English
Death camas toxicosis in horses is an uncommon but potentially life-threatening form of plant poisoning. These highly toxic plants grow across much of North America and may be consumed when pasture forage is sparse or dried plant material contaminates hay.
All parts of death camas contain steroidal alkaloids that disrupt nerve and muscle signaling. Affected horses may develop profuse salivation, colic, lethargy, trembling, weakness, incoordination, a slow heart rate, and difficulty breathing within hours of exposure.
Suspected poisoning requires immediate veterinary attention. Although many horses recover with prompt supportive care, severe cases can progress to collapse, respiratory failure, and death.
Read on to learn how to identify death camas, recognize signs of toxicosis, and understand the diagnosis, treatment, prognosis, and prevention of poisoning in horses.
Death Camas Poisoning in Horses
Death camas refers to a group of highly poisonous perennial plants traditionally classified within the genus Zigadenus. More than 20 species occur primarily throughout North and Central America, with many of the most toxic species concentrated in the western United States. [1]
These plants are named for their resemblance to edible camas species in the genus Camassia. Owners may also confuse their bulbs and grass-like leaves with wild onions or other harmless bulb-forming plants. This similarity has historically resulted in accidental poisoning in people. Livestock exposure generally occurs when animals graze young plants or consume contaminated hay. [1]
Death camas poisoning is uncommon in horses because the plant is intensely bitter and is usually avoided when adequate forage is available. However, horses may ingest it when pasture growth is limited, particularly in early spring when death camas emerges before surrounding grasses. [2]
In equine cases, contaminated hay appears to be a more common source of exposure than direct grazing. Once dried and incorporated into forage, the plant may be more difficult for horses to avoid and for owners to identify. [2]
Clinical signs typically begin within several hours to one day after ingestion. Most affected horses recover within 24 to 48 hours with prompt supportive care, and fatalities appear to be rare in this species.
However, severe poisoning can lead to coma, respiratory failure, and death. Any suspected exposure should be treated as a veterinary emergency. [2]
Other Names for Death Camas
Common names for death camas include:
- Death camas
- Deathcamas
- Poison camas
- Poison onion
- Poison lily
- Poison sego
- Star lily
Table 1. Death Camas Poisoning in Horses at a Glance
| Category | Key Information |
|---|---|
| Definition |
|
| Primary Cause |
|
| Common Exposure Sources |
|
| Onset |
|
| Symptoms |
|
| Severity |
|
| Treatment |
|
| Recovery Time |
|
| Prognosis |
|
| Prevention |
|
Identification
Death camas is a bulb-forming perennial with a grass-like appearance. Plants produce a single erect, unbranched flowering stem surrounded by narrow leaves. Because the leaves emerge early in the growing season and resemble those of grasses or edible camas plants, death camas may be difficult to recognize before flowering. [2][3][4]
Flowers, Star Lily
Depending on the species and growing conditions, plants typically reach 8 to 48 in (20 to 120 cm) in height. Most are considerably shorter in early spring when the leaves first emerge. The stem is upright, smooth, and sparsely leafed. [2]
The leaves arise primarily from the base of the plant. They are long, narrow, and linear to lance-shaped and may be folded or slightly keeled near the base. Smaller, bract-like leaves may also occur along the flowering stem. Their grass-like appearance contributes to the risk of accidental grazing when death camas grows among desirable forage. [2]
Flowers develop in terminal clusters arranged as racemes or branching panicles. Individual flowers are usually white, cream, greenish-white, or yellowish-green, although some species may have a slight purple tinge. Each flower typically has six petal-like segments with one or two visible glands near the base. Depending on the species, the flowers may appear star-shaped or shallowly bell-shaped. [2]
Following flowering, the plant forms three-lobed seed capsules containing several light-brown seeds. The seeds and fruits contain particularly high concentrations of toxic alkaloids. However, young leaves are considered the most hazardous source of grazing exposure because they emerge in early spring before many surrounding forage plants and may be eaten by hungry animals. [2][5]
Death camas grows in a wide range of environments, including dry grasslands, prairies, alpine meadows, bogs, pinewoods, beaches, shrublands, and mountain valleys. Some species have broad geographic distributions, while others are restricted to particular habitats or regions. [2]
Several of the most toxic species, including Zigadenus nuttallii, Zigadenus venenosus, and Zigadenus paniculatus, occur primarily in the western half of the United States. Other species are found across northern North America, the Rocky Mountains, the Appalachians, the Ozarks, and parts of the southeastern United States. [2][5]
Most death camas species begin growing in early spring, flower and set seed, then wither by early summer. This short growing period can make pasture identification difficult later in the season. Although the above-ground foliage may no longer be visible, dried plant material can be difficult to detect when incorporated into hay. [2][4][6]
Positive identification may require assistance from a veterinarian, botanist, or agricultural extension specialist. Because several species differ in appearance and taxonomy, horse owners should avoid relying on a single identifying feature. Any unidentified bulb-forming plant with narrow leaves and pale clustered flowers should be considered potentially hazardous until confirmed otherwise. [2][4]
What's your top priority with your horse's health?
