anthrax (redirected from cutaneous anthrax)

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.

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anthrax

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.

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anthrax

1. a highly infectious and often fatal disease of herbivores, esp cattle and sheep, characterized by fever, enlarged spleen, and swelling of the throat. Carnivores are relatively resistant. It is caused by the spore-forming bacterium Bacillus anthracis and can be transmitted to man

2. a pustule or other lesion caused by this disease

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Anthrax

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 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.

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 Infectious disease