Ricinus communis
Castor bean
Small evergreen tree up to 2.5x2 metres. Large leaves 5 - 9 pointed palmate leaves 45 - 60cm in diameter. The leaves are serrate with prominent veins, brilliant green or reddish bronze colour. The flowers grow as upright clusters with the red female flowers at the top. These develop into a 3 lobed fruit that is green/red with a soft spiny exterior. These are about 2.8cm long and the beans that develop inside these are about 1.3cm, brown, often mottled or streaked and look like a well fed tick.
Several native plants could be mistaken for castor plants. Seven finger (Schefflera digitata, pate) has similarly shaped leaves, but they are usually glossy and green, not red. It also tends to grow in the bush rather than out in the sun.
Fairly frequent on waste ground in northern areas near Auckland, Waikato and Bay of Plenty but cultivated in colder climates including the Manawatu.
The toxic protein ricin is concentrated in the beans. It is a potent cytotoxin which inhibits protein synthesis by irreversibly inactivating ribosomes. Ricin is a water soluble protein which is inactivated by heat therefore the commercial castor oil derived from the beans is not toxic. The beans also contain another toxic protein which causes haemagglutination, and a neurotoxic alkaloid (ricinine) has been extracted from the leaves. The seeds are the primary source of ricin, the rest of the plant is less toxic. There is only a problem when the coat of the seed is damaged, e.g. if it was chewed and opened. Poisonings tend to occur in spring and summer as this coincides with the formation of the beans. Poisonings can occur when there has been contamination of foodstuffs with the castor beans e.g. in hay. Care should be taken as to rid pastures of this plant before harvest or at least remove its flowers. The plant should never be grown in gardens where young children could gain access to the beans. Ricin is toxic enough to have been used as an "untraceable" assassination weapon. Experimental methods for detecting ricin have been described.
All. Single oral lethal dose: horse 0.1g/kg, ox 2g/kg, calf 2.5g/kg, sheep 1.25g/kg, goat 5.5g/kg, pig 1.4g/kg, piglet 2.4g/kg, rabbit 1g/kg, goose 0.4g/kg, hen 14g/kg. Ricin has the potential to be used for bioterrorism, in which case an aerosol is the most likely route of exposure. The toxic dose is much lower by this route.
In people a burning sensation in the mouth and throat, nausea, vomiting, sedation and gastroenteritis have been reported. In 18 - 24 hours after ingestion (can be a latent period of 2 - 3 days) there is depression and a mild increase in temperature. In animals the signs are associated with gastroenteritis and also staggering convulsions, coma and death. The gastrointestinal signs include vomiting, diarrhoea (may be bloody), abdominal pain, stomach irritation. Cardiovascular; circulation collapse, increased heart rate, profuse sweating, maybe haemaglobinuria, eventually collapse, convulsions and death usually within 36 hours. Inhalation (onset of symptoms is likely within 8 hours) of ricin is expected to produce cough, dyspnea, arthralgias, and fever and may progress to respiratory distress and death, with few other organ system manifestations.
There can also be a chronic form cause by inhalation of dust and castor bean pomace causing dermatitis and inflammation of the nose and eyes.
Haemorrhage and oedema of gastrointestinal tract. Haemolysis and degenerative change in the kidney. The gut can be fluid filled with patchy inflammation of the gastric and intestinal mucosa occasionally with punciform haemorrhage. The mesenteric lymph nodes may be swollen. The liver, kidney and spleen may also be swollen and oedematous or may be unaffected. The lungs may also be oedematous with froth in the trachea.
Based on clinical signs: The effects maybe immediate or delayed.
Rhododendron, acorn, ethylene glycol, Oxalis species, arum lily, tutu, other plant poisonings, nitrate/nitrite, superphosphate, heavy metals, copper, OP poisoning, metaldehyde, anticoagulant rodentcide, 1080
Remove the bean gastric lavage/emesis, maintain circulation with fluids/ blood transfusions. Alkalising the urine may help to prevent haemoglobin products in the kidney. Sedation may be indicated.
Poor.
Remove plants from pasture. There is research into vaccine for people, but no products yet.
Audi J. Belson M. Patel M. Schier J. Osterloh J. Ricin poisoning: a comprehensive review. JAMA. 294(18):2342-51, 2005
Bradberry SM. Dickers KJ. Rice P. Griffiths GD. Vale JA. Ricin poisoning. Toxicological Reviews. 22(1):65-70, 2003
Connor, HE, The Poisonous plants in New Zealand, 2nd ed.,1977, Government Publications Ltd., Wellington
Doan LG. Ricin: mechanism of toxicity, clinical manifestations, and vaccine development. A review. Journal of Toxicology - Clinical Toxicology. 42(2):201-8, 2004
Parton K, Bruere A.N. and Chambers J.P. Veterinary Clinical Toxicology, 3rd ed. 2006. Veterinary Continuing Education Publication No. 249
