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To date, the most severe Ebola outbreak in history began in Guinea in 2013 and
spread to West African neighbors Liberia and Sierra Leone. Before being
declared extinguished in 2016, over 28,000 cases and 11,000 deaths occurred. A
few cases were imported to the United States, revealing issues with medical
readiness for imported viral hemorrhagic fevers. Ebola, depending on the strain,
typically has a case fatality rate of 50% to 80% in African nations, raising
concerns regarding its intentional release by terrorists. A recombinant Ebola
vaccine tested in Guinea during the outbreak has shown great promise in
preventing spread of disease to close contacts.

Ricin
The distinction between biologic agents, which are living organisms capable of
causing infections, and chemical agents, which are nonliving poisons, is obvious.
Toxins such as ricin, however, are chemical poisons produced by biologic
organisms and occupy a somewhat nebulous niche between chemical and biologic
(infectious) agents. Although discussed with biologic agents, it should be kept in
mind that they cause intoxication (poisoning) rather than infection, do not
replicate in hosts, and do not produce communicable, or contagious, conditions.
Ricin is a toxin derived from the castor bean, and its production is not
technologically challenging. It is quite toxic if ingested, and far more so if
injected or inhaled. It is infamous as a homicidal weapon of espionage used by
the Bulgarian secret service in London during the Cold War against defector
Georgi Markov. More recently, in February 2004, it was discovered in a U.S.
Senate office building, apparently having been delivered through the mail. At
least 16 persons required decontamination, although no one became ill. Ricin is
an inhibitor of cellular protein synthesis via enzymatic attack on the 28S
ribosomal subunit.
The clinical presentation of ricin intoxication depends on the route of exposure.
Exposures due to aerosols produce dose-dependent symptoms. Four to 8 hours
after inhalation, fever, chest tightness, cough, dyspnea, nausea, and arthralgias
can occur, followed within 36 hours by progressive cough, dyspnea, cyanosis, and


pulmonary edema resulting in respiratory failure. If ingested, necrosis of the GI
epithelium, local hemorrhage, and hepatic, splenic, and renal necrosis can be
expected followed by vascular collapse and death. If injected, severe local
necrosis of muscle and regional lymph nodes with moderate visceral organ
involvement are seen.
Patients with ricin poisoning are not contagious. Establishing a diagnosis of
ricin intoxication may be challenging: Early postexposure (0 to 24 hours) nasal or
throat swabs and respiratory secretions may be submitted for toxin assay for



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