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Anthrax

  • Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Mar 23, 2016
 

Practice Essentials

Anthrax is a zoonotic infection caused by Bacillus anthracis. Most anthrax is cutaneous (95%); the remaining cases are inhalational (5%) and gastrointestinal (< 1%). Anthrax caused by inhalation is usually fatal, and symptoms usually begin days after exposure. Bioterrorism must be suspected in any case of inhalational anthrax. See the image below.

Skin lesion of anthrax on face. Image courtesy of Skin lesion of anthrax on face. Image courtesy of the Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.

See Clues on the Skin: Acute Poisonings, a Critical Images slideshow, to help diagnose patients based on their dermatologic presentations.

Signs and symptoms

Depending on the route of exposure to B anthracis spores (ie, handling of sick animals or contaminated wool, hair, or hides; inhalation; or ingestion of contaminated meat products), patients may present with cutaneous, respiratory, or GI complaints, respectively.

Cutaneous anthrax

  • Develops 1-7 days (usually 2-5 days) after skin exposure
  • Lesions most commonly develop at lacerations, abrasions, or fly bites on exposed areas of the upper extremities and, to a lesser extent, the head and neck
  • Begins as a pruritic papule that enlarges within 24-48 hours to form a 1-cm vesicle and subsequently becomes an ulcer surrounded by an edematous halo [1]
  • Lesions are usually approximately 2-3 cm in diameter and have a round, regular, and raised edge
  • The skin in infected areas may become edematous and necrotic but not purulent
  • Lesions are painless but on occasion are slightly pruritic
  • Regional lymphadenopathy of the nodes draining the infected area may occur and may be painful
  • The anthrax ulcer and surrounding edema evolve into a black eschar within 7-10 days and last for 7-14 days before separating and leaving a permanent scar
  • Lymphadenopathy may be persistent
  • With neck lesions, edema and lymphadenopathy may impinge on the trachea and cause stridor and respiratory distress

Oropharyngeal anthrax

  • Develops 2-7 days after ingestion
  • Fever and neck swelling occur in the presence of an oral cavity lesion
  • The lesion starts as an edematous area that becomes necrotic and forms a pseudomembrane within 2 weeks
  • Sore throat, dysphagia, respiratory distress, and oral bleeding also occur
  • Soft-tissue edema and dramatic cervical lymph node enlargement follow

Intestinal anthrax

  • Develops 2-5 days after ingestion
  • Abdominal pain and fever
  • Nausea, vomiting, malaise, anorexia, hematemesis, bloody (or, less often, watery) diarrhea
  • Shock

Inhalational anthrax

Inhalational anthrax begins abruptly, usually 1-3 days (range, 1-60 days) after exposure, and follows a biphasic course. Initial manifestations include the following:

  • Myalgia
  • Malaise
  • Fatigue
  • Nonproductive cough
  • Sensation of retrosternal pressure (occasional)
  • Fever

Transient clinical improvement may occur after the first few days, followed by rapid progression and clinical deterioration in which the following signs and symptoms may be present:

  • High fever
  • Severe shortness of breath
  • Tachypnea
  • Cyanosis
  • Profuse diaphoresis
  • Hematemesis
  • Chest pain, which may be severe enough to mimic acute myocardial infarction
  • Decreased level of consciousness, meningismus, and coma (with meningeal involvement)
  • Shock

See Clinical Presentation for more detail.

Diagnosis

B anthracis is present in high numbers in appropriate specimens, and can be demonstrated by staining or culture. Laboratory personnel must take level II biohazard precautions to avoid contracting anthrax from specimens.

Diagnostic studies may include the following:

  • Staining of cutaneous ulcer exudate with methylene blue or Giemsa stain
  • Punch biopsy at the edge of the lesion, examined by silver staining and immunohistochemical testing (for patients with prior antibiotic treatment)
  • Blood culture and Gram stain (for patients with systemic symptoms)
  • ELISA serology for B anthracis toxins or IgG response to B anthracis protective antigen
  • Chest radiography – In inhalational anthrax, typically shows widening of the mediastinum and pleural effusions, whereas the parenchyma may appear normal
  • Chest CT – In inhalational anthrax, detects hemorrhagic mediastinal and hilar lymph nodes and edema, peribronchial thickening, and pleural effusions
  • Lumbar puncture (for patients with meningeal symptoms) – CSF is grossly hemorrhagic, with grossly hemorrhagic with few polymorphonuclear neutrophils (PMNs) and numerous gram-positive bacilli

See Workup for more detail.

