Castor Bean (Ricinum communis)

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CASTOR BEAN
(Ricinum communis)
A.K.A
Rosary Pea, Jequirity Bean
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Castor-Bean-PlantCastor Bean Plant Leaves

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Castor bean is a herbaceous 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.

Distribution:
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 commercially 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 stream beds, dumping grounds, barnyards or along roadsides.

Conditions of Poisoning:
All parts of the plants are toxic, but most dangerous are the seeds. One rosary pea has caused death, One or two castor bean seeds are a near lethal dose for adults. 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. Artificial respiration may not preserve life for long because of rapid onset of concurrent vasomotor paralysis.

CALL YOUR VET FOR IMMEDIATE TREATMENT
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 Lone Star English Setter Club provides this information
as a partial reference of the potential poisons that could harm your dog.
We are not veterinarian’s and DO NOT provide medical help.

If you think that your animal is ill or may have ingested a poisonous substance,
contact your local veterinarian or
the ASPCA’s 24-hour emergency poisoning hotline directly

 1-888-426-4435