Jesse P. Goff

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.

Prevalence of subclinical hypocalcemia in dairy herds.

The prevalence of subclinical hypocalcemia in the transition cow is unknown. Cows with subclinical hypocalcemia have no clinical signs of hypocalcemia but may be more susceptible to other diseases. The objective of this study was to determine the prevalence of subclinical hypocalcemia in the US dairy herds. As a part of the United States Department of Agricultures National Animal Health Monitoring System 2002 Dairy study, serum samples were collected from 1462 cows within 48 h of parturition. The samples were sorted by lactation number: 1st (n=454), 2nd (n=447), 3rd (n=291), 4th (n=166), 5th (n=72), and 6th (n=32). Subclinical hypocalcemia (<2.0 mM) increased with age and was present in 25%, 41%, 49%, 51%, 54%, and 42% of 1st-6th lactation cows, respectively. Cows with serum calcium concentrations >2.0 mM had significantly lower serum non-esterified fatty acids indicating better energy balance than those with subclinical hypocalcemia. Subclinical hypocalcemia may make cows more susceptible to secondary diseases but more research will be required to determine if this is true.

Pathophysiology of Calcium and Phosphorus Disorders

Hypocalcemia and hypophosphatemia are relatively common in periparturient cows. This article reviews the etiologic factors that contribute to the development of these conditions. The physiologic role of magnesium in calcium homeostasis and the physiologic effect of dietary cation-anion difference at the cellular level are discussed in depth. A theory to explain the development of periparturient hypophosphatemia is developed.

Calcium, Phosphorus, and Magnesium Homeostasis in Ruminants

Significant advances have been made in the last 30 years in the understanding of Ca, PO4, and Mg homeostasis in ruminants. Despite these advances, the primary cellular or molecular lesions responsible for failure of homeostasis have yet to be identified. Suggested causes, such as primary hormone deficiencies, have been eliminated, and we now believe that aging and nutrition can reduce the ability of intestine, bone, and kidney to respond rapidly to the hormone signals responsible for homeostasis during rapid increases in demand for these minerals. Further research is required before these lesions can be identified and new knowledge applied to the development of economical, effective programs that prevent milk fever and hypomagnesemic tetany. Until then, diseases such as milk fever will continue to affect 8 to 9 per cent of our dairy cows, and dairy farmers will continue to spend millions of dollars a year for treatment of the primary disease and the many secondary problems that result from these diseases.

Adapting to the transition between gestation and lactation : Differences between rat, human and dairy cow

Adequate blood calcium concentrations are vital for the normal function of mammals. Mechanisms for maintaining normal blood calcium function adequately most of the time; however, occasionally they fail and calcium homeostasis is compromised. Milk fever or periparturient hypocalcemia in dairy cattle is a well-documented example of a breakdown in the mechanisms of calcium homeostasis. This disease occurs at the time of parturition and is unique to adult dairy animals. The disease results from the inability of animals to cope with the sudden demand for calcium in support of colostrum formation. Animals developing the disease become hypocalcemic and require intravenous calcium to survive. The precise metabolic disorder(s) responsible for the onset of milk fever is still being debated. This report will highlight some of the current concepts related to the causes and prevention of milk fever in dairy cattle, as well as contrasting differences in calcium demands that exist between dairy cattle, humans and rats at the onset of lactation.

Treatment of calcium, phosphorus, and magnesium balance disorders.

In food animal practice, the majority of the calcium, phosphorus, and magnesium balance disorders are due to low blood concentrations of one or more of these minerals. The purpose of this article is to review methods that can be used to restore normal blood concentrations of these minerals. Low plasma calcium is often accompanied by changes in plasma phosphorus and magnesium. Initial discussions will consider each mineral separately, followed by pros and cons of combined therapies. In all cases the doses of the treatments described in this article are those appropriate for the 600-kg cow.

Protection of calves with a vaccine against Cryptosporidium parvum.