Management

Treatment of anthrax varies as follows:

  • Cutaneous anthrax – 7-14 days of outpatient therapy with oral doxycycline, or any quinolone (eg, ciprofloxacin, levofloxacin) in patients who are unable to take penicillin
  • With doxycycline, a loading regimen should be used (200 mg PO/IV every 12 hours for 72 hours); in severely ill patients, 200 mg IV/PO every 12 hours may be continued for the duration of therapy
  • Nonbioterrorist inhalational anthrax and anthrax meningitis – Penicillin in meningeal doses is the preferred agent; use any quinolone in patients unable to take penicillin
  • Bioterrorist anthrax - Any quinolone or doxycycline for 1-2 weeks; clindamycin may be added for its anti-exotoxin effect
  • Postexposure prophylaxis – Doxycycline or any quinolone; continue for 60 days to prevent inhalational anthrax
  • When other therapies for inhalational anthrax or prevention are unavailable or inappropriate – Raxibacumab, in combination with appropriate antibiotics [2]
  • Patients with septic and hemorrhagic shock, or progressive respiratory insufficiency – ICU admission for hemodynamic monitoring and management and respiratory support

See Treatment and Medication for more detail.

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Background

Anthrax is a zoonotic infection caused by Bacillus anthracis (see the image below). Most anthrax is cutaneous (95%). The remaining cases of the disease are inhalational (5%) and gastrointestinal (< 1%). Cutaneous anthrax results from exposure to the spores of B anthracis while handling sick animals or contaminated wool, hair, or animal hides. Pulmonary anthrax results from inhaling anthrax spores. GI anthrax results from ingesting meat products that contain anthrax. Anthrax is present in areas where animals, particularly herbivores, graze. Anthrax caused by inhalation is usually fatal, and symptoms usually begin days after exposure. This delay makes the initial exposure to B anthracis difficult to track.

Polychrome methylene blue stain of Bacillus anthra Polychrome methylene blue stain of Bacillus anthracis. Image courtesy of Anthrax Vaccine Immunization Program Agency, Office of the Army Surgeon General, United States.

Anthrax was described in the early literature of the Greeks, Romans, Egyptians, and Hindus. The term anthrakis means coal in Greek, and the disease is named after the black appearance of its cutaneous form.[3] The fifth plague described in the Old Testament book of Genesis may be among the earliest descriptions of anthrax. At the end of the 19th century, Robert Koch's experiments with anthrax led to the original theory of bacteria and disease. John Bell's work in inhalational anthrax led to wool disinfection processes and the term woolsorter's disease.

A modern concern is use of anthrax as a biologic warfare agent. During the first Gulf War, Iraq reportedly produced 8500 L of anthrax. A total of 150,000 US troops were vaccinated with anthrax toxoid. In the weeks following the terrorist attacks of September 11, 2001, 22 confirmed or suspected cases of anthrax infection were disseminated via the US postal system; the spores mailed in these letters were ultimately traced to a US army medical research institute. Since there have been no cases of naturally occurring inhalational anthrax in the US since 1976, alarm should be raised for the occurrence of even a single infection.

For patient education information, see the Bioterrorism and Disaster Medicine Center, as well as Biological Warfare, Anthrax, and Personal Protective Equipment.

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Pathophysiology

Anthrax is primarily a disease of herbivores (eg, cattle, sheep, goats, horses). Pigs are not immune, but they are more resistant, as are dogs and cats. Birds are usually naturally resistant to anthrax. Buzzards and vultures are naturally resistant to anthrax but may transmit the spores on their talons and beaks.

Anthrax (B anthracis) is a large, spore-forming, gram-positive rod. Persistence of spores is aided by nitrogen and organic soil content, environmental pH greater than 6, and ambient temperature greater than 15°C. Spores can exist indefinitely in the environment. Optimal growth conditions result in a vegetative phase and bacterial multiplication. Drought or rainfall can trigger anthrax spore germination, while flies and vultures spread the spores.

