a. Clinical Syndrome.

(1) Characteristics. 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.

(2) Clinical Features. 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. In monkeys, inhalation toxicity is characterized by a dose dependent preclinical period of 24-36 hours followed by anorexia and progressive decrease in physical activity. Death occurs 36-48 hours post challenge. In mice, histopathologic change is characterized by necrotizing, suppurative airways lesions: rhinitis, laryngitis, tracheitis, bronchitis, bronchiolitis, and interstitial pneumonia with perivascular and alveolar edema. Histopathologic change in the airways is seen as early as 3 hours post challenge. 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.

b. Diagnosis.

(1) Routine Laboratory Findings. Laboratory findings are generally nonspecific. Neutrophilic leukocytosis beginning between 12-18 hours was reported in a case of human lethal intramuscular intoxication that was purposely inflicted. Leukocytosis, beginning 12-18 hours after challenge, also occurs following aerosol exposure of laboratory animals.

(2) Differential Diagnosis. 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. The temporal onset of botulinum intoxication would be similar, but include ptosis and general muscular paralysis with minimal pulmonary effects. Staphylococcal enterotoxin B intoxication would likely have a more rapid onset after exposure and a lower mortality rate but could be difficult to distinguish. Nerve agent intoxication is characterized by acute onset of cholinergic crisis with dyspnea and profuse secretions.

(3) Specific Laboratory Diagnosis. Based on animal studies, ELISA (for blood) or immunohistochemical techniques (for direct analysis of tissues) may be useful in confirming ricin intoxication. Postmortem pathologic change is route specific: inhalation results in airways lesions; ingestion causes gastrointestinal hemorrhage with necrosis of liver, spleen, and kidneys; and intramuscular intoxication causes severe local muscle and regional lymph node necrosis with moderate involvement of visceral organs. Ricin is extremely immunogenic; sera should be obtained from survivors for measurement of antibody response.

c. Therapy. Management 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.

d. Prophylaxis. 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. Ricin is not dermally active, therefore, respiratory protection is the most critical means of prevention.

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