Anthrax is an infection caused by the bacterium
It can occur in four forms: skin, lungs, intestinal, and injection.
Symptoms begin between one day and two months after the infection is
contracted. The skin form presents with a small blister with
surrounding swelling that often turns into a painless ulcer with a
black center. The inhalation form presents with fever, chest pain,
and shortness of breath. The intestinal form presents with diarrhea
which may contain blood, abdominal pains, and nausea and vomiting.
The injection form presents with fever and an abscess at the site of
Anthrax is spread by contact with the bacterium's spores, which often
appear in infectious animal products. Contact is by breathing,
eating, or through an area of broken skin. It does not typically
spread directly between people. Risk factors include people who
work with animals or animal products, travelers, postal workers, and
military personnel. Diagnosis can be confirmed based on finding
antibodies or the toxin in the blood or by culture of a sample from
the infected site.
Anthrax vaccination is recommended for people who are at high risk of
infection. Immunizing animals against anthrax is recommended in
areas where previous infections have occurred. Two months of
antibiotics such as ciprofloxacin, levofloxacin, and doxycycline after
exposure can also prevent infection. If infection occurs treatment
is with antibiotics and possibly antitoxin. The type and number of
antibiotics used depends on the type of infection.
recommended for those with widespread infection.
Though a rare disease, human anthrax, when it does occur, is most
common in Africa and central and southern Asia. It also occurs
more regularly in
Southern Europe than elsewhere on the continent, and
is uncommon in
Northern Europe and North America. Globally, at
least 2,000 cases occur a year with about two cases a year in the
United States. Skin infections represent more than 95% of
cases. Without treatment, the risk of death from skin anthrax is
24%. For intestinal infection, the risk of death is 25 to 75%,
while respiratory anthrax has a mortality of 50 to 80%, even with
treatment. Until the 20th century, anthrax infections killed
hundreds of thousands of people and animals each year.
been developed as a weapon by a number of countries. In
plant-eating animals, infection occurs when they eat or breathe in the
spores while grazing.
Carnivores may become infected by eating
1 Signs and symptoms
2.3 Mode of infection
6.2 Monoclonal antibodies
7.1 United States
7.2 United Kingdom
8.3 First vaccination
9 Society and culture
9.1 Site cleanup
9.2 Biological warfare
9.2.1 Sverdlovsk incident (2 April 1979)
9.2.3 Decontaminating mail
10 Other animals
12 External links
Signs and symptoms
Skin lesion from anthrax
Skin anthrax lesion on the neck
Cutaneous anthrax, also known as Hide porter's disease, is when
anthrax occurs on the skin. It is the most common form (>90% of
anthrax cases). It is also the least dangerous form of anthrax (low
mortality with treatment, 20% mortality without). Cutaneous
anthrax presents as a boil-like skin lesion that eventually forms an
ulcer with a black center (eschar). The black eschar often shows up as
a large, painless, necrotic ulcer (beginning as an irritating and
itchy skin lesion or blister that is dark and usually concentrated as
a black dot, somewhat resembling bread mold) at the site of infection.
In general, cutaneous infections form within the site of spore
penetration between two and five days after exposure. Unlike bruises
or most other lesions, cutaneous anthrax infections normally do not
cause pain. Nearby lymph nodes may become infected, reddened, swollen,
and painful. A scab forms over the lesion soon, and falls off in a few
weeks. Complete recovery may take longer. Cutaneous anthrax is
typically caused when B. anthracis spores enter through cuts on the
skin. This form is found most commonly when humans handle infected
animals and/or animal products.
Cutaneous anthrax is rarely fatal if treated, because the
infection area is limited to the skin, preventing the lethal factor,
edema factor, and protective antigen from entering and destroying a
vital organ. Without treatment, about 20% of cutaneous skin infection
cases progress to toxemia and death.
Respiratory infection in humans is relatively rare and presents as two
stages. It infects the lymph nodes in the chest first, rather than
the lungs themselves, a condition called hemorrhagic mediastinitis,
causing bloody fluid to accumulate in the chest cavity, therefore
causing shortness of breath. The first stage causes cold and flu-like
symptoms. Symptoms include fever, shortness of breath, cough, fatigue,
and chills. This can last hours to days. Often, many fatalities from
inhalational anthrax are when the first stage is mistaken for the cold
or flu and the victim does not seek treatment until the second stage,
which is 90% fatal. The second (pneumonia) stage occurs when the
infection spreads from the lymph nodes to the lungs. Symptoms of the
second stage develop suddenly after hours or days of the first stage.
