Veterinary Medicine Library

Castor Bean (Ricinus communis)

| Description | Distribution | Conditions of poisoning | Control | Toxic principle | Clinical signs | References

Castor Bean


Castor bean is a herbacious annual which can reach to nearly 15 feet tall when growing in open spaces in warm climates. Large leaves are alternate, palmately lobed with 5-11 toothed lobes. Leaves are glossy and often red or bronze tinted when young. Flowers appear in clusters at the end of the main stem in late summer. The fruit consists of an oblong spiny pod which contains three seeds on average. Seeds are oval and light brown, mottled or streaked with light and dark brown and resemble a pinto bean. The plant itself is fast growing, but the seeds require a long frost-free season in order to mature.

Castor Bean - early growth Castor Bean - mid-summer Castor Bean Castor Bean Flowers
     Early growth In mid-summer stalk and flower bud        flowers


Castor bean is native to the tropics (Africa) but is planted as a garden plant throughout the U.S. for its large, striking appearance. It is now commerically grown in the U.S. in Illinois, Missouri, Kansas, Oklahoma, Oregon and California. As a result, it is naturalized in the south where winters are mild and most often is found near streambeds, dumping grounds, barnyards or along roadsides.

Conditions of poisoning

All parts of the plants are toxic, but most dangerous are the seeds. The most susceptible animal species include cattle, horses, sheep, pigs, fowl, rabbits and other small animals. Seeds ingested at 0.2% of body weight have caused toxicosis in cattle and 0.01% of body weight was toxic to horses.

Toxic principle

The principle toxin of castor bean is ricin which is a lectin, also termed a toxalbumin. Ricin may comprise up to 3% of the seed weight. Toxalbumins are very toxic plant-derived compounds that combine carbohydrate and protein moieties or components. Ricin is water soluble and is not present in castor oil. Taken orally, ricin is readily absorbed from the stomach and intestine. Another phytotoxin in castor bean, ricinine, is reportedly goitrogenic, but the significance of this compound is not clearly established.

Clinical signs

Signs appear after a characteristic lag period of a few hours to days, usually between 12 hours and 48 hours. Signs support nausea and include evidence of abdominal pain, bloody diarrhea, tenesmus, and dehydration. Additional signs may be anorexia, cessation of rumination, excessive thirst, weakness, muscle twitching, dullness of vision, convulsions, dyspnea, opisthotonus and coma. At postmortem severe inflammation of the stomach and intestine are evident.

Sometimes convulsions and decreased tendon reflexes are observed. After convulsions, death may result from paralysis of the respiratory center. Artifical respiration may not preserve life for long because of rapid onset of concurrent vasomotor paralysis.

In ducks, there is an ascending paralysis which may be confused with botulism. Sometimes thousands of ducks as well as geese are poisoned.

For horses, signs include trembling, sweating, dyspnea, incoordination, vigorous heart contractions, shivering, cold extremities, depression, increased body temperature, weak pulse, constipation or diarrhea, and convulsions.

Cattle may have diarrhea stained with blood.

Pigs have frequent vomiting.

Poultry show signs of depression, roughened feathers, droopy wings, greyish wattles and combs, and emaciation. Egg production ceases and premature moulting may begin.

Other References:

Caster bean entry in Wikipedia

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