Review/Oorsig Volume 22, Issue 03 - Page 23

Volume 22 • Issue 03 • 2018 vital reserves. Thus milk fever can be induced by just a brief and temporary interruption in gastro-intestinal function. • • • A decreased appetite at partus, high oestrogen levels at partus, sudden dietary changes and a relatively alkalotic state may all participate in causing a state of ruminal and intestinal stasis. Fat cows will tend to have a lower intake in the immediate post partum period and seem to be more prone to milk fever than lean cows. Stressful situations will also lead to a decreased feed intake. Calcium intake during the dry period Feeding more than 100g of Calcium daily during the last few weeks of the dry period is associated with an increased incidence of milk fever. If calcium intake is excessive the cow’s daily requirement for calcium can be met almost entirely by passive absorption of dietary calcium. Active transport of dietary calcium from intestine to blood and bone calcium resorption mechanisms are then depressed and become quiescent. Because the production of PTH and 1,25 (OH)2 D seems to be adequate in most cows with milk fever it is thought that target tissues in these cows that received too much Ca through the diet have defective hormone receptors that either do not recognize the hormone or there may be fewer receptors present in the target tissues. Magnesium levels A hypomagnesaemia will negatively influence the production and / or secretion of both PTH and 1,25(OH)2D. Magnesium is also a co-factor in the action of PTH and 1,25(OH)2D3 on the bone and small intestine (see above). Both the above factors may lead to an increased incidence of milk fever if there is a deficiency of magnesium in the diet. Furthermore Mg plays a role in the release of Ca from the endoplasmic reticulum in muscle cells, and a reduced Mg level can therefore exacerbate the symptoms. Age The ability of the cow to increase intestinal calcium resorption decreases with age. This is the result of bo