Mycobacterium kansasii is known to cause a chronic pulmonary infection that closely resembles pulmonary tuberculosis.[1, 2] The most common symptoms associated with pulmonary M kansasii infection include cough, sputum production, weight loss, breathlessness, chest pain, hemoptysis, and fever or sweating. Additionally, cutaneous M kansasii infection can spread locally into the lymphatics, mimicking sporotrichosis, and is characterized by nodules, pustules, verrucous lesions, erythematous plaques, abscesses, and ulcers.
In advanced HIV-infected or other immunocompromised patients, M kansasii infection may manifest as disseminated disease, affecting multiple systems and potentially leading to conditions such as meningitis, pericarditis, osteomyelitis, and scalp abscesses. Diagnosis of M kansasii infection hinges on the isolation of the organism from sputum or other clinical samples. Unlike other nontuberculous mycobacteria (NTM), M kansasii is seldom considered a mere colonization or environmental contaminant.
Before initiating antimicrobial therapy, it is crucial to test all clinical isolates of M kansasii for susceptibility to rifampin and clarithromycin. For patients with rifampin-susceptible M kansasii, the first-line treatment regimen includes rifampin and ethambutol, supplemented with either isoniazid or a macrolide such as clarithromycin or azithromycin. Conversely, for patients with rifampin-resistant M kansasii or those intolerant to rifampin, an alternative regimen based on in vitro susceptibility should be employed. This regimen typically comprises a fluoroquinolone, ethambutol, and a macrolide, with the option to substitute isoniazid in place of the macrolide.
Treatment for M kansasii should continue for at least 12 months. However, extended treatment may be necessary for patients who do not achieve sputum conversion within 4 months. This approach ensures comprehensive management of the infection, aiming to mitigate the risk of persistent or recurrent disease.
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. Mycobacterium 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), there has been 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. Mycobacterium 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 (I to VII), are described. Types I and II are common clinical isolates, with type I being the most prevalent M kansasii isolate from human sources worldwide. The remaining types (III-VII) mostly are recovered from environmental samples only and very rarely are found in human samples.[1]
Mycobacterium 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]
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. Mycobacterium kansasii infection typically has 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]
International
Mycobacterium 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]
Mortality/Morbidity
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.
Race
M kansasii infection has no reported racial predilection.
Sex
M kansasii infection is more common in men, with a male-to-female ratio of 3:1.
Age
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%. A systemic review and meta-analysis of 24 studies showed a post-treatment sputum conversion rate of 80.2% (95% CI= 58.4%-95.2%) among patients with M kansassii infection.[13]
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.[14, 15]
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.
The adverse effects of any medications used for treatment are as follows:
Visual problems may occur with administration of ethambutol.
Rifampin has drug interactions with other drugs which are metablised in the liver, such as oral contraceptives, and reduces their efficacy . Therefore, it is important to ask the physician about any need to adjust the dose of any other concomitantly used drugs.
In most cases, Mycobacterium 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%).[16]
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.
Mycobacterium 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.
Mycobacterium 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 also has 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[17] :
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.
The workup of Mycobacterium kansasii infection necessitates a nuanced approach due to its pathogenic profile, which significantly differs from other nontuberculous mycobacteria (NTM).[18] Mycobacterium kansasii is recognized for its potential to cause symptomatic infections that closely resemble tuberculosis, thereby requiring precise and timely diagnostic strategies to ensure effective treatment. Unlike other NTM, M kansasii rarely is considered a benign colonizer or environmental contaminant, which underscores the importance of distinguishing true infection from mere exposure.[18]
In clinical practice, the diagnosis of M kansasii infection begins with the collection and analysis of respiratory specimens, as the bacterium most commonly presents in pulmonary forms. The standard protocol involves the evaluation of at least 3 sputum samples using acid-fast bacilli (AFB) staining and culture techniques. This approach may be expanded to include more invasive procedures such as bronchoalveolar lavage or biopsies from sterile sites if initial sputum samples are inconclusive or if the clinical presentation suggests more extensive disease.[18] Blood cultures also are integral, particularly for detecting M kansasii bacteremia, which is essential for diagnosing disseminated forms of the infection. This is especially relevant in immunocompromised patients, such as those with HIV, where approximately 10% exhibit M kansasii bacteremia.
