This is a popular urban legend and factually incorrect.
Ricin is a cytotoxin that inhibits protein synthesis in mammalian cells by (permanently) inactivating the ribosomes, shutting them down. It causes wholesale cell death and tissue/organ failure as a result. The direct cause of death can vary widely and depends on where the ricin is in the body and the method by which you came in contact with it. Because of the very fine-grained nature of its toxic effect, it usually takes anywhere from hours to days before symptoms of poisoning are noticeable, usually requiring a critical mass of cells in a region of your body to die before you notice since cell death is a normally occurring phenomenon in the body. Of course, if you notice any symptoms at all, you are usually toast. This has made it a popular assassins weapon, since a lethal poisoning may take a day or more to manifest symptoms.
Among the reasons ricin is interesting is that it is not very specific to any particular kind of cell and will happily deactivate eukaryotic ribosomes most places it finds them. Most cytotoxins show a great deal more specificity.
Ricin.
Ricin is a glycoprotein toxin (66,000 daltons) from the seed of the castor plant. It blocks protein synthesis by altering the rRNA, thus killing the cell. Ricin's significance as a potential biological warfare agent relates to its availability world wide, its ease of production, and extreme pulmonary toxicity when inhaled.
Overall, the clinical picture seen depends on the route of exposure.
All reported serious or fatal cases of castor bean ingestion have taken approximately the same course: rapid onset of nausea, vomiting, abdominal cramps and severe diarrhea with vascular collapse; death has occurred on the third day or later.
Following inhalation, one might expect nonspecific symptoms of weakness, fever, cough, and hypothermia followed by hypotension and cardiovascular collapse. The exact cause of death is unknown and probably varies with route of intoxication. High doses by inhalation appear to produce severe enough pulmonary damage to cause death.
[Hypotension and cardiovascular collapse: Tachycardia, arrhythmias, ECG may show ischaemic changes. Cardiac arrest.]
In oral intoxication, fever, gastrointestinal involvement, and vascular collapse are prominent, the latter differentiating it from infection with enteric pathogens. With regard to inhalation exposure, nonspecific findings of weakness, fever, vomiting, cough, hypothermia, and hypotension in large numbers of patients might suggest several respiratory pathogens.
Therapy is supportive and should include maintenance of intravascular volume. Standard management for poison ingestion should be employed if intoxication is by the oral route. There is presently no antitoxin available for treatment.
There is currently no prophylaxis approved for human use. Active immunization and passive antibody prophylaxis are under study, as both are effective in protecting animals from death following exposure by intravenous or respiratory routes.