10 Plants Toxic to Horses

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Maple (Acer spp.)

Where it’s found

Thirteen species of maple trees are found throughout the Northern Hemisphere, with a larger distribution in the eastern United States and Canada. The red maple (Acer rubrum) is among the most common, as are the sugar maple (Acer saccharum), silver maple (Acer saccharinum), and box elder (Acer negundo). Only a few species have been associated with the development of clinical signs.

What is the toxin and how does it work?

The toxin is unknown but it damages the red blood cells, making them unable to carry oxygen.

Threat to horses

Most of the case reports and experimental studies are specific to the red maple tree. Other species, especially hybrid species with Acer rubrum in the lineage, may be associated with intoxication. Silver and sugar maples also have been implicated by some research scientists; box elder has not.

  • Ingestion of dry or wilted leaves causes signs; ingestion of fresh leaves does not.
  • Dry and wilted leaves may remain toxic for up to four weeks, but generally do not retain their toxicity over the winter.
  • Generally, leaves dropped after Sept. 15 are considered more toxic, but wilted leaves from branches dropped during summer storms may be just as harmful.
  • It takes about 1.5 lbs to 2 lbs of dried or wilted leaves per 1,000 lbs of a horse’s body weight to cause clinical signs.
  • All organ systems in a horse’s body are affected by the blood cells’ lack of oxygen. The kidneys and liver may be harmed by the red blood cell breakdown products.

Signs

These can occur as early as a few hours after ingestion or be delayed for four to five days. Depression, lethargy, and anorexia usually occur first and are followed by reddish-brown urine and pale yellowish gums and mucous membranes. Later signs include dark-brown muddy gums and mucous membranes, difficulty breathing, inability to rise, and death.

Treatment

Use activated charcoal and mineral oil to decontaminate. Aggressive IV fluids to correct dehydration and protect the kidneys, blood transfusions, ascorbic acid (Vitamin C), nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids may all be necessary.

Prognosis

Good if animals are treated before signs begin. Once evidence of red blood cell damage occurs, aggressive in-hospital treatment will be needed for survival.

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Foxglove (Digitalis spp.), oleander (Nerium oleander), rhododendron (Rhododendron spp.)

Where they’re found

Each of these plants is found to some extent throughout the United States. Different cultivars of foxglove and rhododendron grow and overwinter in just about every state. Oleander is not hardy enough to overwinter in Northern climates but is often found as a houseplant or ornamental container-grown plant.

What is the toxin and how does it work?

Foxglove, oleander, and rhododendron contain toxins known as cardenolides or cardiac glycosides. Cardenolides interfere with the electrical conductivity of the heart, resulting in irregularities in heart rate and rhythm.

Threat to horses

  • Ingestion of any of these plants is associated with death in horses.
  • Cardenolide concentrations are found in all parts of the plant but are highest in the fruit, flowers, and immature leaves. Dried leaves retain their toxicity.
  • Oleander: ingestion of 30 to 40 oleander leaves is deadly.
  • Foxglove: estimated that ingestion of 100 – 120 grams (3-4 ounces) fresh leaves results in clinical signs and death.
  • Rhododendron: toxic dose in horses is not well established but ingestion of 1-2 pounds of green leaves has resulted in signs.

Signs

Signs generally begin just a few hours after ingestion, and most horses are simply found dead. Other early signs include weakness; edema of the head, neck, and eyes; and a slow heart rate that progresses to irregularity. Seizures and inability to rise often occur before death.

Treatment

Rapid development of illness and signs generally make treatment impossible. Veterinarians can use activated charcoal and mineral oil to decontaminate if done so early after ingestion. Other drugs such as atropine and lidocaine that focus on specific cardiac conduction abnormalities may be useful in hospitalized cases. Digoxin-specific Fab fragments have been used successfully in small animals but are cost-prohibitive in horses.

Prognosis

Very poor once signs have developed. Early and aggressive therapy before signs improves the prognosis.

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Bracken fern (Pteridium aquilinum)

Where is it found?

Bracken fern is found throughout the United States in open pastures and woodlands. It prefers moist, acidic soils.

What is the toxin and how does it work?

Bracken fern contains a type I thiaminase enzyme. It works by degrading or destroying thiamine (Vitamin B1) and creating a thiamine analog (fake thiamine) that interferes with nerve function and other bodily processes.

