Negative energy balance Flashcards
What factors need considering in NEB?
- glucose
- C3 molecules (more important in ruminants than glucose)
- krebs (citric acid) cycle
- gluconeogenesis
- vitamins
- co-enzymes
Describe glucose levels in early lactation
Insufficient in early lactation –> gluconeogenesis and lipolysis d/t drop in insulin. Lack of glucose –> cascade of problems
Consequences of NEB
- glucose deficit
- reserve mobilisation (fat and protein)
- ketosis complex
- fat mobilisation syndrome
Describe ketosis complex
- excessive build up of ketone bodies in blood d/t accumulation of acetyl-CoA (as precursors are turned into glucose?)
- increased ketones –> reduces appetite –> vicious cycle
- aka acetonaemia which is not same as acidosis
T/F; cows don’t develop ketoacidosis
True
When does ketosis complex occur?
- post-partum (2-10 weeks after calving)
- lactation incidence 3-7%, some farms higher
- subclinical ketosis higher, esp poorly managed farms
- RISK FACTORS: hypoCa, hypoMg, RFM, lame, twins
How does hypoCa lead to ketosis complex?
HypoCa –> gut stasis –> fat mobilisation –> ketosis complex
Categorisation - ketosis complex
- primary vs secondary
- wasting form vs neurological form
Describe primary ketosis
- VFI cannot meet energy demands
- excessive breakdown of body fat and mm
- sometimes d/t specific nutritional deficiencies affecting energy metabolism (choline, biotin, vit B12)
= ‘starvation ketosis’
Describe secondary ketosis
- any condition causing cow’s appetite to decrease:
- LDA/RDA
- (endo)metritis
- lameness
- (mastitis)
Describe ‘wasting form’ of ketosis
- gradual reduction in appetite, cows refuse to eat concentrates
- marked loss of body weight
- firm, dry faeces
- occasional bouts of staggering
Describe ‘neurological form’ of ketosis
- sudden onset ‘abnormal’ behaviour
- walk in circles, aimless wandering, head pushing, apparent blindness
- develop depraved appetite, lick skin and objects, chewing
- hyperaesthesia, uncoordinated gait
+/- 10% of ketosis cows
Dx - ketosis
- CS
- blood glucose (low end)
- Beta hydroxybutyric acid (BHBA): >1.4 mmol/l subclinical, >2.5mmol/l clinical
- milk and urine ketone levels
- serum NEFAs can be elevated
Tx - ketosis
- IV dextrose 100g, quick
- ** IV dextrose, 200g, slow drip (5 hours) ***
- corticosteroids sometimes
- appetite stimulants (transfaunation)
- propylene glycol 250ml, BID, until cow fights you off!
Describe fatty liver syndrome
= fat cow syndrome = fat mobilisation syndrome
- excessive wt loss
- fat mobilised as NEFA (lipase) is deposited in liver (fat can also be turned into KB, ATP and VLDL but these are less preferable pathways)
CS - fatty liver syndrome (FLS)
- BCS recumbent
- neuro signs
- death
- typically have concurrent condition (RFM, (endo)metritis, although low grade in severity, that doesn’t respond to tx)
Outline relationship b/w FLS and pregnancy toxaemia
- start last few weeks of gestation
- most prevalent at parturition
- twins
- reduced VFI is primary cause
- fat animals are at risk
- cattle and sheep mainly
Describe pregnancy toxaemia of cattle
- beef
- usually autumn calving herds (relates to feed available, palatability, quality)
- internal parasitism increases the risk
- when it occurs shortly before calving, cows/ heifers are agitated, incoordinated, have difficulty rising, scant faeces
- when +/- 6 weeks before calving, the tend to be depressed, rest the same
Describe pregnancy toxaemia of sheep
- uncommon in maiden ewes
- breed and age variations relate to fecundity
- fatality approaches 100%, in clinical cases
- outbreaks in flock also have higher lamb mortality
- Associated with (sometimes): hypoMg, hypoCa
CS - pregnancy toxaemia of sheep
- affected ewes separate from flock, apparently blnd
- constipation common and grinding of teeth
- periods of drowsiness and abnormal posture (‘stargazing’) and incoordination
- ewes become more recumbent, severe depression, coma
- recovered ewes show evidence of ‘woolbreak’
Dx - FLS and pregnancy toxaemia
- BLOOD: NEFA, glucose, liver enzymes, fatal uraemia in sheep
- MILK; fat > 5%, protein 1.6%
- LIVER BIOPSY (research): >15% fat
Tx - FLS and pregnancy toxaemia
- as for ketosis + IVFT
- consider: insulin, steroids, choline, biotin, cobalt amine, BST (illegal in EU)
- provide high quality feed, glucose precursor rich
- depends on case, usually poor response
How does insulin with IVFT dextrose help?
allows glucose to enter cells faster
Tx - sheep - FLS and pregnancy toxaemia
- **drench q4-8 hours with rehydration solution (like scouring calves) **
- induce parturition or CS
- affected flocks IMMEDIATELY place on supplementary concentrates/ cereal and early cases tx with propylene glycol
Control/prevention - FLS and pregnancy toxaemia in cattle
- prevent overly fat or poor BCS at calving
- transition cow ration to reduce concurrent dz
- early lactation cows: balance, high energy dense (glucose) ration, aim to minimise rumen acidosis
- good quality forage, maize silage
- strategic BCS recording
- fat cows to walk moderate distance for feed/water
- consider: sodium propionate, niacin, biotin, cobalt
- high risk cows: monensin bolus (KEXXTONE)
Control/prevention - FLS and pregnancy toxaemia in sheep
- BCS monitoring
- twins and triplets ID for supplementary feeding at end of gestation
- provide shelter and supplement hay/silage for ewes during inclement weather and careful planning of husbandry events to minimise stress at high risk periods
2 features of negative energy balance (NEB)
- ketosis
- fat mobilisation syndrome
