.

Anthrax
Classification and external resources

Photomicrograph of a Gram stain of the bacterium

Bacillus anthracis, the cause of the anthrax disease
ICD-10
A22.minor
ICD-9
022
DiseasesDB
1203
MedlinePlus
001325
eMedicine
med/148
MeSH
D000881
Anthrax is an acute disease caused by the bacterium Bacillus anthracis. Most forms of the
disease are lethal, and it affects both humans and animals. There are effective vaccines against
anthrax, and some forms of the disease respond well to antibiotic treatment.
Like many other members of the genus Bacillus, Bacillus anthracis can form dormant
endospores (often referred to as "spores" for short, but not to be confused with fungal spores)
that are able to survive in harsh conditions for decades or even centuries. [1] Such spores can be
found on all continents, even Antarctica.[2] When spores are inhaled, ingested, or come into
contact with a skin lesion on a host, they may become reactivated and multiply rapidly.
Anthrax commonly infects wild and domesticated herbivorous mammals that ingest or inhale the
spores while grazing. Ingestion is thought to be the most common route by which herbivores
contract anthrax. Carnivores living in the same environment may become infected by consuming
infected animals. Diseased animals can spread anthrax to humans, either by direct contact (e.g.,
inoculation of infected blood to broken skin) or by consumption of a diseased animal's flesh.
Anthrax spores can be produced in vitro and used as a biological weapon. Anthrax does not
spread directly from one infected animal or person to another; it is spread by spores. These
spores can be transported by clothing or shoes. The body of an animal that had active anthrax at
the time of death can also be a source of anthrax spores.
Until the twentieth century, anthrax infections killed hundreds of thousands of animals and
people worldwide each year.[3] French scientist Louis Pasteur developed the first effective
vaccine for anthrax in 1881.[4][5][6] Thanks to over a century of animal vaccination programs,
sterilization of raw animal waste materials, and anthrax eradication programs in North America,

Australia, New Zealand, Russia, Europe, and parts of Africa and Asia, anthrax infection is now
relatively rare in domestic animals (with only a few dozen cases reported each year). [citation needed]
Anthrax is especially rare in dogs and cats, as is evidenced by a single reported case in the USA
in 2001.[7] Anthrax typically does not cause disease in carnivores and scavengers, even when
these animals consume anthrax-infected carcasses. Anthrax outbreaks do occur in some wild
animal populations with some regularity.[8] The disease is more common in countries without
widespread veterinary or human public health programs.
Bacillus anthracis bacterial spores are soil-borne. Because of their long lifespan, spores are
present globally and remain at the burial sites of animals killed by anthrax for many decades.
Disturbed grave sites of infected animals have caused reinfection over 70 years after the animal's
interment.[9]

Signs and symptoms

Pulmonary
Respiratory infection in humans initially presents with cold or flu-like symptoms for several
days, followed by severe (and often fatal) respiratory collapse. Historical mortality was 92%,
but, when treated early (seen in the 2001 anthrax attacks), observed mortality was 45%.[10]
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.[11] Illness progressing to the fulminant phase has a 97% mortality regardless of
treatment.
A lethal infection is reported to result from inhalation of about 10,00020,000 spores, though this
dose varies among host species.[12] As with all diseases, it is presumed that there is a wide
variation to susceptibility with evidence that some people may die from much lower exposures;
there is little documented evidence to verify the exact or average number of spores needed for
infection. Inhalational anthrax is also known as Woolsorters' or Ragpickers' disease. These
professions were more susceptible to the disease due to their exposure to infected animal
products. Other practices associated with exposure include the slicing up of animal horns for the
manufacture of buttons, the handling of hair bristles used for the manufacturing of brushes, and
the handling of animal skins. Whether these animal skins came from animals that died of the
disease or from animals that had simply laid on ground with spores on it is unknown. This mode
of infection is used as a bioweapon.
Gastrointestinal
Gastrointestinal infection in humans is most often caused by consuming anthrax-infected meat
and is characterized by serious gastrointestinal 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 bowel system, it spreads
through the bloodstream throughout the body, while also continuing to make toxins.
Gastrointestinal infections can be treated but usually result in fatality rates of 25% to 60%,
depending upon how soon treatment commences.[13] This form of anthrax is the rarest form. In
the United States, there have only been two official cases, the first reported in 1942 by the CDC
and the second reported in 2010 that was treated at the Massachusetts General Hospital. [14][15][16] It
is the only known case of survival from GI anthrax in the U.S.A.
Cutaneous

