Anthrax= الجمرة الخبيثة |
ANTHRAX
Etiology and Epidemiology
Anthrax is a zoonotic infectious disease caused by Bacillus anthracis, a large aerobic, spore-forming Gram-positive rod. Anthrax occurs naturally in ruminant mammals, such as sheep, cattle, and goats. Human disease is seen most often in agrarian, livestock-dependent regions. Consequently, human anthrax usually follows agricultural or industrial exposure, either through direct handling of infected animals or contaminated soil or through the processing of hides, wool, hair, or meat.2 The clinical presentation of human anthrax depends on the route of inoculation. In 95 percent of human cases, the disease is acquired through percutaneous inoculation of anthrax spores. Human anthrax can also be acquired as inhalational and gastrointestinal disease. Each form has distinctive clinical, epidemiologic, and prognostic features.3 Anthrax has potential as a class A bioweapon.
Clinical Findings
HISTORY
After an incubation period of 1 to 7 days, patients may experience low-grade fever and malaise and develop a
ANTHRAX AT A GLANCE
CUTANEOUS LESIONS
Cutaneous anthrax develops when spores enter minor breaks in the skin, especially on exposed parts of the hands, legs, and face . In the hospitable environment of human skin, spores revert to their rod forms and produce their toxins. A dermal papule, often resembling an arthropod bite reaction, develops over several days, and then progresses through vesicular, pustular, and escharotic phases. Lesions are surrounded by varying degrees of edema. Depending on the manner of inoculation, one to several lesions may appear, and there may be regional lymphadenitis, malaise, and fever. Individual lesions may appear pustular, leading to the name “malignant pustule,” but they do not suppurate. In anthrax, true pustules are rare; a primary pustular lesion is unlikely to be cutaneous anthrax. The lesion enlarges into a glistening pseudobulla that becomes hemorrhagic with central necrosis and may be umbilicated . The necrotic ulcr is usually painless, which is an important feature in differentiating it from a brown recluse spider bite. There may be small satellite papules and vesicles that may extend along lymphatics in a sporotrichoid manner. An area of brawny, non-pitting edema (“malignant edema”) often surrounds the main lesion. Lesional progression is due to toxins and is unaffected by antibiotic therapy. Fatigue, fever, chills, and tender regional adenopathy may cause an ulcero-glandular syndrome. The eschar dries and separates in 1 to 2 weeks.
RELATED PHYSICAL FINDINGS
Cutaneous anthrax may cause fever, tachycardia, and hypotension.
Histopathology
The prominent features are hemorrhagic edema, dilated lymphatics, and epidermal necrosis. Bacilli may be found in the eschar. Anthrax is toxin mediated and induces scant inflammatory infiltrate. Immunohistochemical stains are quite useful.14
Treatment
Naturally occurring anthrax is treated with penicillin or doxycycline. Weaponized anthrax, on the other hand, may be resistant to these antibiotics, and, therefore, a fluoroquinolone is recommended for the initial treatment of confirmed or suspected bioterrorism-associated anthrax, even in pregnant women and children. Once drug sensitivities have been established, the patient may be switched to another antibiotic as clinically indicated. Antibiotics will kill activated B. anthracis bacilli but will not alter tissue damage already caused by toxins
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