Hemolytic Anemia

Hemolytic anemia in horses refers to a condition in which red blood cells are destroyed faster than the body can replace them, leading to a deficiency of these essential oxygen-carrying cells. The term hemolytic derives from the Greek words for blood and destruction, accurately describing the pathological process underlying this serious condition. In horses, hemolytic anemia can result from various causes including immune-mediated destruction, infections, toxins, and certain drugs, with immune-mediated hemolytic anemia representing one of the most common and clinically significant forms. The resulting anemia compromises oxygen delivery to tissues throughout the body, producing clinical signs that range from subtle exercise intolerance to life-threatening cardiovascular collapse.

Hemolytic anemia occurs in horses of all breeds, ages, and uses, though certain forms affect specific populations more commonly. Immune-mediated hemolytic anemia can develop as a primary autoimmune disorder or secondary to underlying diseases, infections, or drug reactions. Neonatal isoerythrolysis, a specific form of hemolytic anemia affecting newborn foals, occurs when maternal antibodies attack foal red blood cells and is more common in certain breeds including Thoroughbreds, Standardbreds, and mules. Infectious causes such as equine infectious anemia and piroplasmosis produce hemolytic anemia through different mechanisms but with similar clinical consequences. Geographic distribution of certain infectious forms follows the distribution of causative organisms and their vectors.

The impact of hemolytic anemia on equine health depends on the severity and rapidity of red blood cell destruction. Acute severe cases can cause life-threatening anemia requiring emergency intervention, including blood transfusions to maintain adequate oxygen-carrying capacity. Chronic forms may produce more subtle signs of exercise intolerance, poor performance, and general debilitation that affect quality of life and athletic function. The underlying cause significantly influences prognosis, with some forms being readily treatable while others, particularly those associated with equine infectious anemia, carry much graver implications. Economic impacts include veterinary costs, lost training time, and potential loss of the animal.

Many forms of hemolytic anemia in horses respond well to appropriate treatment, making early recognition and accurate diagnosis essential for optimal outcomes. Immune-mediated forms often improve with immunosuppressive therapy, while infectious causes require specific antimicrobial treatment. Removal of offending drugs or toxins allows recovery in those cases. Supportive care including blood transfusions can sustain horses through acute crises while specific treatments take effect. The key to successful management lies in identifying the underlying cause and implementing appropriate targeted therapy along with supportive care. With proper treatment, many horses with hemolytic anemia make complete recoveries and return to their previous level of function.

The primary causes of hemolytic anemia in horses are diverse and can be broadly categorized into immune-mediated, infectious, toxic, and miscellaneous causes. Immune-mediated hemolytic anemia occurs when the immune system mistakenly produces antibodies against the horse's own red blood cells, targeting them for destruction by splenic macrophages or causing intravascular hemolysis. This autoimmune process can develop as a primary disorder of unknown trigger or secondary to underlying conditions including infections, neoplasia, or drug reactions. Understanding the specific cause is essential for appropriate treatment selection and accurate prognostic assessment.

Genetic and breed predispositions for hemolytic anemia vary by the specific form of the condition. Neonatal isoerythrolysis shows higher incidence in Thoroughbreds, Standardbreds, and mules due to higher frequencies of blood group incompatibilities between mares and foals in these populations. Certain blood types, particularly the Aa and Qa antigens, are more commonly associated with isoerythrolysis reactions. Primary autoimmune hemolytic anemia does not appear to have significant breed predisposition in horses. Inherited enzyme deficiencies that can cause hemolytic anemia in other species have not been well-documented in horses.

Environmental and management factors contribute to hemolytic anemia through exposure to infectious agents, toxins, and certain plants. Geographic location influences exposure to infectious causes including piroplasmosis in tropical and subtropical regions and equine infectious anemia in areas with high biting fly populations. Toxic causes include exposure to red maple leaf toxicity, which is common in North America during late summer and fall when wilted leaves become palatable. Onion toxicity can occur in horses with access to gardens or fields containing wild onions. Heavy metal toxicity, particularly lead or copper, can cause hemolysis in exposed horses.

