Ricin Exposure

Updated: May 27, 2021
Author: Ferdinando L Mirarchi, DO, FAAEM, FACEP; Chief Editor: Zygmunt F Dembek, PhD, MS, MPH, LHD 


Practice Essentials

Ricin is a toxin contained in the seeds (beans) of the castor oil plant (Ricinus communis). The plant is found primarily in Asia and Africa but has taken root in all temperate and subtropical regions around the world and is widely grown as a garden ornamental. See the image below.

Castor bush. Castor bush.

Ricin is present in all parts of the plant but is most highly concentrated in the beans or seeds. The beans are covered by a hard, relatively impervious outer shell that must be chewed or broken in some way in order for the toxalbumin to be released and, thus, present a toxic hazard. In addition, castor beans are notably antigenic and may cause severe cutaneous hypersensitivity and systemic reactions.

Although castor beans are an uncommon cause of poisoning, they remain a concern because their toxin is among the most lethal naturally occurring toxins known today, is easily accessible, is inexpensive, and is easy to prepare; hence, it is attractive to terrorists. The Centers for Disease Control and Prevention (CDC) classification scheme for major biological agents that terrorists could use to harm civilians categorizes ricin as a category B agent (ie, second highest priority) because it is moderately easy to disseminate while causing moderate-to-high morbidity in humans.[1]

Ricin has documented use in politically motivated assassination. Indeed, ricin has been used for homicidal purposes for centuries, although it has never been released or used in battle as a biological weapon of war.[1, 2]

Although ricin is not the ideal biologic warfare agent, it remains a threat. It would not be the agent of choice for an aerosol attack but remains a major concern as a food and water contaminant. With the increasing number of biologic threats, hoaxes, and “how-to” Internet resources available, this threat has the potential to become reality. Therefore, it is essential for physicians to be familiar with the diagnosis and treatment of poisonings due to ricin.

Exposure to ricin can result in toxicity or allergic reactions. Clinical manifestations of ricin toxicity depend on the route of exposure—that is, respiratory (inhaled aerosol), gastrointestinal (GI [ingested]), parenteral (injected), or dermal (absorption)—and on the delivered dose.

For example, ingestion can produce delayed gastroenteritis, which may be severe and hemorrhagic. Other complications of ricin toxicity include severe multisystem organ damage; shock, disseminated intravascular coagulation (DIC), seizures, coma, and death.

Treatment of ricin exposure is supportive; no antidote or approved vaccine is available. (See Treatment.)

See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and poisonings.

For patient education resources, see the First Aid and Injuries Center, as well as Biological Warfare, Ricin, and Personal Protective Equipment.


In attempting to evaluate and discuss agents that can be used as weapons of mass destruction (WMDs), a key question to consider is, What can  cause a maximum cre dible event? (A maximum credible event is one that could cause a large loss of life in addition to disruption, panic, and an overwhelming use of civilian healthcare resources.)

For an agent to be considered capable of causing a maximum credible event, it should be highly lethal, inexpensively and easily producible in large quantities, stable in aerosol form, and readily dispersible (1-5 µm in size). The ideal agent also is communicable from person to person and has no treatment or vaccine.

When these criteria are applied to ricin, the use of this agent as a WMD appears limited; nevertheless, the risk should not be underestimated. Indeed, ricin is produced easily and inexpensively; is highly toxic; can be disseminated as an aerosol, by injection, or as a food and water contaminant; is stable in aerosolized form, and has no treatment or approved vaccine. However, a considerably larger amount of ricin would be needed to produce the desired effect of a WMD than would be needed with a living replicating biologic agent or a chemical weapon.

For example, the amount of ricin necessary to cover a 100-km2 area and cause 50% lethality, assuming an aerosol toxicity of 3 µg/kg and optimum dispersal conditions, is approximately 4 metric tons, whereas only 1 kg of Bacillus anthracis is required to yield the same effects. Ricin, however, would have efficacy as a disabling agent. Its use as a food and water contaminant easily could incapacitate many and overwhelm local healthcare resources.

