KETOSIS IN ANIMALS
Anita Sewaga, Rashmi Singhb, Ankitaa
a: Ph.D. Scholar, b: Assistant Professor
Department of Veterinary Medicine PGIVER, Jaipur,
RAJUVAS, Bikaner, Rajasthan.
Ketosis is a multi-factorial disorder of energy metabolism, due to negative energy balance results in hypoglycemia, ketonemia (the accumulation in blood of acetoacetate, β-hydroxybutyrate [BHB] and their decarboxylation products acetone and isopropanol), and ketonuria.
Hepatic Insufficiency in Ketosis
- In type I, or “spontaneous” ketosis, the gluconeogenic pathways are maximally stimulated, and ketosis occurs when the demand for glucose outstrips the capacity of the liver for gluconeogenesis because of an insufficient supply of glucose precursors.
- In type II ketosis, manifest with fatty liver, gluconeogenic pathways are not maximally stimulated, and consequently mitochondrial uptake of NEFAs is not as active, and NEFAs become esterified in the cytosol, forming triglyceride. The capacity of cattle to transport triglyceride from the liver is low, resulting in accumulation and fatty liver. The occurrence of a fatty liver can further suppress hepatic gluconeogenic capacity.
- In type III ketosis, cattle are fed a diet (typically a high-maize ration) that results in a higher ruminal production of butyrate, which is directly metabolized by ruminal epithelial cells to butyrate.
Types of Bovine Ketosis
- Primary ketosis (production ketosis)
- Secondary ketosis
- Alimentary ketosis
- Starvation ketosis
- Ketosis resulting from a specific nutritional deficiency
Primary Ketosis (Production Ketosis)- Primary ketosis occurs in cows in good to excessive body condition those have high lactation potential and are being fed good-quality rations but that are in a negative energy balance.
Secondary Ketosis– Secondary Ketosis Secondary ketosis occurs where the presence of other disease results in a decreased food intake.
Alimentary Ketosis- Alimentary ketosis (also called type III in some classification systems) is a result of excessive amounts of butyrate in silage and possibly also a result of decreased food intake resulting from the poor palatability of high-butyrate silage. Silage made from succulent material may be more highly ketogenic than other types of ensilage because of its higher content of preformed butyric acid.
Starvation Ketosis- Starvation Ketosis Starvation ketosis occurs in cattle that are in poor body condition and that are fed poor quality feed stuffs. There is a deficiency of propionate and protein from the diet and a limited capacity of gluconeogenesis from body reserves. Affected cattle recover with correct feeding.
Nutritional Deficiency– Ketosis Resulting from Specific Nutritional Deficiency Specific dietary deficiencies of cobalt and possibly phosphorus may also lead to a high incidence of ketosis.
Pathogenesis: In early lactation, at which time negative energy balance leads to adipose mobilization, and milk synthesis creates a high glucose demand. Adipose mobilization is accompanied by high blood serum concentrations of nonesterified fatty acids (NEFAs). During periods of intense gluconeogenesis, a large portion of serum NEFAs is directed to ketone body synthesis in the liver. Thus, the clinicopathologic characterization of ketosis includes high serum concentrations of NEFAs and ketone bodies and low concentrations of glucose.
Ketone Formation: Ketones arise from two major sources: butyrate in the rumen and mobilization of fat. In response to a negative energy balance and low serum concentrations of glucose (and consequently low serum concentrations of insulin), cows will mobilize adipose tissue, with consequent increases in serum concentrations of nonesterified fatty acids (NEFA) and subsequent increases in serum concentrations of β-hydroxybutyrate (BHB), acetoacetate, and acetone.
Clinical findings: Two major clinical forms of bovine ketosis are described—wasting and nervous present in varying degrees of prominence.
Wasting form
The wasting form is the more common of the two and is manifest with a gradual but moderate decrease in appetite and milk yield over 2 to 4 days. In component-fed herds, the pattern of appetite loss is often very specific in that the cow first refuses to eat grain, then ensilage, but may continue to eat hay. The appetite may also be depraved. Woody appearance of animal because of the apparent wasting and loss of cutaneous elasticity presumably resulting from disappearance of subcutaneous fat. The temperature and the pulse and respiratory rates are normal, and although the ruminal movements may be decreased in amplitude and number, they are within the normal range unless the course is of long duration. The characteristic sweet odor of ketones is detectable on the breath and often in the milk.
