Apr 19, 2014
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Animal Health & Nutrition

RSS By: Rick Lundquist, Dairy Today

Rick Lundquist is an independent nutrition and management consultant based in Duluth, Minn. He provides livestock production advice.

Vitamin E: What's the Requirement?

Dec 30, 2013

Inconclusive research leads to expensive guessing.

Vitamin E can be one of the most expensive supplements in our rations, and in my opinion, we don’t know the cow’s requirement.

Vitamin E is an antioxidant and is supplemented to reduce oxidative stress in tissues caused when reactive oxygen species (ROS) accumulate. These ROS have been shown to be associated with an increased incidence of retained placenta and metabolic diseases. The National Research Council (NRC) recommends supplementing 1000 IU of vitamin E prepartum and 500 IU postpartum. Researchers at Ohio State have suggested that levels as high as 4,000 IU prepartum may be beneficial.

So, what does this cost the dairy producer? Vitamin E production is controlled by very few players in the world – primarily the Chinese. The market goes up and down as these producers manipulate the market. The approximate cost for 1000 IU of vitamin E, by the time it gets to the farm has varied over the past 6 years from as low as 3¢/cow/day to over 10¢/cow/day. So, 4000 IU could cost as much as 40¢/cow.

There have been no definitive titration studies done with vitamin E under different physiological or environmental conditions to really pinpoint a requirement. We went from 300 IU to 500 to 1000 and then jumped to 4,000 IU as recommended supplemental levels. What if you’re feeding fresh forage, which can be loaded with vitamin E, or only ensiled forages with very little vitamin E?

I recently read a University of Florida study, where the effect of heat stress and vitamin E levels were examined. The hypothesis was that heat stress increased oxidative stress in the animals and vitamin E may help alleviate this. Cows were supplemented with levels from 500 to 3000 IU vitamin E pre and postpartum under cooled or heat stressed conditions.

The results were pretty much inconclusive, although feeding more vitamin E did increase the level of E in the blood. Feeding the high level of vitamin E to mature cows under heat stress increased milk, but first-calf heifers actually produced less milk with higher vitamin E supplementation, whether heat stressed or not. Based on blood NEFA levels, the first-calf heifers were under less metabolic stress than cows. The researchers theorized that supplementing too much vitamin E to the less stressed heifers may have caused greater radical formation which reduced performance. Wow, too much vitamin E?

There’s no question that vitamin E is a required nutrient. Dairy producers spend a lot of money on vitamin E, based on what I consider less than adequate research.
We’ve really dialed in on protein and carbohydrate requirements in recent years. I think we should do the same with vitamin E. Since the U.S. doesn’t produce any, maybe we could make it a national security issue.

 

Lundquist & Associates, Nutrition Professionals, is based in Duluth, MN. Contact Rick at siestadog@aol.com.


 

A Classic Case of Milk Fat Depression

Oct 28, 2013

Nutritionist Rick Lundquist explains how ration changes lowered this herd’s milk fat numbers before a diet modification restored them.


I was reading a paper about milk fat depression published in the October 2013 Journal of Dairy Science. One of my client’s dairies had just experienced a case of milk fat depression. This rarely occurs, but, when it does, there’s no doubt what’s happening. The timeline on this dairy followed the experimentally induced milk fat depression in this study almost to a "T."

Milk fat depression occurs when all the stars align in the diet and hence, the rumen, even in well formulated diets. High fat (especially unsaturated fat), combined with high starch or low fiber alter the biohydrogenation pathways in the rumen, producing trans fatty acids that inhibit milk fat synthesis in the mammary gland. Rumensin seems to accentuate these changes.

According to the researchers, the timeline for milk fat depression follows dietary induced changes in rumen microbial populations. Unsaturated fatty acids in the ration cause changes in microbial pathways as soon as two to three days after ration changes. But full milk fat depression takes about 14-19 days as microbial shifts are complete. Milk fat can be restored by changing the diet (reducing oil, increasing forage) and the recovery follows a similar pattern, as rumen microbial populations adjust to the new diet.