Symptoms include high fever, extreme shortness of breath, shock, and
rapid death within 48 hours in fatal cases. Historical mortality rates
were over 85%, but when treated early (seen in the 2001 anthrax
attacks), observed case fatality rate dropped to 45%.
Distinguishing pulmonary anthrax from more common causes of
respiratory illness is essential to avoiding delays in diagnosis and
thereby improving outcomes. An algorithm for this purpose has been
Gastrointestinal (GI) infection is most often caused by consuming
anthrax-infected meat and is characterized by diarrhea, potentially
with blood, abdominal pains, acute inflammation of the intestinal
tract, and loss of appetite. Occasional vomiting of blood can
occur. Lesions have been found in the intestines and in the mouth and
throat. After the bacterium invades the gastrointestinal system, it
spreads to the bloodstream and throughout the body, while continuing
to make toxins. GI infections can be treated, but usually result in
fatality rates of 25% to 60%, depending upon how soon treatment
commences. This form of anthrax is the rarest form.
Photomicrograph of a
Gram stain of the bacterium
the cause of the anthrax disease
Bacillus anthracis is a rod-shaped, Gram-positive, aerobic bacterium
about 1 by 9 μm in size. It was shown to cause disease by
Robert Koch in 1876 when he took a blood sample from an infected cow,
isolated the bacteria, and put them into a mouse. The bacterium
normally rests in spore form in the soil, and can survive for decades
in this state. Herbivores are often infected whilst grazing,
especially when eating rough, irritant, or spiky vegetation; the
vegetation has been hypothesized to cause wounds within the
gastrointestinal tract permitting entry of the bacterial spores into
the tissues, though this has not been proven. Once ingested or placed
in an open wound, the bacteria begin multiplying inside the animal or
human and typically kill the host within a few days or weeks. The
spores germinate at the site of entry into the tissues and then spread
by the circulation to the lymphatics, where the bacteria multiply.
The production of two powerful exotoxins and lethal toxin by the
bacteria causes death. Veterinarians can often tell a possible
anthrax-induced death by its sudden occurrence, and by the dark,
nonclotting blood that oozes from the body orifices. Most anthrax
bacteria inside the body after death are outcompeted and destroyed by
anaerobic bacteria within minutes to hours post mortem. However,
anthrax vegetative bacteria that escape the body via oozing blood or
through the opening of the carcass may form hardy spores. These
vegetative bacteria are not contagious. One spore forms per one
vegetative bacterium. The triggers for spore formation are not yet
known, though oxygen tension and lack of nutrients may play roles.
Once formed, these spores are very hard to eradicate.
The infection of herbivores (and occasionally humans) by the
inhalational route normally proceeds as follows: Once the spores are
inhaled, they are transported through the air passages into the tiny
air sacs (alveoli) in the lungs. The spores are then picked up by
scavenger cells (macrophages) in the lungs and are transported through
small vessels (lymphatics) to the lymph nodes in the central chest
cavity (mediastinum). Damage caused by the anthrax spores and bacilli
to the central chest cavity can cause chest pain and difficulty in
breathing. Once in the lymph nodes, the spores germinate into active
bacilli that multiply and eventually burst the macrophages, releasing
many more bacilli into the bloodstream to be transferred to the entire
body. Once in the blood stream, these bacilli release three proteins
named lethal factor, edema factor, and protective antigen. The three
are not toxic by themselves, but their combination is incredibly
lethal to humans. Protective antigen combines with these other two
factors to form lethal toxin and edema toxin, respectively. These
toxins are the primary agents of tissue destruction, bleeding, and
death of the host. If antibiotics are administered too late, even if
the antibiotics eradicate the bacteria, some hosts still die of
toxemia because the toxins produced by the bacilli remain in their
system at lethal dose levels.
Color-enhanced scanning electron micrograph shows splenic tissue from
a monkey with inhalational anthrax; featured are rod-shaped bacilli
(yellow) and an erythrocyte (red)
Gram-positive anthrax bacteria (purple rods) in cerebrospinal fluid:
If present, a Gram-negative bacterial species would appear pink. (The
other cells are white blood cells.)
The spores of anthrax are able to survive in harsh conditions for
decades or even centuries. Such spores can be found on all
continents, including Antarctica. Disturbed grave sites of
infected animals have been known to cause infection after 70
Occupational exposure to infected animals or their products (such as
skin, wool, and meat) is the usual pathway of exposure for humans.