Skin reaction to anthrax

A skin lesion caused by anthrax

Cutaneous (on the skin) anthrax infection in humans 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 2
and 5 days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections
normally do not cause pain.[13]
Cutaneous anthrax is typically caused when Bacillus anthracis spores enter through cuts on the
skin. This form of Anthrax is found most commonly when humans handle infected animals
and/or animal products (e.g., the hide of an animal used to make drums).
Cutaneous anthrax is rarely fatal if treated,[10] 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.
Cause
Bacteria

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 sample. If present, a Gramnegative bacterial species would appear pink. (The other cells are white blood cells).
Main article: Bacillus anthracis
Bacillus anthracis is a rod-shaped, gram-positive, aerobic bacterium about 1 by 9 micrometers 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 it into a mouse. [17] The bacterium normally rests in
endospore form in the soil, and can survive for decades in this state. Herbivores are often
infected whilst grazing or browsing, 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 endo-spores 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 endo-spores germinate at the
site of entry into the tissues and then spread via the circulation to the lymphatics, where the
bacteria multiply.
It is the production of two powerful exo-toxins and lethal toxin by the bacteria that causes death.
Veterinarians can often tell a possible anthrax-induced death by its sudden occurrence, and by the

dark, non-clotting blood that oozes from the body orifices. Most anthrax bacteria inside the body
after death are out-competed and destroyed by anaerobic bacteria within minutes to hours
postmortem. However, anthrax vegetative bacteria that escape the body via oozing blood or
through the opening of the carcass may form hardy spores. 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) via the inhalational route normally
proceeds as follows: Once the spores are inhaled, they are transported through the air passages
into the tiny air particles 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 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. All three are non-toxic by themselves, but the combination is
incredibly lethal to humans.[18] 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. This is because the toxins
produced by the bacilli remain in their system at lethal dose levels.
The lethality of the anthrax disease owes itself to the bacterium's two principal virulence factors:
(i) the poly-D-glutamic acid capsule, which protects the bacterium from phagocytosis by host
neutrophils, and (ii) the tripartite protein toxin, called anthrax toxin. Anthrax toxin is a mixture of
three protein components: (i) protective antigen (PA), (ii) edema factor (EF), and (iii) 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.
In order to enter the cells, the edema and lethal factors use another protein produced by B.
anthracis called protective antigen. Protective antigen 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 EF or LF forming a resistant complex. [18]
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. [19] 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.[18] To be specific, LF inactivates neutrophils (a type of
phagocytic cell) by the process just described so that they cannot phagocytose bacteria.

Throughout history, it was believed that lethal factor caused macrophages to make TNF-alpha
and interleukin 1, beta (IL1B). 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 TNF-alpha and IL1B ultimately leads to septic shock and death. However, recent
evidence indicates that anthrax also targets endothelial cells (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 (low
blood volume), and septic shock.
Exposure
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 exposures are not sufficient to
develop anthrax infections. It is presumed that the body's natural defenses can destroy low levels
of exposure. These people usually contract cutaneous anthrax if they catch anything. Throughout
history, the most dangerous form of 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, 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. The autopsy was done at UCLA hospital. 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.[20]
In November 2008, a drum maker in the United Kingdom who worked with untreated animal
skins died from anthrax.[21] Gastrointestinal anthrax is exceedingly rare in the United States, with
only one case on record, reported in 1942, according to the Centers for Disease Control and
Prevention.[14] In December 2009 an outbreak of anthrax occurred amongst heroin addicts in
Glasgow, Scotland, resulting in ten deaths.[22] The source of the anthrax is believed to be dilution
of the heroin with bone meal in Afghanistan.[23]
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.[24] 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, states, "It is a mystery. We really don't
know why it happened."[25]

