Ricinus communis

RICINUS COMMUNIS

Ricinus Communis (Castor Bean, Castor-Oil-Plant, Palma Christi)

Ricinus

Toxic principle

  • Ricin a tozxalbumin is the principal toxin.
  • Toxalbumins are very toxic proteinaceous compounds of plant origin.
  • Ricin is 100 times less toxic orally than parenterally; the difference is apparently not a result of the effects of trypsin or pepsin.
  • Toxicosis is not only associated with plant, but most often with seed and seed products.
  • Orally, ricin is readily absorbed from the stomach and intestine.
  • Ricin is water soluble and not present in castor oil.
  • Being a protein, and a fairly large molecule, ricin is heat labile. In castor bean cake, meal, etc. the ricin is generally inactivated by heating.
  • Aging also reduces toxicity.
  • Another phytotoxin in castor bean, ricinine, is reportedly goitrogenic.
  • The importance of this compound is not clearly established.
  • Ricin acts as an antigen and protective antibodies may be elicited.
  • Castor oil is not poisonous.
  • It has been suggested that anaphylactic reactions may occur in all species.

Signs

  • Signs appear after a characteristic lag period of a few hours to days, usually onset is between 12 hours and 48 hours.
  • Nausea, gastrointestinal irritation, abdominal pain, diarrhea which is often bloody, tenesmus, dehydration and at postmortem severe inflammation of the stomach and intestine.
  • Anorexia, cessation of rumination.
  • Excessive thirst.
  • Weakness, muscle twitching.
  • Dullness of vision, convulsions, dyspnea, opisthotonus, coma and death.
  • Sometimes clonic convulsions and decreased tendon reflexes are described.
  • 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.
  • Clotting time may be prolonged, possible hypoprothrombinemia.
  • Cyanosis.

Treatment

  • Early - Use of emetics in appropriate species followed by activated charcoal and a saline cathartic unless contraindicated (as in marked diarrhea) is useful.
  • A gastrointestinal tract protectant such as kaolin-pectin and fluid therapy are useful. Appropriate fluid and electrolyte therapy can greatly increase chances of survival.
  • Judicious use of anticonvulsants if necessary.
  • Maintain (or establish) respiration, fluid, and electrolyte balance.
  • Oral antacids to alleviate local irritation.
  • Ascorbic acid increases survival rates.
  • Forced alkaline diuresis has been suggested to prevent nephrosis.
Last modified: Thursday, 22 December 2011, 11:28 AM