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.
Animals that are over fat also have a tendency towards insulin resistance. Excess fat tissues release higher levels of leptin (the satiety hormone), which further reduces appetite causing the body to upregulate fat breakdown using ketones as the energy source. This would not be too much of a problem later in lactation, however when you take into account that ketones are a far less efficient energy source, ketone production is hard on the liver, and this is all happening during a high stress period – you can understand how these animals very quickly get into an energy deficiency crisis.
THREE DISTINCT PATHWAYS LEAD TO THIS ONE PROBLEM
In a similar way to diabetes these are often referred to as types:
• Type I: Inadequate feeding – meaning insufficient energy in the diet.
This will cause the body to take emergency action and begin mobilizing body fat reserves for energy in the form of ketones, never a good thing.
Diets at this time need to be formulated to supply high levels of readily available energy, relative to protein, and for obvious reasons fats should not be added to the diet at this stage, as they are not a readily available form of energy and can further hamper the liver in metabolizing volatile fatty acids. Target an increase in carbohydrate and starch, relative to any increase in potentially high crude protein containing grasses or silages. Grains are excellent sources of starch. However, it is important in any mixed ration to have sufficient fibre to maintain rumen pH stability. Rumen buffers added to the premix can help ensure stable rumen pH.
• Type II: Over conditioning – too much body fat can be a real complicating issue for this disease and is probably the leading cause of both ketosis and related fatty liver disease.
Unfortunately, excess conditioning is not always easy to identify in goats. While dairy cattle accumulate fat under the skin, goats tend to accumulate this fat internally in their body cavities. Hence an overweight goat is not always so obvious.
• Type III: Poor quality silage – this is probably the least recognized, yet very important.
Poor quality silage, particularly when fed around transition time can be a game changer (in the worst way). This is the silage that we all know too well, the stuff with the sickly smell. It was probably baled or bunkered when the rain threatened the crop, or the contractor turned up too early. Being harvested at a higher than optimal moisture content, this silage didn’t go through efficient lactic acid fermentation but instead, because of the higher moisture content, it has gone through a butyric acid fermentation cycle.
Consider that it takes as little as 50 grams of butyric acid to cause severe ketosis in a goat during the transition period. A little more care and good practice around silage making can ensure a crop that delivers high levels of energy, which will lead to better production as well as lessen the risk of ketosis.
TAKING ACTION TO PREVENT KETOSIS
As a farmer it is important to carefully plan the feed requirements during the lead up to transition and the early lactation period. How you manage the nutrition at the different stages of this period will need to change constantly as the requirements change, but every stage of this period is equally important in order to maintain a healthy productive animal into the next lactation.
Correct transitioning should see us preparing the animal for the stresses leading up to the birth and then supplying adequate nutrition to support the heavy demands of early lactation. A failure at any stage will have serious consequences and will increase potential losses and negatively impact production during the following lactation.
THINGS THAT SHOULD BE DONE:
1. Plan feed demands well in advance, ensuring feed levels will be adequate and of the right quality for each part of the season; the dry period, the transition, and the early lactation periods. If feeding silages, make sure that these are lactic acid fermented silages. With correct fermentation good quality silage will not contain butyric acid. The correct silage inoculant can be very beneficial to ensure a correct fermentation and a better quality final product.
2. Make sure animals are well conditioned without being over conditioned at the end of lactation and during the dry period.
3. Plan to feed increased levels of energy leading up to birth, and then plan to rapidly increase energy levels once lactation is underway, while all the time taking precautions against acidosis.
4. Give careful consideration to the correct balance of minerals, vitamins, and amino acids required, both being delivered through the feeds naturally, as well as supplementation of additional quantities into the feed. These will be very important co-factors in efficiently utilizing the feed, as well as ensuring against health problems.
Certain key amino acids and vitamins, while not taking the place of adequate feeding, are essential to the production of energy and the utilization of dietary protein. In the scientific world these are called methyl donors; they are essential at the cell level in energy production as well as the utilization of protein. Methyl donors of most importance to ruminants are choline, methionine, betaine, vitamin B12, and vitamin B2.
Unfortunately, these amino acids and B group vitamins when supplemented to ruminants in their raw form are rapidly broken down by the rumen microflora. To be really beneficial they need to be absorbed within the intestine. So if they are not fed in a rumen-protected form they are of little use. When added to ruminant feeds, they are normally added in protected form through the application of a fat coating and this allows them to flow through the rumen untouched, to be absorbed further down the digestive tract. When fed in protected form, choline, methionine, and betaine, have been shown to be very beneficial in optimizing liver function. These key amino acids aid the liver in better synthesizing fatty acids without the risk of fat accumulation. Rumen protected B group vitamins such as riboflavin (B2) and Cobalamin (B12) are also highly beneficial co-factors in this process.
Article by Chris Balemi, Agvance Nutrition
