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Pyrrolizidine Alkaloidosis (Senecio Poisoning, Ragwort Poisoning)


Rob Bildfell

, DVM, DACVP, Carlson College of Veterinary Medicine, Oregon State University

Reviewed/Revised Oct 2020 | Modified Nov 2022

Typically, pyrrolizidine alkaloidosis is a longterm poisoning that results in liver failure. It is caused by many toxic plants, most commonly of the genera Senecio, Crotalaria, Heliotropium, Amsinckia, Echium, Cynoglossum, and Trichodesma. These plants grow mainly in temperate climates, but some (for example, Crotalaria species) require tropical or subtropical climates. The plants most often implicated are ragwort (Senecio jacobea), woolly groundsel (Senecio redellii, S. longilobus), rattleweed (Crotalaria retusa), and seeds of yellow tarweed (Amsinckia intermedia).

Individual susceptibility varies greatly within species, with young, growing animals the most susceptible. Cattle, horses, farmed deer, and pigs are most susceptible.

These plants, which under normal conditions are avoided by grazing animals, may be eaten during drought conditions. Some animals may eat these plants preferentially as roughage when they are available on extremely lush pasture. Animals are also poisoned by eating the plant material in hay, silage, or pellets. Seeds from Crotalaria, Amsinckia, and Heliotropium species, which have been harvested with grain, have caused pyrrolizidine alkaloidosis in horses.

Short-term poisoning is characterized by sudden death from liver damage and loss of blood from ruptured blood vessels. Animals rarely eat large amounts of these plants because of their poor taste. Longterm exposure is more typical, with the liver reflecting the cumulative and progressive effects of repeated ingestion of small amounts of toxin. Signs may not be seen for several weeks or months after initial exposure. The animal may have stopped eating the offending plant months earlier.

In horses, signs include loss of condition and appetite, dullness, and constipation or diarrhea. The animal may show straining and pain on defecation, and pass bloodstained feces. Fluid can build up within the abdomen, and jaundice may develop. Some animals become progressively weaker and reluctant to move. Liver damage can result in toxic substances accumulating in the blood, which affect brain function. In these animals, signs can also include head pressing, aimless wandering, lack of coordination, or frenzied and aggressive behavior. Animals may crave and eat nonfood substances (such as chalk, ashes, paint chips, clay, plaster, dirt or bones). Death may occur suddenly or after a prolonged coma caused by severe liver disease and high levels of ammonia in the blood.

Diagnosis is based on history, signs, and microscopic examination of liver and kidney tissue collected at necropsy.

Further intake of toxic plant material must be prevented. Animals showing signs rarely recover. Because high protein intake may prove harmful, rations high in carbohydrates are recommended. Veterinary treatment may include methionine in 10% dextrose solution, administered intravenously. Because the liver has a decreased ability to regenerate after pyrrolizidine alkaloid poisoning, the outlook is guarded.

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