Threat to horses

  • Thiamine is necessary for nerve function. The primary problem with low thiamine in horses is the development of neurological disease.
  • Both fresh and dried bracken fern is toxic if ingested.
  • Some horses develop a taste for bracken fern and seek it out in the pasture and hay.
  • Horses must consume large amounts of bracken fern for days to weeks before signs develop. If the plant composes 20 percent to 25 percent of their diet, signs develop in about three weeks. If it composes 100 percent of their diet, signs occur in seven to 10 days.

Signs

Signs are related to neurological dysfunction and include depression, blindness, gait abnormalities, muscle twitching, and seizures.

Treatment

Administer IV or IM thiamine for days to weeks. Other treatment is primarily supportive and includes nonsteroidal anti-inflammatory agents, IV fluids, and drugs to prevent seizures.

Prognosis

Generally very good if treatment is begun before neurological problems develop. The onset of seizures and blindness is associated with a poor prognosis.

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Black walnut (Juglans nigra)

Where it is found

Black walnut trees have been cultivated in the United States since 1868. They are commonly found in the eastern half of the United States except the northernmost border.

What is the toxin and how does it work?

The toxin is unknown. Many believe that juglone, present in black walnut roots and leaves, is the culprit, but scientists are unable to reproduce toxicosis by oral or dermal exposure to juglone.

Threat to horses

Black walnut shavings are harmful if ingested; leaves, bark, flowers, and nuts are not.

  • Black walnut shavings, often purchased from furniture manufacturers, should not be used as bedding for horses. Examine new bedding that comes from an unknown source for the presence of black walnut shavings, which are much blacker in color than pine shavings.
  • Horses placed on bedding composed of as little as 20 percent fresh black walnut shavings made from either new or old wood develop laminitis (founder) within just a few hours.
  • Early removal of the horse from the bedding generally results in cessation of signs, but laminitis may continue unabated.

Signs

  • Early: Depression, limb edema, stiff gait, laminitis
  • Mid: Colic, increased body temperature
  • Late: Rotation of coffin bone (severe laminitis)

Treatment

Removal of the horses from the shavings as soon as signs are noticed often stops the progression of laminitis. Wash the horse’s feet and limbs with cold water to remove any remaining shavings and help decrease signs of laminitis. Further treatment is based on the signs and generally includes an NSAID—such as flunixin or phenylbutazone—mineral oil, and good farrier care.

Prognosis

Generally very good if horse is removed within a few hours of exposure. Once laminitis develops, the prognosis for a full recovery decreases.

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Tansy ragwort (Senecio spp.)

Where it is found?

More than 70 different species of Senecio are present in the United States (including Oregon). This daisy-like weed is found in hay fields, pastures, ditches, and other unimproved areas. Due to weather conditions and the lack of the tansy's insect predators, tansy growth in Western Oregon has increased in the past few years. Tansy is also toxic to cattle and can cause abortion in both horses and cattle.

What is the toxin and how does it work?

Senecio species plants contain pyrrolizidine alkaloids, which are metabolized to pyrroles in the liver. Pyrroles inhibit cellular division, resulting in production of abnormal liver cells (megalocytes). As the megalocytes die, they are replaced with fibrotic tissue. Not all Senecio species have the same amount of toxin but all contain at least some concentration of pyrrolizidine alkaloids and all are considered harmful.

Threat to horses

  • Both fresh and dried plants are toxic if ingested.
  • The plant is not particularly palatable and most cases occur on overgrazed pastures or in the spring when green grass is scarce.
  • Pyrrolizidine alkaldoids are most harmful to a horse’s liver.
  • Damage to the liver accumulates over time and is irreversible.

Signs

Generally aren’t present until the liver has failed. Once the liver fails, anorexia, weight loss, photosensitization, depression, blindness, unusual behaviors, and jaundice swiftly follow. Signs generally develop after a total ingestion of 50 lbs to 150 lbs, or about 1 percent to 5 percent of a horse’s body weight, for several weeks.

Treatment

There is no treatment once signs are present. If ingestion is suspected and complete liver failure has not developed, supportive care is recommended, but the horse may never return to its previous healthy state. IV fluids, electrolytes, glucose, and B vitamins are useful, as is protecting the horse from the sun.

