Also called Fat cow syndrome, ketosis is an important clinical and sub clinical disease, as several metabolic disorders and diseases, common in the periparturient and early lactation period including milk fever, retained foetal membranes and displaced abomasums are linked to ketosis.
Hypoglycaemia is the major factor involved in the onset and development of clinical signs of ketosis.
There is a gradual loss of body condition over several days or even weeks. There is also a moderate to marked decline in milk yield over five to six days before the onset of obvious clinical signs and can persist (up to 5 litres per day) for up to two weeks after diagnosis.
The disease is most commonly seen in high-yielding dairy cows in early lactation. Secondary ketosis due to inappetance as a result of another disease can be seen at any stage of lactation. Beef cows may also suffer from ketosis during pregnancy, although this is less commonly recognised.
- Causes of Acetonaemia >
- Effects of Acetonaemia >
- Diagnosis of Acetonaemia >
- Treatment & Control of Acetonaemia >
- Medication/Vaccination for Acetonaemia >
Causes of Acetonaemia
To satisfy the requirements of milk production, the cow can draw on two sources of nutrients, food intake and body reserves. During early lactation, the energy intake is insufficient to meet the energy output in milk and the animal is in a negative energy balance.
In conventional farming, this is considered to be a normal metabolic situation in high-yielding dairy cows. Cows in early lactation are, therefore, in a vulnerable situation, and any stress that causes a reduction in feed intake may lead to the onset of clinical ketosis.
If the feed intake of the cow is not sufficient to meet the demand for energy, there is insufficient ruminal production of propionic acid, the main precursor of glucose in ruminants, which results in hypoglycaemia.
Hypoglycaemia leads to a mobilization of free fatty acids and glycerol from the fat stores. However, the liver cannot deal with the acetyl-CoA, which results from the oxidization of these fatty acids, because of a lack of energy. The excess acetyl-CoA is converted into the ketone bodies acetoacetate and β -hydroxybutyrate and, to a small extent, acetone. Tissues other than the liver can use ketone bodies, but if their production exceeds the rate at which they are used by muscle and other tissues, they accumulate, and ketosis is the result. Ketone bodies are excreted in milk and urine.
The reduction of propionic acid production is usually the result of underfeeding or a reduced feed intake caused by inappetance. A period of inappetance is normal around calving, but may be exacerbated in the early post-partum period by a deterioration of forage quality, sudden changes in diet or excessive fatness at calving.
Other risk factors are month (more likely in winter), increasing parity, milk fever, ketosis in the previous lactation, increased 305-day milk yield in the previous lactation and the average milk protein percentage in the previous lactation. Cows with milk fever have a greater decrease in feed intake after calving which exacerbates the negative energy balance, increasing the risk of ketosis.
Figure 1. Energy metabolism in the ruminant
Effects of Acetonaemia
Cows will have raised blood ketone levels and may excrete ketones in urine and milk. It is important to recognise that many cases of ketosis are sub-clinical, with the cow’s performance and health compromised, but without overt clinical signs.
The clinical signs of ketosis include a refusal to eat grain and concentrate feeds and a sudden drop in milk output. There is a sweet smell of acetone in the breath and milk. Some cows may exhibit nervous signs, which include excessive salivation, abnormal chewing movements, licking of walls, gates or metal bars, incoordination with apparent blindness and a degree of aggression. The nervous signs often only last for a few hours. The affected cows have fatty infiltration and degeneration of the liver.
Cows with ketosis are at greater risk of developing retained foetal membranes, displacement of the abomasum and are more likely to have prolonged calving to conception intervals and lower fertility.
Secondary ketosis
Secondary ketosis is common and is the result of diseases causing a reduction in appetite in early lactation, such as displaced abomasum, mastitis, metritis, etc. In areas of cobalt deficiency, ketosis may be diagnosed in grazing cattle. Cobalt is required for rumen microbial synthesis of vitamin B12 and is also essential for adequate utilization of propionic acid. Ketosis has also been reported as the major presenting sign in a dairy herd with fasciolosis.
Ketosis in beef cows
Whereas ketosis in early lactation mainly affects high-yielding dairy cows, ketosis or pregnancy toxaemia in late pregnancy mainly affects beef cows. Cows of all ages can be affected, but over fat animals and those carrying twins are most at risk.
