trace minerals in dairy cattle

Proper dairy herd management should be designed to optimize the production of high quality milk, while minimizing any adverse effects on the health and welfare of dairy cattle. Two key ingredients in accomplishing these goals are adequate nutrition programs and sound mastitis control programs.

Although historically these management areas may have been considered as separate entities, mounting evidence accumulated over the past 15 years has demonstrated a dramatic impact of proper micronutrient nutrition on udder health and milk quality.

In particular, adequate supplementation of selenium, zinc, and copper in dairy cattle diets has been shown to be important for improving udder health and reducing somatic cell counts in milk (Harmon and Torre, 1997).

In general, optimizing dietary trace minerals in the prepartum period of heifers and in the dry or non-lactating period of older cows can reduce the prevalence of infection and incidence of clinical mastitis at calving and in early lactation. Such positive benefits translate into economic returns to the dairy farmer.


Selenium

Extensive evidence supports a critical role for vitamin E and selenium (Se) in protection of the body from infection (Erskine, 1993). Vitamin E is important in protecting the membranes of cells from oxidative damage; and Se is a component in the enzyme glutathione peroxidase.

Glutathione peroxidase is an enzyme within cells that is critical for the protection of cells from internal damage when the body is fighting an infection. Deficiencies of Se or vitamin E will reduce the ability of phagocytic cells, a first line of defense against udder infection, to kill ingested bacteria.

In fact, Grasso et al. (1990) showed that the killing of Escherichia coli by milk neutrophils (phagocytic cells) from Se-deficient cows was decreased. Erskine et al. (1989) showed that experimental E. coli mastitis was less severe and of shorter duration in Se-supplemented (2 mg per head per day) than in Se-deficient cows.

Selenium-supplemented cows also had lower peak bacterial numbers in milk and reduced milk loss resulting from infection.

Deficiencies in dietary Se and vitamin E have been shown to result in increased incidence of mastitis.

Supplemental dietary Se and vitamin E were shown to lower the frequency and shorten the duration of clinical mastitis (Smith et al., 1984).

A later Ohio study (Smith et al., 1985) evaluated mastitis incidence in heifers either supplemented with vitamin E and Se or those receiving no supplemental vitamin E and Se from 60 days prepartum and throughout lactation. Prepartum dietary supplementation was with approximately 1,000 IU vitamin E per head per day and 2 mg Se per head per day.

In addition, supplemented heifers received a subcutaneous injection of Se (sodium selenite) at 21 days prepartum. Lactation supplementation was 600 to 800 IU vitamin E and 2 mg Se per head per day. Vitamin E and Se supplementation resulted in:


1. 42% reduction in prevalence of infection at calving.

2. 57% reduction in clinical mastitis in early lactation and 32% reduction throughout lactation.

3. 40 to 50% reduction in duration of infections.

4. Significantly lower somatic cell counts for the lactation.

Overall, vitamin E and Se improved udder health, and the effect was most evident at calving and early lactation. In studies in commercial dairy herds, herd prevalence of intramammary infection was shown to decrease with increasing mean activity of blood glutathione peroxidase.


Zinc

The link between dietary zinc (Zn) and ruminant immune function dates to the early 1970s when an inherited, lethal trait in Black Pied Danish calves of Friesian descent was found to result in symptoms including hair loss, parakeratosis around the mouth, eyes, and jaw, diarrhea, conjunctivitis, rhinitis, and bronchopneumonia (Brummerstedt et al., 1971).

Symptoms typically began at 4 to 6 weeks of age, and most affected calves died at approximately 4 months of age. At necropsy the calves were found to have atrophy of the thymus and Peyer’s patches. These symptoms, similar to those in humans possessing inborn errors of Zn metabolism, improved with oral administration of Zn oxide (Brummerstedt et al., 1971).

