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Ricinus communis: Castor bean
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Family
Euphorbiaceae
Common Names
Castor bean, castor oil plant, higuerilla, palma Christi
Plant Description
Originating in northeastern Africa and southwestern Asia, Ricinus is a monotypic genus that has become widely distributed in most tropical and mild temperate areas of the world. It is grown as a crop plant for its oil, and numerous cultivars have been developed for use as a fast growing ornamental. It is a weed in tropical areas.
Ricinus communis is a perennial except in temperate areas where it is an annual. It is an erect, branching, fast growing herb that attains heights of 15 - 20 feet (5 - 8m) in the tropics. Stems are hollow, hairless, turning red with maturity. Leaves are simple, large, alternate, long petioled, palmate with 5 - 11 lobes, hairless, glossy green, in some cultivars turning red. Inflorescences are terminal panicles with the staminate (male) flowers on top and the pistillate (female) flowers below. Flowers have 3 - 5 fused sepals, no petals and many stamens. The fruits are spiny capsules with 3 characteristically mottled seeds. The immature fruits are bright red in some cultivars, turning brown when mature (Fig. 341, Fig. 342, and Fig. 343).
Figure 341. Ricinus communis.
Figure 342. Ricinus hybrid spiny seed capsule.
Figure 343. Castor beans.
Toxic Principle and Mechanism of Action
Ricin, a glycoprotein (toxalbumin) or lectin present in the seeds, and ricinine, a piperidine alkaloid found in the leaves and seeds are the principle toxic compounds present in the plant [1,2]. Castor oil, commercially extracted from the seeds, contains 90% ricinoleic acid, an unsaturated fatty acid with purgative properties if taken orally. The primary site of action of ricin is on the digestive system epithelium, although the majority of ricin is degraded and passes through the digestive tract with minimal effect. When injected, however, ricin is one of the most toxic biological substances known. Ricin consists of 2 chains of amino acids (A and B chains) linked by a single disulphide bond [3]. The B chain binds to cell receptor sites and facilitates the entry of the A chain into the cell where it enzymatically hydrolyses ribosomal protein thus inhibiting DNA and RNA synthesis [1]. The lectin abrin found in Abrus precatorius similarly affects ribosomal protein synthesis. Once bound to cells the ricin inhibits protein synthesis, prevents intestinal absorption, and is directly irritating to the digestive tract causing a hemorrhagic diarrhea.
Ricinine has strong hemagglutinating properties, and may through its action on neuroreceptors be responsible for the seizures and muscular weakness seen in some animals chewing and swallowing castor beans [4].
Risk Assessment
Castor beans pose the greatest risk to animals and children as the seeds are attractive and are often collected and brought into the domestic environment [5]. Castor bean seed necklaces are commonly acquired by tourists. Intact seeds because of their hard coat will pass through the digestive tract without effect. Seeds that are well chewed and swallowed allow the ricin to exert its toxic effects. Castor bean cake, a product after the castor oil has been extracted, is a source of protein for cattle rations and is toxic unless heat treated. Dogs eating the untreated cake in cattle rations or where it is used as a fertilizer can be poisoned [6].
Clinical Signs
After a delay of 6 hours or more from the time the seeds were chewed and swallowed, severe diarrhea that may be hemorrhagic is the most common clinical effect. Abdominal pain and straining is common. Vomiting, weakness, dehydration, muscle tremors and sudden collapse may develop in severe cases. Serum liver enzymes are often elevated due to hepatic degeneration. In a series of 98 dogs with castor bean poisoning, the most common signs were diarrhea, vomiting, and depression, with 9% of the cases dying or were euthanized [7].
If an animal is witnessed eating castor bean seeds, vomiting using apomorphine should be induced as quickly as possible. Treatment of castor bean poisoning should be directed at preventing dehydration and shock. Activated charcoal orally and intravenous fluid and electrolyte therapy should be maintained until the animal’s digestive system recovers.
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Affiliation of the authors at the time of publication
Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA.
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