Virulence depends on the bacterial capsule and the toxin complex. The capsule is a poly-D-glutamic acid that protects against leukocytic phagocytosis and lysis. Experiments by Sterne demonstrated that the capsule is vital for pathogenicity.

Anthrax toxins

Anthrax toxins are composed of 3 entities: a protective antigen, a lethal factor, and an edema factor. The protective antigen is an 83-kd protein that binds to cell receptors within a target tissue. Once it is bound, a fragment is cleaved free to expose an additional binding site. The binding of edema factor at this site results in the formation of edema toxin; the binding of lethal factor results in the formation of lethal toxin.

Edema toxin acts by converting adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Cellular cAMP levels are increased, leading to cellular edema within the target tissue. Lethal factor is not well understood; it may inhibit neutrophil phagocytosis, lyse macrophages, and cause release of tumor necrosis factor and interleukin-1. Death from anthrax occurs as a result of the effects of lethal toxin. Near death or just after death, animals bleed from all body orifices.

Cutaneous anthrax

Humans are relatively resistant to cutaneous invasion by B anthracis, but the organisms may gain access through microscopic or gross breaks in the skin. In cutaneous anthrax, a malignant pustule develops at the infection site. This pustule is a central area of coagulation necrosis (ulcer) surrounded by a rim of vesicles filled with bloody or clear fluid. A black eschar forms at the ulcer site. Extensive edema surrounds the lesion.

The organisms multiply locally and may spread to the bloodstream or other organs (eg, spleen) via the efferent lymphatics. B anthracis remains in the capillaries of invaded organs, and the local and fatal effects of the infection are due, in large part, to the toxins elaborated by B anthracis. Dissemination from the liver, spleen, and kidneys back into the bloodstream may result in bacteremia. Secondary hemorrhagic intestinal foci of anthrax result from B anthracis bacteremia.

Intestinal anthrax

Primary intestinal anthrax predominantly affects the cecum and produces a local lesion similar to the lesion produced in the cutaneous form. In this illness, spores invade the GI mucosa. In some cases, necrosis and ulceration at the site of infection produce GI hemorrhage (see the image below).

Histopathology of large intestine showing marked h Histopathology of large intestine showing marked hemorrhage in the mucosa and submucosa. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.

As spores are transported to mesenteric lymph nodes, replication and bacteremia begin. Ascites and ileus follow as the lymphatic system becomes occluded with the large number of bacilli. Peritoneal fluid is turbid with the presence of leukocytes and red blood cells from hemorrhagic adenitis. Vascular stasis occurs, and the stomach and intestine become edematous.

Oropharyngeal anthrax

Oropharyngeal anthrax is a variant of intestinal anthrax and occurs in the oropharynx after ingestion of meat products contaminated by anthrax. Oropharyngeal anthrax is characterized by throat pain and difficulty in swallowing. The lesion at the site of entry into the oropharynx resembles the cutaneous ulcer.

Inhalational anthrax

Inhalational anthrax occurs after a person inhales spores into the lungs. Primate studies suggest that the minimum infective dose ranges from 4000-8000 inhaled spores. Inhaled spores are ingested by pulmonary macrophages and then carried to hilar and mediastinal lymph nodes (see the image below). The incubation period is 1-6 days.

Histopathology of mediastinal lymph node showing a Histopathology of mediastinal lymph node showing a microcolony of Bacillus anthracis on Giemsa stain. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.

The spores undergo germination and multiplication and begin to elaborate toxins. Anthrax in the lungs does not cause pneumonia, but it does cause hemorrhagic mediastinitis and pulmonary edema. Hemorrhagic pleural effusions frequently accompany inhalational anthrax. After the lymph nodes become overwhelmed, bacteremia and death quickly ensue. Without treatment, the mortality rate of inhalational anthrax is approximately 95%.

Bacteremic anthrax with hematogenous spread most commonly follows inhalational anthrax. In bacteremic anthrax, hemorrhagic lesions may develop anywhere on the body. Septicemic anthrax refers to overwhelming infection resulting from bloodstream invasion secondary to inhalation or intestinal anthrax.

