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Pyrrolizidine alkaloids (PAs) are naturally occurring compounds that are toxic to horses and found in many species of plants.
Some common plants that contain high concentrations of PAs include Ragwort (Senecio spp.), Rattlepod, Hound’s tongue, Heliotrope, and Fiddlenecks.
Chronic pyrrolizidine alkaloid poisoning, also referred to as ragwort toxicosis, occurs when horses consume large amounts of these plants for a prolonged period.
This severe and often fatal condition affects the horse’s liver and bile system and causes photosensitization (sensitivity to light), which can result in skin damage and pain.
Signs of chronic exposure may not occur until several weeks or months after initial ingestion. Common symptoms observed in horses include lack of appetite, behavioral changes, head-pressing, colic, and exercise intolerance.
Diagnosing ragwort poisoning in horses is challenging as no specific test is currently available, and signs develop months after exposure to the toxic plant.
To date, no antidote is available. Horses that present clinical signs usually have irreversible liver damage and typically require humane euthanasia.
Pyrrolizidine Alkaloids in Plants
Pyrrolizidine alkaloids (PAs) are a group of naturally occurring organic compounds that are toxic to horses. Plants produce these compounds as a defense mechanism against herbivores and microbial pathogens. [1]
Like other toxic plants, these species are generally unpalatable to grazing animals and are not usually eaten in large quantities if other food is available. However, to protect your horse, it is best to remove any known PA-containing plants from horse pastures.
The concentration of toxic alkaloids varies across different plant species and between individuals of the same species. The concentration also varies between different structures within the plant anatomy. [1]
Pyrrolizidine alkaloids are among the leading causes of photodermatitis in horses, which is characterized by extreme skin sensitivity to sunlight. This hypersensitivity is a secondary complication of liver and bile system damage. [1][2]
When a horse’s liver function is compromised by 80% or more, the organ is unable to eliminate phylloerythrin, which accumulates in the blood. When exposed to sunlight, the excess phylloerythrin causes skin damage that, in turn, results in secondary photosensitization and dermatitis. [2]
Relevant Plant Species
Over 6,000 species of plants are known to produce pyrrolizidine alkaloids that are toxic to horses. They include: [2][3]
- Ragwort (Senecio spp.)
- Hound’s tongue (Cynoglossum officinale)
- Fiddlenecks (Amsinckia intermedia)
Ragwort (Senecio spp.)
There are over 1,200 species of Ragwort worldwide. North America has 70 Ragwort species, of which approximately 25 contain toxic amounts of pyrrolizidine alkaloids. [2]
It is prudent for horse owners and caretakers to assume that all Ragwort species are poisonous for horses.
Senecio spp. can be found in a number of different environments. Some species take root in high-altitude, damp, subalpine regions, while others favor dry, rocky terrains.
General characteristics of Senecio spp. include: [2]
- Flower heads: single layer of green bracts (the leaves that support the flower stalk) that touch each other but do not overlap
- Leaves: alternate leaves, typically lanceolate (flat, long, oblong and pointed) to ovate (shorter with rounded tips) in shape, with symmetrical teeth (the jagged edges of leaves)
- Flowers: bright yellow disk florets surrounded by a ray of yellow petals
- Seeds: dense ring of white pappus (the seeds’ wind-dispersal mechanism) at one end
The concentration of pyrrolizidine alkaloids (PAs), the toxic compounds in Senecio, varies significantly. Mature plants pose a greater threat than young plants. Mature Ridell’s ragwort (S. ridellii) contains the highest PA concentration of species in this family (18% of its dry matter). [2]
Hound’s tongue (Cynoglossum officinale)
Hound’s tongue (Cynoglossum officinale) is a widespread weed commonly found in both cultivated areas and wastelands. It can reach up to 3 feet (1 meter) in height. [4]
General characteristics of Hound’s tongue include: [2][4]
- Leaves: The hound’s tongue’s basal leaves are large and tongue-shaped, reaching up to 20 inches (0.5 meters) in length. Higher leaves are lanceolate in shape
- Flowers: small clusters of reddish-purple flowers are found in clusters on the plant’s terminal stalks
