Anthrax Medication

Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD more...

Updated: Sep 27, 2011

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Medication Summary
Antibiotics, Other
Corticosteroids
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Medication Summary

Before October 2001, the first-line treatment of anthrax infection and prophylaxis was penicillin; however, this is not the case for bioterrorism-related cases because of the concern for genetically engineered penicillin-resistant anthrax strains. The Centers for Disease Control and Prevention (CDC) recommends ciprofloxacin or doxycycline. Doxycycline should not be used in suspected meningitis because it has poor penetration of the central nervous system.

Quinolones are not routinely indicated for pediatric patients because of the risk of musculoskeletal disorders. However, in 2008, the US Food and Drug Administration (FDA) approved use of levofloxacin in children as young as 6 months for the treatment of inhalational (and inhalational exposure to) anthrax.^[6]Treatment duration is 60 days, but safety has not been evaluated beyond 14 days.

Women who are pregnant or breastfeeding can use amoxicillin. Resistance exists to third-generation cephalosporins, trimethoprim, and sulfisoxazole. For patients with severe anthrax, therapy with corticosteroids and intravenous antibiotics is recommended.

Individuals with inhalational anthrax should receive a multidrug regimen of either ciprofloxacin or doxycycline along with at least one more agent, including a quinolone, rifampin, tetracycline, vancomycin, imipenem, meropenem, chloramphenicol, clindamycin, or an aminoglycoside. After susceptibility testing and clinical improvement, the regimen may be altered.

Cases of gastrointestinal and cutaneous anthrax can be treated with ciprofloxacin or doxycycline for 60 days. Penicillin such as amoxicillin or amoxicillin-clavulanate may be used to complete the course if the strain is susceptible.

Measures to prevent anthrax infection after exposure include vaccination, decontamination, and prophylactic treatment. For people who have been exposed to anthrax but do not have symptoms, 60 days of ciprofloxacin, a tetracycline (including doxycycline), or penicillin is given to reduce the risk or progression of disease due to inhaled anthrax. Vaccination is recommended as part of postexposure treatment by the CDC; however, this is not a licensed use for this vaccine.

Class Summary

Empirical antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

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Penicillin G (Pfizerpen)

Penicillin interferes with the synthesis of bacterial cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Penicillin is the drug of choice for nonbioterrorism-related anthrax. Treatment should begin with intravenous dosing.

Penicillin V potassium

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Penicillin G procaine

Penicillin reduces the incidence or progression of anthrax following exposure to aerosolized B anthracis. Available safety data for penicillin G procaine best support a duration of therapy of 2 weeks or less. Treatment for inhalational anthrax (postexposure) must be continued for a total of 60 days. Physicians must consider risks and benefits of continuing administration of penicillin G procaine for more than 2 weeks or switching to an effective alternative treatment.

In adults, administer by deep IM injection only into the upper outer quadrant of a buttock. In infants and small children, the midlateral aspect of the thigh may be a better site for administration.

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Doxycycline (Adoxa, Doryx, Vibramycin)

Doxycycline is a second-generation tetracycline that is more active than tetracycline against many pathogens and is not hepatotoxic. Its adverse-effect profile and pharmacokinetics are different than those of tetracycline. Doxycycline reduces the incidence or progression of anthrax, including inhalational anthrax (postexposure) following exposure to aerosolized B anthracis.

Doxycycline inhibits protein synthesis and, thus, bacterial growth by binding with 30S and, possibly, 50S ribosomal subunits of susceptible bacteria. Although tetracyclines have an adverse effect on teeth in children younger than 8 years, the delay in bone development is apparently reversible; balancing these risks against the lethality of inhalational anthrax, the US Food and Drug Administration recommends a pediatric dosing regimen for inhalational anthrax (postexposure).

Administer IV therapy only when oral administration is not indicated, and do not give over a prolonged period (may increase the risk of thrombophlebitis and other complications). Switch to oral doxycycline or another antimicrobial drug product as soon as possible to complete a 60-day course of therapy.

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Amoxicillin (Moxatag)

Amoxicillin interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

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Ampicillin

Ampicillin has bactericidal activity against susceptible organisms. It is an alternative to amoxicillin for patients who are unable to take medication orally.

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Ciprofloxacin (Cipro, Proquin XR)

Ciprofloxacin is the drug of choice for anthrax when mutant strains are suspected (as in biological warfare). It is indicated for inhalational anthrax post exposure. Ciprofloxacin inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA gyrase in susceptible organisms. It has high resistance potential. Initiate treatment immediately following suspected or confirmed anthrax exposure.

