “Conditions” homeostatic mechanisms to be more efficient at Ca uptake/mobilisation
- Hard to get diet [Ca] low enough with normal feeds
- Ca binding feedstuffs available
– Work well but moderate cost
– Becoming popular in UK

Other methods
- Mg supplementation
– Mg required for production of PTH
– Generally not very effective alone
- Prophylactic treatment
– Ca boluses most appropriate
– Often targeted e.g. at older cows

31
Q

Why is dry cow feeding vital?

A

To:
- Maintain DMI around calving, and prevent problems with early lactation negative energy balance
- Prevent clinical and subclinical hypocalcaemia

32
Q

How to maximise DMI - the ration

A
  • Increase palatability
  • Improve taste e.g. molasses
  • “Open” ration
  • Approximately 50% dry matter
  • Allow 10% refusals (left over) for true ad lib feeding
  • Remove left over feed
  • Make ration fresh daily
  • “Push up” regularly
  • Keep feed face/trough clean
33
Q

How to maximise DMI - feed face design

A
  • Adequate feed face (length)
  • Ensure neck rail not pushing on neck
  • Shiny feed surface
  • Good access to feedface
  • Dividers to reduce bullying (must be comfortable)
34
Q

How to maximise DMI - other

A
  • Ensure adequate water access
  • Maintain appropriate body condition
  • Maintain appropriate environment (e.g. avoid heat stress)
35
Q

Dry cow ration

A
  • Dry cows are not lactating so require less energy
  • Maximising intakes is still important
  • The ration contains a much higher proportion of straw
36
Q

How to reduce sorting

A
  • Cows may “sort” the ration
  • Compare before and after
  • Avoid with short chop length for long fibre

Y4 Farm - Production diseases (18 decks)

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