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, may be fatal.
Anthrax can 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.
Diagnosis
Other than Gram stain of specimens, there are no specific direct identification techniques for
identification of Bacillus species in clinical material. These organisms are Gram-positive but
with age can be Gram-variable to Gram-negative. A specific feature of Bacillus species that
makes it unique from other aerobic microorganisms is its ability to produce spores. Although
spores are not always evident on a Gram stain of this organism, the presence of spores confirms
that the organism is of the genus Bacillus.
All Bacillus species grow well on 5% Sheep blood agar and other routine culture media. PLET
(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 sp. will 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 media must be
incubated in 5% CO2.
B.anthracis appears as medium-large, gray, flat, irregular with swirling projections, often
referred to as "medusa head" appearance, and is non-hemolytic on 5% sheep blood agar. It is

non-motile, is susceptible to penicillin and produces 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. [26] Anthrax is
also a Biphasic disease.
Prevention
Vaccines
Main article: Anthrax vaccines
Vaccines against anthrax for use in livestock and humans have had a prominent place in the
history of medicine, from Pasteurs pioneering 19th century work with cattle (the second
effective vaccine ever) to the controversial 20th century use of a modern product (BioThrax) to
protect American troops against the use of anthrax in biological warfare. 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 (USA) 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.[27] 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. [28] New second-generation vaccines currently being
researched include recombinant live vaccines and recombinant sub-unit vaccines.
Prophylaxis
If a person is suspected as having died from anthrax, every precaution 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 and then burnt. A blood sample taken in a
sealed container and analyzed in an approved laboratory should be used to ascertain if anthrax is
the cause of death. 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. Bacillus anthracis bacillii
range from 0.55.0 m in size. Anyone working with anthrax in a suspected or confirmed victim
should wear respiratory equipment capable of filtering this size of particle or smaller. The US
National Institute for Occupational Safety and Health (NIOSH) and Mine Safety and Health
Administration (MSHA) approved high efficiency-respirator, such as a half-face disposable

respirator with a high-efficiency particulate air (HEPA) filter, is recommended. [29] All possibly
contaminated bedding or clothing should be isolated in double plastic bags and treated as
possible bio-hazard waste. The victim should be sealed in an airtight body bag. Dead victims that
are opened and not burned provide an ideal source of anthrax spores. Cremating victims is the
preferred way of handling body disposal. No embalming or autopsy should be attempted without
a fully equipped biohazard laboratory and trained and knowledgeable personnel.
Delays of only a few days may make the disease untreatable and treatment should be started even
without symptoms if possible contamination or exposure is suspected. Animals with anthrax
often just die without any apparent symptoms. Initial symptoms may resemble a common cold
sore throat, mild fever, muscle aches and malaise. After a few days, the symptoms may progress
to severe breathing problems and shock and ultimately death. Death can occur from about two
days to a month after exposure with deaths apparently peaking at about 8 days after exposure. [30]
Antibiotic-resistant strains of anthrax are known.
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 (USPS)
installed BioDetection Systems (BDS) in their large scale mail cancellation 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.
Treatment
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 effective soap and water. Waste water should be
treated with bleach or other anti-microbial agent. Effective decontamination of articles can be
accomplished by boiling contaminated articles 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.
Antibiotics
Early antibiotic treatment of anthrax is essentialdelay significantly lessens chances for
survival.
Treatment for anthrax infection and other bacterial infections includes large doses of intravenous
and oral antibiotics, such as fluoroquinolones (like ciprofloxacin), doxycycline, erythromycin,
vancomycin, or penicillin. FDA-approved agents include ciprofloxacin, doxycycline, and
penicillin.[31]

In possible cases of inhalation anthrax, early antibiotic prophylaxis treatment is crucial to prevent
possible death.
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.[32] If death occurs from anthrax the body should be
isolated to prevent possible spread of anthrax germs. Burial does not kill anthrax spores.
In recent years there have been many attempts to develop new drugs against anthrax, but existing
drugs are effective if treatment is started soon enough.
Monoclonal antibodies
On December 14, 2012, the U.S. Food and Drug Administration approved raxibacumab injection
to treat inhalational anthrax. Raxibacumab is a monoclonal antibody that neutralizes toxins
produced by B. anthracis that can cause massive and irreversible tissue injury and death. A
monoclonal antibody is a protein that closely resembles a human antibody that identifies and
neutralizes foreign material like bacteria and viruses.[33]
History
Etymology
The name comes from anthrax [], the Greek word for 'coal', because of the black skin
lesions developed by victims with a cutaneous anthrax infection. It was discovered and analyzed
by Robert Koch (1876).
Alternative names: siberian plague, charbon, splenic fever, malignant edema, woolsorter's
disease
Discovery
Robert Koch, a German physician and scientist, first identified the bacterium that caused the
anthrax disease in 1875.[17][34] His pioneering work in the late nineteenth century was one of the
first demonstrations that diseases could be caused by microbes. In a groundbreaking series of
experiments, he uncovered the life cycle 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 Medicine for his discovery of the bacterium causing tuberculosis.

