Ketosis in Cattle: Introduction (Acetonemia, Ketonemia) Etiology and Pathogenesis Epidemiology Clinical Findings Diagnosis Treatment Prevention and

Control Ketosis is a common disease of adult cattle. It typically occurs in dairy cows in early lactation and is most consistently characterized by partial anorexia and depression. Rarely, it occurs in cattle in late gestation, at which time it resembles pregnancy toxemia of ewes. In addition to inappetence, signs of nervous dysfunction, including pica, abnormal licking, incoordination and abnormal gait, bellowing, and aggression are occasionally seen. The condition is worldwide in distribution, but is most common where dairy cows are bred and managed for high production. Etiology and Pathogenesis: The pathogenesis of bovine ketosis is incompletely understood, but it requires the combination of intense adipose mobilization and a high glucose demand. Both of these conditions are present 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 (NEFA). During periods of intense gluconeogenesis, a large portion of serum NEFA is directed to ketone body synthesis in the liver. Thus, the clinicopathologic characterization of ketosis includes high serum concentrations of NEFA and ketone bodies and low concentrations of glucose. In contrast to many other species, cattle with hyperketonemia do not have concurrent acidemia. The serum ketone bodies are acetone, acetoacetate, and β-hydroxybutyrate (BHB). There is speculation that the pathogenesis of ketosis cases occurring in the immediate postpartum period is slightly different than that of cases occurring closer to the time of peak milk production. Cases of ketosis in very early lactation are usually associated with fatty liver. Both fatty liver and ketosis are probably part of a spectrum of conditions associated with intense fat mobilization in cattle. Ketosis cases occurring closer to peak milk production, which usually occurs at 4-6 wk postpartum, may be more closely associated with underfed cattle experiencing a metabolic shortage of gluconeogenic precursors than with excessive fat mobilization. The exact pathogenesis of the clinical signs is not known. They do not appear to be associated directly with serum concentrations of either glucose or ketone bodies. There is speculation that they may be due to metabolites of the ketone bodies.

Lactating cows with hyperketonemia (subclinical ketosis—serum BHB concentrations >12 mg/dL) are at increased risk of developing clinical ketosis. and metritis. as are aggression and bellowing. and an “empty” appearing abdomen are usually the signs of ketosis noticed first. CNS disturbances are noted in a minority of cases. compared with cows with lower serum BHB concentrations. other than being associated with dairy breeds. On physical examination. a thorough physical examination should be performed because frequently ketosis occurs concurrently with other peripartum diseases. Positive milk tests for acetoacetate and/or acetone usually indicate clinical ketosis. lethargy. All of these tests are read by observation for a particular color change. In a given animal. these results indicate subclinical ketosis.0) at calving are at increased risk of ketosis. cows with ketosis often refuse grain before forage. but because the disease is so common. The majority of commercially available test kits are based on the presence of acetoacetate or acetone in milk or urine. Rabies and other CNS diseases are important differential diagnoses. In group-fed herds. cows are afebrile and may be slightly dehydrated. These include abnormal licking and chewing. These signs occur in a clear minority of cases. Due to the large surge in plasma NEFA at calving.75 out of 5. compared with those with lower body condition scores. A dipstick . such as partial anorexia. being hyperactive in some cases and hypoactive in others. but those designed to detect acetoacetate or acetone in urine are not suitable for milk testing. finding animals with these signs is not unusual. Especially common concurrent diseases include displaced abomasum. but incidence in individual herds varies substantially. urine ketone body concentrations are always higher than milk ketone body concentrations. reduced milk production. Cows with excessive adipose stores (body condition score ≥3. Ketosis occurs in all parities (although it appears to be less commin in primiparous animals) and does not appear to have a genetic predisposition. Milk tests for acetone and acetoacetate are more specific than urine tests. a positive test for ketones is very common during this period.Epidemiology: All dairy cows in early lactation (first 6 wk) are at risk of ketosis. Trace to mildly positive results for the presence of ketone bodies in urine do not signify clinical ketosis. Incoordination and gait abnormalities occasionally are seen. Dipstick tests are convenient. When a diagnosis of ketosis is made. In many cases there are no other physical abnormalities. Diagnosis: The clinical diagnosis of ketosis is based on presence of risk factors (early lactation). If rations are offered in components. Rumen motility is variable. with cows sometimes chewing incessantly on pipes and other objects in their surroundings. The incidence in lactation is estimated at 5-16%. clinical signs. Caution should be exercised in the use of such tests within 48 hr after calving. Clinical Findings: In cows maintained in confinement stalls. Without clinical signs. Cow-side tests for the presence of ketone bodies in urine or milk are critical for diagnosis. reduced feed intake is usually the first sign of ketosis. and ketone bodies in urine or milk. retained fetal membranes.