Workers who are exposed to dead animals and animal products are at the
highest risk, especially in countries where anthrax is more common.
Anthrax in livestock grazing on open range where they mix with wild
animals still occasionally occurs in the United States and elsewhere.
Many workers who deal with wool and animal hides are routinely exposed
to low levels of anthrax spores, but most exposure levels are not
sufficient to develop anthrax infections. A lethal infection is
reported to result from inhalation of about 10,000–20,000 spores,
though this dose varies among host species. Little documented
evidence is available to verify the exact or average number of spores
needed for infection.
Historically, inhalational anthrax was called woolsorters' disease
because it was an occupational hazard for people who sorted wool.
Today, this form of infection is extremely rare in advanced nations,
as almost no infected animals remain.
Mode of infection
Inhalational anthrax, mediastinal widening
Anthrax can enter the human body through the intestines (ingestion),
lungs (inhalation), or skin (cutaneous) and causes distinct clinical
symptoms based on its site of entry. In general, an infected human
will be quarantined. However, anthrax does not usually spread from an
infected human to a noninfected human. But, if the disease is
fatal to the person's body, its mass of anthrax bacilli becomes a
potential source of infection to others and special precautions should
be used to prevent further contamination. Inhalational anthrax, if
left untreated until obvious symptoms occur, is usually fatal.
Anthrax can be contracted in laboratory accidents or by handling
infected animals, their wool or their hides. It has also been used
in biological warfare agents and by terrorists to intentionally infect
as exemplified by the 2001 anthrax attacks.
The lethality of the anthrax disease is due to the bacterium's two
principal virulence factors: the poly-D-glutamic acid capsule, which
protects the bacterium from phagocytosis by host neutrophils, and the
tripartite protein toxin, called anthrax toxin.
Anthrax toxin is a
mixture of three protein components: protective antigen (PA), edema
factor (EF), and lethal factor (LF). PA plus LF produces lethal
toxin, and PA plus EF produces edema toxin. These toxins cause death
and tissue swelling (edema), respectively.
To enter the cells, the edema and lethal factors use another protein
produced by B. anthracis called protective antigen, which binds to two
surface receptors on the host cell. A cell protease then cleaves PA
into two fragments: PA20 and PA63. PA20 dissociates into the
extracellular medium, playing no further role in the toxic cycle. PA63
then oligomerizes with six other PA63 fragments forming a heptameric
ring-shaped structure named a prepore. Once in this shape, the complex
can competitively bind up to three EFs or LFs, forming a resistant
complex. Receptor-mediated endocytosis occurs next, providing the
newly formed toxic complex access to the interior of the host cell.
The acidified environment within the endosome triggers the heptamer to
release the LF and/or EF into the cytosol. It is unknown how
exactly the complex results in the death of the cell.
Edema factor is a calmodulin-dependent adenylate cyclase. Adenylate
cyclase catalyzes the conversion of ATP into cyclic AMP (cAMP) and
pyrophosphate. The complexation of adenylate cyclase with calmodulin
removes calmodulin from stimulating calcium-triggered signaling, thus
inhibiting the immune response. To be specific, LF inactivates
neutrophils (a type of phagocytic cell) by the process just described
so they cannot phagocytose bacteria. Throughout history, lethal factor
was presumed to cause macrophages to make
TNF-alpha and interleukin 1,
TNF-alpha is a cytokine whose primary role is to regulate
immune cells, as well as to induce inflammation and apoptosis or
programmed cell death. Interleukin 1, beta is another cytokine that
also regulates inflammation and apoptosis. The overproduction of
IL1B ultimately leads to septic shock and death.
However, recent evidence indicates anthrax also targets endothelial
cells that line serous cavities such as the pericardial cavity,
pleural cavity, and peritoneal cavity, lymph vessels, and blood
vessels, causing vascular leakage of fluid and cells, and ultimately
hypovolemic shock and septic shock.
Various techniques may be used for the direct identification of B.
anthracis in clinical material. Firstly, specimens may be Gram
Bacillus spp. are quite large in size (3 to 4 μm long),
they may grow in long chains, and they stain Gram-positive. To confirm
the organism is B. anthracis, rapid diagnostic techniques such as
polymerase chain reaction-based assays and immunofluorescence
microscopy may be used.
