Hypocalcemia / Eclampsia / Lactation Tetany

Hypocalcemia in horses refers to abnormally low levels of calcium in the blood, a metabolic emergency that can have life-threatening consequences when severe or rapidly developing. This condition is also known as eclampsia when occurring in lactating mares or lactation tetany when specifically related to the calcium demands of milk production. The terms reflect the various circumstances under which horses develop critically low calcium levels, though the underlying metabolic derangement and clinical consequences are similar regardless of the precipitating cause. Calcium is essential for numerous physiological processes including muscle contraction, nerve function, blood clotting, and cardiac rhythm, making its deficiency a true medical emergency.

Hypocalcemia affects horses of various types and ages depending on the underlying cause. Lactation-associated hypocalcemia most commonly affects mares during the first few months after foaling, when the demands of milk production may exceed calcium intake and mobilization capabilities. Transport tetany occurs in horses subjected to prolonged transportation, particularly those that are pregnant or lactating, with stress and reduced feed intake contributing to calcium depletion. Endurance horses and those engaged in prolonged intense exercise may develop hypocalcemia due to calcium losses through sweat combined with inadequate replacement. Any condition that disrupts calcium homeostasis can potentially lead to clinically significant hypocalcemia.

The impact of hypocalcemia on equine health ranges from mild, subclinical disturbances to acute life-threatening crises depending on the severity and rapidity of calcium decline. Calcium is crucial for normal neuromuscular function, and its deficiency produces characteristic signs including muscle tremors, stiffness, incoordination, and potentially tetanic spasms. Cardiac effects can include arrhythmias that may become fatal if uncorrected. The condition known as synchronous diaphragmatic flutter, colloquially called thumps, occurs when the diaphragm contracts synchronously with the heartbeat due to hypocalcemia-induced nerve irritability. Without treatment, severe hypocalcemia progresses to recumbency, seizures, and death.

The treatability of hypocalcemia is excellent when the condition is recognized promptly and appropriate calcium supplementation is administered. Intravenous calcium solutions can rapidly restore normal blood calcium levels and reverse clinical signs, often with dramatic improvement occurring during or immediately after treatment. However, successful outcome depends on timely recognition and intervention, as delayed treatment allows progression to potentially irreversible complications. Understanding the situations that predispose horses to hypocalcemia enables prevention through appropriate management and early intervention. This condition exemplifies the importance of maintaining mineral homeostasis and the serious consequences that can result from its disruption.

The primary causes of hypocalcemia in horses relate to imbalances between calcium losses, demands, and intake. Lactation represents the most significant calcium-demanding physiological state, as mares transfer substantial quantities of calcium into milk for foal nutrition. A lactating mare may lose twenty to thirty grams of calcium daily through milk production, creating demands that can exceed dietary intake and the body's ability to mobilize calcium from bone stores. This is particularly problematic in the first months of lactation when milk production peaks and foals nurse frequently. Mares that produce particularly abundant milk or those with twins are at heightened risk.

Physiological stress from transportation, prolonged exercise, or other demanding circumstances can precipitate hypocalcemia through multiple mechanisms. Transport stress causes reduced feed intake, altered intestinal absorption, and increased calcium losses through sweat and urine. The combination of stress hormones and reduced nutritional intake disrupts normal calcium homeostasis. Endurance exercise produces significant calcium losses through sweat, with horses losing substantial electrolytes including calcium during prolonged exertion. Combined with reduced intestinal blood flow during exercise that impairs absorption, exercise-induced hypocalcemia can develop in horses engaged in demanding athletic activities.

Dietary factors contribute to hypocalcemia risk, including inadequate calcium intake, improper calcium-to-phosphorus ratios, and conditions that impair calcium absorption. Diets high in phosphorus relative to calcium can interfere with calcium metabolism, as can diets high in oxalates that bind calcium and prevent absorption. Sudden dietary changes, particularly during high-demand periods like lactation, may not allow adequate time for metabolic adaptation. Horses grazing on certain pasture types, including those high in oxalate-containing plants, may be at increased risk. Vitamin D deficiency, while uncommon in horses with adequate sunlight exposure, can impair calcium absorption and homeostasis.

