Mycobacterium Kansasii Treatment & Management

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