In our case, butterfat was running about 3.7% prior to the ration changes. We were running low on alfalfa haylage due to a loss of first cutting. Because of this, we had to increase the proportion of corn silage in the diet. Then our whole cottonseed contract ran out, so tallow replaced the fat provided by the cottonseed. We were also feeding about 400 mg of Rumensin. Dietary fiber was similar before and after the changes, although the physically effective fiber had changed due to less haylage and no cottonseed.

Cows were ruminating well and manure looked normal, but butterfat started slipping a few days after cottonseed was replaced with tallow plus additional corn silage and protein. Butterfat was down to less than 3.0% within three weeks.

It was apparent that the combination of more corn silage, lower effective fiber and the tallow had caused a microbial shift that resulted in production of milk fat robbing fatty acids. Corn and corn silage can contribute a lot of unsaturated corn oil.

We brought in some hay, reduced the tallow and replaced it with a rumen inert bypass fat. We also bought some more cottonseed. Butterfat began turning in a few days, with a full recovery in about two weeks.

In retrospect, we should have replaced the whole cottonseed with a rumen inert fat rather than tallow. Even though we may know how to fix milk fat depression, the rumen microbial population is slow to adjust, so two to three weeks of low butterfat can be expected.

Reference: Rico, D. E. and K. J. Harventine. 2013. Induction of and recovery from milk fat depression occurs progressively in dairy cows switched between diets that differ in fiber and oil concentration. J. Dairy Sci. 96:6621-6630.

Fighting Aflatoxin with the Fungi that Produce It

Sep 19, 2013

Nutritionist Rick Lundquist’s dairy client used a new technology to prevent the development of aflatoxin in his corn silage crop - and it appears that it worked.

Last month in this column, I discussed the problems many producers were having with aflatoxin contamination of their 2013 corn silage crop.

Some dairies in the Southwest had to dump milk that tested over the legal limit. Many dairies are feeding clay products and limit-feeding the corn silage to reduce the risk of aflatoxin.

One of my clients used a new technology to prevent the development of aflatoxin in his corn silage crop - and it appears that it worked. He actually applied Aspergillus flavus, the fungi that produce aflatoxin, to his corn crop while it was growing in the field.

Aspergillus flavus and Aspergillus parasiticus are fungi that are ubiquitous in soil and produce spores that are spread by wind and insects. The spores attach to crops such as corn, cotton and peanuts and then germinate if environmental conditions are right. The fungi can also live on crop residues from previous growing seasons, especially under no-till management. Temperature between 77 and 108 F are optimum for development. The fungi grow under these conditions and can produce alfatoxin on plants stressed from heat, drought or insects.

My client applied a commercial product called Afla-Guard (manufactured for Syngenta), which contains a strain of Aspergillus flavus that does not produce aflatoxin. The product is on a barley carrier. Moisture activates the fungi to produce spores, which are then spread by wind and insects throughout the field and on the crop. The "nontoxic" strain of the fungi compete with and displace the naturally occurring toxin producing strain, thereby reducing the risk for aflatoxin development in the crop. Research by USDA-ARS showed up to 85% reduction in aflatoxin with the product.

The product is applied by ground or aerial broadcast methods. For corn, recommendations are for application between about 14 days before tassling (or when about 10-12 visible leaf collars appear) up to active silking.

My client’s costs for the product and for the aerial application were less than $1.00 per ton of silage. This is less than what we would spend on binders trying to deal with aflatoxin in the feed. His silage tested very low or completely clean for aflatoxin. We didn’t have any control plots, but the local lab commented that his was one of the very few corn silage samples in that area that didn’t have aflatoxin. 

We’re Seeing High Aflatoxin Levels in 2013 Corn Silage

Aug 26, 2013

What you can do if you have corn silage that’s contaminated with aflatoxin.

Corn silage tests on the 2013 crop have shown high levels of aflatoxin in some areas. While most of the country still has corn in the field, tests coming in from the Southwest are showing high or very high levels of aflatoxin. Some dairies feeding 2013 silage have had to dump milk.