Risk factors for hypocalcemia include lactation, particularly in high-producing mares; pregnancy, especially late gestation when fetal calcium demands increase; transportation, particularly when prolonged or when feed access is limited; intense exercise, especially endurance riding; hot weather that increases sweating; pre-existing nutritional imbalances; and concurrent illnesses that reduce feed intake or affect calcium metabolism. Alkalosis from various causes can decrease ionized calcium levels even when total calcium remains normal. Older mares may have reduced ability to mobilize calcium from bone stores efficiently, potentially increasing lactational hypocalcemia risk.

The pathophysiology of hypocalcemia involves disruption of normal calcium homeostasis, which is tightly regulated through the interactions of parathyroid hormone, calcitonin, and vitamin D metabolites. When blood calcium falls, parathyroid hormone normally stimulates calcium release from bone, increases kidney calcium reabsorption, and promotes vitamin D activation for enhanced intestinal absorption. In hypocalcemia, these compensatory mechanisms are overwhelmed by excessive calcium demands or losses. The resulting low ionized calcium concentration affects cell membrane stability and nerve-muscle function. Nerves become hyperexcitable, leading to spontaneous firing and muscular contractions. Cardiac muscle function is also affected, with potential for dangerous arrhythmias. The neuromuscular effects produce the characteristic clinical signs of muscle tremors, stiffness, and eventually tetany.

Early warning signs of hypocalcemia in horses may be subtle and include mild nervousness, slight muscle stiffness, and reduced performance or endurance during exercise. Affected horses may show subtle changes in gait, appearing slightly stiff or uncomfortable. Lactating mares may seem restless or uncomfortable, potentially showing reduced tolerance for nursing. Horses may demonstrate mild anxiety or altered behavior that owners familiar with their normal demeanor might detect. During or after transportation, horses may seem unusually tired or slow to recover their normal energy. Because these early signs are nonspecific, hypocalcemia may not be immediately suspected until more characteristic symptoms develop.

Common symptoms of established hypocalcemia include muscle tremors and fasciculations, often beginning in the large muscle groups of the hindquarters and flanks. Affected horses develop a stiff, stilted gait that may progress to obvious difficulty walking. Trismus, or jaw stiffness, may be observed, with horses showing difficulty opening their mouths normally. Increased sensitivity to stimuli and exaggerated responses to sound or touch reflect the neuromuscular hyperexcitability caused by low calcium. Sweating disproportionate to ambient temperature or exercise level commonly occurs. Horses may show reluctance to move or obvious discomfort when forced to walk.

Behavioral changes in hypocalcemic horses often include anxiety, restlessness, and altered mentation. Affected animals may appear frightened or distressed without apparent cause. Some horses become ataxic, with incoordination that may initially be mistaken for neurological disease. Colic-like signs including pawing, looking at flanks, and assuming uncomfortable postures may be observed. Lactating mares may become irritable with their foals or resistant to nursing. As the condition progresses, horses may show signs of abdominal discomfort or apparent confusion.

Physical signs of hypocalcemia include the hallmark finding of synchronous diaphragmatic flutter, commonly known as thumps. This condition produces visible or palpable rhythmic contractions of the flanks synchronous with the heartbeat, caused by the phrenic nerve firing in response to the electrical activity of the heart due to hypocalcemia-induced nerve hyperexcitability. Elevated heart rate is common, and cardiac arrhythmias may develop. Respiratory rate may be increased. Third eyelid prolapse may be observed. Elevated body temperature from muscle activity commonly occurs. Decreased intestinal sounds may indicate reduced gut motility.

Symptom progression in untreated hypocalcemia follows a predictable pattern of worsening neuromuscular dysfunction. Muscle tremors intensify and spread to involve more muscle groups. Stiffness progresses to obvious reluctance or inability to move normally. Tetanic episodes may occur, with sustained muscle contractions that can be extremely painful. Recumbency develops as the horse becomes unable to support its weight due to muscle dysfunction. Once recumbent, affected horses may be unable to rise despite efforts to do so. Seizure-like activity may occur in severe cases. Without intervention, cardiac arrhythmias may progress to cardiac arrest.

Emergency symptoms requiring immediate veterinary care include obvious thumps, recumbency or inability to stand, severe muscle tremors or tetanic episodes, seizures, apparent collapse, severe cardiac arrhythmias detected on examination, and any combination of the above symptoms in a horse with known risk factors for hypocalcemia. A lactating mare showing any neuromuscular abnormalities should be considered a potential hypocalcemia emergency. Horses that become recumbent during or after transport warrant immediate evaluation. Any horse showing rapidly progressive muscle stiffness, tremors, or neurological signs should receive emergency veterinary attention, as hypocalcemia can progress to fatal outcomes within hours if untreated.

