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1 Department of Radiology and Center for Imaging Science, Samsung Medical
Center, Sungkyunkwan University School of Medicine, 50, Ilwon-Dong,
Gangnam-Ku, Seoul 135-710, South Korea.
2 Division of Pulmonary and Critical Care Medicine, Department of Medicine,
Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul
135-710, South Korea.
3 Department of Pathology, Samsung Medical Center, Sungkyunkwan University
School of Medicine, Seoul 135-710, South Korea.
Received June 4, 2004;
accepted after revision August 17, 2004.
Supported by grant R11-2002-103 from the Korea Science & Engineering
Foundation.
Abstract
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MATERIALS AND METHODS. We retrospectively reviewed thin-section CT scans (2.5-mm collimation, both axial and coronal reformation images) of 24 cases (male-female ratio, 13:11; mean age, 61 years; age range, 43-82 years) of the cavitary form of culture-proven Mycobacterium avium-intracellulare complex pulmonary infection including two cases with lobectomy specimens. Any changes in CT findings detected on the follow-up CT scans that were available for seven patients (follow-up interval, 6-24 months; mean, 12 months) were also assessed.
RESULTS. Thin-section CT findings were bronchiectasis (24/24 patients, 100%), a patent bronchus running into a cavitary lesion (the "feeding bronchus" appearance) (18/24, 75%), nodules less than 10 mm (17/24, 71%), centrilobular nodules (17/24, 71%), nodules of 10-30 mm (13/24, 54%), peribronchial nodules (8/24, 33%), lobular consolidation (6/24, 25%), bronchial wall thickening (4/24, 17%), and consolidation (2/24, 8%). Two lobectomy specimens showed large cavitary consolidations with the feeding bronchus appearance on pathologic specimens. In two patients, small peribronchial nodules had changed into cavitary nodules with the feeding bronchus appearance on follow-up CT, which represented inflamed focal cystic bronchiectasis.
CONCLUSION. In the cavitary form of M. avium-intracellulare complex pulmonary infection, the feeding bronchus appearance is another very frequent thin-section CT finding. This appearance may suggest that peribronchial nodules of M. avium-intracellulare complex infection evolve into inflamed focal cystic bronchiectasis manifesting as cavitary lesions.
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Several previous studies suggested that the bronchiectasis was not a preexisting condition but resulted from nontuberculous mycobacterial infection [5-10]. To our knowledge, nothing has been described in the English-language literature concerning the possible relation between bronchiectasis and the centrilobular nodules and cavitary lesions in both forms of nontuberculous mycobacterial pulmonary infection or how these lesions develop and evolve.
We retrospectively reviewed thin-section CT images of 24 cases of the cavitary form of Mycobacterium avium-intracellulare complex (MAC) pulmonary infection in immunocompetent patients with CT-pathologic correlation of two lobectomy specimens to suggest a possible hypothesis about how bronchiectasis and centrilobular nodules and cavitary lesions develop and evolve in MAC pulmonary infection.
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Chest CT scans were obtained with a LightSpeed QX/i scanner (GE Healthcare) without IV injection of contrast medium. All CT data were reconstructed using a high-spatial-frequency algorithm. Helical volumetric scanning data using MDCT (120 kVp, 70 mA, 2.5-mm collimation, pitch of 6, and 2-mm reconstruction interval) were obtained through the thorax. The data obtained were reconstructed with a 2.5-mm thickness for transaxial images and a 1.2- to 2.0-mm thickness for coronal images. The scanning data were displayed directly on monitors (four monitors, 1,536 x 2,048 image matrices; 8-bit viewable gray-scale; and 60-foot-lamberts luminescence) of a PACS workstation (Path-Speed, GE Healthcare Integrated Imaging Solutions).
Thin-section CT scans were retrospectively reviewed by two independent chest radiologists with 7 and 4 years of experience, respectively. Both axial and coronal reformation images of thin-section CT scans were reviewed on the PACS workstation using the cine mode with scrolling a mouse up and down, which facilitated more accurate evaluation of the relation between an airway and a cavitary lesion. Final conclusions were reached by consensus. Thin-section CT scans were evaluated with regard to the presence or absence of bronchiectasis, a patent bronchus toward a cavitary lesion, well-defined small nodules (< 10 mm in diameter), branching centrilobular nodules (tree-in-bud pattern), nodules of 10-30 mm in diameter, peribronchial nodules, lobular consolidation (polygonal, 10-25 mm in diameter), bronchial wall thickening, and subsegmental or segmental consolidation.
Two lobectomy specimens were reviewed by a pathologist with 10 years of experience and correlated with the findings of the corresponding thin-section CT scans.
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Two patients who underwent lobectomy showed large cavitary consolidations with a centrally located, thickened, patent bronchus (the feeding bronchus appearance) on both thin-section CT and pathologic specimens (Figs. 1A, 1B, 1C, 1D, and 1E). On histopathologic examination, bronchial or peribronchial wall thickening with lymphocytic infiltration and peribronchial caseating granulomas surrounding an ectatic or narrowed bronchus were found (Figs. 1A, 1B, 1C, 1D, 1E, 2A, 2B, and 2C). Destruction and displacement of bronchial cartilages with inflammatory wall thickening were also noted in the bronchial wall with some intraluminal necrotic debris (Figs. 2A, 2B, and 2C).
In two of seven patients whose follow-up CT scans were available, small peribronchial nodules had changed into cavitary nodules with the feeding bronchus appearance, which represented inflamed focal cystic bronchiectasis (Figs. 4A, 4B, 4C, 4D, 4E, 5A, 5B, and 5C). The remaining five patients showed slight improvement (n = 2) or no significant interval change (n = 3) of the overall pulmonary lesions.