Risk factors for developing hemolytic anemia include concurrent illness that may trigger secondary immune-mediated disease, recent medication administration that could cause drug-induced hemolysis, and pasture access to potentially toxic plants. Pregnant mares that have been previously sensitized to foal blood types through prior pregnancy or blood transfusion are at risk of producing foals with neonatal isoerythrolysis. Horses in geographic areas endemic for blood parasites face ongoing risk of infectious hemolytic anemia. Recent stress, surgery, or other immune-modulating events may precipitate autoimmune conditions in predisposed individuals.

The disease mechanism of hemolytic anemia involves accelerated destruction of red blood cells through various pathways depending on the underlying cause. In immune-mediated hemolysis, antibodies bind to red blood cell surface antigens, marking cells for destruction by splenic macrophages or activating complement-mediated lysis directly within blood vessels. Intravascular hemolysis releases free hemoglobin that can damage kidneys and causes characteristic red or brown discoloration of urine and serum. Extravascular hemolysis in the spleen and liver produces breakdown products including bilirubin that cause the icterus characteristic of hemolytic conditions. The bone marrow responds by increasing red blood cell production, but when destruction outpaces production, anemia develops.

Early warning signs of hemolytic anemia may be subtle and easily overlooked, particularly in chronic or slowly progressive cases. Decreased energy level, reluctance to work, and mild exercise intolerance often represent the first detectable changes. Horses may appear slightly dull or less enthusiastic than normal without obvious signs of illness. Slight pallor of the mucous membranes may be apparent on close examination but can be missed without direct comparison to normal color. Changes in coat quality, including dullness and poor condition, may develop insidiously over time. Because horses are prey animals that instinctively hide weakness, early hemolytic anemia often goes unrecognized until more obvious signs develop.

The most common symptoms of hemolytic anemia include pale or yellow mucous membranes, weakness, elevated heart rate, rapid breathing, and depression. Pallor results directly from reduced red blood cell numbers and decreased hemoglobin concentration. Icterus, or jaundice, produces yellow discoloration of the gums, whites of the eyes, and vulvar mucosa due to accumulation of bilirubin from red blood cell breakdown. Tachycardia and tachypnea represent cardiovascular and respiratory compensation for reduced oxygen-carrying capacity. General depression and lethargy reflect inadequate oxygen delivery to the brain and other organs. Exercise intolerance may be profound, with horses becoming exhausted after minimal exertion.

Behavioral changes in horses with hemolytic anemia often reflect their compromised energy status and general malaise. Affected horses frequently show decreased appetite, ranging from reduced interest in grain to complete anorexia in severe cases. Social behavior may change, with horses becoming withdrawn and less interactive with herd mates. Previously energetic horses may stand quietly with lowered heads, showing little response to environmental stimuli. Some horses become irritable or reactive due to discomfort or anxiety associated with their declining condition. Changes in normal daily patterns, such as increased lying down or failure to come to the gate at feeding time, should prompt investigation.

Physical signs of hemolytic anemia extend beyond the obvious pallor and icterus. Elevated heart rate, often exceeding 60 beats per minute at rest, reflects cardiovascular compensation for reduced oxygen delivery. Heart murmurs may develop secondary to anemia-induced changes in blood viscosity and flow dynamics. Respiratory rate increases as the body attempts to maximize oxygen uptake. The spleen may be enlarged and palpable on rectal examination due to increased red blood cell destruction and sequestration. Fever may be present with infectious causes or as a component of the underlying disease process. Discolored urine ranging from pink to dark brown may occur with intravascular hemolysis releasing free hemoglobin.

Symptom progression in hemolytic anemia depends heavily on the rate and severity of red blood cell destruction. Acute, rapidly progressive hemolysis can produce life-threatening anemia within hours to days, with rapid deterioration from mild weakness to recumbency and cardiovascular collapse. Chronic hemolysis may produce slowly progressive symptoms over weeks to months as the body partially compensates for gradual red blood cell loss. Recurrent episodes characterize some forms, with periods of relative stability interrupted by acute crises. Without treatment, progressive cases continue to worsen as red blood cell destruction outpaces bone marrow production capacity.

Emergency symptoms requiring immediate veterinary attention include severe weakness or inability to stand, profound pallor with white or gray mucous membranes, dark red or brown urine indicating severe intravascular hemolysis, rapid weak pulse, and signs of cardiovascular shock. Horses with packed cell volumes below 12-15 percent face immediate life-threatening risk and may require emergency blood transfusion. Rapid breathing at rest, particularly with nostril flaring, indicates severe compromise. Any horse showing acute onset of weakness, jaundice, and dark urine should be evaluated immediately, as some causes of hemolytic anemia, including red maple toxicity, can progress rapidly to fatal outcomes.

