eMedicine Specialties > Infectious Diseases > Bacterial Infections

Anthrax

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
Contributor Information and Disclosures

Updated: Aug 18, 2008

Introduction

Background

Anthrax was described in the early literature of the Greeks, Romans, and Hindus. The fifth plague described in the book of Genesis may be among the earliest descriptions of anthrax.

Most of the terms associated with anthrax relate to cutaneous or respiratory anthrax. Cutaneous anthrax results from exposure to the spores of Bacillus anthracis after handling sick animals or contaminated wool, hair, or animal hides. Pulmonary anthrax results from inhaling anthrax spores. Intestinal anthrax results from ingesting meat products that contain anthrax. Anthrax is present in areas where animals, particularly herbivores, graze.

Polychrome methylene blue stain of <em>Bacillus a...

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

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Polychrome methylene blue stain of <em>Bacillus a...

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


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.

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. Dissemination from the liver, spleen, and kidneys back into the bloodstream may result in bacteremia. In bacteremic anthrax, hemorrhagic lesions may develop anywhere on the body. Bacteremic anthrax with hematogenous spread most commonly follows inhalation anthrax.

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. Anthrax in the spore stage can exist indefinitely in the environment. Optimal growth conditions result in a vegetative phase and bacterial multiplication. Secondary hemorrhagic intestinal foci of anthrax result from B anthracis bacteremia.

Primary intestinal anthrax predominantly affects the cecum and produces a local lesion similar to the lesion produced in the cutaneous form. Oropharyngeal anthrax is a variant of intestinal anthrax and occurs in the oropharynx after ingesting 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.

Inhalation anthrax occurs after inhaling spores into the lungs. 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. Hemorrhagic pleural effusions frequently accompany inhalation anthrax.

Anthrax meningitis may occur after bacteremic seeding from any form of anthrax.

Septicemic anthrax refers to overwhelming infection resulting from bloodstream invasion secondary to inhalation or intestinal anthrax. Death from anthrax occurs as a result of the effects of lethal toxins. Near death or just after death, animals bleed from all body orifices.

Frequency

United States

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.

International

Anthrax is uncommon in Western Europe, but the disease is not uncommon in the Middle East, the Indian subcontinent, Africa, Asia, and Latin America. Anthrax used in bioterrorism (ie, weapon-grade anthrax) may be dispersed as an aerosol for mass effect or by focal spore contamination via letters or packages.

Mortality/Morbidity

Most cases of anthrax are the cutaneous type, are mild, and resolve with or without treatment. However, other forms of anthrax are potentially fatal.

  • Septicemic anthrax and inhalation anthrax carry the highest mortality rates. Inhalation anthrax may be fatal with or without antibiotic therapy. In 2001, the mortality rate of treated inhalation anthrax was 45%.1
  • Cutaneous anthrax is readily curable if treated early with appropriate antibiotics (mortality rate <1%).
  • Intestinal anthrax is difficult to diagnose and is associated with higher morbidity (mortality rate 20-60%).

Race

  • No racial predilection for, or protection from, anthrax exists.

Sex

  • No sex predilection exists.

Age

  • No inherent age predilection exists, but, 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 be affected if anthrax is used as a bioterrorist weapon.

Clinical

History

  • Cutaneous anthrax
    • Cutaneous anthrax develops 1-7 days (usually 2-5) after skin exposure and penetration of B anthracis spores.
    • This form most commonly affects the exposed areas of the upper extremities and, to a lesser extent, the head and neck.
    • Hematogenous dissemination occurs in 5-10% of untreated cases.

      Cutaneous anthrax. Image courtesy of Anthrax Vacc...

      Cutaneous anthrax. Image courtesy of Anthrax Vaccine Immunization Program Agency, Office of the Army Surgeon General, United States.

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      Cutaneous anthrax. Image courtesy of Anthrax Vacc...

      Cutaneous anthrax. Image courtesy of Anthrax Vaccine Immunization Program Agency, Office of the Army Surgeon General, United States.


      Skin lesions of anthrax on neck. Image courtesy o...

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

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      Skin lesions of anthrax on neck. Image courtesy o...

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


      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.

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      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.


      Seven-month-old infant with anthrax. In this infa...

      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.

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      Seven-month-old infant with anthrax. In this infa...

      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...

      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.

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      Fourth patient with cutaneous anthrax in New York...

      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 cutan...

      Note the hemorrhage that is associated with cutaneous anthrax lesions. The early ulcer has a moist base. Courtesy of American Academy of Dermatology.

