Fiddleneck toxicosis in horses is a form of poisoning caused by ingestion of plants from the Amsinckia genus. Horses may ingest the plant while grazing or consume its dried material and seeds in contaminated hay or grain.

Pyrrolizidine alkaloids in fiddleneck species damage the liver gradually, and affected horses may not show signs of poisoning for weeks or months after exposure. Because liver injury can progress after the original exposure, early recognition of contaminated feed or pasture is important even when the horse still appears healthy.

Clinical signs are often vague and may include reduced appetite, weight loss, or changes in behavior before more obvious evidence of liver dysfunction develops. Recognizing potential sources of fiddleneck and preventing further ingestion are critical to protecting exposed horses.

Keep reading to learn how to identify fiddleneck, recognize signs of poisoning, and reduce the risk of equine exposure.

Fiddleneck Poisoning in Horses

Fiddleneck, or Amsinckia spp., is a hairy, yellow-flowered weed associated with liver disease in horses. It belongs to the Boraginaceae family and grows in dry, open areas. [1][2][3]

Horses may consume the plant while grazing or can ingest it in contaminated hay and grain. The plant contains pyrrolizidine alkaloids (PAs), which are compounds that can cause cumulative liver damage. [1][2][3]

Repeated exposure leads to progressive liver fibrosis (scarring) and impaired function. Severe exposures can lead to liver failure.

Since the effects of PAs are cumulative, clinical signs often appear long after ingestion, making it difficult to connect a horse’s illness with a particular pasture or feed supply. [1][2][3]

Traditional names for fiddleneck poisoning include: [1]

  • Walking disease
  • Walla Walla hard liver disease
  • Winter-wheat poisoning

Historical reports of these outbreaks helped connect fiddleneck seed contamination in feed with progressive liver disease in horses. [1]

Common Names for Fiddleneck

  • Rancher’s fireweed
  • Fingerweed
  • Yellow burweed
  • Yellow tarweed
  • Coast fiddleneck
  • Yellow forget-me-not

Table 1. Fiddleneck poisoning in horses at-a-glance

Category Key Information
Definition
  • Cumulative plant toxicosis caused by pyrrolizidine alkaloids in fiddleneck plants (Amsinckia spp.).
Common Causes
  • Consumption of fiddleneck seeds mixed into grain.
  • Ingestion of dried plant fragments or seeds in contaminated hay.
  • Grazing fiddleneck when forage is limited by overgrazing or competition between horses.
Onset
  • Most cases develop gradually after repeated, long-term ingestion.
  • Signs may be delayed for months, sometimes up to a year or longer after exposure.
  • Acute poisoning can occur after a large exposure over a short period.
Symptoms
  • Reduced appetite, weight loss, sluggish behavior, and oral ulcers.
  • Jaundice, abdominal discomfort or distension, swelling of the legs or underside, diarrhea, and red urine.
  • Frequent yawning, excessive drowsiness, head pressing, aimless wandering, incoordination, and abnormal gait.
  • Persistent licking, agitation, delirium, and reduced awareness of fences or obstacles.
  • Photosensitization affecting pale or non-pigmented skin.
Severity
  • Severity depends on the alkaloids and concentrations present, the amount and duration of exposure, and the horse’s age and condition.
  • Jaundice, head pressing, severe incoordination, persistent aimless walking, or inability to rise require prompt veterinary attention.
Treatment
  • Stop feeding contaminated hay or grain and prevent further access to fiddleneck immediately.
  • There is no specific antidote; treatment focuses on supportive care and preserving remaining liver function.
  • Veterinary care may include intravenous fluids, electrolytes, glucose, and nutritional support.
  • Protect horses with photosensitization from sunlight and treat damaged skin or secondary infection as directed.
Recovery Time
  • Severely affected horses may require months of care and may not return to their former level of fitness.
  • Follow-up examinations and laboratory testing are needed because apparent improvement may not indicate complete resolution of liver damage.
Prognosis
  • Some horses with limited liver injury may stabilize and recover after exposure ends, but prognosis is poor once advanced liver disease develops.
  • Prognosis is guarded to poor once substantial fibrosis, liver failure, persistent neurologic abnormalities, or severe debilitation develops.
Prevention
  • Inspect hay fields, pastures, fence lines, and disturbed ground for fiddleneck.
  • Check hay and grain for unfamiliar weeds, plant fragments, or seeds before feeding.
  • Maintain adequate forage supplies, avoid overgrazing, and use pasture rotation to reduce consumption of toxic plants.
  • Hand-pull small fiddleneck populations and mow before seed production where appropriate.
  • Remove suspect feed immediately, retain samples, identify exposed horses, and seek veterinary assessment.

