NEB

Question 1

What 2 syndromes must be considered wrt NEB?

Answer 1

• ketosis
• fat mobilisation syndrome
  > 1* v 2*
• eg. LDA -> 2* ketosis (but also ketosis PDF LDA!)
• eg. Metritis -> 2* ketosis (and vice versa)
• eg. 1* ketosis d/t insufficient nutrient supply

Question 2

What substances are important wrt NEB?

Answer 2

• glucose (C6)
• C3 molecules (building Blocks)
• kerbs citric acid cycle
• gluconeiogensis
• vitamins and coenzymes for gluconeiogensis

Question 3

When will glucose levels be insufficient?

Answer 3

Early lactation

Question 4

What initiates gluconeiogensis and lipolysis?

Answer 4

Hypoglycaemia

Question 5

What is glucose necessary for?

Answer 5

Vital for brain and milk yield (milk yield insulin independent)
- other organs insulin dependent

Question 6

Krebs cycle - how do ketone bodies form?

Answer 6

• B oxidation of fatty acids releases Acetyl CoA molecules
• these enter the Krebs cycle to join with C4 making C6.
• if shortage of C4 ketone bodies produced to use up excess CoA

Question 7

Consequences of

Answer 7

• glucose deficient -> mobilisation of reserves -> BOTH fat and protein
• fat cow skinny cow pendulum (overconditioned -> NEB -> skinny-> poor fertility -> long dry period -> overconditioned) INIEFFICIENT

Question 8

Do cows get ketoacidosis?

Answer 8

No rare cf, cats etc.

- ketosis complex

Question 9

What is ketosis complex?

Answer 9

• excessive build up of ketone bodies in blood d/t accumulation of acetyl-coA
• ketones elevation v appetite (vicious cycle)
• also called acetonaemia.. NOT THE SAME AS ACIDOSIS
• cows don’t develop ketoacidosis (cats do)
  > change in volatile fatty acid composition d/t high carbs etc. causes acidosis NOT ketones!!! OPPOSITE THIGNS

Question 10

How common is ketosis complex?

Answer 10

• post partum 2-10w after calving
• lactation incidence 3-7%
• sub clinical ketosis much higher esp if poorly managed
• hypocalceamia, hypomagnesaemia, RFM, lameness, twin carrying cows

Question 11

How can ketosis be divided?

Answer 11

• 1* v 2*

- neurological v wasting form

Question 12

What is 1* ketosis

Answer 12

= starvation ketosis

• voluntary feed intake not meeting energy demands
• excessive catabolism
• sometime d/t specific deficient (choline, biotin, Vit B12)

Question 13

Causes of 2* ketosis

Answer 13

• any condition causing loss of appetite
• LDA/RDA
• endometriosis
• lameness
• mastitis (usually picked up)

Question 14

What is the wasting form of ketosis

Answer 14

• gradual reduction in appetite (esp refusing to eat concentrates)
• marked loss of body weight
• firm, dry feaces
• occasional transient bouts of staggering (can dip in and out of NEURO form)

Question 15

How is the neurological form of ketosis complex identified?

Answer 15

• sudden onset abnormal behaviour
• walk in circles, aimless wandering, head pushing, apparent blindness
• develop depraved appetite, lick things, chewing
• hyoeraesthesia
• uncoordinated gait
  +- 10% if ketosis cows get this

Question 16

Diagnosis of ketosis

Answer 16

• clinical signs
• blood glucose low
• blood beta-hydroxybutyrate (BHBA)
  >1.4mmol/l subclin
  > 2.5mmol/l Clin
• milk and urine ketone levels
• serum NEFAs elevated

Question 17

Why do cows not get ketoacidosis ?

Answer 17

50% levels cf. cats so not high enough to cause acidosis

Question 18

Tx ketosis

Answer 18

• IV dextrose (glucose) 100g quick
• IV dextrose (glucose) 200d slow drip
• steroids (NB: -> v milk yield, abortion though these cows empty so less of a problem)
• appetite stimulants eg. transfaunation
• propylene glycol 250ml BID unti the cow fights you off!

