Atypical Myopathy (AM) and Seasonal Pasture Myopathy (SPM) are highly fatal muscle disorders in horses caused by the ingestion of seeds of the box elder or sycamore maple trees.
Seeds of these species contain a compound called hypoglycin A that converts into a toxin once ingested by horses, leading to rapid muscle degeneration.
Clinical signs appear within 12-24 hours of ingestion and include lethargy, muscle weakness, tremors, stiffness, rapid heart rate, and recumbency.
Treatment options are limited as no antidote is currently available. Even with prompt veterinary intervention most horses do not recover. Both box elder and sycamore poisoning have mortality rates ranging from 75 to 90%.
Preventive strategies include removing or fencing off box elder and sycamore maple trees, avoiding overgrazing, limiting turnout during high-risk seasons, and ensuring horses receive a balanced diet. If exposure is suspected, early veterinary intervention provides the best chance of survival.
Causes of Atypical and Seasonal Pasture Myopathies
Horses are at risk of developing Atypical or Seasonal Pasture Myopathies if they consume seeds from box elder or sycamore maple trees. Both species of trees produce seeds that contain hypoglycin A, a protoxin that converts into a toxin after ingestion by horses. [1]
Atypical Myopathy (AM) affects horses in Europe, Australia, and New Zealand and is caused by ingestion of seeds from Acer pseudoplatanus trees, more commonly known as the sycamore maple. [1]
Seasonal Pasture Myopathy (SPM) occurs in North America and is the result of horses feeding on Acer negundo seeds. These trees are commonly referred to as box elders. [1][2]
These conditions are similar in presentation and etiology, both resulting in severe muscle damage with a poor prognosis and high fatality rate.
Box Elder
Box elder, scientifically known as Acer negundo, is a small perennial species of maple tree native to North America. It grows in the southern prairies in western Canada and it can be found across the United States, especially in the north east. [3]
Box elder is dioecious, meaning that male and female flowers are produced on separate trees. The male flowers are long, drooping clusters, while female flowers are shorter and produce winged seeds known as samaras, which are toxic to horses.
The seeds of the box elder maple drop from September to March in most regions. [3]
Key characteristics of this tree species include: [2][3][4][5]
- Habitat: primarily grows close to water sources, including floodplains, near lakes or river shores, and occasionally, along streams in hardwood forests
- Size: mature trees reach up to 50-65 feet (15-20 meters) in height and up to 3.3 feet (1 meter) in diameter
- Bark: young trees and branches have smooth, olive-green bark that develops into gray-brown with shallow cracks as the tree matures
- Leaves: compound, with three to seven leaflets that are ovate at the bottom and pointed at the tip
- Seeds: box elders produce winged seeds (samaras) in clusters. Each seed is 1-2 inches (2.5-5 cm) long
Sycamore Maple
Acer pseudoplatanus, commonly known as the sycamore maple, is a large species of maple native to Central Europe from the Aceraceae family. It is found throughout central and eastern Europe and the mountainous regions of southern Europe. [6]
Note that the sycamore maple is a distinct species from the North America sycamore tree (Platanus occidentalis), which is not toxic to horses.
The tree is dioecious, with male and female flowers on separate trees. Flowering in spring, the sycamore maple produces small, green-yellow flowers in hanging clusters that release seeds that are toxic to horses. Each seed has a wing that helps it to be carried away by the wind, aiding in dispersal.
The seeds of the sycamore maple drop from September to October in most regions. [6]
Other characteristics of this species include: [6]
- Habitat: maple sycamores grow easily in many soil types, making them a popular choice for an urban park or street ornamental
- Size: mature trees reach up to 100-115 feet (30-35 m) in height and up to 24-31 inches (60-80 cm) in diameter
- Bark: young trees and branches have smooth, gray bark that develops into deep gray with deep cracks as the tree matures
- Leaves: large with five pointed lobes, dark green color, up to 7 x 10 inches (18 x 26 cm) in size
- Seeds: paired samaras, each with a wing; samaras grow to 0.2-0.4 inches (5-10 mm) diameter, 1.2-2 inches 3-5 cm (3-5 cm) long
Toxicology
Both atypical and seasonal pasture myopathy are highly fatal acute muscle disorders in horses.
- Atypical Myopathy (AM) is caused by ingesting sycamore maple seeds and occurs primarily in Europe and New Zealand
- Seasonal Pasture Myopathy (SPM) is caused by ingestion of box elder maple seeds and generally affects horses in North America
The two conditions tend to have varied prevalence based on geography. This is due to the range and distribution of the associated trees. [1]
Both species of seeds contain the protoxin hypoglycin A. Hypoglycin A is a naturally occurring amino acid which is not toxic on its own. However, when ingested by horses, it is broken down into the toxic metabolite methylene cyclopropyl acetic acid (MCPA). [1][7]
Once formed, MCPA inhibits cellular enzymes called mitochondrial dehydrogenases that break down fatty acids and aid in energy production of cells. The inhibition of these enzymes causes a condition known as acquired multiple acyl-CoA dehydrogenase deficiency (MADD). [1][7]
MADD disrupts the normal breakdown of fatty acids for energy, leading to lipid (fat) accumulation in the muscles. This results in rapid muscle degeneration. [1][7][8][9][10]
The onset of clinical signs typically occurs 12 to 24 hours after the ingestion of a toxic amount of seeds, and progresses rapidly. Both conditions have an extremely high mortality rate that ranges between 75 and 90%. The majority of fatalities occur within 72 hours from the onset of symptoms. [1]
Risk Factors
Both kinds of myopathies are more frequent during autumn months when seeds of the sycamore maple and box elder tree fall.