Pathophysiology and Etiology

Ricin is composed of two hemagglutinins and two toxins, in a structure resembling those of botulinum toxin, cholera toxin, diphtheria toxin, tetanus toxin, and insulin. The toxins are dimers comprising a 32-kd A chain and a 34-kd B chain, which are polypeptides joined by a disulfide bond. The B chain binds to cell surface glycoproteins and affects entry into the cell by an unknown mechanism. The A chain acts on the 60S ribosomal subunit and prevents the binding of elongation factor-2; this inhibits protein synthesis and leads to cell death.[3]

Castor beans are commonly encountered as ornamental items (eg, in prayer beads, bracelets, or necklaces) or in maracas. They are also used in the production of castor oil, a brake and hydraulic fluid constituent. The aqueous phase of the production process, termed the “waste mash,” contains 5-10% ricin. Extracting this 66-kd toxin is not difficult and is readily accomplished by means of chromatography, a common undergraduate chemistry skill. Castor beans are legal to possess and easily obtained through the Internet. Possession of ricin toxin requires registration with the  CDC or United States Department of Agriculture (USDA).[4]



United States statistics

Castor bean ingestions are extremely uncommon. In 2019, the American Association of Poison Control Centers (AAPCC) recorded 197 cases of single exposures to toxalbumins (a class of toxic agents that includes both ricin and abrin, the toxin from jequirity beans).[5] Of those patients, 71 were treated in a health care facility. Despite the fact that mastication of just one seed liberates enough ricin to kill a child, only 1 death was  reported, and only 1 case was considered to have a major adverse outcome.[5] Gastrointestinal absorption of the toxin is poor,[6] which is probably the explanation for the favorable outcomes.

Cases of suicide by intravenous injection of castor bean extract have been reported.[7]

Attempts to weaponize ricin have a long history. The United States tested ricin for military application during World War I. One 1918 report stated: "These experiments show...easily prepared preparations of ricin can be made to adhere to shrapnel bullets...there is no loss in toxicity of firing...every wound inflicted by a shrapnel bullet coated with ricin would produce a serious casualty..."[8]

Between 1991 and 1997, three criminal cases were related to ricin. In 1991 in Minnesota, four members of the Patriots Council, an extremist group that held antigovernment and antitax ideals and advocated the overthrow of the US government, were arrested for plotting to kill a US marshal with ricin.[9] The ricin was produced in a home laboratory. They planned to mix the ricin with the solvent dimethyl sulfoxide (DMSO) and then smear it on the door handles of the marshal’s vehicle. The plan was discovered, and the four men were convicted.

In 1995, a man entered Canada from Alaska on his way to North Carolina.[9] Canadian custom officials stopped the man and found him in possession of several guns, $98,000, and a container of white powder, which was identified as ricin. Finally, in 1997, a man shot his stepson in the face. Investigators discovered a makeshift laboratory in his basement and found agents such as ricin and nicotine sulfate.

In 2003, ricin was found in US Senator Bill Frist’s office, and, in January of that same year, individuals connected to Al Qaeda were arrested in a London apartment while trying to manufacture ricin.[10] In February 2008, a man was poisoned in a hotel room in Las Vegas, Nevada. In separate incidents during 2013, ricin-tainted letters were sent to US Senator Roger Wicker, US President Barack Obama, the US Central Intelligence Agency, Fairchild Air Force Base, and US Federal Judge Fred Van Sickle.[11]

International statistics

In 1978 a Bulgarian dissident named Georgi Markov was assassinated on a street in London when a small pellet containing ricin was injected into his thigh. The highly publicized case of Markov illustrates the rapidly fatal nature of parenteral exposure.[12] Markov, an exiled Bulgarian broadcaster, was waiting for a bus when he was jabbed with an umbrella in the lower extremity. He then developed severe gastroenteritis and high fevers and died 3 days later.

