The castor bean plant (Ricinus communis) or palma christi is a common ornamental houseplant with large, palmated, lobed leaves that may be found in almost any location in the United States. The plant is also grown for the manufacturing of castor oil. This same plant has a more sinister side and may be used to produce a potent phytotoxin called ricin.

Although all parts of the castor bean plant are toxic, ricin is concentrated in the seed of the plant. The seeds are very large and mottled, typically with a light brown color. The seeds are produced in a capsule that breaks open at maturity. The seed coat is very hard and the seed will pass harmlessly through the digestive tract unless the seed coat is broken due to chewing or crushing before ingestion.

People and horses account for most cases of poisoning. Cattle and sheep appear to be more resistant to the toxic effects of the castor bean. Most toxicities in the horse occur when castor-bean seeds contaminate concentrates.

The ricin molecule is composed of two glycoprotein chains A and B. One of the chains facilitates endocytosis (entry into a cell) while the other chain, once it has gained entry into a cell, will inhibit protein synthesis within the ribosomes and cause cell death. These proteins may be antigenic in sensitive animals thereby resulting in anaphylaxis. In the horse; as little as 0.1 mg/kg of ground castor bean seeds may be lethal. Ricin is water soluble and not fat soluble, therefore there is no risk of ricin being present in castor oil.

To eliminate the possibility of poisoning, the flowering head of the castor bean plant should be snipped from the plant.

Typically there is a latent period of 18 to 24 hours between the ingestion of the beans and the onset of clinical symptoms. In the early stages of toxicity, there is a slight depression and an elevation of body temperature of 3 to 4ºF. Affected animals will become thirsty, there may be mild colic pains, and sweating will develop. As the toxicity progresses, vomiting will occur as well as a profuse catarrhal to bloody (hemorrhagic) diarrhea. Animals become weak, incoordinated and will often tremble. The heart rate will become erratic and may result in terminal convulsions.

Affected animals will have an elevated packed cell volume. Accumulation or pooling of body fluids in the intestines leads to hypovolemic shock.

When diagnosed early, treatment consists of evacuating the gastrointestinal tract through emesis and intestinal lavage. Additional treatment is symptomatic and largely involves the replacement of fluid loss.

Diagnosis is difficult unless one receives a history of exposure to castor beans.


References:

Fowler, Murray. Plant Poisoning in Small Companion Animals. Ralston Purina Co. 1981. Pp. 9-11.

Gupta, Ramesh. Veterinary Toxicology. Elsevier. 2007. P. 1124.

Kahn, Cynthia Editor. The Merck Veterinary Manual. Merck and Co. 2005. Pp. 2468 – 2469.

Stegelmeier, Bryan. “Identifying Nephrotoxic Plants and how to Minimize Poisoning”. DVM Newsmagazine. November. 2007. P. 10E.