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