In New Zealand, contact with and exposure to anthrax is managed by general medicines. Anthrax is an acute infection caused by Bacillus anthracis, a large gram-positive spore-forming rod whose hardy spores survive in soil for decades and can be aerosolized as a biological weapon. The disease produces four distinct clinical syndromes depending on portal of entry — cutaneous (95% of naturally occurring cases), inhalation, gastrointestinal, and injection (in heroin users).
Anthrax (ICD-10: A22) is a zoonotic infection caused by Bacillus anthracis, a large (1-1.5 µm × 3-10 µm) gram-positive, aerobic, spore-forming rod. The organism produces three plasmid-encoded virulence factors: protective antigen (PA), lethal factor (LF), and edema factor (EF). PA forms a heptameric channel in host cell membranes through which LF and EF translocate into the cytoplasm. Lethal toxin (PA + LF) cleaves mitogen-activated protein kinase kinases and triggers macrophage death; edema toxin (PA + EF) raises intracellular cAMP and produces massive fluid extravasation.
The key symptoms of Contact with and exposure to anthrax are: A painless papule appearing 1-7 days after exposure that progresses through vesicle, then ulceration, then a depressed black eschar surrounded by massive non-tender edema — the pathognomonic feature of cutaneous anthrax., Marked extension of edema beyond the primary lesion, sometimes involving an entire limb or the face, often with regional lymphadenopathy disproportionate to the modest skin lesion., Initial flu-like illness with fever, malaise, dry cough, mild chest discomfort, and fatigue lasting 2-5 days in inhalation anthrax — clinically indistinguishable from viral upper respiratory infection at this stage., Abrupt clinical deterioration after the initial phase of inhalation anthrax with high fever, severe dyspnea, hypotension, profuse diaphoresis, and progressive shock over hours to days., Cyanosis, stridor, and respiratory failure from massive hemorrhagic mediastinal lymphadenopathy and pleural effusion in inhalation anthrax — the classic widened mediastinum on chest imaging., Severe sore throat, dysphagia, and a pseudomembranous lesion at the base of the tongue or tonsillar pillar with massive cervical edema (oropharyngeal anthrax)., Severe abdominal pain, fever, hematemesis, and bloody diarrhea with ascites in intestinal anthrax, with peritonitis if untreated..
Diagnosis of anthrax begins with clinical recognition of the four syndromes and epidemiologic suspicion. Cutaneous anthrax presents a near-pathognomonic picture: painless papule progressing through vesicle to black eschar with massive non-tender edema. Inhalation anthrax masquerades as influenza early in its course; the diagnostic clue is rapid clinical deterioration with a widened mediastinum on chest imaging — a finding that, in the right exposure context, demands immediate empirical therapy. Gram stain of blood, lesion swab, sputum, cerebrospinal fluid, or pleural fluid shows large gram-positive rods, often in chains. Blood cultures grow B. anthracis on standard media within 12-24 hours; growth is rapid but the organism is a select agent requiring BSL-3 containment, so laboratories must be informed in advance. Real-time PCR for the pagA gene (protective antigen) and capB gene (capsule biosynthesis) confirms diagnosis within hours and is available through the Laboratory Response Network. Antigen-capture immunoassays for protective antigen support rapid diagnosis. Serology by ELISA for IgG to protective antigen documents recent exposure for post-event surveillance but is too slow for acute management. Imaging: chest X-ray and CT in inhalation anthrax show the classic widened mediastinum, hemorrhagic mediastinal adenopathy, and pleural effusions. Differential diagnosis depends on form: cutaneous anthrax mimics brown recluse spider bite, ecthyma gangrenosum, tularemia, plague, and necrotizing soft-tissue infection; inhalation anthrax mimics influenza early and dissecting aortic aneurysm or pulmonary embolism later; oropharyngeal anthrax mimics severe streptococcal pharyngitis with peritonsillar abscess; intestinal anthrax mimics severe gastroenteritis with peritonitis. Because anthrax kills so quickly, empirical antibiotic therapy must start on clinical suspicion without waiting for laboratory confirmation. All suspected and confirmed cases must be reported to public health within 24 hours.
Prognosis varies dramatically by clinical form and treatment timing. Cutaneous anthrax treated with appropriate antibiotics has a case fatality rate under 1% — among the lowest of any acute bacterial infection. Inhalation anthrax untreated has a case fatality of 85-90% over 4-10 days; with optimal modern combination antibiotic therapy plus toxin-neutralizing monoclonal antibodies and intensive care, mortality falls to roughly 45% in the limited modern experience. Gastrointestinal anthrax carries mortality of 25-60% depending on form and access to care. Injection anthrax (heroin users) has mortality of 20-30% with surgical debridement and antibiotics. Anthrax meningitis is almost uniformly fatal even with optimal therapy (over 90% mortality). The 2001 US letter attack cohort demonstrated that early recognition, combination antibiotic therapy, and aggressive critical care can save inhalation anthrax patients who in earlier decades would have died — 6 of 11 inhalation cases survived in that outbreak. Survivors of severe systemic anthrax may face long-term consequences including chronic lung damage, cognitive impairment from post-sepsis encephalopathy, and post-traumatic stress disorder. The decisive prognostic factor across forms is timely initiation of combination antibiotic therapy plus antitoxin in systemic disease.
Suspected anthrax warrants immediate infectious disease consultation, hospitalization, and public-health notification. Inhalation, gastrointestinal, injection, and disseminated cutaneous anthrax require intensive care unit admission. Critical care, ENT, neurosurgery, and surgical teams collaborate as indicated. Self-treatment of suspected anthrax is not appropriate; even a localized cutaneous lesion mandates evaluation because of select-agent reporting and risk of progression.
Find specialists →Cutaneous anthrax eschar typically separates and heals over 6-8 weeks, often leaving a depressed scar. Antibiotic therapy continues for 7-10 days in localized cutaneous disease and 60 days in systemic disease. Inhalation anthrax survivors typically spend 2-4 weeks in intensive care followed by 3-6 months of pulmonary rehabilitation. Gastrointestinal anthrax requires 2-6 weeks for clinical recovery. Full return to baseline energy can take 6-12 months after severe systemic disease.
Strict bed rest during acute systemic disease. Gradual return to activity after at least 48 hours afebrile and clinically improving. Cardiopulmonary recovery from inhalation anthrax can take 3-6 months; pulmonary rehabilitation helps restore exercise tolerance. Patients on the 60-day antibiotic course can resume normal activity once acute illness has resolved, with avoidance of strenuous exercise during fluoroquinolone therapy if tendinopathy symptoms develop.
Suspected anthrax should bypass primary care for emergency department or infectious disease referral. Hospitals with Laboratory Response Network affiliation maintain anthrax preparedness protocols. In bioterrorism scenarios, treatment and prophylaxis are coordinated by local public health authorities and the CDC. Patients with workplace exposure to wool, hides, or livestock should be evaluated in occupational health.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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