ANTHRAX is an infection caused by the bacterium _
_. It can occur in four forms: skin, inhalation, 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 nausea,
vomiting, diarrhea, or abdominal pain. The injection form presents
with fever and an abscess at the site of drug injection .
Anthraxis spread by contact with the spores of the bacteria , which
are often from 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.
Anthraxvaccination is recommended for people who are at high risk.
Immunizing animals against anthrax is recommended in areas where
previous infections have occurred. Two months of antibiotics, such as
doxycycline or ciprofloxacin , 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.
Antitoxinis recommended for those with
Anthraxamong humans is most common in Africa and central and
Southern Asia. It also occurs fairly regularly in Southern Europe,
but 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
Carnivoresmay become infected by eating infected animals.
* 1 Signs and symptoms
* 1.1 Skin
* 1.2 Lungs
* 1.3 Gastrointestinal
* 2 Cause
* 2.1 Bacteria
* 2.2 Exposure
* 2.3 Mode of infection
* 3 Diagnosis
* 4 Prevention
* 4.1 Vaccines
* 5 Treatment
* 5.2 Monoclonal antibodies
* 6 History
* 6.1 Etymology
* 6.2 Discovery
* 6.3 First vaccination
* 7 Society and culture
* 7.1 Site cleanup
* 7.2.1 Sverdlovsk incident (2 April 1979)
* 7.2.3 Decontaminating mail
* 8 Other animals
* 9 References
* 10 External links
SIGNS AND SYMPTOMS
Skin lesionfrom anthrax Skin anthrax lesion on the neck
Cutaneous anthrax, also known as _Hide porter's disease_, is when
anthrax occurs on the skin. It 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. Cutaneous anthrax is
the most common and least dangerous form of anthrax.
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 initially
presents with cold or flu-like symptoms for several days, followed by
pneumonia and severe (and often fatal) respiratory collapse.
Historical mortality rates were over 85%, but, when treated early
(seen in the
2001 anthrax attacks
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 developed.
Gastrointestinal (GI) infection in humans is most often caused by
consuming anthrax-infected meat and is characterized by serious GI
difficulty, vomiting of blood , severe diarrhea, acute inflammation of
the intestinal tract, and loss of appetite. 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.
Gram stainof the bacterium Bacillus
anthracis_, the cause of the anthrax disease Main article: Bacillus
Bacillusanthracis_ is a rod-shaped,
bacterium about 1 by 9 μm in size. It was shown to cause disease by
Robert Kochin 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 endospore 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 endospores
into the tissues, though this has not been proven. Once ingested or
placed in an open wound, the bacterium begins multiplying inside the
animal or human and typically kills the host within a few days or
weeks. The endospores germinate at the site of entry into the tissues
and then spread by the circulation to the lymphatics, where the
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 the
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 will still die of toxemia because the toxins produced by
the bacilli remain in their system at lethal dose levels.
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 toxinis 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.
Edemafactor 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-alphaand interleukin 1,
TNF-alphais 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
IL1Bultimately 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 the peritoneal cavity , lymph vessels, and blood
vessels, causing vascular leakage of fluid and cells, and ultimately
hypovolemic shock and septic shock.
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-positiveanthrax 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 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 years.
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.
Anthraxin 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. 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 autopsy.
In November 2008, a drum maker in the United Kingdom who worked with
untreated animal skins died from anthrax. 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. In December 2009, an outbreak of anthrax
occurred amongst heroin addicts in the
Scotland, resulting in 14 deaths. The source of the anthrax is
believed to be dilution of the heroin with bone meal in Afghanistan.
Also 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 drumming circle . The woman apparently inhaled
anthrax 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
MODE OF INFECTION
Inhalational anthrax, mediastinal widening
Anthraxcan 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, may be fatal.
Anthraxcan be contracted in laboratory accidents or by handling
infected animals or their wool or hides. It has also been used in
biological warfare agents and by terrorists to intentionally infect as
exemplified by the
2001 anthrax attacks
2001 anthrax attacks.
Various techniques may be used for the direct identification of _B.
anthracis_ in clinical material. Firstly, specimens may be Gram
stained . _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.
All _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
formation. _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. _B. anthracis_ bacilli range from 0.5–5.0 μm in
size. Anyone working with anthrax in a suspected or confirmed person
should wear respiratory equipment capable of filtering this size of
particle 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 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
Pasteurdeveloped the first effective vaccine in 1881. Human
anthrax vaccines were developed by the
Soviet Unionin 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 spore (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 (
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.
Anthraxcannot 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 Sciencessubmitted 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.
Raxibacumabis 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_.
Obiltoxaximabis approved to treat
inhalational anthrax in conjunction with appropriate antibacterial
drugs, and for prevention when alternative therapies are not available
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
Bartholomaeus Anglicus' work _De proprietatibus rerum_
(_On the Properties of Things_, 1240).
Anthraxhas 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 the 1905
Nobel Prize in Physiology or Medicinefor 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
Bradfordwith his family as a child, carried out important research
for the local
AnthraxInvestigation Board. Eurich also made valuable
contributions to a
Home OfficeDepartmental 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).
sheep against anthrax
Anthraxposed a major economic challenge in
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 Pasteurwas 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 prepared by
Pasteurtwice, 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,
Pasteurmade strenuous efforts to
export the vaccine beyond France. He used his celebrity status to
PasteurInstitutes across Europe and Asia, and his nephew,
Adrien Loir, travelled to
Australiain 1888 to try and introduce the
vaccine to combat anthrax in
New South Wales
New South Wales. Ultimately the vaccine
was unsuccessful in the challenging climate of rural
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
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 straincontains two virulence plasmids ,
which separately encode for a three-protein toxin, called anthrax
toxin , and a polyglutamic acid capsule .
Vollum strain, developed but never used as a
biological weapon during the
Second World War
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.
Anthraxspores 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
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 dioxidehas 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
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 Islandis 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 Powellgiving a presentation to the United Nations
Security Council , holding a model vial of anthrax
Anthraxspores 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.
Anthraxwas first tested as
a biological warfare agent by
Unit 731of the Japanese Kwantung Army
Manchuriaduring 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 Islandin 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 Downfor "
Operation Vegetarian" – antilivestock attacks
against Germany to be made by the
Royal Air Force
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
and stored 100 to 200 tons of anthrax spores at
Vozrozhdeniya Island. They were abandoned in 1992 and destroyed in
American military and
British Armypersonnel are routinely vaccinated
against anthrax prior to active service in places where biological
attacks are considered a threat.
Sverdlovsk Incident (2 April 1979)
Sverdlovsk anthrax leak
Despite signing the 1972 agreement to end bioweapon production, the
government of the
Soviet Unionhad 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
KGBcontinued from 1979 until Russian President 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 Unionhad 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 Unionviolating the 1972
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 weapons program.
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 Daschleof South Dakota
Patrick Leahyof 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
Anthraxis especially rare in dogs and cats, as is evidenced by a
single reported case in the United States in 2001.
occur in some wild animal populations with some regularity.
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 heat wave.
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