Micobactérias

Mycobacterium kansasii

Long, banded acid-fast bacilli

Identification & Growth

Identification

Photochromogen: produces yellow pigment after light exposure
Slow growth (2–4 weeks), heat-stable catalase positive

Growth Conditions

Löwenstein-Jensen, 37 °C, 2–4 weeks, with a photochromogenicity test

Clinical Significance

Cavitary pulmonary disease closely resembling tuberculosis, especially in COPD and silicosis

Intrinsic Resistance

Resistant to pyrazinamide; susceptible to rifampicin, ethambutol and macrolides

Bench Alerts

Test rifampicin and clarithromycin by MIC (CLSI M24); disk diffusion does not apply
Differentiate from tuberculosis before starting treatment — management differs

Clinical Notes

Clinical presentations

Chronic cavitary pulmonary disease resembling pulmonary tuberculosis, predominantly in men with pre-existing structural lung disease.
Disseminated disease in patients with advanced HIV infection and other severe forms of immunosuppression.
Less common extrapulmonary infections, including lymphadenitis, tenosynovitis and skin and soft-tissue infection.

Specimens and collection

Serial sputum samples for smear and liquid/solid culture, applying ATS/IDSA diagnostic criteria for pulmonary NTM disease.
Bronchoalveolar lavage when spontaneous expectoration is insufficient or results are inconclusive.
Mycobacterial blood culture and lymph node or tissue biopsy in disseminated or extrapulmonary disease, correlated with immune status.

Epidemiology and at-risk populations

Slow-growing, photochromogenic mycobacterium associated with urban water sources, predominantly distributed in urban and industrial areas.
Prior structural lung disease (COPD, prior tuberculosis, pneumoconiosis) is the main predisposing factor for pulmonary disease.
Regarded as one of the most pathogenic NTM species when isolated from a pulmonary site, usually with significant clinico-radiologic correlation.

Resistance and therapeutic implications

CLSI M24 recommends susceptibility testing primarily for rifampin, with clarithromycin and other agents tested according to clinical indication.
Rifampin resistance, although uncommon, drives regimen substitution and reinforces the need for susceptibility testing in treatment failure.
Isolates are intrinsically resistant to pyrazinamide, which distinguishes management from tuberculosis despite the similar clinico-radiologic picture.

Bench and reporting notes

Slow-growing, acid-fast, photochromogenic bacillus that produces yellow pigment when exposed to light after growth in the dark.
Species confirmation by molecular probes, sequencing or validated mass spectrometry is essential to differentiate it from other photochromogenic NTM.
Isolation from a respiratory specimen should be correlated with clinical, radiologic and microbiologic criteria before establishing a diagnosis of disease.

Sources

Educational decision-support content. It does not replace laboratory validation, current guidelines or review by the responsible professional.

FAQ: Frequently Asked Questions

How to identify Mycobacterium kansasii in the lab?

Mycobacterium kansasii is identified through photochromogen: produces yellow pigment after light exposure, slow growth (2–4 weeks), heat-stable catalase positive.

What are the intrinsic resistances of Mycobacterium kansasii?

This organism is naturally resistant to resistant to pyrazinamide; susceptible to rifampicin, ethambutol and macrolides. These drugs should not be reported as susceptible.

Where is Mycobacterium kansasii commonly found?

It is typically associated with cavitary pulmonary disease closely resembling tuberculosis, especially in copd and silicosis.

Antibiogram InterpreterCheck BrCAST 2026 breakpoints Rugai InterpreterBiochemical identification tools