At autopsy, a 1.5-mm metallic sphere was found at the wound site.[12] It had two tiny holes and could hold a volume of 0.28 mL. No toxin was isolated. Because of the small volume available and the rapid demise of the patient, ricin was believed to be the only capable inciting agent. The British government Chemical Defense Establishment at Porton Down recreated the scenario by injecting a pig with a similar dose of ricin. The pig died in a similar manner 26 hours later.[12] The ricin theory as the agent of death in the Markov case was given additional validation when ricin was recovered from a pellet used in another murder under similar circumstances.[13]

In December 2002, six terrorist suspects were arrested in Manchester, England; their apartment was serving as a “ricin laboratory.”[9] Among them was a 27-year-old chemist who was producing the toxin. Later, on January 5, 2003, British police raided two residences around London and found traces of ricin, which led to an investigation of a possible Chechen separatist plan to attack the Russian embassy with the toxin; several arrests were made.[14]


Although studies are limited and accurate statistics are not known, the prognosis for patients who develop symptoms appears to be generally good with appropriate supportive care. Fatalities have occasionally been reported after ingestion of chewed castor beans. Chewing and swallowing as little as 1 bean may produce death in a child; however, swallowing an intact bean without chewing is unlikely to cause serious sequelae.

Mortality and morbidity depend on the route and amount of exposure. Very little actual human data exist regarding the toxicity of specific dosages, but some information may be extracted from studies on nonhuman primates and mammals.

For gastrointestinal (GI) exposure, the lethal dose for 50% of the exposed population (LD50) is 30 µg/kg in rodents. Ricin’s lethality is diminished when ingested. Castor bean ingestions were once considered fatal, but multiple case reports prove otherwise. Many documented cases are related to ingestions of multiple seeds and voluntary ingestion of ricin without fatality. If ingested in sufficient amounts, ricin can cause severe gastroenteritis, GI hemorrhage, and hepatic, splenic, and renal necrosis. Death may occur from circulatory collapse.

For aerosol exposure, the LD50 for rodents is 3 µg/kg. Aerosol exposure causes weakness, fever, cough, and pulmonary edema within 18-24 hours and severe respiratory distress and death within 36-72 hours. In rodents, aerosol exposure is characterized by necrotizing airway lesions causing tracheitis, bronchitis, bronchiolitis, and interstitial pneumonia with perivascular and alveolar edema.

Parenteral exposure can be rapidly fatal, with an LD50 similar to that of aerosol exposure. When injected, ricin can cause severe local necrosis of muscle and regional lymph nodes, along with organ involvement and death.

Dermal exposure to ricin is of little concern, because the amount absorbed is insignificant. To be absorbed dermally, ricin must be enhanced with a strong solvent such as DMSO. Absorption would depend on the type of solvent and length of exposure, but for the most part, the dose of ricin from dermal exposure probably is too low to produce toxicity.




In the case of an isolated attack involving ricin (eg, an assassination attempt), no historical markers may be present. If a number of patients are affected simultaneously, by either ingestion or inhalation, the subsequent cluster of patients presenting with similar symptoms over a brief time may alert an astute clinician to the possibility of an intentional act. This is especially true in the case of an inhalation incident (ingestion initially may mimic food poisoning).

The usual significant factors associated with toxic environmental exposures should be addressed, including the following:

  • Identification of the toxic substance

  • Time and duration of exposure

  • Symptoms

  • Treatment thus far

  • Associated injuries

  • Preexisting conditions

In cases of ingestion, an effort should be made to obtain a sample of the exact bean ingested, if possible; this greatly facilitates the identification process. It is important to be aware that beans are often known by various names, both common and scientific. In the United States, the castor oil plant (see the first image below) grows wild in the southwest, mainly along streams and riverbeds; gardeners in colder areas grow the plant as an ornamental annual. Castor beans (see the second image below) are oblong and brown in color with speckled dark brown spot. Castor beans are easily purchased in many horticulture and plant shops and over the Internet.

Castor bush. Castor bush.
Castor beans. Castor beans.

