COW AND CALF NUTRITION INEXTRICABLY LINKED
The lead up to another calving period means the next few weeks offer an opportunity to meet the nutritional demands of your cows. Good nutrition
The lead up to another calving period means the next few weeks offer an opportunity to meet the nutritional demands of your cows. Good nutrition
Early lactation, spanning both calving and mating, is a stressful time for cows as energy demand is very high at a time when cows may
The arrival of another busy calving period means the next few weeks represent a critical time for cows and calves alike. Both need the best
The end of lactation when cows are dried off is one of the few times during the seasonal calendar when both farmers and their cattle can take a breather from the daily grind of milking. The dry period is a critical phase in the seasonal cycle of every dairy cow, as it allows them time to rebuild the mammary tissue required for milk production in the next season. This is also a critical time for cows to build up their natural immunity before the next calf is born.
Milk producing cells within the udder are rapidly dying and being replaced while the cow is lactating. During the dry period the udder rapidly regenerates these cells in order to build maximum milk production capacity, in anticipation of the next lactation. Planning sufficient time to allow these processes to take place will ensure your herd is less likely to suffer from the effects of mastitis, which is an infection caused by bacteria or injury to the udder.
A farmer’s decisions at dry off can influence a herd’s mastitis prevalence for up to the following 6 to 12 months. As you know, it’s good practice to dry off lighter cows earlier; this is when body condition scores are imperative. This can also be a good time to either treat (dry cow therapy) or cull cows that have a history of mastitis.
Mastitis is an inflammation of the mammary gland, which is caused by either infection or trauma, and leads to decreased milk production. Contagious mastitis can spread quickly during milking, as milk from an infected quarter can be spread to the teat skin via dirty gloves, teat cup lines and cross flow of milk between teat cups.
While there is no milk being produced during dry off, the average dry cow will require as little as 10kg of dry matter in order to maintain their condition. If the cow is light in body weight, she may need more feeding. However, overfeeding during this period in the hope of building condition may risk additional metabolic issues around calving.
In order to build resilience and strength for a stress-free season, the dry period can be an important time to get mineral levels right. Minerals such as selenium, zinc, and copper, can increase the bodies resistance to udder infections early in the next lactation, while also ensuring better reproductive outcomes later in the season.
Every farm is different. Herds are drying off at different times, and they will have different diets and differing deficiency challenges. By using a custom mineral blend in conjunction with Agvance, farmers can defend against the likelihood of infections, by supporting the specific nutritional needs of their herd at this key time.
Prior to the 1600’s the liver was considered to be the most important organ in the body, much more so than the heart and the brain. Throughout the ages this organ has been steeped in myth, in the case of the Romans, the liver held a key place in their religious rituals. Roman priests closely studied sacrificed animal livers, these signs could indicate such things as, prosperity, famine, wars, or curses.
Today, the heart and the brain seem to have more emphasis placed on their importance. However, the ancients may have known more than we give them credit for, we should not be too quick to dismiss the liver. Regardless of the heart and brain, without a functional liver most living creatures would not survive very well, or for very long.
The liver is fascinating, and in many ways, I find it to be the most complex of all the bodies organs. It is a single organ with a massive number of functions, below are just a few of the key functions.
Key functions of the liver
• The production of bile – bile clears waste products.
• Produces many blood proteins, e.g. albumin, ferritin, cholesterol etc.
• Produces lipoproteins that carry different fats throughout the body.
• Controls energy – rapidly converts glucose to glycogen (storage) and then rapidly converts glycogen back to glucose as the body calls for more energy.
• Regulates amino acids, the building blocks of protein within the blood.
• Regulating (storing and releasing) hemoglobin levels of minerals such as iron, copper, etc
• Conversion of excess ammonia to urea (a major issue in ruminant digestion)
• Clears toxins from the blood (think feed toxins, aflatoxins, mycotoxins, ergot toxins)
• Important in the immune response in that the liver detects and clears bacteria and viruses arriving from the gut.
• Regulates blood clotting
• Clears bilirubin (broken down red blood cells) from the blood.
These are just a few of the key processes involving the liver. You can see from the list that these are all very essential processes. They are all reliant on a healthy liver, with enough capacity to consistently carry out every single function.
When I started working with farmers 40 years ago, if you asked a farmer what fertilizer he used, he would invariably tell you how much Super he was applying. Back then fertilizer was either straight super or potassic super. Most farmers could readily rattle off the units of P being applied per acre. It was common to see soil ‘Olsen P’ levels in excess of 60 on loam soils and as high as 110 on some pumice soils. Pasture commonly came back at levels in excess of 0.55% P on a dry matter basis.
At the time, if you had the courage to suggest to a farmer that he consider cutting back the phosphorus he used… he would give you a very nervous look.
Jump forward to the present day, farmers haven’t just been weaned off their P addiction, many have gone cold turkey. Because of environmental constraints around feed brought onto the farm, many farms see little or no P fertilizer being applied. As the fertilizer budget is reduced, this situation has seriously decreased plant P levels. Adding to the issue is that NZ cows used to be fed mainly grass. They are now fed a variety of feeds, many being P deficient yet supplying high soluble sugar or starch level. Where it used to be rare to see a case of phosphorus deficiency it is now becoming a common problem.
A DEVELOPING CONCERN
There is hardly a day goes by when we don’t hear from a farmer describing what they think are normal calcium deficient downer cows. When questioned, the symptoms often don’t quite fit, these cows don’t always respond so well to normal treatment. Sometimes a bottle of calcium in the vein will get them up, only for many to go back down again later. Often these cows will only respond to a calcium phosphorus combination into the vein, or if given calcium borogluconate can tend to go down again.
All farmers will recognise a downer cow by the symptoms presented, and they know that this disease is brought about through a low level of calcium in the blood during a stress period.
This issue is commonly called milk fever and the cow involved a downer cow. What farmers won’t always recognise is that the cows that present with clinical symptoms are just a small part of a much bigger issue. This is why most researchers into the disease will use terminology such as hypocalcemia, as this broader term better conveys the true issue (calcium deficiency), and the fact that the disease takes many forms and effects many processes critical to early lactation.
For every incidence of a downer cow there will be many more cases where the cow stays on her feet but suffers the wider effects of the deficiency. Calcium deficiency can commonly exhibit in such things as calving problems, metritis, retained fetal membranes, mastitis, poor immunity, poor conception and the list goes on. Few of these things are as dramatic as the downer cow, yet they are equally important.
THE BODY’S CALCIUM BALANCING SYSTEM
The majority of feed sources supply more than adequate levels of calcium, yet calcium is among the most poorly absorbed elements. The body controls calcium uptake very tightly as an imbalance can lead to serious complications. This is done through the release of hormones, particularly, parathyroid hormone and vitamin D (a hormone not a vitamin), and calcium storage is controlled by another hormone called calcitonin. The body’s hormonal system responds quickly to manipulate the available calcium level based on demand. This system works really well, provided the diet is right and the cow has not been subject to longer term deficiencies. And also provided they are not under or over conditioned cows, as these cows are not as good metabolically at regulating these hormones.
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.
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.
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.