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Clinical Observations |
1 Department of Radiology and Center for Imaging Science, Samsung Medical
Center, Sungkyunkwan University School of Medicine, 50, Ilwon-dong,
Gangnam-gu, Seoul 135-710, South Korea.
2 Department of Diagnostic Pathology, Samsung Medical Center, Sungkyunkwan
University School of Medicine, 50, Ilwon-dong, Gangnam-gu, Seoul 135-710,
South Korea.
3 Division of Pulmonary and Critical Care Medicine, Department of Medicine,
Samsung Medical Center, Sungkyunkwan University School of Medicine, 50,
Ilwon-dong, Gangnam-gu, Seoul 135-710, South Korea.
Received August 20, 2004; accepted after revision October 6, 2004.
Address correspondence to J. Han.
OBJECTIVE. Our objective was to assess the CT findings for endobronchial actinomycosis associated with broncholithiasis.
CONCLUSION. Endobronchial actinomycosis associated with broncholithiasis manifests as a proximal obstructive calcified endobronchial nodule associated with distal postobstructive pneumonia of the involved lobe or segment on CT. The possibility of endobronchial actinomycosis should be entertained when broncholithiasis is seen on CT in tuberculosis-endemic areas.
Actinomycosis is a chronic suppurative pulmonary infection usually caused by Actinomyces israelii, which are normal inhabitants of the human oropharynx and frequently found at gingival margins of persons with poor oral hygiene [1]. The disease is believed to be acquired by the spread of endogenous organisms from these sites [2], usually directly from the oropharynx into the lungs by aspiration.
Rare cases of predominantly endobronchial actinomycosis have also been reported [3–16]. Case reports of CT findings of endobronchial actinomycosis associated with broncholithiasis, however, have involved few patients [15, 16]. We retrospectively assessed chest CT findings for nine patients with histopathologically proven endobronchial actinomycosis.
Materials and Methods
Between December 1997 and August 2004, nine patients (six men and three women; age range, 38–66 years; mean, 52 years) with histopathologically proven endobronchial actinomycosis were identified from the file archives of the Department of Pathology in our institute. Approval from the institutional review board was not needed for review of pathologic reports and radiologic images in our institute. We retrospectively reviewed the patients' clinical, CT, and histopathologic findings.
The chief complaints of the patients before admission were cough (n = 8), sputum (n = 8), and hemoptysis or blood-tinged sputum (n = 5). One patient was asymptomatic. All patients were immunocompetent. Five patients were smokers, and one was alcoholic. Two patients were receiving oral hypoglycemic drug therapy for diabetes, and two reported a history of pulmonary tuberculosis.
Unenhanced and contrast-enhanced helical chest CT images were obtained for all patients using a helical CT scanner (HiSpeed Advantage, GE Healthcare). The parameters of helical chest CT were 7-mm collimation and a table feed of 10 mm/sec. Contrast-enhanced chest CT scans were obtained after injection of 30 g of iodinated contrast medium (100 mL of iopamidol [Iopamiron 300, Bracco]) at a rate of 3 mL/sec with a power injector (OP 100, Medrad). For one patient, four serial CT scans obtained during a 21-month interval were available.
Chest CT findings were analyzed retrospectively and jointly by two experienced chest radiologists (with 7 and 4 years' experience in chest radiology). The decisions on the CT findings were reached by consensus. Chest CT findings were assessed specifically for the distribution and pattern of abnormalities of the airway and the lung, the presence or absence of pleural change, and mediastinal or hilar lymphadenopathy. Findings suggestive of previous tuberculous infection such as calcified mediastinal or hilar lymph nodes, calcified parenchymal nodules, or pleural calcification were also assessed. Uncalcified mediastinal or hilar lymph nodes measuring greater than 10 mm in the short axis were regarded as significantly enlarged.
Actinomycosis was diagnosed at bronchoscopic biopsy in three patients and at surgery in six (lobectomy [n = 5] or segmental resection [n = 1]). Confirmative diagnosis was based on histopathologic findings of Actinomyces colonies or sulfur granules (yellowish aggregates of clustered mycelia) or of filamentous organisms staining positively with Gomori's methenamine silver within the tissue specimen [17]. The CT and histopathologic findings for the resected lungs of six patients were correlated by a pathologist with 9 years' experience and by a chest radiologist.
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CT Findings
All nine patients showed a proximal endobronchial calcified nodule
(broncholith) on CT (Figs. 1A,
1B,
1C,
1D,
1E,
1F,
1G,
1H and
2A,
2B,
2C,
2D). The broncholiths were in
the right lower lobe (n = 4), right middle lobe (n = 2),
left upper lobe (n = 1), left lower lobe (n = 1), or right
main bronchus (n =1). The proximal airways were narrowed (n
=2) or obstructed (n = 7) by the broncholiths, which ranged from 8 to
17 mm in widest diameter (mean, 13 mm).
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Bronchiectasis within the consolidation was noted in four patients; one showed patent bronchiectasis, and the remaining three showed mucoid impaction within dilated bronchi.
Significantly enlarged mediastinal or hilar lymph nodes (range, 10–18 mm in the short axis) were seen in seven patients. Adjacent pleural thickening (n = 2) or minimal pleural effusion (n = 1) was also noted.