Physical examination of a horse with suspected hypocalcemia focuses on identifying the characteristic neuromuscular signs while assessing cardiovascular stability and overall condition. Careful observation for muscle fasciculations, tremors, and abnormal gait patterns helps identify neuromuscular involvement. The flanks are specifically examined and palpated for synchronous diaphragmatic flutter, a highly suggestive finding for hypocalcemia. Cardiac auscultation assesses heart rate and rhythm, identifying tachycardia or arrhythmias. Mucous membrane color and capillary refill time indicate cardiovascular perfusion status. The jaw is gently manipulated to assess for trismus. Rectal temperature may be elevated due to muscle activity. History regarding lactation status, recent transport, exercise, and feeding is critical for context.

Diagnostic tests for hypocalcemia center on measurement of serum calcium levels, which can confirm the diagnosis when found to be below normal reference ranges. Total calcium and ionized calcium should ideally both be measured, as ionized calcium represents the physiologically active fraction and may be low even when total calcium is normal in certain acid-base disturbances. Normal serum calcium in horses ranges from approximately 11 to 14 mg/dL, with clinical signs typically appearing when levels fall below 6 to 8 mg/dL. Blood chemistry panels also provide information about other electrolytes including phosphorus, magnesium, and potassium that may be concurrently deranged. Magnesium levels are particularly important as hypomagnesemia can cause similar signs and often accompanies hypocalcemia.

Advanced diagnostics may be employed in cases where the cause of hypocalcemia is not immediately apparent or when complications are suspected. Electrocardiography can document and characterize cardiac arrhythmias associated with electrolyte disturbances. Complete blood count and comprehensive metabolic panels assess overall health status and identify concurrent conditions. Urinalysis may reveal information about calcium excretion. In refractory or recurrent cases, parathyroid hormone levels and vitamin D metabolite concentrations may be measured to evaluate the regulatory systems controlling calcium homeostasis. Ultrasound examination may be useful for evaluating complications or concurrent conditions.

Differential diagnosis for hypocalcemia includes other conditions that cause similar neuromuscular signs in horses. Tetanus produces muscle stiffness and spasms but has distinct features including characteristic facial expression and history of wound contamination. Exertional rhabdomyolysis causes muscle stiffness and reluctance to move but typically includes muscle swelling and discoloration of urine. Hypomagnesemia can produce similar clinical signs and commonly occurs alongside hypocalcemia. Colic may be considered when abdominal discomfort is prominent. Neurological diseases including botulism, equine protozoal myeloencephalitis, and cervical spinal cord disease may enter the differential. The combination of appropriate clinical signs with documented low serum calcium confirms the diagnosis, though concurrent electrolyte abnormalities should also be identified and addressed.

Emergency and immediate treatment for hypocalcemia consists of intravenous calcium supplementation, which often produces dramatic improvement in clinical signs within minutes to hours. Calcium solutions, typically calcium borogluconate or calcium gluconate, are administered slowly by intravenous infusion while carefully monitoring the heart for arrhythmias. Rapid administration of calcium can cause dangerous cardiac effects, necessitating slow infusion over ten to thirty minutes with continuous cardiac monitoring. The dosage is calculated based on the horse's body weight and the severity of hypocalcemia. Multiple treatments may be necessary in severe cases, as calcium redistributes into tissues and continuing losses may exceed single-dose replacement.

Medical management beyond initial calcium replacement addresses underlying causes and prevents recurrence. Concurrent magnesium deficiency should be identified and corrected, as magnesium is necessary for proper parathyroid hormone function and calcium homeostasis. Other electrolyte abnormalities detected on blood chemistry should be addressed. Oral calcium supplementation may be initiated once the acute crisis is resolved to support ongoing needs, particularly in lactating mares. Dietary evaluation and modification may be recommended to ensure adequate calcium intake relative to demands. Anti-inflammatory medications may be administered if muscle damage has occurred.

