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Rationale: While the history of pulmonary tuberculosis (PTB) is a risk factor for developing both chronic obstructive pulmonary disease (COPD) and lung cancer, it remains unclear whether the histor...

Patients with refractory Mycobacterium avium complex lung disease (MAC-LD) undergo long-term macrolide therapy, but macrolide resistance develops infrequently.The aim of this study was to determine whether reinfection was a factor in the low incidence of macrolide resistance in patients with refractory MAC-LD.Among 481 patients with treatment-naive MAC-LD who started antibiotic treatment between January 2002 and December 2013, we identified 72 patients with refractory disease, characterized by persistently positive sputum cultures despite ≥12 months of treatment. Molecular analyses of the 23S ribosomal RNA gene responsible for macrolide resistance and serial mycobacterial genotyping were performed using stored MAC isolates.The median duration of treatment was 32 months (interquartile range, 24-41 mo) in 72 patients. After treatment for a median of 33 months (interquartile range, 21-44 mo), macrolide resistance developed in 16 (22%) patients. Molecular analysis of isolates from 15 patients revealed that 80% (12 of 15) had a point mutation at position 2,058 or 2,059 of the 23S ribosomal RNA gene. Of the 49 patients who had stored pre- and post-treatment isolates, mycobacterial genotyping revealed that reinfection by new MAC strains occurred in 36 (73%) patients. New MAC strains were found in 24 (49%) patients, and mixed infections with original and new strains occurred in 12 (24%) patients. Only 13 (27%) patients had persistent infections with their original MAC strains.Refractory MAC-LD is commonly caused by reinfection with new strains rather than persistence of the original strain, which may explain the infrequent development of macrolide resistance in refractory MAC-LD. Clinical trial registered with www.clinicaltrials.gov (NCT00970801).

Background: Pulmonary paragonimiasis is a subacute to chronic inflammatory disease of the lung caused by lung flukes that result in prolonged inflammation and mechanical injury to the bronchi. However, there are few reports on the bronchoscopic findings of pulmonary paragonimiasis. This report describes the bronchoscopic findings of pulmonary paragonimiasis. Methods: The bronchosocpic findings of 30 patients (20 males, median age 50 years) with pulmonary paragonimiasis between May 1995 and December 2007 were reviewed retrospectively. Results: The diagnoses were based on a positive serologic test results for Paragonimus-specific antibodies in 13 patients (43%), or the detection of Paragonimus eggs in the sputum, bronchial washing fluid, or lung biopsy specimens in 17 patients (57%). The bronchoscopic examinations revealed endobronchial lesions in 17 patients (57%), which were located within the segmental bronchi in 10 patients (59%), lobar bronchi in 6 patients (35%) and main bronchi in 1 patient (6%). The bronchoscopic characteristics of endobronchial lesions were edematous swelling of the mucosa (16/17, 94%) and mucosal nodularity (4/17, 24%), accompanied by bronchial stenosis in 16 patients (94%). Paragonimus eggs were detected in the bronchial washing fluid of 9 out of the 17 patients with endobronchial lesions. The bronchial mucosal biopsy specimens showed evidence of chronic inflammation with eosinophilic infiltration in 6 out of 11 patients (55%). However, no adult fluke or ova were found in the bronchial tissue. Conclusion: Bronchial stenosis with mucosal changes including edematous swelling and mucosal nodularity is the most common bronchoscopic finding of pulmonary paragonimiasis.