Mycobacterium Kansasii

Updated: Jun 11, 2020
Author: Janak Koirala, MD, MPH, FACP, FIDSA; Chief Editor: Michael Stuart Bronze, MD 



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 became 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. However, with better control of HIV/AIDS with antiretroviral therapy (ART), recently published studies report a declining trend in most of world.


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. Seven genotypes, or subtypes, are described. Types I and II are common clinical isolates, while the remaining types (III-VII) are mostly recovered from environmental samples only and are very rarely found in human samples. Type I is the most prevalent M kansasii isolate from human sources worldwide.[1]

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.[2]

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.[3]



United States

The prevalence of M kansasii, an unusual pathogen in the pre-AIDS era, increased with the HIV pandemic. With the advent of HIV/AIDS in the United States, M kansasii became 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. A 5-year study of 3 northern California counties in the 1990s found that M kansasii infection was more common in census tracts with a lower median income.[4] This study estimated an overall incidence of 2.4 cases per 100,000 adults per year in the general population of northern California, 115 cases per 100,000 persons with HIV infection per year, and 647 cases per 100,000 persons with AIDS per year.

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. 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< 0.001).[5] A 2017 review of a US national hospitalization database found that M kansasii made up only 3% of all clinical isolates of NTM, with a higher frequency of isolation in the western states.[6]


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.[7] In the United Kingdom, it has been reported as the most common cause of NTM lung infection in patients without HIV infection.[8] 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.[9]

An increasing incidence of NTM infections has been reported in other countries, including Israel, Korea, Spain, Portugal, France, Brazil, and Japan.[2] However, recent reports suggest downward trends of M kansasii in several countries. M kansasii was found to be the most common cause of NTM pulmonary disease in sub-Saharan Africa.[10]


The likelihood of mortality associated with M kansasii infection depends on various factors, including the presence of comorbid diseases, treatment compliance, rifampin 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.[11] Estimates for NTM disease in Ontario, Canada, from 2001-2013 found 1-year and 5-year survival rates for ​M kansasii infection to be 84% and 64%, respectively.[12] A retrospective study of South African gold miners treated for M kansasii infection reported mortality rates of 2% in those without HIV infection and 9% in patients with HIV infection.[7]

Untreated pulmonary M kansasii disease progresses and can lead to death in more than 50% of infected individuals.


M kansasii infection has no reported racial predilection.


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


M kansasii infection is more common in the older population and is rare in children.

The age predilection shifts in conjunction with age predilections of HIV infection.


Untreated M kansasii infection persists in sputum and progresses both clinically and radiographically. Untreated pulmonary M kansasii disease progresses and can lead to death in more than 50% of infected individuals.

Before rifampin was available, treatment success rates with antimycobacterial drugs were disappointing when compared to tuberculosis. With the advent of rifampin, 4-month sputum conversion rates with rifampin-containing regimens were 100% in 180 patients from 3 studies. Researchers report that long-term relapse rates in patients on these regimens are less than 1%.

In patients infected with HIV, predictors of survival include higher CD4 counts, antiretroviral therapy, negative smear microscopy results, and adequate treatment for M kansasii infection.[13, 14]

Patients with cavitary lung disease have a slower response to treatment. Patients with CNS infection have high rates of morbidity and mortality despite appropriate treatment.

Patient Education

Explain the adverse effects of any medications used for treatment, as follows:

  • Visual problems may occur with administration of ethambutol.

  • Rifampin reduces the efficacy of oral contraceptives.

For excellent patient education resources, visit eMedicineHealth's Lung Disease and Respiratory Health Center. Also, see eMedicineHealth's patient education articles Tuberculosis and Bronchoscopy.




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.[11]

Healthy host

The most common symptoms of pulmonary M kansasii infection include cough (91%), sputum production (85%), weight loss (53%), breathlessness (51%), chest pain (34%), hemoptysis (32%), and fever or sweats (17%).[15]

Cutaneous M kansasii infection resembles sporotrichosis secondary to local lymphatic spread. Cutaneous lesions may include nodules, pustules, verrucous lesions, erythematous plaques, abscesses, and ulcers.

Immunocompromised host

M kansasii infection manifests late in the course of HIV disease. The lung is the organ most commonly involved. Commonly reported symptoms include fever, chills, night sweats, productive or nonproductive cough, weight loss, fatigue, dyspnea, and chest pain.

Almost 20% of patients with HIV infection who develop M kansasii infection eventually develop disseminated disease.

M kansasii meningitis similar to M tuberculosis meningitis has been reported in patients infected with HIV and may carry a higher mortality rate despite appropriate antibiotic therapy.

