Mycobacterium gordonae

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Background

Advanced laboratory diagnostic techniques have improved the isolation and identification of nontuberculous mycobacteria. Mycobacterium gordonae, a commonly found species of mycobacteria, is named after its discoverer, the American bacteriologist Ruth E. Gordon. It is classified in Runyon group 2 as a scotochromogenic organism. Cultures grow slowly, are smooth, and are pigmented yellow. M gordonae is referred to as the tap water bacillus because it is a frequent isolate in tap water.[1]

M gordonae is ubiquitous and may be found in soil, water (eg, ground, tap, bottled), whirlpools, unpasteurized milk, mucous membranes of healthy persons, urine, and gastric fluid. It is the most commonly encountered nontuberculous mycobacterium in water, with concentrations as high as 1000 colony-forming units per liter.

After analyzing the molecular epidemiology of M gordonae infections in hospital environments, Yoshida et al concluded that effective and continuous surveillance is necessary.[2]

New cases of M gordonae disease should always be published to increase the knowledge of this disease. Many isolates represent contamination of the specimen or colonization, but not true disease. Discussing positive culture findings with microbiology laboratory personnel is useful. The authors are willing to discuss any possibly new case of M gordonae infection and are willing to offer support to write up cases of actual disease.

Pathophysiology

M gordonae is one of the least pathogenic of the mycobacteria. It is usually a contaminant or colonizer in patients who are not infected with HIV. However, in patients with HIV infection who are severely immunosuppressed (count of < 100 CD4+ cells/µL), M gordonae may infect the lungs, blood, bone marrow, and other organs. In the few published case reports of M gordonae disease, pathogenicity was not always established because of the presence of single isolates, the lack of confirmation by a reference laboratory, or the rapid improvement of pulmonary infiltrates, which are not characteristic features of infections from other mycobacterial species.

Epidemiology

Frequency

United States

M gordonae disease is rare. While more than 100 cases have been reported, most documentation supports contamination or colonization rather than pathogenicity. Nosocomial pseudo-outbreaks have been described from tap water, ice machines, antimicrobial and laboratory solutions, instrumentation, fiberoptic bronchoscopes and colonoscopes (especially if the working channel is not adequately exposed to disinfectant), aerosol devices, and (possibly) continuous ambulatory peritoneal dialysis fluid.

International

Worldwide distribution of M gordonae infection is probable. Additional studies with adequate documentation are warranted to investigate the pathogenicity of M gordonae.

Mortality/Morbidity

M gordonae infection carries a mortality rate of less than 0.1%. M gordonae may be a marker of severe immunosuppression in patients infected with HIV. One death was reported in a patient who was HIV positive and had severe immunosuppression, acute respiratory distress syndrome, and multiple isolates of M gordonae.

Race

M gordonae infection has no recognized racial predilection.

Sex

M gordonae infection has no known sexual predilection.

Age

M gordonae infection has no determined age predilection.

History

Physical

Causes

HIV infection with severe immunosuppression (< 50 CD4+ cells/µL) is a risk factor for M gordonae infection.

Laboratory Studies

Imaging Studies

Other Tests

The "3-2-1" rule is useful for a more accurate determination of disease as opposed to contamination or colonization without pathogenicity. To prove disease, one would want to see at least 3 cultures with M gordonae, 2 cultures with one positive acid-fast bacilli smear, or one culture from a sterile source such as blood, bone marrow, or pleural fluid.

Procedures

Histologic Findings

Acid-fast stains are positive for M gordonae, and/or granulomas are present.

Medical Care

Collect more data to establish the presence of disease. Clinical response to specific antimycobacterial therapy indicates possible disease presence. As with other mycobacterial organisms, slow resolution of radiographic infiltrates is expected.

Consultations

Medication Summary

While the most effective treatment regimen has not been established, in vitro susceptibilities suggest clarithromycin and, possibly, azithromycin, quinolones (eg, levofloxacin, moxifloxacin), and ethambutol as treatment options. Rifabutin may be beneficial, and rifampin has shown variable results.

In vivo activity of doxycycline and trimethoprim-sulfamethoxazole is not known.

M gordonae has been shown to be resistant to isoniazid, pyrazinamide, and streptomycin.

The recommended duration of therapy is not established.

Clarithromycin (Biaxin)

Clinical Context:  Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Very active drug for nontuberculous mycobacterial disease, but acquired resistance from monotherapy is a concern.

