Mycobacterium Kansasii



Mycobacterium kansasii is an acid-fast bacillus (AFB) that is readily recognized based on its characteristic photochromogenicity, which produces a yellow pigment when exposed to light. In 1953, Buhler and Pollack first described the bacterium. Under light microscopy, M kansasii appears relatively long, thick, and cross-barred.

The most common presentation of M kansasii infection is a chronic pulmonary infection that resembles pulmonary tuberculosis. However, it may also infect other organs. M kansasii infection is the second-most-common nontuberculous opportunistic mycobacterial infection associated with AIDS, surpassed only by Mycobacterium avium complex (MAC) infection. The incidence of M kansasii infection increased with the burgeoning of the HIV/AIDS epidemic.


Unlike other nontuberculous mycobacteria (NTM), M kansasii is not readily isolated from environmental sources. However, it has been isolated from a small percentage of specimens obtained from water supplies in areas with high endemicity. Most likely, M kansasii is acquired via either aspiration or local inoculation from the environment. Little evidence exists of person-to-person transmission. Molecular characterization of M kansasii shows that it is a homogeneous group of organisms. Five genotypes, or subtypes, are described. Types I and II are common clinical isolates, while the remaining types (III, IV, V) are recovered from environmental samples only. Type I probably is the most prevalent M kansasii isolate from human sources worldwide.

M kansasii infection of the lung causes a pulmonary disease similar to tuberculosis. Its histopathologic appearance is similar to that of tuberculosis and may include acute suppuration, nonnecrotic tubercles, or caseation. In persons with AIDS or in patients with other forms of immunocompromise, many of its characteristic histologic features may be absent.[1]

After skin inoculation, M kansasii can cause local disease of the skin and subcutaneous tissue. It may spread from the local site and cause lymphadenitis, infection of a distant organ, or disseminated disease.[2]



United States

The prevalence of M kansasii, an unusual pathogen in the pre-AIDS era, increased with the HIV pandemic. M kansasii is the second-most-common cause of NTM disease in patients with AIDS. M kansasii infection has typically been described as a disease of urban dwellers and of patients with high incomes and better standards of living. One study of 3 northern California counties found that M kansasii infection was more common in census tracts with a lower income (median income [3]

M kansasii infection occurs throughout the United States, with the highest incidence in the Midwest and the Southwest. A national laboratory surveillance from 1982-1983 estimated the prevalence of M kansasii infection to be 0.3 case per 100,000 persons. The above study done in northern California estimated an overall incidence of 2.4 cases per 100,000 adults per year in the general population, 115 cases per 100,000 persons with HIV infection per year, and 647 cases per 100,000 persons with AIDS per year.[3] This was confirmed by another laboratory-based data analysis at San Francisco General Hospital, which showed a decrease in NTM infection from 319 cases in 1993 to 59 in 2001 (P < .001). Mycobacterium avium was found to be the most common isolate in both HIV-positive and HIV-negative patients, followed by M kansasii.[4]


M kansasii infection has been reported in most areas of the world. The incidence appears to be relatively high in England and Wales and among South African gold miners.[5] In the United Kingdom, it has been reported as the most common cause of NTM lung infection in patients without HIV infection.[6]

An increasing incidence of NTM infections, including M kansasii, has been reported in other countries, including Israel, Korea,[1] Portugal, France, and Japan.

Based on the analysis of identification data received by the NTM-Network European Trials Group (NET) for 20,182 patients in 30 countries across 6 continents in 2008, M kansasii was the sixth most common NTM isolated from pulmonary samples. Mycobacterium avium complex (MAC) was the most common NTM in most countries.[7]


The likelihood of mortality associated with M kansasii infection depends on various factors, including the presence of comorbid diseases, treatment compliance, rifampicin use, and extent of infection. One US center's experience, which included 302 patients over more than a 50-year period (1952-1995), showed a mortality rate of 11%, but this included both immunocompromised and nonimmunocompromised patients.[8]


M kansasii infection has no reported racial predilection.


M kansasii infection is more common men, with a male-to-female ratio of 3:1.



In most cases, M kansasii causes lung disease that is clinically indistinguishable from tuberculosis. Symptoms may be less severe and more chronic than Mycobacterium tuberculosis infection. Asymptomatic M kansasii infection occurs in a small proportion (16%) of affected patients.[8]



Immunocompromised patients, including patients with HIV/AIDS, are at a high risk for M kansasii infection.

Laboratory Studies

Imaging Studies

Approximately 90% of patients with M kansasii disease have cavitary infiltrates on chest radiography, as depicted below. Among patients without cavitary lung lesions, clinical symptoms and high-resolution computed tomography (HRCT) scanning are important adjuncts in defining the presence of lung disease.

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Chest radiograph in a patient with Mycobacterium kansasii pulmonary infection shows left lower lung infiltrates.