M kansasii bacteremia, pericarditis with cardiac tamponade, oral ulcers, chronic sinusitis, osteomyelitis, and scalp abscess have been reported in patients with AIDS.

Disseminated M kansasii infection has also been reported in other immunocompromised hosts (eg, patients with myelodysplastic syndrome, patients on hemodialysis).

Cutaneous M kansasii infections in immunocompromised hosts usually have atypical clinical features (eg, cellulitis, seroma). These features, along with atypical histology (eg, absence of granuloma), may delay diagnosis.


Common physical findings of M kansasii infection include the following:

  • Fever

  • Pulmonary crackles and wheezing

  • Lymphadenopathy

Analysis of a series of 49 patients coinfected with HIV showed the following physical findings at the time of initial isolation of M kansasii:[16] ​

  • Pulmonary disease

    • Fever (45%)

    • Lung crackles (40%)

    • Lymphadenopathy (25%)

    • Wheezes (20%)

    • Hepatosplenomegaly (5%)

  • Disseminated disease

    • Fever (60%)

    • Hepatosplenomegaly (40%)

    • Lung crackles (25%)

    • Lymphadenopathy (10%)

    • Cutaneous lesions (10%)

    • Wheezes (5%)

Patients with cutaneous M kansasii infection may develop nodules, pustules, verrucous lesions, erythematous plaques, abscesses, or ulcers.

Other signs depend on the site of infection. For example, other manifestations, such as septic arthritis, tenosynovitis, osteomyelitis, and pleurisy, among others, have been reported.


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

Predisposing conditions for M kansasii infection include pulmonary conditions resulting from pneumoconioses (especially silicosis, gold mining, and coal mining), healed chronic infections (eg, tuberculosis, mycosis, chronic obstructive pulmonary disease, bronchiectasis), heavy smoking, and chronic obstructive pulmonary disease.

Other risk factors include cancer, diabetes mellitus, long-term steroid use, alcoholism, peptic ulcer disease, coronary artery disease, and prior pneumonia.





Laboratory Studies

Diagnosis of M kansasii infection requires isolation of the organism. Unlike other nontuberculous mycobacteria (NTM), M kansasii is believed to rarely represent colonization or an environmental contaminant. Patients with M kansasii isolated from sputum had similar clinical symptoms, although they did not meet ATS/IDSA criteria for diagnosis.[17]

Initially, evaluate at least 3 sputum samples by AFB staining and mycobacterial cultures. Bacteriologic examination may include AFB stain and culture of specimens (eg, bronchoalveolar lavage, aspirates from sterile sites, tissues).

Blood culture may be useful to detect M kansasii bacteremia and to establish a diagnosis of disseminated infection. Approximately 10% of patients with HIV infection who are also infected with M kansasii have blood cultures positive for M kansasii.

Nucleic acid probes and polymerase chain reaction (PCR) are useful for early identification of growing M kansasii colonies. They are highly sensitive and specific, providing species identification directly from liquid culture media. Other molecular methods of identification such as multiplex PCR, MALDI-TOF, and biochip assay, among others, are currently under development.

Susceptibility testing

The Clinical and Laboratory Standards Institute (CLSI) recommends that all initial isolates of M kansasii be tested only for clarithromycin and rifampin susceptibility.[18] Rifampin-susceptible isolates are also susceptible to rifabutin. If the isolate is resistant to rifampin (>1mcg/mL), further susceptibility to rifabutin, clarithromycin, amikacin, ethambutol, trimethoprim-sulfamethoxazole, ciprofloxacin/levofloxacin, moxifloxacin, and linezolid should be determined. Rifampin-resistant isolates should be sent to an experienced reference laboratory for further testing.[19] The CLSI does not recommend testing initial isolates for isoniazid susceptibility routinely since results do not correlate with the clinical outcome. 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 (0.5-5 mcg/mL) to predict a clinical failure.[20] Isoniazid and streptomycin are tested as secondary agents but do not have recommended breakpoints per CLSI.[18] Ciprofloxacin susceptibility results mirror those of susceptibility for both ofloxacin and levofloxacin.

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.

Chest radiograph in a patient with Mycobacterium k Chest radiograph in a patient with Mycobacterium kansasii pulmonary infection shows left lower lung infiltrates.
Chest CT scan in a patient with Mycobacterium kans Chest CT scan in a patient with Mycobacterium kansasii pulmonary infection.
Chest radiograph in a patient with classic right u 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 lo 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.

The characteristic radiological feature of M kansasii pulmonary infection has been described as a right-sided, apical or subapical, thin-walled cavitary infiltrate.[11] 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.[8]

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

Baseline laboratory workup for M kansasii infection should include complete blood cell count (CBC), renal profile, and liver profile.

Patients with M kansasii infection should be counseled about HIV infection and tested for HIV infection.