What's your top priority with your horse's health?
Toxicology of Death Camas
All parts of death camas are poisonous to horses. The plants contain a group of cevanine-type steroidal alkaloids related to those found in Veratrum species. [2][5]
Identified compounds include: [2][5]
- Zygacine
- Zygadenine esters
- Germidine
- Neogermidine
- Protoveratridine
The exact combination and concentration of toxins vary among species, individual plants, growth stages, and environmental conditions. [2][5]
Seeds and fruits generally contain the highest alkaloid concentrations. Bulbs may also be highly toxic, particularly after the above-ground portions of the plant have withered. In practical grazing situations, young leaves represent the greatest grazing hazard because they emerge before abundant spring grass is available and are the plant parts most likely to be eaten by livestock. [2][5]
The toxic alkaloids interfere with voltage-sensitive sodium channels found in nerves and muscles. Under normal conditions, these channels open to allow sodium ions to move across the cell membrane, then close so the cell can reset before receiving another signal. Death camas alkaloids bind to open sodium channels and delay their closure. [2][5]
This allows excessive movement of sodium, calcium, and potassium across the cell membrane. As a result, a single nerve stimulus may trigger repeated electrical discharges rather than one controlled response. Nerves and muscles become abnormally excitable before eventually weakening or becoming depressed. [2][5]
The vagal sensory nerves appear particularly sensitive to these alkaloids. Excessive vagal stimulation contributes to a slowed heart rate and low blood pressure, along with dilation of peripheral blood vessels. The same disruption produces effects that may resemble organophosphate poisoning, including: [3][5]
- Salivation
- Frequent urination
- Increased intestinal activity
- Frequent defecation
Neurologic effects include lethargy, trembling, weakness, and incoordination, particularly in the pelvic limbs. In severe cases, progressive nervous system depression can lead to hypothermia, recumbency, coma, and respiratory failure. [3][5]
Death due to death camas poisoning has historically been attributed to cardiac failure, but central respiratory depression is now considered the more likely cause. Severe hypotension (low blood pressure), impaired breathing, and generalized weakness may all contribute to collapse. [3][5]
No toxic dose has been established specifically for horses. Experimental and field estimates in sheep and cattle suggest that serious or fatal poisoning can occur following ingestion of relatively small amounts of highly toxic species. These figures should not be directly applied to horses, particularly because species susceptibility, body size, and plant alkaloid concentrations vary widely. [2][4][7]
Horses rarely consume large quantities of fresh death camas because all parts of the plant are bitter. This natural aversion likely explains why severe and fatal cases are uncommon in equids. However, bitterness may offer less protection when plants are dried, fragmented, and mixed into hay.
Symptoms of Death Camas Poisoning in Horses
Clinical signs of death camas poisoning usually develop several hours after ingestion, although onset may be delayed for as long as one day. The disease generally follows an acute course lasting one to two days.
Hypersalivation is often the first noticeable sign in horses. Saliva may become profuse and frothy, with long strings hanging from the mouth. [2][4][7][8]
Lethargy commonly develops at approximately the same time, and affected horses may stand quietly with a lowered head and drooping ears. [2][4]
Early gastrointestinal and nervous system signs may include: [2][4][7][8]
- Reduced appetite
- Colic
- Bruxism or teeth grinding
- Hunched posture
- Increased intestinal sounds
- Frequent defecation
- Frequent urination
As toxicity progresses, abnormal nerve and muscle activity becomes more apparent. Horses may initially tremble before developing generalized weakness and incoordination. Ataxia is often most noticeable in the pelvic limbs.
Progressive signs may include: [2][4][7][8]
- Muscle trembling
- Pelvic limb ataxia
- Generalized weakness
- Reluctance or difficulty moving
- Drooping ears
- Low body temperature
- Bradycardia (low heart rate)
- Hypotension (low blood pressure)
In severe cases, weakness may progress until the horse has difficulty remaining upright. Advanced cardiovascular and neurologic dysfunction can cause collapse, recumbency, and impaired breathing.