The utilization of molecular diagnostic techniques such as nucleic acid probes and polymerase chain reaction (PCR) has significantly enhanced the sensitivity and specificity of M kansasii detection. These methods allow for the rapid identification of the organism directly from liquid culture media, facilitating timely initiation of appropriate therapy. Ongoing advancements in molecular diagnostics, including techniques like multiplex PCR, MALDI-TOF MS, and biochip assays, are further refining the ability to detect and identify M kansasii with greater accuracy and speed.
In cases where initial non-invasive tests (eg, sputum analysis) fail to confirm NTM pulmonary disease despite persistent clinical suspicion, more targeted diagnostic measures such as CT-directed bronchial washings are recommended. These procedures are particularly valuable for obtaining diagnostic material from patients who are unable to produce sputum or when sputum samples do not yield conclusive results. The comprehensive approach to diagnosing M kansasii not only aids in confirming the presence of the pathogen but also in delineating the extent of infection, which is crucial for guiding subsequent therapeutic decisions.
The clinical approach to diagnosing M kansasii infection involves isolating the pathogen, as M kansasii typically is not considered a mere colonization or environmental contaminant, unlike other nontuberculous mycobacteria (NTM).[18] Clinically, patients presenting with M kansasii in sputum samples often exhibit symptoms consistent with NTM infections, though they may not meet the ATS/IDSA diagnostic criteria for NTM diseases.[19]
Initial diagnostic steps include the evaluation of at least 3 sputum samples using acid-fast bacilli (AFB) staining and mycobacterial cultures, which may extend to include specimens like bronchoalveolar lavage, aspirates from sterile sites, and tissues.[18]
Blood cultures are particularly useful for identifying M kansasii bacteremia, which aids in diagnosing disseminated infections. It is noteworthy that approximately 10% of HIV-positive patients co-infected with M kansasii have positive blood cultures.
Techniques such as nucleic acid probes and polymerase chain reaction (PCR) are employed for the early detection of M kansasii colonies, offering high sensitivity and specificity. These methods facilitate species identification directly from liquid culture media. Additional molecular identification methods, including multiplex PCR, MALDI-TOF, and biochip assays, are under development.
For individuals suspected of having NTM pulmonary disease, diagnostic evaluations may utilize sputum, induced sputum, bronchial washings, bronchoalveolar lavage, or transbronchial biopsy samples. Initial diagnostic efforts should favor less invasive techniques to minimize procedural risks.
Respiratory samples should be processed within 24 hours of collection, or refrigerated at 4°C if processing is delayed. Oropharyngeal swab culture or serology testing is not recommended for diagnosing NTM pulmonary infections.
In cases where sputum cultures return negative but clinical suspicion for NTM infection remains high, CT-directed bronchial washings should be considered to obtain more targeted samples.
Patients undergoing diagnostic evaluation for NTM infection who are on antibiotics that may inhibit NTM growth, such as aminoglycosides, macrolides, tetracyclines, cotrimoxazole, and linezolid, are advised to discontinue these medications two weeks prior to sample collection.
A validated rapid method should be employed for detecting NTM in respiratory samples. All samples should be stained with auramine-phenol after liquefaction and concentration, followed by microscopic examination.
Respiratory tract samples should be cultured on both solid and liquid media in an ISO15189-accredited clinical laboratory for up to 8 weeks, with an extension to 12 weeks if necessary.
The routine use of non-culture-based detection methods is currently not recommended.
All NTM isolates from respiratory samples must be identified to at least the species level using validated molecular techniques or mass spectrometry.