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      Note the hemorrhage that is associated with cutan...

      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 Am...

      Note the central ulcer and eschar. Courtesy of American Academy of Dermatology.

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      Note the central ulcer and eschar. Courtesy of Am...

      Note the central ulcer and eschar. Courtesy of American Academy of Dermatology.


      An example of a central ulcer and eschar with sur...

      An example of a central ulcer and eschar with surrounding edema. Courtesy of American Academy of Dermatology with permission from Boni Elewski, MD.

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      An example of a central ulcer and eschar with sur...

      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 Acade...

      Note the black eschar. Courtesy of American Academy of Dermatology. Courtesy of Gorgas Course in Clinical Tropical Medicine.

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      Note the black eschar. Courtesy of American Acade...

      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 A...

      Anthrax with facial edema. Courtesy of American Academy of Dermatology.

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      Anthrax with facial edema. Courtesy of American A...

      Anthrax with facial edema. Courtesy of American Academy of Dermatology.

  • Oropharyngeal anthrax
    • Ingestion of B anthracis spores may result in oropharyngeal anthrax 2-7 days after exposure.
    • Patients with oropharyngeal anthrax may report unilateral sore throat and/or difficulty swallowing.
  • Intestinal anthrax
    • Ingesting B anthracis spores may cause intestinal anthrax 2-5 days following ingestion.
    • Patients with intestinal anthrax report nausea, vomiting, malaise, anorexia, abdominal pain, hematemesis, and bloody diarrhea, which are accompanied by fever.
  • Inhalation anthrax
    • Inhalation anthrax begins abruptly, usually 1-3 days (range, 1-60 d) after inhaling anthrax spores that are 1-5 µm in diameter. The number of spores needed to cause inhalation anthrax varies. As evidenced by recent anthrax cases in the United States, fewer spores of weapon-grade anthrax may be required to cause inhalation anthrax.
    • This form presents initially with nonspecific symptoms, including a low-grade fever and a nonproductive cough.
    • Patients may report substernal discomfort early in the illness.
    • Patients may improve temporarily before rapidly deteriorating clinically with hemorrhagic mediastinitis.
    • After the initial improvement, inhalation anthrax progresses rapidly, causing high fever, severe shortness of breath, tachypnea, cyanosis, profuse diaphoresis, hematemesis, and chest pain, which may be severe enough to mimic acute myocardial infarction.
  • Septicemic anthrax
    • Septicemic anthrax refers to overwhelming infection by anthrax bacilli. This form of anthrax may complicate inhalation anthrax.
    • Internal organs become darkly colored with widespread petechiae and hemorrhage.
    • The anthrax bacilli multiply in the blood and proliferate to outnumber red blood cells. Another name for anthrax is black blood, which refers to the very dark color of the blood of animals or humans with overwhelming septicemic anthrax.
    • Because humans are relatively resistant to invasion by B anthracis, most cases of septicemic anthrax occur following inhalation anthrax. The number of organisms released from the liver or spleen into the bloodstream overwhelms host defenses and produces massive amounts of lethal toxin that cause shock and death.
  • Anthrax meningitis: Anthrax meningitis may complicate any form of anthrax, with bacteremia and hematogenous spread to the CNS.

