Cause
During the dry period (late gestation, non-lactating), dairy cattle have relatively low calcium requirements, with a need to replace approximately 30 g of calcium per day due to utilization for fetal growth and fecal and urinary losses. At parturition, the requirement for calcium is greatly increased due to initiation of lactation, when mammary drainage of calcium may exceed 50g per day. Due to this large increase in demand for calcium, most cows will experience some degree of hypocalcemia for a short period following parturition as the metabolism adjusts to the increased demand. When the mammary drain of plasma calcium causes hypocalcemia severe enough to compromise neuromuscular function, the cow is considered to have clinical milk fever. Mechanism
In normal calcium regulation, a decrease in plasma calcium levels causes the parathyroid glands to secrete parathyroid hormone (PTH), which regulates the activation of Vitamin D3 in the kidney. These two compounds act to increase blood calcium levels by increasing absorption of dietary calcium from the intestine, increasing renal tubular reabsorption of calcium in the kidney, and increasing resorption of calcium from bones.It has been found that tissue is less responsive to parathyroid hormone prepartum, compared to postpartum. It is believed that hypocalcemia causing milk fever is due to a lower level of responsiveness of the cows tissues to circulating parathyroid hormone.The resultant decreased plasma calcium causes hyperexcitability of the nervous system and weakened muscle contractions, which result in both tetany and paresis. Prevention
Diet
Proper dietary management will prevent most cases of milk fever.
Some scientists believed that udder inflation could cause stimulation that then prevents calcium loss. Other scientists suggested that udder inflation prevented milk secretion, reducing calcium loss overall. This may prevent calcium being taken from the blood plasma. Later Theories
The true cause of milk fever was first suggested by Prof John Russell Greig and Henry Dryerre in March 1925, at the Moredun Research Institute in Scotland. This idea was later confirmed experimentally by Little and Wright in May 1925. By 1933, Pulles began treatments with magnesium chloride and calcium chloride, which is the basis for modern pharmaceutical treatments. References
External links
Prevention of Milk Fever, University of Kentucky
Parturient Paresis in Cows (Milk fever, Hypocalcemia), The Merck Veterinary Manual