First vaccination
Further information: Anthrax vaccines

In May 1881 Louis Pasteur performed a public experiment 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 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 non-vaccinated group died,
while all of the animals in the vaccinated group survived. [35] 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.[36]
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
poly-glutamic 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, UK.
This is the same strain that 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 [37] to have been isolated from William A. Boyles, a 46year-old scientist at the U.S. Army Biological Warfare Laboratories at Camp (later Fort) Detrick,
Maryland, USA (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 poly-glutamic acid capsule expressing plasmid.
Site cleanup
Anthrax spores can survive for very long periods of time in the environment after release.
Methods for cleaning anthrax-contaminated sites commonly use oxidizing agents such as
peroxides, ethylene oxide, Sandia Foam,[38] chlorine dioxide (used in the Hart Senate Office
Building), and liquid bleach products containing sodium hypochlorite. These agents slowly
destroy bacterial spores. A bleach solution for treating hard surfaces has been approved by the
EPA.[39] Bleach and vinegar must not be combined together directly, as doing so could produce
chlorine gas. Rather some water must first be added to the bleach (e.g., two cups water to one
cup of bleach), then vinegar (e.g., one cup), and then the rest of the water (e.g., six cups). The pH
of the solution should be tested with a paper test strip; and treated surfaces must remain in
contact with the bleach solution for 60 minutes (repeated applications will be necessary to keep
the surfaces wet).
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 demand.
To speed the process, trace amounts of a non-toxic catalyst composed of iron and tetro-amido
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.[40]
Using the catalyst method, a complete destruction of all anthrax spores can be achieved in under
30 minutes.[40] A standard catalyst-free spray destroys fewer than half the spores in the same
amount of time. They can be heated, exposed to the harshest chemicals, and they do not easily
die.[vague]
Cleanups at a Senate office building, several contaminated postal facilities and other U.S.
government and private office buildings showed that decontamination is possible, but it is timeconsuming and costly. Clearing the Senate office building of anthrax spores cost $27 million,
according to the Government Accountability Office. Cleaning the Brentwood postal facility
outside Washington cost $130 million and took 26 months. Since then newer and less costly
methods have been developed.[41]
Clean up 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 graze and browse. 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's not clear if similar treatment has
been applied to US test sites.

Biological warfare

Colin Powell giving a presentation to the United Nations Security Council

Anthrax spores can and have been used as a biological warfare weapon. Its first modern
incidence occurred when Scandinavian rebels, supplied by the German General Staff used
anthrax with unknown results against the Imperial Russian Army in Finland in 1916. [42] Anthrax
was first tested as a biological warfare agent by Unit 731 of the Japanese Kwantung Army in
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.
There is a long history of practical bioweapons research in this area. For example, in 1942,
British bioweapons trials[43] 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. [44]
[45]
The Gruinard trials involved testing the effectiveness of a submunition of an "N-bomb"a
biological weapon. Additionally, five million "cattle cakes" impregnated with anthrax were
prepared and stored at Porton Down for "Operation Vegetarian"an anti-livestock weapon
intended for attacks on Germany by the Royal Air Force.[46] The infected cattle cakes were to be
dropped on Germany in 1944. However, neither the cakes nor the bomb was used; the cattle
cakes were incinerated in late 1945.
Weaponized anthrax was part of the U.S. stockpile prior to 1972, when the United States signed
the Biological Weapons Convention.[47] President Nixon ordered the dismantling of US
biowarfare programs in 1969 and the destruction of all existing stockpiles of bioweapons. In the
period 19781979 the Rhodesian government used anthrax against cattle and humans during its
war with black nationalists.[48] The Soviet Union created and stored 100 to 200 tons of anthrax
spores at Kantubek on Vozrozhdeniya Island. They were abandoned in 1992 and destroyed in
2002.
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 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, ten 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.[49] Extensive cover-ups and destruction of records by the KGB continued 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.[49][50][51]
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, there
were suspicions by NATO governments that the Soviet Union had developed a sex-specific
weapon.[52] 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 that all
stray dogs be shot and that people not have contact with sick animals. There was also a voluntary
evacuation and anthrax vaccination program established for people from 1855.[53]
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.[53] In addition to the medical problems that 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 that the exposure was from
aerosol anthrax from a military weapons facility.[54] In 1992, President Yeltsin admitted that 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
weapons program.[52]
Anthrax bioterrorism
In theory, anthrax spores can be cultivated with minimal special equipment and a first-year
collegiate microbiological education, but in practice the procedure is difficult and dangerous. To
make large amounts of an aerosol form of anthrax suitable for biological warfare requires
extensive practical knowledge, training, and highly advanced equipment.[citation needed]
Concentrated anthrax spores were used for bioterrorism in the 2001 anthrax attacks in the United
States, delivered by mailing postal letters containing the spores.[55] The letters were sent to
several news media offices as well as to two Democratic senators: Tom Daschle of South Dakota
and Patrick Leahy of Vermont. As a result, 22 were infected and five died. [18] 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.[56] These events also spawned many anthrax hoaxes.

