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anthrax

 
(ăn'thrăks') pronunciation
n.
  1. An infectious, usually fatal disease of warm-blooded animals, especially of cattle and sheep, caused by the bacterium Bacillus anthracis. The disease can be transmitted to humans through contact with contaminated animal substances, such as hair, feces, or hides, and is characterized by ulcerative skin lesions.
  2. pl., -thra·ces (-thrə-sēz'). A lesion caused by anthrax.

[Middle English antrax, malignant boil, from Latin anthrax, carbuncle, from Greek.]


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Infectious disease of warm-blooded animals, caused by Bacillus anthracis, a bacterium that, in spore form, can retain its virulence in contaminated soil or other material for many years. A disease chiefly of herbivores, the infection may be acquired by persons handling the wool, hair, hides, bones, or carcasses of affected animals. Infection may lead to death from respiratory or cardiac complications (within 1 – 2 days if acute), or the animal may recover. In humans, anthrax occurs as a cutaneous, pulmonary, or intestinal infection. The most common type, which occurs as an infection of the skin, may lead to fatal septicemia (blood poisoning). The pulmonary form of the disease is usually fatal. Sanitary working environments for susceptible workers are critical to preventing anthrax; early diagnosis and treatment are also of great importance. In recent decades, various countries have attempted to develop anthrax as a weapon of biological warfare; many factors, including its extreme potency (vastly greater than any chemical-warfare agent), make it the preferred biological-warfare agent. Concerns about anthrax mounted in 2001 after it was found in letters mailed to members of the U.S. government and news agencies.

For more information on anthrax, visit Britannica.com.

An acute infectious zoonotic disease caused by the bacterium Bacillus anthracis and primarily associated with herbivorous mammals. Carnivorous mammals, birds, reptiles, amphibians, fish, and insects are generally resistant to anthrax infection. However, carnivorous and omnivorous mammals often succumb after ingestion of infected meat containing the anthrax toxins, which can cause swelling in the throat and suffocation. Humans primarily present with cutaneous lesions, appearing as black scabs or eschars, after contact with infected animals, carcasses, or animal products. See also Zoonoses.

Anthrax is responsible for the deaths of thousands of domesticated and wild herbivorous animals annually. Parts of Africa, Asia, southern Europe, and North and South America are subject to repeated outbreaks. In the Western Hemisphere, anthrax is well controlled in livestock.

Bacillus anthracis is a gram-positive, rod-shaped, endospore-forming bacterium, approximately 1.0–1.2 micrometers in diameter and 3–8 μm long. The spores resist drying, cold, heat, and disinfectants, and can remain viable for many years in soil, water, and animal hides and products. Bacillus anthracis possesses three virulence factors: lethal toxin, edema toxin, and a poly-D-glutamic acid capsule. Lethal toxin is composed of two proteins, lethal factor and protective antigen. The protective antigen is produced by the anthrax bacillus at a molecular weight of 83 kDa, but must be cleaved by either serum or target cell surface proteases to 63 kDa before it complexes with lethal factor to form lethal toxin. The edema toxin is composed of edema factor and protective antigen, and it is believed to complex in a manner similar to that seen for lethal toxin. Protective antigen plays a central role in that it is required for transport of lethal factor and edema factor into host target cells. The macrophage appears to be the primary host target cell for lethal toxin, whereas the neutrophil appears to be the target cell for edema toxin in addition to other cells involved in edema formation. The third virulence factor is the capsule, which inhibits phagocytosis through its negatively charged poly-D-glutamic acid composition. All three toxin components are encoded by a plasmid, pXO1, whereas the enzymes required for capsule synthesis are encoded for by the pXO2 plasmid. Strains lacking either or both plasmids are avirulent, such as the veterinary vaccine Sterne strain, which lacks the pXO2 plasmid. See also Edema.

Anthrax consists of two clinical forms, cutaneous and septicemic. The cutaneous form begins as a blisterlike lesion that eventually becomes an intensely dark, relatively painless, edematous lesion forming a black eschar. The lesions rapidly become sterile after antibiotic therapy and take several weeks to resolve, even with treatment. The cutaneous form is reported only in humans, rabbits, swine, and horses.