Surgical intervention is not applicable to primary hypocalcemia treatment, though supportive procedures may be necessary in horses that have sustained injuries secondary to falls or during tetanic episodes. Horses that become recumbent may require assistance rising once calcium levels are restored. Padding, positioning, and support during recumbency help prevent pressure injuries and compartment syndrome. In lactating mares with severe hypocalcemia, temporary separation from the foal and reduction or cessation of nursing may be recommended to reduce calcium demands while the mare recovers.

Supportive care for hypocalcemic horses includes stress reduction, quiet environment, and careful handling to avoid stimulating tetanic episodes in animals with hyperexcitable nervous systems. Intravenous fluid therapy supports hydration and provides a vehicle for electrolyte replacement. Pain management may be necessary if muscle cramping has been severe or if the horse has sustained injuries. Monitoring should continue for several hours after initial treatment to ensure response is sustained and to detect any relapse requiring additional treatment. Nutritional support including access to high-quality, calcium-appropriate feeds helps rebuild stores.

Rehabilitation following hypocalcemia focuses on addressing underlying causes and preventing recurrence while supporting the horse's return to normal function. Lactating mares may require modified management including reduced nursing frequency, supplemental feeding of the foal, or dietary calcium supplementation. Horses that experienced hypocalcemia during transport or exercise require evaluation of management practices and conditioning programs. Gradual return to normal activity is appropriate once calcium levels have stabilized and the horse has recovered from any muscle damage or other complications. Follow-up blood work confirms normalization of calcium and other electrolytes.

Treatment decision factors include the severity of hypocalcemia, the underlying cause, the horse's response to initial therapy, and the presence of complications. Most cases of hypocalcemia respond well to appropriate calcium supplementation, but refractory cases may require investigation for concurrent conditions affecting calcium metabolism. The horse's use and value influence decisions about ongoing management modifications. Lactating mares must be managed to balance their own health needs against the nutritional needs of their foals. Owner education regarding recognition of early signs and predisposing factors helps prevent recurrence and ensures prompt treatment if hypocalcemia recurs.

The recovery timeline for hypocalcemia is often remarkably rapid when treatment is initiated promptly, with many horses showing dramatic improvement during or within hours of intravenous calcium administration. Muscle tremors and stiffness typically begin resolving within thirty minutes to two hours of treatment. Horses that were recumbent may be able to stand within hours of therapy, though some require additional time depending on the severity and duration of hypocalcemia before treatment. Complete normalization of all clinical signs usually occurs within twenty-four to forty-eight hours in uncomplicated cases. However, horses that experienced prolonged severe hypocalcemia may have sustained muscle damage or other complications that extend recovery time.

Post-treatment care and monitoring following hypocalcemia includes observation for relapse, which can occur as supplemented calcium redistributes into tissues while underlying causes may continue to drain calcium stores. Serial blood calcium measurements over the first twenty-four to forty-eight hours confirm sustained response to treatment. Lactating mares require ongoing monitoring as they continue to lose calcium through milk production. Dietary modifications should be implemented to improve calcium intake and prevent recurrence. Horses should be monitored for complications including muscle soreness or stiffness from tetanic episodes, injuries sustained during falls or recumbency, and cardiac effects.

Prognosis factors for hypocalcemia recovery are generally favorable, as most horses respond well to appropriate treatment and make full recoveries. Outcomes depend on the severity of hypocalcemia at presentation, the duration of clinical signs before treatment, the presence of complications, and successful identification and management of underlying causes. Horses treated early before progression to recumbency or severe tetany have excellent prognoses. Those that become recumbent may have more variable outcomes depending on the duration of recumbency and any secondary complications. Horses with underlying conditions that predispose to ongoing calcium loss may require long-term management to prevent recurrence.

Long-term outlook for horses that have recovered from hypocalcemia is generally excellent. Most horses return to their previous level of function without lasting effects once calcium levels are normalized and any underlying causes addressed. Lactating mares can typically continue nursing their foals with appropriate dietary management and monitoring. Performance horses can return to competition once recovered, though management practices during transport and competition may need modification to prevent recurrence. Horses that have experienced one episode of hypocalcemia should be considered at risk for future episodes under similar circumstances, necessitating vigilant management during high-risk periods.

