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.
Such spores can be found on all continents, even Antarctica.
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 each year worldwide, particularly in the concentration camps during WWII.
French scientist Louis Pasteur developed the first effective vaccine for anthrax in 1881.
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.
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.
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.
Signs and symptoms
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%.
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.
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.
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 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.
Skin reaction to 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.
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, 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.
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.
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.
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.
These toxins cause death and tissue swelling (edema), respectively.
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.
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 non infected 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.
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.  Anthrax is also a Biphasic disease
There are several vaccines in current use.
If a person or animal 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.
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.
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.
Antibiotic-resistant strains of anthrax are known.
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.
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.
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.
Alternative names: siberian plague, charbon, splenic fever.
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.
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.
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, chlorine dioxide, and liquid bleach products containing sodium hypochlorite.
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.
Clean up of anthrax-contaminated areas on ranches and in the wild is much more problematic.
Carcasses should 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.
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