The septicemic form arises from various initial sites of infection, including cutaneous, oropharyngeal, gastrointestinal, or inhalational exposures. The course of septicemic disease depends on the exposure route and the susceptibility of the animal host. The vast majority of systemic anthrax cases in herbivorus animals occur from trauma to mucosal linings of the mouth and upper alimentary canal caused by ingested fibrous foods. Inhalation anthrax is believed to be initiated by phagocytosis of spores within the lungs by alveolar macrophages. Spore-laden macrophages pass through lymphatic channels to the sinuses of regional lymph nodes or migrate to the spleen, where the spores germinate within the macrophages, multiply, and overwhelm and escape the macrophages to invade the efferent lymphatics. For other portals of entry, mesenteric lymph nodes become involved. The bacilli move to the spleen, where they induce pronounced splenomegaly (enlargement of the spleen), and finally enter the bloodstream, where they induce secondary sites of infection, massive bacillemia, toxemia, and sudden death. Failure of the blood to clot, hemorrhages of skin, hemorrhagic meningitis, and reduced rigor mortis are frequently found in anthrax-infected carcasses. Exposure of contaminated body fluids to the lower atmospheric levels of carbon dioxide results in sporulation of the bacilli. Therefore, opening of infected carcasses should be avoided.

Besides its central role for binding the lethal and edema toxins to target cells, protective antigen plays an important role in the host's protective immune response against anthrax, hence the term protective antigen. Vaccines lacking protective antigen are not protective. For United States and United Kingdom human anthrax vaccines, protective antigen bound to aluminum salts is the principal immunogen. However, veterinary vaccines are composed of viable spores of B. anthracis Sterne strain, a nonencapsulated toxigenic variant. Full protection against anthrax with the veterinary vaccine is afforded by primary and annual booster vaccinations. See also Infectious disease.


Anthrax, a zoonotic disease, is one of the earliest diseases known to man. Worldwide public health surveillance data are not accurate for either animal or human anthrax up to the 1950s, but it is probable that thousands of human cases occurred annually. Since the 1950s, it is estimated that between 2,000 and 5,000 cases of human anthrax have occurred annually.

Anthrax is seen in three forms in humans: cutaneous, inhalational, and gastrointestinal. Cutaneous anthrax begins as a blister on the skin that, within two to six days, develops into a vesicle which, when ruptured, reveals a depressed ulcer covered by a black eschar, or scab. The patient may have a mild fever and slight edema surrounding the lesion. Within one or two weeks the lesion gradually becomes covered with tissue, eventually resulting in a small scar. Treatment is with appropriate antibiotics and hygienic care of the lesion. The mortality rate without treatment is approximately 5 percent.

Inhalational anthrax is a systemic toxic disease that involves the mediastinal lymph nodes. It begins with mild respiratory symptoms, and within one or two days, fever, perspiration, and a falling blood pressure develop rapidly. The result is a toxic shock-like condition, which is followed by death in almost 100 percent of cases. Rapid intravenous treatment with antibiotics may reduce the chance of fatality.

Gastrointestinal anthrax can involve either the oropharyngeal area, which results in swelling, redness, and ulcers, or the gastrointestinal tract, with the development of ulcers, hemorrhage, and edema. With appropriate treatment, the patient recovers within approximately one week. The mortality rate is 5 to 20 percent.

Diagnosis of anthrax is made by clinical history; culturing of secretions from lesions, blood, or spinal fluid; and by epidemiological association with contaminated animal products such as wool, goat hair, hides, dried bones, and tissue from animals that have died from anthrax. Serological tests can also be diagnostic. Meningitis may develop with any form of the disease.

There is a safe and effective human anthrax vaccine. Health education is also important for people that may be exposed to diseased animals or their products. Cutaneous anthrax primarily results from occupational exposure to contaminated animal products. Such exposure may occur in the manufacturing of textiles using goat hair or wool, in handling animal hides or rendered products, and in attending to sick animals. Inhalational anthrax results from the inhalation of spores related to industrial sources. Gastrointestinal anthrax results from eating contaminated meat. A major concern today is the threat of the use of the bacterium that causes anthrax, Bacillus anthracis, as an agent in bioterrorism or biological warfare.