Due to these events, the U.S. Postal Service installed biohazard detection systems at its major
distribution centers to actively scan for anthrax being transported through the mail.[57]
Decontaminating mail
In response to the postal anthrax attacks and hoaxes the US Postal Service sterilized some mail
using a process of gamma irradiation and treatment with a proprietary enzyme formula supplied
by Sipco Industries Ltd.[58]
A scientific experiment performed by a high school student, later published in The Journal of
Medical Toxicology, suggested that 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.[59]
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Antraks adalah penyakit zoonosis yang disebabkan oleh kuman bacillus anthracis, suatu basil
yang dapat membentuk spora dan ditularkan ke manusia melalui kontak dengan binatang yang
terinfeksi atau bahan dari binatang yang terkontaminasi.
Antraks adalah infeksi bakteri yang jarang terjadi, dan biasanya didapatkan dengan menghirup
udara, menelan makanan, masuk melalui kulit yang bersentuhan dengan endospora dari Bacillus
Antrachis
Infeksi antraks pada manusia melalui 3 cara yaitu inhalasi, melalui kulit, dan gastroinstestinal.
Sangat jarang terjadi kasus antraks yang masuk melalui inhalasi. Antraks inhalasi diperkirakan
sebagai penyebab morbiditas dan mortalitas selama penggunaan Bacillus Antrhacis sebagai
senjata biologi. Kutaneus antraks adalah bentuk antraks yang paling sering terjadi, dengan
perkiraan sekitar 2000 kasus yang dilaporkan setiap tahunnya. Epidemi terbesar terjadi
Zimbabwe antara tahun 1979 dan tahun 1985. Meskipun antraks gastrointestinal jarang terjadi,
outbreaks secara terus menerus dilaporkan di Afrika dan Asia setelah memakan daging yang
telah terkontaminasi dan tidak dimasak dengan baik.
Saat ini banyak negara yang mengembangkan pemanfaatan antraks sebgai senjata biologis.
Beberapa peristiwa yang menggunakan bakteri antraks sebgai senjata biologis antara lain
serangan kelompok Aum Shinrikyo tahin 1993 terhadap stasiun kereta api bawah tanah di Tokyo
yang menggunakan spora antraks, untungnya tidak menimbulkan korban jiwa.

Antraks disebut juga Malignant pustule, malignant edema, charbon , Ragpicker disease atau
Woolsorter disease. Penyakit antraks adalah penyakit yang disebabkan oleh Bacillus anthracis
pada binatang (zoonotik) ternak dan binatang buas yang bisa ditularkan ke manusia. Terminologi
kata antraks ( dari bahasa yunani anthrax yang berarti arang atau batubara; dalam bahasa
inggris disebuat coal; dan dalam bahasa Perancis disebut charbon ) mucul karena dikulit
penderita terbentuk luka yang berwarna hitam.
Penyakitini menjadi lrbih menarik perhatian para ahli karena isuterorisme yang berupa spora
antraks melalui kertas atau amplop surat. Spora yang terhisap oleh manusia dapat menyebabkan
antraks paru yang mortalitasnya lebih tinggi dari pada antraks tipe kulit.
Sejarah penyakit ini mulai dikenal pada tahun 1752 sebagai malignant pustule. Pada tahun 1780
Chabert melaporkan lebih detail tentang penyakit antraks pada hewan. Hewan yang sering
terserang adalah sapi, kambing, kuda, dan babi. Oleh sebab itu, penularan penyakit ini sangat
berhubungan dengan pekerjaan peternak, petani, pekerja, ditempat pemotongan hewan, dokter
hewan dan pekerja pabrik yang mengolah hasil-hasil peternakan.
ETIOLOGI
Bacillus anthracis adalah bakteri Garam-positif, tidak bisa geak, berkapsul , dan mampu
membentuk spora. Pembentukan spora terjadi pada keadaan aerob dan sedikit kalsium, yaitu di
alam terbuka seperti ditanah atau udara luar. Kuman vegetatif akan segera mati pada keadaan itu,
sehingga kuman menjadi inaktif dan membentuk spora yang bisa bertahan hidup bertahun-tahun
pada tanah dan produk hewan seperti bulu.
Spora antraks tahan terhadap cuaca panas dan dingin dan kembali aktif setelah masuk kedalam
tubuh hewan. Pada tanah kerig dapat bertahan selama 60 tahun. Spora akan mati pada suhu

