Minerals are critical to the health and performance of grazing livestock, and deficiencies and excesses can cause weight loss, decreased reproductive performance, and a variety of nutritional disorders. Milk fever and grass tetany are two metabolic issues that can occur as a result of mineral imbalances this time of year. It is important to understand various factors that contribute to the potential for these disorders and also to understand associated symptoms and treatments to minimize losses.
Milk Fever (Parturient Paresis)
Milk fever is generally associated with high-producing dairy cattle; however, it can also occur in beef cattle. Milk fever is a result of hypocalcaemia (low calcium). Most forage contains enough calcium (Ca) to meet the minimal requirements of livestock (around 40 grams per day). However, a dramatic increase in calcium (Ca) requirements occurs with the onset of lactation in the dam, and requirements are typically unable to be met simply by increasing Ca intake. Colostrum contains 2.0 – 2.3g/L of Ca, which drains reserves in the cow’s blood stream. Typically, milk fever is seen in mature cows as they have a much greater rate of colostrum production. Hypocalcaemia results in a decrease in smooth muscle function, decreasing rumen and gastrointestinal tract function and ultimately resulting in a decrease in dry matter intake. In addition, decreases in uterine motility and immunity raise the risk of uterine infections and decreased fertility.
Normal levels of Ca in the blood will be between 8.5 and 11 mg/dL; however, levels drop dramatically in a cow experiencing milk fever, resulting in clinical symptoms (Table 1). This decrease in Ca in the blood supply directly impacts the animal’s ability to regulate muscle contractions and relaxation, which is the most identifiable clinical signs of milk fever.
Cattle must be able to increase absorption of calcium in the small intestine and mobilize stored calcium from bones to effectively meet increased requirements of lactation. Mobilization of bone calcium is regulated by parathyroid hormone (PTH), which is produced by glands in the neck. When blood calcium levels drop, PTH is activated. As this occurs, a secondary hormone derived from vitamin D in the kidney stimulates the intestine to increase absorption of dietary calcium. If calcium intake from the diet was sufficient prior to calving, mechanisms for stimulating calcium mobilization may not be stimulated. Therefore, a decrease in calcium intake is actually recommended late in gestation to prime those systems and increase their functionality prior to the onset of lactation. However, it is difficult to get calcium levels in the diet low enough to actually prevent milk fever.