Treatment: Treatment is aimed at reestablishing normoglycemia and reducing serum ketone body concentrations. Propylene glycol (250-400 g/dose. Some feed additives. Dietary particle size will influence the optimal proportions of carbohydrate fractions. This solution is very hyperosmotic and. propylene glycol. Bolus IV administration of 500 mL of 50% dextrose solution is a common therapy. This dose may be administered twice per day. Cows tend to reduce feed consumption in the last 3 wk of gestation. IM. including niacin. . Nutritional management should be aimed at minimizing this reduction. when cows frequently become too fat. Bolus glucose therapy generally results in rapid recovery. Ketosis cases occurring within the first 1-2 wk after calving frequently are more refractory to therapy than those cases occurring nearer to peak lactation. if administered perivascularly. PO. Use of insulin in this manner is an extra-label. so care should be taken to assure that it is given IV. Rations should be relatively high in nonfiber carbohydrate concentration. After calving. Glucose and glucocorticoid therapy may be repeated daily as necessary. Insulin suppresses both adipose mobilization and ketogenesis. The dry period is generally too late to reduce body condition score. To be effective. A critical area in ketosis prevention is maintaining and promoting feed intake. Overdosing propylene glycol leads to CNS depression. Fatty Liver Disease of Cattle . is more sensitive than milk tests for acetone and acetoacetate and may be useful for monitoring incidence of subclinical ketosis. results in severe tissue swelling and irritation. Body condition should be managed in late lactation. Feed intake should be monitored and rations adjusted to maximize dry matter and energy consumption in late gestation. calcium propionate. However. diets should promote rapid and sustained increases in feed and energy consumption. Neutral-detergent fiber concentrations should usually be in the range of 28-30% with nonfiber carbohydrate concentrations in the range of 38-41%. generally results in a more sustained response. especially in mild cases or in combination with other therapies.) Prevention and Control: Prevention of ketosis is via nutritional management. may be beneficial in preventing and managing ketosis. It is likely that optimal energy and fiber concentrations in rations for cows in the last 3 wk of gestation vary from farm to farm. unapproved use. and rumen-protected choline. Other therapies that may be of benefit in refractory ketosis cases are continuous IV glucose infusion and tube feeding. Administration of glucocorticoids including dexamethasone or isoflupredone acetate at 5-20 mg/dose. Controversy exists over the optimal dietary characteristics during this period. the effect frequently is transient and relapses are common. a long-acting insulin preparation given IM at 150-200 IU/day may be beneficial. but contain enough fiber to maintain rumen health and feed intake. [~8-14 oz]) acts as a glucose precursor and may be effective as ketosis therapy. resulting in excessive adipose mobilization prepartum. (See also fatty liver disease of cattle. In these cases. Reducing body condition in the dry period may even be counterproductive. available in Japan and Europe. especially in cases occurring near peak lactation. sodium propionate.designed to detect BHB in milk. but should be given in combination with glucose or a glucocorticoid to prevent hypoglycemia.

they all eat the same rations. All of them seem depressed. Ewes are most commonly affected in the days prior to parturition and when they're carrying twins or triplets. It typically affects dairy cows in negative energy balance during periods of high milk. dietary intake can't keep pace with demand. they're all pastured on the same ground.these supplements should be fed in the last 2-3 wk of gestation. The cows freshened about two weeks ago and are now back in the business of producing milk. The operator has called you in because he expects his production to be in the neighborhood of 60 pounds of milk per day per cow. and the body begins to use fatty acids and ketone bodies as its fuel source. Just today. three of the smaller ones started to tremble and stumble around when brought to the parlor for milking. but these five cows have been putting out less and less for the past five days. and the smallest ones. A physical examination shows you that the five cows you're there to see are thinner than the ones producing normally. (In case of multiple pregnancies the energy demands of the fetuses cause metabolic derangements in the mother. are camped in and look unsteady on their feet. DIAGNOSIS These five cows have developed ketosis. including rabies. You have a pretty good idea what this might be so you take a urine sample for a quick confirmation. Furthermore. You also take a small blood sample to test its glucose level.) The most common etiology of ketosis in both cattle and sheep is fairly straightforward: high demand for energy depletes the body's supply of free and stored glucose. they've been losing condition in spite of eating their ration. as well as during the period of ketosis susceptibility. One is noted head-pressing in the corner of her pen. and housed in the same barn. KETOSIS IN A FRESHENED DAIRY COW You are called out to a small dairy operation in Central Virginia to examine five of the operator's cows out of a herd of 60 head. You notice a strong acetone odor on the breath of the three cows who seem the most affected. a ruminant metabolic disorder that often affects high producing dairy cows (bovine ketosis) and ewes in late pregnancy (pregnancy toxemia). . The entire herd is up-to-date on vaccinations.

