Myopathies are diseases that primarily cause damage to muscles. They may be present at birth (congenital) or occur due to nutritional imbalances, injury, or ingestion of a poisonous substance. Myositis is an inflammatory reaction in muscle. Common causes include infections, parasitic diseases, and immune-mediated conditions.
Muscle disorders can appear with a variety of signs ranging from muscle stiffness and pain to muscle atrophy, weakness, exercise intolerance, and muscle fasciculations (twitching). The most common signs are muscle pain, stiffness, and reluctance to move due to rhabdomyolysis, which may or may not be related to exercise.
Muscle weakness or damage can also occur as a sign of many different disorders (such as nerve trauma or influenza). Only conditions in which myopathy or myositis are primarily involved are discussed in this section.
Nutritional Myopathies of Horses
Disorders related to vitamin E, selenium (an element required in small amounts for normal nutrition), and fat metabolism can all affect the muscles, leading to inflammation and degeneration.
Selenium or Vitamin E Deficiency
Degeneration of muscle is sometimes associated with a deficiency of selenium or vitamin E. The condition may cause rapid, unexpected death in adult horses. Other affected horses may show a staggering gait, difficulty swallowing, swelling of the cheek and tongue muscles, difficulty breathing, and a rapid heartbeat. Physical changes involve the skeletal muscles and the heart muscle. Blood tests are used to confirm a selenium or vitamin E deficiency and muscle damage (indicated by increases of muscle-associated enzymes). Treatment includes providing selenium and vitamin E.
In foals, this nutritional myopathy may be seen at birth or shortly thereafter and may be accompanied by inflammation of fatty tissue or “yellow fat disease.” Stiffness and pain are noticeable when feeling for the firm, fat masses below the skin, and severely affected foals may be unable to suckle. Treatment involves addressing the underlying dietary deficiency. Vitamin E supplementation appears to be effective.
Exertional Myopathies in Horses
Exertional myopathies in horses involve muscle fatigue, pain, or cramping associated with exercise. Most exercise-associated myopathies result in death of skeletal muscle, which is called exertional rhabdomyolysis. Once considered a single disease, it is now understood that there are several conditions that appear similar but have different causes.
Signs are usually seen shortly after the horse begins to exercise. Excessive sweating, increased breathing rate, rapid heartbeat, reluctance or refusal to move, and firm, painful hindquarters are common. The severity varies between horses and even between episodes in the same horse. Severe episodes may involve muscle damage with kidney failure and reluctance to stand. A diagnosis of exertional rhabdomyolysis is confirmed using blood tests.
Exertional rhabdomyolysis can be sporadic, with single or very infrequent episodes occurring with exercise. It can also be chronic, with repeated episodes, often occurring after mild exertion. Horses of any breed may develop sporadic exertional rhabdomyolysis.
Sporadic Exertional Rhabdomyolysis (Tying Up)
The most common cause of sporadic exertional rhabdomyolysis is exercise that exceeds the horse’s physical condition (level of training, health, etc.). Respiratory disease and deficiencies of sodium, calcium, vitamin E, or selenium in the diet may also play a role. Affected horses generally have no previous history of the condition.
Signs include muscle cramping and stiffness following exercise. Blood tests will reveal elevated levels of certain enzymes. As soon as the condition is diagnosed, exercise should stop and the horse should be moved to a stall with comfortable bedding and access to fresh water. Treatment should aim to relieve anxiety and muscle pain and to correct dehydration and metabolic imbalances. Appropriate tranquilizers or pain relievers may be prescribed to relieve pain and inflammation. Most horses are relatively free of pain within 18 to 24 hours.
Severe rhabdomyolysis can lead to kidney problems. In severely affected animals, regular blood and urine tests are advised to assess the kidney damage. Treatments that induce urination (diuretics) are not recommended except in certain cases (such as in horses receiving intravenous fluid treatment). Your veterinarian will monitor your horse’s kidney function and develop an appropriate treatment plan.
Horses should be kept on a hay diet and stall rest for a few days. The horse should continue to rest with regular access to a paddock until the blood muscle enzyme levels are normal. Because the cause is generally temporary, most horses recover with rest, a gradual return to normal training levels, and dietary changes. Horses ridden for endurance should be encouraged to drink electrolyte-supplemented water during an endurance ride. They should be watched especially closely in hot, humid weather for signs of dehydration or muscle cramping.