Bacillus species grow well on 5% sheep blood agar and other
routine culture media. Polymyxin-lysozyme-EDTA-thallous acetate can be
used to isolate B. anthracis from contaminated specimens, and
bicarbonate agar is used as an identification method to induce capsule
Bacillus spp. usually grow within 24 hours of incubation at
35°C, in ambient air (room temperature) or in 5% CO2. If bicarbonate
agar is used for identification, then the medium must be incubated in
5% CO2. B. anthracis colonies are medium-large, gray, flat, and
irregular with swirling projections, often referred to as having a
"medusa head" appearance, and are not hemolytic on 5% sheep blood
agar. The bacteria are not motile, susceptible to penicillin, and
produce a wide zone of lecithinase on egg yolk agar. Confirmatory
testing to identify B. anthracis includes gamma bacteriophage testing,
indirect hemagglutination, and enzyme-linked immunosorbent assay to
detect antibodies. The best confirmatory precipitation test for
anthrax is the Ascoli test.
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If a person is suspected as having died from anthrax, precautions
should be taken to avoid skin contact with the potentially
contaminated body and fluids exuded through natural body openings. The
body should be put in strict quarantine. A blood sample should then be
collected and sealed in a container and analyzed in an approved
laboratory to ascertain if anthrax is the cause of death. Then, the
body should be incinerated. Microscopic visualization of the
encapsulated bacilli, usually in very large numbers, in a blood smear
stained with polychrome methylene blue (McFadyean stain) is fully
diagnostic, though culture of the organism is still the gold standard
for diagnosis. Full isolation of the body is important to prevent
possible contamination of others. Protective, impermeable clothing and
equipment such as rubber gloves, rubber apron, and rubber boots with
no perforations should be used when handling the body. No skin,
especially if it has any wounds or scratches, should be exposed.
Disposable personal protective equipment is preferable, but if not
available, decontamination can be achieved by autoclaving. Disposable
personal protective equipment and filters should be autoclaved, and/or
burned and buried. Anyone working with anthrax in a suspected or
confirmed person should wear respiratory equipment capable of
filtering particles of their size or smaller. The US National
Institute for Occupational Safety and Health – and Mine Safety and
Health Administration-approved high-efficiency respirator, such as a
half-face disposable respirator with a high-efficiency particulate air
filter, is recommended. All possibly contaminated bedding or
clothing should be isolated in double plastic bags and treated as
possible biohazard waste. The body of an infected person should be
sealed in an airtight body bag. Dead people who are opened and not
burned provide an ideal source of anthrax spores. Cremating people is
the preferred way of handling body disposal. No embalming or autopsy
should be attempted without a fully equipped biohazard laboratory and
trained, knowledgeable personnel.
Vaccines against anthrax for use in livestock and humans have had a
prominent place in the history of medicine. The French scientist Louis
Pasteur developed the first effective vaccine in 1881.
Human anthrax vaccines were developed by the
Soviet Union in the late
1930s and in the US and UK in the 1950s. The current FDA-approved US
vaccine was formulated in the 1960s.
Currently administered human anthrax vaccines include acellular
(United States) and live vaccine (Russia) varieties. All currently
used anthrax vaccines show considerable local and general
reactogenicity (erythema, induration, soreness, fever) and serious
adverse reactions occur in about 1% of recipients. The American
product, BioThrax, is licensed by the FDA and was formerly
administered in a six-dose primary series at 0, 2, 4 weeks and 6, 12,
18 months, with annual boosters to maintain immunity. In 2008, the FDA
approved omitting the week-2 dose, resulting in the currently
recommended five-dose series. New second-generation vaccines
currently being researched include recombinant live vaccines and
recombinant subunit vaccines. In the 20th century the use of a modern
product (BioThrax) to protect American troops against the use of
anthrax in biological warfare was controversial.
Preventative antibiotics are recommended in those who have been
exposed. Early detection of sources of anthrax infection can allow
preventive measures to be taken. In response to the anthrax attacks of
October 2001, the
United States Postal Service
United States Postal Service (USPS) installed
biodetection systems (BDSs) in their large-scale mail processing
facilities. BDS response plans were formulated by the USPS in
conjunction with local responders including fire, police, hospitals
and public health. Employees of these facilities have been educated
about anthrax, response actions, and prophylactic medication. Because
of the time delay inherent in getting final verification that anthrax
has been used, prophylactic antibiotic treatment of possibly exposed
personnel must be started as soon as possible.
