A REVIEW of the scientific literature indicates that there is a link between nutrition and mastitis in the dairy cow. The major impact of nutrition on udder health is via suppression of the immune system.
The teat end is the first barrier against invading pathogens. The anatomical and physical characteristics of the teat canal (tightness of closure and keratin lining) inhibit penetration of udder pathogens. Approximately 40% of the keratin lining is removed at each milking (Figure 1) and, therefore, it requires constant regeneration. Consequently, it is important to ensure that the teat canal is closed post milking.
This is the reason why it is recommended that cows should stand for 30 minutes post milking before returning to the cow housing.
After bacteria breach the teat end, they are taken up and destroyed by leukocytes through the process called inflammation. Leukocyte chemotaxis is one of the major factors involved in migration of these cells towards the centre of inflammation. Several experimental infection studies have shown a strong relationship between early leukocyte influx and outcome of infection.
Nutrition
Feeding should always be aimed at meeting the nutritional requirements of the dairy cow during the various stages of lactation cycle. During the transition period the dairy cow can experience negative energy balance which can have a major impact on the immune response.
Cows in negative energy balance are at a higher risk of ketosis. Clinical ketosis is associated with a two-fold increase in the risk of clinical mastitis and ketotic cows experience more severe clinical mastitis.
In a review of hyperketonaemia and the impairment of udder defence, Suriyasathaporn postulated that cows in the negative energy balance period seem to show an impairment of udder defence mechanisms. The presence of ketone bodies reduced: (a) capacity for phagocytosis by polymorphonuclear neutrophil (PMN) and macrophages, (b) generation of chemo-attractant and (c) capacity for blood leukocytes to migrate into the infected gland.
In relation to the generation of chemo-attractant, PMNs move randomly, and towards specific stimuli from cytokines, in the infected udder (directed migration).
Both types of migration are faster for cells from cows with low beta-hydroxy butyric acid (BHBA) levels than for cells from cows with high BHBA levels in their blood. If cells move slowly, they are out competed by bacteria, resulting in clinical mastitis (Figure 2).
In a Canadian study, 28.6% of cows with pre-partum ketosis subsequently developed clinical mastitis compared with 8.7% of cows without pre-partum ketosis (Table 1).
Trace minerals and vitamins
Trace minerals and vitamins that can affect udder health are selenium and vitamin E, copper, zinc, vitamin A and ß-carotene.
Vitamin E and selenium (Se) are integral components of the antioxidant defence of tissues and cells. Cattle consuming stored forages are likely to be low in vitamin E, unless supplemented, and vitamin E deficiencies are frequently observed in peripartum dairy cows.
Vitamin E and Se deficiency leads to impaired PMN activity. Dietary supplementation of cows with Se and vitamin E results in a more rapid PMN influx into milk following intramammary bacterial challenge and increased intracellular kill of ingested bacteria by PMN, as well as lowering the frequency and shortening the duration of clinical mastitis.
In Norway, as in many European countries, content of Se in soil is low. A recent survey of 254 Norwegian Red heifers and dry cows found that the relative risk of mastitis treatment in herds with low blood Se concentration was 1.3 to 1.4 times higher during the first 30 days of lactation than in herds with high concentrations of Se.
A meta-analysis of 14 papers between 1984 and 2003 to estimate the magnitude and significance of the weighted summarised effect of vitamin E status on udder health found that vitamin E supplementation was on average associated with a 14% reduction in the risk of intramammary infection (IMI), a reduction in milk SCC by a factor of 0.70 and a 30% decrease in the risk of occurrence of clinical mastitis (CM).
These results support the hypothesis that vitamin E supplementation during the dry and early lactation periods is associated with lower IMI, SCC and CM. However, consideration of vitamin E alone is not recommended as all the components of the antioxidant system appear to interact.
Copper deficiency reduces the number of circulating T cells, B cells, and neutrophils. Supplemental dietary copper reduced the severity of mastitis following experimental challenge with Escherichia coli, but the duration of mastitis was unchanged.
Zinc is required for keratin formation. Cows receiving supplemental zinc methionine had significantly (P < 0.03) more teat canal keratin.
Zinc deficiency is associated with reduced phagocytosis and killing by macrophages and results in a decrease in blood lymphocyte population. Several studies have examined the effect of supplemental zinc methionine on SCC and in most cases supplementation statistically or numerically reduced SCC. In some studies SCCs were reduced by about 22%.
Organic forms of zinc appear to be better absorbed and retained by the animal. In a recent study, Popovic replaced 33% of the supplemental inorganic zinc sulphate with organic zinc from 45 days precalving until 100 days post-calving. Cows receiving the organic zinc had significantly lower SCC (Table 2).
Low concentrations of plasma vitamin A and ß-carotene were associated with severity of mastitis. In cows fed vitamin A plus ß-carotene starting three weeks before calving, and continued through 10 weeks of lactation, mean SCC was reduced during week 2 to 8 of lactation.
Conclusion
Nutrition can influence the cow’s resistance to mastitis. However, it does not influence the exposure of teat ends to pathogens.
Mastitis control begins with implementation of the five-point control programme as well as providing a clean, dry environment for cows.
Ensuring that the cow has adequate energy, minerals and vitamins for maximal milk production is essential for maintenance of udder health and immune status.
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A list of references is available on request.