Zinc supplementation has been used to reduce effects of infectious pododermatitis in Friesian cattle (Suttle and Jones, 1989). However, studies to determine whether in vivo Zn status affects cellular immune function in the ruminant are lacking. Droke and Spears (1993) found that severe Zn deficiency was required to increase numbers of blood neutrophils and decrease numbers of lymphocytes. Serum IgG response to lysozyme or in vivo response to phytohemagglutinin injection was not altered.

Zinc deficiency in ruminants has been postulated to weaken skin and other stratified epithelia (i.e., keratinocytes) as well as reducing the magnitude of increase of basal metabolic rate following infectious challenge (reviewed in Suttle and Jones, 1989).

Because the mammary gland is essentially a skin gland and the importance of the keratin lining of the streak canal in prevention of infection is known (Capuco et al., 1992), speculation that Zn supplementation may enhance resistance to mastitis is tempting. Moderate to severe blood hypozincemia during mastitis, particularly acute coliform or endotoxininduced mastitis, has been documented (Lohuis et al., 1990; Verheijden et al., 1983).

Zinc is a cofactor for many proteins and enzymes involved in the acute phase response to infection and inflammation (Prasad, 1979; Vallee and Galdes, 1984). Mastitis-associated hypozincemia in cattle is likely linked to the magnitude of the acute phase response, but the possibility that blood or tissue levels of Zn could be a limiting factor in the bovine acute phase response has not been explored. Consequently the precise roles of Zn supplementation in mammary health are not clear.

Most studies in this area have focused on reduction of somatic cell counts (SCC) during supplementation of organic forms of Zn, which are reported to be more bioavailable to the ruminant compared with inorganic Zn (Madsen, 1993). A summary (Kellogg, 1990) of eight trials evaluating effects of Zn methionine compared with equivalent amounts of Zn oxide and methionine showed that supplementation of Zn methionine (180 or 360 mg Zn, 360 or 720 mg methionine) resulted in 22% decrease in SCC when feeding the lower level. Feeding the higher level of Zn methionine lowered SCC by 50%.

However, decreased SCC were not observed in another study of Zn methionine supplementation (Moore et al., 1988).

Galton (1990) saw no effect of Zn methionine on rate of new infections resulting from experimental challenge with Streptococcus agalactiae, although SCC were significantly decreased in supplemented cows. In contrast, Spain (1993) reported beneficial effects of Zn proteinate (providing 50% of a total 800 mg Zn per cow per day as Bioplex Zinc; Alltech, Inc.) on rate of new, naturally occurring intramammary infections. No effects of Zn proteinate supplementation on SCC or milk yield were observed compared with Zn oxide.

However, numbers of new infections were reduced approximately 50% in the Bioplex Zn proteinate group compared to the Zn oxide supplemented animals (5 vs 11 new infections). The majority of isolates were environmental mastitis pathogens. Spain (1993) suggested that Bioplex Zn is beneficial in enhancing resistance to mastitis pathogens because of the postulated role of Zn in maintaining skin integrity and the keratin lining of the streak canal.


Copper

The importance of copper (Cu) as an essential trace element has been recognized for nearly 60 years, with the early discovery that Cu was necessary for normal hemoglobin synthesis in young rabbits and rats (Hart et al., 1928). Since that time, the importance of Cu for normal growth, production and reproductive performance has been established.

The biological role of Cu is exerted through a number of Cu-containing proteins including ceruloplasmin and superoxide dismutase (SOD) (Prohaska and Lukasewycz, 1990). When Cu is inadequate in animals, physiological and metabolic functions related to the Cu-enzymes may be impaired and, during clinical deficiency, symptoms will appear.

In addition, inadequate Cu status may influence the magnitude of tissue injury that occurs during inflammation. Although low Cu content of feedstuffs is a common cause of Cu inadequacy, reduced bioavailability of Cu in ruminants may occur when dietary sulfur, molybdenum (Mo), Zn, or iron is high (Hemken et al., 1993). Recent evidence in cattle suggests that Cu proteinate (Bioplex Cu) is stored more readily than inorganic Cu (Hemken et al., 1993) and Cu proteinate may be absorbed in the organic form (Du et al., 1995).

