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MANAGING DCAD LEVELS IN NEW ZEALAND SPRINGER COWS

I recently wrote an article on the unseen impact of milk fever and how widely spread this issue can be without correct mineral support. The challenge of calcium deficiency is a fairly large topic and it’s important to now cover the other key information farmers should consider in managing the pasture dominant diets of our dairy herds at this critical time.

Pasture still makes up a significant portion of the diet for many of New Zealand’s springer cows. Our lush pasture and high growth levels lead to higher than optimal levels of potassium. Levels in the plant can often supply potassium in excess of 300% of a cow’s daily nutritional requirement. High potassium not only restricts the animal’s ability to uptake other essential minerals, it also changes the acid/alkali balance of the body which can seriously impact the body’s ability to release hormones critical to calcium utilisation during calving and early lactation.

The DCAD system of feeding involves adding acid forming salts to the diet of springer cows in an attempt to further drive this metabolic acid/alkali balance slightly more towards the acid range, thus facilitating the release of the hormones required to release calcium. Provided this feeding system is correctly implemented, when compared to other options, this approach is also very cost effective.

CALCIUM OR NO CALCIUM?

The calibration used in the correct formulation of these diets is expressed in total milliequivalents (mEq). An unmodified pasture-based springer cow diet can typically have a DCAD anywhere from +350 to +550 mEq’s or even higher, dependent on the level of pasture being fed. The aim is to get the mEq level of the diet down as low as possible. Under New Zealand conditions that normally means somewhere between -15 to +120 mEq’s. This is achieved by manipulating the feed sources in the diet and then adding a specific blend of acid forming salts. With the correct blend, palatability is maintained while reducing the total feed DCAD levels substantially.

KEEPING KETOSIS AWAY FROM DAIRY GOATS

Ketosis in any of its forms can lead to sudden and catastrophic loss levels around kidding time.

A number of goat farms this year experienced significant losses around kidding time and during early lactation. Farmers were puzzled as to the cause and unfortunately these losses happened rapidly, before any remedial action could be taken.

Such acute losses at this time typically come down to one thing, a catastrophic energy deficit experienced during a critical stress period, namely kidding and early lactation. This disease goes under a number of names and confusingly can take a number of different forms. The most acute form is often called pregnancy toxemia in goats, or sleepy sickness. In dairy cattle it is more commonly called ketosis, or fatty liver disease.

These different forms can be made up of a range of symptoms but all emanate from the same root cause – a lack of glucose production. When the body fails to produce enough glucose for energy it kicks into survival mode and begins to break down fat tissue for energy, releasing ketones.

To fully understand this disease and its differing manifestations we need to have a good understanding of the stresses involved during the lead up to kidding and early lactation. At this time there is a rapidly increasing requirement for energy and the body needs to have the capacity to meet these needs within a very small period of time.

UNDERSTANDING KETOSIS IN DAIRY GOATS

Ketosis is a metabolic disease common to all living creatures, but particularly problematic in high production ruminants. It will usually only appear at critical stress times, namely kidding/calving and early lactation.

Ketosis is related to the body’s inability to synthesize sufficient glucose from fatty acids produced in the rumen to supply its energy demands. The body then starts to mobilize body fat (some humans would say that’s a good thing). The mobilized fat is broken down into what are called non-esterified fatty acids (NEFA’s). When these non-esterified fatty acids reach the liver, they are either oxidized into energy forming substances (ketones) or removed out again as very low-density lipoproteins (VLDL’s). This process is complex and is largely regulated by hormones such as insulin, ghrelin and leptin (the satiety hormone). The problem is, when the production of ketone bodies is upregulated in favour of the more efficient glucose energy cycle, it can lead to a significant energy deficit. A serious side effect of the over utilization of fat for energy is fatty liver disease; when fat goes into the liver in greater volumes than the livers capacity to process it, and this causes a fat buildup that can quickly lead to liver failure. Once established this condition is very hard to reverse, particularly in small ruminants with more limited liver capacity.

WHY MAKE STINK SILAGE

On so many farms the familiar smell of silage is the sickly cloying smell of butyric acid.