Total aflatoxin in feeds and foods like corn grain, cottonseed and peanuts is restricted by the FDA to 20 ppb. Aflatoxin B1 is the most toxic form of aflatoxin in feed and food. It is converted to aflatoxin M1 (AFM1) in milk. This is a less toxic metabolite, but nonetheless, it is more strictly regulated than B1 because of the high volume of dairy products consumed by humans. The FDA limits AFM1 to 0.5 ppb in milk, ensuring the safety of dairy products. About 1-3% of aflatoxin in feed is transferred to milk. So if, for example, a TMR contains an ingredient that is 100 ppb and it is 20% of the TMR, the AFM1 in milk could potentially be between .2 and .6 ppb.

The risk for aflatoxin in feeds and foods is higher in warm, humid areas or in drought stricken areas. It can develop in the seed or during storage.

So what do you do if you have a bunch of corn silage contaminated with aflatoxin? Unfortunately, if the aflatoxin levels are very high, the options are few.

1. Minimize your risk from other sources – corn grain, cottonseed, peanut products.

2. Since there may be hot spots in a pit of corn silage, we really don’t know at any one time how much aflatoxin is in the silage we are feeding. Test both the corn silage and the TMR regularly if you think there is a risk of contamination. Send the feed to a certified lab and identify the feed, since labs may use different testing procedures for cereal grains, forages or TMRs.

3. Limit the amount of silage in the TMR to reduce the risk of transfer to milk.

4. Bentonite clay has been shown to bind aflatoxin from the gastrointestinal tract. Refined clay products such as Novasil and AB20 (called smectite or montmorillonite clays) are more effective. An inclusion rate of .5% of the dry matter has been shown to be effective, although higher levels may be required. Recent research has shown that trace mineral and vitamin depletion when feeding clays may not be an issue, as previously thought. However, higher vitamin E levels may be warranted as a precaution. Non-clay binders may be more wide-spectrum but are not as specific for aflatoxin.

5. Ammoniation has been used in Arizona as an approved method to detoxify cottonseed over 20 ppb for dairy cattle. This is also effective for corn silage, although more difficult to apply after it is ensiled.

6. It takes about 12-24 hours for aflatoxin in contaminated feed to appear in milk. It takes about 1-4 days for milk to clear after the feed has been removed or an effective binder is fed. 

Ask What Changed when You’re Troubleshooting Problems

Jul 29, 2013

A CSI-like investigation -- not a knee-jerk reaction -- led us to find a herd-health culprit in the commodity barn.

A string of displaced abomasums in fresh cows, all within a couple of days, prompted a recent call from a client. "We need to change the ration" was the initial response to this crisis.

Well, we had been feeding the same close-up and fresh ration for quite a while, long before the DA’s occurred. That hadn’t changed, so why would it be the cause of these recent digestive problems?

If you’re a nutritionist reading this, you’re probably familiar with this situation.

Troubleshooting an issue like this can be kind of like investigating a CSI case. You have to look at all the evidence before you hopefully find the culprit. Sometimes you never do. Sometimes the problems go away without ever pinpointing the exact cause.

But the first question we need to ask is, "What has changed?" The ration on paper didn’t change.

1. Was there a mixing error or a substitute feeder?
2. Did we have a forage change?
3. Did we change, run out of or substitute an ingredient?
4. Was moldy feed fed?
5. Were the bunks dirty?
6. Were the pens overcrowded?
7. Was there a big weather change?

Obviously, there are many other issues that could contribute to a problem like this. Every dairy is different. But a knee-jerk reaction probably won’t solve the problem.

Back to my client. In my experience, inadequate fiber is rarely the cause of early lactation DA’s. It’s usually the result of something that caused the animals to go off feed, even for a day. Cyclical feed intake caused by subclinical milk fevers or metritis often ends in a DA. Or it may be one or more of the things I listed above.

In our case, we found the potential culprit in the commodity barn. After several days of high rainfall and hot humid weather, the whole cottonseed in the back of the commodity barn had gotten wet. There was a pile of moldy, maggot-infested cottonseed behind the fresh stuff and it had been fed for at least a couple of days. This affected all the cows in the herd, but especially fresh cows. It took a couple of days after the cottonseed was tossed out until things got back to normal.

If we had changed the ration, without looking any further, the DA’s would have eventually gone away after the nasty cottonseed was fed up. But we would have convicted the wrong culprit.

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