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purpose of is to present facts, not to train. Please help
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Anthrax and antibiotics
Anthrax cannot be spread directly from person to person, but a
person's clothing and body may be contaminated with anthrax spores.
Effective decontamination of people can be accomplished by a thorough
wash-down with antimicrobial soap and water. Waste water should be
treated with bleach or another antimicrobial agent. Effective
decontamination of articles can be accomplished by boiling them in
water for 30 minutes or longer. Chlorine bleach is ineffective in
destroying spores and vegetative cells on surfaces, though
formaldehyde is effective. Burning clothing is very effective in
destroying spores. After decontamination, there is no need to
immunize, treat, or isolate contacts of persons ill with anthrax
unless they were also exposed to the same source of infection.
Early antibiotic treatment of anthrax is essential; delay
significantly lessens chances for survival.
Treatment for anthrax infection and other bacterial infections
includes large doses of intravenous and oral antibiotics, such as
fluoroquinolones (ciprofloxacin), doxycycline, erythromycin,
vancomycin, or penicillin. FDA-approved agents include ciprofloxacin,
doxycycline, and penicillin.
In possible cases of pulmonary anthrax, early antibiotic prophylaxis
treatment is crucial to prevent possible death.
In recent years, many attempts have been made to develop new drugs
against anthrax, but existing drugs are effective if treatment is
started soon enough.
In May 2009,
Human Genome Sciences submitted a biologic license
application (BLA, permission to market) for its new drug, raxibacumab
(brand name ABthrax) intended for emergency treatment of inhaled
anthrax. On 14 December 2012, the US Food and Drug Administration
approved raxibacumab injection to treat inhalational anthrax.
Raxibacumab is a monoclonal antibody that neutralizes toxins produced
by B. anthracis. On March, 2016, FDA approved a second anthrax
treatment using a monoclonal antibody which neutralizes the toxins
produced by B. anthracis.
Obiltoxaximab is approved to treat
inhalational anthrax in conjunction with appropriate antibacterial
drugs, and for prevention when alternative therapies are not available
Globally, at least 2,000 cases occur a year.
The last fatal case of natural inhalational anthrax in the United
States occurred in California in 1976, when a home weaver died after
working with infected wool imported from Pakistan. To minimize the
chance of spreading the disease, the deceased was transported to UCLA
in a sealed plastic body bag within a sealed metal container for
Gastrointestinal anthrax is exceedingly rare in the United States,
with two cases on record, the first was reported in 1942, according to
the Centers for Disease Control and Prevention.
During December 2009, the New Hampshire Department of Health and Human
Services confirmed a case of gastrointestinal anthrax in an adult
female. The CDC investigated the source and the possibility that it
was contracted from an African drum recently used by the woman taking
part in a drum circle. The woman apparently inhaled anthrax [in
spore form] from the hide of the drum. She became critically ill, but
with gastrointestinal anthrax rather than inhaled anthrax, which made
her unique in American medical history. The building where the
infection took place was cleaned and reopened to the public and the
woman recovered. Jodie Dionne-Odom, New Hampshire state
epidemiologist, stated, "It is a mystery. We really don't know why it
In November 2008, a drum maker in the United Kingdom who worked with
untreated animal skins died from anthrax. In December 2009, an
outbreak of anthrax occurred amongst heroin addicts in the
Stirling areas of Scotland, resulting in 14 deaths. The source of
the anthrax is believed to be dilution of the heroin with bone meal in
See also: List of anthrax outbreaks
The English name comes from anthrax (ἄνθραξ), the Greek word
for coal, possibly having Egyptian etymology, because of
the characteristic black skin lesions developed by victims with a
cutaneous anthrax infection. The central, black eschar, surrounded by
vivid red skin has long been recognised as typical of the disease. The
first recorded use of the word "anthrax" in English is in a 1398
translation of Bartholomaeus Anglicus' work De proprietatibus rerum
(On the Properties of Things, 1240).
Anthrax has been known by a wide variety of names, indicating its
symptoms, location and groups considered most vulnerable to infection.
These include Siberian plague, Cumberland disease, charbon, splenic
fever, malignant edema, woolsorter's disease, and even la maladie de
Robert Koch, a German physician and scientist, first identified the
bacterium that caused the anthrax disease in 1875 in
part of Poland). His pioneering work in the late 19th century
was one of the first demonstrations that diseases could be caused by
microbes. In a groundbreaking series of experiments, he uncovered the
lifecycle and means of transmission of anthrax. His experiments not
only helped create an understanding of anthrax, but also helped
elucidate the role of microbes in causing illness at a time when
debates still took place over spontaneous generation versus cell
theory. Koch went on to study the mechanisms of other diseases and won
Nobel Prize in Physiology or Medicine
Nobel Prize in Physiology or Medicine for his discovery of
the bacterium causing tuberculosis.
