Ketosis / Acetonemia (cattle)

Ketosis, also known as acetonemia in cattle, is a common and economically significant metabolic disorder characterized by elevated levels of ketone bodies in the blood, milk, and urine as a result of inadequate glucose supply to meet the body's energy demands. This condition develops when animals cannot consume enough feed to meet their energy requirements and must mobilize excessive amounts of body fat as an alternative fuel source. The incomplete oxidation of these fatty acids in the liver results in the accumulation of ketone bodies, including beta-hydroxybutyrate, acetoacetate, and acetone, which produce the characteristic sweet, fruity odor often detectable on the breath of affected animals.

Ketosis primarily affects high-producing dairy cattle in the first weeks to months of lactation, when the energy demands of milk production exceed the animal's capacity to consume and digest sufficient feed. In sheep, a similar condition known as pregnancy toxemia or twin lamb disease occurs in late pregnancy, particularly in ewes carrying multiple fetuses. Dairy goats are also susceptible to both lactational and pregnancy-related forms of the disease. The condition represents one of the most common metabolic disorders in dairy cattle, with subclinical ketosis affecting 20-60% of cows in many herds during the early postpartum period, while clinical ketosis affects approximately 2-15% of cows.

The economic impact of ketosis on dairy production is substantial and multifaceted. Direct losses include decreased milk production, which may be reduced by 10-25% in clinically affected cows, as well as veterinary treatment costs and the value of milk discarded during treatment. Subclinical ketosis, even without obvious clinical signs, significantly impairs productivity. The condition also predisposes animals to numerous other disorders including displaced abomasum, mastitis, metritis, and reduced fertility, creating a cascade of health problems that compound the economic impact. Studies have estimated the cost of each clinical ketosis case at several hundred dollars when all direct and indirect effects are considered.

With appropriate management and early intervention, ketosis is highly treatable, and most affected animals can recover fully with supportive care and energy supplementation. Prevention through optimal nutritional management during the transition period from dry cow to early lactation is preferable to treatment and forms a cornerstone of modern dairy herd health management. Understanding the underlying physiology, recognizing early signs, and implementing evidence-based prevention protocols can dramatically reduce the incidence and impact of this common metabolic disorder.

The primary cause of ketosis is negative energy balance, a state in which the energy demands of the animal exceed the energy supplied by feed intake. In dairy cattle, this occurs most commonly in early lactation when the metabolic demands of rapidly increasing milk production outpace the cow's ability to increase feed intake sufficiently to meet those demands. A high-producing dairy cow may produce 50 liters or more of milk daily in early lactation, requiring enormous amounts of glucose for lactose synthesis, yet her appetite and digestive capacity have not fully recovered from the effects of late pregnancy and calving. This mismatch creates an energy deficit that the body attempts to compensate for by mobilizing fat reserves.

Genetic and breed predisposition to ketosis is well documented, with higher-producing animals generally at greater risk due to their higher energy demands. Within breeds, heritability estimates for ketosis susceptibility range from 0.10 to 0.20, indicating moderate genetic influence on disease risk. Cows that have experienced ketosis in previous lactations are more likely to experience it again. Some bloodlines appear to have more efficient feed intake capacity or fat mobilization regulation, making them more resistant to ketosis. Selection for ever-higher milk production without accompanying selection for feed intake and metabolic efficiency has contributed to the high prevalence of ketosis in modern dairy cattle.

Environmental and management factors strongly influence ketosis risk, particularly nutritional management during the dry period and transition phase. Over-conditioning of dry cows leads to excessive fat mobilization at calving and increased ketosis risk. Inadequate feed access, poor feed quality, or sudden dietary changes around calving reduce energy intake when it is most critically needed. Heat stress reduces feed intake and exacerbates negative energy balance. Social stress from grouping changes, excessive handling, or overcrowding further suppresses appetite. Any condition that reduces dry matter intake in the periparturient period increases ketosis risk, including lameness, mastitis, metritis, and other concurrent diseases.

Risk factors for developing ketosis include increasing parity, with multiparous cows at higher risk than first-lactation heifers, though heifers face their own challenges with simultaneous growth and production demands. Body condition at calving is a critical risk factor, with both over-conditioned (body condition score greater than 3.5) and thin cows at increased risk. High previous-lactation milk production predicts high demands in the current lactation. Calving difficulties and their aftermath, including retained placenta and metritis, increase risk. In sheep, multiple fetuses dramatically increase pregnancy toxemia risk, with ewes carrying triplets at highest risk.