Although a patient is unlikely to be aware of contamination of ingested foods or beverages, an effort should be made to determine approximately when exposure occurred and to what degree (including how many beans were chewed and whether any were swallowed).

After ingestion of castor beans, symptoms develop within 8-24 hours (see the image below). The clinical picture can include gastrointestinal (GI) symptoms that can progress to hypotension, liver and renal failure, and death. After inhalation of ricin, illness can develop within 8 hours. Symptoms include cough, dyspnea, arthralgias, fever, respiratory distress, and death. After injection of ricin, symptoms develop within 6 hours, including weakness and myalgias with progression to fever, hypotension, multiple organ failure, and death.[15]

Chemical Terrorism Agents and Syndromes. Signs and symptoms. Chart courtesy of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright University of North Carolina at Chapel Hill, www.unc.edu/depts/spice/chemical.html. (PDF)

It is important to determine whether the patient has received any treatment before presentation. Inquiries should be made regarding any other potential exposures or injuries. A victim of an attack may relate the pain of an antecedent injection, but this may be overlooked during the history. Inquiries should also be made regarding past medical history, medications, and allergies.

Physical Examination

With any exposure to ricin, a complete physical examination is essential. Airway patency should be assessed. Oral or upper airway swelling severe enough to cause airway compromise is extremely uncommon, and breathing is usually unaffected. Circulation may be affected as shock develops, secondary to severe gastroenteritis. Severe cutaneous hypersensitivity or systemic allergic reactions may occur. An urticarial, immunoglobulin E–mediated allergic reaction may occur, with tongue or facial swelling, bronchospasm, and acute upper airway obstruction.

In parenteral exposure, the site should be inspected for induration, erythema, and the possibility of a retained foreign body. These physical findings may be present before or simultaneously with systemic manifestations.

In aerosol exposure, the presentation is that of a rapidly progressive acute lung injury. Physical findings are consistent with the stage of progression, from normal physical examination results through hypoxia, cyanosis, labored breathing, tachypnea, tachycardia, and progressive respiratory failure.

In GI exposure, physical examination should yield findings consistent with gastroenteritis and volume depletion. If the dose was sufficient and the disease had progressed, frank hematemesis, bloody diarrhea, or melena may be present.



Diagnostic Considerations

Diagnosis of an aerosolized attack or food and water contamination with ricin is similar to that of an attack with any of the biologic or chemical agents that serve as weapons of mass destruction (WMDs). It primarily depends on the clinical and epidemiologic setting. In cases of isolated injection, the diagnosis is extremely difficult.

The clinical presentation of acute lung injury in a large number of patients in a particular area should suggest a pulmonary irritant. The clinical presentation of severe gastroenteritis or hemorrhagic gastroenteritis in a large number of patients in a particular area should suggest a food and water contaminant.

Several other agents (eg, staphylococcal enterotoxin B, Q fever, tularemia, pneumonic plague, inhalational anthrax, chemical agents such as phosgene) should be included in the differential diagnosis.

Ricin poisoning is expected to progress despite antibiotic therapy. Chest radiography reveals no evidence of mediastinitis, as would be expected with pulmonary anthrax. Staphylococcal enterotoxin B does not progress to a life-threatening syndrome, and phosgene produces acute respiratory distress syndrome (ARDS), which is mediated by exertion. Phosgene also has the characteristic odor of newly mown hay or grass and is moderately water soluble but may be quite irritating to mucous membranes in higher concentrations.