Beef cows often get over fat on good summer pastures. If the same cows do not have access to high quality forage during the winter months, when they are in late pregnancy, they will succumb to ketosis due to a low energy intake. Affected cows are usually 7-9 months pregnant, and the initial clinical signs are the same as for ketosis in early lactation. However, many cows become recumbent fairly quickly and most die three to fourteen days later. Cows affected close to parturition often die during parturition.
Diagnosis of Acetonaemia
Diagnosis is confirmed by the clinical signs of milk drop, inappetance and elevated ketones in the blood, urine or milk.
Treatment & Control of Acetonaemia
There are three main aims of treatment:
- To restore blood glucose levels as quickly as possible;
- To replenish oxaloacetate, the essential intermediate in the tricarboxylic acid cycle (TCA), so that fatty acids are completely oxidised and the production of ketone bodies reduced;
- To increase the availability of dietary glucogenic precursors, notably propionic acid.
It is important that the cow's appetite is returned to normal as soon as possible after treatment, so access to high quality fodder is important. Provision of highly palatable feed, such as molassed feed can help encourage the cow to eat.
Most cows with ketosis (pregnancy toxaemia) in late pregnancy are so severely affected that medical treatments invariably fail to succeed. Immediate removal of the calf by caesarean section may save the cow. This should be followed by the treatments mentioned above (Eddy, 1992As at least 60% of the diet fed to dairy cows should consist of fresh or conserved roughage, this should be of excellent quality during early lactation to meet the energy and protein requirements. This is especially important in the winter diet which is based on home-grown, conserved forages and it may be difficult to supply sufficient energy and where cows are high yielding. A high level of roughage in the diet has the advantage of promoting good rumen digestion.
Transition cow management (the late dry period up to the first 1-2 weeks of lactation) is critical in prevention of a range of metabolic diseases including ketosis, and as such should be highlighted in the herd health plan.
The aims of the transition period are to allow cows to develop a strong immune system, maintain normocalcaemia, minimise the negative energy balance, prevent calving related diseases and develop a rumen adapted to the post-partum diet.
The following points should be considered:
- Cows should not be too fat at calving. A condition score of 2.5-3.0 would be optimal, and anything higher would be considered too fat and at greater risk of ketosis.
- Concentrates fed during lactation should be introduced in small amounts, approximately two weeks before calving, to allow adjustments of the rumen microflora. Dietary changes during early lactation should be made gradually.
- Efforts should be made to ease the transition from gestation to lactation by offering highly palatable forage at parturition and providing suitable calving accommodation and assistance where necessary.
- Roughage high in butyric acid should be avoided in early lactation. Forage quality should be checked every year. In cobalt deficient areas, measures should be taken to ensure adequate cobalt intake.
- A sufficient supply of high quality forage is essential for beef cows in late pregnancy. Pregnancy scanning of the beef herd may identify twin-bearing cows with greater needs.
- Metabolic profiles using blood samples taken from groups of dry cows and cows in early lactation can help veterinarians monitor the herd health and detect sub-clinical disease. Dietary changes can then be made if necessary to reduce disease. Milk tests are also being developed to test for ketosis.
- The heritability for ketosis is relatively high. Additionally, there may be some variation in breed predisposition to ketosis although management has a much greater effect on farm than breeding.
- Housing also seems to have an effect on the level of ketosis in the herd. Research from Norway indicates that a significantly higher proportion of herds with tie stalls experienced ketosis compared to those with free stall herds (relative risk = 1.59). The reason for this is not known.
Medication/Vaccination for Acetonaemia
- Treat cases with intravenous glucose followed by an oral glucose precursor for several days.
- Severe cases should be treated with glucocorticoid drugs on veterinary advice.
- Homeopathy has been suggested for the treatment of clinical ketosis.
- In the case of ketosis (pregnancy toxaemia) in late pregnancy, the veterinarian may have to carry out a caesarean section to save the cow.
This info was adapted from Defra’s Compendium of Animal Health & Welfare in Organic Farming, which is a collaborative effort led by Duchy College, Cornwall with VEERU at The University of Reading and The Faculty of Veterinary Medicine, University of Glasgow.
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