The same smell that gets you ordered to take a shower when you come in for breakfast after feeding out, the smell that makes most townies hold their noses. That smell has become so familiar over the years that many farmers naturally associate it to silage – it is prevalent across most farms during periods when silage is being fed. The funny thing is, good silage shouldn’t really have any smell at all. The familiar sickly smell is actually a sign of secondary fermentation that has caused butyric acid to form within the silage. And that smell is costing you money as it is a sign that the silage has lost some of its nutritional value. A good quality fermentation should be purely based on lactic acid, and lactic acid actually has very little smell.

WHAT’S GOING ON IN THE SILAGE?
As mentioned butyric acid is formed during secondary fermentation, produced by aerobic clostridial bacteria this fermentation is indicative of decomposition of the naturally formed (anaerobic) lactic acid. Aerobic fermentation degrades much of the original protein in the grass. Some farmers are naturally confused because butyric acid fermented silage is so common here in New Zealand they inherently associate the butyric acid smell to silage.

Added to this dilemma butyric acid fermented silage, while still being nutritionally degraded, can be very stable. Its high acidity levels can make it largely immune to moulds and any further degradation. However at this point the cost has already been paid, this butyric acid fermented silage has lost much of its protein as this has been used up during fermentation.

GOOD SILAGE MAKING IS A FINE ART.

TRANSITIONING WELL, DELIVERS RESULTS

Minerals and the Transition Period
The Transition cow mob, more commonly referred to by farmers as the springer cow mob, has the potential to respond to a higher level of thought and attention. Making key decisions around feeding and supplementation of this mob can have a bigger impact on a dairy farm’s profitability than any other single set of management decisions made throughout the rest of the season. A well transitioned cow will normally produce more total milk, have less disease issues, and a better reproductive outcome, than cows that don’t receive as much attention around this time.

Most experts agree that the transition period begins 21 days prior to the day the cow gives birth, into 21 days of lactation. For any cow this is a period of vast metabolic change. During this time their hormone levels are going through rapid developments as the body gets ready to mobilise many of the key minerals required, as well as preparing her body to mobilise the vast amounts of energy required during birth and lactation. Transition is normally the single highest stress period a cow will experience each year.

A TIME NOT TO DO THINGS BY HALVES

Both the period prior to calving and the period after calving are equally important to ensure the cow will produce at her potential, remain healthy and conceive again when mated. In my experience farmers will tend to either concentrate on the period leading up to calving or the period after – most commonly the period after calving gets most attention. And this can create a problem. In this article we will concentrate on the transitioning of cows only, rather than heifers (first calvers) where the focus need only be on ramping up the feed rate prior to calving. Transitioning cows is a very different process, a cow that is not transitioned correctly leading up to calving is a cow that will calve with her metabolic processes operating well short of full potential. She will be more exposed to both clinical and subclinical metabolic disease through either being calcium deficient or lacking the ability to mobilise sufficient calcium, ketosis, fatty liver disease, or possibly a combination of these problems.

A NEW GENERATION OF ORGANIC SELENIUM

NEW ZEALAND SOILS ARE LOW IN SELENIUM

Selenium is an essential trace element for ruminants and required for growth, fertility and the prevention of mastitis and calf scours. However, selenium deficiency is prevalent in soils around the country. This presents an issue every farm manager would benefit from understanding better. A new generation of organic selenium supplementation (called Excential Selenium 4000) will be introduced into New Zealand this year. It’s an exciting development, providing a significant improvement to previous options for selenium supplementation on the farm. But first we need to understand the relevance and impact of selenium deficiency.

WHY IS SELENIUM IMPORTANT?

Specific enzymes (selenoproteins) require the incorporation of selenium to ensure their activity in the animal. These enzymes reduce the presence of oxide radicals (produced during normal metabolic activity and elevated during stressful periods) that cause cell damage and subsequent malfunction of tissues. Protection against these harmful by-products is especially important in high-energy demanding cells such as heart, muscle and mammary gland cells.