In addition to the conditions listed in the differential diagnosis, other problems to be considered include the following:

  • Cholera

  • Necrotizing fasciitis

  • Trichothecene mycotoxin

  • Pyrolysis byproducts of Teflon, Kevlar

  • Paraquat

  • Acute arsenic toxicity

  • Acute inorganic mercury, thallium, or iron ingestion

  • Acute radiation sickness

  • Chemotherapeutic drugs

  • Capillary leak syndromes (eg, autoimmune vasculitis and Stevens-Johnson syndrome [SJS])

  • Pneumonia

  • Myocardial infarction

  • Plague

  • Salmonella infection

  • Shigella infection

  • Streptococcus aurea infection

  • Undifferentiated sepsis

Differential Diagnoses



Approach Considerations

In the face of credible threats, clinicians should consider ricin poisoning in patients who present with gastrointestinal (GI) or respiratory illness. Efforts should be made to notify poison control centers, public health, and local law enforcement agencies. Clinicians must have a low threshold of suspicion for patients who present with nonspecific systemic illness, especially when a large number of patients with similar symptoms are present.

Laboratory Studies

Baseline laboratory information should be obtained. Useful tests include the following:

  • Complete blood count (CBC) with differential

  • Blood typing and screening

  • Electrolytes

  • Blood urea nitrogen (BUN) and creatinine

  • Glucose

  • Amylase and lipase

  • Liver function tests (LFTs)

  • Lactic acid

  • Blood, urine, and sputum culture

Coagulation studies (eg, prothrombin time [PT], activated partial thromboplastin time [aPTT], international normalized ratio [INR], and fibrinogen) may be necessary if the gastroenteritis becomes hemorrhagic.

Critically ill and hypotensive patients and those that meet criteria for the systemic inflammatory response syndrome (SIRS) or sepsis should have arterial blood gas (ABG) values and cortisol levels measured. Arterial blood gas studies may reveal hypoxemia.

An enzyme-linked immunoassay (ELISA) can detect ricin in human urine and serum at concentrations of 100 pg/mL or higher. Testing for ricin can be done at a regional public health center laboratory by performing a polymerase chain reaction (PCR) assay on 25 mL of urine. Acute and convalescent serum may be collected to determine measurements of antibody response.

Additional analytic methods may be available for ricin detection through the US Army Medical Research Institute for Infectious Diseases and the Centers for Disease Control and Prevention (CDC).

Other Studies

Chest radiography

In general, imaging studies are not necessary, because the beans generally are not detectable by means of plain radiography. However, a chest radiograph may reveal infiltrates or a picture suggestive of acute respiratory distress syndrome (ARDS). Radiography may also be useful in parenteral exposures to evaluate for a retained foreign body.


If bronchoscopy is performed, the bronchial aspirate may be rich in protein when compared to plasma, as is observed in any condition causing high-permeability pulmonary edema.



Approach Considerations

Emergency department (ED) management begins with universal precautions and the ABCs (airway, breathing, and circulation); a “D” may be added for decontamination (including the removal of garments). If the history and presenting findings suggest that ingestion is possible, gut decontamination should be considered as well.

Treatment depends on the route of exposure. Treatment is supportive, and no antidote for ricin is available. All symptomatic patients should be admitted to the hospital. After ingestion and inhalation, the clinical course typically progresses over 4-36 hours, and monitoring in an intensive care unit (ICU) may be warranted. Children with severe systemic toxicity should be transferred to a center capable of handling critically ill children. This should occur after the child has been stabilized and whole-bowel decontamination initiated.

Because there is no definitive antidote for ricin poisoning, the only effective way of managing ricin toxicity is to prevent it. Candidate vaccines and ricin inhibitors (eg, pteroic acid, neopterin, pterin tautomer, and guanine tautomer) are being investigated either as antidotes or as means of facilitating immunotoxin treatment. Some promising results have been obtained; however, vaccine trials still require additional testing for safety and efficacy.

Supportive Care

Universal precautions must be strictly adhered to at all times. The risk of secondary aerosolization is minimal. Protective masks, which are effective in preventing toxicity, should be used when an overt aerosol attack is suspected.


The first priority in treating a patient with castor bean poisoning is to establish that the patient’s airway is patent and that breathing and circulation are adequate. Supportive care based on clinical symptoms is the primary therapy.

Any symptomatic patient should be admitted and monitored, and aggressive intravenous (IV) volume resuscitation should be initiated. Hypotension should be treated with isotonic fluids and packed red blood cells as needed. A vasopressor-type agent (eg, dopamine or norepinephrine) should be employed when needed.


