Calcium Metabolism of Peri-Parturient Dairy Cattle and Prevention of Milk Fever by Strategic Calcium Supplementation

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Calcium Metabolism of Peri-Parturient Dairy Cattle and Prevention of Milk Fever by Strategic Calcium Supplementation

Punita Kumaria, A K Singhb, Ravindra Kumarc, Shailendra Rajaka and Nandani Kumaria

a: Assistant Professor cum Junior Scientist, Ranchi veterinary College, BAU, Ranchi

b: Assistant Professor, FVAS, RGSC, BHU

c: Head, Department of Livestock Production Management, RVC, BAU, Ranchi

Introduction

The transition period (3 weeks before to 3 weeks after parturition) is critically important for health, production and profitability of dairy cows. This period is characterized by tremendous metabolic and endocrine adjustments that the cows must experience from late gestation to the early lactation. The most important physiological changes occurring during this period are the reduction in dry matter intake around parturition and a sudden increase in nutrients that the cows need for milk production.

Milk fever (parturient paresis) is a hypocalcemic disorder associated with the onset of lactation in dairy cows. Hypocalcaemia may be clinical or subclinical. Clinical hypocalcemia, also known as milk fever and is a particular concern for the newly calved cow. Most of cases of milk fever occur within 24 hours of calving. Generally cows with milk fever are recumbent and are unable to rise as a result of low blood Ca, whereas cows with subclinical stage have no clinical signs of hypocalcemia. Hypocalcemia reduces dry matter intake, milk production and fertility and increases the risk of secondary diseases such as ketosis, retained fetal membranes, displaced abomasum and mastitis and the incidence of dystocia and uterine prolapse.

Milk Fever and Subclinical Hypocalcemia

Clinical manifestation of parturient hypocalcaemia is a disease of considerable importance for dairy cow’s welfare and economy of the farmers however it appears when the sudden demand for Ca of colostrum and milk production cannot be met by dietary Ca absorption, bone Ca mobilization and renal Ca resorption. Most dairy cows have some degree of hypocalcemia (milk fever or subclinical) during the early postpartum. Hypocalcemia occurs because Ca leaves the extracellular fluid pool to enter the mammary gland faster than it can be replaced by intestinal Ca absorption, bone Ca mobilization and renal Ca resorption. Blood Ca in the adult cows is maintained between 8.5 and 10 mg/dl (2.0 and 2.5 mmol/L). Maintenance of blood Ca within the acceptable range is a balancing act between the Ca demand of milk production and the cow’s homeostatic mechanisms to maintain blood Ca. Clinical signs of milk fever often are not seen until serum Ca concentration is about 4 mg/dl whereas subclinical hypocalcemia appears when <7.5mg/dl serum Ca concentration.

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Intestinal Ca absorption and bone Ca resorption are controlled by parathyroid hormone, which is secreted by the parathyroid glands and 1, 25-dihydroxyvitamin D3, which is produced in the kidney. As there is a decline in blood Ca concentration, parathyroid hormone concentration is increased. When blood Ca is within the normal range, parathyroid hormone secretion is decreased. Parathyroid hormone initiates renal production of 1, 25-dihydroxyvitamin D3 to permit Ca homeostasis. In addition, renal resorption of Ca is enhanced by parathyroid hormone. Metabolic alkalosis blunts the response of the cow to parathyroid hormone and predisposes dairy cows to milk fever and subclinical hypocalcemia. Metabolic alkalosis largely occurs as the result of diets high in cations, especially sodium and potassium and low in anions, especially chlorine and sulfur. Pre-calving diets high in anions and low in cations or containing anionic salts such as ammonium sulfate, magnesium sulfate and ammonium chloride can decrease the occurrence of hypocalcemia. In addition, many strategies including feeding a precalving diet containing a low Ca concentration, administration of vitamin D at approximately 1 week before calving and supplementation of Ca at calving have been used for the prevention of hypocalcemia.