Unfortunately, there is often a selenium deficiency in animals due to limited uptake from the diet. These deficiencies can be pronounced in ruminants grazing on pastures grown on selenium-deficient soils, such as here in NZ. Resulting challenges may include suboptimal milk production and fertility, mastitis and premature, weak calves. In places with severe selenium deficiency calves have poor growth rates, difficulties standing, and sudden deaths can occur. To prevent this, it is important to provide additional selenium via the diet and assess regularly the selenium status of the herd by analysing blood and milk.

SELENIUM DEFICIENCY – A NUTRITIONAL SOLUTION

Selenium can be added to the diet in either inorganic or organic forms. The advantage of using organic selenium over inorganic sources (e.g. sodium selenite or selenate) is its ability to be incorporated directly into animal proteins. This incorporated selenium (in the form of L-Selenomethionine) acts as a storage depot of selenium inside the animal. L-Selenomethionine is the only selenium compound that can be directly, without conversion, built into animal structural proteins (i.e. muscle and liver). This ensures optimal selenium supply, even during stressful periods (e.g. calving, lactation, heat) when selenium intake is required most by the animal.

MINERAL BALANCE FOR IN CALF DAIRY COWS

The challenge is not getting them in-calf. It is keeping them in calf.
It is still a trend among some dairy farmers to concentrate on mineral supplementation only through the months of early lactation, and up to the completion of the mating period. In my view this misses the point.

Generally speaking while the energy and protein levels of the pasture may improve as the season progresses, the mineral levels in lush green spring pasture are often very low, and can reach their lowest level in the spring to early summer months. Cutting minerals at such a critical time can be likened to ‘saving cents while sacrificing dollars’. A fully formulated trace element supplement designed to be delivered throughout the season can cost anywhere from 50 cents to $1.70 per dairy cow per month depending on the types of mineral used and the levels required.

WE ASK A LOT OF OUR COWS AND IT IS AMAZING WHAT THEY WILL ENDURE AND STILL REMAIN PRODUCTIVE.

Given the usually challenging climatic conditions experienced on most New Zealand dairy farms during the spring, the average farmer certainly expects a lot from their cows. Firstly they go through the trauma of giving birth, then we extract large volumes of milk pretty much from day one, and then the cow is expected to become pregnant again. This all happens within a very tight window of time. Is it any wonder that cows struggle to recover when one stress event so closely follows the next?

DAIRY GOATS. THE HIGH PERFORMANCE RUMINANT

It is tempting, given the limited research around goat nutrition to assume a goat’s nutritional requirements fit somewhere between that of sheep and cattle. This assumption would be a mistake. When it comes to mineral nutrition goats have very different requirements.

Based on a goat’s production level when related to body weight and feed intake, these small ruminants are probably better compared to the ruminant equivalent of an F1 racing car. Just as you wouldn’t run a high performance car on low octane fuel, you shouldn’t feed your goat the same way as you would cattle and sheep. Goats have different and very specific nutritional requirements. If these requirements are not met, the animal will not perform to its full potential, and worse still will be subject to a higher level of disease.

The interesting thing about goats is that their requirement is both higher and lower depending on the element in question. While their milk is in many ways more nutritious than that of a dairy cow, nature has at the same time designed the animal to survive under very different conditions, and on a very different diet from that of a cow.

SO WHAT ARE THE MINERAL REQUIREMENTS OF DAIRY GOATS?

Lets start with one of the key macro elements, phosphorous. Goats typically have a lower requirement for phosphorous to that of dairy cattle. They seem to be better at recycling it and while they have higher levels in their saliva, losses during rumination are lower than that of a cow.

In contrast calcium requirements are quite high and should be set at least twice that of phosphorous in the diet.

FACIAL ECZEMA PREVENTION

Facial eczema is a cause of major production losses in dairy herds.

When moisture, high ground temperatures and humidity all occur together, the offending fungus present all year round becomes a problem. Under these conditions the fungus grows rapidly and spores are produced containing the toxin Sporidesmin which damages the liver and prevents removal of chlorophyll break down products from the body. This ultimately causes photosensitisation or ‘sunburn’ when the cow is exposed to sunlight. This is usually seen 10 days after exposure to the spores. The first thing you may notice is a drop in milk production and affected cows may seek shade, have swollen legs or brisket, fat ears, red skin or burnt teats.