Nervous form (nervous ketosis)
- Walking in circles
- Straddling or crossing of the legs
- Head pushing or leaning into the stanchion
- Apparent blindness
- Aimless movements and wandering
- Vigorous licking of the skin and inanimate objects
- Depraved appetite
- Chewing movements with salivation Hyperesthesia may be evident.
- The nervous signs that occur in some cases of bovine ketosis are thought to be caused by the production of isopropanol, a breakdown product of acetone in the rumen, although the requirement of nervous tissue for glucose to maintain normal function may also be a factor in these cases.
Subclinical Ketosis (Hyperketonemia): Subclinical ketosis is defined as an increase in blood/plasma/serum BHB above the normal reference range or ketonuria in a cow without detectable clinical signs of disease. Potential milk production in cows with subclinical ketosis is reduced by 1% to 9%.
Clinical pathology:
- Hypoglycemia, ketonemia, and ketonuria are characteristic of the disease.
- Glucose Plasma glucose concentrations are reduced from the normal of approximately 50 to 65 mg/dL to 20 to 40 mg/dL
- BHB is the quantitatively highest circulating ketone body in cattle.
- Normal cows have plasma BHB concentrations less than 1.0 mmol/L;
- Cows with subclinical ketosis have blood or plasma/serum concentrations greater than 1.0, 1.2, or 1.4 mmol/L
- Cows with clinical ketosis usually have serum/plasma BHB concentrations in excess of 2.5 mmol/L, with values rarely reaching 10.0 mmol/L.
Diagnosis: In a affected animal, urine ketone body concentrations are always higher than milk ketone body concentrations. Biochemical examination reveals hypoglycemia, ketonemia and ketonuria.
Rothera’s Test for ketone bodies, Acetoacetic acid reacts with Sodium nitroprusside to give a violet color.
Necropsy findings: The disease is not usually fatal in cattle, but fatty degeneration of the liver and secondary changes in the anterior pituitary gland and adrenal cortex may be present.
Differential Diagnosis:
Wasting form:
- Abomasal displacement
- Traumatic reticulitis
- Primary indigestion
- Cystitis and pyelonephritis
Nervous form:
- Rabies
- Hypomagnesemia
- Bovine spongiform encephalopathy
Treatment:
- Treatment of ketosis is aimed at reestablishing normoglycemia and reducing serum ketone body concentrations.
- Dextrose 50% solution @ 500-800 ml should be administered intravenously.
- Dexamethasone, Predinisolone @ 10 ml I/M
- Insulin @ 200 IU can be administered.
- Propylene glycol administered orally (250–400 g/dose [8–14 oz]) once per day acts as a glucose precursor and is effective as ketosis therapy.
- Cyanocobalamin (vitamin B12, 1 to 4 mg daily IV)
Prevention and Control: Prevention of ketosis is via nutritional management. Body condition should be managed in late lactation, when cows frequently become too fat. Modifying diets of late lactation cows to increase the energy supply from digestible fiber and reduce the energy supply from starch may aid in partitioning dietary energy toward milk and away from body fattening. Monensin sodium is approved for use in preventing subclinical ketosis and its associated diseases. Where approved, it is recommended at the rate of 200–300 mg/head/day. Ionophores alter bacterial flora of the rumen, leading to decreases in gram-positive bacteria, protozoa, and fungi and increases in gram-negative bacteria. The net effect of these changes in bacterial flora is increased propionate production and a decrease in acetate and butyrate production providing increased gluconeogenic precursors.
Economic Significance: Economic Significance Clinical and subclinical ketosis are major causes of loss to the dairy farmer. In rare instances the disease is irreversible and the affected animal dies, but the main economic loss results from the loss of production while the disease is present, the possible failure to return to full production after recovery, and the increased occurrence of periparturient disease. Decreased milk yields; lower milk protein and milk lactose; increased risk for delayed estrus and lower first-service conception rates; lower pregnancy rates; increased intercalving intervals; increased risk of cystic ovarian disease, metritis, and mastitis; and increased involuntary culling.