Drug susceptibility testing and reporting
The Clinical and Laboratory Standards Institute (CLSI) specifically recommends that initial isolates of M kansasii undergo susceptibility testing for clarithromycin and rifampin only.[20] If an isolate is found to be susceptible to rifampin, it typically also is susceptible to rifabutin.[18] Conversely, if resistance to rifampin is detected (concentration >2mcg/mL), expanded testing should include rifabutin, clarithromycin, amikacin, ethambutol, trimethoprim-sulfamethoxazole, and the fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin), as well as doxycycline, minocycline, and linezolid.[21] Isolates resistant to rifampin should be forwarded to a specialized reference laboratory for further analysis.[22]
Routine isoniazid susceptibility testing is not advised by CLSI for initial isolates, as it does not reliably predict clinical outcomes. The concentration levels used for Mycobacterium tuberculosis (0.2 or 1 mcg/mL) are lower than those required for M kansasii (0.5-5 mcg/mL), which are necessary to accurately forecast clinical failure.[23] Both isoniazid and streptomycin are tested as secondary agents, yet CLSI has not specified breakpoints for these drugs.[20] It is noted that susceptibility results for ciprofloxacin are reflective of those for ofloxacin and levofloxacin.
Adherence to CLSI guidelines is essential for drug susceptibility testing and reporting. Before initiating treatment for M kansasii, rifampin susceptibility testing is essential and should be repeated for any subsequent isolates if the patient's response to treatment is inadequate or if M kansasii is recultured post culture conversion.
In the clinical evaluation of individuals suspected of having NTM pulmonary disease, it is recommended to send at least 2 sputum samples collected on different days for mycobacterial culture.[18] If these sputum samples consistently return negative results, or if the patient is unable to produce sputum, CT-directed bronchial washings should be considered for mycobacterial culture. Routine transbronchial biopsies are not recommended in the diagnostic workup of suspected NTM pulmonary disease.
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.[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):
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]
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.[24]
Unlike other NTM, in appropriate clinical setting Mycobacterium kansasii is considered pathogenic and treated with anti-NTM therapy. This bacterium is known to cause severe pulmonary disease similar to tuberculosis.[18]
Rifampin is considered as the mainstay of therapy for M kansasii. The standard treatment regimen for M kansasii typically includes rifampin, ethambutol, and either isoniazid or a macrolide as a third agent.
Antimicrobial susceptibility testing should be perfomed and the treatment regimen should be based on the suceptibility results. Should there be resistance to rifampin, alternative medications are available for treating M kansasii.
Initial treatment with clarithromycin and rifampin generally is effective. The observed high resistance rates to doxycycline, ciprofloxacin, and SXT warrant particular attention.
A systematic review and meta-analysis of 17 cross-sectional studies found the following resistance rates of M kansasii to various antibiotics: clarithromycin (0%), rifampin (1%), amikacin (0%), ciprofloxacin (14%), linezolid (0%), moxifloxacin (0%), rifabutin (1%), doxycycline (96%), and SXT (49%). These findings highlight the critical need for careful management and monitoring of these antibiotics, along with additional research to determine the precise mechanisms of resistance in M kansasii.[25]
Patients with M kansasii infection are treated with at least 3 drugs. Rifampin is the cornerstone of treatment for M kansasii infection. The initial drug regimen includes rifampin, which has been shown to yield low failure rates (1.1%) and low long-term relapse rates (< 1%).[26] Although more commonly used as an alternative in HIV-infected patients to reduce drug interaction, rifabutin shows more in vitro activity compared with rifampin.[27]
The 2020 ATS/ERS/ESCMID/IDSA Guidelines for nontuberculous mycobacterial (NTM) infections recommends susceptibility-based treatment for rifampin rather than empiric use of antimicrobial agents.[21] These guidelines recommend the following regimens for treatment of M kansasii infection:
First-line regimen
For patients with rifampin-susceptible M kansasii, the recommended treatment regimen includes:
Rifampin: Administered at 10 mg/kg/day, not exceeding 600 mg per day,
Ethambutol: Administered at 15 mg/kg/day, AND
Isoniazid with pyridoxine: Administered at 5 mg/kg/day, with a maximum of 300 mg per day, and pyridoxine at 50 mg/day,
Alternatively, a macrolide such as clarithromycin at 500 mg twice daily or azithromycin ranging from 250 to 500 mg daily can be used instead of isoniazid with pyridoxine.
