Comparison of 0.46% calcium diets with and without added anions with a 0.7% calcium anionic diet as a means to reduce periparturient hypocalcemia.

Most studies demonstrating that diets with low dietary cation-anion difference (DCAD) reduce hypocalcemia in cows add enough anions to the diet to reduce urine pH below 7.0. One objective of these experiments was to determine whether there is any benefit to periparturient plasma Ca concentration if diet anion addition results in a lesser degree of acidification of the cow and urine pH does not go below 7.0. Another method for reducing hypocalcemia involves feeding a prepartal diet that is Ca deficient. This places the cow in negative Ca balance before calving, stimulating parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D secretion before calving and thus promoting Ca homeostasis at calving. As practiced in the field, low-Ca diets are often about 0.5% Ca. Our second objective was to determine whether a 0.46% Ca diet would be sufficiently low in Ca to stimulate PTH secretion before calving. A meta-analysis of the literature suggests that a 0.5% Ca, low-DCAD diet will reduce hypocalcemia better than a 0.7% Ca diet. A third objective was to compare periparturient plasma Ca in cows fed 0.46 or 0.72% Ca diets with similar DCAD. In experiment 1, anions (primarily chloride) or anions plus Ca were added to a 1.4% K basal diet to create the following diets: 0.46% Ca and +167 mEq/kg of DCAD, 0.46% Ca and -13 mEq/kg of DCAD, and 0.72% Ca and -17 mEq/kg of DCAD. In experiment 2, the same amounts of anion were added to a 2.05% K basal diet to create the following diets: 0.46% Ca and +327 mEq/kg of DCAD, 0.46% Ca and +146 mEq/kg of DCAD, and 0.72% Ca and +140 mEq/kg of DCAD. In experiment 1, cows fed the diet with 0.46% Ca and +167 mEq/kg of DCAD had significantly lower plasma Ca concentration after calving than cows fed the 0.46 or 0.72% Ca diets with anions. Periparturient plasma Ca concentrations did not differ in cows fed the low-DCAD diets with 0.46 or 0.72% Ca. Urine pH was reduced from 8.27 in the diet with 0.46% Ca and +167 mEq/kg of DCAD to 7.07 and 7.41 in the 0.46 and 0.72% Ca anion diets, respectively. Precalving plasma PTH and 1,25-dihydroxyvitamin D concentrations were similar in cows fed the 0.46% Ca diets and the 0.72% Ca diets, suggesting that the 0.46% Ca diets were not low enough in Ca to place the cow in negative Ca balance before calving. In experiment 2, adding the anion supplements to a 2.05% K diet did not reduce urine pH below 8.0. Periparturient plasma Ca concentrations did not differ in cows in any group in experiment 2. Precalving diets that are 0.46% Ca fed ad libitum are too high in Ca to stimulate Ca homeostasis before calving. Adding anions to a diet can benefit periparturient cow plasma Ca concentration, but only if it alters acid-base status enough to reduce urine pH below 7.5.

The monitoring, prevention, and treatment of milk fever and subclinical hypocalcemia in dairy cows.

The periparturient cow undergoes a transition from non-lactating to lactating at calving. The animal is tremendously challenged to maintain calcium homeostasis. Those that fail can develop milk fever, a clinical disorder that is life threatening to the cow and predisposes the animal to a variety of other disorders. Guidelines for monitoring the incidence of hypocalcemia and methods for treating milk fever are reviewed. The physiological factors that cause milk fever and strategies for prevention of milk fever are discussed, focusing on the effects diet cation-anion difference can have on tissue sensitivity to parathyroid hormone. Another major risk factor for milk fever is hypomagnesemia, which is observed when animals are fed inadequate amounts of magnesium, or some factor is present in the diet that prevents adequate absorption of magnesium. Moderate hypomagnesemia impairs the ability of the cow to maintain calcium homeostasis and hypocalcemia occurs.

Macromineral disorders of the transition cow.

Four macrominerals have the distinction of being involved in the "downer cow" syndrome, which is, unfortunately, often associated with parturition in cows. Inadequate blood calcium (Ca), phosphorus (P), magnesium (Mg), or potassium (K) concentrations can cause a cow to lose the ability to rise to her feet because these minerals are necessary for nerve and muscle function. Less severe disturbances in blood concentrations of these minerals can cause reduced feed intake, poor rumen and intestine motility, poor productivity, and increased susceptibility to other metabolic and infectious disease. Mechanisms for maintaining blood Ca, P, Mg, and K concentrations perform efficiently most of the time, but occasionally these homeostatic mechanisms fail and metabolic diseases such as milk fever occur. Understanding how and why these mechanisms fail may allow the practitioner to develop strategies to avoid these disorders.

Effect of mastectomy on milk fever, energy, and vitamins A, E, and beta-carotene status at parturition.

The objective of this study was to compare blood profiles of intact and mastectomized periparturient cows to discriminate those metabolic changes associated with the act of parturition from the metabolic changes caused by lactation. Mastectomized and intact cows had similar increases in plasma estrogens and cortisol concentrations around the time of calving. Mastectomy eliminated hypocalcemia and the rise in 9,13-di-cis retinoic acid observed in intact cows. Mastectomy reduced but did not eliminate decreases in plasma phosphorus, alpha-tocopherol, and beta-carotene associated with parturition in intact cows, suggesting the mammary gland is not the sole factor affecting plasma concentrations of these compounds. Dry matter intake was similar in both groups before calving. The day of calving, dry matter intake was lower in intact cows than in mastectomized cows, but after calving the mastectomized cows exhibited a pronounced decline in feed intake. Plasma nonesterified fatty acid (NEFA) concentrations rose rapidly in intact cows at calving and did not return to baseline level for > 10 d. In contrast, NEFA concentrations in mastectomized cow plasma rose moderately at calving and returned to baseline level 1 to 2 d after calving. This study provides evidence that hypocalcemia in the cow is solely a result of the calcium drain of lactation. The act of parturition affects blood phosphorus, dry matter intake, and NEFA concentration independent of the effect of lactation.