Elsevier

Clinics in Chest Medicine

Volume 23, Issue 3, September 2002, Pages 613-621
Clinics in Chest Medicine

Management of disease due to Mycobacterium kansasii

https://doi.org/10.1016/S0272-5231(02)00016-3Get rights and content

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Pathogenesis and epidemiology

Infection by M kansasii probably occurs via an aerosol route. Although it is not known with certainty, tap water is likely a major reservoir for M kansasii causing human infection. The organism has been isolated from tap water in the same communities where patients with M kansasii disease have been identified [2], [31]. Isolates of the same phage type as those isolated from patients have been recovered from drinking water distribution systems in the Netherlands [3], [4], and environmental

Clinical aspects of M kansasii disease

Pulmonary disease is the most frequent clinical manifestation of M kansasii infection in immunocompetent patients. Of all NTM, M kansasii lung disease most closely parallels the clinical course of M tuberculosis. M kansasii primarily affects middle-aged white men, but it can affect adult patients of any sex, race, or age. Risk factors for M kansasii infection include pneumoconiosis, chronic obstructive lung disease (COPD), previous mycobacterial disease, malignancy, and alcoholism [1], [10],

Diagnosis of M kansasii disease

M kansasii is isolated from respiratory specimens using standard mycobacteriology laboratory techniques. Identification of M kansasii isolates usually is accomplished with a highly sensitive and specific commercial DNA probe (Accuprobe; GenProbe, Inc. San Diego, CA) in larger reference and state health laboratories. This method, along with high-performance liquid chromatography (HPLC) analysis of mycolic acid esters, has generally replaced utilization of colony morphology and pigmentation for

M kansasii in vitro drug susceptibility

Untreated (“wild”) strains of M kansasii are inhibited by rifampin, rifabutin, isoniazid, ethambutol, ethionamide, amikacin, streptomycin, clarithromycin, and probably ciprofloxacin at concentrations readily achievable in the serum with usual therapeutic doses [20], [21], [22], [23]. M kansasii is also usually susceptible in vitro to sulfamethoxazole, amikacin, the newer quinolones, and clarithromycin [20], [21], [22], [23]. Isolates are usually resistant to high concentrations in vitro and

Treatment of M kansasii disease

There have been several retrospective and prospective studies of various treatment regimens for M. kansasii lung disease that form a reasonable basis for drug therapy recommendations [22], [24], [25], [26]. The key to successful therapy of M kansasii lung disease is inclusion of rifampin in a multidrug regimen. For antimycobacterial drug regimens without rifampin, the sputum conversion rates at 6 months have ranged from 52–81% [22], [27]. Relapse rates were approximately 10% even in patients

Treatment monitoring

Serial sputum AFB analysis is the most important element of disease monitoring in M kansasii lung disease. The sputum analysis is an indication of patient response to therapy and allows determination of the time that sputum converted to negative on therapy (which will dictate the length of therapy in some patients). Additional routine sputum analysis will indicate relapse of disease in patients who had previously converted sputum to AFB negative. Patients who have relapsed microbiologically

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