Misc Flashcards
What are the 2 main consequences of NEB in the periparturient cows?
Ketosis
Fat mobilisation syndrome
NEB can be 1ry or 2ry
Why has selecting for increased milk yield led to incr susceptibility to NEB?
Early lactation- glucose insufficient. Glucose goes to udder independent of insulin control, therefore drains the cows glucose.
What is the ketosis complex?
Excessive build up of ketone bodies due to accumulation of acetyl-coA due to lack of C3 molecules. Reduces appetite- vicious cycle. Happens post partum 2-10wks after calving
What causes primary ketosis?
Vol feed intake can’t meet energy demands. Excessive breakdown of body fat and muscle.
What causes secondary ketosis?
Any condition that makes cows lose appetite. E.g. LDA/RDA, (endo)metritis, lameness, (mastitis)
What is the ketosis wasting form?
Gradual reduction in appetite, refuses to eat concentrates, marked loss of body wt, firm dry faeces, occasional transient bolus of staggering.
What is the ketosis neurological form?
Sudden onset of abnormal behaviour. Walks in circles, aimless wandering, head pushing, apparent blindness. Develop depraved appetite, licking of skin and objects, chewing. Hyperaesthesia, incoordinated gait. About 10% of ketosis cases.
How is ketosis in cows diagnosed?
Clinical signs. Blood glucose (low end). Blood beta-hydroxybutyrate >1.4 subclinical >2.5mmol/l clinical. Milk and urine ketone levels. Serum NEFAs can bee elevated
What is the treatment for ketosis?
IV dextrose 100g quick or 200g slow. Corticosteroids. Appetite stimulants. Propylene glycol 250ml bid (rich in C3 molecules) until cow fights you off.
What is fatty liver syndrome?
Excessive weight loss. Fat mobilised as NEFA (due to low glucose), deposited in liver. Typically BCS >4 if early on, or was BCS 4 2wks ago but now 2- skinny. Inappetence to anorexia. May become recumbent, get neuro signs and die. Often concurrent condition e.g. RFM or (endo)metritis that doesn’t respond to tx.
What is pregnancy toxaemia?
Similar to FLS but presented at a diff stage and typically in diff animal. Last few weeks of gestation, prevalent around parturition, twins. Reduced feed intake 1ry cause, fat animals at risk (lots to mobilise)
How does pregnancy toxaemia present in cattle?
Typically beef. More common in autumn calving. Internal parasitism may incr risk.. When shortly before calving, cows/heifer agitated, incoordinated, difficulty rising, scant faeces. When +/- 6 weeks before calving tend to be depressed.
How does pregnancy toxaemia present in sheep?
Uncommon in maiden ewes. Case fatality about 100% in clinical cases (fat–> kidney, fatal uraemia). Can be outbreaks. May be associated with hypomag and hypocal. Separate themselves, apparently blind, constipation common, grinding teeth, periods of drowsiness and abnormal posture and incoordination. Recumbent, severe deoression, coma. Recovered ewes show wool break
How do you diagnose FLS and pregnancy toxaemia?
Blood- NEFA (>0.7mmol/l), glucose (5%, protein 1.6 Liver biopsy (>15% fat)
How is FLS and preg tox treated?
Tx as for ketosis combined with IVFT. Consider insulin, steroids, choline, biotin, cobalt amine, BST. High quality feed, glucose precursor rich. Usually poor response to tx- too late