Ethambutol (Myambutol)

Clinical Context:  Standard drug for nontuberculous mycobacterial disease. Diffuses into actively growing mycobacterial cells and impairs cell metabolism by inhibiting synthesis of one or more metabolites, which, in turn, causes cell death. No cross-resistance demonstrated. Mycobacterial resistance is frequent with previous therapy. Use in these patients in combination with second-line drugs that have not previously been administered. Administer qd until permanent bacteriological conversion and maximal clinical improvement is observed. Absorption not significantly altered by food.

Levofloxacin (Levaquin)

Clinical Context:  May be useful. Aide effects are very rare (eg, GI or CNS abnormalities, tendinitis). For treatment of mycobacterial infection in combination with rifampin and other antituberculosis agents.

Rifampin (Rifadin, Rimactane)

Clinical Context:  For use in combination with at least one other antituberculous drug. Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. Cross-resistance may occur. Often used for nontuberculous mycobacterial disease.

Rifabutin (Mycobutin)

Clinical Context:  Ansamycin antibiotic derived from rifamycin S. Inhibits DNA-dependent RNA polymerase, preventing chain initiation in susceptible strains of Escherichia coli and Bacillus subtilis but not in mammalian cells. If GI upset occurs, administer dose bid with food. May be more active with nontuberculous species.

Azithromycin (Zithromax)

Clinical Context:  Treats mild-to-moderate microbial infections. Dosing qwk is possible.

Class Summary

Empiric antimycobacterial therapy must be comprehensive.

Further Inpatient Care

Further Outpatient Care

Inpatient & Outpatient Medications

Transfer

Complications

Prognosis

Author

Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Disclosure: Nothing to disclose.

Coauthor(s)

Cynthia de Luise, PhD, MPH, Director, Epidemiology, Pfizer, Inc

Disclosure: Pfizer Salary Employment

Specialty Editors

Thomas E Herchline, MD, Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

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

Aaron Glatt, MD, Chief Administrative Officer, Executive Vice President, Mercy Medical Center, Catholic Health Services of Long Island

Disclosure: Nothing to disclose.

Chief Editor

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

Disclosure: Nothing to disclose.

References

  1. Lalande V, Barbut F, Varnerot A, Febvre M, Nesa D, Wadel S, et al. Pseudo-outbreak of Mycobacterium gordonae associated with water from refrigerated fountains. J Hosp Infect. May 2001;48(1):76-9. [View Abstract]
  2. Yoshida S, Suzuki K, Iwamoto T, Tsuyuguchi K, Tomita M, Okada M, et al. [Detection of molecular epidemiology of Mycobacterium gordonae isolates]. Kekkaku. Jul 2010;85(7):609-14. [View Abstract]
  3. American Thoracic Society. Diagnosis and treatment of disease caused by nontuberculous mycobacteria. This official statement of the American Thoracic Society was approved by the Board of Directors, March 1997. Medical Section of the American Lung Association. Am J Respir Crit Care Med. Aug 1997;156(2 Pt 2):S1-25. [View Abstract]
  4. Jun HJ, Jeon K, Um SW, Kwon OJ, Lee NY, Koh WJ. Nontuberculous mycobacteria isolated during the treatment of pulmonary tuberculosis. Respir Med. Dec 2009;103(12):1936-40. [View Abstract]
  5. Konishi M, Uno K, Kasahara K, Mori K, Yoshimoto E, Maeda K, et al. [A case of pulmonary Mycobacterium gordonae infection progressed for no therapy]. Nihon Kokyuki Gakkai Zasshi. May 2007;45(5):436-40. [View Abstract]
  6. Lessnau KD, Milanese S, Talavera W. Mycobacterium gordonae: a treatable disease in HIV-positive patients. Chest. Dec 1993;104(6):1779-85. [View Abstract]
  7. Sneath PH, Mair NS, Sharpe ME, eds. The Mycobacteria. Genus Mycobacterium. In: Bergey's Manual of Systematic Bacteriology. Vol 2. 2nd ed. Baltimore, Md: Williams & Wilkins; 1986:1447.
  8. Sánchez-Morgado JM, Gallagher A, Johnson LK. Mycobacterium gordonae infection in a colony of African clawed frogs (Xenopus tropicalis). Lab Anim. Jul 2009;43(3):300-3. [View Abstract]
  9. Umeda Y, Matsuno Y, Imaizumi M, Mori Y, Iwata H, Takiya H. Extralobar pulmonary sequestration infected with Mycobacterium gordonae. J Thorac Cardiovasc Surg. Jan 2009;137(1):e23-4. [View Abstract]
  10. Weinberger M, Berg SL, Feuerstein IM, Pizzo PA, Witebsky FG. Disseminated infection with Mycobacterium gordonae: report of a case and critical review of the literature. Clin Infect Dis. Jun 1992;14(6):1229-39. [View Abstract]