Chronic Exertional Rhabdomyolysis
Some horses have multiple episodes of rhabdomyolysis that occur after even light exercise. Four forms of chronic exertional rhabdomyolysis have been identified from samples of muscle tissue (biopsies)—two forms of polysaccharide storage myopathy, malignant hyperthermia, and recurrent exertional rhabdomyolysis.
Type 1 polysaccharide storage myopathy is frequently seen in Quarter horse-related breeds, Morgans, and draft horses but is also present in at least 20 other horse breeds. It is caused by a dominantly inherited gene mutation and can be diagnosed with genetic testing of blood or hair samples. Affected horses often develop episodes of rhabdomyolysis at a young age with little exercise. Rest for a few days before exercise is a common triggering event. Signs include a tucked-up abdomen, a camped-out stance, muscle twitching, sweating, abnormal gait, stiffness in hindlimbs, and reluctance to move. Pawing or colic signs may also occur. Draft horses may have more dramatic signs that include loss of muscle mass, progressive weakness, and lying down.
Type 2 polysaccharide storage myopathy occurs in light breeds such as Arabians, Morgans, Thoroughbreds, a variety of Warmbloods, and some Quarter horses. Diagnosis is based on a muscle biopsy showing specific abnormalities and is supported by negative test results to the genetic test for Type 1 disease. In Quarter horses <1 year old, it may cause difficulty in rising, chronic episodes of muscle stiffness, soreness, and muscle atrophy. Signs may be noticed as a gait abnormality, exercise intolerance, and loss of muscle mass during periods of rest.
Malignant hyperthermia is caused by a different dominantly inherited gene than Type 1 polysaccharide storage myopathy and can also be diagnosed with a genetic test performed on hair roots or blood. The mutation causes both anesthesia-related and non-anesthesia-related rhabdomyolysis in Quarter horses. Signs related to inhalation anethesia include increased heart rate, increased rate of breathing, increased body temperature, and muscle rigidity. Exertional rhabdomyolysis in Quarter horses with the mutation can result in sudden death preceded by excessive sweating and the signs described for anethesia-related events.
Recurrent exertional rhabdomyolysis is most often seen in Thoroughbreds (in which it may be an inherited condition), Standardbreds, and Arabian horses. It is likely due to problems with regulation of calcium within muscle cells. Muscle contraction is intermittently disrupted in otherwise healthy horses, particularly horses that are fit or have a nervous temperament.
Your veterinarian can perform tests to determine the cause of the condition, including blood and urine tests, dietary analysis, exercise testing, and muscle biopsy. An exercise challenge test is useful to detect less severe cases. Determining the severity of the condition during mild exercise is helpful in deciding how quickly to resume training.
Management of this condition is best done by minimizing the factors that lead to an episode and regulating calcium within muscle cells through the use of medication. Techniques to minimize excitement include decreasing stall confinement by using turn-out or a hot walker, exercising and feeding horses with this condition before other horses, providing the company of compatible horses, and careful use of low-dose tranquilizers during training. A high-fat, low-starch diet is helpful.
Unlike horses with polysaccharide storage myopathy, horses that have recurrent exertional rhabdomyolysis often require higher-calorie diets. At these high caloric intakes, specialized feeds designed for horses with this condition are necessary. Simply adding vegetable oil or rice bran cannot supply enough calories for athletes in intense training. Your veterinarian can recommend a diet for a horse with recurrent exertional rhabdomyolysis.
Hyperkalemic Periodic Paralysis
Hyperkalemic periodic paralysis is a hereditary condition that affects American Paint horses, Appaloosas, Quarter Horses, and Quarter Horse crossbreeds. About 4% of Quarter Horses are affected by this condition, which results from an abnormally high level of potassium in the blood. Horses descended from the stallion named Impressive with signs of this condition are strongly suggestive. Diagnosis requires DNA testing of mane or tail hair.
Signs are not always obvious but may include intermittent muscle spasms and weakness. They are usually first identified in foals and young horses up to 3 years of age. A brief period in which muscles stay contracted for much longer than normal and have difficulty in relaxing is often the first sign. In some horses, the third eyelid also slips out of place. Muscle spasms begin on the flanks, neck, and shoulders and may spread to other parts of the body. Most horses remain standing during mild attacks, but weakness with swaying, staggering, dogsitting, or lying down may be seen. Severe attacks last anywhere from 15 minutes to an hour or longer. Breathing and heart rate may increase, but horses remain alert and attentive. Some horses have difficulty breathing due to upper respiratory muscle paralysis. Once an episode is over, the horse can walk or stand normally.