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Chest CT scan in a patient with Mycobacterium kansasii pulmonary infection.

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Chest radiograph in a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreed....

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CT thorax of a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD....

The characteristic radiological feature of M kansasii pulmonary infection has been described as a right-sided, apical or subapical, thin-walled cavitary infiltrate.[8] In a separate study, which included only patients without HIV infection, a comparison of chest radiography findings in patients with M kansasii infection with those in patients with tuberculosis showed that M kansasii infection occurred more frequently as unilateral, right-sided infiltrates. Cavities were observed in both cases, whereas pleural effusions and air space shadowing involving multiple bronchopulmonary segments were less common in M kansasii infection.[6]

Analysis of chest radiographs in a series of 16 patients infected with HIV and M kansasii pulmonary infection showed the following abnormalities (in decreasing order of frequency):

  1. Alveolar opacities
  2. Cavity
  3. Thoracic lymphadenopathy
  4. Pleural effusions
  5. Interstitial opacities

Other Tests


Histologic Findings

The variable histopathologic findings of M kansasii disease may include acute suppuration, nonnecrotic tubercles, or caseation. In general, the findings are similar to tuberculosis.

Examination of lung tissue and lymph nodes usually shows caseating granulomas. Skin lesions may show granulomas with areas of necrosis or foci of acute and chronic inflammation without well-formed granulomas. Other tissues may show caseating or noncaseating granulomas.

AFB are commonly seen in tissues from lungs and lymph nodes. They are found less commonly in tissues from other sites.

In patients with AIDS or other immunocompromised states, many of the histologic characteristics usually associated with M kansasii infection may be absent. Cytologic and histologic material may show a wide range of inflammatory reactions, including granulomas with and without necrosis, neutrophilic abscesses, spindle-cell proliferation, and focal granular eosinophilic necrosis.[13]

Diagnostic criteria based on American Thoracic Society/Infectious Disease Society of America Guidelines

In 1997, the American Thoracic Society (ATS) established diagnostic criteria for NTM lung disease, regardless of the host's HIV status.[14] These guidelines were revised and approved by the American Thoracic Society and Infectious Disease Society of America (IDSA) in 2007.

M kansasii is considered a highly pathogenic mycobacterium, and many experts advise that M kansasii isolated from lungs or elsewhere almost always warrants treatment, especially in patients with HIV/AIDS and in other immunocompromised groups. The authors of the ATS/IDSA guidelines also acknowledge and suggest that the treatment decisions for M kansasii should be made carefully, even if some specimens are not positive for M kansasii or if multiple specimens are not available, and they recommend expert consultation in the decision-making process.

The general diagnostic criteria for all NTM pulmonary infections based on 2007 ATS/IDSA guidelines are summarized below.[15]

Clinical criteria

Both of the following clinical criteria are required to establish a diagnosis of NTM lung disease:

Microbiologic criteria

One of the following microbiologic criteria is required for diagnosis of NTM lung disease:

The ATS/IDSA guideline also recommends the followings for diagnosis:

Medical Care

In general, M kansasii shows good in vitro susceptibility to rifampin/rifabutin, amikacin, streptomycin, and clarithromycin. Rifampin-resistant strains are usually cross-resistant to rifabutin and, therefore, need separate susceptibility testing. In vitro susceptibility of isoniazid should be interpreted carefully, as it does not correlate with clinical outcome. In patients with no prior exposure to isoniazid, the drug is useful in the treatment of M kansasii infection, regardless of poor susceptibility results. Isoniazid susceptibility testing in laboratories is performed at lower concentrations (0.2 or 1 mcg/mL), which were designed for M tuberculosis, whereas M kansasii susceptibility requires a higher concentration (5mcg/mL) . Pyrazinamide should not be used to treat M kansasii infection.

Patients in whom M kansasii infection is diagnosed should be treated with at least 3 drugs. The initial drug regimen should include rifampin, which has been shown to yield low failure rates (1.1%) and low long-term relapse rates (< 1%).[16] Rifampin is the cornerstone of treatment for M kansasii infection. Although more commonly used as an alternative in HIV-infected patients to reduce drug interaction, rifabutin shows more in vitro activity compared with rifampin.[17]

The 2007 ATS/IDSA guidelines for nontuberculous mycobacterial (NTM) infections recommended the following regimens for treatment of M kansasii infection:[15]

More recent in vitro data for M kansasii suggest increasing resistance to fluoroquinolones, including ciprofloxacin and moxifloxacin (30% and 40% resistance, respectively).[18] However, clarithromycin remains active against M kansasii, with 100% of isolates displaying susceptibility in vitro.[17, 18] Many clinicians prefer a combination of clarithromycin with rifampin (or rifabutin) and ethambutol.

Patients with M kansasii pulmonary infection should be closely monitored with routine clinical examinations and regular sputum for AFB smears and cultures for mycobacteria during the treatment period. The antimycobacterials can be stopped after AFB sputum results are negative for at least 12 months.