Anthrax meningitis

Anthrax meningitis may complicate any form of anthrax, with bacteremia and hematogenous spread to the CNS. It also has occurred without a primary focus. The meninges are characteristically hemorrhagic and edematous (see the image below). The mortality rate is near 100%.

Anthrax infection. Histopathology of hemorrhagic m Anthrax infection. Histopathology of hemorrhagic meningitis in anthrax. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
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Etiology

Anthrax is caused by B anthracis, a gram-positive bacillus. B anthracis has a diameter of 1-1.5 µm and a length of 3-10 µm. It is usually straight but may be slightly curved. The ends of the bacilli are truncated, not rounded. Anthrax bacilli tend to form into long chains and may appear similar to streptobacilli on cultures.

B anthracis produces a capsule that is easily visualized using a methylene blue or India ink stain (see the image below). Ground-glass–appearing colonies are adherent and appear gray or white on blood agar. Colonies measure 4-5 mm in diameter and have characteristic comma-shaped protrusions.

Polychrome methylene blue stain of Bacillus anthra Polychrome methylene blue stain of Bacillus anthracis. Image courtesy of Anthrax Vaccine Immunization Program Agency, Office of the Army Surgeon General, United States.

Bacilli grow optimally in enhanced carbon dioxide and are nonmotile. The organism shows preferential growth on phenylethyl alcohol blood agar with characteristic gelatin hydrolysis and salicin fermentation. B anthracis is catalase positive. Capsule formation may help differentiate B anthracis from other nonpathogenic bacilli. Anthrax is differentiated from other gram-positive rods on culture by lack of motility in broth and lack of hemolysis on blood agar. See Table 1 below.

Table 1. Microbiological Differences Between B anthracis and Non– B anthracis Bacilli (Open Table in a new window)

B anthracis Non–B anthracis bacilli (pseudoanthrax bacilli)
Nonmotile long chains Generally motile short chains
Capsule formation on bicarbonate agar No capsule formation in bicarbonate
No growth on penicillin agar



(10 mcg/mL)



Usually good growth on penicillin agar
Growth in gelatin resembles inverted fir tree Growth in gelatin absent or resembles atypical fir tree
Gelatin liquefaction slow Gelatin liquefaction usually rapid
No hemolysis of sheep RBCs Hemolysis of sheep RBCs
Ferments salicin slowly or not at all Usually ferments salicin rapidly
Pathogenic to laboratory animals Nonpathogenic to laboratory animals
Adapted from Cunha CB. Anthrax: Ancient Plague, Persistent Problem. Infect Dis Pract. 1999;23(4):35-9.

Anthrax toxins

Anthrax exotoxins are produced in the vegetative phase and are composed of proteins (see Table 2 below). Lethal toxin is the single most important virulence factor and is the primary cause of death. Lethal toxin is a combination of protective antigen and lethal factor. Edema factor and lethal toxin inhibit phagocytosis and polymorphonuclear neutrophil (PMN) function. The other major anthrax virulence factor is its antiphagocytic poly-D-glutamic acid capsule.

Table 2. Toxins and Protein Toxins of Bacillus anthracis (Open Table in a new window)

Edema factor (EF) + lethal factor (LF) = Host cell penetration by B anthracis
EF + protective antigen (PA) = Edema toxin
LF + PA = Lethal toxin (primary virulence factor of B anthracis)
Edema toxin + lethal toxin = Inhibited PMN function and phagocytosis

Risk factors

Studies of inhalational anthrax based on several cases in patients with no known exposure in the October 2001 postal anthrax release found the following determinants of risk:

  • Bacterial virulence factors
  • Balance between infectious aerosol production and removal
  • Pulmonary ventilation rate
  • Duration of exposure
  • Host susceptibility factors

Dilution ventilation of the indoor environment is an important determinant of the risk for infection. Enhanced room ventilation, germicidal irradiation with ultraviolet light, and other engineering control measures may be used to decrease the risk for infection.