The pathophysiology of ketosis begins with the mobilization of non-esterified fatty acids (NEFA) from adipose tissue in response to negative energy balance and low blood glucose. These fatty acids travel to the liver where they can be oxidized for energy, re-esterified and exported as very-low-density lipoproteins, or partially oxidized to ketone bodies. When fatty acid delivery exceeds the liver's capacity for complete oxidation and export, ketogenesis increases and ketone bodies accumulate in the blood. While ketone bodies can serve as alternative fuel sources for some tissues, high concentrations cause metabolic acidosis and have direct toxic effects on various organ systems. Fatty infiltration of the liver may develop, impairing hepatic function and reducing the liver's ability to produce glucose through gluconeogenesis.

Early warning signs of ketosis often begin subtly and may be detected through routine monitoring programs before clinical signs become apparent. Decreased feed intake, particularly reduced consumption of concentrates while maintaining forage intake, is often the first noticeable change. Milk production may begin declining or fail to increase as expected in early lactation. Some cows show subtle changes in milk composition, with increased fat percentage relative to protein. Body condition begins declining more rapidly than expected, and some animals may appear dull or slightly depressed. The characteristic sweet, fruity odor of acetone may be detectable on the breath, in the milk, or in the urine even before other clinical signs are apparent.

Common symptoms of clinical ketosis in dairy cattle are traditionally described in two forms: the wasting form and the nervous form. The wasting form is more common and characterized by progressive loss of body condition, selective appetite (eating hay but refusing grain), decreased milk production, and firm, dry feces. Affected cows appear dull and depressed, often standing with an arched back and reluctance to move. The characteristic acetone odor is often prominent. Milk production may decrease by 25% or more. In severe cases, cows become weak and may become recumbent. The nervous form, while less common, produces dramatic signs including apparent blindness, incoordination, abnormal licking of objects, aggressive behavior, bellowing, and head pressing against fixed objects. These neurological signs are thought to result from the effects of ketone bodies and low glucose on brain function.

Behavioral changes associated with ketosis are often among the first signs noticed by observant animal caretakers. Affected cattle frequently separate themselves from the group and spend more time lying down. They may approach the feed bunk but eat little, showing decreased time spent eating and fewer meals per day. Rumination time decreases. In the nervous form, behavior may become erratic and unpredictable, with some animals showing apparent hallucinations or inappropriate responses to stimuli. Cows may resist being milked or show unusual reactions in the milking parlor. Attention to changes in normal behavior patterns, particularly around feeding time, often provides the earliest opportunity for intervention.

Physical signs of ketosis include weight loss and declining body condition, which may be rapid in severe cases. The coat may appear rough and dull. Dehydration may develop if the animal is not drinking adequately. Rumen contractions are typically decreased in frequency and strength. The feces are often dry and firm, reflecting reduced feed intake and altered gastrointestinal function. In advanced cases, muscle wasting becomes apparent, particularly over the hindquarters and topline. Body temperature is usually normal unless a concurrent infection is present. The characteristic ketotic odor, reminiscent of nail polish remover or sweet apple cider, is often detectable by experienced personnel.

Symptom progression in untreated ketosis follows a gradual worsening course over days to weeks if left unaddressed. Initial mild reductions in feed intake and milk production progress to more obvious clinical disease. Body condition continues to decline as fat mobilization accelerates. Ketone levels in blood and urine continue to rise, increasing the toxic effects on various organ systems. Fatty liver may develop, further impairing the animal's ability to recover through normal metabolic pathways. In severe cases, profound weakness, recumbency, and potentially death may occur, though fatal outcomes are relatively uncommon with modern dairy management and veterinary care.

Emergency symptoms requiring immediate veterinary intervention include any signs of the nervous form of ketosis, as affected animals may injure themselves or handlers due to their erratic behavior. Recumbent cows that cannot rise require immediate assessment and treatment. Severe depression or obtundation suggests advanced disease requiring intensive care. Any cow with clinical ketosis that fails to respond to initial treatment within 24-48 hours should be re-evaluated for concurrent conditions. In pregnant sheep with pregnancy toxemia, emergency intervention is critical as the condition progresses rapidly and can be fatal within days without treatment.

