Milk fever is a metabolic disorder caused by insufficient calcium, commonly occurring around calving. Milk fever, or Hypocalcaemia, is when the dairy cow’s calcium requirement exceeds the bodies ability to mobilize calcium. Milk fever generally occurs within the first 24 hours post-calving, but can still occur two to three days post-calving
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Milk fever, both clinical and sub-clinical is the most harmful macro mineral deficiency that can effect transition cows. Because Calcium (Ca) is essential for muscle tone and contraction, Poor bone mobilization of calcium can result in slow calving’s and cows going down with milk fever. Poor muscle tone also contributes to displaced abomasum and weak uterine muscle contractions which are involved in retained placentas. Further to this milk fever can lead to immune suppression and a reduction in DMI (dry matter intake) and appetite which can further increase negative energy balance around time of calving leading to further problems such as;
• Fatty liver
• Ketosis
• Reduced milk yield (up to 1,000 L per cow)
• Metritis
• Mastitis
• Lower fertility
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The day she calves, a cow will commonly produce 10 litres of colostrum, containing about 23 grams of calcium. She will need another 23 grams for maintenance resulting in a total requirement which is about 12 times the amount of Ca circulating in her blood at any point in time. Where does she get the extra Ca she needs for lactation? Most cows adapt to the demand by increasing the absorption of Ca from the diet, mobilizing Ca from bone and reducing urinary Ca excretion. Cows that don't adapt effectively will end up with low blood calcium levels (hypocalcemia). Strategies to prevent these problems are aimed at feeding the dry cow to prepare her systems for the increased Ca demand at calving.
Limiting total dietary Ca intake to less than 30 grams/head/day in the close-up dry period has been the most commonly recommended strategy to help reduce the incidence of milk fever. High ration calcium levels result in decreased absorption rates. In addition, when higher Ca intakes keep blood Ca levels high, excretion increases and the hormonal mechanism for mobilizing Ca from bone is effectively shut down.
K+ absorbed from forages causes the blood and urine of the cow to become alkaline. High blood pH inhibits the ability of the cow to mobilise Ca from the bone a mechanism that is vital post calving. To help avoid this
• Use forage from fields that had little or no manure applied
• Use later cut silage such as Autumn silage as it is generally lower in K
• Use mature crops such as straw that are naturally low in K to substitute silage out of the diet
Another strategy commonly used on farm is dietary cation-anion balance (DCAB). Cations, including sodium (Na+ ) and potasium (K+ ), carry positive charges and increase pH in the blood. Anions, including chlorine (Cl- ) and sulphur (S2-), carry negative charges and have an acidifying (pH lowering) effect in the blood. When the balance between cations and anions results in a net negative charge (negative DCAB), blood pH is lowered. To neutralize the lower blood pH caused by negative DCAB, the cow mobilizes buffers, including Ca phosphate and bicarbonate from bone. These two strategies are both aimed at activating mechanisms which allow the cow to quickly draw from bone Ca reserves when her demand for Ca increases abruptly at calving. This can be easily done on farm using magnesium chloride flakes and pre-calver salts.
Mg has a vital role in Calcium (Ca) metabolism and body Ca mobilisation. Increasing dietary Mg from 0.3 to 0.4% of your cows’ total diet will help reduce the risk of milk fever. In the majority of cases this will mean adding at least 25g of Mg to the diet of your cows from supplements.
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Dock Road
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