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