Although Koch arguably made the greatest theoretical contribution to
our understanding of anthrax, other researchers were more concerned
with the practical questions of how to prevent the disease. In
Britain, where anthrax affected workers in the wool, worsted, hides
and tanning industries, it was viewed with fear. John Henry Bell, a
doctor based in Bradford, first made the link between the mysterious
and deadly "woolsorter's disease" and anthrax, showing in 1878 that
they were one and the same. In the early twentieth century,
Friederich Wilhelm Eurich, the German bacteriologist who settled in
Bradford with his family as a child, carried out important research
for the local
Anthrax Investigation Board. Eurich also made valuable
contributions to a
Home Office Departmental Committee of Inquiry,
established in 1913 to address the continuing problem of industrial
anthrax. His work in this capacity, much of it collaboration with
the factory inspector G. Elmhirst Duckering, led directly to the
Anthrax Prevention Act (1919).
Louis Pasteur inoculating sheep against anthrax
Anthrax posed a major economic challenge in
France and elsewhere
during the nineteenth century. Horses, cattle and sheep were
particularly vulnerable, and national funds were set aside to
investigate the production of a vaccine. The noted French scientist
Louis Pasteur was charged with the production of a vaccine, following
his successful work in developing methods which helped to protect the
important wine and silk industries.
In May 1881,
Pasteur – in collaboration with his assistants
Jean-Joseph Henri Toussaint, Émile Roux and others – performed a
public experiment at Pouilly-le-Fort to demonstrate his concept of
vaccination. He prepared two groups of 25 sheep, one goat, and several
cows. The animals of one group were injected with an anthrax vaccine
Pasteur twice, at an interval of 15 days; the control
group was left unvaccinated. Thirty days after the first injection,
both groups were injected with a culture of live anthrax bacteria. All
the animals in the unvaccinated group died, while all of the animals
in the vaccinated group survived.
After this apparent triumph, which was widely reported in the local,
national and international press,
Pasteur made strenuous efforts to
export the vaccine beyond France. He used his celebrity status to
Pasteur Institutes across Europe and Asia, and his nephew,
Adrien Loir, travelled to
Australia in 1888 to try and introduce the
vaccine to combat anthrax in New South Wales. Ultimately the
vaccine was unsuccessful in the challenging climate of rural
Australia, and it was soon superseded by a more robust version
developed by local researchers John Gunn and John McGarvie Smith.
The human vaccine for anthrax became available in 1954. This was a
cell-free vaccine instead of the live-cell Pasteur-style vaccine used
for veterinary purposes. An improved cell-free vaccine became
available in 1970.
Society and culture
The virulent Ames strain, which was used in the 2001 anthrax attacks
in the United States has received the most news coverage of any
anthrax outbreak. The
Ames strain contains two virulence plasmids,
which separately encode for a three-protein toxin, called anthrax
toxin, and a polyglutamic acid capsule.
Nonetheless, the Vollum strain, developed but never used as a
biological weapon during the Second World War, is much more dangerous.
The Vollum (also incorrectly referred to as Vellum) strain was
isolated in 1935 from a cow in Oxfordshire. This same strain was used
during the Gruinard bioweapons trials.
A variation of Vollum, known as "Vollum 1B", was used during the 1960s
in the US and UK bioweapon programs. Vollum 1B is widely believed
to have been isolated from William A. Boyles, a 46-year-old scientist
at the US Army Biological Warfare Laboratories at Camp (later Fort)
Detrick, Maryland, (precursor to USAMRIID), who died in 1951 after
being accidentally infected with the Vollum strain.
The Sterne strain, named after the Trieste-born immunologist Max
Sterne, is an attenuated strain used as a vaccine, which contains only
the anthrax toxin virulence plasmid and not the polyglutamic acid
capsule expressing plasmid.