Animal anthrax occurs primarily in herbivores and results from ingestion of Bacillus anthracis in soil or feed. Infected animals develop gastrointestinal anthrax with systemic infection and die with secretions issuing from their bodily orifices. There is a safe and effective animal vaccine, and antibiotic treatment can be curative if started early enough.

(SEE ALSO: Communicable Disease Control; Terrorism; Veterinary Public Health; Zoonoses)

— PHILIP S. BRACHMAN




[ܒænܖthræks]

ˈænܖthræks n.a serious bacterial disease causing severe skin ulceration or a form of pneumonia. Anthrax spores can survive for long periods of time in harsh conditions, making anthrax a possible biological weapon.

See the Introduction, Abbreviations and Pronunciation for further details.

anthrax (ăn'thrăks), acute infectious disease of animals that can be secondarily transmitted to humans. It is caused by a bacterium (Bacillus anthracis) that primarily affects sheep, horses, hogs, cattle, and goats and is almost always fatal in animals. The bacillus produces toxins that kill cells and cause fluid to accumulate in the body's tissues.

Anthrax spores, which can survive for decades, are found in the soil, and animals typically contract the disease while grazing. Transmission to humans normally occurs through contact with infected animals but can also occur through eating meat from an infected animal or breathing air laden with the spores of the bacilli. The disease is almost entirely occupational, i.e., restricted to individuals who handle hides of animals (e.g., farmers, butchers, and veterinarians) or sort wool.

In the cutaneous, or skin, form of the disease, which is not usually fatal to humans, the bacillus enters the skin through a scratch, cut, or sore. Pustules occur on the hands, face, and neck; if the disease is not treated with antibiotics, the bacteria can migrate to the blood vessels, causing septicemia (blood poisoning) and death. Gastrointestinal anthrax is more likely to be fatal. Nausea, vomiting, and fever can be followed by abdominal bleeding, tissue death, and septicemia. Pulmonary, or inhalation, anthrax begins with flulike symptoms and ultimately causes lesions in the lungs and brain. It is rarer, but is usually fatal if not treated early. Because of this, individuals without symptoms who have been exposed to inhaled anthrax are treated with antibiotics for 60 days.

Anthrax is a well-known, ancient disease; the fifth plague visited upon the Egyptians in Genesis (see plagues of Egypt) resembles the disease. Pure cultures of the anthrax bacillus were obtained in 1876 by Robert Koch, who demonstrated the relationship of the microbe to the disease. Confirmation of the bacillus as the cause of anthrax was provided by Louis Pasteur, who also developed a method of vaccinating sheep and cattle against the disease. Anthrax is now uncommon in the United States because of widespread vaccination of animals and disinfection of animal products such as hides and wool.

Anthrax spores have been used experimentally by various nations as a biological warfare agent, but effective delivery of anthrax to a population is difficult, and such use is now banned by international convention. Because anthrax has been tested as a biological weapon, the United States has developed a vaccine for military use, but it requires several injections and annual boosters. An accidental release of anthrax from a military laboratory near Sverdlovsk (now Yekaterinburg) in the Soviet Union resulted in 68 deaths from pulmonary anthrax in 1979. In 2001 a number of people in the United States were exposed to spores that were sent through the mails and contracted anthrax; several persons died. Although these bioterror attacks occurred shortly after the terrorist attacks on the World Trade Center and the Pentagon, it did not appear to be linked to them.

Bibliography

S. D. Jones, Death in a Small Package (2010).


Science Q&A:

What is anthrax?

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Bacillus anthracis, the etiologic agent of anthrax, is a large, gram-positive, non-motile, spore-forming bacterial rod. The three virulence factor of B. anthracis are edema toxin, lethal toxin, and a capsular antigen. Human anthrax has three major clinical forms: cutaneous, inhalation and gastrointestinal. If left untreated, anthrax in all forms can lead to septicemia (blood poisoning) and death.