Management practices to prevent hypocalcemia focus on maintaining adequate calcium nutrition during high-demand periods and minimizing stress that disrupts calcium homeostasis. Lactating mares should receive diets providing abundant calcium to meet the demands of milk production, with calcium intake beginning to increase in late gestation to prepare for the upcoming lactational demands. Feeding practices should ensure mares consume their entire ration, as selective eating may result in inadequate mineral intake. Stress should be minimized during the peripartum period and early lactation when hypocalcemia risk is highest. Transportation should be avoided when possible during high-risk periods.

Nutritional prevention of hypocalcemia requires attention to calcium content and availability in the diet. Legume hays such as alfalfa provide higher calcium levels than grass hays and may be beneficial for lactating mares. The calcium-to-phosphorus ratio should be maintained at approximately 1.5 to 2 parts calcium to 1 part phosphorus, as high phosphorus levels can interfere with calcium metabolism. Commercial feeds formulated for lactating mares typically provide appropriate mineral balances. Mineral supplements may be indicated when dietary analysis reveals inadequate calcium intake. Vitamin D status, while rarely deficient in horses with adequate sun exposure, should be considered in horses kept primarily indoors.

Exercise and conditioning considerations for hypocalcemia prevention include appropriate training and preparation for endurance exercise, adequate electrolyte replacement during prolonged exertion, and recognition of environmental conditions that increase sweat losses. Endurance horses should have access to electrolyte supplements during competition. Conditioning programs should gradually increase workload to allow physiological adaptation. Hot weather exercise requires additional attention to electrolyte replacement. Horses should not compete at levels beyond their conditioning and preparation.

Environmental factors in hypocalcemia prevention include managing transport stress, maintaining comfortable housing conditions, and avoiding sudden changes that disrupt normal eating patterns. Transportation duration should be minimized when possible, and horses should have access to feed and water during transport. Extreme temperature stress should be avoided or managed with appropriate shelter, ventilation, or blanketing. Herd dynamics should be monitored to ensure lactating mares can eat without competition. Quiet, predictable routines help reduce stress that could affect appetite and calcium homeostasis.

Preventive health care for at-risk horses includes pre-transport or pre-competition veterinary evaluation and blood work to establish baseline calcium and electrolyte status. Prophylactic oral calcium supplementation may be recommended for high-risk individuals before stressful events. Mares with history of lactational hypocalcemia require careful management and monitoring with subsequent pregnancies. Regular monitoring of body condition and milk production in lactating mares helps identify potential problems early. Education of owners regarding risk factors and early warning signs enables rapid recognition and treatment should hypocalcemia develop despite preventive efforts.

Daily management adjustments for horses that have experienced hypocalcemia or are at ongoing risk involve ensuring consistent adequate calcium nutrition and minimizing physiological stress. Lactating mares require daily attention to feed consumption, with any reduction in appetite warranting close monitoring for developing hypocalcemia. Multiple feeding opportunities throughout the day help ensure adequate intake. Water should be freely available and fresh, as hydration affects calcium homeostasis. Daily observation for early signs of hypocalcemia including mild stiffness, nervousness, or changes in nursing behavior enables early intervention before clinical deterioration.

Housing and turnout considerations for at-risk horses balance the benefits of turnout for stress reduction against the need for observation and controlled nutrition. Lactating mares often do well with turnout that allows natural movement and grazing behavior while ensuring access to appropriate supplemental feeds. Housing should protect from temperature extremes that increase metabolic stress. Foaling mares should be in facilities allowing close observation during the high-risk peripartum period. Endurance horses may benefit from housing arrangements that facilitate controlled feeding and electrolyte supplementation.

Exercise modifications for horses with hypocalcemia history depend on the underlying cause of the condition. Lactating mares generally do not require exercise restriction beyond what is appropriate for their reproductive status. Endurance horses that have experienced exercise-induced hypocalcemia may need modifications to training programs, competition distances, and electrolyte replacement protocols. Return to exercise following a hypocalcemia episode should be gradual once the horse has fully recovered and any underlying causes have been addressed. Exercise in extreme heat requires additional attention to electrolyte replacement.

Monitoring and ongoing care requirements for at-risk horses include regular assessment of condition, behavior, and any signs suggesting calcium imbalance. Periodic blood work may be recommended during high-risk periods such as peak lactation or heavy competition schedules. Body weight monitoring helps ensure adequate nutrition. Owners should be educated to recognize early warning signs of hypocalcemia and have veterinary contact information readily available for rapid response. Records of any previous hypocalcemia episodes, including circumstances and treatment, help guide ongoing management.