Patients with extrapulmonary and disseminated M kansasii infections should be treated in a similar manner to those with pulmonary disease.

Treatment for CNS disease is similar to the pulmonary infection and includes rifampin or rifabutin, with ethambutol, and either isoniazid or clarithromycin. CNS infection due to M kansasii has been reported to have high rates of morbidity despite treatment.[19]

Surgical Care

Surgical treatment is unnecessary in M kansasii infection, as it responds very well to antimycobacterial therapy.



A dietitian should evaluate malnourished patients.


Activity is not limited in patients with M kansasii infection and should be performed as tolerated.

Medication Summary

The 2007 ATS/IDSA guideline for the treatment of M kansasii pulmonary disease recommends a regimen containing rifampin (600 mg), ethambutol (15 mg/kg) and isoniazid (300 mg) with pyridoxine (50 mg) daily for a total duration that includes at least 12 months of negative sputum culture results.[15]

Patients who are infected with rifampin-resistant M kansasii or who are intolerant of rifampin should be treated with a 3-drug regimen based on susceptibility results. For example, for rifampin-resistant M kansasii, rifampin should be substituted with clarithromycin.

Other agents with useful activity against M kansasii include fluoroquinolones (moxifloxacin, sparfloxacin), aminoglycosides (streptomycin, amikacin), sulfamethoxazole, and linezolid.[15, 20]

Patients with severe M kansasii infections and disseminated infections should also be treated with 3-drug regimens similar to that instituted for pulmonary infection . Rifampin should not be used concurrently with HIV protease inhibitors or nonnucleoside reverse transcriptase inhibitors (NNRTIs) because rifampin significantly enhances their metabolism. Rifabutin at a lower dose (150 mg/d) should be substituted for rifampin in patients receiving protease inhibitors.

Most M kansasii isolates are pyrazinamide-resistant in vitro. Pyrazinamide is unacceptable as an alternative drug for M kansasii infection.

Rifampin (Rifadin, Rimactane)

Clinical Context:  Considered the most important drug. Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. Cross-resistance may occur. Treat for 6-9 mo or until 6 mo have elapsed from conversion to sputum culture negativity.

Isoniazid (INH, Laniazid)

Clinical Context:  Best combination of effectiveness, low cost, and minor adverse effects. First-line drug unless known resistance or another contraindication is present. Therapeutic regimens of < 6 mo demonstrate unacceptably high relapse rate.

Coadministration of pyridoxine is recommended if peripheral neuropathies secondary to INH therapy develop. Prophylactic doses of 6-50 mg of pyridoxine daily are recommended.

Ethambutol (Myambutol)

Clinical Context:  Impairs cell metabolism by inhibiting synthesis of 1 or more metabolites, which in turn, causes cell death. No cross-resistance demonstrated.

Mycobacterial resistance is frequent with previous therapy. Use in combination with second-line drugs that have not been administered previously.

Administer q24h until permanent bacteriologic conversion and maximal clinical improvement are observed. Absorption is not significantly altered 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 occurs, administer dose bid with food.

Clarithromycin (Biaxin)

Clinical Context:  Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.


Clinical Context:  Recommended by some experts during the initial phase, especially with positive sputum smear results and positive blood cultures. For treatment of susceptible mycobacterial infections.

Use in combination with other antituberculous drugs (eg, INH, EMB, rifampin).

Amikacin (Amikin)

Clinical Context:  Occasionally necessary during initial treatment phase, especially with positive sputum smear results. Irreversibly binds to 30S subunit of bacterial ribosomes. Blocks recognition step in protein synthesis. Causes growth inhibition. Use patient's IBW for dosage calculation.

Moxifloxacin (Avelox)

Clinical Context:  Inhibits bacterial DNA synthesis and growth. Activity is similar to that of ciprofloxacin and levofloxacin.

Class Summary

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

Further Inpatient Care

Further Outpatient Care





Janak Koirala, MD, MPH, FACP, FIDSA, Professor and Division Chair, Division of Infectious Diseases, Department of Internal Medicine, Southern Illinois University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

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.

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.


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Chest radiograph in a patient with Mycobacterium kansasii pulmonary infection shows left lower lung infiltrates.

Chest CT scan in a patient with Mycobacterium kansasii pulmonary infection.

Chest radiograph in a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL.

CT thorax of a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL.

Chest radiograph in a patient with Mycobacterium kansasii pulmonary infection shows left lower lung infiltrates.

Chest CT scan in a patient with Mycobacterium kansasii pulmonary infection.

Chest radiograph in a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL.

CT thorax of a patient with classic right upper lobe cavitary lung disease secondary to Mycobacterium kansasii infection. Courtesy of Raj Sreedhar, MD, SIU School of Medicine, Springfield, IL.