Gil, Enrique. Bovine Ketosis and Pregnancy Toxaemia. Library. College of Agricultural Sciences (UNMP). Balcarce. Argentina. 1994.

Summary.
Bovine ketosis or acetonaemia is generally considered to be the second most serious malady affecting dairy cattle (after milk-fever). And it is also a serious problem in other ruminant animals as well.
Pregnancy toxaemia, which is primarily a problem in ewes, is often considered to be a different disease than ketosis, although metabolically speaking ketosis develops in these animals.
In dairy cows, clinical ketosis is most apt to occur during a period within a week to six weeks after calving, the bulk of the cases occurring by one month after calving. Ketosis generally occurs during the winter month when cattle are being fed harvested forage and other feeds, thus indicating that pasture tends to be antiketotic.
With respect to pregnancy toxaemia the incidence of clinical cases is primarily restricted to pregnant ewes. The most severe cases are usually in ewes with multiple foetuses; such cases generally develop a few days to a few weeks prior to lamming.
Clinical symptoms of ketosis generally develop gradually, and are evidenced by a variable reduction in: food intake, a variable and rapid drop in milk production, and a loss of alertness. The animals may show signs of incoordination, as evidenced by a staggering, swaying gait. The breath may have a strong smell of ketones (acetone). The liver upon autopsy, will be soft, greasy and yellow indicating fatty infiltration.
Biochemical changes occurring. Briefly ketosis may be defined as the presence in the blood and urine of the "ketone bodies" a group of compounds including acetoacetic acid, ß-hydroxybutyric acid, acetone, and isopropanol. When carbohydrate utilisation is deficient (for example in diabetes or in starvation after carbohydrate reserves are depleted), the energy requirements of the body must be met by the use of more fat. Furthermore, a supply of carbohydrate sufficient to maintain the citric acid cycle is necessary in order to permit the smooth entry of acetic acid into the cycle. When carbohydrate metabolism is decreased not only is the cycle impaired for lack of materials of which it is composed (pyruvate and oxaloacetate), but the increased demand for energy from fat also produces more acetic acid to be oxidised. If the products of fatty acid catabolism exceeds the capacity of the tissue to oxidise them, these acetic acid residues condense and form ketones. The ketone bodies then accumulate in the blood and are excreted in the urine. That oxaloacetic deficiency is the primary cause of ruminant ketosis has been clearly demonstrated. Also the failure of the adrenals to produce sufficiently high levels of glucocorticoids results in the depletion of blood glucose and carbohydrate reserves, giving rise to the ketotic condition.
Reduction of ketosis. Restoration of normal carbohydrate metabolism in order to reduce the excess utilisation of fat and to restore the function of the citric cycle is followed by the disappearance of ketosis. In ketosis it's important to consider the lipotropic factor. Choline is probably the most important of these factors. When lecithin is added to the diets, increased accumulation of fat is prevented in the liver. The choline contained in the lecithin molecule is the effective agent; in fact the role of choline in the formation of phospholipids such as lecithin may be the basis for its lipotropic action. Choline is a major donor of methylic groups (CH₃). A source of labile methyl is an important factor in fat metabolism in the liver. Choline may promote the formation of some lecithin containing lipoproteins in the liver which are essential in mitochondrial activity or in the oxidation of fatty acids. It is very possible that these lipoproteins synthesised in the liver are the form in which fatty acids are transferred or transported from the liver to the depots. Of all the aminoacids synthesised by the ruminal flora this sulphur containing aminoacid is one of the most limiting substances produced by the ruminal bacteria, very possibly due to the competing effect in the production of sulphidric acid (H₂S).
Bovine ketosis treatment. A wide variety of treatments have been applied with varying success. Intravenous glucose is by far the most effective, but often fails to sustain the animal and there is a high degree of relapse. The feeding of methanogenic inhibitors is also effective. Rapid response in rumen propionate follows administration of any methanogenic inhibitors. It is possible that dietary limitations influence propionate metabolism or gluconeogenesis, and could play a role in the development of primary ketosis. These factors could be Vitamin B₁₂ or any factor limiting the supply of oxaloacetate.
Effect of Acidosis on Animal Metabolism. When the body depends entirely on fats for metabolism, the level of acetoacetic acid and other keto acids in the body fluids rise. Obviously the result is blood acidosis. There is a Sodium concentration decrease as half the acid is excreted combined with ammonia synthesised in the kidney or with cations, mainly sodium derived from the extracellular fluids. The high acidosis in blood also inhibits the regular exchange of gases limiting the oxygen carrying capacity of the red blood cells, which in turn affect the nervous system of the animal. Intravenous injections of bycarbonate may help to aliviate the problem.

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