Clinical examination of animals suspected of having ketosis combines recognition of characteristic clinical signs with detection of ketone bodies in body fluids. The veterinarian assesses the animal's body condition, noting any recent weight loss, and evaluates appetite and mentation. Physical examination includes auscultation of the rumen for decreased motility, assessment of hydration status, and evaluation for concurrent conditions that may have precipitated or complicated the ketosis. The characteristic acetone odor on breath, in milk, or in urine, when present, is highly suggestive of ketosis. A thorough history regarding stage of lactation, calving events, feed intake patterns, and recent management changes helps establish the diagnosis.

Diagnostic tests for ketosis primarily involve detection and quantification of ketone bodies in blood, milk, or urine. Blood testing for beta-hydroxybutyrate (BHB) is considered the gold standard, with levels above 1.2-1.4 mmol/L indicating subclinical ketosis and levels above 2.9-3.0 mmol/L consistent with clinical ketosis. Handheld electronic meters designed for measuring blood ketones in diabetic humans have been validated for use in cattle and provide rapid cowside results. Milk and urine test strips that detect acetoacetate and acetone provide convenient screening tools, though they are somewhat less sensitive and specific than blood BHB measurement. These tests may produce false-negative results in some subclinical cases, as BHB may be the predominant ketone body.

Differential diagnosis for ketosis includes other conditions that cause decreased feed intake, reduced milk production, and weight loss in early lactation cows. Displaced abomasum, which often occurs concurrently with ketosis, causes reduced feed intake and may produce a similar clinical picture. Hardware disease (traumatic reticuloperitonitis) causes pain, reduced feed intake, and decreased production. Hepatic lipidosis may accompany severe ketosis and can be difficult to distinguish. Metritis and mastitis may trigger or accompany ketosis. In pregnant sheep, hypocalcemia must be differentiated from pregnancy toxemia, though the two conditions may occur together. Primary ketosis must be distinguished from secondary ketosis caused by other diseases that reduce feed intake.

Herd-level diagnostics for ketosis are increasingly implemented in dairy operations to identify the prevalence of subclinical disease and evaluate the effectiveness of transition cow management programs. Systematic monitoring of fresh cows through blood or milk ketone testing in the first two weeks postpartum provides herd-level data on ketosis prevalence. Testing protocols typically call for sampling all cows between 3-14 days in milk or targeting high-risk animals. Prevalence of subclinical ketosis (BHB greater than 1.2 mmol/L) above 15-20% suggests significant room for improvement in transition management. Integration of ketosis monitoring data with other herd health and production information helps identify risk factors and optimize prevention strategies.

Emergency and immediate treatment for severe clinical ketosis focuses on rapidly restoring blood glucose levels and providing alternative energy substrates. Intravenous dextrose (500 mL of 50% dextrose solution) provides immediate glucose that raises blood sugar and suppresses fat mobilization and ketogenesis. The glucose effect is temporary, typically lasting only a few hours, but provides immediate relief of hypoglycemia and its effects. Severely affected animals, particularly those with nervous signs or recumbency, may require repeated dextrose infusions. Concurrent treatment with corticosteroids, typically dexamethasone, stimulates gluconeogenesis and reduces milk production, helping redirect glucose from the mammary gland to other body needs.

Medical management of ketosis continues after initial stabilization with oral energy supplements to provide sustained glucose precursors. Propylene glycol is the most commonly used treatment, typically administered orally at 250-500 mL once or twice daily for several days. Propylene glycol is absorbed from the rumen and converted to glucose in the liver, providing sustained energy supply. Glycerol is an alternative oral energy supplement with similar properties. Some protocols include oral or injectable B vitamins, particularly niacin and B12, to support metabolic function. Insulin administration may be used in some treatment protocols to enhance glucose utilization and reduce lipolysis. All treatments in food-producing animals must be administered according to label directions or under veterinary supervision with appropriate withdrawal times observed.

Surgical options are not directly applicable to ketosis treatment, but surgical intervention may be required for concurrent conditions. Displaced abomasum, which commonly accompanies ketosis, typically requires surgical correction. The decision regarding timing of surgery must consider the cow's metabolic status, with some cases benefiting from stabilization before surgery while others may improve more rapidly after the abomasum is corrected. Cesarean section may be necessary in pregnant sheep or goats with pregnancy toxemia if viable fetuses are present and induction of parturition is not successful.