Perform a complete HIV evaluation if the patient tests positive for HIV. This evaluation should include CD4 counts and HIV viral load.


Bronchoscopy, tissue biopsy, thoracentesis, or pericardiocentesis may be needed to recover the pathogen and establish diagnosis. In some cases, transthoracic needle aspiration or open-lung biopsy may be necessary.

Bone marrow and liver biopsies may be useful in establishing disseminated M kansasii infection.

Needle aspiration or biopsy of a skin lesion (eg, nodule) may be useful for establishing M kansasii skin infections.[3]

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.[21]



Medical Care

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%).[22] 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.[23]

The 2007 ATS/IDSA guidelines for nontuberculous mycobacterial (NTM) infections recommended the following regimens for treatment of M kansasii infection:[24]

  • First-line regimen: This consists of rifampin (10 mg/kg/day; maximum, 600 mg) plus ethambutol (15 mg/kg/day) plus isoniazid (5 mg/kg/day; maximum 300 mg) plus pyridoxine (50 mg/day), with the treatment duration continuing until sputum culture results are negative for 12 months.

  • Alternative regimen: In patients with rifampin-resistant M kansasii disease, a 3-drug regimen should be used based on in vitro susceptibilities. These 3 drugs should include clarithromycin or azithromycin, moxifloxacin, ethambutol, sulfamethoxazole, or streptomycin.

In general, M kansasii shows good in vitro susceptibility to rifampin/rifabutin, amikacin, streptomycin, and clarithromycin. The CLSI recommends testing all initial clinical isolates of M. kansasii against rifampin and clarithromycin only. Rifampin-susceptible isolates are also susceptible to rifabutin and do not need separate testing. However, rifampin-resistant strains need separate susceptibility testing for rifabutin. In vitro susceptibility of isoniazid should be interpreted carefully, as it does not correlate with clinical outcome (see more under Susceptibility testing). In patients with no prior exposure to isoniazid, it is useful in the treatment of M kansasii infection, regardless of poor susceptibility results. Pyrazinamide should not be used to treat M kansasii infection.

More recent in vitro data for M kansasii suggest increasing resistance to fluoroquinolones, including ciprofloxacin and moxifloxacin (30% and 40% resistance, respectively).[25] However, clarithromycin remains highly active against M kansasii.[23, 25] Many clinicians prefer a combination of clarithromycin (or azithromycin) with rifampin (or rifabutin) and ethambutol. This regimen is also recommended in British Thoracic Society guidelines.[26]

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.[27]

Surgical Care

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


See the list below:

  • Infectious disease specialists, especially in patients who are co-infected with HIV or in drug-resistant cases
  • Pulmonologist if bronchoscopy with bronchoalveolar lavage and transbronchial biopsies are needed
  • Dermatologist if skin is involved and biopsy is desired
  • Thoracic surgeon if open-lung biopsy is necessary (rare)
  • In treatment-resistant cases, consulting the National Jewish Hospital Medical and Research Center in Denver, Colorado; the Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia; or other local experts may be useful.


A dietitian should evaluate malnourished patients.


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


Unlike for tuberculosis, respiratory isolation is not recommended for M kansasii and other NTM infections.

Long-Term Monitoring

Monitor patient care clinically and with chest radiography to assess response to therapy and clinical improvement. Induced sputum sample collection at regular intervals for AFB stain and culture are useful.

Monitor patients for drug toxicity, including periodic monitoring for the following:

  • Visual acuity, visual symptoms, and color vision in patients receiving ethambutol

  • Uveitis due to rifabutin, indicated by eye pain, decreased visual acuity, and anterior chamber fluid level

  • Liver enzymes for hepatotoxicity caused by drugs such as isoniazid, rifampin, rifabutin, and clarithromycin

  • Monitor renal function (for nephrotoxicity) and audiogram (for ototoxicity) at regular intervals if the patient is receiving aminoglycosides (amikacin or streptomycin)

  • Monitoring and education of patients to avoid drug interactions (The macrolides [clarithromycin, azithromycin] increase levels of many drugs metabolized in the liver, while rifampin and rifabutin decrease levels of other drugs metabolized in the liver.)



Guidelines Summary

Below is a summary of the British Thoracic Society[26] and American Thoracic Society/Infectious Diseases Society of America (ATS/IDSA) guidelines for diagnosis and treatment of NTM infections, which are relevant to ​M kansasii infection.[26, 24]

British Thoracic Society Guidelines for the Workup and Treatment of Nontuberculous Mycobacterial Pulmonary Disease

Workup for nontuberculous mycobacterial infections

Sputum, induced sputum, bronchial washings, bronchoalveolar lavage, or transbronchial biopsy samples can be used to evaluate individuals suspected of having nontuberculous mycobacterial (NTM) pulmonary disease.