- Fruit: large with thick, fleshy walls that, once mature, split into four brown individual seeds (nutlets)
Fiddleneck (Amsinckia intermedia)
Fiddleneck or Tarweed (Amsinckia intermedia) is an annual weed that can be found in fields and wastelands. It reaches 3 feet (1 meter) in height. [2][5]
The fiddleneck plant is sparsely branched and covered in small, lightly colored hairs. As the plant matures and its flowers start to blossom, the coiled stem unfurls, giving the plant its characteristic “fiddleneck” appearance. [2][5]
Other characteristics include: [5]
- Leaves: lanceolate alternate, hairy leaves
- Flowers: small yellow or orange funnel-shaped petaled-flowers characterized by a “fiddleneck” shape, with all the flowers clustering on one side of the stalk
- Fruit: mature fruits split into 2 – 4 black, ridged seeds (nutlets)
Toxicology
After ingesting plants containing pyrrolizidine alkaloids, the toxic compounds are rapidly absorbed by the horse’s gastrointestinal tract. Once absorbed, pyrrolizidine alkaloids are passed into the liver by way of the portal vein (the blood vessel that carries blood from the GI tract to the liver, spleen, and pancreas). [6][7]
In the liver, the alkaloids are broken down into reactive pyrrole compounds, which damage liver cells and can ultimately cause liver tumors and cancers. [6][7]
Pyrrolizidine alkaloid toxicity is cumulative, meaning its effects build in the liver over time. As such, affected horses may not show any symptoms for long periods of time after initial exposure, even if the horse has already ingested a deadly dosage of toxin.
This makes diagnosis, early treatment, and prevention difficult, as the toxic plant responsible for onset of poisoning symptoms may not be present in the pasture by the time medical intervention is needed. [6][7]
It is possible for horses to develop acute PA toxicity after ingesting a large quantity of PA-containing plants in a short period of time. This form of poisoning is very rare compared to chronic toxicity in horses. [3]
Symptoms in Horses
Horses that ingest a toxic amount of ragwort or related plants over time exhibit symptoms related to liver and biliary system dysfunction, including: [6][8]
- Weight loss
- Anorexia (reduced appetite)
- Aimless walking
- Dull coat
- Ataxia (uncoordinated gait)
- Head pressing
- Excitability
- Jaundice (yellow eyes or gums)
- Colic
- Exercise intolerance
- Ventral edema (fluid build-up in abdomen)
- Diarrhea
- Laryngeal hemiplegia (larynx paralysis)
What's your top priority with your horse's health?
What's your top priority with your horse's health?
Secondary Photosensitization
Photosensitization, also referred to as light-induced dermatitis, is a painful skin condition that causes extreme sensitivity to sunlight. Pyrrolizidine alkaloids-induced photosensitization is categorized as a secondary photosensitization since it is caused by the underlying liver damage rather than direct exposure to a phototoxic agent. [2][6]
Horses with photosensitization may exhibit aversion to bright light or sunlight (photophobia), often squinting or avoiding exposure to direct sunlight. [6][9]
Common skin symptoms of photosensitization in horses include: [6][9]
- Patchy, gradual hair loss (alopecia)
- Skin edema (fluid build-up and swelling)
- Skin lesions
- Itching, particularly on the ears, eyelids, and muzzle
- Red skin
- Formation of pus blisters
- Scabs
The photosensitive reaction can also affect the horse’s lips, gums, and tongue. This can cause oral lesions, sores, ulcers, that make eating uncomfortable. [6][9] Difficulty eating may also lead to unplanned weight loss and poor body condition in severe cases.
Acute Symptoms
Acute toxicosis occurs when horses ingest large amounts (1-5% of their body weight) of alkaloid‐containing plants over a few days.
While rare due to the unpalatable nature of pyrrolizidine alkaloids, ingestion of large doses of these toxic plants can lead to acute hemorrhagic necrosis of the horse’s liver. In this condition, liver tissue dies rapidly, resulting in severe bleeding into the abdomen. [7][10]
Acute ragwort poisoning is rapidly fatal. Symptoms in horses include: [7][10]
- Lethargy
- Coma
- Sudden death
Diagnosis
Diagnosis of chronic pyrrolizidine alkaloid toxicosis is challenging as the ingestion of toxic amounts of PA-containing plants generally occurs months prior to the onset of symptoms. Symptoms appear only when the liver is already irreversibly damaged.
