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Question answered:15/10/01 Warning! this question is over two years old.
The MERCK Manual
provides the following information on anthrax. "The causative organism, Bacillus anthracis, is a large, gram-positive, facultatively anaerobic, encapsulated rod. The spores resist destruction and remain viable in soil and animal products for decades. Human infection is usually through the skin but has occurred after ingestion of contaminated meat. Inhaling spores under adverse conditions (eg, the presence of an acute respiratory infection) may result in pulmonary anthrax (woolsorter's disease), which is often fatal. Pulmonary anthrax follows rapid multiplication of spores in the mediastinal lymph nodes. Rarely, GI anthrax may follow ingestion of contaminated meat when a break is present in the pharyngeal or intestinal mucosa, which facilitates invasion of the intestinal wall".
Signs and Symptoms
"The incubation period varies from 12 h to 5 days (generally, 3 to 5 days).
The cutaneous form begins as a painless, pruritic, red-brown papule; as it enlarges, it is surrounded by a zone of brawny erythema and gelatin-like edema. Considerable peripheral erythema, vesiculation, and induration are present. Central ulceration follows, with serosanguineous exudation and formation of a black eschar. Local lymphadenopathy may occur, occasionally with malaise, myalgia, headache, fever, nausea, and vomiting.
Initial symptoms of pulmonary anthrax are insidious and resemble influenza. Fever increases, and within a few days, severe respiratory distress develops, followed by cyanosis, shock, and coma. Severe haemorrhagic necrotizing lymphadenitis develops and spreads to the adjacent mediastinal structures. Serosanguineous transudation, pulmonary edema, and pleural effusion occur. Haemorrhagic meningoencephalitis and/or GI anthrax may develop. Lung x-ray may show diffuse patchy infiltration; the mediastinum is widened because of enlarged hemorrhagic lymph nodes.
In GI anthrax, the released toxin induces a haemorrhagic necrosis extending to the draining mesenteric lymph nodes. Septicaemia with potentially lethal toxicity ensues".
Diagnosis
"The occupational and exposure history is important. Cultures or Gram stains from cutaneous lesions may be used to isolate B. anthracis, and throat swabs and sputum may be used in the pulmonary form. When primary cultures do not grow, the organism may be isolated by mouse inoculation.
Diagnosis of GI anthrax depends on recognition of clinical symptoms. Occasionally, organisms can be seen by Gram stain of vomitus or feces. Clinically, GI anthrax presents with nausea, vomiting, anorexia, and fever progressing to bowel necrosis with concurrent septicemia and death. An oropharyngeal form of anthrax presents as a mucocutaneous lesion in the oral cavity with sore throat, fever, adenopathy, and dysphagia. This proceeds to necrosis and death".
In regards to morbidity and mortality eMedicine offers the following.
Cutaneous anthrax
- With treatment, mortality is approximately 1%.
Inhalational anthrax
- Without treatment, the mortality rate of inhalational anthrax is approximately 95%.
Gastrointestinal anthrax
- Death is rapid without antibiotic therapy and aggressive volume resuscitation.
References
- THE MERCK MANUAL. Bacterial Diseases. Section 13, chapter 157. http://www.merck.com/pubs/mmanual/section13/chapter157/157c.htm
- Cranmer H, Martinez M. CBRNE - Anthrax Infection. http://www.emedicine.com/emerg/topic864.htm
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