A number of additional risk factors may increase the likelihood of a horse ingesting toxic amounts of hypoglycin A containing seeds, including: [1][11]
- Turn out: horses that are turned out for more than 12 hours a day are more likely to eat seeds in the pasture.
- Feed accessibility: horses that do not have access to abundant and healthy forage are more likely to ingest sycamore maple or box elder seeds
- Seasonality: cold weather may be a factor as horses with a negative energy balances require higher calories and may seek out more vegetation from the ground
- Age: young horses, especially those new to the paddock, are at a higher risk of toxicosis
- Size: miniature horses and ponies are at higher risk because their lower body weight means a smaller amount of toxin can cause illness
Symptoms
Atypical and seasonable pasture myopathy primarily affect the horse’s musculoskeletal and respiratory systems as the associated muscle groups deteriorate. [1]
Symptoms present within 24 hours from ingestion and progress rapidly. The most common symptoms include: [1][11]
- Lethargy
- Acute muscular weakness
- Muscle tremors
- Stiffness
- Reluctance to move
- Recumbency (inability to stand)
- Rapid breathing (tachypnea)
- Difficulty breathing (dyspnea)
Less frequently, atypical and seasonal pasture myopathy can affect other organ systems. In these cases symptoms may include: [1]
- Mild tachycardia (increased heart rate)
- Heart murmurs
- Bloody or brown urine
- Dysuria (pain and discomfort while urinating)
- Distended bladder
- Changes in appetite
- Colic
- Dysphagia (difficulty swallowing)
- Dry feces
- Colon impaction
Rarely, affected horses may present ventral edema (swollen abdomen), laminitis, and mild diarrhea.
Diagnosis
Atypical and seasonal pasture myopathies present a significant diagnostic challenge, as the symptoms of both conditions closely resemble those of a number of other conditions. Diagnosis relies on a comprehensive approach that includes history of exposure, clinical signs, and laboratory findings.
Due to the high fatality rate and rapid progression of symptoms, cases are often diagnosed postmortem. [1]
Initial diagnosis is based on history of exposure and clinical presentation. To confirm diagnosis, veterinarians may run a number of laboratory diagnostic tests including: [1][11]
- Blood work: common findings in serum analysis include increases in serum creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activity; complete blood count shows excessive percentage of red blood cells in blood
- Urinalysis: urine samples are tested for the presence of blood, indicating abnormal hemolysis, the breakdown of red blood cells in the muscles
- Muscle biopsy: a sample of muscle tissue is examined under microscope for evidence of lipid accumulation and cell death
Differential Diagnosis
For cases without a known history of exposure, a number of conditions that may present similar symptoms to AM and SPM should be considered. These include: [1][11]
- Ionophore toxicosis (i.e. monensin, lasalocid)
- Nutritional myopathies
- Recurrent exertional rhabdomyolysis
- Polysaccharide storage myopathy
- Post-anaesthetic myopathy
- Immune-mediated myopathy
- White snakeroot (Eupatorium rugosum) toxicosis
- Laminitis
- Colic
- Pleuropneumonia
Post-mortem examination
Since horses usually succumb to AM or SPM before diagnosis, many cases are investigated post-mortem. Veterinarians may submit the horse for necropsy (autopsy) to confirm diagnosis of box elder or sycamore maple poisoning.
Common findings on necropsy include: [1][11][12]
- Hemorrhage in postural and respiratory muscles
- Dark brown urine in the bladder
- Muscle discoloration
- Swelling under the skin (subcutaneous edema) in the neck and sternum
Rarely, hemorrhage in the heart muscle (myocardium) may be present.
Treatment
Unfortunately, survival rates of atypical and seasonal pasture myopathies are extremely low. To date, no specific antidote for either condition is available. Treatment focuses on providing supportive care to minimize further damage and promote recovery. [1][11]
Early intervention is critical in improving the horse’s chances of survival, but it’s important for horse owners to be aware that most equines do not survive this form of poisoning. Treatment mainly aims at limiting further muscle damage, restoring blood volume, correcting metabolic disturbances, and providing pain relief. [1][11]
The first step in treating AM and SPM is removing the animal from the pasture to minimize the risk of further exposure. The animal should be stabled in a comfortable and quiet environment. [11]
Supportive care may include: [1]
- IV fluids
- Stall rest
- Nasogastric feeding
- Pain management
- Dietary support
Detoxification by way of activated charcoal or cathartics is rarely performed as it is only recommended in cases of witnessed, single acute ingestions of seeds.