1000C dalam waktu 10 menit, pada karbol 5% dalam waktu 40 hari, pada formalin 10% dalam
waktu 4 jam, dan pada hidrogen peroksida dalam waktu 1 jam.
Bakteri vegetatif mudah mati oleh antibioti, disinfektan, atau antiseptik. Kuman mati pada suhu
540C dalam waktu 30 menit.
PENULARAN
penularan pada manusia biasanya melalui cara-car dibawah ini
1.
2.
3.
4.

Kontak dengan kulit maniusia yang lesi, lecet dan abrasi

Mengonsumsi daging yang terkontaminasi kuman vegetatif atau spora melalui tangan.
Menghisap spora di tempat kerja yang berkaitan dengan produk hewan
Digigit serangga yang baru saja menggigit hewan infektif(jarang)

GEJALA DAN TANDA

Jumlah spora yang bisa mengakibatkan manifestasi klinis pada manusia adalah beberapa ribu
sampai 40.000 spora. Masa inkubasinya 7 hari dengan rata-rata 2-5 hari. Secara klinis antraks
dpat dibedakan menjadi :
1. Antraks kulit
Tipe ini merupakan tipe terbanyak, yang mencakup 90% kasus antraks di indonesia.
Antraks tipe ini bermula dengan rasa gatal yang kemudian menjadi vesikel, lalu pecah,
dan terbentuk ulkus yang ditutupi kerak hitam kering(eschar)
2. Antraks Gastrointestinal
Gejala antraks tipe ini bermula dengan sakit perut yang hebat, mual, muntah dan demam.
Penderita tertular akibat menelan daging yang terkontaminasi spora. Mortalitasnya cukup
tinggi yaitu 25-75%
3. Antraks Paru
Tipe ini paling jarang ditemukan. Penularan terjadi karena spora terisap oleh penderita.
Gejalanya tidak khas, bisa berupa batuk, lesu, lemah dan tanda-tanda bronkitis lainnya.
Angka kematian tipe ini adlaah yang paling tinggi sekitar 75-90%
4. Antraks otak
Tipe ini sangat jarang, biasanya merupakan komplikasi dari tipe-tipe lainnya.

PENGOBATAN

Obat pilihan utama untuk antraks adalah penisilin. Bila pasien hipersensitif tehadap penisilin,
obat ini dapat diganti dengan tetrasiklin, kloramfenikol, atau eritromisin. Untuk antraks tipe
kulit diberikan penisilin prokain 2x1.2 juta unit/hari selama 5-7 hari yang dilakukan secara
intramuskular, atau benzil penisilin 4x250.000 unit/hari secara intramuskular dengan melakukan
skin test terlebih dahulu
Untuk antraks tipe saluran pencernaan, dapat diberikan tetrasiklin 1 gram/hari dan untuk antraks
tipe paru diberikan IVFD penisilin G 18-24 unit/hari ditambah streptomisin 1-2 gram.

PENCEGAHAN
Upaya yang dapat dilakukan dalam pencegahan antraks adalah sebagai berikut :
1. Penyemblihan hewan hanya dilakukan di rumah potong, diluar tempat itu harus ada izin
dinas peternakan setempat.
2. Hewan yang dicurigai sakit antraks tidak boleh disemblih
3. Daging hewan yang dicurigai sakit antraks tidak boleh dikonsumsi
4. Tidak boleh sembarangan memandikan orang yang meninggal karena sakit antraks
5. Dilarang memproduksi barang yang berasal dari kulit, tanduk, bulu, atau tulang hewan
yang sakit atau mati karena antraks
6. Melapor ke puskesmas atau dians peternakan setempat apabila menemukan ada hewan
yang diduga menderita antraks
7. Melakukan vaksinasi antraks pada hewan ternak