Biological Terorism

Anthrax
 Biological Terrorism The Perfect Biological Weapon
 Easily concealed
 Potent
 Easily delivered The small quantity of anthrax needed for a lethal inhalation
dose makes concealment, transportation, and dissemination very easy. An
anthrax aerosol is odorless and invisible, making it a very stealthy killer.
Only a millionth of a gram of anthrax is a lethal dose. A kilogram can
eradicate hundreds of thousands of individuals living in a metropolitan area.
Another characteristic making anthrax an effective biological agent, is that
anthrax spores can be stored for decades without losing their viability .Why
should we be worried about biological terrorism?
 Many of the agents used as biological weapons occur in nature and are
therefore available for use among both the military and civilians. The ease
with which biological weapons can be delivered also makes dissemination of
these agents easy. In 1995, two members of a militia group in Minnesota
were convicted of possession of ricin, a biological agent that they had
produced themselves. The ease with which harmful biological agents may
be obtained is probably best exemplified by the 1996 episode in which
Bubonic plague cultures were obtained through the postal service by a man
in Ohio.   
 Epidemiology
 Anthrax is caused by the bacterium Bacillus anthracis. Bacillus anthracis is derived
from the Greek word, anthrakis, which translates into "coal" because it causes dark,
coal-like eschars on affected areas. Anthrax is most common in South and Central
America, Southern and Eastern Europe, Asia, Africa, the Caribbean, and the Middle
East

 Anthrax has a long history

 Anthrax is believed to be the fifth Egyptian plague, dating back to around 1500 BCE
 There have been recorded cases of anthrax in ancient Rome
 Anthrax is considered to be the first "germ" discovered to cause disease in humans
 Bacillus anthracis was used as the model for Koch's postulates 
 In 1881, in a famous experiement, Louis Pasteur vaccinated some sheep with a live
attenuated version of anthrax. He then challenged vaccinated and unvaccinated with
a virulent culture. All the vaccinated survived while the unvaccinated did not.
 Louis Pasteur also used a live attenuated anthrax strain to develop the first anthrax
vaccine for use in humans
 Metchnikoff used anthrax to examine the ability of macrophages to kill microbes .
 
 Symptoms appear two to five days after ingestion, and include nausea,
abdominal pain, vomiting, and malaise, eventually progressing to bloody
diarrhea, acute abdomen, or sepsis. Massive edema and mucosal necrosis
occur at the sites of infection. Due to the ulceration of the gastrointestinal
mucosa, blood-tinged vomiting usually occurs. Ascites eventually develop
two to four days after the onset of symptoms.
 Anthrax has a long history

 Anthrax is believed to be the fifth Egyptian plague, dating back to

around 1500 BCE
 There have been recorded cases of anthrax in ancient Rome
 Anthrax is considered to be the first "germ" discovered to cause
disease in humans
 Bacillus anthracis was used as the model for Koch's postulates 
 In 1881, in a famous experiment, Louis Pasteur vaccinated some
sheep with a live attenuated version of anthrax. He then challenged
vaccinated and unvaccinated with a virulent culture. All the
vaccinated survived while the unvaccinated did not.
 Louis Pasteur also used a live attenuated anthrax strain to develop
the first anthrax vaccine for use in humans
 Metchnikoff used anthrax to examine the ability of macrophages to
kill microbes
 Pathology
 3 types of anthrax infection occur in
humans:
 Inhalation
 Gastrointestinal
 Cutaneous
 Inhalation
 Naturally occurring inhalational anthrax was historically a disease associated
with wool sorters at industrial mills. Only 18 cases were reported in the US
from 1900 to 1978.

This form of the disease is a result of the deposition of spore-bearing particles

of 1 to 5 mm into the alveolar spaces. Macrophages, which act as a host
defense mechanism, lyse and destroy some of the spores. Infection in the lung
is extremely rare. The surviving spores are transported to the mediastinal and
peribronchial lymph nodes. Germination may occur in the mediastinal lymph.
nodes up to 60 days after infection. Disease immediately follows germination
Anthrax bacilli replicate in the lymph nodes. Hemorrhage, edema, and necrosis
are the results of bacterial toxins released during replication. The first stage of
illness is flu-like with fever, myalgia, dyspnea, cough, headache, vomiting,
chills, abdominal pain, and chest pain. Sudden fever, dyspnea, diaphoresis,
and shock characterize the second stage of illness. In the second stage of
illness, cyanosis and hypotension result in a rapid death. Death usually results
2-3 days after the onset of symptoms.
Treatment

Why is early intervention necessary?                                     

Therapy is most efficacious if initiated during the incubation period.
The disease progresses rapidly once symptoms are recognized
 Gastrointestinal
Gastrointestinal infection is associated with ingestion of undercooked contaminated
meat. There are 2 distinct syndromes of gastrointestinal anthrax: oral-pharyngeal
and abdominal. The oral-pharyngeal form of the disease results from the
deposition and germination of spores in the upper gastrointestinal tract.

Gastrointestinal anthrax cases are uncommon, however, there have

been reported outbreaks in Africa and Asia. Abdominal anthrax is more
common than the oral-pharyngeal form. The consumption of
contaminated buffalo meat resulted in 24 cases of oral-pharyngeal
anthrax in Thailand in 1982. Five years later, 14 cases were reported in
Thailand with both oral-pharyngeal and abdominal disease occurring.
Gastrointestinal anthrax has not been reported in the United States.

 
 Symptoms appear two to five days after ingestion, and include nausea,
abdominal pain, vomiting, and malaise, eventually progressing to bloody
diarrhea, acute abdomen, or sepsis. Massive edema and mucosal necrosis
occur at the sites of infection. Due to the ulceration of the gastrointestinal
mucosa, blood-tinged vomiting usually occurs. Ascites eventually develop
two to four days after the onset of symptoms.
 Cutaneous
Infection develops following exposure to anthrax-infected animals. Cuts
or breaks in the skin make a person more susceptible to infection. After
the spore germinates in skin tissues, toxin production initially results in
macular or papular skin lesions. The macules or papules enlarge into
ulcers which are usually 1-3 cm in diameter. Vesicles may also develop
which discharge clear or serosanguinous fluid. This is followed by the
development of painless black eschars surrounded by massive edema
and a number of purplish vesicles. The eschars eventually dry and fall off
within 1 to 2 weeks.
                               
Antibiotics are used to treat infection, and although treatment does not prevent the
formation of eschars, it does prevent progression to systemic disease. If the
infection is treated with antibiotics, death is rare. However, if antibiotics are not
used, there is a 20% death rate.
Approximately 2000 cases of cutaneous anthrax are reported annually, making it the
most common naturally occurring form of anthrax. The largest epidemic occurred
between 1979 and 1985 in Zimbabwe with more than 10,000 cases of cutaneous
anthrax reported. Only 224 cases were reported in the US from 1944 to 1994.