Signs of severe poisoning may include: [2][4][7][8]
- Marked respiratory effort
- Convulsions or spasmodic movements
- Coma
- Respiratory failure
Many horses develop only salivation, lethargy, and gastrointestinal discomfort before recovering. Fatality rates are considered low in horses compared with sheep, which may develop more severe disease after grazing heavily infested areas. Most equine cases resolve within 24 to 48 hours when exposure ends and appropriate supportive care is provided. [2][4][7][8]
When to Call the Veterinarian
Contact a veterinarian immediately if a horse consumes unfamiliar hay or grazes an area containing death camas and develops:
- Sudden profuse salivation
- Lethargy
- Colic
- Trembling
- Weakness
- Incoordination
These signs can also occur with several other serious toxicities, including organophosphate exposure, carbamate insecticide poisoning, botulism, and slaframine intoxication.
Urgent veterinary assessment is particularly important if the horse develops a slow heart rate, low blood pressure, marked weakness, difficulty standing, labored breathing, convulsions, or collapse. Respiratory depression and cardiovascular instability can become life-threatening even though fatalities are relatively uncommon in horses.
Exposure Risk Factors
Death camas poisoning is relatively uncommon in horses because the plant is naturally bitter and generally avoided when adequate forage is available. Most cases occur when horses have little alternative grazing or inadvertently consume the plant in hay. Contaminated hay is considered one of the most significant sources of exposure in horses. [1][2]
The greatest risk for grazing horses occurs in early spring. Death camas is one of the first plants to emerge after winter dormancy, often appearing well before surrounding grasses begin active growth.
Hungry horses turned out onto sparse pastures may sample the young leaves because little other forage is available. Once desirable grasses become established later in the season, horses generally ignore the plant. Owners should account for this risk when transitioning horses to spring pasture. [2][4][6]
Toxicity varies depending on the species of death camas, the plant part consumed, stage of growth, and environmental conditions. Seeds and fruits contain the highest concentrations of alkaloids, while young leaves represent the greatest practical hazard because they are the portions most likely to be grazed during early spring.
Bulbs may also become highly toxic under certain conditions, particularly after the aerial portions of the plant have died back. [2][5]
Environmental factors may influence alkaloid concentrations. Soil moisture stress has been associated with increased toxin production in some species, and seasonal changes can alter the distribution of alkaloids within different plant parts. This means the toxicity of an individual plant may vary from year to year, even within the same pasture. [2][5]
Several species of death camas occur throughout North America, but the greatest livestock risk is associated with Zigadenus nuttallii, Zigadenus venenosus, and Zigadenus paniculatus, which are found primarily in the western United States. Horse owners in these regions should be particularly vigilant when inspecting spring pastures or purchasing hay harvested from native rangelands. [2][5]
Diagnosis
Diagnosis of death camas poisoning is based primarily on exposure history, compatible clinical signs, and plant identification within the horse’s environment because no widely available laboratory test can confirm poisoning in a living horse.
A veterinarian first determines whether the horse recently grazed pasture containing death camas or consumed hay originating from areas where the plant commonly grows.
Since horses frequently ingest the plant accidentally rather than intentionally, careful examination of both pasture and forage is an important part of the investigation. Finding characteristic bulbs, leaves, seed capsules, or flowering stalks supports the diagnosis. [2][5]
Although the clinical signs of toxicosis are not unique to death camas poisoning, their combination following suspected plant exposure is highly suggestive. If gastric lavage is performed shortly after ingestion, plant fragments may be recovered and examined to support identification.
Specialized laboratories may be able to detect steroidal alkaloids in gastrointestinal contents or ocular fluid, although these techniques are not routinely available in clinical practice. [2][5]
In fatal cases, postmortem examination often reveals only subtle abnormalities. Pulmonary congestion, pulmonary edema, scattered hemorrhages, and reddening of the stomach lining may be present, while microscopic lesions are generally nonspecific.
Identifying plant material within the gastrointestinal tract can provide important diagnostic evidence. [2][5]
Treatment & Management
There is no specific antidote for death camas poisoning. Treatment focuses on limiting further absorption of toxins, supporting cardiovascular and respiratory function, and managing clinical signs until the alkaloids are eliminated from the body. Because the disease is typically short-lived, prompt supportive care often results in a favorable outcome. [5][7]
The first priority is to prevent further exposure by removing affected horses from contaminated pasture or discontinuing suspected hay immediately. Any remaining forage should be retained for inspection rather than discarded, as identifying the source of exposure may help protect other horses on the property.
