1. Hypocalcemia in dairy cattle
Sophie Rosevear
Jess Neal
Tara Hall
Alex Doddridge

2. Introduction 99% of a cow’s calcium is stored in the skeleton.
Calcium is essential for many physiological processes; neuromuscular function, blood clotting and hormonal secretion.
Failure to maintain calcium homeostasis (hypocalcaemia, milk fever, parturient paresis) affects productivity of the cows and profitability of the dairy industry.
Calcium homeostasis is stressed in dairy cattle as their main function is to produce high milk yields. Also, during the transition period the demand for calcium dramatically increases.

3. Calcium Homeostasis
Cows can only obtain calcium from dietary sources and absorb calcium through the epithelial cells of the small intestine.
Calcium is removed from the body through:
Urine
Faeces, and
Milk production.
Plasma calcium levels should be mg/dL for a healthy adult cow. This is regulated by intestinal and renal absorption, and bone turnover.
Calcium is removed from the body via urine and faeces and is also lost through milk production.

4. Calcium Homeostasis II
A decline in calcium levels stimulates the parathyroid gland to release parathyroid hormone (PTH). This increases calcium reabsorption from the glomerular filtrate.
PTH also triggers production of 1 α-hydroxylase which converts circulating vitamin D to 1,25-dihydroxyvitamin D.

5. Calcium Homeostasis III
When the calcium levels return to normal, the secretion of PTH decreases via a negative feedback loop.
Calcitonin is secreted by the thyroid in response to calcium levels increasing beyond the ‘setpoint’.
Osteocytic osteolysis is stimulated if both the demand for calcium and the PTH levels remain high.

6. Calcium Homeostasis IIII

7. Development of hypocalcaemia
Dairy cows:
Lactate for 10 months of the year.
Pregnant from about 3 months into lactaction (3 monthas after last calving).
Calve once a year, 8 weeks into their dry period.
During the ‘dry period’, calcium levels required for foetal growth are quite low compared to the demands of lactation.
The onset of lactation requires a high level of calcium, this can cause an imbalance from the high output of calcium in the colostrums and the influx of calcium to maintain the plasma levels.

8. Development of hypocalcaemia II
~50% of adult dairy cows develop subclinical hypocalcaemia within the first few weeks of lactation.
5-20% of dairy cows each year will not adapt and recover calcium balance.
This is a severe metabolic disease known as milk fever and normally occurs hours after parturition, but can occur several weeks before and after.
Prolonged release of PTH increases reabsorption of calcium (intestinal, renal and bone).

9. Clinical signs and pathology of disease
Initially:
Anorexia
Listlessness
Muscle weakness
Body temperature declines
Sternal recumbancy

10. Clinical signs and pathology of disease II
“Crush Syndrome”
If parturient, the birthing process is suspended.
Weak pulse and heart sounds, tachycardia.
Loss of consciousness with body temperature as low as 32°C.
Death can occur within hours without treatment.

11. Predisposing factors
Age
Breed
Metabolic Alkalosis
Hypomagnesia

12. Control (Prevention) The Dietry Cation-Anion Difference (DCAD) Method
Reduce dietry cations, increase anions  Lowers blood pH
Feed a calcium deficient diet
Decreases plasma calcium
Higher dietry magnesium
Maintains adequate levels of Magnesium in the blood.

13. Effect of DCAD
Source: Horst et al (full ref in reference list)

14. Treatment Treat as early as possible.
Fastest: IV injection of Calcium salts  (commonly Ca borogluconate).
Administer the Ca at a rate of 1 g/min
Subcutaneous injection
Blood flow is often compromised, so absorption is variable
A single subcutaneous site should be limited to 1–1.5 gCa (50–75 mL).
 Intramuscular administration
Limited to 0.5–1.0 g Ca/injection site to avoid tissue necrosis.
Oral treatments are not reccomended.

15. Conclusion
Hypocalcaemia in dairy cows is an economically important disease.
Loss of production
Cost of control
Treatment measures.
It reduces a dairy cow’s productive life.
Prevention is better than cure  complications are difficult to prevent once the clinical signs are present.
Future research will bring a greater understanding of the regulatory mechanisms and control of calcium homeostasis in the dairy cow.

16. 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
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
Goff, J.P. 2008, ‘The monitoring, prevention, and treatment of milk fever and subclinical hypocalcaemia in dairy cows’, The Veterinary Journal vol. 176, pp
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
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
Hamali, H. 2008, 'Post estrus hypocalcemia in a repeat breeder half-breed holstein cow', Journal of Animal and Veterinary Advances vol. 10, pp
Horst, R.L. (1986), ‘Regulation of calcium and phosphorus homeostasis in the dairy cow’, Journal of Dairy Science vol. 69, pp
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
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

17. Kimura, K. , Reinhardt, T. A. and Goff, J. P
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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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