Knowde Enhanced TDS
Identification & Functionality
- Animal Feed & Nutrition Functions
- Technologies
Features & Benefits
- Animal Feed & Nutrition Features
- Metabolic Disease
- METABOLIC disease is most commonly seen around the periparturient period of a cow, due to the marked nutritional, metabolic, hormonal and immunological changes (Goff and Horst, 1997).
- Metabolic diseases not only lead to direct costs, such as treatments and veterinary bills, but have knock-on, indirect costs on infertility and displaced abomasums, to name but a few. Not only do the cows have to cope with their metabolic insufficiencies, but, during the periparturient period, dairy cows experience a natural state of immunosuppression, increasing susceptibility to infections (Kehrli et al, 1989a).
- Neutrophils undergo a weakening of their capacity to phagocytose (Kehrli et al, 1989), meaning the fight against bacteria is less effective. Inappetent cows produce non-esterified fatty acids (NEFAs), which impair lymphocyte proliferation and polymorpho-nuclear neutrophilic leukocyte function (Ster et al, 2012).
- NEFAs bind to magnesium when mobilized in the bloodstream and so promote a state of hypomagnes-aemia, which, in turn, can lead to hypocalcaemia. If a cow is unable to maintain blood concentrations of calcium, magnesium, phosphorus and glucose using homeostatic mechanisms then metabolic disease develops, often setting off a cascade of disease.
- Below the more common metabolic diseases are adressed – namely ketosis and fatty liver. These diseases combine and should not be diagnosed and treated as single entities, as the causes are often multi-factorial.
- It is vital to carry out a full physical examination before any treatments, as cows may have concurrent pathology/ disease, such as fractures or ruptured tendons from falling/slipping, and these will need to be euthanised for welfare reasons immediately.
Ketosis
- Type one ketosis occurs when there is not enough propionate to meet the glucose needs of the cow, as it is the major precursor for gluconeogenesis. There is little conversion of NEFAs to triglycerides, resulting in minimal fat infiltration of the liver, meaning the liver’s function is unimpaired. Ensuring a diet is sufficient in propionate avoids the use of other glucose precursors and subsequent mobilization of peripheral adipose tissue. This can be achieve by adding FF CaPro to the diet.
- Type two ketosis occurs when there is a primary problem such as fatty liver, metritis or hypocalcaemia and the cow is, therefore, unable or unwilling to eat sufficiently for its needs.
Fatty liver
Fatty liver disease is initiated by the ratio of growth hormone: insulin being high at calving, which, in turn, stimulates the mobilization of NEFAs from adipose tissue to support the lactation energy requirements. Adipose lipogenesis ceases and there is an increased sensitivity to lipolytic signals, such as epinephrine.
Resistance to insulin develops, meaning all energy can be used for milk production. Consequently, stressors and poor nutritional management cause a decrease in voluntary DMI and a large increase in NEFAs immediately post-calving (Bertoni et al, 1998). The NEFAs are primarily absorbed by the liver, where they undergo three separate processes, as shown by figure 1.
- Assuming there is sufficient propionate in the diet, by addition of FF CaPro, the free fats are oxidized into acetyl coenzyme A (CoA) and enter the Krebs cycle, which leads to the production of glucose.
- If there is insufficient propionate, the acetyl CoA is metabolized to ketone bodies (acetoacetate and beta-hydroxybutyrate; BHB) which are then used as energy sources. Excess levels of these in the blood demonstrate more are being produced than are being used by the peripheral tissues. Ketones produced in the Iiver are limited to utilization by heart, skeletal muscle, kidney, lactating mammary glands and intestinal tissues (Herdt, 1988). These tissues have the enzymes necessary to convert ketones back to acetoacetate and then to acetoacetyl CoA (Littledike et al, 1981).
- If the uptake of NEFAs is greater than the number being oxidized then the NEFAs are re-esterified and ideally exported from the liver via low density lipoproteins. Ruminants are not very good at this, so the fats are slowly exported into the bloodstream and instead accumulate in the liver, reducing its capacity for gluconeogenesis. As a consequence, more peripheral fats are mobilized. The process is a vicious circle and results in a fatty liver with rounded edges that show how swollen the liver is and an abnormal color.
- Energy Requirements
- In ruminants, glucose metabolism is unique as they absorb no preformed glucose from the gut. The main source of glucose is gluconeogenesis of volatile fatty acids (VFAs), primarily propionate, which are produced by bacterial fermentation in the rumen. The VFAs are absorbed and, via the bloodstream, end up in the liver where gluconeogenesis takes place.
- It is commonly written all dairy cows suffer from ketosis at some point in their early lactation for a variety of reasons, with resulting economic losses to the farmer from treatment costs, decreased milk production, impaired reproduction efficiency and increased involuntary culling (Reist et al, 2000).
- A 650kg cow walking to the field daily and producing 40 liters of milk a day will need around 285MJ/ day. If the energy content of the foodstuff is 10MJ/kg/dry matter (DM), such as grass, the cow will need to ingest 28.5kg DM, which is 4.4 per cent of the cow’s bodyweight – far exceeding the expected dry matter intake (DMI) of three per cent bodyweight.
- The resulting negative energy balance will lead to type one ketosis, which is commonly seen from six weeks to eight weeks postparturition when feed intake (energy intake) is outstripped by milk output (energy output).
- Signs And Diagnosis
- The clinical signs for ketosis are often non-specific, such as anorexia with accompanying weight loss, decreased milk production and scant feces. The smell of acetone (“pear drops”) is often reported, but is not a specific diagnosis. Some cows demonstrate nervous signs such as pica, ataxia and head pressing, which can last for one to two hours. This is due to the ketones being broken down in the rumen, although the lack of glucose available to nervous tissue to maintain normal function may be a contributing factor (Radostits et al, 2007).
- Measuring the BHB levels in the blood can give a definitive answer, with a level more than 1.4mmol/ml commonly accepted as a cut-off. Blood NEFA levels can be measured to see the extent of fat mobilization. Liver parameters, such as glutamate dehydrogenase, may demonstrate liver damage caused by fat infiltration. A liver biopsy is the definitive diagnosis for fatty liver, with following histopathology or seeing if the liver floats in copper sulfate.
Applications & Uses
- Markets
- Treatment
- Once diagnosed, a few treatment options are available, which are very similar for both fatty liver and ketosis. Any underlying/primary disease processes should be identified and treated alongside the accompanying ketosis.
- The initial priority is to get the cow back on an even energy balance, or at least provide sufficient propionate (FF CaPro), so ketone bodies are not formed, nor fat is deposited in the liver.
Regulatory & Compliance
- Certifications & Compliance