Supportive care is directed toward maintaining circulation, hydration, and organ function. Intravenous fluid therapy may be indicated for horses with dehydration or hypotension. Because the alkaloids stimulate the vagus nerve and commonly produce bradycardia, atropine may be administered to improve heart rate when clinically appropriate. [5][7]
If ingestion is recognized early, a veterinarian may perform gastric lavage to remove plant material from the stomach before additional toxin absorption occurs. Activated charcoal administered through a nasogastric tube may help reduce gastrointestinal absorption of alkaloids. Cathartics may also accelerate intestinal transit, although their effectiveness has not been specifically evaluated for death camas poisoning. [5][7]
Prognosis
The prognosis for horses with death camas poisoning is generally favorable with prompt supportive care. Unlike many poisonous plants that cause irreversible organ damage, death camas produces an acute toxic syndrome that typically resolves as the alkaloids are eliminated from the body. [2][5]
Most affected horses recover completely within 24 to 48 hours after ingestion. Salivation, gastrointestinal signs, weakness, and incoordination generally improve rapidly once further exposure is prevented and cardiovascular function stabilizes. Long-term complications are uncommon in horses that survive the initial poisoning episode. [2][5][7]
The prognosis is more guarded in horses that develop severe hypotension, respiratory depression, prolonged recumbency, or coma. Although fatalities are uncommon in horses compared with sheep, severe poisoning can still be life-threatening if supportive treatment is delayed or unavailable. [2][5]
Prevention
Preventing death camas poisoning begins with careful pasture and forage management. Since horses rarely consume the plant when adequate grazing is available, maintaining productive pastures and avoiding overgrazing substantially reduces the likelihood of exposure.
Horse owners should inspect pastures each spring before turnout, particularly following winter. Young death camas plants are often easiest to identify before surrounding grasses have grown. Remove the plants before they flower and produce seed, taking care to extract the entire bulb where practical. Agricultural extension services or local forage specialists can assist with plant identification when uncertainty exists.
Owners should also inspect hay for contamination, especially if the harvest is from native rangelands or regions where death camas commonly occurs. Because dried plants remain toxic and are more difficult to recognize than fresh vegetation, purchasing hay from reputable suppliers familiar with local poisonous plants can reduce the risk of accidental exposure.
Avoid turning hungry horses onto unfamiliar pastures in early spring when death camas is actively growing and alternative forage is limited. Providing supplemental hay before turnout can reduce exploratory grazing of undesirable plants.
In areas where death camas forms dense populations, integrated pasture management may be necessary. Mechanical removal of individual plants is effective for small infestations.
Herbicide application early in the growing season, before flowering stalks emerge, may also be an option for heavily infested pastures as part of a broader weed management program. Any chemical control program should follow local regulations and label directions while ensuring treated pastures remain safe for grazing.
Although poisoning is relatively uncommon in horses, death camas remains a highly toxic plant throughout much of North America. Routine pasture inspections, careful hay selection, and adequate forage availability remain the most effective strategies for preventing exposure and protecting equine health.
Frequently Asked Questions
Here are some frequently asked questions about death camas poisoning in horses:
Death camas poisoning in horses is an acute and potentially life-threatening condition caused by eating toxic death camas plants. All parts of the plant contain steroidal alkaloids that disrupt normal nerve and muscle signaling, affecting the digestive system, nervous system, heart rate, blood pressure, and breathing. Poisoning is uncommon because fresh death camas tastes bitter, but exposure can occur when grazing is sparse or dried plant material contaminates hay.
Death camas can be identified as a bulb-forming perennial with narrow, grass-like leaves and a single upright flowering stem. Its clustered flowers are usually white, cream, greenish-white, or yellowish-green, and the plant later produces three-lobed seed capsules. Because death camas can resemble grasses, edible camas, and wild onions, owners should ask a veterinarian, botanist, or agricultural extension specialist to confirm the identification rather than relying on one feature alone.
Horses are most likely to encounter death camas in early spring, when its young leaves emerge before many desirable grasses begin growing. The plant occurs in varied habitats across North America, including grasslands, prairies, meadows, shrublands, pinewoods, and mountain valleys. Risk is greatest when hungry horses graze sparse or unfamiliar pastures, although contaminated hay can cause exposure at any time of year.
The first signs of death camas poisoning in horses commonly include profuse or frothy salivation, lethargy, reduced appetite, and colic. Affected horses may also grind their teeth, stand with a hunched posture, urinate or defecate frequently, or have increased intestinal sounds. As poisoning progresses, trembling, weakness, incoordination, a slow heart rate, low blood pressure, and labored breathing may develop.
