How to prevent milk fever in dairy cows
Prevention strategies include manipulation of the cow’s close-up diet post-calving
Hypocalcaemia, or milk fever, is a common occurrence in dairy operations. While clinical hypocalcaemia is generally easy to spot and producers often have a treatment plan in place, sub-clinical cases are less easy to detect, especially if blood calcium levels are not routinely measured.
The initiation of lactation requires a tremendous increase in the cow’s calcium requirement to meet demands for milk synthesis. About 20 to 30 grams of calcium per day are needed for milk production compared with 8 to 10 grams per day for fetal development just prior to calving. Thus, metabolic adaptations must take place to support the increased need for calcium. If they do not take place soon enough or are of insufficient magnitude, the concentration of calcium in the blood drops below a critical threshold and clinical and subclinical hypocalcaemia (milk fever) can result.
Milk fever can have lasting knock-on effects in the cow’s production cycle, and every effort should be made to reduce its incidence. This article explores management practices, feeding best practices and on-farm tools that can be used to help minimize clinical cases and/or catch subclinical cases.
The abundance of calcium
Calcium is the most abundant mineral in the body with the vast majority being found in bone. The remainder (only ~1 percent) is vital for nerve function, muscle contraction and cell signalling. There is internal regulation of blood calcium levels involving parathyroid hormone (PTH), calcitonin and Vitamin D3 (1, 25-dihydroxycholecalciferol), known as calcitriol.
Regulation involves calcium moving into or out of the skeleton, as well as dietary uptake of calcium from the small intestine. In situations of low blood calcium, PTH is secreted resulting in a greater amount of skeletal calcium that is resorbed and released into the blood. Parathyroid hormone release stimulates renal production of calcitriol, which then increases the absorption of calcium from the small intestine.
Magnesium is also involved in appropriate PTH response to low blood calcium levels, hence the importance of adequate levels of this mineral in the diet of dry cows. Heifers appear to have higher concentrations of PTH, as well as lower colostrum and milk production, compared with multiparous cows and, therefore, often don’t succumb to hypocalcaemia.
Clinical versus subclinical milk fever
Dry period diets often high in potassium, which increases blood alkalinity, result in insensitivity of target tissues to PTH. This lack of response by tissues to PTH results in reduced calcium release from bones, reduced renal activation of calcitriol, and reduced renal reabsorption of calcium.
Clinical milk fever is certainly becoming much more widely recognized in terms of the provision of treatment plans, and there are usually three stages of increasingly worsening symptoms associated with this form of the disease, with treatment during Stage 1 being critical to survival.
Subclinical milk fever is defined as low blood calcium concentrations without clinical signs and, unfortunately, because of its non-symptomatic nature, is often not dealt with as efficiently as its clinical counterpart.
Blood calcium concentrations of <2 mmol/l indicate subclinical milk fever, and a semi-recent study found that nearly one in two multiparous cows had blood calcium levels below this threshold, indicating a near 50 percent incidence of subclinical hypocalcaemia compared with ~8 percent for clinical milk fever. It also noted a relationship between high circulating NEFA (an indication of NEB) and low blood calcium levels.
Milk fever has a range of effects on the cow that increases the risk of other diseases and issues, such as abomasal displacement, as well as reducing feed intake so that greater body fat mobilization occurs in early lactation, increasing the risk of ketosis.
Milk fever also reduces all muscle contraction, including the teat sphincter muscle responsible for closure of the teat orifice after milking, thus increasing the risk of mastitis. As if this wasn’t enough, it can result in a direct impairment of immune cell response.
Most prevention strategies are concerned with manipulation of the close-up diet to try to ensure the cow’s metabolism is ready to deal with the rapid and substantial increase in calcium demand following calving.
Dietary calcium restriction in the close-up dry period
This has been the traditional approach and has included such practices as feeding diets very low in calcium and adding materials to the diet, such as zeolite, in order to prevent calcium from being absorbed. However, it is difficult to formulate low calcium diets unless whole crop or corn silage is being fed and the animal still requires a certain level of dietary calcium to maintain bone integrity.
Dietary potassium restriction in the close-up dry period
Again, this may be difficult to achieve under practical conditions and may result in reduced intake of forage, which is undesirable in the period close to calving. One of the keys to preventing hypocalcaemia is to keep dietary potassium as close to NRC requirements as possible during the dry period (~1 percent of the diet).
Dietary cation-anion difference (DCAD)
A more effective and practical approach has been to look at the overall balance between key cations and anions that determine blood pH. Dairy cows are often in a state of metabolic alkalosis, which predisposes them to hypocalcaemia. The idea behind DCAD is to reverse the alkalosis and generate mild metabolic acidosis during, at most, the three weeks prior to calving. This is done by monitoring dietary levels of sodium, potassium, chloride and sulphur and can be calculated as follows:
DCAD (mEq/kgDM) = (Na%*434.98)+(K%*255.74)-(Cl%*282.06)+(S%*623.74)
Target DCAD for a close-up dry cow is ~ -100mEq/kg DM. Animals on DCAD diets must be closely monitored via urine pH and must receive sufficient dietary magnesium (~0.4 percent) and dietary calcium at 1 percent. Close-up dry cows on a DCAD diet should have a target urine pH of <7, preferably nearer 6 (optimal is 6.2 to 6.8 for Holstein cattle).
Anionic salts are a common method of manipulating the DCAD but can have issues with palatability. Again, close monitoring of urine pH will show whether the salts have been effective, including whether too many anions are being fed resulting in a more acidic pH (<5.5).
Additional oral calcium supplementation
Oral calcium drenches post-partum have shown benefit to reducing incidence of milk fever.
Dosing with vitamin D3 for a short period of time prior to calving has had mixed results. The amount required to elicit a response often has negative impact elsewhere in the body, and there remain problems associated with timing of administration.
Subclinical hypocalcaemia can be diagnosed by blood calcium levels; however, monitoring of the metabolic "state" of the animal with regards to blood pH, which affects susceptibility to milk fever, can be carried out more practically using urine pH analysis.
Although urine pH does not indicate an animal’s risk of hypocalcaemia per se, it does give an indication of whether DCAD diets are effective. Urine should be measured mid-stream to avoid contamination with other secretions and can be collected no earlier than two days following the addition of anionic salts or any dietary change designed to reduce pH.
Most people tend to re-test urine about a week after introduction of dietary intervention.
Hypocalcaemia occurs when the cow cannot satisfy the huge increase in calcium demand following the onset of lactation. Blood calcium drops, and cows can succumb to both clinical and/or sub-clinical hypocalcaemia. While clinical hypocalcaemia is generally easier to spot, subclinical hypocalcaemia can be missed, which can have serious consequences in terms of health and production.
Numerous dietary strategies exist to try to reduce the risk of hypocalcaemia, including low calcium and potassium diets and the DCAD diet. Any strategy needs careful and accurate monitoring, and urine pH analysis is a key tool in determining not only an animal’s risk of hypocalcaemia but also whether prevention strategies are working.
References available upon request.