Chapter

Anthrax

Arthur E. Brown and Thira Sirisanthana

in Oxford Textbook of Medicine

Fifth edition

Published on behalf of Oxford University Press

ISBN: 9780199204854
Published online May 2012 | e-ISBN: 9780199570973 | DOI: http://dx.doi.org/10.1093/med/9780199204854.003.070620_update_002

Series: Oxford Textbooks

Anthrax

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Anthrax is primarily a disease of herbivorous mammals, caused by the Gram-positive rod Bacillus anthracis, which causes human infection when its spores enter the body, most commonly from handling infected animals or animal products. The disease occurs in most countries of the world, but not in those where the condition is controlled in livestock by vaccination programmes. Anthrax is a leading agent of biological warfare.

Pathophysiology—after entry into the body, anthrax spores are phagocytosed by macrophages and carried to regional lymph nodes, where they germinate to produce vegetative bacilli that enter the blood stream. These produce anthrax toxin, which has effects including impairment of cellular water homeostasis and of many intracellular signalling pathways.

Clinical features—anthrax occurs in three clinical forms based on the route of exposure. (1) Cutaneous—lesions are usually found on exposed areas of skin; a small papule develops at the site of infection, enlarges and ulcerates, with the painless ulcer becoming covered with a black leathery eschar surrounded by nonpitting oedema before healing in 2 to 6 weeks; associated systemic symptoms are usually mild. (2) Gastrointestinal—acquired by eating contaminated food and comprising (a) oropharyngeal anthrax, presenting with fever, neck swelling, sore throat, oropharyngeal ulcer, and dysphagia, OR (b) terminal ileal/caecal anthrax, presenting with fever, nausea, vomiting, and abdominal pain, followed by rapidly developing ascites and bloody diarrhoea. (3) Inhalation—aerosol exposure leads to a nonspecific viral-type prodrome which progresses to a fulminant stage of severe respiratory distress, cyanosis, stridor, and profuse sweating; up to half of patients develop anthrax meningitis; shock and death typically follow in hours or days.

Diagnosis—may be very difficult in the absence of a known outbreak, particularly for inhalation anthrax, where a clinical clue is widening of the mediastinum caused by lymphadenopathy. Confirmation is by laboratory identification of B. anthracis. Serological testing can be used for retrospective diagnosis.

Treatment—this is with supportive care and antibiotics, which are effective against the multiplying (vegetative) form of B. anthracis, but not against the spore form. Mild cases of cutaneous anthrax are usually treated with oral penicillin. For gastrointestinal, inhalational and meningeal anthrax, at least two antibiotics should be given intravenously, e.g. ciprofloxacin or doxycycline along with another antimicrobial expected to be effective (e.g. penicillin, ampicillin, rifampin, vancomycin, chloramphenicol, imipenem, clindamycin, and clarithromycin).

Prognosis—the mortality of untreated cutaneous anthrax is 10 to 20%, but fatalities are rare with appropriate antibiotic treatment. Almost all cases of inhalation anthrax and anthrax meningitis are fatal; initiation of treatment after the start of fulminant disease is rarely effective.

Prevention—routine immunization of livestock should be instituted in endemic areas with continuing cases of animal anthrax. Carcasses of animals suspected of dying from anthrax must be disposed of appropriately. Anthrax vaccines should be offered to members of high-risk groups, e.g. those at occupational risk, laboratory workers and some military groups. Postexposure prophylaxis should be given following suspected exposure to aerosolized anthrax spores (e.g. ciprofloxacin for 60 days).

Chapter.  5422 words.  Illustrated.

Subjects: Medical Microbiology and Virology ; Infectious Diseases

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