Physical examination of horses with suspected hemolytic anemia provides important initial information but cannot determine the specific cause. Veterinarians assess mucous membrane color, noting pallor indicating anemia and icterus suggesting hemolysis. Heart rate and rhythm evaluation typically reveals tachycardia and may identify murmurs associated with anemia. Respiratory rate and effort assessment documents compensation for reduced oxygen-carrying capacity. Rectal examination may reveal an enlarged spleen. Body condition assessment notes any recent weight loss. A thorough history including recent medications, pasture access, travel history, and exposure to potential toxins guides further diagnostic testing.

Complete blood count analysis is essential for confirming anemia and characterizing its severity and nature. Packed cell volume or hematocrit measures the percentage of blood volume composed of red blood cells, with values below 30 percent indicating anemia and values below 15 percent representing life-threatening levels. Red blood cell morphology examination may reveal changes suggesting specific causes, including spherocytes in immune-mediated disease or parasites in infectious hemolysis. Reticulocyte counts or other measures of bone marrow response help distinguish regenerative anemia with active replacement from non-regenerative forms. White blood cell counts and platelet numbers provide additional diagnostic information and may suggest underlying causes.

Advanced diagnostic testing targets identification of the specific cause of hemolytic anemia. Coombs testing detects antibodies bound to red blood cells, supporting diagnosis of immune-mediated hemolytic anemia. Blood smear examination may identify parasites such as Babesia or Theileria in endemic areas. Serum chemistry panels evaluate liver function, which is commonly affected in hemolytic conditions, and kidney function, which may be compromised by hemoglobin toxicity. Serology or PCR testing for equine infectious anemia, piroplasmosis, or other infectious agents may be indicated based on geographic risk and clinical suspicion. Bone marrow biopsy may be performed when non-regenerative anemia suggests marrow pathology.

Differential diagnosis for hemolytic anemia requires consideration of multiple potential causes. Immune-mediated hemolytic anemia may be primary or secondary to underlying conditions requiring investigation. Equine infectious anemia produces hemolytic anemia through immune-mediated mechanisms but carries much different regulatory and prognostic implications. Piroplasmosis should be considered in horses from endemic areas or with travel history. Red maple toxicity must be considered in horses with pasture access to maple trees, particularly in late summer and fall. Drug-induced hemolysis requires review of recent medication administration. Neonatal isoerythrolysis affects only newborn foals from sensitized mares. Other causes of anemia including blood loss and bone marrow failure must be distinguished from hemolytic disease.

Emergency and immediate treatment for severe hemolytic anemia focuses on stabilizing the patient and restoring adequate oxygen-carrying capacity. Blood transfusion is the primary emergency intervention for horses with life-threatening anemia, typically indicated when packed cell volume falls below 12-15 percent or when clinical signs indicate inadequate tissue oxygenation despite higher values. Fresh whole blood from a compatible donor provides both red blood cells and plasma components. Cross-matching should be performed when possible, particularly for horses that may have received previous transfusions. Intravenous fluid therapy supports cardiovascular function and helps dilute potentially nephrotoxic free hemoglobin in cases of intravascular hemolysis. Oxygen supplementation may benefit severely affected horses.

Medical management of hemolytic anemia depends on identifying and addressing the underlying cause. Immune-mediated hemolytic anemia typically responds to immunosuppressive therapy, with corticosteroids such as dexamethasone representing the first-line treatment. Initial high-dose corticosteroid administration is gradually tapered over weeks to months as the condition stabilizes. Additional immunosuppressive agents including azathioprine may be added for refractory cases. Infectious causes require specific antimicrobial therapy, such as imidocarb dipropionate for piroplasmosis. Toxic causes necessitate removal of the toxin source and supportive care while the horse recovers. Drug-induced hemolysis requires immediate discontinuation of the offending medication.

Surgical options are limited for most causes of hemolytic anemia, though splenectomy has been considered in cases of refractory immune-mediated disease. However, splenic removal is major surgery with significant risks and eliminates an important immunological organ, making it a last resort rather than routine treatment. Plasma exchange procedures, which can remove pathogenic antibodies, have been explored but are not widely available in equine medicine. Most hemolytic anemia treatment remains medical rather than surgical in nature.