Prognosis

Very poor to death once liver failure has occurred. Poor for cases of suspected ingestion that are caught earlier.

Control

Information on how to control problem weeds like tansy can be found in the Pacific Northwest Weed Management Handbook.

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Yew (Taxus spp.)

Where it's found

Western yew is common along the West Coast, and eastern yew is common along the East Coast and parts of the central United States. Japanese yew is found throughout much of the United States.

What is the toxin and how does it work?

Yew contains the toxic alkaloid taxine, which primarily affects the heart and respiratory system.

Threat to horses

  • All parts of the plant except the fleshy portion of the red berries are poisonous.
  • The leaves are toxic even when dried.
  • Horses are often poisoned from ingesting discarded yew cuttings found in their pasture or from eating yew-made barn decorations such as wreaths and swags.
  • Ingestion of even a small amount results in signs. Depending on the individual horse, it takes anywhere from a few mouthfuls to 1 lb of leaves per 1,000 lbs of a horse’s body weight to cause death.

Signs

Sudden death is the most common sign. Other signs occur within an hour after ingestion. These signs include a slowed heart rate, difficulty breathing, trembling, lack of coordination, impaired movement, and inability to rise. Death generally follows 15 to 30 minutes after the onset of signs.

Treatment

Rapid development of illness and signs generally make treatment impossible. Veterinarians can use activated charcoal to decontaminate if done so early after ingestion. Other drugs such as atropine and lidocaine that focus on specific cardiac conduction abnormalities may be useful in horses that didn’t ingest a lethal dose.

Prognosis

Very poor to fatal. Sudden death is the normal outcome.

Water hemlock (Cicuta spp.)

Where it's found

Water hemlock is often referred to as the most violently toxic plant in the United States. While found throughout the nation, the plant is less common in the Gulf Coast states. As its name suggests, water hemlock prefers wet areas, such as irrigation ditches, marshes, damp areas in pastures, and riverbanks.

What is the toxin and how does it work?

Water hemlock contains the toxins cicutoxin and cicutol, which affect the neurons in the brain and central nervous system.

Threat to horses

  • The plant’s roots contain the highest concentration of toxins, however horses rarely ingest these. It’s more likely that horses would eat the leaves and stems, which are also poisonous, when grazing in low-lying, moist areas.
  • The amount of toxins in the leaves and stems decreases as the plant ages and further decreases as the plant dries.
  • It takes about 0.2 to 2 lbs hemlock root per 1,000 lbs of a horse’s body weight to cause death.

Signs

These usually occur within an hour after ingestion. Because the toxins target the central nervous system, signs generally include agitation, nervousness, twitching, and seizures. Other signs include excessive salivation, dilated pupils, skeletal muscle weakness, cardiac abnormalities, difficult breathing, and death from respiratory paralysis.

Treatment

Veterinarians can use activated charcoal to decontaminate if the horse isn’t experiencing seizures and it can safely be accomplished. In the case of seizures, veterinarians can use pentobarbital to slow the activity of the horse’s brain and nervous system.

Prognosis

Very poor to fatal once signs have developed. Most horses are found dead within two to three hours after ingestion. Horses alive after eight hours of developing clinical signs are likely to recover, but usually have some residual cardiac and skeletal muscle damage.

Poison hemlock (Conium maculatum)

Where it's found

Poison hemlock is found throughout the United States except for northern Minnesota, North and South Dakota, and eastern Montana. The plant grows in ditches, uncultivated areas, and near water such as swamps and lowlands. Poison hemlock looks similar to water hemlock. The only way to truly tell the difference between the two is by their roots.

What is the toxin and how does it work?

Poison hemlock contains a number of alkaloid compounds including coniine, N-methyl coniine, and gamma-coniine. (Alkaloids are neurotoxins that affect both the central and peripheral nervous systems.)

Threat to horses

  • The poisonous parts of the plant are the leaves, stems, and seeds. These parts increase in toxicity as the plant matures, especially with seeds, and decrease as the plant dies.
  • Most horses will avoid eating this plant; however, it can contaminate hay.
  • It takes about 2 to 8 lbs of plant material per 1,000 lbs of a horse’s body weight to cause death.

