Serum Mineral Status and Periparturient Disease
Posted: November 7, 2005
We are very familiar with a cow’s inability to maintain blood calcium (Ca) concentration around the time of calving and the resulting disease of milk fever. Similarly, if the cow is unable to maintain blood magnesium (Mg) concentration, hypomagnesemia (i.e., grass tetany) occurs. Both low blood phosphorus (P) and potassium (K) are associated with muscular weakness and downer cow problems. Deficiencies of the trace minerals copper (Cu), zinc (Zn) and selenium (Se) are often associated with immune system dysfunction.
Most veterinarians and dairy producers are familiar with the use of blood mineral concentration determinations as an aid in disease diagnosis. Although it is useful to know what is responsible for a disease process, a preferred option is to determine if a cow is metabolically unstable and will ultimately succumb to some disease process.
Mineral evaluation was generally not considered predictive or sensitive to dietary influences since homeostatic controls maintain stable blood concentrations. However, homeostatic controls become unstable around the time of calving with increasing losses of nutrients in colostrum and milk and declining dry matter intake.
Mineral-associated diseases occur when homeostatic control mechanisms are not capable of returning blood mineral concentrations back to stable concentrations. Given this situation, determining blood mineral concentrations around the time of calving may be useful in predicting potential for disease postpartum. Potential predictive relationships of serum mineral concentrations to postpartum disease were investigated.
In the weeks prior to calving presence of subclinical hypocalcemia, defined as blood Ca concentration below 8.0 mg/dl and not showing signs of clinical milk fever, increased a cow’s risk for experiencing any postpartum disease by more than 3-times that of a cow not experiencing subclinical hypocalcemia prepartum. Consistent with other studies, cows with postpartum hypocalcemia also had more postpartum disease problems, especially ketosis.
As one might expect, cows that experienced any disease event postpartum also had reduced dry matter intake over the first 5 weeks postpartum. In contrast to what has been published, cows that experienced one or more diseases postcalving did not have significantly lower intake prior to calving. Though, cows that went on to become sick had slightly lower intake one or two weeks prior to calving. There were differing effects of specific diseases on dry matter intake, but intake was consistently lower for sick cows compared to those not experiencing postpartum disease.
Of interest was the observation that high blood K concentration prepartum was also associated with increased risk of postpartum disease. This seems reasonable given the adverse interrelationship between K and Ca homeostasis related to hypocalcemia induction. A somewhat surprising observation was the strong association between low blood Na concentration pre- and postpartum with postpartum disease risk.
This observation seems contradictory given our understanding of cations and Ca homeostasis. However, low blood Na may reflect inadequate salt intake and reduced dry matter intake, which may lead to increased postpartum disease incidence. These data suggest that measuring blood mineral concentrations prior to calving may be useful in predicting potential risk for postpartum disease. With the observed associations with Na and K, further investigation of the potential role electrolytes and fluid balance in postpartum disease is warranted.Robert Van Saun, Extension Veterinarian, Department of Veterinary Science, Penn State