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We have been told that you have to drench Propylene Glycol!
This is based on the fact that propylene glycol in a drench that stimulates the insulin response. The mode of action of our dry propylene glycol is different. We start feeding this product already in the close-up ration. In this way we supply a glucose precursor which helps to keep blood glucose level up already before the cow becomes ketotic. This results in a reduced NEFA mobilisation. In this way we prevent an overload of fatty acids entering the liver. In this situation there is less burden on the liver and less keton body production. We prevent massive keton body production around calving. Drenching is done at calving when the cow is already (sub)clinically ketotic.
What is the difference between primary and secondary ketosis?
Primary Ketosis is caused by a sudden energy deficiency around calving, which is caused by the onset of milk production, growth of the embryo and reduced rumen capacity. Secondary Ketosis is caused by a health problem e.g. acidosis, infection, hoof problems etc. which reduces the feed intake and therefore causes an energy deficiency.
What kind of symptoms can I expect when transition is not going smoothly?
Typical symptoms are: reduced appetite, dull listless behaviour, long birth process, retained placenta , early metritis, ruminal stasis , DA’s (displayed abomasum), slow starters, ketosis, milk production is low, mastitis, milk fever.
Why do we see a high percentage of metabolic disorders during transition?
Many cows suffer from acute energy and calcium shortage around calving because they have to switch over from ‘maintenance’ with low nutritional demands to ‘production’ with high demands. This sudden change-over is the problem.
What is Ketosis?
- Reduced matter intake: at the end of the dry period the feed intake is reduced by 25-30%. The cow is faced with an acute energy shortage.
- Mobilization body fat: the cow tries to compensate the reduced dry matter intake by mobilizing body fat. The cow switches to a high fat metabolization.
- Fatty liver syndrome: the liver cannot metabolize this high amount of fatty acids, because not enough enzymes are produced. Not all fatty acids are completely metabolized (production of keton bodies), fat storage in liver occurs and glucose production is reduced which induces more fat mobilization (downward spiral). Keton bodies reduce feed intake.
- Reduced milk production: reduced milk yield. Higher fat level in the milk. Lower protein level in the milk.
- Reduced fertility: reduced insulin concentration in the blood. Reduced LH-hormone production. Reduced growth rate of egg-cell. Reduced development potential of egg-cell (After-effect). Less ovulations. Embryonic death. Reduced pregnancy percentage. Index insemination/pregnant is increased. Higher calving interval.
- Lower resistance: reduced resistance increases the risk of mastitis, uterus inflammation and claw-inflammation (secondary infections).