Since patients with CF have chronic bacterial pulmonary infections as their disease progresses, the clinical signs and symptoms of NTM are often difficult to distinguish from the underlying disease. Such potential underestimation of the contribution of NTM to the decline of lung function in cystic fibrosis may be an added risk to the eventual outcome of these patients. A variety of microorganisms traditionally considered colonizers of the airways, have been increasing in frequency and assuming new clinical significance5, 6, and previously unknown types of known organisms are taking on a new and ominous clinical significance.7 To the practicing clinician NTM appears to be increasing in incidence among the CF population, but the significance of this observation has not been firmly established. The concept of "colonization," defined as the isolation of the organism from the respiratory tract without evidence of tissue invasion, was supported by several investigators in the past, mainly in association with M. avium-complex infection.8, 9 With the emergence of high resolution CT scanning (HRCT), it now appears that many of these patients have features of parenchymal involvement, usually of a nodular pattern, suggesting that the term "colonization," at least in some patients, may be erroneous10, this notion has also been supported by direct bioptic evidence11, indicating the possibility that the full significance of infection with NTM may be underappreciated in patients with CF. It has been proposed that rather than using terminologies such as colonization and active disease, the distinction should be between patients who require immediate therapy on the basis of the rapid progression of their disease and those in whom the decision can be delayed.12 The repeated isolation of the same Mycobacterium from a patient with CF may be indicative of indolent infection and these patients may be at risk of developing clinical symptoms that will ultimately require treatment. This observation is supported by a series of autoptic studies13 indicating that patients with CF who have multiple positive sputum cultures for NTM are more likely to have histologic evidence of granulomatous mycobacterial disease. An additional study11 reports of a patient who had bioptic evidence of granulomas with NTM infection resulting in fulminant disease some 14 years later, suggesting that frank infections may be subclinical for a long period of time. The predictable but variable progression of the lung disease inherent to CF cannot be easily uncoupled from a possible contribution that chronic infection with NTM may add to the slope of such decline. Thus the role of such silent infections in exacerbating the decline of pulmonary function in such patients remains to be elucidated. From the clinical perspective subtle changes on serial high resolution computerized tomography of the chest (HRCT) may enable earlier diagnosis and intervention prior to the development of cavitation and/or irreversible lung damage.10 Of the NTM, Mycobacterium abscessus is a member of the rapidly growing mycobacteria. With improvements in identification, it is now known that this organism accounts for approximately 80% of rapidly-growing mycobacterial respiratory disease isolates.9 Prior to the 1990s, there were few reports of clinically important NTM infection complicating CF of which seven were cases of M. abscessus.11 Although the natural history of this disease can vary, it appears to follow a more fulminant course in patients with underlying lung diseases such as cystic fibrosis.14 The treatment of M. abscessus is complex. The isolates are uniformly resistant to standard antituberculosis drugs and are generally susceptible only to parenteral antibiotics and the newer oral macrolides. The organism is notoriously difficult to eradicate. In a report of 154 patients infected with rapidly growing mycobacteria14, only 10 patients infected with M. abscessus exhibited a "cure," the latter being defined as a return of respiratory symptoms to baseline and reversion of sputum to smear and culture negativity for at least 1 year. It has been noted for many years that the rates of infection and morbidity with and from NTM in non-CF patients have been increasing.1, 9 This notion has been recently supported by a report on the prevalence of mycobacterial infection in Ontario. The prevalence rose significantly (p<0.001) from 9.1/100,000 in 1997 to 16.5/100,000 in 2002, and 14.2/100,000 in 2003. A coincidental significant (<0.001) decline in the rate of M. tuberculosis infection from 6.9/100,000 in 1997 to 5.4/100,00 in 2003 was noted15. Whether such a trend of increasing prevalence of NTM also occurs in CF has not been formally addressed in the literature.