Mycobacterium Xenopi



Researchers first described Mycobacterium xenopi in 1959 after isolating it from skin lesions of the South African toad Xenopus laevis.M xenopi, a slow-growing, nontuberculous mycobacterium, is often considered to be a saprophyte or an environmental contaminant. It grows optimally at 45°C (113°F) and has been found, occasionally in large numbers, in hospital hot water supplies at the outlet valves of water heaters.[1, 2] M xenopi colonization occurs from ingestion or inhalation of, or cutaneous exposure to, organisms in water, soil, or airborne particles. Colonization of hospital water systems is associated with infection, disease, and nosocomial isolation. 


M xenopi has low pathogenicity, and host impairment is required to contract disease from the organism. Most M xenopi infections occur in the lungs, usually in patients with preexisting lung disease or with predisposing conditions (eg, extrapulmonary malignancy, alcoholism, diabetes mellitus, HIV infection). Extrapulmonary and disseminated disease may develop in patients with AIDS or other immunodeficiencies.

For pulmonary disease, inhalation of infected airborne particles is the usual route of infection. For skin and soft tissue infections, direct contact through penetrating injuries and surgical procedures provide the route. Person-to-person transmission of nontuberculous mycobacterial disease has never been documented.



United States

Surveillance data for M xenopi infection are not available because such infection is not a reportable disease. More than 500 cases have been reported, but only approximately 70 cases seem to document true disease.


Prevalence is unknown.


Subjects with documented M xenopi infections are divided into the following broad categories:


No racial predilection has been identified.


No predilection for either sex has been demonstrated.


No age predilection has been reported.


Infection with M xenopi may result in pulmonary infection, usually in older adults with COPD, in patients who are immunocompromised with disseminated disease, or in patients with extrapulmonary disease involving the lymphatic system, skin, bones, or joints.[3, 4] Onset of symptoms is insidious, and the infection may progress slowly or increase and decrease over the course of months or years.

Presenting symptoms

See the list below:

Presenting symptoms of immunocompromised patients with disseminated disease

See the list below:

Possible presenting symptoms of patients with HIV infection

See the list below:


Physical findings relate to underlying long-term illness and are not specific for M xenopi infection. More than 95% of patients have abnormal lung findings.


Predisposing factors include the following:

Sirolimus therapy inhibits interleukin 12–induced proliferation of activated T lymphocytes and may be a risk factor.

Varghese et al have described a patient data set in which the risk factors for M xenopi infection were pre-existing lung diseases such as emphysema.[5]

Laboratory Studies

Serum electrolyte tests may reveal hyponatremia, most likely due to inappropriate secretion of antidiuretic hormone syndrome.

CBC counts may reveal leukocytosis, leucopenia, anemia, reactive thrombocytosis, or thrombocytopenia, or they may be entirely within reference ranges.

Mycobacterial examination of sputum,[6] blood, urine, bronchoalveolar lavage fluid, and tissue biopsies may reveal M xenopi.

American Thoracic Society criteria are used for diagnosing nontuberculous mycobacterial lung disease in HIV-seropositive or HIV-seronegative patients. Use the following criteria when diagnosing symptomatic patients who have infiltrative, nodular, or cavitary lung disease and those with high-resolution CT scan findings that reveal multifocal bronchiectasis and/or multiple small nodules:

Imaging Studies

Chest radiography

The classic appearance of M xenopi is cavitary apical pulmonary disease. The cavities have thin walls with little surrounding parenchymal infiltration.

Bronchogenic spread of disease is rare and appears as patchy, irregular, alveolar or interstitial opacities.

Adenopathy and pleural effusions are rare and are not isolated findings.

The nonclassic form develops in about 25% of patients and appears as multiple patchy alveolar, interstitial pneumonitis, or interstitial opacities without defined borders (predominantly in the lower lung fields).

M xenopi may occasionally manifest as a solitary pulmonary nodule, usually in asymptomatic individuals who come to medical attention because of possible malignancy. Surgical resection demonstrates changes without evidence of tumor.

Chest CT scanning

This defines the features more precisely by possibly revealing bronchiectasis and 5- to 15-mm nodular opacities.

Carillo et al compared CT scan findings of M xenopi infection with those of Mycobacterium avium-intracellulare infection. In their patient population, they observed a more fibrocavitary and nodular pattern in patients with M xenopi infection compared to classic descriptions of it being more bronchiectatic. They also described findings consistent with ground-glass opacifications and consolidations.[8]

Positron emission tomography (PET)–CT imaging

This often reveals solitary pulmonary nodules that may mimic carcinoma.


