B5: Rumen Acidosis. B6: Ketosis, B7: Hypocalcemia Flashcards
Rumen acidosis. Types
- Subclinical
- Clinical
Rumen acidosis. Causes
- excess concentrates (RAC - readily available CHs: starch, sugars) in 1st phase of lactation —> increase of propionic acid —> drop of pH —> lactic acid increases (pH≤5,5)
- amount of saliva decreased —> buffering decreased
Normal pH of rumen
6,2 - 6,8
Rumen acidosis. Symptoms
- decrease of appetite
- rumen atony, bloat
- diarrhoea (osmotic, caused by lactic acid)
- lactic acidemia
- metabolic acidosis
- laminitis
- liver abscesses
Rumen acidosis. Prevention
- fibre supply — minimum 18% of DM
- buffers (sodium bicarbonate, magnesium oxide)
- sufficient concentrates feeding close to calving (2-4 kg) to adapt microflora to huge amount of starch given PP
Ketosis. Definition. What’s behind ketosis?
- production of ketone bodies > usage of ketone bodies
- ketone bodies can be found in blood, urine, milk (5:10:1)
- negative energy balance in first 8 weeks PP -> fat mobilisation -> increase of FAs level -> end product of FAs metabolism is acetyl-coenzyme A but it can’t enter Krebs cycle because oxaloacetae is missing because it is involved into GNG to maintain blood glucose level for milk fat production, lactose production and ovarian function -> acetyl CoA is transformed into ketone bodies
Consequences of high ketone bodies concentration
- ketonuria —> energy loss —> NEB is worsened
- acidosis
- reduced performance, milk production and fertility
How does the BCS of cows influence the incidence of ketosis?
Ketosis type 1: BCS ≤ 3-3,5 (undernutrition)
- can develop 3-6 weeks PP
Ketosis type 2: BCS > 3-3,5 (fatty cow syndrome)
- can develop 1-2 weeks PP
- more common than type 1
In both cases hypoglycemia
In case of type 2 will lead to insulin resistance —> hyperglycemia —> hypoglycemia (reduced appetite)
Fat cow —> higher leptin —> inhibition of neuroleptide Y release —> reduced food intake —> NEB
How to prevent ketosis ?
- feeding management of dry cows !!!
- keep them on maintenance level (feeding intensity = 1)
To reduce NEB:
- by-pass sugar
- by-pass fat (hot pressed rapeseed cake, heat-treated full fat soya, propylene glycol, glycerol, by-pass AAs)
Control of ketosis
Based on milk and urinary ketone bodies
Hypocalcemia. Types
- Subclinical (more common)
- Clinical (milk fever)
Consequences of hypocalcemia
- inhibition of muscle function
- NEB
- displaced abomasum
- decreased milk yield
- metritis
- dystocia
What’s behind the hypocalcemia?
- LACTATION
- insufficient PTH activity !!!
- last 2 weeks before parturition cows get alkaline daily ration (high value of CAB (cation-anion balance) caused by high K) (WHY WOULD WE DO THIS IF IT INCREASES CHANCE OF HYPOCALCEMIA LATER???)
- due to high CAB value after calving the PTH activity is limited —> calcium can’t be mobilised from the bones; also can’t be absorbed from GI because of lower vit D level and calcium reabsorption from urinary tract is also inhibited —> hypocalcemia
How to prevent the hypocalcemia?
- goal: to reduce CAB
- acidic diet: ammonium chloride, magnesium sulphate
Milk urea level
- (MUN - milk urea nitrogen)
- this concept reflects protein to energy ratio in the ration
- optimum: 3,5 - 6 mmol/l