Question 19

Other names for fatty liver syndrome

Answer 19

• fat cow syndrome

- fat mobilisation syndrome

Question 20

Causes of fatty liver syndrome

Answer 20

• excessive weight loss
• fat mobilised as NEFAs (lipase) deposited
• can also become ketones, ATP, VLDLs but accumulates in liver

Question 21

Common presentation of fatty liver syndrome

Answer 21

• fat cow (>4 BCS)
• or very quickly losing weight cow
• inappetence or anorexia
• recumbent, NEURO signs and death
• typically have concurrent condition (RFM, endometrittis,, although low grade in severity, no response to Tx)

Question 22

When will a fat cow get skinny if pregnant?

Answer 22

Last few weeks of gestation - periparturient

- should not be fat when calving down!!!

Question 23

How is FLS related to pregnancy toxaemia?

Answer 23

• start last weeks gestation
• most prevalent around parturition
• twins
• v feed intake
• fat
• cattle and sheep

Question 24

Which cattle are PDF pregnancy toxaemia?

Answer 24

Beef or dairy crossed to beef

• esp Autumn calving herds
• internal parasitism ^ risk

Question 25

Clinical signs pregnancy toxaemia

Answer 25

``` > if shortly before calving - agitated - incoordinated - difficulty rising - scant feaces > if -+ 6 weeks around calving tend to be depressed - otherwise the same ```

Question 26

Which sheep do not commonly get pregnancy toxaemia?

Answer 26

- maiden ewes rare

Question 27

PDF for pregnancy toxaemia in sheep

Answer 27

- breed and age variation related to fecundity - case fatality can be 100% if clinical (cattle more subclincial) - outbreaks in flock higher mortality in lambs - may be assoc hypomagnesaemia, hypocalceamia

Question 28

Clinical signs pregnancy toxaemia sheep

Answer 28

- separate from flock appearing blind - constipation and bruxism - drowsiness and abnormal posture (stargazing) in coordination - ewes become recumbent - depression and coma - recovered ewes : WOOLBREAK

Question 29

Diagnosing FLS and pregnancy toxaemia

Answer 29

``` > Bloods - NEFA >0.7mmol/l - glucose Milk - fat >5% - protein 1.6 > liver biopsy >15% fat ```

Question 30

Tx FLS and pregnancy toxaemia

Answer 30

- as for ketosis + IVFT - consider insulin, steroids, choline, biotin, cobalt amine, BST [illegal uk growth hormone ] - high quality feed, glucose precursor rich

Question 31

Px FLS and pregnancy toxaemia?

Answer 31

Usually poor response to Tx

Question 32

Tx sheep FLS / pregnancy toxaemia

Answer 32

- emergency ceaser - Tx uraemia - drench q4-8hrs rehydration fluids as for scouring calves - immediately placed on supplementary feeding/better silage/concentrates - early cases Tx propylene glycol (C3 molecules)

Question 33

Control and prevention of FLS and pregnancy toxaemia

Answer 33

- Prevent fat and thin animals at calving - transition cow ration to reduce concurrent disease - early lactation cows fed balanced, high energy dense (glucose) ration *NB: balance risk of rumen acidosis these things will ^ risk** - good quality forage and maize silage - BCS recording - force fat cows to walk between housing and food - consider use of sodium propionate, niacin, biotin, cobalt - high risk cows : monensin bolus (KEXXSTONE) elanco $$$ not blanket Tx

Question 34

Control and prevention in sheep

Answer 34

- as with cattle for BCS Recoring - ID twins and triplets and feed accordingly towards end of gestation - provision of shelter and supplementary hay/silage - minimise stress at high risk periods

Question 35

When are animals shifted into NEB?

Answer 35

- periparturient cows and other mammals

Question 36

What is considered a high yielding farm? Range?

Answer 36

5,000 average - 10,000L/cow/year high yield