Medications
Additional treatment options may include administration of the following medications or supplements: [1] [11] [12]
- Insulin: to counteract hyperglycemia
- Antioxidant supplementation: Vitamins E and C may aid in reducing cell damage
- NSAIDs: used to manage pain and inflammation
- Butorphanol: administered in cases of severe pain
- Electrolytes: muscle damage can lead to electrolyte imbalances; the horses’ electrolyte levels should be closely monitored and targeted supplementation administered when necessary
- IV fluid therapy: to prevent dehydration and support detoxification
Prognosis and Prevention
Prompt veterinary intervention is the best way of increasing an affected horse’s chances of survival. However, the prognosis for both atypical and seasonal pasture myopathies is very poor with a mortality rate that ranges between 75 and 90%. [1]
Prevention
Due to the severity of both conditions, the rapid progression of symptoms, the lack of an antidote, and the very high mortality rate, prevention is the only way of ensuring the wellbeing of horses at risk of exposure to box elder or sycamore maple.
Preventive strategies include: [1][2][11]
- Vegetation control: if possible, remove sycamore maple or box elder trees from pastures so there is no risk of exposure; trim low-hanging tree branches to minimize seed exposure
- Fencing: if complete removal is not possible, fence off affected areas and remove seeds from the fence perimeter frequently to minimize the number of seeds in pasture
- Pasture rotation and management: by maintaining horses in healthy pastures, they are less inclined to consume seeds or other toxic plants, favoring safe, palatable grasses instead.
- Turnout management: limiting turnout to less than 12 hours a day for horses grazing on pastures where poisonous trees are nearby during high-risk seasons
- Seasonal adjustments: avoiding introducing horses to new pastures near these trees just prior to or during high-risk seasons when trees are dropping seeds
- Dietary management: ensuring horses receive a good quality, balanced diet reduces the chances of horses feeding on unsafe items that are otherwise unpalatable
Summary
Atypical Myopathy (AM) and Seasonal Pasture Myopathy (SPM) are severe muscle disorders in horses caused by ingestion of seeds from box elder or sycamore maple trees. Seeds from these species contain hypoglycin A, which is metabolized into the toxic compound MCPA, causing rapid muscle degeneration in horses
- Clinical signs typically appear within 12-24 hours from ingestion and include lethargy, muscle weakness, tremors, stiffness, tachycardia, and recumbency
- Treatment options are limited; they focus on limiting further exposure, supportive care, and pain relief
- The prognosis for both conditions is very poor, with mortality rates ranging from 75 to 90%
- Both AM and SPM predominantly occur during autumn when seeds fall to the ground
- Risk factors include prolonged turnout, inadequate feed accessibility, cold weather, body size, and age
- Prevention strategies include removing or fencing off trees, providing abundant high-quality feed, and limiting turnout duration
References
- Hovda, L. R. Blackwell’s Five-Minute Veterinary Consult Clinical Companion Equine Toxicology. Wiley Blackwell. 2022.
- Renier, A. Boxelder Seeds Cause Seasonal Pasture Myopathy in Horses. University of Minnesota. 2021.
- CABI. Acer Negundo (Box Elder). CABI Compendium. CABI. 2019. doi: 10.1079/cabicompendium.2862.
- Acer Negundo (Box Elder) | Native Plants of North America. The University of Texas at Austin.
- Range Map Acer Negundo. Louisiana State University, Baton Rouge. 1999.
- Pasta, S. et al. Acer Pseudoplatanus in Europe: Distribution, Habitat, Usage and Threats. European Commission. 2016.
- Abdenur, J. E. et al. Multiple Acyl-CoA-Dehydrogenase Deficiency (MADD): Use of Acylcarnitines and Fatty Acids to Monitor the Response to Dietary Treatment. Pediatric Research. Nature Publishing Group. 2001. doi: 10.1203/00006450-200107000-00013.
- Bochnia, M. et al. Hypoglycin A Content in Blood and Urine Discriminates Horses with Atypical Myopathy from Clinically Normal Horses Grazing on the Same Pasture. PLOS ONE. Public Library of Science. 2015. doi: 10.1371/journal.pone.0136785.
- Romani, A. M. P. Physiology and Pathology of Mitochondrial Dehydrogenases. Secondary Metabolites – Sources and Applications. IntechOpen. 2018. doi: 10.5772/intechopen.76403.
- Valberg, S. J. et al. Seasonal Pasture Myopathy/Atypical Myopathy in North America Associated with Ingestion of Hypoglycin A within Seeds of the Box Elder Tree. Equine Veterinary Journal. 2013. doi: 10.1111/j.2042-3306.2012.00684.x.
- Votion, D.-M. The Story of Equine Atypical Myopathy: A Review from the Beginning to a Possible End. International Scholarly Research Notices. Hindawi. 2012. doi: 10.5402/2012/281018.
- Finno, C. J. et al. Seasonal Pasture Myopathy in Horses in the Midwestern United States: 14 Cases (1998–2005). Journal of the American Veterinary Medical Association. American Veterinary Medical Association. 2006. doi: 10.2460/javma.229.7.1134
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