Hypocalcaemia and milk fever in cows

Protection of dairy cows against hypocalcaemia and post parturient paresis (milk fever)


According to FAO data in the report from 2013 titled “Milk and dairy products in human nutrition”, cow’s milk on a global scale is a significant source of many important nutrients (including calcium) in human diet. All components of milk come either in an unprocessed form, or after a transformation in the body of a cow form components of the feed ration consumed by cows. This fact is reflected in the popular belief among breeders, that proper nutrition allows producing a substantive volume of high quality milk. This issue would not be complicated if it only required balancing the nutrients provided in feed with the components secreted in milk. This is not the case, because the body of a cow cannot be regarded as. e.g. a shampoo factory, which product is a simple combination of mixed ingredients. A dairy cow’s body is a place of complex transformations and processes, which can heavily influence the effectiveness and the result of milk production. This is also the case with the transfer of calcium to the udder. This element provided in the feed is used by cows not only to produce milk, but also to build the skeleton, and for many other metabolic functions. The entire homeostasis (balance) of calcium in the body of a cow, i.e. the balance between the Ca absorbed from the gastrointestinal tract, and deposited in the skeleton (own bones and in the skeleton of a foetus, during pregnancy), returned in faeces, urine and milk, is controlled by hormones, which is affected by many factors spread over time. An disadvantageous phenomenon from the point of view of mineral balance occurs directly after giving birth – after the dry period, when due to the lack of milk production the need for calcium is low and the endocrine system rearranges to anabolism of this component (process when Ca is deposited in the skeleton and absorption of Ca is limited due to stimulation with calcitonine – fig. 1), suddenly followed by secretion of milk rich in calcium, resulting in a drastic reduction of concentration of this macroelement in blood – hypocalcemy (Ca level in blood plasma < 7 mg/dl). Simply increasing the amount of calcium in the dose after labour does not help, as the high levels of the hormone calcitonin, somewhat “inherited” after the dry period, blocks the absorption and retention of calcium in the organism. Clinical, acute hypocalcemia results in a deadly disease – post parturient paresis, called the milk fever (calcium is responsible, inter alia, for correct transmission of nerve impulses, hence the symptoms are cramps and paralysis of muscles making the cow unable to maintain a standing position). With a smaller decrease in the concentration of calcium in the blood (subclinical hypocalcemia), similarly dangerous consequences occur, such retained placenta, dislocation of the abomasum, atony of the rumen or mastitis. Milk fever occurs during the transition period, within 24 hours after calving. This applies to high-yielding dairy cows, which are usually in the third or subsequent lactation. Milk fever occurs in 6% of dairy cattle, and subclinical (subacute) form of hypocalcemia may affect up to 50% of cows. Animals suffering from post-parturient paralysis include dairy cows, sheep, goats, and less frequently – beef cattle. As a rule, incidence of this disorder increases with the age of animals.

The basic milk fever prevention includes good nutrition management practice around the calving period, including acidifying diets. Insufficient release of calcium reserves from the bones and poor absorption of calcium from feed are considered as the primary causes of group of diseases associated with hypocalcemia. Dietary Cation-Anion Difference (DCAD) and Ca concentration in the feed during the dry period are key for the correct and effective release of calcium reserves from bones induced by the parathormone (antagonist to calcitonine) around the calving period. Several studies have shown that metabolic alkalosis and excess of calcium during the dry period are one of the most important causes of hypocalcemia. Excessive supply and blood concentration of cations (K, Na, Ca, and Mg) and insufficient concentration of anions: chlorine (Cl), sulphates and phosphates are the primary cause of blood pH increase. Having this in mind, one can formulate practical principles for mineral nutrition during the dry period, which somewhat indirectly are an important element in the prevention of hypocalcaemia by controlling blood pH: Mg – 0.40-0.50% dw.; K – max. 1.5 % dw.; Cl – recommended minimum chlorine concentration depends on the content of potassium in the feed ration, and the recommended difference is minimum 5 g of Cl in 1 kg of dry weight., (e.g. K 1.2% dw. = Cl min. 0.7% dw.), Cl content can be effectively increased by the addition of chlorides (e.g. ammonium chloride), which notably are reluctantly taken by animals (so called bitter salts); Ca <0.55% dw. (approx. 50g/animal – low level counteracts hypocalcaemia (excess of Ca), which decreases the amount of calcitonin, and stimulates the secretion of parathyroid hormone); Na – 0.12-0.15% dw.; P – 0.30-0.36% dw.; S – 0.22-0.30% dw. – the amount of S can be effectively increased by the addition of sulphates (e.g. magnesium sulphate). What plays an important role in enhancing the supply of the organism with calcium is the form of vitamin D3 – 1,25-dihydroxycholecalciferol (1.25 – D3 –fig. 1)

Acc. to American and German specialists, when dry cows are provided with anionic salts, high doses of calcium (> 100 grams per day) should be introduced as early as 2 weeks prior to calving. However, if “bitter salts” are not applied, administering Ca, Mg and P in quantities as during the lactation is recommended just before calving. Special preparations administered orally in liquid form aid supplementing readily absorbed forms of these elements. They guarantee providing cows with the recommended level of these vital macroelements.

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