Transcript Hypocalcemia in dairy cattle edited

HYPOCALCAEMIA
in dairy cattle
Sophie Rosevear, Jessie Neal, Tara Hall and Alex Doddridge
Introduction
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Calcium is essential, it is involved in many physiological processes.
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Dairy cows have been heavily selected for the ability to produce high milk
yields.
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There is a fine calcium balance in the dairy cow.
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When demand for energy and calcium suddenly increases this balance is
disrupted.
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Calcium homeostasis fails = milk fever (also called periparturient paresis)
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Affects productivity and longevity of high producing dairy cows
Calcium
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
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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
ketosis
Predisposing factors
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Age
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.
Breed
Breeds such as Channel Island, Swedish Red and White, and Jerseys are all more susceptible to milk fever than
Holsteins.
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.
Hypomagnesaemia
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)
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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
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Reducing calcium in diet prior to calving to increase calcium efficency
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Diets less than the required concentration of calcium can cause a slight decline in plasma calcium
stimulating increased release of parathyroid hormone
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Done days prior to parturition, these mechanisms, including osteoclastic bone resorption, are already
active and the cow is able to utilise, with maximum efficiency.
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Demand for calcium is more easily overcome and hypocalcaemia can be avoided.
Higher dietary Magnesium
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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.
Treatment
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Should be implemented as early as possible
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Restore the plasma calcium.
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Fastest: IV injection of calcium salts, usually calcium borogluconate,
(recommended 2g Ca/100 kg bodyweight)
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Administer the Ca at a rate of 1 g/ min
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While listening to the heart
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Oral gels containing calcium salts are given before, during and around 12-24
hours after parturition, as a preventative treatment measure.
CONCLUSION
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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.
REFERENCES
Bigras-Poulin, M. & Tremblay, A. 1998, ‘An epidemiological study of calcium metabolism in non-paretic postparturient Holstein cows’,
Preventive Veterinary Medicine vol. 35, pp. 195-207
DeGaris, P. J. and Lean, I. J. 2007, 'Milk Fever in dairy cows: A review of pathophysiology and control principles', The Veterinary Journal vol.
176, no. 1, pp. 58-69
El-Samad, H., Goff, J.P. and Khammash, M. 2002, ‘Calcium homeostasis and parturient hypocalcaemia: An integral feedback perspective’,
Journal of Theoretical Biology vol. 214, pp. 17-29
Goff, J.P. 2008, ‘The monitoring, prevention, and treatment of milk fever and subclinical hypocalcaemia in dairy cows’, The Veterinary
Journal vol. 176, pp. 50-57
Goff, J.P., Reinhardt, T.A. and Horst, R.L. 1991, ‘Enzymes and factors controlling vitamin D metabolism and action in normal and milk fever
cows’, Journal of Dairy Science vol. 74, no. 11, pp. 4022-4032
Goff, J.P., Ruiz, R. and Horst, R.L. 2004, ‘Relative acidifying activity of anionic salts commonly used to prevent milk fever’, Journal of Dairy
Science vol. 87, pp. 1245-1255
Hamali, H. 2008, 'Post estrus hypocalcemia in a repeat breeder half-breed holstein cow', Journal of Animal and Veterinary Advances vol.
10, pp. 1301-1304
Hangping, C., ZhongHua, W. and Fuchang, Li 2010, 'Effects of dietary calcium levels on calcium homoeostasis in lactating dairy cows',
Chinese Journal of Animal Nutrition vol. 22, no. 5, pp 1286-1292
Horst, R.L. 1986, ‘Regulation of calcium and phosphorus homeostasis in the dairy cow’, Journal of Dairy Science vol. 69, pp. 604-616
Horst, R.L., Goff, J.P. and Reinhardt, T.A. 1994, ‘Calcium and vitamin D metabolism in the dairy cow’, Journal of Dairy Science vol. 77, pp.
1936-1951
Horst, R.L., Goff, J.P. and Reinhardt, T.A. 2005, ‘Adapting to the transition between gestation and lactation: Differences between rat,
human and dairy cow’, Journal of Mammary Gland Biology and Neoplasia vol. 10, no. 2, pp. 141-156
REFERENCES continued
Kimura, K., Reinhardt, T.A. and Goff, J.P. 2006, ‘Parturition and hypocalcaemia blunts calcium signals in immune cells of dairy cattle’,
Journal of Dairy Science vol. 89, pp. 2588-2595
Kronqvist, C., Emanuelson, U., Sporndly, R. and Holtenius, K. 2011, 'Effects of prepartum dietry calcium level on calcium and magnesium
metabolism periparturient in dairy cows', Journal of Dairy Science vol. 94, no. 3, pp. 1365-1373
Lean, I. J., DeGaris, P. J., McNeil, D. M. and Block, E. 2006, 'Hypocalcemia in dairy cows: meta-analysis and dietary cation anion
difference theory revised', Journal of Dairy Science vol. 89, pp. 669-684
McNeill, D. M., Roche, J. R., McLachlan, B. P. and Stockdale, C. R. 2002,'Nutritional strategies for the prevention of hypocalcaemia at
calving for dairy cows in pasture-based systems, Australian Journal of Agricultural Research, vol. 53, no. 7, pp. 755-770
Oba, M., Oakley, A.E. and Tremblay, G.F. 2011, ‘Dietary Ca concentration to minimise the risk of hypocalcaemia in dairy cows is affected
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Peacock, M. 2010, ‘Calcium Metabolism in Health and Disease’, Clinical Journal of the American Society of Nephrology vol.5, pp. s23-s30
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Questions?