Physical

  • Cutaneous anthrax
    • Cutaneous anthrax begins as a pruritic papule that enlarges within 24-48 hours to form an ulcer surrounded by a satellite bulbus/lesion edematous halo. The cutaneous anthrax lesion is usually approximately 2-3 cm in diameter and has a round, regular, and raised edge.
    • Regional lymphadenopathy of the nodes draining the infected area may occur.
    • The cutaneous anthrax ulcer is characteristically pruritic but not painful. The adenopathy associated with cutaneous anthrax may be painful.
    • The membrane/exudate of the ulcer contains numerous anthrax bacilli.
    • 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. The edema surrounding the ulcer may persist through the eschar stage.
    • Lymphadenopathy associated with cutaneous anthrax may persist long after disappearance of the ulcer/eschar.
    • If the lesions of cutaneous anthrax affect the neck, neck swelling due to edema and enlarged cervical lymph nodes may impinge on the trachea and cause stridor and respiratory distress and, if severe, may be accompanied by asphyxiation.
  • Oropharyngeal anthrax
    • Oropharyngeal anthrax is the proximal GI manifestation of intestinal anthrax. Mouth lesions may affect the hard palate or pharyngeal walls.
    • The anthrax ulcer in the oropharynx may be accompanied by a membrane and is associated with local edema and cervical adenopathy.
    • Death may result from asphyxiation due to neck edema or toxemia.
  • Intestinal anthrax
    • Patients with intestinal anthrax may have severe abdominal pain, hematemesis, and/or bloody diarrhea.
    • Multiple anthrax ulcerative lesions are found throughout the GI tract secondary to hematogenous spread.
    • Primary intestinal anthrax causes a local lesion that resembles the ulcer of oropharyngeal anthrax.
    • Intestinal anthrax is difficult to recognize, and shock and death may occur 2-5 days after onset.
  • Inhalation anthrax
    • Chest radiographs and CT scans reveal a widened mediastinum.
    • In patients with potential inhalation anthrax exposure who have a flulike illness and substernal discomfort, obtain a chest CT scan.
    • Pulmonary infiltrates are usually absent because inhalation anthrax presents primarily as hemorrhagic mediastinitis, not pneumonia, which may be associated with bloody pleural effusions.
    • Inhalation anthrax is usually fatal; the patient often succumbs to shock and to the effects of lethal toxin.
  • Septicemic anthrax: This is the most severe form and may complicate any other form of anthrax, particularly inhalation anthrax.
  • Anthrax meningitis
    • Cerebrospinal fluid (CSF) anthrax is distinguished by hemorrhagic leptomeningitis.
    • Anthrax is present in other locations of the body, and patients develop hemorrhagic leptomeningitis (Cardinal's cap).

Causes

Anthrax is caused by B anthracis, a gram-positive bacillus. B anthracis measures 1 µm by 3 µm and 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. Ground-glass–appearing colonies are adherent and appear gray or white on blood agar. B anthracis is catalase-positive. Bacilli grow optimally in enhanced carbon dioxide and are nonmotile. Capsule formation may help differentiate B anthracis from other nonpathogenic bacilli.

The most important presumptive test for B anthracis is the lack of motility in broth and hemolysis on blood agar.

Table 1. Microbiological Differences Between B anthracis and Non– B anthracis Bacilli

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Table
B anthracis Non– B anthracis bacilli (pseudoanthrax bacilli)
Nonmotile long chainsGenerally motile short chains
Capsule formation on bicarbonate agarNo capsule formation in bicarbonate
No growth on penicillin agar
(10 mcg/mL)		Usually good growth on penicillin agar
Growth in gelatin resembles inverted fir treeGrowth in gelatin absent or resembles atypical fir tree
Gelatin liquefaction slowGelatin liquefaction usually rapid
No hemolysis of sheep RBCsHemolysis of sheep RBCs
Ferments salicin slowly or not at allUsually ferments salicin rapidly
Pathogenic to laboratory animalsNonpathogenic to laboratory animals
B anthracis Non– B anthracis bacilli (pseudoanthrax bacilli)
Nonmotile long chainsGenerally motile short chains
Capsule formation on bicarbonate agarNo capsule formation in bicarbonate
No growth on penicillin agar
(10 mcg/mL)		Usually good growth on penicillin agar
Growth in gelatin resembles inverted fir treeGrowth in gelatin absent or resembles atypical fir tree
Gelatin liquefaction slowGelatin liquefaction usually rapid
No hemolysis of sheep RBCsHemolysis of sheep RBCs
Ferments salicin slowly or not at allUsually ferments salicin rapidly
Pathogenic to laboratory animalsNonpathogenic 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 B anthracis 

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Table
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 polymorphonuclear function and phagocytosis
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 polymorphonuclear function and phagocytosis

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

More on Anthrax

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Differential Diagnoses & Workup: Anthrax
Treatment & Medication: Anthrax
Follow-up: Anthrax
Multimedia: Anthrax
References
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Further Reading

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Keywords

anthrax, cutaneous anthrax, inhalation anthrax, Bacillus anthracis, B anthracis, respiratory anthrax, inhalational anthrax, pulmonary anthrax, intestinal anthrax, bacteremic anthrax, B anthracis bacteremia, primary intestinal anthrax, oropharyngeal anthrax, anthrax meningitis, septicemic anthrax, bioterrorist anthrax, anthrax bacilli, hemorrhagic leptomeningitis, woolsorter's disease, black bane, charbon, murrain, black blood

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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, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Douglas A Drevets, MD, Assistant Professor, Department of Medicine, Section of Infectious Disease, Oklahoma University Health Sciences Center
Douglas A Drevets, MD is a member of the following medical societies: American Association of Immunologists, American Society for Microbiology, Central Society for Clinical Research, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, 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; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist  Speaking and teaching

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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