Signs of death camas poisoning in horses usually appear within several hours of ingestion, although onset may be delayed for up to one day. The condition generally follows an acute course lasting one to two days. Because signs can progress from salivation and gastrointestinal discomfort to collapse or respiratory failure, suspected poisoning requires immediate veterinary attention.
A veterinarian should be called immediately when a horse develops sudden profuse salivation, lethargy, colic, trembling, weakness, or incoordination after eating unfamiliar hay or grazing a potentially contaminated pasture. A slow heart rate, difficulty standing, labored breathing, convulsions, collapse, or coma indicate a particularly urgent situation. Owners should not administer medications or attempt gastrointestinal decontamination without veterinary direction because other poisonings can cause similar signs and may require different treatment.
Death camas poisoning in horses is diagnosed primarily from the exposure history, clinical signs, and identification of the plant in the pasture or hay. There is no widely available laboratory test that can confirm the condition in a living horse, so veterinarians evaluate the animal and inspect possible forage sources. Plant fragments recovered from the stomach or specialized testing for toxic alkaloids may provide additional evidence in some cases.
Death camas poisoning in horses is treated with supportive care because there is no specific antidote. The horse must be removed from contaminated pasture or hay immediately, and the suspected forage should be retained for inspection. Depending on the timing and severity of exposure, a veterinarian may use gastric lavage, activated charcoal, intravenous fluids, or medications to support heart rate and circulation while the toxins are eliminated.
Horses can recover from death camas poisoning, particularly when exposure is recognized quickly and supportive veterinary care is provided. Most affected horses improve within 24 to 48 hours, and long-term complications are uncommon because the toxins do not usually cause permanent organ damage. The prognosis is more guarded when a horse develops severe low blood pressure, respiratory depression, prolonged recumbency, or coma.
Death camas poisoning can kill a horse, although fatalities appear to be uncommon compared with some other livestock species. Severe poisoning may cause profound weakness, collapse, coma, and respiratory failure. Death is believed to result primarily from depression of the brain mechanisms that control breathing, making rapid veterinary treatment essential.
Every part of the death camas plant is poisonous, but seeds and fruits generally contain the highest concentrations of toxic alkaloids. Bulbs can also be highly toxic, particularly after the above-ground portions have withered. Young leaves create the greatest practical grazing risk because they emerge early in spring and may be eaten when other forage is limited.
Hay can contain toxic death camas when the plant is harvested with forage crops. Drying does not destroy the alkaloids, and fragmented plant material may be difficult for horses and owners to recognize once mixed into a bale. Contaminated hay is considered one of the most significant sources of death camas exposure in horses, so suspected hay should be removed from feeding and examined.
Death camas poisoning can be prevented by maintaining adequate forage, avoiding overgrazing, and inspecting pastures each spring before turnout. Horses should not be released hungry onto sparse or unfamiliar pasture, and providing hay before turnout can reduce exploratory grazing. Death camas plants should be removed before they produce seed, while hay should be purchased from reputable suppliers who monitor forage for poisonous plants.
Summary
Death camas is a highly poisonous plant that can cause acute gastrointestinal, neurologic, cardiovascular, and respiratory signs in horses. Prompt veterinary care generally results in a favorable outcome.
- Exposure most often occurs through contaminated hay or grazing young plants when pasture forage is sparse
- Profuse salivation, lethargy, colic, trembling, weakness, incoordination, bradycardia, and hypotension are characteristic signs
- Treatment may include gastric lavage, activated charcoal, intravenous fluids, atropine, and other supportive measures because no specific antidote is available
- Pasture inspections, adequate forage, careful hay sourcing, and removal of death camas plants help prevent poisoning
References
- Eschbacher. E. Five plants poisonous to horses in Wyoming. Barnyards & Backyards. 2008.
- Burrows. G. E. and Tyrl. R. J. Toxic Plants of North America. 2nd ed. John Wiley & Sons. 2013.
- McQuinn. S. and Price. S. D. Horse Owner's Guide to Toxic Plants. Skyhorse Publishing. 2020.
- Death camas (Toxicoscordion venenosum). Colorado State University.
- Plumlee. K. H. Ed. Clinical Veterinary Toxicology. 1st ed. Mosby. 2004.
- Death Camas: Near animal fatality. Klickitat County Noxious Weed Control Board.
- Waldridge. B. M. Ed. Nutritional Management of Equine Diseases and Special Cases. 1st ed. Wiley-Blackwell. 2017.
- Deathcamas Poisoning in Horses. HorseDVM. 2026.