Whenever possible, less invasive sampling should be attempted first to minimize procedural risks.

Respiratory samples should be processed within 24 hours of collection (or refrigerated at 4°C if delays are anticipated).

Oropharyngeal swab culture or serology testing should not be used to diagnose NTM pulmonary infection.

If sputum cultures are negative but clinical suspicion of NTM infection is high, consider performing CT-directed bronchial washings to obtain targeted samples.

If individuals undergoing diagnostic evaluation for NTM infection are taking antibiotics that may impair NTM growth (eg, aminoglycosides, macrolides, tetracyclines, cotrimoxazole, linezolid), consider discontinuing these antibiotics 2 weeks before collecting samples.

A validated rapid method should be used to detect NTM in respiratory samples.

All respiratory samples should be stained using auramine-phenol after liquefaction and concentration and then examined by microscopy.

Respiratory tract samples should be cultured (following decontamination) on solid and liquid media in a ISO15189-accredited clinical laboratory for 8 weeks, extending to 12 weeks if necessary.

Routine use of non–culture-based detection methods is not recommended at the present time.

All NTM isolates from respiratory samples should be identified to at least species level using validated molecular or mass spectrometry techniques.

Drug susceptibility testing and reporting

Drug susceptibility testing and reporting should follow the Clinical Laboratory Standards Institute (CLSI) guidelines.

For M kansasii, rifampin susceptibility testing should be performed on an isolate prior to initiation of treatment and on subsequent isolates if the patient fails to respond to treatment or recultures M kansasii after culture conversion.

Rifampin-resistant M kansasii isolates should be tested against a wider panel of antibiotics to guide, but not dictate, treatment regimens.

A minimum of 2 sputum samples collected on separate days should be sent for mycobacterial culture when investigating an individual suspected of having NTM pulmonary disease.

Individuals suspected of having NTM pulmonary disease whose sputum samples are consistently culture-negative for mycobacteria should have CT-directed bronchial washings sent for mycobacterial culture.

Individuals suspected of having NTM pulmonary disease who are unable to expectorate sputum should have CT-directed bronchial washings sent for mycobacterial culture.

Transbronchial biopsies should not be performed routinely in individuals suspected of having NTM pulmonary disease.

Treatment recommendations for M kansasii infection

Rifampin-sensitive M kansasii pulmonary disease should be treated with rifampin, ethambutol, and isoniazid or a macrolide (clarithromycin or azithromycin) using a daily oral regimen.

Rifampin-resistant M kansasii pulmonary disease should be treated with a three-drug regimen guided, but not dictated by, drug susceptibility test results using a daily oral regimen.

Antibiotic treatment for M kansasii pulmonary disease should continue for a minimum of 12 months after culture conversion.

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.[28] These guidelines were revised and approved by the American Thoracic Society and Infectious Disease Society of America (IDSA) in 2007.[24]

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.[24]

Clinical criteria

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

  • Pulmonary symptoms, nodular or cavitary opacities on chest radiography, or a HRCT scan that shows multifocal bronchiectasis with multiple small nodules

  • Appropriate exclusion of other diagnoses

Microbiologic criteria

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

  • Positive culture results from at least 2 separate expectorated sputum samples (If these culture results are nondiagnostic, consider repeat sputum AFB smears and cultures.)

  • Positive culture result from at least one bronchial wash or lavage

  • Transbronchial or other lung biopsy sample with mycobacterial histopathologic features (granulomatous inflammation or AFB) and positive culture for NTM; alternatively, a biopsy sample showing mycobacterial histopathologic features (granulomatous inflammation or AFB) and one or more sputum or bronchial washings that are culture-positive for NTM

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

  • Expert consultation should be obtained when NTM that are either infrequently encountered or that usually represent environmental contamination are recovered.

  • Patients with suspected NTM lung disease but who do not meet the diagnostic criteria should be observed until the diagnosis is firmly established or excluded.

  • A diagnosis of NTM lung disease does not automatically necessitate the institution of therapy, which is a decision based on potential risks and benefits of therapy in individual patients.



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.[24]

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, bedaquiline, and oxazolidinones (tedizolid or linezolid).[24, 29, 30] However, clinical experience for their use in the treatment of M kansasii infection are very limited.

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.


Class Summary

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

Rifampin (Rifadin, Rimactane)

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.

Ethambutol (Myambutol)

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.

Isoniazid (INH, Laniazid)

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.

Rifabutin (Mycobutin)

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)

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

Azithromycin (Zithromax, Zmax)

Macrolide that inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Used once daily as an alternative to clarithromycin.


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)

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)

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