KEY STRATEGIES TO FE PREVENTION:
1) GRAZING

• Spore counting & then selectively grazing safe paddocks – obtain spore count information from your local vet or get spore counts done on pasture samples from your own farm and send them to your vet for testing
• Avoid hard grazing of paddocks as the toxin is concentrated at the bottom of the sward
• No topping of grass as this allows build-up of leaf litter
• Provide alternative feeds (maize, silage, brassica crops, hay) during high risk times

2) ZINC DOSING

Zinc forms a stable complex with sporidesmin preventing damage to the liver. For best protection zinc dosing should be started 2-3 weeks before spore counts start to rise (December – January.)

HEAT STRESS PREVENTION

TOUCHY COWS, SUMMER PRODUCTION DROPPING OFF?

Typically during the summer months when temperatures and humidity levels are high, dairy cows face health challenges. Rye grass staggers occur from late November until the end of April, but tend to be worst from late January to early February, when we experience hot, dry spells followed by rain. Heat stress also becomes an issue where the cow’s ability to lose heat by sweating and breathing declines owing to the high relative humidity levels. Natural grass toxins which form when plants come under environmental stress, can also affect the animals grazing them.

Are your cows becoming hot and bothered this summer? Settle them down with Ascocool seaweed extract, a fully water soluble seaweed extract that helps to calm cows in the heat of summer.

Read further research here

WHY USE SEAWEED EXTRACT?

Agvance’ concentrated Seaweed Extract – called Ascocool can assist in alleviating these summer time health issues. It originates from the North Atlantic brown seaweed called Ascophyllum Nodosum where research trials have shown that this particular seaweed helps in the following ways:
1) Binds naturally occurring toxins & moulds that build up in grasses & stored feed under hot, dry humid conditions, causing heat stress and problems in central nervous system
2) Increases immunity
3) Potential to act as a powerful prebiotic owing to poly & mono-saccharides being present that allow for more efficient breakdown of feed
4) Contains a wide range of amino acids

Check out our Ascocool brochure here

Salmonella in Dairy Cows | Agvance Nutrition New Zealand

SALMONELLA IN NZ DAIRY COWS

Salmonella link to coarse grade and palleted Magnesium Oxide in Feeds
Over the past few weeks, a number of vets have been reporting Salmonella outbreaks on dairy farms. Our investigations on some of these farms indicate that these outbreaks seem to correlate to use of pelleted Magnesium Oxide being fed in palm kernel based feeds. Although one of the farmers we interviewed, reported some salmonella before feeding the PKE containing the coarsely ground magnesium oxide, he reported that after introducing the feed the disease took off. On discussions with some in the feed industry it would seem that coarsely ground magnesium supplements may have been widely used throughout the feed mill industry over the past 2 seasons. This magnesium is a little different to that used in the past and the pelleted magnesium associated with the outbreaks of salmonella reported in Taranaki. Prior to the last two seasons this coarsely ground form of magnesium oxide was formerly only sold into the fertiliser market and has large particle sizing, ranging from 2mm – 5mm. We believe the same risk factors are involved as those reported in the Taranaki outbreak of 2011 at that time associated to a prilled magnesium oxide product used in those feeds.

A case controlled study was performed in 2011 – 2012 to identify herd-level risk factors for acute Salmonellosis. It is our belief that the most recent outbreak has many of the same issues in common with the earlier outbreak. This summary, identified a number of risk factors that contributed to this sudden outbreak of the infection across a large number of herds, most particularly highlighted was the strong connection between feeding granulated magnesium supplements and prevalence of the disease.

click here to read study

CONTRIBUTING FACTORS IDENTIFIED IN THIS REPORT WERE AS FOLLOWS:

1) Continuous feed troughs – consumption of supplementary feed from shared troughs varies amongst individual cows where dominant cows will consume more than their allotted daily feed allowance, with submissive cows consuming less. Fluctuations in feed intake could affect the rumen microflora balance, allowing salmonella to multiply and cause infection. Reduce risk by using individual troughs.