Decontamination begins by removing garments and cleaning the body. If available, a 0.5% sodium hypochlorite solution should be used, with a contact time of 15 minutes. It should not be instilled into open abdominal, brain, or spinal cord injuries or into the eyes; however, it can be instilled into noncavity wounds and then removed via suction into disposable containers. This discarded solution is neutralized and nonhazardous in 5 minutes.

To make a 0.5% sodium hypochlorite solution, mix 1 part bleach and 9 parts water. Make it fresh daily with a pH in the alkaline range. In the absence of this solution, copious amounts of soap and water may be used.

Care with specific routes of exposure

For dermal exposure, a weak sodium hypochlorite solution (0.1-0.5%), soap and water, or both typically suffice to decontaminate the skin.

For gastrointestinal (GI) exposure, institute gastric decontamination with superactivated charcoal and volume replacement. Laboratory evaluation should include chemistry panels, a complete blood count (CBC), a liver function panel, blood urea nitrogen (BUN) and creatinine levels, urinalysis, and blood type and screening.

For percutaneous exposure, treatment should be based on excision of the injection site, if possible, within the shortest amount of time. Baseline laboratory information should be obtained, including arterial blood gas values and fibrinogen. Although antibiotics play no role in the treatment of ricin, withholding such therapy in an acutely septic-appearing patient would be difficult. Antibiotics may serve to prevent infection resulting from the percutaneous mechanism. Tetanus immunization status should be updated if unknown.

For aerosol or pulmonary exposure, standard critical care treatment should be directed toward acute lung injury and pulmonary edema. A low threshold should be maintained to secure the patient’s airway and ensure adequate oxygenation and ventilation. A chest radiograph, which may show infiltrates, should be obtained. The clinical course progresses despite antibiotic therapy.

The only post-exposure measure that is effective against pulmonary ricinosis is passive immunization with anti-ricin neutralizing antibodies. The efficacy of this antitoxin treatment depends on antibody affinity and the time of treatment initiation within a limited therapeutic time window. Small-molecule compounds that interfere directly with the toxin or inhibit its intracellular trafficking may also be beneficial against ricinosis. Another approach relies on the co-administration of antitoxin antibodies with immunomodulatory drugs, thereby neutralizing the toxin while attenuating lung injury. Immunomodulators and other pharmacological-based treatment options should be tailored according to the particular pathogenesis pathways of pulmonary ricinosis.[16]

Whole-bowel irrigation

In theory, rapid elimination of the bean from the GI tract before erosion of the outer shell may decrease or prevent the release of potent toxins. Accordingly, whole-bowel irrigation (WBI) has been suggested as a means of ensuring rapid and complete decontamination of the GI tract; however, the clinical use of WBI has not been demonstrated.

WBI is accomplished by continuously instilling a polyethylene glycol electrolyte lavage solution through the GI tract until the effluent from the rectum is clear or all of the beans have been recovered. Inserting a nasogastric tube and setting a continuous flow rate will accomplish WBI best. Irrigation rates vary according to age, as follows:

  • Age 0-5 years - Flow rate, 500 mL/h
  • Age 6-12 years - Flow rate, 1000 mL/h
  • Age > 12 years - Flow rate, 1500-2000 mL/h

It is advisable to consult with a medical toxicologist at the nearest regional poison control center before undertaking WBI.

Further inpatient care

IV fluids should be continued at a rate that maintains adequate hydration and replacement of electrolytes. Beans should be counted to ensure complete recovery. Patients should remain under observation for at least 4-6 hours; after this period, they may be safely discharged if they are asymptomatic. Antispasmodics, such as loperamide, are contraindicated.


Surgical consultation for local excision and removal is warranted for parenteral exposures when a retained foreign body is located.

All exposures should be reported to the regional poison control center. The American Association of Poison Control Centers (AAPCC) is the only national organization currently tracking all potentially poisonous ingestions and may be helpful in bean identification. Expert consultation with a trained toxicologist is also recommended and can be obtained at the regional poison control center.


