Excerpt from CBRNE - Anthrax Infection

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Background

The term anthrax means coal in Greek, and the disease is named after the appearance of its cutaneous form. Anthrax is described in the Old Testament, by the poet Virgil, and by the Egyptians. At the end of the 19th century, Robert Koch's experiments with anthrax led to the original theory of bacteria and disease. John Bell's work in inhalational anthrax led to wool disinfection processes and the term woolsorter's disease.

Anthrax is caused by inhalation, skin exposure, or gastrointestinal (GI) absorption. Disease caused by inhalation is usually fatal, and symptoms usually begin days after exposure. This delay makes the initial exposure to Bacillus anthracis difficult to track.

An additional concern is use of anthrax as a biologic warfare agent. During the Gulf War, Iraq reportedly produced 8500 L of anthrax. A total of 150,000 US troops were vaccinated with anthrax toxoid. Since October 2001, 22 confirmed or suspected cases of anthrax infection, disseminated via the US postal system, have been identified.

Pathophysiology

Anthrax (B anthracis) is a large, spore-forming, gram-positive rod. Persistence of spores is aided by nitrogen and organic soil content, environmental pH greater than 6, and ambient temperature greater than 15°C. Drought or rainfall can trigger anthrax spore germination, while flies and vultures spread the spores.

B anthracis has a diameter of 1-1.5 µm and a length of 3-10 µm. It grows in culture as gray-white colonies that measure 4-5 mm in diameter and have characteristic comma-shaped protrusions. Anthrax is differentiated from other gram-positive rods on culture by lack of hemolysis and motility and by preferential growth on phenylethyl alcohol blood agar with characteristic gelatin hydrolysis and salicin fermentation.

Virulence depends on the bacterial capsule and the toxin complex. The capsule is a poly-D-glutamic acid that protects against leukocytic phagocytosis and lysis. Experiments by Sterne demonstrated that the capsule is vital for pathogenicity.

Anthrax toxins are composed of 3 entities: a protective antigen, a lethal factor, and an edema factor. The protective antigen is an 83-kd protein that binds to cell receptors within a target tissue. Once bound, a fragment is cleaved free to expose an additional binding site. This site can combine with edema factor to form edema toxin or with lethal factor to form lethal toxin. Edema toxin acts by converting adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Cellular cAMP levels are increased, leading to cellular edema within the target tissue. Lethal factor is not well understood, but recent work suggests that it may inhibit neutrophil phagocytosis, lyse macrophages, and cause release of tumor necrosis factor and interleukin 1.

Frequency

United States

During the last 20 years, the indigenous US incidence has been less than 1 case per year. From 1955-1994, US cases totaled 235, with 224 cases of cutaneous anthrax, 11 cases of inhalational anthrax, and 20 fatalities. The last fatal case during this period occurred in 1976, when a home craftsman died of inhalational anthrax after working with yarn imported from Pakistan.

Before October 2001, the Centers for Disease Control and Prevention (CDC) investigated several threats in the United States, including Indiana, Kentucky, Tennessee, and California. Since October 2001, 22 confirmed or suspected cases of anthrax infection have been identified. Cases were reported from Florida, New York, New Jersey, the District of Columbia, and Connecticut. There were 11 confirmed cases of inhalational anthrax (5 deaths) and 7 confirmed and 4 suspected cases of cutaneous anthrax (no deaths). Seven cases were associated with occupational exposures in the postal service, and 2 cases had documented exposures to contaminated mail in the business office of a media company. No sources of exposure were identified for 2 women who were presumably exposed to secondarily contaminated mail. No reports in the literature have documented direct human-to-human transmission.

International

In 1958, approximately 100,000 cases of anthrax occurred worldwide. Exact figures do not exist because of reporting difficulties in Africa. Anthrax is endemic in Africa and Asia despite vaccination programs. Sporadic outbreaks have occurred as a result of both agricultural and military disruptions. During the 1978 Rhodesian civil war, failure of veterinary vaccination programs led to a human epidemic, causing 6500 anthrax cases and 100 fatalities. A mishap at a military microbiology facility in the former Soviet Union in 1979 resulted in at least 66 deaths. Human anthrax often is associated with agricultural or industrial workers who come in contact with infected animal tissue.

Mortality/Morbidity

Anthrax is primarily zoonotic. Human anthrax cases are due to exposure through agriculture or industry. Those at highest risk are shepherds, farmers, and workers in facilities that use animal products, especially previously contaminated goat hair, wool, or bone. Most anthrax disease is cutaneous (95%). The remaining cases of the disease are inhalational (5%) and GI ( <1%). Without treatment, the mortality rate of inhalational anthrax is approximately 95%.

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