Deficiencies in protein, energy, vitamins, and minerals are known to compromise immune function (Beisel, 1982). A relationship between Cu and immune function has been shown by decreased natural resistance to infection in animals that were Cu deficient (Jones and Suttle, 1983;Woolliams et al., 1986). Reports by Jones and Suttle (1988) support a relationship between Cu status and disease susceptibility. Low liver Cu levels have been linked circumstantially with the occurrence of abomasal ulceration and pathogenic bacterial infections in beef calves in aWyoming survey (Libbey et al., 1985).

The phagocytosis and killing of microorganisms are important functions of white blood cells such as the macrophage and neutrophil. This is especially important in the protection of the bovine mammary gland against infection by bacterial pathogens (Craven andWilliams, 1985). The ability of peripheral blood granulocytes to kill ingested Candida albicans was reduced in Cu-deficient ewes (Jones and Suttle, 1981) and in Cu-deficient steers (Boyne and Arthur, 1981).

Furthermore, leukocyte and erythrocyte SOD activities were significantly decreased in the hypocupremic ewes and cattle (Arthur and Boyne, 1985). Kentucky studies (Xin et al., 1991) showed that neutrophils from dairy steers made Cu deficient by feeding 10 ppm Mo (as ammonium molybdate) had significantly lower capacity to kill S. aureus than neutrophils from Cu-supplemented (20 ppm) animals. The low Cu status resulted in a significant decrease in SOD activities in whole blood, neutrophils, and erythrocytes and significantly lower Cu levels in the liver and neutrophils.

Torre et al. (1996) extended these studies to the dairy cow. They found that mild Cu insufficiency (prepartum and postpartum diets containing 6 to 7 ppm Cu) in lactating Holstein heifers resulted in a 30% reduction in bactericidal capacity of blood neutrophils compared with cells from heifers which had received a dietary supplement of 20 ppm Cu as sulfate.

Liver Cu concentrations can be influenced by numerous factors including species, age of animal, disease conditions, and dietary composition. Dietary Cu is accumulated in the liver with a nearly linear response in liver Cu concentration to dietary Cu supplementation. Studies by Xin et al. (1991) at Kentucky indicated that liver Cu concentration, but not total plasma Cu, was a good indicator of Cu status of animals with subclinical Cu deficiency.

Although liver Cu concentrations in these studies approached deficiency levels (18.1 ppm at trial termination), no influence on growth was observed. This is a significant observation, because it suggests that a subclinical Cu deficiency may compromise host defense mechanisms in the absence of clinical symptoms or an effect on growth. Although Puls (1988) reported that 87.5 to 350 ppm Cu in the liver reflects an adequate Cu status, the level at which host defenses or antioxidant activities may be compromised is not clear.


COPPER AND UDDER HEALTH

Studies (Harmon et al., 1994a) at the University of Kentucky have attempted to elucidate the role of Cu status on inflammation and infection of the mammary gland. Holstein heifers were assigned in pairs (by date of expected calving) to two dietary treatments from 84 days prepartum through 105 days of lactation. No supplemental Cu had been fed since the cattle were about 5 months of age.

The diets were basal diet (6 to 7 ppm Cu) with no supplemental Cu (-Cu) and basal diet plus 20 ppm supplemental Cu (+Cu) as Cu sulfate. The NRC recommendation for dairy cattle is 10 ppm. Liver and blood Cu contents and postpartum milk bacteriology were monitored. Two quarters of each cow were challenged with 25 μg E. coli endotoxin at 35 days of lactation and with viable S. aureus at 70 days of lactation; responses were measured for 6 and 15 days, respectively.

Analysis of the data showed that liver Cu levels in the +Cu and -Cu cows were 209 and 14 ppm at calving and 474 and 29 ppm at 105 days postpartum.

However, plasma Cu in both groups of heifers was within a normal range.

