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Nutrition and mastitis: More than just minerals and vitamins

Bill Weiss Published on 22 August 2014

Mastitis is inflammation of the mammary gland usually caused by a bacterial infection. Poor nutrition does not cause mastitis, but poor nutrition can make it easier for bacteria to become established in the mammary gland, resulting in increased rates of mastitis.

The mammary glands of cows are frequently exposed to potential pathogens, but most cows on most days do not get mastitis because their immune systems are adequate to prevent infection. Nutrition (good and bad) affects many components of the immune system.

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Nutrition can impact immune function via two broad mechanisms. First, immune cells have specific requirements for certain nutrients, and diets that do not provide adequate amounts of those nutrients can impair immunity while still providing adequate nutrients for other functions, such as producing milk.

In other words, a diet might support high levels of milk production but at the same time increase the risk of mastitis because of suboptimal immune function. The second way proper nutrition can enhance immune function and reduce mastitis risk is by reducing the prevalence of metabolic conditions that inhibit or suppress immunity.

Provide nutrients to enhance immunity

Most of the research looking at nutritional effects on immune function and mastitis involve trace minerals and vitamins associated with the antioxidant system of cows. These include selenium, vitamin E, copper and zinc.

In most situations, formulating diets to meet the NRC recommendations for those nutrients will be adequate to optimize immune function. However, diets that contain more than about 0.25 percent sulfur (the amount of sulfur provided by drinking water should be included) can reduce absorption of both selenium and copper, and NRC requirements probably are not adequate in those situations.

Using a copper source that has been shown to have greater bioavailablity than copper sulfate and replacing inorganic selenium with selenium yeast should be considered in that situation.

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The other situation where NRC requirements for some nutrients may not be adequate for optimal immune function is during the pre-fresh period (approximately the last two or three weeks of gestation). Increased supplementation of vitamin E (2,000 to 4,000 IU per day) has been shown to reduce mastitis and improve immune function.

Based on available data, increased supplementation (i.e., more than the amounts supplemented during the dry period) of the other antioxidant nutrients during the pre-fresh period is not warranted at this time. The NRC has not established a recommendation for B-carotene but supplementation (300 to 600 mg per day) in the pre-fresh period may enhance immunity and reduce mastitis.

Plasma concentrations of B-carotene decrease markedly a few days before parturition (similar to vitamin E), and low plasma concentrations of B-carotene have been identified as a risk factor for some diseases. If cows are fed pasture or good-quality silage, the basal diet is probably adequate in B-carotene, and supplementation is not needed.

In addition to the antioxidant nutrients, vitamin D and vitamin A affect immune functions in cows, but studies have not shown that supplementation above NRC recommendations improves cow health.

Use good nutrition to eliminate immune suppressors

In well-managed herds that have controlled contagious mastitis, two-thirds to three-fourths of all clinical mastitis cases occur the first two months of lactation, and most of those occur in the first few weeks of lactation. One reason for this (but not the only reason) is that many metabolic disorders are associated with parturition, and these metabolic disorders have negative effects on immune function.

Surveys of U.S. dairy cows indicate that up to 45 percent of cows suffer from subclinical or clinical ketosis, and up to 50 percent of cows suffer from subclinical or clinical hypocalcemia during the early postpartum period. Cows that suffer from either of those ailments have a much higher risk of developing mastitis.

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Cows with hypocalcemia spend more time lying down, increasing teat-end exposure to pathogens. Making this worse is that calcium is needed by muscles, and the teat-end sphincter in cows with hypocalcemia may contract slower and less completely, allowing bacteria to enter the mammary gland.

Additionally, calcium is needed for immune cells to function properly, and these cells do not work as well when cows have hypocalcemia.

Reducing the prevalence of hypocalcemia by formulating dry cow diets to provide proper amounts of calcium, phosphorus, vitamin D and magnesium, and to contain the correct cation-anion balance, should reduce the incidence of mastitis via improved calcium status.

If herds have higher-than-expected incidence of mastitis in early lactation, monitoring blood calcium concentrations at calving may help discover an underlying cause of the mastitis.

Cows that have ketosis or excessive mobilization of body fat in early lactation (these very often happen together) are much more likely to get mastitis than are healthy cows. When cows mobilize body fat, the concentrations of non-esterified fatty acids (NEFA) in blood increase, and NEFA has been shown to directly inhibit the function of certain immune cells.

High concentrations of plasma NEFA during the transition period are a good marker for cows at high risk for developing mastitis. One study found that cows with NEFA concentrations greater than 1.2 mEq per L shortly after calving were two times more likely, and cows with concentrations greater than 1.6 mEq per L were four times more likely to develop clinical mastitis in early lactation than cows with lower concentrations.

If mastitis is an issue in early lactation, measuring NEFA on several transition cows may help determine a potential reason. Elevated concentrations of ketones also have direct negative effects on immune function and increase the risk for clinical mastitis.

However, unlike NEFA, we do not have a clear-cut point for when concentrations of ketones (usually measured as BHBA) become a good marker for risk of mastitis, but cows with BHBA concentrations higher than about 1.2 mM per L are at greater risk for other health disorders.

Properly managing body energy change in the transition cow is important for many reasons, but one is to reduce the risk of mastitis in early lactation. Some key points are:

  1. 1.Prevent cows from becoming too fat in late lactation or during the dry period. This may require a late-lactation or fat cow pen.
  2. 2. Prevent a large decrease in feed intake during the pre-fresh period. A large decrease in intake causes the cow to mobilize fat, elevating NEFA, and can cause fatty liver and ketosis. The prepartum drop in intake can be mitigated by feeding a high-fiber, lower-energy diet to the dry cows.
  3. 3. Promote a rapid increase in energy intake during the immediate post-fresh period. Feed a well-balanced diet (moderate concentrations of both fiber and starch) based on high-quality forage.

Keep concentrations of supplemental fat in the diet low for the first week or two after calving. Overcrowding fresh cows also restricts their intake, so give cows lots of room plus plenty of access to the feedbunk.

Good nutrition can help reduce mastitis, especially in early lactation. Key summary points are: Meet the transition cow’s requirements for trace minerals and vitamins. Use good nutrition to prevent hypocalcemia. Manage body energy change in transition cows by maintaining intake prepartum and doing everything possible to increase intake postpartum. PD

Bill Weiss
  • Bill Weiss

  • Department of Animal Sciences
  • Ohio Agricultural Research and Development Center
  • Ohio State University
  • Email Bill Weiss

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