Alternative regimen
For patients with rifampin-resistant M kansasii or those intolerant to rifampin, the treatment should include:
A fluoroquinolone (eg, moxifloxacin),
Ethambutol,
A macrolide (either clarithromycin or azithromycin),
Isoniazid may be used instead of a macrolide, depending on susceptibility results.
Duration of treatment
The treatment duration generally is 12 months. Treatment should not be extended beyond this unless sputum conversion has not occurred by the fourth month. Some authorities suggest continuing treatment for 12 months following sputum culture conversion to ensure complete eradication of the infection.[18]
Dosing frequency is as follows:
For cavitary pulmonary disease secondary to M kansasii, a daily dosing regimen is recommended.
For non-cavitary pulmonary disease, such as nodular and bronchiectatic lesions, treatment can be administered daily or three times a week when using a regimen that includes rifampin, ethambutol, and a macrolide.
Alternative regimens should be administered daily to ensure efficacy.[21]
The current guidelines including the CLSI recommend testing the 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.
In general, M kansasii shows good in vitro susceptibility to rifampin/rifabutin, amikacin, streptomycin, and clarithromycin. In vitro data for M kansasii suggested increasing resistance to fluoroquinolones, including ciprofloxacin and moxifloxacin (30% and 40% resistance, respectively) whereas clarithromycin remained highly active against M kansasii.[27, 28] Many clinicians prefer a combination of a macrolide (either clarithromycin or azithromycin) or isoniazid with rifampin (or rifabutin) and ethambutol. This regimen is recommended in both 2020 ATS/ERS/ESCMID/IDSA and 2017 British Thoracic Society guidelines.[18, 21] Due to the high rates of toxicity, parenteral therapy with streptomycin is recommended only in the setting of rifampin resistance and when an effective oral regimen is not available.
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.
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.[29]
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.
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). Audiometric assessments should also be done for patients receiving azithromycin.
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.)
The following organizations have released guidelines for the management of Mycobacterium kansasii. Key diagnostic and treatment recommendations have been reviewed and integrated throughout the article.
British Thoracic Society (2017): Management of non-tuberculous mycobacterial pulmonary disease.[18]
ATS/ERS/ESCMID/IDSA (2020): Treatment of nontuberculous mycobacterial pulmonary disease.[21]
The guidelines for the treatment of M kansasii pulmonary disease recommend a regimen containing rifampin (600 mg), ethambutol (15 mg/kg) and isoniazid (300 mg) with pyridoxine (50 mg) daily for a total duration of 12 months, or when sputum conversion does not occur within 4 months, at least 12 months after the sputum culture becomes negative.[21]
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 can be substituted with clarithromycin and administered with isoniazid and a fluoroquinolone.
Other agents with useful activity against M kansasii include fluoroquinolones (moxifloxacin, sparfloxacin), aminoglycosides (streptomycin, amikacin), sulfamethoxazole, bedaquiline, and oxazolidinones (tedizolid or linezolid).[30, 31, 32] 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.
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.
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.
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.
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.
Clinical Context:
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Clinical Context:
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.
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).
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.
Janak Koirala, MD, MPH, FACP, FIDSA, Professor Emeritus, Division of Infectious Diseases, Department of Internal Medicine, Southern Illinois University School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Aaron E Glatt, MD, MACP, FIDSA, FSHEA, Chairman, Department of Medicine, Chief, Division of Infectious Diseases, Hospital Epidemiologist, Mount Sinai South Nassau; Professor of Medicine, Icahn School of Medicine at Mount Sinai
Disclosure: Nothing to disclose.
Chief Editor
Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London
Disclosure: Nothing to disclose.
Additional Contributors
Klaus-Dieter Lessnau, MD, FCCP, Former 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
Gail L. Woods, M.D. et al. Susceptibility Testing of Mycobacteria, Nocardiae, and Other Aerobic Actinomycetes; Approved Standard. Second Edition. Wayne, PA: Clinical and Laboratory Standards Institute; 2011. M24A2:
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.
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