To minimize the risk of accidental ingestion of plant toxins such as ricin, efforts should be made to keep all potentially poisonous and injurious plants and plant-related products away from children. Homes should be purged of all potentially toxic plant items, just as they are purged of medications and cleaning supplies. In addition, children should be specifically instructed never to eat wild plants, beans, or berries.

For a biologic attack involving ricin, the only effective management is prevention; unfortunately, no prophylaxis exists. In an aerosol attack, protective masks are effective in preventing toxicity and should be used.

Currently, investigations of vaccines are ongoing. Candidate vaccines include RVEc (developed by the US Army Medical Research Institute of Infectious Diseases) and RiVax (Soligenix, Princeton, NJ).[17, 18, 19, 20] RVEc has been tested in human volunteers, who subsequently developed antibodies to the toxin. However, two of the 10 volunteers experienced severe adverse reactions. The study was discontinued and a reliable method of determining antigen concentration is under development.[21]

RiVax been found to be safe in healthy human volunteers, in whom they stimulated the production of antibodies.[22]  [23] A Phase 1B study of RiVax has also been successully completed.[24] In animal testing, rhesus macacques vaccinated with RiVax were protected against ricin aerosol exposure.[25] Further human testing is necessary.

Ricin inhibitors are also being studied. Certain 6-substituted pterins (eg, pteroic acid) have shown promise in this setting. A study by Pruet et al suggested that 7-carboxy pterin and derivatives thereof may prove useful as part of a program to make effective ricin toxin A chain inhibitors.[26]

O’Hara et al found that passive administration of 10 µg of GD12—a murine monoclonal immunoglobulin G (IgG) antibody to an epitope on the A chain of ricin toxin—or a chimeric derivative (cGD12) to mice via intraperitoneal injection protected the animals against a systemic ricin challenge.[27] After exposure, the two antibodies, administered up to 6 hours after toxin challenge, were each capable of rescuing mice from toxin-induced death, suggesting that GD12 might have both prophylactic and therapeutic potential for ricin intoxication.



Medication Summary

Tetanus status should be updated if unknown. If exposure is via the parenteral route, antibiotics may be helpful in preventing secondary bacterial infection.

Antibiotics, Other

Class Summary

With regard to ricin toxicity, the only possible indication for antibiotics is for the parenteral mechanism of exposure. Direct the choice of antibiotic to cover skin flora.


Cefazolin is a first-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth.

Alpha/Beta Adrenergic Agonists

Class Summary

Before or simultaneously with the use of vasopressors, perform adequate volume resuscitation of patients with isotonic fluids and packed red blood cells; do not use these agents in place of volume resuscitation. The choice of agent is usually determined by physician preference. There is no criterion standard vasopressor for treatment of hypotension caused by ricin toxicity.


Dopamine is probably the best-known and most widely used pressor agent. A standard mixture of 200 mg in 250 mL produces a concentration of 800 µg/mL; administer intravenously (IV).

Norepinephrine (Levophed)

Norepinephrine is often a second-line agent but can be used as a first-line agent. It can be given with dopamine. A standard mixture of 4 mg in 250 mL produces a concentration of 16 µg/mL; administer IV.

Vaccine, Inactivated (Bacterial)

Class Summary

Toxoids are used to induce active immunity. Tetanus status should be updated if unknown.

Diphtheria and tetanus toxoid (Tenivac)

Diphtheria and tetanus toxoid is used to induce active immunity against tetanus in selected patients.

Antidotes, Other

Class Summary

Antidotes are used to inhibit or reduce absorption of the toxin.

Activated charcoal (CharcoCaps, EZ-Char, Actidose Aqua)

Activated charcoal is employed as a component of emergency treatment in poisoning caused by drugs and chemicals. The network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Charcoal does not dissolve in water. For maximum effect, it should be administered within 30 minutes after the ingestion of the poison.