Anthrax spores can survive for very long periods of time in the
environment after release. Chemical methods for cleaning
anthrax-contaminated sites or materials may use oxidizing agents such
as peroxides, ethylene oxide, Sandia Foam, chlorine dioxide (used
in the Hart Senate Office Building), peracetic acid, ozone gas,
hypochlorous acid, sodium persulfate, and liquid bleach products
containing sodium hypochlorite. Nonoxidizing agents shown to be
effective for anthrax decontamination include methyl bromide,
formaldehyde, and metam sodium. These agents destroy bacterial spores.
All of the aforementioned anthrax decontamination technologies have
been demonstrated to be effective in laboratory tests conducted by the
US EPA or others. A bleach solution for treating hard surfaces has
been approved by the EPA.
Chlorine dioxide has emerged as the preferred biocide against
anthrax-contaminated sites, having been employed in the treatment of
numerous government buildings over the past decade. Its chief
drawback is the need for in situ processes to have the reactant on
To speed the process, trace amounts of a nontoxic catalyst composed of
iron and tetroamido macrocyclic ligands are combined with sodium
carbonate and bicarbonate and converted into a spray. The spray
formula is applied to an infested area and is followed by another
spray containing tert-butyl hydroperoxide.
Using the catalyst method, a complete destruction of all anthrax
spores can be achieved in under 30 minutes. A standard
catalyst-free spray destroys fewer than half the spores in the same
amount of time.
Cleanups at a Senate office building, several contaminated postal
facilities, and other US government and private office buildings
showed decontamination to be possible, but it is time-consuming and
costly. Clearing the Senate office building of anthrax spores cost
$27 million, according to the Government Accountability Office.
Cleaning the Brentwood postal facility in Washington cost
$130 million and took 26 months. Since then, newer and less
costly methods have been developed.
Cleanup of anthrax-contaminated areas on ranches and in the wild is
much more problematic. Carcasses may be burned, though it often
takes up to three days to burn a large carcass and this is not
feasible in areas with little wood. Carcasses may also be buried,
though the burying of large animals deeply enough to prevent
resurfacing of spores requires much manpower and expensive tools.
Carcasses have been soaked in formaldehyde to kill spores, though this
has environmental contamination issues. Block burning of vegetation in
large areas enclosing an anthrax outbreak has been tried; this, while
environmentally destructive, causes healthy animals to move away from
an area with carcasses in search of fresh grass. Some wildlife workers
have experimented with covering fresh anthrax carcasses with
shadecloth and heavy objects. This prevents some scavengers from
opening the carcasses, thus allowing the putrefactive bacteria within
the carcass to kill the vegetative B. anthracis cells and preventing
sporulation. This method also has drawbacks, as scavengers such as
hyenas are capable of infiltrating almost any exclosure.
The experimental site at
Gruinard Island is said to have been
decontaminated with a mixture of formaldehyde and seawater by the
Ministry of Defence. It is not clear whether similar treatments
had been applied to US test sites.
Colin Powell giving a presentation to the United Nations Security
Council, holding a model vial of anthrax
Anthrax spores have been used as a biological warfare weapon. Its
first modern incidence occurred when Nordic rebels, supplied by the
German General Staff, used anthrax with unknown results against the
Imperial Russian Army in Finland in 1916.
Anthrax was first tested
as a biological warfare agent by
Unit 731 of the Japanese Kwantung
Manchuria during the 1930s; some of this testing involved
intentional infection of prisoners of war, thousands of whom died.
Anthrax, designated at the time as Agent N, was also investigated by
the Allies in the 1940s.
A long history of practical bioweapons research exists in this area.
For example, in 1942, British bioweapons trials severely contaminated
Gruinard Island in Scotland with anthrax spores of the Vollum-14578
strain, making it a no-go area until it was decontaminated in
1990. The Gruinard trials involved testing the effectiveness
of a submunition of an "N-bomb" – a biological weapon
containing dried anthrax spores. Additionally, five million "cattle
cakes" (animal feed pellets impregnated with anthrax spores) were
prepared and stored at
Porton Down for "Operation Vegetarian" –
antilivestock attacks against Germany to be made by the Royal Air
Force. The plan was for anthrax-based biological weapons to be
dropped on Germany in 1944. However, the edible cattle cakes and the
bomb were not used; the cattle cakes were incinerated in late 1945.
Weaponized anthrax was part of the US stockpile prior to 1972, when
the United States signed the Biological Weapons Convention.