The +Cu cows had more (P < 0.05) uninfected quarters (60%) than the -Cu cows (36%) at calving. The +Cu and -Cu cows had 6 and 28% of quarters with intramammary infections (IMI) by major pathogens (P < 0.01); however, there was no difference in coagulase-negative staphylococci IMI. Major pathogen IMI were 0 and 14% on day 7.

The -Cu cows tended to have higher SCC than +Cu on day 1 (P<0.10) and day 3 (P<0.07) after endotoxin challenge (3,954 vs 2,624 × 103/ml; 1,213 vs 877×10³/ml). Mean clinical severity scores (P<0.05) and the number of abnormal quarters (P<0.01) were lower in +Cu cows on day 1 (Harmon et al., 1994b).

No differences in milk production or other measures of inflammation were observed. In contrast, no differences in SCC, clinical scores, or other measures were found between groups in response to S. aureus challenge.

This study demonstrated that inadequate Cu status is possible in the absence of Cu supplementation of normal diets of heifers. The failure to provide Cu supplementation in heifer diets is likely a common occurrence in some dairy herds. These data suggest that inadequate Cu status may result in increased infection prevalence at calving and an increase in clinical severity following challenge, perhaps accompanied by increased SCC, compared with that observed in cows with an adequate Cu status.


Copper proteinate, mastitis, and mineral status

Studies were recently completed (unpublished data) at the University of Kentucky to evaluate effects of Bioplex Cu on Cu status, infections of heifers at calving, and response to E. coli J-5 vaccination. Thirty-one primigravid Holstein heifers were maintained on a basal diet (-Cu; 6–7 ppm Cu) or diets supplemented (10 ppm) with either Bioplex Cu proteinate (BioCu; Alltech, Inc.) or Cu sulfate (CuSO₄) beginning 120 days prepartum through about 60 days of lactation.

All animals were vaccinated with E. coli J-5 bacterin at -60 days, -30 days and at calving. Liver biopsies and blood samples were taken during the trial for liver and blood minerals and plasma ceruloplasmin (Cp). Serum was analyzed for titers to E. coli J-5. Table 1 shows mean liver Cu analyses throughout the trial.

The BioCu supplement showed an advantage over CuSO₄ at restoring Cu stores, particularly at the critical periparturient period. Liver Cu was higher (P<0.07) in the BioCu group than in the CuSO₄ group at calving. Interestingly, evaluation of overall mean liver and plasma Cu contents and plasma Cp activities tend to support the idea that organic Cu supplements have increased bioavailability over that of inorganic forms in periparturient heifers (Table 2).

As expected, the overall mean liver Cu was about 2-fold higher in both BioCu and CuSO₄ groups than that in -Cu animals. However, plasma Cu was highest (P<0.07) in BioCu animals, especially at calving (Table 3). This is in contrast to Cp activities which only responded to the CuSO₄ (Table 3). Ceruloplasmin is reported to be the major Cu transport protein produced in the liver. The blood Cu and Cp data suggest the BioCu can affect plasma Cu levels without marked stimulation of Cp. The suggestion is that BioCu may be taken up and(or) transported via a different mechanism than inorganic forms of Cu.


Table 1. Mean liver Cu levels (ppm Cu in dry matter) in heifers with no supplementation (−Cu) or supplemented with 10 ppm Cu proteinate (Bioplex Cu) or CuSO₄ from 120 days pre- to 60 days postpartum.





Table 4 gives a summary of infection status at calving for all 31 heifers.A higher proportion of quarters were confirmed uninfected and fewer were infected with coagulase-negative staphylococci (considered a minor pathogen) in BioCu (P<0.01) compared with -Cu and CuSO₄ groups. The higher percentage of uninfected quarters in BioCu-supplemented heifers compares with previous studies at Kentucky which showed similar results when 20 ppm CuSO₄ was supplemented in the diets of prepartum heifers.