mobilization of lipids leads to accumulation and metabolism of free fatty acids in the liver. Primary ketosis This form is seen in cattle with high body condition on good quality feed. in cattle they're classified as follows: 1. The wasting form involves mobilization of fat stores and loss of body condition. resulting in ketosis. High protein content. a displaced abomasum. and erratic behavior. or other painful conditions can all can put a cow off feed during a period of high demand. mastitis. Hepatic insufficiency secondary to the degeneration can lead to a spiral of more metabolic derangements. so the cow mobilizes what little fat she has to meet her needs. Ketosis is further classified according to its root cause and by its clinical presentation. low digestibility. 3.Lipolysis depletes the body's fat stores and results in rapid loss of body condition. wasting and nervous. Ulcers. 2. the cows are not eating well due to another disease or condition that prevents them from meeting their intake requirements. Further. The nervous form involves the effects of ketones on the central nervous system. Starvation ketosis Cattle in poor condition on poor quality feed simply can't energy demands through diet. often resulting in excessive retention of lipid by the hepatocytes (fatty degeneration). . Ketosis presents in two major forms. In this case. Secondary ketosis In this case. Ketosis may also result from specific nutritional deficiencies or high butyrate levels in silage. and genetic predisposition are all factors in this form of ketosis. insufficient dry matter intake. the cows are eating but are not meeting their energy demands and a negative energy balance results. ataxia. The presence of high levels of ketones leads to trembling. particularly in cattle.

this is a condition caused by a separate disease that causes the ewe to go off feed. resulting in negative energy balance. As you can tell from the higher-magnification image. The classifications used for sheep are as follows: 1. Primary pregnancy toxemia Ewes typically experience a decrease in feed intake in the last two months of pregnancy. things are much worse than in the relatively mild case of Willow the obese cat. The ewe can't consume enough to maintain its body weight and negative energy balance results. The hepatocytes are so distended that their cytoplasm is barely visible. 3. Secondary pregnancy toxemia As with cattle. If these sheep are stressed at this stage (by shearing. The normal. This . regular architecture of the liver has been so badly distorted that the venous and biliary supply has almost certainly been compromised. putting them at risk of negative energy balance. This low power image shows a field of hepatocytes that are heavily infiltrated with lipid. The lipid inclusions of some hepatocytes are sequestered in several small vacuoles. forced to the margins of the cell membranes by the sheer volume of fat within the cells. the ketosis is caused by a decrease in feed intake due to excess intra-abdominal fat compressing the rumen. or transportation). not in early lactation. 2. crutching. This allows staining of cytoplasm between the vacuoles. "Fat ewe" pregnancy toxemia In this case. lending a "webby" appearance to the tissue. the result may be the onset of ketosis. Sheep with decreased liver function are also at higher risk for the disorder.Sheep experience similar forms of ketosis but they will typically show clinical signs in late pregnancy.

More frequently. In every case there will be some increase in the fat content of the liver. basophilic "dots" are the nuclei of the hepatocytes. particularly in early lactation. which means death. but the deficit has knockon effects such as an increased incidence of metabolic and infectious disease." Cells that are not as fully infiltrated have a cloudy appearance where their multiple vacuoles overlap. and poor fertility including poor conception rates. Necrotic cells become an inflammatory stimulus and hepatitis and cirrhosis (scarring) will result. . Close This Window Farm Animal Practice Ketosis and fatty liver in cattle Tony Andrews Tony Andrews is an independent consultant in farm animal management and disease. leads to fat mobilisation. All these factors can result in increased fat utilisation and raised plasma fatty acids and ketone body levels. The liver function can be compromised to the point of causing total liver failure. If this sort of damage is extensive and prolonged. Abstract PROBABLY two-thirds of nutritional problems in cattle centre on energy balance. suboestrus and cystic ovarian disease. there are no overt signs of disease. He is an RCVS Specialist in Cattle Health and Production. the degree of which appears to be related to the level of milk production. which in turn can lead to diseases such as clinical ketosis or fat cow syndrome. displaced to the margins of the more distended cells. He has a considerable interest in nutritional problems and has recently undertaken projects involving the use of recombinant bovine somatotrophin in the treatment of fat cow syndrome and pregnancy toxaemia in ewes. anoestrus. excessive loss of condition. giving an appearance similar to an adipocyte's "signet ring. however. as described in this article. Thus. the development of fatty liver appears to precede ketosis and contribute to its onset and that of a number of other energy deficiency syndromes. the magnitude of the energy deficit and/or the cow's body condition score at calving. Energy deficiency.sample is so completely infiltrated with fat that at first glance it resembles a field of brown fat more than it does liver! The dark. hepatocytes begin to die.

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