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A ProMED-mail post
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http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
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http://www.isid.org>
Date: Wed 17 Apr 2013
Source: Chicago Tribune, Reuters report [edited]
<
http://www.chicagotribune.com/news/sns-rt-us-usa-obama-letterbre93g0ou-20130417,0,2770928.story>
A letter addressed to President Barack Obama contained a substance
that preliminarily tested positive for the deadly poison ricin,
authorities said on Wed 17 Apr 2013.
News that the letter to Obama was being investigated came as a flurry
of other reports of suspicious letters and a package caused the
evacuation of parts of 2 Senate buildings and set nerves in Washington
on edge.
The letter contained "a granular substance that preliminarily tested
positive for ricin," an FBI statement said. But the statement added:
"There is no indication of a connection to the attack in Boston,"
where 3 people were killed in bombings at the Boston Marathon on
Monday [15 Apr 2013].
The USA Secret Service said the letter to Obama was received at a mail
screening facility on Tue 16 Apr 2013. The mail facility that received
the letter was not located near the White House itself, Secret Service
spokesman Edwin Donovan said in a statement. "The Secret Service is
working closely with the US Capitol Police and the FBI in this
investigation," Donovan said.
Parts of the Russell and Hart Senate office buildings were cleared
while officials investigated suspicious letters and a package, a
Capitol Police spokesman said.
CNN read a statement from a spokesman to Senator Richard Shelby,
saying that Capitol Police were investigating a suspicious package
that had been delivered to their office.
Senator Carl Levin said one of his Michigan regional offices had
received a suspicious-looking letter, but it was not opened.
Authorities are investigating, Levin said in a statement.
On Tue 17 Apr 2013, USA authorities intercepted a letter sent to
Mississippi Senator Roger Wicker that preliminary tests showed
contained the deadly poison ricin.
[Byline: Susan Cornwell]
- --
Communicated by:
ProMED-mail
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promed@promedmail.org>
[ProMED-mail awaits more information regarding the presumed ricin.
The following is extracted (citations removed) from: Lutwick LI,
Gradon J, Zellen J: Category B Biotoxins. In Lutwick LI, Lutwick SM
(eds), Beyond Anthrax: Bioterror - The Weaponization of Infectious
Diseases. Springer-Humana, New York, 2009, New York, pp. 181-206:
"Ricin is found in castor beans from the plant _Ricinus communis_ and
is a residual product of the production of castor oil. The oil has
applications as a purgative, an engine lubricant, and as a component
of brake and hydraulic fluid. The industry is no longer active in the
United States but the oil is produced in large quantities in other
areas of the world. Importantly, the oil, if properly prepared, does
not contain the toxin.
"One million tons of castor beans are used each year for producing the
oil. The waste mash from the oil production process can have as much
as 5 percent ricin by weight and is easily and inexpensively isolated
via a simple process in a low technology setting using materials
easily obtainable. Ricin is easily prepared in liquid or crystalline
forms or as a readily aerosolized, lyophilized powder. The toxin is
stable and can be poisonous in its native form in the beans.
"Ricin is a 66 kD [kiloDalton] globular protein with a toxic mode of
action of inhibiting protein synthesis in eukaryotic cells. The
mechanism is due to the enzymatic removal of a single adenine residue
from (amino acid 4324) close to the 3-prime end of 28S ribosomal RNA.
The removal prevents elongation factor-2 from binding. Structurally it
is made up of 2 approximately equal molecular weight subunits, the A
and B chains, linked by a disulfide bond. The B chain facilitates
binding to cell surfaces and entry into the cell through binding to
terminal galactose moieties of cellular membrane glycolipids and
glycoproteins.
"The clinical presentation of ricin poisoning depends on whether the
exposure is parenteral, inhaled, or ingested. In mice, the dose found
to be lethal to 50 percent (LD50) of animals was found to be 3-5
microg/kg in inhalation or intravenous exposures and 20-25 microg/kg
in intraperitoneal, subcutaneous, or intragastric administration. The
time to death in the mice was 60 hours for inhalation, 90 hours for
intravenous, and 80-100 hours for the other exposures. It is important
to note that there is a variation of as much as 2 logarithms
[100-fold] in the microg/kg dose of ricin between animals, with the
horse seeming to be the most sensitive and the frog and chicken the
least.
"The 1st symptoms of toxicity generally occur 6-12 hours after
exposure but can occur as early as 3 hours. This is longer than many
of the chemical agents affecting the lung and more rapid than
infectious agents. In humans, as seemed to have occurred in the Georgi
Markov assassination, multiorgan failure occurred with a prominently
elevated white blood cell count. [Markov was a Bulgarian communist
defector who was killed in London in 2003 by a ricin pellet injected
into his leg from a modified umbrella point -- see
<
http://edition.cnn.com/2003/WORLD/europe/01/07/terror.poison.bulgarian/index.html>.]
"As a weapon of bioterrorism, ricin would most likely be dispersed as
an aerosol although contamination of food and water supplies is also
feasible. Although easily obtained, massive quantities of toxin are
necessary to create a large scale effect. Because signs and symptoms
are non-specific, detection of an attack would require a high index of
suspicion based on clinical and epidemiologic factors. The finding of
a geographic cluster of patients with acute lung injury should arouse
suspicion of an attack via an aerosolized agent, although the list of
potential culprits is extensive and includes chemical as well as
biologic agents. Ricin cases do not exhibit mediastinitis, as with
anthrax, and they do not demonstrate any response to antibiotic
therapy as would be expected with an infectious etiology. Pulmonary
edema may develop one to 3 days after ricin exposure, in contrast to
staphylococcal enterotoxin B or phosgene where time to development of
pulmonary edema is 12 and 6 hours respectively.
"There are limited data describing the outcome from an inhalation
exposure. In the 1940s, sublethal and accidental exposures were said
to have occurred and were manifest 4-8 hours after exposure with
fever, cough, shortness of breath, and nausea. Studies in rodents
suggest an inhaled ricin aerosol could lead to necrosis of the upper
and lower airway, respiratory distress syndrome and respiratory
failure. Chest x-ray would be expected to show bilateral infiltrates.
In animal studies death occurred in 36 to 72 hours and was dose
dependent. In primates, symptoms and time to death were also dose
related and associated with alveolar flooding, fibropurulent
pneumonia, and necrotizing tracheitis. Death occurred 36 to 48 hours
after challenge following a 8-24 hour preclinical period." - Mod.LL
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