Important host susceptibility risk factors for inhalational anthrax include the following:

  • Prior exposure to radiation
  • Alcoholism
  • Underlying pulmonary disease
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Epidemiology

United States statistics

Natural incidence is rare, but infection is an occupational hazard among veterinarians, farmers, and individuals who handle animal wool, hair, hides, or bone meal products. During the last 30 years, the indigenous US incidence of any anthrax infection has been less than 1 case per year. From 1955–1994, US cases totaled 235, with 224 cases of cutaneous anthrax, 11 cases of inhalational anthrax, and 20 fatalities. The last fatal case during this period occurred in 1976, when a home craftsman died of inhalational anthrax after working with yarn imported from Pakistan.

Before October 2001, the Centers for Disease Control and Prevention (CDC) investigated several threats in the United States, including Indiana, Kentucky, Tennessee, and California. In October 2001, 22 confirmed or suspected cases of anthrax infection were identified. Cases were reported from Florida, New York, New Jersey, the District of Columbia, and Connecticut. There were 11 confirmed cases of inhalational anthrax (5 deaths) and 7 confirmed and 4 suspected cases of cutaneous anthrax (no deaths).

Seven cases were associated with occupational exposures in the postal service, and 2 cases had documented exposures to contaminated mail in the business office of a media company. No sources of exposure were identified for 2 women who were presumably exposed to secondarily contaminated mail. No reports in the literature have documented direct human-to-human transmission.

International statistics

Anthrax is uncommon in Western Europe, but the disease is not uncommon in the Middle East, the Indian subcontinent,[4] Africa, Asia, and Latin America. In 1958, approximately 100,000 cases of anthrax occurred worldwide. Exact figures do not exist because of reporting difficulties in Africa. Anthrax is endemic in Africa and Asia despite vaccination programs.

Sporadic outbreaks have occurred as a result of both agricultural and military disruptions. During the 1978 Rhodesian civil war, failure of veterinary vaccination programs led to a human epidemic, causing 6500 anthrax cases and 100 fatalities. A mishap at a military microbiology facility in Sverdlovsk in the former Soviet Union in 1979 resulted in at least 66 deaths.[3] Human anthrax often is associated with agricultural or industrial workers who come in contact with infected animal tissue.

Race-, sex-, and age-related differences in incidence

There is no racial, sexual, or age predilection for anthrax. However, because anthrax is often related to industrial exposure and farming, the disease most often affects young and middle-aged adults. Persons of any age can of course be affected if anthrax is used as a bioterrorist weapon.

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Prognosis

Most cases of anthrax are the cutaneous type, are mild, and resolve with or without treatment. If treated early with appropriate antibiotics, the mortality rate of cutaneous anthrax is less than 1%. However, other forms of anthrax are potentially fatal, with inhalational anthrax carrying the worst prognosis. Inhalational anthrax and its subsequent systemic infection (eg, septicemia, hemorrhagic leptomeningitis) have a mortality rate approaching 100%. If treatment is initiated during the incubation period of 1-6 days and before the manifestation of symptoms, mortality can decrease to 1%. In the US cases in 2001, the mortality rate of treated inhalational anthrax was 45%.[5]

Oropharyngeal or intestinal anthrax carries a less favorable prognosis than cutaneous anthrax but a more favorable prognosis than inhalational anthrax. Patients with oropharyngeal anthrax may develop airway obstruction (as may those with inhalational anthrax or cutaneous anthrax involving the neck). Intestinal anthrax is difficult to diagnose and is associated with higher morbidity (mortality rate 20-60%).

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Contributor Information and Disclosures
Author

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Hilarie Cranmer, MD, MPH, FACEP Director, Global Women's Health Fellowship, Associate Director, Harvard International Emergency Medicine Fellowship, Department of Emergency Medicine, Brigham and Women's Hospital; Director, Humanitarian Studies Program, Harvard Humanitarian Initiative; Assistant Professor, Harvard University School of Medicine

Hilarie Cranmer, MD, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Massachusetts Medical Society, Physicians for Human Rights, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Robert G Darling, MD, FACEP Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Mauricio Martinez, MD Assistant Medical Director, Department of Emergency Medicine, Winchester Medical Center

Mauricio Martinez, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Barry J Sheridan, DO Chief, Department of Emergency Medical Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Akbayram S, Dogan M, Akgün C, et al. Clinical findings in children with cutaneous anthrax in eastern Turkey. Pediatr Dermatol. 2010 Nov-Dec. 27(6):600-6. [Medline].

