HYPOCALCEMIA
IN
DAIRY CATTLE
Dr A. Murondoti (BVSc,
MSc,PhD
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
.
PREDISPOSING FACTORS
Breed-Jersey, Swedish red and white and
Channel Island are more susceptible
Susceptibility linked to fewer intestinal
receptors
Milk production level
Lactation number
Age
Feeding regime
ASSOCIATION WITH OTHER DAIRY DISEASES
LDA and RDA
Mastitis
Retained fetal membranes
Uterine prolapse
Ketosis
Dystocia
Metritis, Endometritis (Immunosuppresion)
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 8.5-10 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.
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.
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.
Calcium Homeostasis IIII
Definition & Mechanism
Ca homeostasis
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.
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 12-24 hours after parturition, but can occur several
weeks before and after.
Prolonged release of PTH increases reabsorption of calcium
(intestinal, renal and bone).
CLINICAL SIGNSchanism
Signs
Low milk
Excitement stage
Restlessness, hypersensitivity, tremors, S-shape neck, teeth
grinding, stiff gait, and fall easily, protrude tongue,
salivation
Sternal recumbancy
Recumbancy, neck turned into flank, hypothermia, increased
heart rate but with decreased intensity, dry muzzle, dilated
pupil, ruminal stasis and constipation
Lateral recumbancy
Limbs stuck out, hypothermic, die within 12-24 hrs
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.
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.
Prevention
Calcium Chloride
Acidogenic salt which lowers blood ph and
make issue more responsive to PTH
Calcium propionate
Propionate part useful in hepatic
Gluconeogenesis
Hydrochloric acid
Source of anions which have acidifying effects
Prevention contd
Vit D and Parathyroid hormone
Not helpful because of negative
feedbackmechanisms and cow may fail to
recover from hypocalcemia
DCAD
Effect of DCAD
Source: Horst et al. 2005 (full ref in reference list)
Dietary Management
1. DCAD
How it affects milk fever?
If anions > cations acidic blood
↑ PTH
↑ responsiveness to PTH
↑1, 25(OH)2D3 (↑ intestinal absorption)
↑ ostoclast resorption
If cations > anions alkaline blood
Opposite to above
Dietary Management
2. Adding dietary anions
Used when it is hard to decrease dietary Ca
Do not use when Ca intake is low (< 100 g)
Palatability problems
Cl- and SO4- salts of Ca, ammonium, Mg
S is not recommended (why? Toxicity, not
documented)
Phosphate salts is not recommended (why? Weak
acidifier, weak absorption, inhibit renal synthesis of
1,2(OH)2D3)
Dietary Management
1. DCAD
Dietary Management
3. Removing dietary cations
Be careful not to go below requirements
Support: diet low in Na & K prevented milk fever
Alfalfa use should be limited if it contains high K
Dietary Management
1. DCAD
http://ahdairy.com/our-products/dcad-balancers/dcad-calculator.aspx
Target
Transition period: -50 to -100 meq/kg DM
Fresh, lactation: +200-300+ meq/kg DM
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.
References
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postparturient Holstein cows’, Preventive Veterinary Medicine vol. 35, pp. 195-207
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
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