Supportive care for animals with ketosis includes ensuring adequate water intake, providing palatable and high-quality feeds to encourage eating, and minimizing stress. A quiet, comfortable environment supports recovery. Frequent small meals may be better accepted than large quantities offered at once. Highly palatable feeds, such as fresh grass or high-quality alfalfa hay, may stimulate appetite in animals refusing other feeds. Addressing any concurrent conditions that may be suppressing appetite is essential. Body condition and feed intake should be monitored closely, and adjustments to treatment made based on response. Complete recovery may take several days to a week or more.

Herd treatment protocols following identification of clinical ketosis cases should include intensified monitoring of other fresh cows and review of transition management practices. Prophylactic treatment with propylene glycol or other energy supplements may be warranted for high-risk cows, including those with previous ketosis history, over-conditioned cows, and cows showing early signs of reduced feed intake. Investigation of factors that may have contributed to the case, such as dietary changes, feed quality issues, or housing problems, should be undertaken. Subclinical ketosis testing of other fresh cows helps assess whether the case represents an isolated occurrence or a herd-level problem.

Treatment decisions for ketosis balance the costs of treatment against the value of the animal and the expected production loss. For most dairy cattle with ketosis, treatment is straightforward and cost-effective, and animals typically return to normal production. Animals that develop complicated ketosis with severe fatty liver may have prolonged recovery and never fully regain previous production levels. Repeated episodes of ketosis in the same animal may warrant consideration of culling after completing the current lactation. In pregnant sheep with pregnancy toxemia, prognosis is more guarded and depends on severity at diagnosis and whether viable fetuses can be delivered. Economic considerations must include the value of any unborn offspring as well as the dam.

Recovery timeline for uncomplicated ketosis with appropriate treatment is generally favorable, with most animals showing significant improvement within 24-72 hours of initiating treatment. Feed intake typically begins improving within the first day or two as blood glucose levels stabilize and ketone levels decline. Milk production recovery is more gradual, often taking one to two weeks to return to expected levels, and some production loss for the lactation may be permanent. Complete resolution of elevated ketone levels may take several days to a week. Body condition recovery is the slowest component, requiring adequate nutrition over weeks to months to restore lost reserves. Overall, most animals with uncomplicated ketosis can be expected to complete the lactation successfully with appropriate treatment.

Post-treatment care and monitoring are essential to ensure continued recovery and identify any complications or recurrence. Feed intake should be monitored daily, with attention to whether the animal is consuming both forages and concentrates. Milk production should be tracked to assess recovery. Follow-up ketone testing three to five days after treatment helps confirm that the condition is resolving. Any failure to improve or recurrence of elevated ketones warrants re-evaluation for concurrent conditions such as displaced abomasum or metritis. Body condition should be monitored, with the goal of gradual improvement over the lactation. Animals that have experienced ketosis should receive continued attention to energy nutrition.

Prognosis for animals with ketosis depends on the severity and duration of the condition, the promptness of treatment, and whether complications are present. Animals with mild subclinical or clinical ketosis detected and treated early have excellent prognoses. Those with severe or prolonged ketosis, particularly with fatty liver, have more guarded prognoses and may experience lasting effects on production and health. Development of downer cow syndrome or severe fatty liver significantly worsens prognosis. Animals that develop concurrent displaced abomasum, severe metritis, or other complications face combined challenges to recovery. Recurrence in subsequent lactations is possible, particularly if underlying risk factors are not addressed.

Return to production considerations following recovery from ketosis include expectation of some permanent milk production loss for the lactation. Studies suggest that clinical ketosis cases may produce 200-500 kg less milk over the lactation compared to unaffected herdmates. Fertility may be impaired, with longer intervals to first breeding and conception. Immune function is compromised by ketosis, and affected animals may have higher rates of mastitis and other infectious diseases. Despite these effects, most cows recovering from ketosis can complete successful lactations and should be maintained in the herd unless there are other reasons for culling. Prevention of recurrence through optimal dry cow and transition management is the focus going forward.

Vaccination protocols are not applicable to ketosis prevention as this is a metabolic disorder rather than an infectious disease. However, maintaining overall herd health through appropriate vaccination programs reduces the incidence of infectious diseases that can trigger secondary ketosis by reducing feed intake. Prevention of calving-related infections through dry cow management and appropriate calving hygiene supports transition cow health.