In contrast, BioCu and CuSO₄ animals had higher (P<0.05) percentage quarters infected with major pathogens than the -Cu group. Preliminary results of titers to E. coli J-5 do not suggest an obvious advantage among the dietary treatments.


Table 2 Overall mean (±SEM) liver and plasma Cu contents and plasma ceruloplasmin activities in heifers that received no Cu (−Cu), Cu proteinate (Bioplex Cu), or CuSO₄ supplementation 120 days prepartum to 60 days postpartum.


^a Significant treatment effect, P<0.01.
^b Significant treatment effect, P<0.02.



Table 3. Plasma Cu contents and plasma ceruloplasmin (C_p) activities in heifers that received no Cu (−Cu), Cu proteinate (Bioplex Cu), or CuSO₄ supplementation 120 days prepartum to 60 days postpartum.





Organic mineral sources and somatic cell counts

Several studies have demonstrated a reduction in SCC in dairy cattle which were supplemented with mineral proteinates. Harris (1995) reported results of a 90 day field trial in which one group of 70 cows received a total mixed ration (TMR) supplemented with 400 mg Zn per cow per day as Bioplex Zinc proteinate (Alltech, Inc.) and the control group was fed the normal TMR.

The mean SCC in the Zn proteinate group decreased 24% and the SCC in the control group increased 36%. Somatic cell count was 57% lower in the group supplemented with Zn proteinate at trial end. Adjustment for the lower SCC in the Zn proteinate group at initiation of the trial would still show an estimated 30 to 40% lower SCC in the Zn proteinate cows.

Boland et al. (1996) reported the results of three different trials in which a combination of mineral proteinates were supplemented to normal dairy cow diets; the control diet was the same as the proteinate-supplemented diet but without the mineral proteinates. The mineral proteinates (Alltech, Inc.) provided the following supplemental minerals per cow per day in the diets during all three trials: Cu, 100 mg; Zn, 300 mg; Se, 2 mg).

Blood mineral profiles were normal for both groups suggesting mineral status was adequate in both groups and unaffected by the supplements. In the groups receiving mineral proteinates in the three trials the SCC were reduced by 52, 45 and 35% over the duration of the trials. In the last trial SCC were reduced 52% during the final 4 weeks.

Boland et al. (1996) indicated that these data showed a greater reduction in SCC the longer the treatment continued. Overall, the results of these studies suggest a beneficial effect of organic mineral supplementation on SCC in the herd and, thus, on udder health.


Table 4. Quarter infection status (% quarters) of heifers at calving (days 1–3) that received no Cu (−Cu) supplement or supplementation with 10 ppm Cu as Bioplex Cu or CuSO₄ for 120 days prepartum.


CNS = coagulase-negative staphylococci.
Major pathogens = S. aureus, Streptococcus spp. and coliforms.
* Quarters from which duplicate milk samples yielded dissimilar culture results.
^a,b Values within a row with different superscripts differ, P<0.01.
^c,d,e Values within a row with different superscripts differ, P<0.05.



Summary

Adequate Se in dairy cow diets certainly is important for optimizing health of the periparturient and lactating dairy cow. Increasing evidence suggests that Cu and Zn also play an important role in host defense and in limiting tissue damage during inflammation.

These ideas, combined with the fact that there is a massive influx of neutrophils into the mammary gland during inflammation, suggest that trace mineral inadequacy in the dairy cow could limit protection against intramammary infection and may increase the opportunity for tissue damage.

Copper may play a role in mammary gland resistance through altered antioxidant capacity and function of inflammatory cells or perhaps by influencing factors which regulate inflammation. The resulting impact could be altered clinical severity as well as reduced incidence of mastitis.

New evidence suggests that Cu proteinates may be taken up and(or) transported via a different mechanism than inorganic Cu sources in the dairy cow, and Cu proteinate appears to provide some advantage to Cu status in the periparturient cow.

These nutritional approaches are important for optimizing udder health and milk quality, but a good nutritional program must be instituted in concert with sound management practices which reduce exposure of dairy cattle to mastitis pathogens.



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