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Chapter: Microbiology and Immunology: Bacteriology: Bacillus

Clinical Syndromes - Bacillus anthracis

Human anthrax is of the following clinical types: (a) cutaneous anthrax, (b) gastrointestinal anthrax, (c) inhalational anthrax, and (d) anthrax meningitis.

Clinical Syndromes

Human anthrax is of the following clinical types: (a) cutaneous anthrax, (b) gastrointestinal anthrax, (c) inhalational anthrax, and (d) anthrax meningitis.

 Cutaneous anthrax

Cutaneous anthrax is the most common form of anthrax and constitutes more than 95% of the naturally occurring anthrax. The condition is caused by the entry of spores through the skin lacerations, abrasions; or through fly bites, usually on the face, neck, or arms. This is commonly found in farmers and in per-sons handling infected carcasses. The cutaneous anthrax may progress through the following stages:

·           Papule: The lesion begins as a painless, pruritic papule atthe site of inoculation of spores. The papule, which is the primary lesion, becomes a 1–2-cm vesicle within 2 days.

·           Vesicle: The vesicle is filled with clear or serosanguineousfluid containing numerous large, Gram-positive bacilli and very rare leukocytes. A characteristic nonpitting, gelatinous edema surrounds the lesion. The vesicle enlarges, and satel-lite vesicles may develop. Subsequently, the vesicle ruptures, undergoes necrosis, and enlarges, forming an ulcer covered by a characteristic black eschar (Fig. 28-3).

·           Eschar: The skin in the surrounding areas may becomeedematous and necrotic, but not purulent. The name anthrax, meaning coal, comes from the eschar, which is black colored (Fig. 28-3). The lesion is called “malignant pustule” due to its characteristic appearance; however, these lesions are neither malignant nor pustular. Lesions are painless, but on occasion are slightly pruritic. Occasionally, multiple bullae develop along with marked toxic effects, and the lesions especially on the face or neck become massively edematous. 

Cutaneous anthrax may resolve spontaneously with the eschar drying up and falling off in 1–2 weeks with very little scarring. Cutaneous anthrax usually remains localized. Without treatment, the condition spreads to blood and disseminates to cause systemic infec-tion in nearly one-fifth of the cases.

Prompt antibiotic therapy prevents dissemination of the infection, but does not affect the natural history of the lesion. With treatment, the mortality due to cutaneous anthrax is approximately 1%.

 Gastrointestinal anthrax

The condition is caused on ingestion of undercooked meat of infected carcasses containing spores. Abdominal pain and fever are the first symptoms to appear, i.e., 2–5 days after the ingestion of the food. These symptoms are followed by nausea, vomiting, and diarrhea.

The anthrax spores invade the mucosa of the GI tract and reach mesenteric lymph nodes. The spores in lymph nodes germinate to vegetative forms and begin multiplying, caus-ing the occlusion of the lymphatic system. This leads to ascites, hemorrhagic adenitis, and edematous stomach and intestine.

·           Ulcers are the primary intestinal lesions and occur mainly in the terminal ileum or cecum.

·           In some cases, necrosis and ulceration at the site of infection produces GI hemorrhage, leading to bloody diarrhea.

·           Anthrax toxins can also cause renal failure.

·           Without antibiotic therapy, death is rapid. Mortality is very high and is always more than 50%.

Oropharyngeal anthrax is a variant of intestinal anthrax andoccurs in the oropharynx after ingesting meat products con-taminated by anthrax. Oropharyngeal anthrax is character-ized by throat pain and difficulty in swallowing. The lesion at the site of entry into the oropharynx resembles the cutane-ous ulcer.

 Inhalational anthrax

Inhalational anthrax is also known as “wool sorters disease”. The condition occurs after inhaling spores into the lungs. The spores are present in the dust or in the filaments of wool from infected animals, particularly in wool factories. Spores are ingested by alveolar macrophages and are carried to the mediastinal lymph nodes. Anthrax in the lungs does not cause pneumonia, but it does cause hemorrhagic mediastinitis and pulmonary edema.

    Inhalational anthrax is characteristically a biphasic illness.

·           The first phase appears abruptly after an incubation period of 1–6 days. It appears as a nonspecific illness. Low-grade fever and nonproductive cough are the nonspecific pulmo-nary symptoms at this stage of the infection.

·           After an additional 24–48 hours, the second phase of inhalational anthrax becomes apparent. The phase manifests as high fever, shortness of breath, tachypnea, diaphoresis, and hematemesis. It progresses rapidly to characteristic hemorrhagic bronchopneumonia with shock and associated hypothermia.

Death occurs within 24–36 hours. The disease has a high fatality rate.

 Anthrax meningitis

Anthrax meningitis may occur commonly as a result of bac-teremia from the inhalational anthrax but is a less common manifestation of the anthrax. The meninges are characteristi-cally hemorrhagic and edematous. Cerebrospinal fluid (CSF) is typically hemorrhagic and exhibits a polymorphonuclear pleocytosis. Numerous large, encapsulated, Gram-positive bacilli are demonstrated in the CSF. Mortality is as high as 100%, but occasionally, patients treated with antibiotics have survived.

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