In one patient for whom four serial CT scans were available, a calcified subcarinal lymph node showed progressive erosion into the lumen of the right main bronchus, resulting in a partially endobronchial broncholith covered with mucosal thickening 18 months after the initial CT scan (Fig. 3A, 3B, 3C, 3D). Bronchoscopic examination showed an endobronchial calcified nodule. The calcified nodule was removed using the bronchoscopic forceps, and a biopsy specimen was taken of the overlying soft tissue. Histologic examination of the biopsy specimen revealed inflammation with multiple Actinomyces colonies. Follow-up CT 3 months after stone removal showed a small amount of residual soft tissue at the previous site.
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Eight of nine patients showed findings suggestive of previous tuberculous infection, such as other calcified hilar (n = 5), paratracheal (n = 7), or subcarinal lymph nodes (n = 6); calcified parenchymal nodules (n = 7); calcified pleural nodules (n = 1); and paracicatricial bronchiectasis in the upper lobe (n =1). Only one patient showed no other calcified lesions except a broncholith, but the patient reported a history of pulmonary tuberculosis.
Histopathologic Findings
Gross examination of the resected specimens revealed lobar or segmental
consolidation associated with a proximal obstructive calcified nodule. At
histopathologic examination, suppurative zones and sulfur granules containing
branching filamentous structures were seen around the broncholith.
Actinomycotic colonies or sulfur granules were round to oval, basophilic
masses, in the center of which were seen organisms identified as gram-positive
or filamentous structures staining positively with Gomori's methenamine silver
(Fig. 1A,
1B,
1C,
1D,
1E,
1F,
1G,
1H). Distal pneumonic
consolidation seen on CT was histopathologically composed of acute suppurative
inflammation, abscesses with or without Actinomyces colonies, or
organizing pneumonia with a variable degree of fibrosis. In one patient,
histopathologic examination of a segmental resection specimen revealed foreign
bodies of some vegetable nature in the background of inflammation with
multiple Actinomyces colonies. In this patient, a 15-mm broncholith
was also seen in the proximal portion of the necrotic segmental
consolidation.
Discussion
Thoracic actinomycosis is usually caused by aspiration of infected material in the oropharynx [2]. Chronic suppurative pneumonia, which may be associated with pleuritis, abscess, or fibrosis [18–20], occurs. According to Cheon et al. [20], in a study of the CT findings for thoracic actinomycosis, it usually appeared as chronic segmental air-space consolidation containing low-attenuation areas with peripheral enhancement or adjacent pleural thickening.
Rare cases of predominantly endobronchial actinomycosis have also been reported [3–16], some associated with a foreign body [3–7], some without an associated foreign body or broncholith [8–14], and some associated with broncholithiasis [15, 16].
According to Chouabe et al. [3], who presented four cases of endobronchial actinomycosis associated with a foreign body and reviewed the literature, the organism appeared to be carried into the lung along with aspirated foreign material, such as a chicken bone, tooth, grape seeds, or bean. According to case reports of endobronchial actinomycosis without a foreign body or broncholith [8–14], the process appeared endoscopically as an exophytic, yellow-white mass within the airway lumen [12]. This kind of endobronchial actinomycosis may be confused with endobronchial tuberculosis [9] or bronchogenic carcinoma [13].
One of the two case reports on endobronchial actinomycosis associated with broncholithiasis presented Histoplasma capsulatum–induced broncholithiasis [15], and the other case report asserted that the broncholiths had formed because of chronic inflammation associated with actinomycotic infection [16]. By definition, broncholithiasis is an uncommon condition in which a calcified nodule is found either within or eroding into the bronchial lumen [21]. The calcified nodule is usually a hilar lymph node that has undergone dystrophic calcification after inflammation and necrosis in tuberculosis or Histoplasma infection [22]. Constant respiratory movements cause the calcified node eventually to erode through the adjacent bronchial wall. Actinomyces have a tendency to colonize devitalized tissue [15, 23], and our cases seem to have been caused by secondary invasion of tissue previously devitalized by tuberculous infection. In our series, most cases showed evidence of earlier tuberculous infection such as calcified hilar and mediastinal lymph nodes or calcified granulomas. In one case with serial CT scans available, a calcified subcarinal lymph node showed progressive erosion into the lumen of the adherent bronchus and became infected with Actinomyces. Therefore, it is likely that the calcified endobronchial nodule was a preexisting broncholith resulting from a previous tuberculous infection rather than de novo calcification from chronic actinomycotic infection.
The probable pathophysiologic mechanism of endobronchial actinomycosis associated with broncholithiasis is as follows: A preexisting broncholith (or aspirated foreign body) is secondarily infected by Actinomyces, and the subsequent inflammatory process enlarges the endobronchial lesion and progressively obstructs the airway, with distal obstructive pneumonia of the involved pulmonary lobe or segment. Progressive shedding of Actinomyces colonies from the nidus further aggravates distal pneumonic consolidation. In our series, one case showed a foreign body comprising some kind of vegetable and a broncholith, both of which must have acted as nidi for secondary Actinomyces infection.
To our best knowledge, this is the first relatively large series reported on endobronchial actinomycosis associated with preexisting broncholithiasis appearing to have resulted from previous tuberculous infection. Our study suggests that the possibility of endobronchial actinomycosis should be entertained when broncholithiasis is seen on CT in tuberculosis-endemic areas.
In conclusion, endobronchial actinomycosis associated with broncholithiasis manifests as a proximal obstructive calcified endobronchial nodule associated with distal postobstructive pneumonia of the involved lobe or segment on CT. Endobronchial actinomycosis is a possibility when broncholithiasis is seen on CT in tuberculosis-endemic areas.
References
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