Supportive care complements specific treatment and helps horses recover from hemolytic episodes. Rest reduces oxygen demand and cardiac workload during the recovery period. Nutritional support with high-quality, easily digestible feeds provides necessary substrates for red blood cell regeneration. Iron supplementation is generally avoided unless iron deficiency is documented, as iron overload can occur with hemolytic conditions. Monitoring for complications including laminitis, which can develop secondary to systemic inflammation, requires vigilant attention. Prevention of stress and maintenance of stable environmental conditions support recovery.

Rehabilitation and return to work following hemolytic anemia should proceed gradually based on hematologic recovery. Serial complete blood count monitoring ensures packed cell volume has returned to acceptable levels before exercise resumes. Initial return to work involves light activity such as hand walking, with gradual progression to more demanding exercise as condition permits. Monitoring for signs of exercise intolerance or recurrence of symptoms guides exercise progression. Full return to previous performance levels may take weeks to months depending on severity and duration of anemia. Ongoing monitoring for recurrence is important, particularly for immune-mediated cases that may relapse.

Treatment decisions for hemolytic anemia must consider the underlying cause and associated prognosis. Immune-mediated cases generally carry good prognosis with appropriate treatment, though some cases require long-term immunosuppressive therapy. Infectious causes have variable prognosis depending on the specific organism and promptness of treatment. Toxic causes may have poor prognosis if significant organ damage has occurred, particularly with red maple toxicity. Equine infectious anemia has no effective treatment and carries regulatory implications requiring special consideration. Cost of treatment, including potential multiple transfusions and extended hospitalization, should be discussed with owners to ensure informed decision-making.

Recovery timeline for hemolytic anemia varies considerably depending on the underlying cause, severity of anemia, and promptness of treatment. Horses with immune-mediated hemolytic anemia typically show initial improvement within days of starting corticosteroid therapy, with stabilization of packed cell volume followed by gradual increase over one to three weeks. Complete hematologic recovery may take four to eight weeks or longer, during which the bone marrow regenerates the red blood cell population. Cases caused by acute toxicity or drug reactions may recover more quickly once the offending agent is removed, assuming no permanent organ damage has occurred. Chronic or recurrent cases may require extended management periods.

Post-treatment care and monitoring are essential components of successful recovery from hemolytic anemia. Regular complete blood count monitoring, initially every few days and then weekly as the condition stabilizes, tracks the response to treatment and ensures continued recovery. Packed cell volume should show progressive improvement, and reticulocyte production indicates appropriate bone marrow response. Ongoing monitoring for recurrence is particularly important in immune-mediated cases, where relapse can occur during corticosteroid tapering. Gradual reduction of immunosuppressive therapy over weeks to months minimizes relapse risk while avoiding long-term side effects of these medications.

Prognosis factors for hemolytic anemia depend heavily on the underlying cause. Primary immune-mediated hemolytic anemia carries a generally favorable prognosis with appropriate treatment, though some cases prove refractory or recurrent. Secondary immune-mediated disease prognosis depends on the underlying condition. Neonatal isoerythrolysis has good prognosis with aggressive early treatment but can be fatal without intervention. Infectious causes have variable prognosis based on the specific organism and timeliness of treatment. Toxic causes, particularly red maple toxicity, may carry guarded prognosis if significant methemoglobinemia or renal damage has occurred. Severity of initial presentation, including degree of anemia and organ involvement, influences individual prognosis.

Long-term soundness outlook for horses recovering from hemolytic anemia is generally positive for causes that can be effectively treated. Horses that recover from immune-mediated hemolytic anemia typically return to full function without lasting effects, though some require ongoing low-dose immunosuppressive therapy to prevent recurrence. Previously affected horses may be at increased risk for relapse, particularly during periods of stress or concurrent illness. Those recovering from infectious causes should have cleared the underlying infection to prevent ongoing problems. Horses that experienced severe anemia with potential organ damage may have residual effects requiring ongoing monitoring. Most horses that survive acute hemolytic crises and respond to treatment return to their previous level of performance.

