Merck Manual on Anthrax

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Although a strain of Anthrax developed as a weapon may be different

or more virulent, this may serve as a better guide for discussion.

 

Jim Ramholz

 

 

 

ANTHRAX

A highly infectious disease of animals, especially ruminants,

transmitted to humans by contact with the animals or their products.

 

Etiology and Epidemiology

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.

 

Although anthrax is an important animal disease, it is rare in humans

and mainly occurs in countries that do not prevent industrial or

agricultural exposure to infected goats, cattle, sheep, and horses or

their products. Anthrax also occurs in exotic wildlife such as

hippos, elephants, and cape buffalo.

 

Symptoms and Signs

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

hemorrhagic necrotizing lymphadenitis develops and spreads to the

adjacent mediastinal structures. Serosanguineous transudation,

pulmonary edema, and pleural effusion occur. Hemorrhagic

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 hemorrhagic necrosis

extending to the draining mesenteric lymph nodes. Septicemia 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.

 

Prevention and Treatment

An anthrax vaccine, composed of a culture filtrate, is available for

those at high risk (veterinarians, laboratory technicians, employees

of textile mills processing imported goat hair). Repeated vaccination

may be required to ensure protection. Local reactions can occur. A

live toxigenic, unencapsulated avirulent animal vaccine is available

for veterinary use.

 

Treatment of the cutaneous form with procaine penicillin G 600,000 U

IM bid for 7 days prevents systemic spread and induces gradual

resolution of the pustule. Progression of the lesion through the

eschar phase occurs despite antibiotic therapy. Tetracycline 2 g/day

in 4 divided doses po (for children, 25 mg/kg/day in 4 divided doses)

is also effective. Alternatively, erythromycin, ciprofloxacin, or

chloramphenicol may be used. Penicillin or erythromycin is preferred

in young children. Most strains are resistant to cefuroxime.

 

Pulmonary anthrax is almost always fatal, but early and continuous IV

therapy with penicillin G 20 million U/day may be lifesaving. (Usual

dose of penicillin G is 100,000 to 250,000 U/kg/day in 4 to 6 divided

doses.) It is used in combination with streptomycin 500 mg/day q 8 h

IM in adults and 25 mg/kg/day in children. Corticosteroids may be

useful but have not been adequately evaluated. If treatment is

delayed (usually because the diagnosis is missed), death is likely.

 

There is no specific therapy for GI anthrax. Contaminated meat should

be avoided. If ingestion occurs, prophylaxis may be given with

penicillin G 4 million U q 4 h IV for 10 days.