Biosecurity measures are not directly relevant to ketosis prevention, though good overall herd health management reduces stress and supports normal feed intake during the critical transition period. Prevention of contagious diseases that could circulate through the herd and reduce feed intake in susceptible fresh cows indirectly supports ketosis prevention.

Nutritional prevention of ketosis is the cornerstone of control and focuses on optimizing body condition, feed intake, and energy balance during the transition period. Avoiding over-conditioning of dry cows is critical, with target body condition at dry-off and at calving in the range of 3.0-3.25 on a 5-point scale. Far-off dry cow diets should be moderate in energy to prevent continued weight gain. Close-up dry cow diets in the final three weeks before calving should prepare the rumen and metabolic systems for the transition to lactation, with gradually increasing energy density and potential inclusion of glucogenic supplements. Fresh cow diets should maximize energy density while maintaining adequate fiber for rumen health.

Management practices for ketosis prevention include minimizing stress during the transition period through stable grouping, adequate space, and comfortable housing. Fresh cow pens should provide easy access to feed and water with minimal competition. Monitoring of fresh cows for early signs of reduced feed intake allows prompt intervention. Cow comfort factors including stall design, bedding quality, and temperature management affect feed intake and ketosis risk. Some operations implement routine prophylactic treatment of high-risk cows with propylene glycol or other energy supplements during the first one to two weeks postpartum. Regular assessment of transition cow health metrics helps evaluate program effectiveness.

Quarantine and testing protocols for ketosis prevention include routine monitoring of fresh cows for subclinical ketosis through blood or milk ketone testing. Establishing baseline ketosis prevalence and monitoring trends over time helps assess the effectiveness of prevention programs. Cows identified with subclinical ketosis can be treated before progressing to clinical disease. Integration of ketosis monitoring with other fresh cow health assessments, including milk production, feed intake, and disease incidence, provides a comprehensive picture of transition cow health. Targets for herd ketosis prevalence guide management decisions and program refinement.

Daily management and monitoring for ketosis prevention and detection centers on close observation of transition cows during the critical weeks before and after calving. Fresh cows should be observed daily for feed intake, attitude, and signs of illness. Milk production should be monitored, with cows not meeting expectations flagged for closer evaluation. Many operations implement routine ketone testing of all fresh cows or high-risk individuals between days 3-14 postpartum. Any animals identified with subclinical ketosis (BHB 1.2-2.9 mmol/L) should receive prophylactic treatment to prevent progression. Animals with declining body condition or reduced intake should be evaluated for ketosis and other fresh cow diseases.

Housing and environmental management during the transition period significantly affect ketosis risk by influencing feed intake and stress levels. Transition cows benefit from housing that provides adequate bunk space, comfortable resting areas, and access to clean water at all times. Overcrowding in close-up and fresh cow pens should be avoided, as social stress reduces feed intake. Heat abatement through fans, sprinklers, and shade is critical in warm weather, as heat stress dramatically reduces intake. Footing should be excellent to promote mobility and confident movement to the feed bunk. Multiple watering points and feeding locations reduce competition. Grouping strategies should minimize social disruption during the transition period.

Herd health programs addressing ketosis should include regular review of transition cow nutrition and management with appropriate specialists. Nutritionist involvement in formulating and monitoring dry cow, close-up, and fresh cow diets is essential. Veterinary input on health monitoring protocols and treatment guidelines ensures timely intervention. Analysis of herd data including ketosis incidence, displaced abomasum rates, and reproductive performance helps identify areas for improvement. Benchmarking against industry standards and other herds provides context for evaluation. Continuous improvement in transition cow management is the goal.

Record keeping and monitoring for ketosis management should document all cases of clinical disease, subclinical ketosis identified through testing, treatments administered, and outcomes. Linking ketosis data to individual cow factors including parity, body condition at calving, previous ketosis history, and production helps identify high-risk profiles. Herd-level trends in ketosis prevalence should be tracked over time and correlated with management changes. Fresh cow health metrics including milk production, disease incidence, and reproductive performance should be integrated with ketosis data for comprehensive transition cow evaluation. This information guides management decisions and program refinement.