Quality of life and use considerations for horses with hypocalcemia history are generally positive, as most affected horses recover fully and continue normal lives with appropriate management. Mares that have experienced lactational hypocalcemia can typically continue breeding careers with proper nutritional management. Performance horses, including endurance horses, can return to competition with modifications to electrolyte and conditioning protocols as needed. The key to long-term success is recognition of ongoing susceptibility and proactive management during high-risk periods. With appropriate attention, horses with hypocalcemia history typically enjoy excellent quality of life and can continue fulfilling their intended purposes.

High-risk breeds for hypocalcemia have not been definitively established, as the condition relates more to physiological circumstances than to specific breed genetics. However, certain breed types may face elevated risk based on their typical uses and physiological characteristics. Draft breeds and draft crosses may be at increased risk during lactation due to the larger volume of milk production associated with their body size. High-producing dairy-type mare bloodlines, including some warmblood crosses bred for milk production characteristics, may face increased lactational hypocalcemia risk. Arabian and Arabian-cross horses commonly compete in endurance riding, potentially placing them at higher risk for exercise-induced hypocalcemia.

Use and discipline considerations for hypocalcemia risk relate to the physiological demands of different equine activities. Endurance horses face particular risk during competition due to substantial electrolyte losses through prolonged sweating combined with reduced intestinal absorption during exercise. Broodmares, regardless of breed, face heightened risk during lactation, with prolific milkers at greatest risk. Horses frequently transported for competition or other purposes may be more susceptible to transport-related hypocalcemia. Show horses, particularly those that travel extensively during the competition season, require attention to electrolyte management. Any use that involves physical stress, reduced feed intake, or increased calcium demands increases hypocalcemia risk.

Genetic testing and breeding recommendations for hypocalcemia are not specifically indicated, as the condition is not hereditary in the classical sense. However, mares that have experienced severe or recurrent lactational hypocalcemia may pass physiological traits affecting milk production or calcium metabolism to offspring, suggesting that daughters of affected mares may warrant closer monitoring during their own lactations. Selection for extremely heavy milk production without concurrent attention to calcium metabolism efficiency could theoretically increase population-level hypocalcemia susceptibility. Breeding programs should consider overall metabolic health and avoid selecting exclusively for characteristics that might predispose to calcium imbalances.

Commonly co-occurring conditions with hypocalcemia include hypomagnesemia, which frequently accompanies calcium deficiency and produces similar clinical signs. Magnesium deficiency impairs parathyroid hormone function, potentially worsening calcium imbalances. Hypochloremia and other electrolyte disturbances commonly occur in horses with hypocalcemia, particularly in transport or exercise-induced cases where multiple electrolytes are lost through sweat. Metabolic alkalosis can decrease ionized calcium levels and may accompany electrolyte disturbances. In lactating mares, concurrent conditions affecting milk production or foal health may complicate the clinical picture.

Conditions with similar symptoms to hypocalcemia include tetanus, which causes muscle stiffness and spasms but results from Clostridium tetani toxin rather than calcium deficiency. Exertional rhabdomyolysis produces muscle stiffness, reluctance to move, and distress but includes muscle swelling and myoglobinuria. Colic may be considered when abdominal discomfort is prominent. Various neurological conditions can cause incoordination and abnormal behavior. Azoturia and tying-up syndromes may present similarly. Heat exhaustion produces sweating, distress, and altered behavior. The characteristic finding of synchronous diaphragmatic flutter strongly suggests hypocalcemia, and blood calcium measurement provides definitive differentiation from clinical mimics.

Potential complications of hypocalcemia include cardiac arrhythmias that may become life-threatening if severe and untreated, muscle damage from severe or prolonged tetanic contractions, injuries from falls or during recumbency, pressure-related complications in recumbent horses including muscle necrosis and nerve damage, aspiration pneumonia if the horse is unable to protect its airway during episodes, and in pregnant mares, potential adverse effects on fetal health. Secondary infections may develop in debilitated horses. Foal health may be affected when nursing is disrupted by maternal hypocalcemia. Prompt recognition and treatment minimize the risk of these complications, emphasizing the importance of maintaining awareness of hypocalcemia risk in susceptible horses.