Identification

Fiddleneck plants develop from early rosettes into upright or semi-upright stems as they mature, typically reaching between 6 in and 4 ft (15 cm to 1.2 m) in height.

The stems may be branched or unbranched and are covered in soft to stiff hairs, giving the plant a coarse texture. [1][4]

Leaves are arranged alternately along the stem and are typically lance-shaped, with pointed tips and hairy surfaces. Both basal leaves and leaves growing along the stem may be present. [1][4]

The most distinctive feature is the curved flower cluster, which resembles the neck of a fiddle. Small yellow to orange tubular flowers develop as a cluster along one side of this coiled structure. The cluster gradually straightens as it matures. [4][5][6]

Flowering time varies with location and species, with descriptions extending from late winter and spring into summer. [4][5][6]

In coast fiddleneck, mature fruits separate into two to four small, dark, ridged nutlets containing the seeds. These seeds are often found in dry, sandy soils, particularly in disturbed habitats such as pastures, roadsides, and cultivated areas. Seed contamination is a common source of equine poisoning. [1][2]

Several Amsinckia species share the common name fiddleneck. The genus is native to western North America and parts of South America. Species identification can be difficult because related fiddlenecks resemble one another and may hybridize. Common characteristics include: [1][7]

  • Annual growth habit
  • Upright, sparsely branching stems
  • Hairy or bristly stems and leaves
  • Alternate, lance-shaped leaves
  • Small yellow to orange flowers
  • Curved flower clusters that resemble the neck of a fiddle
  • Small nutlets that contain the seeds

When identification is uncertain, retaining a plant sample for assessment by a knowledgeable adviser or botanist is best. While the coiled flowers can help identify fiddlenecks as a group, they cannot establish the alkaloid content of the plant. [1][5][8]

Toxicology of Fiddleneck

All parts of fiddleneck are toxic to horses, and drying does not make contaminated plant material safe. The main risk for horses comes from pyrrolizidine alkaloids (PAs), although fiddlenecks can also accumulate nitrates. [1][2]

Fiddleneck contains several PAs, including: [1][2][7]

  • Echiumine
  • Intermedine
  • Lycopsamine
  • Sincamidine

Although seeds are a common source of fiddleneck poisoning in horses, they do not always contain the highest toxin concentration in every plant or sample. [1][2][7]

After ingestion, PAs are absorbed from the digestive tract and processed by the liver. Liver enzymes convert the toxic forms into reactive metabolites called pyrroles. These metabolites bind to cellular proteins and DNA, damaging liver cells and interfering with normal cell division. [3][5][9]

The liver is particularly vulnerable because it is the main site where these reactive compounds form. With repeated exposure, some damaged liver cells enlarge without dividing normally. This change is called megalocytosis.

Other cells die, and fibrous tissue progressively replaces damaged areas. Together, these changes disrupt the liver’s structure and reduce the amount of functioning tissue. [3][5][9]

A specific toxic dose has not been established for horses. Poisoning severity depends on: [3][5][9]

  • The particular alkaloids present
  • Alkaloid concentrations
  • The quantity eaten
  • The duration of exposure
  • The horse’s age and condition

Fiddlenecks are less potent than some other PA-containing plants, but Amsinckia spp. can still cause serious disease when a horse consumes enough of the plant. [1][3][5]

Symptoms of Fiddleneck Poisoning in Horses

Acute PA poisoning can follow a large exposure over a short period, causing extensive liver cell death. More commonly, horses develop chronic disease after repeated long-term ingestion. Signs may take months to appear, sometimes up to a year or longer, during which time an affected horse may appear healthy. [3][9]

Early signs are subtle and can resemble other causes of poor condition. Affected horses may show signs of: [4][10]

  • Reduced interest in feed
  • Weight loss
  • Unusually quiet or sluggish behaviour
  • Oral ulcers

These findings are not specific enough to confirm poisoning on their own. [10]

As liver dysfunction advances, affected horses may show signs of: [1][3][7][9]

  • Jaundice, or yellow discoloration of the gums and other mucous membranes
  • Swelling of the legs or underside of the body
  • Abdominal distension from fluid accumulation
  • Abdominal discomfort
  • Diarrhea
  • Red urine

