Pulmonary Mycobacterium kansasii Infection in Israel, 1999-2004: Discussion
We noted several clinically significant findings. Series from the United States’ and Spain suggested a higher-than-normal rate of isolation of M kansasii from HIV-positive patients, and a study done between 1981 and 1987 reported a 200-fold higher incidence of disseminated M kansasii infection in people with AIDS (138 per 100,000) than in the general population of the United States. However, in the present study, only a small number of patients received immunosuppressive medications, and none were HIV positive. This was also true for the series of Evans et al. website
Another important finding was the relatively low rate of cavitation in our study compared to that of Evans et al (54% vs 75%). In other series,, rates of cavitary infiltrates were even higher (approximately 90%). This discrepancy might be explained by recent improvements in diagnosis and microbiological isolation of the organism.
The good outcome in our study compared to the earlier study (100% vs 79%) may be attributable to the fewer systemic comorbid diseases in our series compared to the reports of Evans et al. In addition, all deaths caused by mycobacterial disease in this study occurred either before or soon after treatment was started. These data provide support for the use of earlier treatment regimens in M kansasii infection.
Because the concentrations of antituberculous drugs used in susceptibility testing were chosen for their usefulness with M tuberculosis, and because M kansasii is less susceptible to these drugs, some isolates of the latter species may be reported resistant to isoniazid at 0.2 ^g/mL or 1 ^g/mL and to streptomycin at 2 ^g/mL. These isolates are susceptible to higher drug concentrations, and laboratory reports of resistance to the low concentrations of these two drugs have no clinical or therapeutic significance as long as a rifampicin is being used. Therefore, we did not test the M kansasii strains for susceptibility to isoniazid.
The ATS recommends isoniazid, rifampicin, and ethambutol. In patients who cannot tolerate one of these drugs, clarithromycin appears to be a reasonable alternative. The quinolones, especially the new generation, may also be useful for rifampicin-resistant M kansasii strains, although no efficacy trials have been conducted to date. In our study population, we preferred the clarithromycin-containing regimen without the isonia-zid. Almost certainly, the key to successful therapy of M kansasii lung disease is inclusion of rifampicin in a multidrug regimen; whereas companion drugs may not enhance efficacy, they are essential to prevent the emergence of resistance to rifampicin. Both ethambutol and isoniazid appear to be effective for this latter role. Moreover, several studies” found that isoniazid does not contribute greatly to the treatment of M kansasii.