Economic considerations for ketosis prevention and management strongly favor investment in prevention through optimal transition management. The cost of nutritional consulting, appropriate facilities, and monitoring programs is far less than the cumulative costs of clinical and subclinical ketosis including production losses, treatment costs, increased disease incidence, and reproductive failures. Studies estimating the total cost of clinical ketosis at $200-400 per case, and subclinical ketosis at $50-100 per affected cow, underscore the economic importance of prevention. Return on investment for transition cow management programs is among the highest of any dairy management intervention.

High-risk breeds and species for ketosis include those selected for high production, as the energy demands of elevated milk synthesis directly contribute to negative energy balance and ketosis risk. Holstein cattle, as the dominant high-producing dairy breed globally, account for the majority of ketosis cases simply due to their prevalence in dairy herds and their high production levels. Within breeds, individual animals with genetic potential for very high production face elevated risk if management does not support their energy needs. Jersey cattle, while producing less total milk volume, produce milk with higher fat content, and some studies suggest similar or even higher ketosis rates compared to Holsteins. Among sheep, prolific breeds carrying multiple fetuses are at highest risk for pregnancy toxemia.

Production type considerations significantly influence ketosis risk, with the condition primarily affecting animals in active lactation or late pregnancy. Dairy cattle are the most commonly affected group, with peak risk in the first four to six weeks of lactation when the gap between energy demand and intake capacity is greatest. Within dairy populations, the highest-producing cows face the greatest risk. First-lactation animals have lower absolute production but also lower intake capacity, so their risk is moderate. Multiparous cows with high previous-lactation production are at highest risk. Dairy goats face similar lactational ketosis risk, while in sheep, pregnancy toxemia in late gestation is the primary concern, particularly in ewes with multiple fetuses.

Genetic selection and testing for ketosis resistance is an emerging area of interest in dairy cattle breeding. The moderate heritability of ketosis susceptibility suggests potential for genetic improvement. Some genomic evaluation systems now include health traits including ketosis in their indexes, allowing selection for improved metabolic health. Balancing selection for production with selection for health and feed efficiency helps address the root causes of ketosis susceptibility. Selection for improved feed intake capacity may be particularly valuable. Within herds, daughters of cows with repeated ketosis episodes should be considered higher risk and targeted for intensified preventive management. Avoiding mating that concentrates genetics for high production without compensating feed intake capacity is prudent.

Commonly co-occurring conditions with ketosis include a complex of periparturient disorders that share risk factors and pathophysiological mechanisms. Displaced abomasum is strongly associated with ketosis, with elevated ketones impairing abomasal motility and predisposing to displacement. Fatty liver syndrome often accompanies severe ketosis, as excessive lipid mobilization overwhelms the liver's capacity to export triglycerides. Hypocalcemia may occur concurrently, particularly as both conditions peak around calving. Metritis incidence is elevated in cows with ketosis, related to immunosuppression and potentially to impaired uterine involution. Mastitis risk is increased due to compromised immune function. Retained placenta may contribute to ketosis development or share common risk factors. This clustering of conditions is sometimes termed the "transition cow disease complex."

Conditions with similar symptoms to ketosis that must be considered in differential diagnosis include displaced abomasum, which causes reduced feed intake and may produce mild ketosis secondary to decreased intake. Hardware disease (traumatic reticuloperitonitis) causes depression, reduced appetite, and decreased milk production. Severe metritis may cause systemic illness with similar signs. Hypocalcemia produces depression and weakness but typically with different timing relative to calving and response to calcium treatment. In sheep, hypocalcemia must be differentiated from pregnancy toxemia, though concurrent disease is common. Primary versus secondary ketosis must be distinguished, as secondary ketosis caused by another disease may not respond to treatment until the primary problem is addressed.

Complications and sequelae of ketosis include fatty liver syndrome, which develops when lipid accumulation in hepatocytes impairs liver function. Severe fatty liver can progress to hepatic failure and death in extreme cases. Prolonged negative energy balance impairs immune function, increasing susceptibility to infectious diseases throughout lactation. Reproductive performance is compromised, with delayed return to estrus, lower conception rates, and increased embryonic loss. Lameness risk may be elevated due to metabolic effects on hoof tissues and immune function. Animals that experience severe ketosis may never fully recover previous production levels and may have shortened productive life in the herd. Recognition and management of complications is essential for optimizing outcomes in affected animals.