Management practices for preventing hemolytic anemia focus on avoiding known causes and maintaining overall health. Pasture management should eliminate access to toxic plants, particularly red maple trees, with special attention during late summer and fall when wilted leaves become toxic and palatable. Any fallen branches or storm damage should be removed promptly before horses can access wilted leaves. Onions, both wild and cultivated, should be kept away from equine areas. Drug administration should follow appropriate protocols, with monitoring for adverse reactions when using medications known to occasionally cause hemolysis.

Nutritional prevention of hemolytic anemia primarily involves avoiding toxic substances rather than providing specific protective nutrients. Maintaining horses on appropriate, balanced diets supports overall immune function and health. Avoiding nutritional deficiencies that might compromise bone marrow function ensures adequate red blood cell production capacity. Appropriate mineral balance prevents potential hemolytic effects of copper toxicity. Feeding programs should exclude any potentially toxic plants or contaminated feeds. Overall nutritional health supports the body's ability to respond to and recover from hemolytic challenges.

Exercise and conditioning considerations for preventing hemolytic anemia relate primarily to avoiding excessive stress that might trigger immune-mediated disease in susceptible individuals. Appropriate conditioning programs that gradually increase workload allow physiological adaptation without excessive stress. Adequate recovery time between competitions or intense training sessions prevents cumulative stress effects. Monitoring horses carefully following introduction of new exercise demands allows early detection of any developing problems. Exercise programs themselves do not directly cause hemolytic anemia but stress management supports overall immune health.

Environmental factors significantly influence risk of certain forms of hemolytic anemia. Geographic awareness of endemic areas for piroplasmosis and other blood parasites allows appropriate precautions including vector control and testing of horses entering these regions. Tick control in endemic areas reduces exposure to blood parasite vectors. Environmental assessment should identify and eliminate toxic plant species within or adjacent to horse pastures. Proper storage of potentially toxic substances prevents accidental exposure. Vector control through fly management reduces transmission risk for equine infectious anemia.

Vaccination does not prevent most forms of hemolytic anemia, as no vaccines exist for immune-mediated disease or toxic causes. No vaccine is available for equine infectious anemia or piroplasmosis. Prevention of neonatal isoerythrolysis requires identification of at-risk mares through blood typing and antibody screening, with withholding of colostrum and provision of alternative antibody sources for foals from sensitized mares. This targeted prevention approach is highly effective when properly implemented. Regular health maintenance including appropriate vaccination against other diseases supports overall immune function that may reduce risk of secondary immune-mediated conditions.

Daily management for horses recovering from or living with hemolytic anemia requires attention to overall health while minimizing stress and avoiding known triggers. Morning health checks should assess general attitude, appetite, and any visible signs of pallor or icterus. Fresh water must be available at all times to support adequate hydration and kidney function. Feeding schedules should provide consistent, high-quality nutrition appropriate for recovery and ongoing health. Medications, particularly corticosteroids if prescribed, should be administered on schedule with attention to proper dosing and any potential side effects. Environmental stability through consistent routines reduces stress that could potentially trigger relapse.

Housing and turnout considerations for horses with hemolytic anemia should balance normal activity with protection from environmental triggers. Pastures must be carefully evaluated and cleared of any toxic plants, particularly red maple trees and onions. Turnout companions should be calm and compatible to minimize stress from social interactions. Adequate shelter provides protection from weather extremes that could add physiological stress. Housing should be well-ventilated but free from excessive dust that could stress respiratory compensation for anemia. Fly control reduces irritation and, in endemic areas, minimizes exposure to potential disease vectors.

Exercise modifications during recovery from hemolytic anemia should follow veterinary guidance based on hematologic status. During active disease or early recovery, rest may be indicated to reduce oxygen demand on a compromised cardiovascular system. As packed cell volume improves, gradual return to light exercise can begin, typically starting with short hand walking sessions. Progression to turnout, then lunging or light riding, follows continued hematologic improvement and absence of clinical signs. Monitoring for exercise intolerance, excessive respiratory effort, or rapid heart rate during activity guides safe progression. Full return to athletic activity requires normal or near-normal packed cell volume and appropriate veterinary clearance.

Monitoring and ongoing care for horses with history of hemolytic anemia should include regular hematologic evaluation and vigilance for recurrence. Periodic complete blood counts, frequency determined by the specific condition and individual history, track red blood cell parameters. Owner monitoring should include regular mucous membrane assessment and attention to any changes in energy level or appetite. Horses on long-term immunosuppressive therapy require monitoring for medication side effects including increased infection susceptibility, weight gain, and potential laminitis risk. Documentation of any concerning changes allows prompt veterinary evaluation.