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In the 1990s, the use of biological weapons by terrorists became a serious threat to the security of countries around the globe, and the United States in particular. During the Gulf War of 1990 to 1991, and in subsequent United Nations inspection efforts, the government of Iraq's development of advanced anthrax based bioweapons was revealed.

Although the incidents have not been directly linked, following the September 11, 2001 terrorist attacks on the World Trade Center buildings in New York City and the Pentagon in Washington, D.C., anthrax was used as a bioterrorist weapon. Letters containing a powdered form of Bacillus anthracis, the bacteria that causes anthrax, were mailed to representatives of government and the media, among others. Multiple attacks eventually killed five people.

Anthrax refers to a disease that is caused by the bacterium Bacillus anthracis. The bacterium can enter the body via a wound in the skin (cutaneous anthrax), via contaminated food or liquid (gastrointestinal anthrax), or can be inhaled (inhalation anthrax). The latter in particular can cause a very serious, even lethal, infection.

The disease has been present throughout recorded history. Its use as a weapon stretches back centuries. Hundreds of years ago, bodies of anthrax victims were dumped into wells, or were catapulted into enemy encampments. Development of anthrax-based weapons was pursued by various governments in World Wars I and II, including those of the United States, Canada, and Britain.

Humans naturally acquire anthrax from exposure to livestock such as sheep or cattle or wild animals. The animals are reservoirs of the anthrax bacterium.

While all three types of anthrax infections are potentially serious, prompt treatment usually cures the cutaneous form. Even with prompt treatment, the gastrointestinal form is lethal in 25%–75% of those who become infected. The inhaled version of anthrax is almost always lethal.

When Bacillus anthracis is actively growing and dividing, it exists as a large "vegetative" cell. But, when the environment is threatening, the bacterium can form a spore and becoming dormant. The spore form can be easily inhaled. Only 8,000 spores, hardly enough to cover a snowflake, are sufficient to cause the inhalation form of anthrax when the spores resuscitate and begin growth in the lungs.

The growing Bacillus anthracis cells have several characteristics that make them so infectious. First, the formation of a capsule around the bacterium can mask the surface from recognition by the body's immune system. The body can be less likely to mount an immune response to the invading bacteria. Also, the capsule helps fend off antibodies and immune cells that do respond. This protection can allow the organism to multiply to large numbers.

The capsule also contains a protein that protects the bacterium. This "protective antigen" dissolves other protein molecules that form part of the outer coating of host cells. This allows the bacterium to evade the host's immune response by burrowing inside host cells such as the epithelial cells that line the lung.

A toxic component called lethal factor actively destroys the host's immune cells. Finally, another toxic factor called the edema factor (edema is the build up of fluid at the site of infection) disables a host molecule called calmodulin. Calmodulin regulates many chemical reactions in the body.

With the various toxic factors, Bacillus anthracis is able to overcome the attempts of the host to deal with the infection. Bacterial toxins enter the bloodstream and circulate throughout the body. The destruction of blood cells and tissues can be lethal.

The early symptoms of anthrax infections are similar to other, less serious infections, such as the flu. By the time the diagnosis is made, the infection can be too advanced to treat. This can make the recognition of a deliberate anthrax attack difficult to recognize until large numbers of casualties have resulted. While the bacteria can be killed by antibiotics, in particular an antibiotic called ciprofloxacin (cipro), the antibiotic needs to be administered early in an infection.

The ease by which anthrax can be transported (i.e., via the mail) has made anthrax a weapon of frightening severity.

A vaccine for anthrax does exist, although the possibility of serious side effects has limited its use to only those at high risk for infection (i.e., soldiers, workers in meat processing plants, anthrax researchers). Vaccine researchers are exploring the possibility that the edema factor and the capsule could be exploited as targets of vaccines. The idea is that the vaccines would stop the bacteria from getting into host cells. This would make it easier for the immune response to kill the invading bacteria.