Cow’s intestine and bone rapidly adapt to the Ca demand of lactation. As cows age, Ca homeostatic mechanisms react more slowly to the Ca demand of lactation. Oral administration of Ca salts prior to and at parturition has been suggested to prevent hypocalcaemia in dairy cows. The use of a source of Ca that has no adverse effects, such as necrotic lesions in the abomasum, on the digestive tract is preferable.

Method of Supplementation

Traditional method-restriction of dietary calcium

  • Main aim is to limit calcium intakes below 30-50 g per cow per day in last 3 weeks of pre-calving. It is Impossible to do if significant amounts of either grazed grass or grass silage in dry cow diet is offered.
  • Be careful when feeding milking cow rations to “close up” dry cows, as levels of calcium will be high.

Alternative method is to use calcium binders such as zeolite to limit calcium absorption.

Supplementation of calcium by mouth at calving

  • The Scandinavian approach to control milk fever is to give “at risk” cows a large dose of calcium at calving, which supplies a readily available source of calcium just when the cow needs it most.
  • This method can work well in small herds, where altering the “close up” dry cow diet is impractical.
  • A number of products are available either as boluses (eg. Bovikalc, Calcium boluses), drenches (eg. Maxacare Reviva, BoviCal), gels or in-feed products (eg. Mike Lemmy’s, Easy Calver).
  • Giving all older cows a bottle of calcium under the skin at calving is short-acting, and may be counterproductive as it will switch off hormone mechanisms that control blood calcium levels just when needed.
  • Prevent excessive drain of calcium reserves immediately after calving
  • Once the cow calves, their calcium requirements increase by 2-3 folds due to high calcium levels in milk. Excessive or inappropriate milk withdrawal can drain too much calcium from the system resulting in milk fevers especially if cases occur 24 hours or more after calving.
  • Do not milk cows precalving.
  • Remove calf at birth and only provide sufficient colostrums to the calf in the first 24 hours.
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Consider reduced or no milking of cows for 3-4 days after calving. Check cow regularly for mastitis.

Supplementation of calcium propionate as source of calcium and energy

  • Calcium propionate is a satisfactory source of Ca and propionate is the major glucose precursor in ruminants that are in positive energy balance and is anti-ketogenic.
  • Depressed dry matter intake during the transition period leads to a lack of propionate supplied for glucose synthesis in the liver. Nutritionally, propionate can be supplied orally in the form of calcium propionate.
  • Calcium propionate is a white crystalline powder. Molecular formula, molecular weight, density and pH of calcium propionate are C6H10CaO4, 186.22, 0.56 g/cm3 and 8.5 to 10, respectively.
  • Calcium propionate, as a source of both Ca and energy, has been administered to transition dairy cows for prevention and or treatment of hypocalcaemia and ketosis.
  • Calcium propionate can be used by oral drenching, adding to total mixed ration or concentrate mixture and in a paste or gel form.
  • Phosphate supplementation
  • Some milk fever cases do not respond to calcium alone, but also require phosphorous injections.
  • These cows are often described as “creeper” or “crawler” cows as they frequently attempt to get up.
  • Phosphorous is intrinsically linked with calcium in the bone stores, as so prevention of such cases involves the standard approach to milk fevers as highlighted above.
  • Too much phosphorous can also cause problems. Do not feed over 0.5% phosphorous in the dry cow diet.

 

Conclusions

The art of feeding dairy cattle is basic and applied science of dairy cattle nutrition. Huge economic losses occur due to medicines, veterinary services and reduced production of dairy animals due to metabolic diseases. Losses are also associated with increased incidence of secondary diseases, such as ketosis, mastitis, retained placenta, displacement of abomasum, uterine prolapse, limb injuries and pneumonia can further inflate losses. So strategy for supplementation of nutrients is necessary for optimum production and prevention of losses in peri-parturient dairy cattle.

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References

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