Mycobacterium gordonae is a nontuberculous mycobacteria (NTM) that rarely is infectious but commonly has been found as a contaminant.[1] Bronchiectasis may increase the risk for NTM-lung disease, including more pathogenic species like MAC and M abscessus. A study found that patients with bronchiectasis were more likely to have M gordonae isolated in respiratory specimens compared to those without bronchiectasis. This suggests that isolation of M gordonae may indicate underlying chronic airway diseases like bronchiectasis and increase the risk for infection with more pathogenic NTM species.[2]
Advanced laboratory diagnostic techniques have improved the isolation and identification of nontuberculous mycobacteria. M 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.[3]
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 milliliter.
After analyzing the molecular epidemiology of M gordonae infections in hospital environments, Yoshida et al concluded that effective and continuous surveillance is necessary.[4]
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.
M gordonae is one of the least pathogenic of the mycobacteria.[2] It usually is 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.
M gordonae disease is rare. Although 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.[3]
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.
Dissemination is a concern. Death is an unlikely outcome, except in patients who are severely immunocompromised, such as CD4+ cell counts in the single digits.
At least three positive culture results or one positive AFB stain result with two positive culture results are required to consider a diagnosis of true M gordonae disease. One positive culture result from a sterile site probably is not enough to start treatment. All cases of possible M gordonae disease should be published in a medical journal.[1]
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.
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.
The most effective treatment regimen has not been established, but in vitro susceptibilities suggest clarithromycin and, possibly, azithromycin, quinolones (especially levofloxacin), and ethambutol as treatment options. Rifabutin may be beneficial, and rifampin shows variable results.[5]
The recommended duration of therapy is not established, although treating patients until culture results are documented as negative is reasonable.[5]
Whether additional or extended (as with tuberculosis) treatment prevents relapse remains unknown.
M gordonae infections should be treated until symptoms resolve. Prolonging treatment may prevent relapse, but the optimal treatment duration is unknown. Three, 6, and 12 months of therapy have been used.[5] The improvement of objective abnormalities (eg, chest radiograph findings) may also be useful in determining the optimal duration of treatment. If the treatment time is too short, relapse may occur. If the treatment time is too long, the adverse effects of medication may become a concern.
Isolation is not indicated (once active tuberculosis infection is excluded); however, the presence of acid-fast organisms on a stain should prompt immediate isolation unless the patient is clearly not acutely contagious.
Transfer to other facilities is unnecessary. Consultation with an expert from the National Jewish Medical and Research Center in Denver, Colo; Centers for Disease Control and Prevention in Atlanta, Ga; local infectious disease experts; or the department of health may be useful.
Clinical practice guideline on nontuberculous mycobacterial pulmonary disease treatment by the ATS/ERS/ESCMID/IDSA
A clinical practice guideline on treatment of nontuberculous mycobacterial pulmonary disease by the American Thoracic Society (ATS), European Respiratory Society (ERS), European Society of Clinical Microbiology and Infectious Diseases (ESCMID), and Infectious Diseases Society of America (IDSA) is summarized below. Please see the complete clinical practice guideline for more information[5] :
Table. Clinical practice guideline on treatment of nontuberculous mycobacterial pulmonary disease by the ATS, ERS, ESCMID, and IDSA
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.
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.
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.
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.
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.
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.
Klaus-Dieter Lessnau, MD, FCCP, Former 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: Received salary from Pfizer for employment.
Specialty Editors
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.
Aaron E Glatt, MD, MACP, FIDSA, FSHEA, Chairman, Department of Medicine, Chief, Division of Infectious Diseases, Hospital Epidemiologist, Mount Sinai South Nassau; Professor of Medicine, Icahn School of Medicine at Mount Sinai
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; Fellow of the Royal College of Physicians, London
Disclosure: Nothing to disclose.
Additional Contributors
Thomas E Herchline, MD, Professor of Medicine, Wright State University, Boonshoft School of Medicine
Disclosure: Nothing to disclose.
References
Nardell EA. Nontuberculous Mycobacterial Infections. Porter RE. The Merck Manual of Diagnosis and Therapy. Rahway, NJ: Merck & Co Inc; Reviewed/Revised July 2022.
