Monitoring nutrition on farm Flashcards
Which diseases are we trying to avoid?
- ketosis and NEB
- hypocalcaemia
NEB - when are cows at risk?
- just after calving
- at peak lactation
Effects of subclinical ketosis/NEB
- reduced milk quality
- decreased fertility
- impaired immune function (-> metritis/RFM, mastitis)
- role in other dz (e.g. LDA)
BCS - key targets
- 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
Metabolic profiles
- 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
Key indicators of energy balance
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
Using milk parameters
- 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?
How does NEB affect BF:Pr ratio?
- milk protein tends to be lower, and butterfat tends to go up (more circulating fat, some tends to leak into the milk)
How does increased yield affect BF:Pr ratio?
- will dilute the constituents out more so have lower protein and butterfat
How does increased fibre affect BF:Pr ratio?
- same protein, increased butterfat
Ration analysis
- Assess feed intake (“DMI”)
- Calculate ration energy density and therefore daily energy intake
- Compare to cow requirements
- Specialist software available
NEB - effect on transition/calving
- poor DMI
- excess BCS/overfeeding
NEB - effect on early/peak lactation
- poor DMI
- low ration energy density
Rough target DMI for transition (late dry period) cow
> 12kg/d
Rough target DMI for high yielding cow
> 23kg/d
Measuring DMI
- DMI = (kg fed per head – kg leftover refusals per head) * DM% of ration
- or compared to what the ration sheet (“recipe”) says
Improving dry matter intake
- 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
Ration formulation (& why it can go wrong)
- 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
Why can’t we just increase the diet energy density?
- Energy densities of ingredients don’t vary all that much
- Need to maintain fibre intake to keep rumen healthy
Additives/”treatments” to ration formulation
- 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
Hypocalcaemia: Aetiology
- Calcium in milk»_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”
Hypocalcaemia: Pathophysiology
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
Hypocalcaemia: Diagnosis
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
Hypocalcaemia target rate
<5 cases/ 100 cows/ year is a common target
Hypocalcaemia prevention
- Feeding in the final 2-3 weeks before calving is key to preventing hypocalcaemia
DCAB
- 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
DCAB manipulation - “True” or “Full” DCAB
- 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
DCAB manipulation - “Partial” DCAB
- 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
DCAB of grass silage
- can vary substantially, and may be >500mEq/kg DM
Other methods of hypocalcaemia prevention
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
Why is dry cow feeding vital?
To:
- Maintain DMI around calving, and prevent problems with early lactation negative energy balance
- Prevent clinical and subclinical hypocalcaemia
How to maximise DMI - the ration
- 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
How to maximise DMI - feed face design
- 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)
How to maximise DMI - other
- Ensure adequate water access
- Maintain appropriate body condition
- Maintain appropriate environment (e.g. avoid heat stress)
Dry cow ration
- Dry cows are not lactating so require less energy
- Maximising intakes is still important
- The ration contains a much higher proportion of straw
How to reduce sorting
- Cows may “sort” the ration
- Compare before and after
- Avoid with short chop length for long fibre