Episodes can be triggered by sudden dietary changes or foods with high potassium content, such as those containing alfalfa hay, molasses, electrolyte supplements, and kelp-based supplements. Lack of food, anesthesia or heavy sedation, trailer rides, and stress may also cause an episode. However, the condition is often unpredictable. Exercise does not appear to trigger episodes.
Many horses recover from episodes of hyperkalemic periodic paralysis without treatment. Owners may treat early mild episodes with light exercise or feeding of grain or corn syrup. In severe cases, emergency treatment from a veterinarian is necessary. If breathing is severely obstructed due to upper respiratory muscle paralysis, a veterinarian may need to perform a tracheostomy (create a hole in the trachea) to allow the horse to breathe. Sudden death is common in severe cases.
To prevent episodes in affected horses, the level of potassium in the body should be reduced. High-potassium feeds, such as alfalfa hay, brome hay, canola oil, soybean meal or oil, sugar molasses, and beet molasses, should be avoided. Grains such as oats, corn, wheat, and barley; beet pulp; and late cuts of timothy and Bermuda grass should be fed in small meals several times a day. Horses should also have regular exercise and frequent access to a large paddock or yard. Pasture is ideal for horses with this condition, because the high water content of live grass reduces potassium intake. Special feeds for horses with this condition are available without a prescription. For horses with recurrent episodes even with dietary changes, there are some drugs that may be helpful. However, use of these drugs during competition is restricted.
Infectious Myopathies in Horses
Bacteria, viruses, and some parasites can infect muscles. In veterinary terms, these are known as infectious myopathies.
Death of body and heart muscle fibers may occur during viral infections such as equine influenza and equine infectious anemia. In most cases, viral-induced muscle damage is a part of effects on multiple organs. Equine influenza 2 has been found to cause severe rhabdomyolysis, and equine herpesvirus 1 has been reported to induce primary muscle stiffness and clinical signs resembling exertional rhabdomyolysis (see above).
Cysts of the sporozoan parasite Sarcocystis are in the muscles of the esophagus in 90% of horses that are at least 8 years old. And 6% of healthy horses also have them in body muscles. Occasionally, heavy infestations occur through contamination of feed with canine feces, resulting in signs of fever, poor appetite, stiffness, weight loss, muscle tremors, muscle decay, and weakness. Diagnosis of sarcocystosis requires history, clinical signs, laboratory tests, and muscle biopsies. Treatment includes anti-inflammatory drugs, antibiotics, and other medications.
Anaplasma phagocytophilum is a parasite that infects cells in the bloodstream and is passed to horses and other animals by tick bites. In rare cases, horses develop clinical signs that may include severe muscle stiffness, fever, malaise, and limb swelling from fluid accumulation (edema). The diagnosis is based on blood tests combined with the clinical signs. A phagocytophilum may also be directly toxic to muscle cells. Treatment should include antibiotics and supportive care.
Streptococcus equi Rhabdomyolysis
Severe rhabdomyolysis can occur in horses with the bacteria Streptococcus equi equi. A stiff gait is the first clinical sign, which progresses rapidly to severely painful, firm, swollen muscles along the back and hindlimbs. Many horses become unwilling to stand, with unrelenting pain that may warrant euthanasia. It is not clear whether death of muscle cells is a direct toxic effect of S equi or is due to release of inflammatory molecules from white blood cells. A diagnosis is based on blood tests or bacterial culture. The prognosis becomes guarded if animals become unwilling to stand.
Appropriate treatment includes a combination of antibiotics. Flushing infected guttural pouches and draining abscessed lymph nodes will diminish the amount of bacteria that are producing toxins. Anti-inflammatory drugs and possibly high doses of short-acting corticosteroids may diminish the inflammatory response and reduce the clinical signs. Control of unrelenting pain is a major challenge in horses with severe rhabdomyolysis. Horses should be placed in a deeply bedded stall and moved from side to side every 4 hours if they are unable to rise. Some horses may benefit from a sling if they will bear weight on their hindlimbs when assisted to stand.
A variety of clostridial bacteria can potentially infect the site of an injection or deep wound, causing local muscle swelling and body-wide toxic effects in horses. Clostridium septicum, C chauvoei, C sporogenes, and mixed infections are associated with a high fatality rate, whereas C perfringens type A has a mortality rate of 20% if treated quickly. Clostridial spores may lie dormant in muscles, or be deposited directly into tissue during trauma. If suitable conditions exist, the spores begin to grow and release powerful toxins. Within 2 days, horses show depression, fever, fast breathing, and swelling at the site of injury. Tremors, unsteadiness, difficulty breathing, recumbency, coma, and death may occur in the next 12–24 hours. Damage to heart muscle occurs in some horses. Blood tests usually reflect a generalized state of weakness and the effects of the toxins.