Diagnosis is generally based on a possible history of exposure and the presence of clinical signs. [6][11]
Further diagnostic tools are limited and include: [6][11]
- Serum chemistry: bloodwork to assess liver and kidney function and rule out other conditions
- Liver biopsy: to directly assess the extent of liver damage
- Diagnostic imaging: ultrasound is used to detect liver abnormalities
Differential Diagnosis
Because diagnosing this condition can be challenging, using a differential diagnosis approach is helpful to rule out other potential causes of symptoms similar to pyrrolizidine alkaloid toxicosis in horses.
Conditions to rule out include: [6][7]
- Acute or chronic hepatitis
- Theiler’s disease
- Nigropallidal encephalomalacia (yellow star thistle toxicosis)
- Leukoencephalomalacia
- Equine Protozoal Myeloencephalitis (EPM)
- Alsike clover/red clover intoxication
- Cholangiohepatitis
- Liver abscess
- Viral encephalitis
Post-Mortem Findings
In cases where a horse dies prior to diagnosis, owners may elect for a post-mortem examination (necropsy) to confirm the cause of death.
Common findings on necropsy in cases of PA toxicity include: [6]
- Jaundice (yellowish discoloration of the skin, mucous membranes, and eyes)
- Fluid accumulation in the abdomen (ventral edema)
- Gastric impaction
- Pale, abnormally small liver
- Megalocytosis (abnormally large liver cells under the microscope)
- Pulmonary edema (fluid accumulation in the lungs)
- Lung tissue scarring
Treatment
There is currently no antidote available for ragwort toxicosis and the late onset of symptoms limits treatment options.
The main goal of treatment for pyrrolizidine alkaloid poisoning in horses is aimed at: [3][6]
- Elimination of further exposure
- Supportive care
- Dietary management
Supportive care
Supportive care aims to keep the horse alive until the liver is able to regenerate itself. Treatment options include: [6][12]
- Feeding the recovering horse with a highly digestible, low-protein diet
- Increasing roughage in the diet
- Avoiding high-protein forages (i.e. alfalfa)
- Dietary supplementation with branched chain amino acids, B vitamins, vitamin K, and folic acid
- Keeping recovering horses indoors or blanketed to protect from sunlight
- Topical wound treatment
- Intravenous fluid therapy
Monitoring
Horses diagnosed with pyrrolizidine alkaloid toxicosis should be closely monitored to assess the progression of the condition. Monitoring involves: [6]
- Regular weight checks every two to four weeks; these are crucial indicators of the horse’s overall health and response to treatment.
- Regular blood and serum tests to assess liver function
If a horse is diagnosed with pyrrolizidine alkaloid toxicosis, other horses that share the same pasture should also be examined for signs of toxicity.
Prognosis
The outlook for horses with pyrrolizidine alkaloid toxicosis is poor, as the majority of horses are diagnosed only once the liver damage has reached an irreversible stage. Unfortunately, most affected animals are euthanized due to the low probability of recovery. [6][7]
With proper care, a small percentage of horses can recover. However, these animals require long-term rest and supportive care and are unlikely to return to full performance. [6][7]
Prevention of Ragwort Toxicosis
Due to the current lack of specific treatment options, prevention is the best way to ensure the animal’s well-being.
Prevention strategies include: [6]
- Providing adequate amounts of high-quality forage to minimize the risk of horses ingesting PA-containing plants
- Regular inspection of hay and pastures to identify the presence of pyrrolizidine alkaloid-containing plants
- Avoiding/removing hay lots containing toxic plants
Frequently Asked Questions
Here are some frequently asked questions about PA toxicity in horses:
Pyrrolizidine alkaloids are toxic plant compounds that can damage a horse’s liver when eaten over time. Plants produce these compounds as a natural defense against grazing animals and microbes. In horses, PA poisoning is cumulative, meaning damage builds slowly until serious liver disease, photosensitization, neurologic signs, or fatal complications appear.
Pyrrolizidine alkaloids are dangerous to horses because the liver converts them into harmful compounds that injure liver cells. Over time, this damage can become irreversible before obvious signs appear. Affected horses may develop weight loss, jaundice, colic, behavior changes, poor exercise tolerance, and painful sensitivity to sunlight.
Ragwort poisoning is linked to plants that contain high levels of pyrrolizidine alkaloids, including ragwort, hound’s tongue, and fiddleneck. Horse owners should treat all ragwort species as poisonous, since many contain toxic amounts of PAs. These plants may be eaten when pasture is poor, forage is limited, or toxic weeds contaminate hay.