  2. US Food and Drug Administration (FDA). FDA approves raxibacumab to treat inhalational anthrax. December 14, 2012 (press announcement). Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm332341.htm.

  3. Inglesby TV, O'Toole T, Henderson DA, et al. Anthrax as a biological weapon, 2002: updated recommendations for management. JAMA. 2002 May 1. 287(17):2236-52. [Medline].

  4. John TJ, Dandona L, Sharma VP, Kakkar M. Continuing challenge of infectious diseases in India. Lancet. 2011 Jan 15. 377(9761):252-69. [Medline].

  5. Holty JE, Bravata DM, Liu H, et al. Systematic review: a century of inhalational anthrax cases from 1900 to 2005. Ann Intern Med. 2006 Feb 21. 144(4):270-80. [Medline].

  6. Knox D, Murray G, Millar M, et al. Subcutaneous anthrax in three intravenous drug users: a new clinical diagnosis. J Bone Joint Surg Br. 2011 Mar. 93(3):414-7. [Medline].

  7. Migone TS, Subramanian GM, Zhong J, Healey LM, Corey A, Devalaraja M, et al. Raxibacumab for the treatment of inhalational anthrax. N Engl J Med. 2009 Jul 9. 361(2):135-44. [Medline]. [Full Text].

  8. Anthim (obiltoxaximab) [package insert]. Pine Brook, NJ: Elusys Therapeutics, Inc. March 2016. Available at [Full Text].

  9. Anthrasil (anthrax immune globulin intravenous [human]) [package insert]. Winnipeg, MB; Canada: Cangene Corp (Emergent BioSolutions). March 24, 2015. Available at [Full Text].

  10. BioThrax (anthrax vaccine adsorbed) [package insert]. Lansing, MI: Emergent BioSolutions. November, 2015. Available at [Full Text].

  11. [Guideline] Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of america. Clin Infect Dis. 2014 Jul 15. 59(2):e10-52. [Medline].

  12. Barclay L. Anthrax Guidelines Address Nonpregnant, Pregnant Adults. Available at http://www.medscape.com/viewarticle/819274. Accessed: January 19, 2014.

  13. [Guideline] Hendricks KA, Wright ME, Shadomy SV, et al. Centers for Disease Control and Prevention expert panel meetings on prevention and treatment of anthrax in adults. Emerg Infect Dis 2014. Available at http://dx.doi.org/10.3201/eid2002.130687.

  14. Raxibacumab [package insert]. Research Triangle Park, NC: GlaxoSmithKline. December, 2012. Available at [Full Text].

  15. Food and Drug Administration. 17.5 FDA-Approved Medication Guide. Levaquin (levofloxacin). [Full Text].

  16. CDC. Vaccines and Preventable Diseases:Anthrax Vaccination. Vaccines:VPF-VAD/Anthrax/mainpage. [Full Text].

  17. Alqurashi AM. Anthrax threat: a review of clinical and diagnostic measures. J Egypt Soc Parasitol. 2013 Apr. 43(1):147-66. [Medline].

  18. Hicks CW, Sweeney DA, Cui X, Li Y, Eichacker PQ. An overview of anthrax infection including the recently identified form of disease in injection drug users. Intensive Care Med. 2012 Jul. 38(7):1092-104. [Medline]. [Full Text].

  19. Meaney-Delman D, Zotti ME, Creanga AA, Misegades LK, Wako E, Treadwell TA, et al. Special considerations for prophylaxis for and treatment of anthrax in pregnant and postpartum women. Emerg Infect Dis. 2014 Feb. 20(2):[Medline]. [Full Text].

  20. Sweeney DA, Hicks CW, Cui X, Li Y, Eichacker PQ. Anthrax infection. Am J Respir Crit Care Med. 2011 Dec 15. 184(12):1333-41. [Medline]. [Full Text].