In cases of advanced liver disease, affected horses may develop neurologic signs as ammonia and other compounds accumulate in the brain. This condition is called hepatic encephalopathy and can cause major changes in a horse’s movement and behavior. [4][9][10]

Neurological signs associated with fiddleneck poisoning and equine PA toxicosis include: [1][2][3][9]

  • Frequent yawning
  • Excessive drowsiness
  • Head pressing against solid objects
  • Aimless wandering
  • Incoordination and an abnormal gait
  • Persistent licking of objects
  • Restlessness, agitation or episodes of delirium
  • Reduced awareness of fences and other obstacles

Some horses also develop secondary photosensitization, which makes the skin unusually sensitive to sunlight. [7] In healthy horses, the liver processes byproducts of digestion. When the liver is damaged, one of these substances, phylloerythrin, can build up in the body and react with sunlight. This can damage sensitive skin, especially pale or non-pigmented areas. [7]

Affected skin may become red and swollen before crusts form. This reaction resembles severe sunburn, but the underlying cause is liver dysfunction. [7]

When to Call the Veterinarian

Contact a veterinarian promptly if your horse has had access to fiddlenecks and develops: [4][10]

  • Jaundice
  • Unexplained weight loss
  • Photosensitization
  • Head pressing
  • Severe incoordination
  • Persistent aimless walking
  • Inability to rise

These signs can indicate advanced disease and should not be attributed to training problems or temperament. [4][10]

Owners should also seek veterinary assessment when fiddlenecks are found in feed a horse has been eating, even if the horse shows no signs of illness.

Stop using the feed and retain a sample for examination. Record when the feed was first given, its source, and any batch details. The absence of immediate signs does not exclude exposure-related liver injury. [4][10]

Exposure Risk Factors

Fiddleneck grows naturally in dry, open environments and disturbed soils. The genus is common in the southwestern United States and Mexico, and some species extend into the Great Plains. [1][2][3][7]

The greatest exposure risk for horses comes from contaminated feed. Horses often avoid these plants while grazing but may consume dried fragments or seeds mixed with otherwise acceptable feed. Equine fiddleneck toxicosis outbreaks are associated with seeds mixed into grain. [1][2][3][7]

Limited forage availability increases the risk of poisoning in horses. Overgrazed paddocks and competition between horses can lead animals to eat plants they would otherwise reject. [3][8]

Some horses may be more vulnerable to the effects of pyrrolizidine alkaloids after exposure. Young horses, underweight horses, and those with underlying health conditions have a higher risk of developing serious disease. [2][3][5]

Physiologic demands can also influence how existing liver damage becomes clinically apparent. Pregnancy and lactation increase metabolic demands, which may make previously unrecognized liver dysfunction more apparent in an exposed mare. Pyrrolizidine alkaloids can also cross the placenta, creating additional concern for the developing foal. [2][3][5]

Diagnosis

Diagnosis combines the horse’s exposure history with clinical examination. Because signs can develop months after ingestion, owners should investigate all pastures and feed supplies the horse had access to, even when those paddocks or batches of hay are no longer in use. [2]

Plant identification does not establish how much toxin a horse has consumed, but records of feed purchases and changes in management can help connect the onset of illness with possible exposure.

Veterinarians investigating suspected cases of poisoning may recommend a combination of tests, such as: [2][3][9]

  • Blood tests: Used to look for evidence of liver injury, impaired liver function, and other changes associated with chronic disease
  • Ultrasonography: Allows the veterinarian to evaluate the size, appearance, and structure of the liver and look for changes consistent with chronic damage
  • Liver biopsy: Provides a tissue sample that can be examined for characteristic changes such as fibrosis, liver cell damage, and megalocytosis
  • Specialized toxicology testing: May help identify evidence of pyrrolizidine alkaloid exposure when testing is available, although results must be interpreted alongside the horse’s history and clinical findings

Diagnosis is not confirmed by a particular test. The treating veterinarian makes their diagnosis based on the horse’s history, clinical signs, laboratory findings, and evidence of liver damage.

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Treatment & Management

There is no specific antidote for fiddleneck poisoning. The first priority is to prevent further exposure by replacing contaminated feed and removing access to affected grazing areas. [1][3]

Treatment is primarily supportive and focuses on maintaining the horse while the liver recovers. The liver has some capacity to regenerate after injury, but advanced fibrosis is permanent and can substantially limit recovery once enough functional tissue has been lost. [1][3]

Supportive care may include: [1][3]

  • Intravenous fluids to correct dehydration
  • Electrolyte and glucose support
  • Nutritional support to provide energy while minimizing additional metabolic stress

Horses with photosensitization may need to be protected from sunlight while they are recovering. Topical antibiotics and gentle wound care may be required if secondary skin infections are present. [3][7]

Activated charcoal and other gastrointestinal decontamination measures are unlikely to help once clinical disease appears, as this occurs long after fiddleneck has passed through the horse’s digestive system. [3][10]

Prognosis

Prognosis depends on the extent of liver damage, the horse’s clinical condition, and their response to supportive care. Exposure does not always lead to fatal disease, and some animals with limited injury may stabilize and recover.