Ragwort poisoning signs often include weight loss, reduced appetite, dull coat, jaundice, colic, diarrhea, head pressing, excitability, aimless walking, and poor coordination. Some horses also develop ventral edema or exercise intolerance. Symptoms may not appear until weeks or months after toxic plant exposure, once liver damage is already advanced.
Ragwort poisoning can cause photosensitivity when liver damage prevents the body from clearing phylloerythrin, a compound that reacts with sunlight. Horses may squint, avoid bright light, or develop painful skin problems on sun-exposed areas. Common signs include hair loss, swelling, itching, red skin, scabs, pus blisters, and sores around the lips, gums, or tongue.
Symptoms of pyrrolizidine alkaloid poisoning often appear weeks or months after a horse eats toxic plants. This delay happens because PA damage builds gradually in the liver. By the time signs are noticed, the original plants may no longer be visible in the pasture, making diagnosis and early treatment difficult.
Ragwort poisoning is diagnosed using exposure history, clinical signs, bloodwork, liver biopsy, and sometimes ultrasound imaging. Diagnosis can be difficult because there is no single specific test, and symptoms usually appear long after ingestion. Veterinarians may also rule out other causes of liver disease, neurologic signs, colic, or photosensitivity.
Pyrrolizidine alkaloid poisoning has no antidote, so treatment focuses on stopping further exposure and supporting the horse. Care may include a highly digestible, low-protein diet, more roughage, avoiding alfalfa, vitamin support, fluids, indoor housing, blanketing, and wound care. Prognosis is poor once clinical signs appear.
Horses can occasionally recover from PA toxicity, but most cases are diagnosed after severe, irreversible liver damage has already occurred. Recovery requires long-term rest, careful monitoring, supportive care, and strict avoidance of further toxic plant exposure. Even horses that survive are unlikely to return to full athletic performance.
Ragwort poisoning prevention starts with reducing access to PA-containing plants in pasture and hay. Horse owners should provide enough good-quality forage, inspect pastures regularly, remove toxic weeds, and avoid hay lots contaminated with ragwort, hound’s tongue, fiddleneck, or related plants. Shared-pasture horses should also be checked if one horse is affected.
Summary
Pyrrolizidine alkaloids (PAs) are toxic compounds produced by over 6,000 plant species worldwide, including ragwort. When ingested by horses, PAs are metabolized in the liver into reactive compounds, damaging liver cells and potentially leading to hepatic tumors.
- Affected horses can develop secondary photosensitization, resulting in hair loss, skin lesions, swelling, and itchiness
- Chronic exposure to pyrrolizidine alkaloids can result in weight loss, anorexia, exercise intolerance, and behavioral changes
- Diagnosing ragwort poisoning is challenging because horses develop symptoms long after ingesting the toxic plants
- Treatment focuses on supportive care, dietary management, and avoiding further exposure to toxins
- The prognosis is poor, with most cases resulting in euthanasia due to irreversible liver damage
- Prevention strategies include providing adequate forage and regular pasture inspections
References
- Schramm, S. et al., Pyrrolizidine Alkaloids: Biosynthesis, Biological Activities and Occurrence in Crop Plants. Molecules. 2019. doi: 10.3390/molecules24030498.
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- Plumlee, K. H., Ed., Clinical Veterinary Toxicology. Mosby, St. Louis, Mo. 2004.
- Common Hound’s-Tongue - Montana Field Guide.
- Amsinckia (Fiddlenecks, Tarweed Fiddleneck) | North Carolina Extension Gardener Plant Toolbox.
- Hovda, L. R., Blackwell’s Five-Minute Veterinary Consult Clinical Companion Equine Toxicology. Wiley Blackwell. 2022.
- Bildfell, R., Pyrrolizidine Alkaloidosis in Animals - Toxicology. MSD Veterinary Manual. 2022.
- Ragwort Poisoning. Irish Horse Welfare Trust. 2015.
- Wilson, D. A., Ed., Clinical Veterinary Advisor: The Horse. Elsevier Saunders, St. Louis, Mo. 2012.
- Bildfell, R., Pyrrolizidine Alkaloidosis (Senecio Poisoning, Ragwort Poisoning) - Special Pet Topics. MSD Veterinary Manual.
- LLC, H., Pyrrolizidine Alkaloid Toxicity | HorseDVM Diseases A-Z.
- Equinews Editor, Sunburn and Photosensitivity in Horses. Kentucky Equine Research. 2004.
