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Define ketosis in cows, weight loss meal plans - Within Minutes

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JAMES ADAMS BVSc, MRCVS in the first of a two-part article, discusses clinical signs, diagnosis and treatment options for ketosis and fatty liver – two conditions affecting metabolism in cows SummaryThis article covers the most common metabolic diseases a farm vet could be expected to diagnose and treat successfully when working in practice, most frequently when dealing with periparturient dairy cows. This whole article will address the more common metabolic diseases – namely ketosis and fatty liver (to be covered in part one), then hypocalcaemia, hypophosphataemia and hypomagnesaemia, which will be reviewed in part two.
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).
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). 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. 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. The clinical signs for ketosis are often non-specific, such as anorexia with accompanying weight loss, decreased milk production and scant faeces. Once diagnosed, numerous treatment options are available, which are very similar for both fatty liver and ketosis. This transient state of hyperglycaemia causes a 12-fold increase in insulin after 15 minutes (Saki et al, 1996) although periparturient cows remain resistant to its action. Intravenous glucose is rarely justified as a solo treatment option, perhaps except when treating a cow with nervous ketosis and if the animal is at risk from injuring itself or personnel.
Periparturient cows often have fatty liver among other diseases, so corticosteroids should be avoided in these cases.

Propylene glycol (PG) is widely used – as, put succinctly, it increases glucose and insulin, and decreases NEFAs and BHBs (Nielsen and Ingvartsen, 2004), thus reducing the risk of ketosis and fatty liver. Cows receiving PG are known to have a higher proportion of propionate in rumen VFAs, showing there is some ruminal metabolisation (Nielsen and Ingvartsen, 2004). Loiselle et al (2009) showed milking cows once a day produced an improvement in their metabolic profile and Ster et al (2012) indicated immune function was also less impaired. 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).
Inappetent cows produce non-esterified fatty acids (NEFAs), which impair lymphocyte proliferation and polymorpho-nuclear neutrophilic leukocyte function (Ster et al, 2012).
In the short term, this can be achieved by administering a bottle of 400ml 40 per cent dextrose intravenously – something that has been done since hypoglycaemia was established as a cause of ketosis in the 1930s (Herdt, 2000). Cows that are ketotic six weeks post-calving tend to be uncomplicated and purely due to lack of food intake, so these are the most suitable candidates. Shpigel (1996) found response of cows with primary ketosis to treatment with corticosteroids and intravenous glucose is superior, with fewer relapses than a single therapy.
To allow cows to produce such a large volume of energy demanding milk in one time, cows are inherently insulin resistant in early lactation (Bauman, 2000).
The problem is not just seen in cobalt-deficient areas, as it has been noted in high-producing cows in non-deficient areas (Knight, 2001). A summary of ketosis treatment by Gordon et al (2013) stipulates a ketotic animal needs 300g of propylene glycol once a day for five days, and those showing nervous signs require a dextrose bolus.

Reducing milk harvest postpartum while maintaining milk stimuli (such as calf sucking), reduces metabolic stress without compromising productivity of high-yielding cows throughout the course of the lactation. Some cows demonstrate nervous signs such as pica, ataxia and head pressing, which can last for one to two hours. This is logical as cows must synthesise all of their glucose and it is the hypoglycaemia that has caused the metabolic disease. A liver biopsy is the definitive diagnosis for fatty liver, with following histopathology or seeing if the liver floats in copper sulphate. Subsequently, there will be increased insulin secretion from the pancreas, thus decreasing fat mobilisation and subsequent ketosis (Holtenius and Holtenius, 1996). New aspects of ketone bodies in energy metabolism of dairy cows: a review, Zentralblatt fur Veterinarmedizin.
Use of corticosteroids alone or combined with glucose to treat ketosis in dairy cows, Journal of the American Veterinary Medical Association 208(10): 1,702-1,704.

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