Ricin, named in 1888, is one of the most poisonous natural toxins known. The toxin is derived from the beans of the castor plant (R. communis). Both its ubiquitous nature and lethality make it an ideal agent for use in bioterrorism. Ricin is easily derived from the mash created from processing castor beans to make castor oil, which is mainly used as an industrial lubricant. The beans are grown worldwide as an agricultural product and grow wildly in arid regions of the United States. Perhaps one of the most famous cases of suspected ricin poisoning occurred in 1978 with the assassination of Bulgarian exile Georgi Markov in London. His assassins used a specially engineered umbrella that injected a tiny pellet containing ricin into his body.

Pathogenesis

Ricin consists of two hemagglutinins and two toxins, each containing two polypeptide chains (A and B) joined by disulfide bonds. The toxins are very lethal to cells, acting by inhibiting protein synthesis. The assault begins when the B chain binds to cellular receptors and the toxin is taken into the cell. Once inside, the A chain, consisting of endonuclease activity, acts by inhibiting protein synthesis. The basic structure of ricin is similar to botulinum, cholera, diphtheria, and tetanus toxins.

Modes of infection can be through the respiratory tract, gastrointestinal, or parenteral. The incubation period is generally 4-6 hours, but can vary depending on the amount of exposure.

Manifestations

Initial symptoms of ingestion include vomiting, abdominal pain, and diarrhea. Rapid onset of severe dehydration coupled with a decrease in blood pressure follows initial symptoms. Additional symptoms include, fever, intense thirst, sore throat, and dilated pupils. Generally, if a person survives the first 3-5 days, chances of recovery are greatly improved.

Primary symptoms of respiratory infection include fatigue, fever, weakness, nausea, and cough. Symptoms progress to sweating, cyanosis, and pulmonary edema. If left untreated, death due to respiratory failure and cardiovascular collapse occur within 36-72 hours.

The symptoms for inhalational exposure are similar to wide variety of infectious pathogens, including pneumonic plague, influenza, and tularemia. If treatment is sought within the first 24 hours of exposure, swabs of the throat can be collected for toxin assay. Patients with aerosol exposure may be subjected to further testing, including x-rays, bronchoscopy, and antibody response.

Treatment

Treatment is supportive in nature. Cough suppressants and fever reducers help keep the patient more comfortable. Hydration is essential, particularly for patients with severe diarrhea. Respiratory support may be needed for individuals with aerosol exposure.

Prevention

There is no vaccine or antitoxin available.

Category A

Yersinia pestis
Bacillus anthracis
Clostridium botulinum
Francisella tularensis
Smallpox
Ebola
Marburg
 

Images

R. communis
the castor plant