Mycobacterium Kansasii Workup

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