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Levofloxacin (Levaquin)

Levofloxacin is a second-generation quinolone that acts by interfering with DNA gyrase in bacterial cells and promoting breakage of DNA strands. It is highly active against gram-negative and gram-positive organisms. It has low resistance potential.

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Chloramphenicol

Chloramphenicol binds to 50 S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. It is effective against gram-negative and gram-positive bacteria.

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Streptomycin

Streptomycin is an aminoglycoside antibiotic recommended when less potentially hazardous therapeutic agents are ineffective or contraindicated.

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Tetracycline

Tetracycline treats susceptible infections caused by gram-positive and gram-negative bacteria and infections caused by Mycoplasma, Chlamydia, and Rickettsia species. It inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.

Class Summary

These agents are used for severe edema, meningitis, or swelling in the head and neck region.

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Dexamethasone (Baycadron)

This agent is used in various inflammatory diseases. Dexamethasone may decrease inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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Prednisone

Prednisone is useful in inflammatory and allergic reactions. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity.

Class Summary

The FDA approved a standard anthrax vaccine designated "anthrax vaccine adsorbed" (AVA), which is a sterile filtrate of cultures of an avirulent strain that elaborates protective antigen. No controlled trials are available. The efficacy of this vaccine in inhalation (biowarfare) anthrax is questionable.

In December 2008, the FDA approved a supplement to the biologics application for AVA (BioThrax, manufactured by Emergent BioSolutions).^[7]The vaccine administration schedule is now 0 and 4 weeks and 6, 12, and 18 months. Previously, the schedule was 0, 2, and 4 weeks and 6, 12, and 18 months. The newly approved administration route is intramuscular; previously, it was subcutaneous.

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Anthrax vaccine adsorbed (BioThrax)

Anthrax vaccine is used in high-risk situations. Along with prophylactic antibiotics, AVA can be administered in cases of potential exposure.

The virulent components of Bacillus anthracis include an antiphagocytic polypeptide capsule and 3 proteins, including protective antigen (PA), lethal factor (LF), and edema factor (EF). They are not cytotoxic individually, but the combination of PA with LF or EF forms cytotoxic lethal toxin and edema toxin, respectively. The immune mechanism of AVA is unknown but, theoretically, antibodies to PA may provide protection by neutralizing the activities of these toxins.

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.

Specialty Editor Board

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

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

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 Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Hilarie Cranmer, MD, MPH, FACEP; Mauricio Martinez, MD; James Li, MD; Barry J Sheridan, DO; Robert G Darling, MD, FACEP

Additional Contributors

Hilarie Cranmer, MD, MPH, FACEP; Mauricio Martinez, MD; James Li, MD; Barry J Sheridan, DO; Robert G Darling, MD, FACEP

References

Inglesby TV, O'Toole T, Henderson DA, et al. Anthrax as a biological weapon, 2002: updated recommendations for management. JAMA. May 1 2002;287(17):2236-52. [Medline].
John TJ, Dandona L, Sharma VP, Kakkar M. Continuing challenge of infectious diseases in India. Lancet. Jan 15 2011;377(9761):252-69. [Medline].
Holty JE, Bravata DM, Liu H, et al. Systematic review: a century of inhalational anthrax cases from 1900 to 2005. Ann Intern Med. Feb 21 2006;144(4):270-80. [Medline].
Akbayram S, Dogan M, Akgün C, et al. Clinical findings in children with cutaneous anthrax in eastern Turkey. Pediatr Dermatol. Nov-Dec 2010;27(6):600-6. [Medline].
Knox D, Murray G, Millar M, et al. Subcutaneous anthrax in three intravenous drug users: a new clinical diagnosis. J Bone Joint Surg Br. Mar 2011;93(3):414-7. [Medline].
Food and Drug Administration. 17.5 FDA-Approved Medication Guide. Levaquin (levofloxacin). Accessed August 6, 2009. Available at http://www.accessdata.fda.gov/drugsatfda_docs/label/2009/020634s053,020635s058, 021721s021lbl.pdf.
CDC. Vaccines and Preventable Diseases:Anthrax Vaccination. Vaccines:VPF-VAD/Anthrax/mainpage. Accessed July 9, 2009. Available at http://www.cdc.gov/vaccines/vpd-vac/anthrax/default.htm#vacc.

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.

Bioterrorist Agents. Signs and symptoms. Chart courtesy of North Carolina Statewide Program for Infection Control and Epidemiology (SPICE), copyright University of North Carolina at Chapel Hill, www.unc.edu/depts/spice/bioterrorism.html.

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

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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Anthrax Medication

Medication Summary

Antibiotics, Other

Class Summary

Penicillin V potassium

Corticosteroids

Class Summary

Vaccines

Class Summary