Hypocalcemia in dairy cattle edited

in dairy cattle
Sophie Rosevear, Jessie Neal, Tara Hall and Alex Doddridge
Calcium is essential, it is involved in many physiological processes.
Dairy cows have been heavily selected for the ability to produce high milk
There is a fine calcium balance in the dairy cow.
When demand for energy and calcium suddenly increases this balance is
Calcium homeostasis fails = milk fever (also called periparturient paresis)
Affects productivity and longevity of high producing dairy cows
Calcium homeostasis
Failure of homeostasis and
development of hypocalcaemia
• Lactation generates a sudden, very high demand on calcium homeostasis.
• Causing an imbalance between calcium output and influx of calcium to
maintain the extracellular pool (plasma) from bone, kidney and intestine.
• Failure of calcium homeostasis.
• Between 5 and 20% of cows will develop milk fever.
• Occurs within 12 to 24 hours of parturition.
• Milk fever is hypocalcaemia serious enough to present clinical signs, when
plasma calcium levels are between 8 mg/dL and 6 mg/dL.
• If allowed to proceed, many will die if left untreated.
Clinical Signs
Initially hyper excitability followed by anorexia, listlessness and muscle weakness.
Body temperature declines as condition worsens.
Fever is not a clinical symptom.
Sternal recumbency (as shown above)
Ruminal atony and constipation due to a loss of smooth muscle contractile function causing bloat.
‘Crush syndrome’ followed by 'downer cow’ syndrome.
If parturient birthing process is suspended.
Weak heart sounds and tachycardia.
Heart muscle contractile function is compromised.
Followed by laterally recumbency with a temperature as low as 32°C (normal temp 38-38.5°C); it can
appear dead at this latest stage of milk fever.
Death can occur in a few to several hours, and is likely at a rate of 60-70% without treatment.
Hypocalcaemia reduces the ability of immune cells to respond to stimuli and therefore significantly
increases a cows susceptibility to mastitis, retained fetal membranes, displaced abomasum, dystocia and
Predisposing factors
Dairy cows usually in their 3rd or later lactation because that’s when they are producing the most milk
Studies showing that the intestinal receptors for 1,25-dihydroxyvitamin D decline in quantity with age. Older animals
are also less able to mobilise calcium from bone, and have a greater milk production which has been shown to be
positively correlated with risk of hypocalcaemia due to the greater demand for calcium.
Breeds such as Channel Island, Swedish Red and White, and Jerseys are all more susceptible to milk fever than
One study showed that intestinal receptors for 1,25-dihydroxyvitamin D are around 15% less in Jerseys than Holsteins.
Metabolic alkalosis (MA)
Mostly caused by a diet that supplies more cations (K, Na, Ca and Mg) than anions (Cl, SO₄ and PO₄) causing a difference
in electrical charge in body fluids. Hydrogen ions, having a positive charge, must be lost to restore neutrality, leading to
an increase in blood pH.
MA has been shown to blunt the homeostatic response of dairy cows to parathyroid hormone because it is believed
that it causes a change in conformation of the parathyroid hormone receptor in all target tissues. This means bone
calcium is not resorbed as efficiently and renal reabsorption of calcium is not as high. Active vitamin D formation by the
kidneys is also inhibited so intestinal calcium absorption cannot be so effectively enhanced. Thus the cow cannot
benefit from these homeostatic mechanisms and restore plasma calcium.
This is attributed to development of hypocalcaemia as low levels of magnesium also interferes with the ability of
parathyroid hormone to act on its target tissues, particularly in relation to magnesium’s action as a co-factor allowing
parathyroid hormone to stimulate cyclic AMP production (necessary for operation of calcium channels).
Control (prevention)
Prevention of hypocalcaemia, not just milk fever, should be a major goal of dairy farms
The DCAD method
Induce a compensated metabolic acidosis in the cow restoring the ability of parathyroid
hormone to regulate blood calcium levels.
Reduce dietary cations and to increase dietary anions.
Causing a reduction in what is known as the Dietary Cation-Anion Difference (DCAD),
subsequently lowering the pH of the blood.
Source: Horst et al. 2005 (full ref in reference list)
Control of Hypocalcaemia continued …
Feeding a calcium-deficient diet
Reducing calcium in diet prior to calving to increase calcium efficency
Diets less than the required concentration of calcium can cause a slight decline in plasma calcium
stimulating increased release of parathyroid hormone
Done days prior to parturition, these mechanisms, including osteoclastic bone resorption, are already
active and the cow is able to utilise, with maximum efficiency.
Demand for calcium is more easily overcome and hypocalcaemia can be avoided.
Higher dietary Magnesium
A higher dietary magnesium concentration prior to calving ensures that passive diffusion of magnesium
in the rumen can occur and levels of magnesium in the blood will be adequate.
Should be implemented as early as possible
Restore the plasma calcium.
Fastest: IV injection of calcium salts, usually calcium borogluconate,
(recommended 2g Ca/100 kg bodyweight)
Administer the Ca at a rate of 1 g/ min
While listening to the heart
Oral gels containing calcium salts are given before, during and around 12-24
hours after parturition, as a preventative treatment measure.
Economically important
Affects productivity
Reduces a dairy cow's productive life.
It costs the dairy industry not only through loss
of production but also in the cost of control and
treatment measures.
• Prevention is key
• Future research focus on regulatory mechanisms
of calcium metabolism.
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