See the list below:

Histologic Findings

Necrotizing or non-necrotizing granulomatous inflammation is observed in lung biopsy samples.


Similar to other nontuberculous mycobacteria

Medical Care

A physician detecting a positive M xenopi culture result must differentiate among colonization, contamination, and true disease.

Assess bacteriologic data (eg, repeated isolation, organism identification), clinical symptoms, and radiographic findings within the entire clinical context.

Treat with chemotherapy, although optimal therapy is not well established.

Surgical Care

Surgery may be curative for patients who present with solitary pulmonary nodules and for those with localized pulmonary disease who fail to respond to, or who relapse after, chemotherapy.


See the list below:


Patients do not require special diets.


Patients do not require activity restrictions.

Medication Summary

Optimal therapy for M xenopi is not established. Response to therapy varies and does not always correlate with the results of in vitro susceptibility testing. Physicians use combination therapy, with 2-4 drugs prescribed from several months to up to 18 months. M xenopi disease should always be treated with at least 2 active drugs because single-drug therapy increases the probability of acquired resistance.

Clarithromycin (Biaxin)

Clinical Context:  Probably most important drug. To avoid development of resistance, should not be used as monotherapy. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Ethambutol (Myambutol)

Clinical Context:  Probably second most important drug. Diffuses into actively growing mycobacterial cells (eg, tubercle bacilli). 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 been administered previously. Administer q24h until permanent bacteriologic conversion and maximal clinical improvement is observed. Absorption is not altered significantly by food.

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, administer dose bid with food.


Clinical Context:  For treatment of susceptible mycobacterial infections. Use in combination with other antituberculous drugs (eg, isoniazid, ethambutol, rifampin). Total period of treatment for tuberculosis is minimum of 1 y; however, indications for terminating therapy may occur at any time. Recommended when less potentially hazardous therapeutic agents are ineffective or contraindicated.

Rifampin (Rifadin)

Clinical Context:  Probably an important drug for treatment. For use in combination with at least 1 other antituberculous drug. Inhibits DNA-dependent bacteria but not mammalian RNA polymerase. Cross-resistance may occur.

Azithromycin (Zithromax)

Clinical Context:  Similar to clarithromycin but may allow once-per-wk dosing.

Levofloxacin (Levaquin)

Clinical Context:  For treatment of tuberculosis in combination with rifampin and other antituberculosis agents.

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of the clinical setting.

Further Outpatient Care

Monitor the patient monthly for possible adverse effects.

Monitoring includes (but is not limited to) the following:

Further Inpatient Care

Inpatient care is not necessary unless the patient is severely immunocompromised, has disseminated disease, or requires hospitalization for severity of the illness.

Inpatient & Outpatient Medications

Use at least 2 medications to avoid acquired resistance.

Intravenous administration may be required with disseminated disease.


Consider referring difficult cases to a specialist center.

Consider sending cultures to a reference laboratory to test for susceptibility; however, routine susceptibility testing in a patient who has never been treated is not necessary.


To date, no strategy, method, treatment, or therapy prevents M xenopi infection.


See the list below:


Outcome is favorable. Many people are colonized but asymptomatic.

Patient Education

See the list below:


Mansoor Arif, MD, Hospitalist, Department of Medicine, Mount Auburn Hospital; Instructor, Department of Medicine, Harvard Medical School

Disclosure: Nothing to disclose.


Syed Faisal Mahmood, MBBS, Associate Professor of Infectious Diseases, Program Director, Infectious Diseases Fellowship Program, Department of Medicine, Aga Khan University Hospital, Pakistan

Disclosure: Nothing to disclose.

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 Glatt, MD, Chairman, Department of Medicine, Chief, Division of Infectious Diseases, Hospital Epidemiologist, South Nassau Communities Hospital

Disclosure: Nothing to disclose.

Chief Editor

Mark R Wallace, MD, FACP, FIDSA, Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Disclosure: Nothing to disclose.


Martin Backer, MD Fellow in Combined Adult and Pediatric Infectious Diseases, State University of New York Health Sciences Center

Disclosure: Nothing to disclose.

Wesley W Emmons, MD, FACP Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE

Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society

Disclosure: Nothing to disclose.

Sailaja Kolli, MD Fellow, Department of Internal Medicine, Division of Pulmonary and Critical Care, The Brooklyn Hospital Center

Disclosure: Nothing to disclose.

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

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.


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