Examining swollen areas by ultrasonography may reveal areas of fluid and gas accumulation. Samples from affected tissues examined under a microscope may show the bacteria. Samples taken to grow the culture may also help make the diagnosis. Cut tissue from the affected area may reveal abundant fluid with an odor of rancid butter.
Opening the wound and removing infected tissues over the entire affected area is required for successful treatment. Additional treatment includes high doses of injectable antibiotics until the horse is stable (1 to 5 days), combined with or followed by antibiotics by mouth, along with supportive fluid treatment and anti-inflammatory drugs. Extensive skin loss over the affected area is common in surviving horses and will require longterm care.
Staphylococcus aureus, Streptococcus equi, and Corynebacterium pseudotuberculosis are bacteria that commonly cause muscle abscesses. They may develop after penetrating injuries, by spread through the bloodstream, or by spread from a nearby infection. Initially there is an ill-defined inflammation of muscle tissue, which may heal or progress to a well-defined abscess. An abscess may heal, expand, or open to the skin surface with potential for a chronic granuloma with intermittent discharge. Prognosis is usually good for superficial abscesses. Deep abscesses are more difficult to manage successfully. The effect of an abscess on the horse’s gait depends on its location and can vary from mild stiffness to severe lameness. Ultrasonography and culture of fluid from the wound are the best means of diagnosis in superficial sites. Abscesses lying deep within muscles can be difficult to diagnose. Treatment consists of poulticing, lancing, flushing, and draining. Occasionally, surgical removal may be required for complete removal of the abscess. If antibiotics are given, they should be continued for several weeks.
Some myopathies in horses are caused by ingestion of certain plants, drugs, or other toxins.
Certain additives (of a type called ionophores) that are often added to feeds for poultry or livestock other than horses may cause muscle disease. Horses are 10 times more sensitive to ionophores than other species. When equine feed is mistakenly contaminated with ionophores or when horses eat cattle feed, toxicity usually results. Signs include colic, persistent loss of appetite, heart failure with rapid heartbeat, difficulty breathing, diarrhea, stiffness, muscle weakness, and reluctance to stand. Diagnosis requires history of exposure to these drugs and physical signs, along with appropriate laboratory tests. Some animals may die suddenly. Others may develop a longterm heart condition.
Degeneration of skeletal and heart muscles results when some animals consume the toxic portions (often the leaves, fruit, or beans) of certain plants. Coyotillo (Karwinskia humboldtiana), sennas (Cassia species), and white snakeroot (Eupatorium rugosum) have been suggested, but other species also may cause similar damage. Sennas (such as coffee senna and sickle-pod) are common in fields and pastures. Affected animals show weakness and trouble walking, and severely affected animals have unhealthy-looking, degenerated muscles and a strong reluctance to stand. Treatment consists of supplemental feeding and removal of animals from the area in which they ingested the toxic plants.
Some myopathies in horses are caused by problems in the animal’s circulatory system. In ischemic myopathy, the formation of blood clots that block the iliac artery results in extensive damage and death of muscle tissue of the hindlimb due to a lack of blood supply. In post-anesthetic myopathy, complications of general anesthesia may cause changes to muscle tissue due to abnormally low arterial blood pressure induced by gas anesthesia.
Fibrotic and Ossifying Myopathy in Quarter Horses
This condition is seen primarily in working Quarter Horses as a result of injury to the inner thigh muscles after exercise that requires abrupt turns and sliding stops. It can also be caused by trauma or intramuscular injections. Usually, it affects one leg at a time and involves thickening and scarring of connective tissue that progressively worsens. The muscles bond together and eventually harden. The gait is distinctive in affected horses; the forward stride is jerky, and the foot is pulled back a short distance before being placed back on the ground. The hardening of the muscles can be felt in some cases. X-rays and ultrasonography help to establish the degree of bonding and hardening. Treatment involves surgery to cut out the thickened and scarred tissue or to cut the ligament attached at the stifle. Most horses improve after surgery but only about half make a full recovery.
Immune-mediated myositis is characterized by rapid decay of back and hindlimb muscles following injury to blood vessels. This may be an immune-mediated consequence of equine respiratory diseases associated with Streptococcus equi (the bacteria that cause strangles in horses). It is most often seen in Quarter horses less than 8 years old or more than 16 years old. Muscle biopsy provides a diagnosis, and treatment includes antibiotics and steroids. Muscle mass gradually recovers over a few months.