However, the outlook is generally guarded to poor once substantial fibrosis or signs of liver failure have developed. [3][9]

Signs that indicate a particularly serious prognosis include: [3][9]

  • Persistent neurologic abnormalities
  • Severe debilitation
  • Extensive fibrosis

Some severely affected horses improve only after months of care and do not return to their former level of fitness. When disease progresses despite treatment or if neurologic signs cannot be controlled, humane euthanasia may be necessary. [3][9]

Continued monitoring is required even after the exposure source has been removed. Appetite or behavior may improve without demonstrating that liver damage has fully resolved. Follow-up clinical examinations and laboratory findings help the veterinarian assess whether the horse is stabilizing or developing progressive disease. [3][9]

Prevention

Prevention involves avoiding contaminated feed and managing fiddleneck growth where horses graze or forage is harvested. [5][10]

Inspecting hay fields before cutting provides an opportunity to identify PA-containing plants while their leaves and flowers remain recognizable. Owners can control small fiddleneck populations by hand pulling adult plants, and mowing before seed production limits seed dispersal in pastures. [5][10]

Maintain adequate forage supply and avoid overgrazing. Pasture rotation and an appropriate stock of feed help reduce reliance on weedy areas. Regularly inspect fence lines, disturbed ground, and places where horses can reach plants outside their enclosure. [5][6]

Owners should also check hay and grain for unfamiliar weeds, fragments or seeds before feeding. [10] If contamination is discovered in purchased feed, stop feeding the suspect supply, retain samples and review which horses received it. Identifying exposure early allows veterinary assessment before obvious signs of liver failure develop. [3][4][8]

Frequently Asked Questions

Here are some frequently asked questions about fiddleneck poisoning in horses:

Summary

Fiddleneck poisoning occurs when horses ingest pyrrolizidine alkaloids in fiddleneck plants, contaminated forage, grain, or seeds. These toxins cause progressive liver damage that may remain unnoticed for months.

  • All parts of fiddleneck are toxic, and drying does not make contaminated forage safe
  • Repeated exposure can cause liver cell damage, fibrosis, impaired function, and eventual liver failure
  • Affected horses may develop weight loss, jaundice, swelling, photosensitization, and neurologic abnormalities
  • Diagnosis combines exposure history with blood tests, ultrasonography, liver biopsy, or toxicology testing
  • Treatment focuses on removing the exposure source and providing supportive care for liver dysfunction
  • Prognosis is guarded to poor once significant fibrosis, liver failure, or neurologic signs develop
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References

  1. Burrows. G. E. and Tyrl. R. J. Toxic Plants of North America. 2nd ed. Wiley-Blackwell. 2013.
  2. Waldridge. B. M. Ed. Nutritional Management of Equine Diseases and Special Cases. 1st ed. Wiley-Blackwell. 2017.
  3. Hovda. L. R. et al. Eds. Blackwell's Five-Minute Veterinary Consult Clinical Companion Equine Toxicology. Wiley-Blackwell. 2021.
  4. Fiddleneck Poisoning in Horses. HorseDVM.
  5. Stegelmeier. B. L. Pyrrolizidine Alkaloid-Containing Toxic Plants (Senecio, Crotalaria, Cynoglossum, Amsinckia, Heliotropium, and Echium Spp.). Veterinary Clinics of North America: Food Animal Practice. 2011.
  6. Amsinckia (Fiddlenecks, Tarweed Fiddleneck). NC State Extension Gardener Plant Toolbox.
  7. Guide to Poisonous Plants. Colorado State University.
  8. Wright. R. G. et al. Common Plant Poisonings of Horses and Their Investigation. Ontario Ministry of Agriculture, Food and Rural Affairs. 2004.
  9. Wilson. D. A. Ed. Clinical Veterinary Advisor: The Horse. Saunders. 2011.
  10. Bildfell. R. Pyrrolizidine Alkaloidosis in Animals. Merck Veterinary Manual. 2024.