Quality of life considerations for horses with hemolytic anemia are generally favorable when the condition is well-managed. Most horses recovering from acute episodes return to normal lives without ongoing limitations. Those requiring long-term immunosuppressive therapy may have some modifications to management but typically maintain good quality of life. Horses that experience recurrent episodes may require more careful management to minimize triggers. The underlying cause significantly influences long-term quality of life, with infectious causes potentially having different implications than self-limiting toxic or drug-induced cases. Most horses with treatable forms of hemolytic anemia can be expected to live comfortable, functional lives with appropriate management.

Hemolytic anemia in its various forms does not show strong breed predisposition for most causes, though certain breeds face elevated risk for specific types. Neonatal isoerythrolysis occurs more frequently in Thoroughbreds, Standardbreds, and mules due to higher frequencies of the blood group antigens most commonly associated with maternal sensitization. Thoroughbred and Standardbred mares bred to stallions positive for Aa or Qa blood groups face increased risk of producing affected foals if they have been previously sensitized. Mule foals face particularly high risk because donkey blood group antigens are more likely to trigger maternal sensitization in horse mares.

Use and discipline considerations for hemolytic anemia relate primarily to geographic exposure risks and management practices. Performance horses that travel frequently may have increased exposure to blood parasites in endemic regions. Horses used for trail riding in wooded areas have potential exposure to red maple leaves and other toxic plants. Show horses and racehorses under high-stress management may face theoretical increased risk for immune-mediated conditions, though this association is not firmly established. Breeding operations face specific concerns regarding neonatal isoerythrolysis prevention that require attention to mare and stallion blood typing.

Genetic testing recommendations for hemolytic anemia relate specifically to prevention of neonatal isoerythrolysis rather than predisposition to other forms. Blood typing of mares and stallions identifies potential incompatibilities before breeding. Mares that have been previously pregnant or received blood transfusions should be tested for antibodies against common red blood cell antigens. Foals from mares with significant antibody titers should not receive maternal colostrum and should instead receive colostrum from a compatible source or commercial colostrum replacement. This targeted genetic and immunologic testing program effectively prevents neonatal isoerythrolysis when properly implemented. Breeding decisions to avoid high-risk matings can further reduce isoerythrolysis incidence in susceptible populations.

Conditions that commonly co-occur with or complicate hemolytic anemia include various sequelae of red blood cell destruction and underlying diseases that may trigger immune-mediated hemolysis. Liver dysfunction frequently accompanies hemolytic conditions due to the increased bilirubin load from red blood cell breakdown and potential direct effects of underlying diseases. Kidney damage may result from hemoglobin toxicity during intravascular hemolysis. Laminitis can develop secondary to systemic inflammation associated with severe hemolytic episodes. Disseminated intravascular coagulation may complicate severe acute hemolytic crises. Secondary bacterial infections may develop in immunocompromised horses, particularly those on high-dose corticosteroid therapy.

Conditions with similar symptoms that must be differentiated from hemolytic anemia include other causes of anemia and icterus. Blood loss anemia from trauma, gastrointestinal ulceration, or coagulation disorders produces pallor without the icterus characteristic of hemolysis. Primary liver disease can produce icterus without significant anemia through different mechanisms. Bone marrow failure or infiltration produces non-regenerative anemia without evidence of hemolysis. Other causes of exercise intolerance, including cardiovascular and respiratory disease, may mimic mild anemia. Appropriate diagnostic testing, including complete blood count, chemistry panel, and specific testing for hemolysis, differentiates among these possibilities.

Potential complications of hemolytic anemia extend beyond the direct effects of red blood cell destruction. Severe acute anemia can cause cardiovascular collapse and death if not treated promptly. Hemoglobin released during intravascular hemolysis can damage kidney tubules, potentially causing acute kidney injury. Chronic hemolytic conditions may lead to iron overload as iron from destroyed red blood cells accumulates in the liver and other organs. Transfusion reactions can occur in horses receiving blood products, particularly those with prior transfusion history. Long-term corticosteroid therapy for immune-mediated cases carries risks including immunosuppression, weight gain, and laminitis. Relapse of immune-mediated disease remains a concern even after initial successful treatment.