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Legionnaires Disease Medication

  • Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD  more...
Updated: Mar 30, 2016

Medication Summary

Treat Legionnaires disease intravenously, and consider changing to oral antibiotic therapy with a 10- to 14-day course after patients begin to show signs of clinical improvement. A 21-day course is recommended in patients who are immunocompromised, who have severe underlying disease, or who develop severe Legionella pneumonia.

For immunosuppressed patients, fluoroquinolone therapy is recommended for several reasons. The fatality rate of Legionella pneumonia is high in this patient population.



Class Summary

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

Levofloxacin (Levaquin)


Levofloxacin, a fluoroquinolone, is used for pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Azithromycin (Zithromax, Zmax)


Azithromycin is a macrolide antibiotic used to treat mild to moderate microbial infections.

Ciprofloxacin (Cipro, Cipro XR)


Ciprofloxacin is a fluoroquinolone with activity against pseudomonads, streptococci, methicillin-resistant Staphylococcus aureus (MRSA), S epidermidis, and most gram-negative organisms, but with no activity against anaerobes. It inhibits bacterial DNA synthesis and, consequently, bacterial growth.

Doxycycline (Vibramycin, Adoxa, Avidoxy, Doryx, Monodox)


Doxycycline inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

Moxifloxacin (Avelox)


Moxifloxacin inhibits bacterial DNA synthesis and growth. Its activity is similar to that of ciprofloxacin and levofloxacin.

Rifampin (Rifadin)


Rifampin is the drug of choice (DOC) to use with erythromycin. It inhibits DNA-dependent RNA polymerase activity in susceptible cells by interacting with bacterial RNA polymerase (without inhibiting the mammalian enzyme).

Tigecycline (Tygacil)


A glycylcycline that inhibits protein synthesis by binding to the 30S ribosomal subunit of susceptible bacteria. It has demonstrated activity against both gram-positive and gram-negative anaerobes, as well as against gram-positive aerobic strains such as methicillin-resistant staphylococci, streptococci, and enterococci.

Erythromycin base (Ery-Tab, E.E.S., PCE)


Erythromycin inhibits ribonucleic acid (RNA) ̶ dependent protein synthesis, possibly by stimulating dissociation of peptidyl transfer RNA (tRNA) from ribosomes. This inhibits bacterial growth.

Clarithromycin (Biaxin, Biaxin XL)


Clarithromycin is a macrolide antibiotic that inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Contributor Information and Disclosures

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.

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: Received salary from Medscape for employment. for: Medscape.

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.

Additional Contributors

Frank C Smeeks, III, MD Specialty Medical Director of Emergency Medicine, Applied Medico Legal Solutions

Frank C Smeeks, III, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Medical Association, North Carolina Medical Society

Disclosure: Nothing to disclose.


Joseph F John Jr, MD, FACP, FIDSA, FSHEA Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina College of Medicine; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Eric M Kardon, MD, FACEP Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Fred A Lopez, MD Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine

Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Scott Savage, DO Associate Clinical Faculty, Department of Emergency Medicine, Wright State University, Boonshoft School of Medicine

Disclosure: Nothing to disclose.

Lynn E Sullivan, MD Assistant Professor of Medicine, Yale University School of 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

Jeter (Jay) Pritchard Taylor III, MD Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina School of Medicine; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist

Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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This electron micrograph depicts an amoeba, Hartmannella vermiformis (orange), as it entraps a Legionella pneumophila bacterium (green) with an extended pseudopod. After it is ingested, the bacterium can survive as a symbiont within what then becomes its protozoan host. The amoeba then becomes a so-called "Trojan horse," since, by harboring the pathogenic bacterium, the amoeba can afford it protection. In fact, in times of adverse environmental conditions, the amoeba can metamorphose into a cystic stage, enabling it, and its symbiotic resident, to withstand the environmental stress. Image courtesy of the Centers for Disease Control and Prevention and Dr. Barry S Fields.
Table 1. Legionnaires Disease: Six Clinical Predictors and Diagnostic Eliminators in Adults Admitted with Pneumonia a
Diagnostic Predictors Diagnostic Eliminators
Clinical Predictors
  • Fever (>102°F)
Clinical Eliminators
  • Sore throat
  • Severe myalgias
Laboratory Predictors b
  • Highly elevated ESR (>90 mm/h) or CRP (>180 mg/L)
  • Highly elevated ferritin levels (>2 X normal)
  • Hypophosphatemia (on admission/early)
  • Highly elevated CPK (>2 X normal)
  • Microscopic hematuria (on admission)
Laboratory Eliminators
  • Leukopenia
  • Thrombocytopenia
  • Negative chest radiographic findings (no infiltrates)
Legionnaire disease very likely if >3 predictors present Legionnaires disease very unlikely if <3 predictors or >3 diagnostic eliminators present
Abbreviations: CPK = creatinine phosphokinase test; CRP = C-reactive protein; ESR = erythrosedimentation rate.

a Pulmonary symptoms: shortness of breath, cough, and so forth with fever and a new focal/segmental infiltrate on chest radiograph.

b Otherwise unexplained. If finding is due to an existing disorder, it should not be used as a clinical predictor.

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