Further Reading

Books

Heyman, D. A., J. Achterberg, and J. Laszlo. Lessons from the Anthrax Attacks: Implications for U.S. Bioterrorism Preparedness: A Report on a National Forum on Biodefense. Washington, DC: Center for Strategic and International Studies, 2002.

Koehler, T. M. Anthrax. Berlin: Springer Verlag, 2002.

Periodicals

Jernigan, J. A., D. S. Stevens, D. A. Ashford, et al. "Bioterrorism-Related Inhalational Anthrax: The First 10 Cases Reported in the United States." Emerging Infectious Diseases no. 7 (2001).

Electronic

Centers for Disease Control and Prevention. "Anthrax." Division of Bacterial and Mycotic Diseases. October 30, 2001. <http://www.cdc.gov/ncidod/dbmd/diseaseinfo/anthrax_t.htm>(9 December 2002).

An infectious disease transmitted by a bacterium in animals, which can also be transmitted to humans. Often fatal if the bacterium enters the lungs, anthrax is usually treated by antibiotics. Anthrax is a potential weapon in germ warfare and bioterrorism.

  • After the September 11 attacks (2001) in the United States, anthrax spores sent through the mail caused several fatalities.
  • If spores are prepared in a sophisticated way, they can stay in the air and be breathed in by human beings. Anthrax produced in this way is referred to as weaponized anthrax.

  • An infectious and often fatal disease contracted from animals. Cutaneous anthrax is contracted through a break in the skin. Infection spreads through the bloodstream causing shock, cyanosis, sweating, and collapse. Inhalation anthrax is contracted by breathing in anthrax spores, resulting in pneumonia, sometimes accompanied by meningitis, followed by death. Because its spores have a long survival period, the incubation period is short, and the disability severe, anthrax has long been developed as a biological weapon by several nations.

    A peracute disease of all animal species, caused by Bacillus anthracis, and characterized by septicemia and sudden death. The causative bacteria form long-living spores which maintain the disease on a farm for many years. Significant necropsy findings include exudation of dark, tarry blood from the body orifices, failure of the blood to clot, absence of rigor mortis and splenomegaly. A dangerous zoonosis. Easily controlled by vaccination of livestock.

    • alimentary a. — infection resulting from the ingestion of animals dead of anthrax. Largely a human manifestation in developing countries.
    • a. belt — regions where anthrax is enzootic, where soil and climate favor persistence of the organism in soil and where routine efforts to control the disease are not sufficient. Outbreaks commonly follow climatic extremes of flood or drought.
    • cutaneous a. — anthrax due to lodgment of the causative organisms in wounds or abrasions of the skin, producing a black crusted pustule on a broad zone of edema. A common form of the disease in humans.
    • pulmonary a. — infection of the respiratory tract resulting from inhalation of dust or animal hair containing spores of Bacillus anthracis; an occupational disease of humans usually affecting those who handle and sort wools and fleeces (woolsorters’ disease).
    (an′thraks)
    n

    An infectious disease in herbivorous animals caused by a spore-forming Bacillus organism. Primary lesions in human beings may be on the lips or cheeks.

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    • Diseases and Infestations - anthrax: acute infectious livestock disease, transmitted to humans by contact, causing pneumonia or skin ulcerations


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    Anthrax
    Classification and external resources

    Microphotograph 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 other 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 reactivate 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 each year in Australia, Asia, Africa, North America, and Europe, particularly in the concentration camps during WWII.[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 every year. 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 developing countries without widespread veterinary or human public health programs.

    Bacillus anthracis bacterial spores are soil-borne, and, because of their long lifetime, they are still present globally and at animal burial sites of anthrax-killed animals for many decades; spores have been known to have reinfected animals over 70 years after burial sites of anthrax-infected animals were disturbed.[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 10,000–20,000 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 as 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 that had spores on it is unknown. This mode of infection is used as a bioweapon.

    Gastrointestinal

    Gastrointestinal infection in humans is most often caused by eating 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. Some 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, making even more toxins on the way. 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.