Signs

Signs generally occur within one to two hours after ingestion. Nervousness, tremors, twitching, lack of coordination, inability to rise, depression, and decreased heart and respiratory rates are common signs. Seizures occur in rare cases.

Treatment

There’s no specific treatment once signs appear, but supportive care is recommended. Veterinarians can use activated charcoal to decontaminate if the horse isn’t presenting with neurological signs and it can safely be accomplished.

Prognosis

Very poor to fatal. Many horses die from respiratory failure. However, those that survive the acute ingestion usually recover with no residual effects.

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Small flower buttercup (Ranunculus abortivus) and tall buttercup (Ranunculus acris)

Where they're found

The plants are found throughout most of the United States; however, they're rarely found in Western Minnesota, North and South Dakota, and Eastern Montana. Most are weeds found in overgrazed pastures, meadows, and fields. A few varieties are grown as ornamental plants.

What is the toxin and how does it work?

The plants contain the chemical ranunculin, which, when crushed or chewed, becomes the toxin protoanemonin. Protoanemonin is a bitter-tasting oil that irritates the mucous membranes of the gastrointestinal tract.

Threat to horses

  • The plants generally don’t pose a serious threat because the toxin’s bitter taste and ability to cause mouth blisters limits ingestion. However, poisoning can occur in overgrazed pastures where there are little to no other plants for horses to consume.
  • The plants are most harmful when eaten fresh in the pasture or field.
  • The concentration of toxin varies depending on the species and growth stage of the plant. The flower part contains the highest amount of toxin.
  • Dried plant material and contaminated hay aren’t normally toxic because the protoanemonin converts to a nontoxic, nonirritating anemonin.

Signs

These can occur as early as a few hours after ingestion or be delayed up to a day or two, depending on the amount ingested. Nose, lips, face, and skin may blister or swell after direct contact with plant. Blisters in the mouth, oropharynx, and esophagus also are common. Other signs include excessive salivation, an irritated gastrointestinal tract, colic, and bloody diarrhea. Tremors, seizures, and paralysis occur in rare cases.

Treatment

Removal of the horse from the pasture or field as soon as signs are noticed. Veterinarians may use activated charcoal to decontaminate; however, it should be used cautiously due to gastrointestinal tract irritation from the plants’ toxins. Supportive care including fluid therapy, gastrointestinal protectants, and analgesics are recommended.

Prognosis

Excellent with appropriate care. No residual effects have been noted.

Yellow star thistle and Russian knapweed (Centauria spp.)

Where it's found

Centauria spp. is primarily found west of the Mississippi River between the Mexican and Canadian borders. It’s present as a weed in ditches, pastures, and fields.

What is the toxin and how does it work?

The toxin is unknown but suspected to be repin, a sesquiterpene lactone. It affects the neurons in the brain and central nervous system that control chewing. It commonly results in nigropallidal encephalomalacia or the “chewing disease.”

Threat to horses

  • Centauria spp. becomes dangerous when ingested in large amounts for a long period of time. Chronic ingestion of 60 percent to 200 percent of body weight for 30 to 60 days results in the onset of signs.
  • Centauria spp. also becomes a problem when it contaminates dry hay or overtakes a grazing pasture.
  • Only horses are affected by Centauria spp.; even mules and burros do not seem to develop signs when exposed to large amounts.

Signs

Signs don’t occur until the horse has ingested the plant for one to two months. At that time, the horse may experience drowsiness and frequent yawning. Horses will lose the ability to adequately chew food or drink fluids and will become anorexic and dehydrated. Other signs include involuntary facial tics, such as the twitching of the lips and tongue, and clenched facial muscles.

Treatment

There is no treatment once signs are present. The damage to the neurons is irreversible.

Prognosis

Very poor to fatal due to the permanent damage to neurons. Once a horse loses the ability to swallow, it will not return despite aggressive therapy. 

Published: December 8, 2010;    Updated: March 4, 2014

Filed Under: Safety, Equine

 

Author: Lynn Hovda, RPH, DVM, MS, DACVIM. Dr. Hovda is director of veterinary services at SafetyCall International and Pet Poison Helpline in Bloomington, MN. Courtesy of Pet Poison Helpline, 800-213-6680

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