Cryptosporidium parvum causes enteric infection and diarrhea in calves, other species of economically important livestock, and humans. There are no effective treatments currently licensed for this parasite, and preventive measures are difficult. In addition to direct economic losses to the cattle industry, infected calves may contaminate water supplies with oocysts and contribute to human cryptosporidiosis. We have developed a vaccine offering partial protection against C. parvum infection in calves. Nine calves received an oral preparation of lyophilized C. parvum oocysts shortly after birth, and 10 calves served as nonvaccinated controls. All calves received colostrum. At 1 wk of age, all calves were administered 10(4) viable C. parvum oocysts orally. Clinical disease and oocyst shedding were monitored daily. Mean duration of diarrhea was 4 days for control calves and 1.7 days for vaccinated calves. Mean duration of oocyst shedding was 5.3 days for control calves and 2 days for vaccinated calves. These differences were statistically significant and suggest that this vaccine has the potential to reduce diarrhea and oocyst shedding caused by C. parvum.

Calcium and Vitamin D Metabolism During Lactation

Calcium transfer to the fetus in late pregnancy and the subsequent transfer of calcium to milk represent the greatest challenges to calcium homeostasis in adult animals. The adaptation of the maternal calcium homeostatic mechanisms is the result of a complex interplay between calciotropic hormones and the tissues, intestine, bone, and kidney, responsible for providing the large amounts of calcium needed to support fetal skeletal growth and lactation. In this review, we will discuss general calcium homeostasis followed by a review of the specific adaptations required by the human, rat, and cow to meet fetal and lactational demands for calcium. Finally, we will review what is known about the regulation of calcium transfer from the plasma to the milk.

Effect of calcium-energy supplements on calving-related disorders, fertility and milk yield during the transition period in cows fed anionic diets

The objective of this study was to determine the effect of a calcium-energy supplement at calving on the incidence of calving-related disorders (CRD), fertility, BCS and milk yield in cows fed anionic diets and to establish any associations among outcome variables. In Florida, from October to December 1997, 479 cows were assigned to three groups and treated at calving as follows: Group 1: 160 nontreated cows; Group 2: 158 cows, treated orally with 60g Ca as CaCl2; Group 3: 161 cows, treated orally with 110g Ca as calcium propionate (510g) plus propylene glycol (400g). No treatment effect was detected for any of the outcome variables. An association was found between dystocia and age and retained fetal membranes (RFM). Age and RFM were associated with metritis. RFM and displacement of the abomasum were associated with ketosis. Ketosis and age were related to displacement of the abomasum. Parity, BCS, ovarian cysts, RFM and metritis were associated with fertility.

Diet-induced pseudohypoparathyroidism: A hypocalcemia and milk fever risk factor

Subclinical hypocalcemia may affect half of all multiparous cows, and clinical hypocalcemia or milk fever affects approximately 5% of dairy cows each year. This disorder of calcium homeostasis can be induced by several dietary factors. Recent studies implicate high dietary potassium and high dietary cation-anion difference (DCAD) with increased risk of milk fever. The hypothesis tested in this study was that high-DCAD diets fed to prepartum cows reduce tissue sensitivity to parathyroid hormone (PTH), inducing a pseudohypoparathyroid state that diminishes calcium homeostatic responses. Multiparous Jersey cows were fed low- or high-DCAD diets in late gestation, creating a compensated metabolic alkalosis in the high-DCAD cows and a compensated metabolic acidosis in the low-DCAD cows. They then received synthetic PTH injections at 3-h intervals for 48 h. Parathyroid hormone is expected to cause an increase in plasma calcium by increasing renal production of 1,25-dihydroxyvitamin D and increasing bone calcium resorption. Plasma calcium concentration increased at a significantly lower rate in cows fed the high-DCAD diet. Cows fed the high-DCAD diet also produced significantly less 1,25-dihydroxyvitamin D in response to the PTH injections than cows fed the low-DCAD diet. Serum concentrations of the bone resorption marker carboxyterminal telopeptide of type I collagen were numerically lower in cows fed the high-DCAD diet but this difference was not statistically significant. These data provide direct evidence that high-DCAD diets reduce tissue sensitivity to PTH. The metabolic alkalosis associated with high-DCAD diets likely induces a state of pseudohypoparathyroidism in some dairy cows at the onset of lactation, resulting in hypocalcemia and milk fever.