    Cutaneous

    Skin reaction to anthrax
    A skin lesion caused by anthrax

    Cutaneous (on the skin) anthrax infection in humans shows up 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 Gram-negative bacterial species would appear pink. (The other cells are white blood cells).

    Bacillus anthracis is a rod-shaped, Gram-positive, aerobic bacterium about 1 by 9 micrometers in length. It was shown to cause disease by Robert Koch in 1876.[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 over-production 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 degrees 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

    There are several vaccines in current use. The Georgian/Russian vaccine (called STI) is a live-attenuated vaccine based on spores from the Stern strain of B. anthracis. The USA vaccine (also known as AVA, manufactured by Emergent BioSolutions under the brand name BioThrax) is adsorbed onto aluminium-hydroxide.[27]

    The STI vaccine's serious side-effects restrict use to healthy adults.[28]

    BioThrax is licensed by the U.S. Food and Drug Administration (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. On December 11, 2008, the FDA approved omitting the week 2 dose, resulting in the currently recommended five-dose series.[29]

    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. 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 0.5–5.0 μm 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.[30] 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.[31] 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 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 like ciprofloxacin, or doxycycline, erythromycin, vancomycin or penicillin. FDA-approved agents include ciprofloxacin, doxycycline and penicillin.[32]

    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.[33] 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.

    History

    Etymology

    The name comes from anthrax [άνθραξ], the Greek word for 'coal', because of the black skin lesions developed by victims with a cutaneous anthrax infection.

    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

    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 46-year-old scientist at the U.S. Army Biological Warfare Laboratories at Camp (later Fort) Detrick (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 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 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 occurrence of previously dormant anthrax, stirred up from below the ground surface by wind movement in a drought-stricken region with depleted grazing and browsing, may be seen as a form of natural culling and a first step in rehabilitation of the area.

    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 freedom fighters ("the rebel groups") 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 1978–1979 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)

    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 18–55.[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]

    See also

    Notes

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    3. ^ Cherkasskiy, B. L. (1999). "A national register of historic and contemporary anthrax foci". Journal of Applied Microbiology 87 (2): 192–195. doi:10.1046/j.1365-2672.1999.00868.x. PMID 10475946. 
    4. ^ David V. Cohn (11 February 1996). "Life and Times of Louis Pasteur". School of Dentistry, University of Louisville. Archived from the original on 8 April 2008. http://web.archive.org/web/20080408070236/http://louisville.edu/library/ekstrom/special/pasteur/cohn.html. Retrieved 13 August 2008. 
    5. ^ Mikesell, P.; Ivins, B. E.; Ristroph, J. D.; Vodkin, M. H.; Dreier, T. M.; Leppla, S. H. (1983). "Plasmids, Pasteur, and Anthrax" (PDF). ASM News 49: 320–2. http://www.asm.org/ASM/files/CCLIBRARYFILES/FILENAME/0000000221/490783p320.pdf. 
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    9. ^ Guillemin 1999, p. 3
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    External links


    Translations:

    Anthrax

    Top

    Dansk (Danish)
    n. - miltbrand, anthrax

    Français (French)
    n. - (Méd, Vét) charbon, (Méd) anthrax

    Deutsch (German)
    n. - Anthrax, Milzbrand

    Ελληνική (Greek)
    n. - (παθολ.) άνθραξ (κν. κακό σπυρί)

    Español (Spanish)
    n. - ántrax

    Svenska (Swedish)
    n. - mjältbrand, bulnad (med.)

    中文(简体)(Chinese (Simplified))
    痈, 脾脱疽, 炭疽, 炭疽脓疱

    中文(繁體)(Chinese (Traditional))
    n. - 癰, 脾脫疽, 炭疽, 炭疽膿皰

    한국어 (Korean)
    n. - 탄저열

    العربيه (Arabic)
    ‏(الاسم) مرض الجمره الخبيثه : مرض مهلك من امراض الماشيه وقد يصيب الإنسان‏

    עברית (Hebrew)
    n. - ‮מחלה הגורמת למות לכבשים, מועברת לבני-אדם ותוקפת בעיקר את העור והריאות, גחלת‬


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    American Heritage Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved.  Read more
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