President Nixon ordered the dismantling of US biowarfare programs in
1969 and the destruction of all existing stockpiles of bioweapons. In
1978–79, the Rhodesian government used anthrax against cattle and
humans during its campaign against rebels. The Soviet Union
created and stored 100 to 200 tons of anthrax spores at
Vozrozhdeniya Island. They were abandoned in 1992 and destroyed in
American military and
British Army personnel are routinely vaccinated
against anthrax prior to active service in places where biological
attacks are considered a threat.
Sverdlovsk incident (2 April 1979)
Main article: Sverdlovsk anthrax leak
Despite signing the 1972 agreement to end bioweapon production, the
government of the
Soviet Union had an active bioweapons program that
included the production of hundreds of tons of weapons-grade anthrax
after this period. On 2 April 1979, some of the over one million
people living in Sverdlovsk (now called Ekaterinburg, Russia), about
850 miles (1,370 km) east of Moscow, were exposed to an
accidental release of anthrax from a biological weapons complex
located near there. At least 94 people were infected, of whom at least
68 died. One victim died four days after the release, 10 over an
eight-day period at the peak of the deaths, and the last six weeks
later. Extensive cleanup, vaccinations, and medical interventions
managed to save about 30 of the victims. Extensive cover-ups and
destruction of records by the
KGB continued from 1979 until Russian
Boris Yeltsin admitted this anthrax accident in 1992. Jeanne
Guillemin reported in 1999 that a combined Russian and United States
team investigated the accident in 1992.
Nearly all of the night-shift workers of a ceramics plant directly
across the street from the biological facility (compound 19) became
infected, and most died. Since most were men, some
Soviet Union had developed a sex-specific weapon.
The government blamed the outbreak on the consumption of
anthrax-tainted meat, and ordered the confiscation of all uninspected
meat that entered the city. They also ordered all stray dogs to be
shot and people not have contact with sick animals. Also, a voluntary
evacuation and anthrax vaccination program was established for people
To support the cover-up story, Soviet medical and legal journals
published articles about an outbreak in livestock that caused GI
anthrax in people having consumed infected meat, and cutaneous anthrax
in people having come into contact with the animals. All medical and
public health records were confiscated by the KGB. In addition to
the medical problems the outbreak caused, it also prompted Western
countries to be more suspicious of a covert Soviet bioweapons program
and to increase their surveillance of suspected sites. In 1986, the US
government was allowed to investigate the incident, and concluded the
exposure was from aerosol anthrax from a military weapons
facility. In 1992, President Yeltsin admitted he was "absolutely
certain" that "rumors" about the
Soviet Union violating the 1972
Bioweapons Treaty were true. The Soviet Union, like the US and UK, had
agreed to submit information to the UN about their bioweapons
programs, but omitted known facilities and never acknowledged their
In theory, anthrax spores can be cultivated with minimal special
equipment and a first-year collegiate microbiological education.
To make large amounts of an aerosol form of anthrax suitable for
biological warfare requires extensive practical knowledge, training,
and highly advanced equipment.
Concentrated anthrax spores were used for bioterrorism in the 2001
anthrax attacks in the United States, delivered by mailing postal
letters containing the spores. The letters were sent to several
news media offices and two Democratic senators:
Tom Daschle of South
Patrick Leahy of Vermont. As a result, 22 were infected and
five died. Only a few grams of material were used in these attacks
and in August 2008, the US Department of Justice announced they
believed that Dr. Bruce Ivins, a senior biodefense researcher employed
by the United States government, was responsible. These events
also spawned many anthrax hoaxes.
Due to these events, the US Postal Service installed biohazard
detection systems at its major distribution centers to actively scan
for anthrax being transported through the mail.
In response to the postal anthrax attacks and hoaxes, the United
States Postal Service sterilized some mail using gamma irradiation and
treatment with a proprietary enzyme formula supplied by Sipco
A scientific experiment performed by a high school student, later
published in The Journal of Medical Toxicology, suggested a domestic
electric iron at its hottest setting (at least 400 °F
(204 °C)) used for at least 5 minutes should destroy all anthrax
spores in a common postal envelope.
Anthrax is especially rare in dogs and cats, as is evidenced by a
single reported case in the United States in 2001. Anthrax
outbreaks occur in some wild animal populations with some
Russian researchers estimate arctic permafrost contains around 1.5
million anthrax-infected reindeer carcasses, and the spores may
survive in the permafrost for 105 years. There is a risk that
global warming in the Arctic can thaw the permafrost, releasing
anthrax spores in the carcasses. In 2016, an anthrax outbreak in
reindeer was linked to a 75-year-old carcass that defrosted during a
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