 
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Polychrome methylene blue stain of Bacillus anthracis. Image courtesy of Anthrax Vaccine Immunization Program Agency, Office of the Army Surgeon General, United States.
Histopathology of mediastinal lymph node showing a microcolony of Bacillus anthracis on Giemsa stain. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Cutaneous anthrax. Image courtesy of Anthrax Vaccine Immunization Program Agency, Office of the Army Surgeon General, United States.
Skin lesion of anthrax on face. Image courtesy of the Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Skin lesions of anthrax on neck. Cutaneous anthrax showing the typical black eschar. Image courtesy of the Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Histopathology of large intestine showing marked hemorrhage in the mucosa and submucosa. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Histopathology of the large intestine showing submucosal thrombosis and edema. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Inhalation anthrax. Chest radiograph with widened mediastinum 22 hours before death. Image courtesy of P.S. Brachman, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Histopathology of mediastinal lymph node showing mediastinal necrosis. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Hemorrhagic meningitis resulting from inhalation anthrax. Image courtesy of the Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Anthrax infection. Histopathology of hemorrhagic meningitis in anthrax. Image courtesy of Marshall Fox, MD, Public Health Image Library, US Centers for Disease Control and Prevention, Atlanta, Georgia.
Microscopic picture of anthrax showing gram-positive rods. Image courtesy of Ramon E. Moncada, MD.
Seven-month-old infant with anthrax. In this infant, the infection progressed rapidly with significant edema developing the day after exposure. This large hemorrhagic lesion developed within 3 more days. The infant was febrile and was admitted to the hospital on the second day after the symptoms appeared.On September 28, 2001, the infant had visited the mother's workplace. On September 29, nontender massive edema and a weeping erosion developed. On September 30, a 2-cm sore developed over the edematous area. (Note that edema preceded the primary lesion.) On October 2, an ulcer or eschar formed, and the lesion was diagnosed as a spider bite. Hemolytic anemia and thrombocytopenia developed, and the patient was hospitalized. Serum was drawn on October 2; the polymerase chain reaction results were positive for Bacillus anthracis. On October 13, skin biopsy results were positive with immunohistochemical testing for the cell wall antigen.Note that the initial working diagnosis was a Loxosceles reclusa spider bite with superimposed cellulitis. Courtesy of American Academy of Dermatology with permission of NEJM.
Fourth patient with cutaneous anthrax in New York City, October 2001. This dry ulcer was present. Photo used with permission of the patient. Courtesy of American Academy of Dermatology. Courtesy of Sharon Balter of the New York City Department of Health.
Note the hemorrhage that is associated with cutaneous anthrax lesions. The early ulcer has a moist base. Courtesy of American Academy of Dermatology.
Note the central ulcer and eschar. Courtesy of American Academy of Dermatology.
An example of a central ulcer and eschar with surrounding edema. Courtesy of American Academy of Dermatology with permission from Boni Elewski, MD.
Note the black eschar. Courtesy of American Academy of Dermatology. Courtesy of Gorgas Course in Clinical Tropical Medicine.
Anthrax with facial edema. Courtesy of American Academy of Dermatology.
Table 1. Microbiological Differences Between B anthracis and Non– B anthracis Bacilli
B anthracis Non–B anthracis bacilli (pseudoanthrax bacilli)
Nonmotile long chains Generally motile short chains
Capsule formation on bicarbonate agar No capsule formation in bicarbonate
No growth on penicillin agar



(10 mcg/mL)



Usually good growth on penicillin agar
Growth in gelatin resembles inverted fir tree Growth in gelatin absent or resembles atypical fir tree
Gelatin liquefaction slow Gelatin liquefaction usually rapid
No hemolysis of sheep RBCs Hemolysis of sheep RBCs
Ferments salicin slowly or not at all Usually ferments salicin rapidly
Pathogenic to laboratory animals Nonpathogenic to laboratory animals
Adapted from Cunha CB. Anthrax: Ancient Plague, Persistent Problem. Infect Dis Pract. 1999;23(4):35-9.
Table 2. Toxins and Protein Toxins of Bacillus anthracis
Edema factor (EF) + lethal factor (LF) = Host cell penetration by B anthracis
EF + protective antigen (PA) = Edema toxin
LF + PA = Lethal toxin (primary virulence factor of B anthracis)
Edema toxin + lethal toxin = Inhibited PMN function and phagocytosis
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