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According to Moore [5], small nodules on CT scans were shown to be peribronchial granuloma formation on pathologic correlation and new areas of bronchiectasis and progression of existing bronchiectasis were shown on serial CT scans. Tanaka et al. [6] suggested that pulmonary lesions slowly progressed from small nodules in the subpleural spaces to those with thickening of the draining bronchi or with both pleural and bronchial thickening and to cystic bronchiectatic changes. According to Tanaka et al. [8] in a study of CT findings of 46 MAC patients with follow-up scans, the common thin-section CT findings of MAC were centrilobular and peribronchovascular nodules, bronchiectasis, consolidation, and pleural thickening. Many nodules located in lobular bronchioles had dilated bronchioles inside them. Bronchiectasis became more severe in five of 38 follow-up patients. The study suggested that the disease might begin in the terminal bronchiole and spread transbronchially along the draining bronchus to produce lesions such as new nodules, cavities, and bronchiectasis.
According to Fujita et al. [9, 10] in pathologic studies of nine cases of MAC infection with a surgical specimen, pathologic findings included bronchiectasis, bronchiolitis, centrilobular nodules, consolidation, cavity wall and nodules, and extensive granuloma formation throughout the airways. Peribronchial granuloma formation was observed from the large airway to the bronchiole. Destruction of bronchial cartilage and the smooth-muscle layer and airway narrowing were caused by extensive submucosal granulomas, and bronchial ulceration involving their whole walls was frequently observed. In some areas, necrotic materials were detached into the lumen of the bronchiole. Because cartilage and smooth muscle play a major role in maintaining airway lumen, destruction of these fundamental bronchial structures could result in bronchiectasis, and this process was likely the main cause of bronchiectasis in MAC infection.
Well-known thin-section CT findings of nontuberculous mycobacterial infection include bronchiectasis, small and large nodules, branching centrilobular nodules, consolidation, and cavitary lesions [2-16]. However, to the best of our knowledge, the thin-section CT finding of a patent bronchus toward a cavitary lesion (the feeding bronchus appearance) has not been described before in nontuberculous mycobacterial pulmonary infection. The feeding bronchus appearance, which was a centrally located, thickened, mildly ectatic, patent bronchus supplying the cavitary lesion, was another common thin-section CT finding of the cavitary form of MAC infection in our study.
We think this finding might have been missed or overlooked on the conventional discontinuous CT images of the previous literature. A bronchus running in the craniocaudal or caudocranial direction is difficult to trace on axial CT images. With a cine mode review of both axial and coronal thin-section CT images of continuous helical volumetric data on a PACS workstation, the feeding bronchus appearance was likely more readily detectable in our study than the axial-only conventional discontinuous CT images of the previous studies, in which focal cystic bronchiectasis might have been interpreted only as a cavitary lesion. In two cases with follow-up CT scans, central cavitation or focal cystic bronchiectatic change of the peribronchial nodule was seen on serial follow-up examinations.
With these thin-section CT findings in our study and literature review, the following hypothesis about the developmental relation of bronchiectasis and centrilobular nodules and cavitary lesions in MAC infection can be proposed. We suggest that MAC infection begins with bronchial wall thickening, develops into peribronchial thickening or a peribronchial nodule, and forms inflamed cystic bronchiectasis that manifests as a cavitary mass or cavitary consolidation on both CT and pathologic specimens (Fig. 6). During the inflammatory process, the central necrotic portion with destroyed bronchial wall and cartilage seems to be ulcerated and detached into the airway, forming a central cavity. The peripheral portion of the peribronchial nodule extends into the surrounding lung parenchyma. In this circumstance, the central patent bronchus plays the role of a draining bronchus, which disposes of the detached central necrotic debris resulting in cavity formation and bronchogenic spread of the infection.
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From correlating our hypothesis with the known CT findings of nontuberculous mycobacterial infection, we suggest that the nodular bronchiectatic form (bronchiolectasis with branching centrilobular nodules) on thin-section CT represents stage III inflammation (peribronchial thickening or nodule) mainly involving small airways. In addition, we believe that the large cavitary form on thin-section CT represents stage IV inflammation mainly involving relatively large airways and more extensive inflammation.
According to the proposed hypothesis, MAC pulmonary infection is a mainly bronchocentric inflammatory process. Therefore, the hallmarks of the disease seem to be bronchial or bronchiolar wall thickening, peribronchial thickening, or peribronchial nodules. The disease can show diverse manifestations—for example, a nodular bronchiectatic form, a large cavitary form, or a mixed form—even in one patient, according to the size of the involved airways, the duration of the inflammatory process at each location after pathogen inoculation, and the severity of inflammation, and, possibly, on host immunocompetency. Most patients with cavitary lesions of MAC infection in our study showed small nodules and bronchiectasis, which are the main features of the nodular bronchiectatic form.
The possible significance of this hypothesis on the development of bronchiectasis and centrilobular nodules and cavitary lesions in MAC infection is that it might give a comprehensive understanding of the nontuberculous mycobacterial disease process. This process comprises a possible pathologic spectrum from bronchial wall thickening with peribronchial or centrilobular nodules to cavitary lesions or cystic bronchiectasis. In addition, this hypothesis may enable better interpretation of diverse thin-section CT findings and, hence, more accurate diagnosis of nontuberculous mycobacterial pulmonary infection.
In conclusion, in the cavitary form of MAC pulmonary infection, the feeding bronchus appearance is another very frequent thin-section CT finding in addition to bronchiectasis, small and large nodules, branching centrilobular nodules, bronchial or peribronchial thickening or nodules, and consolidation.
This appearance may suggest that early bronchial wall thickenings or peribronchial nodules of MAC infection evolve into inflamed focal cystic bronchiectasis manifesting as cavitary lesions.
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