Pulmonary Nocardiosis with Esophageal Involvement: A Rare Imaging Finding
Corresponding Author: Vishnu Appukuttan Kumari, Department of Imaging and Interventional Radiology, Kerala Institute of Medical Sciences (KIMS HEALTH), Trivandrum, Kerala, India, Phone: +91 9633667094, e-mail: firstname.lastname@example.org
Received on: 31 March 2023; Accepted on: 31 August 2023; Published on: 30 October 2023
Nocardiosis is an opportunistic infection that most commonly affects the lungs. On imaging, pulmonary nocardiosis can mimic tuberculosis, chronic pneumonia, and even malignancies. Mediastinal lymphadenopathy is relatively rare and esophageal involvement is even rarer in nocardiosis. However, it is possible for dissemination to occur to any site in the systemic form of the disease. Here, we present a case of biopsy-proven nocardiosis with esophageal and mediastinal nodal involvement with emphasis on imaging.
How to cite this article: Appukuttan Kumari V, Samed H, Chandranath A, et al. Pulmonary Nocardiosis with Esophageal Involvement: A Rare Imaging Finding. Indian J Respir Care 2023;12(3):272–276.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
Keywords: Case report, Esophageal thickening, High-resolution computed tomography, Mediastinal lymphadenopathy, Nocardiosis, Opportunistic infection
Nocardiosis is an opportunistic infection that most commonly affects the lungs. Pulmonary nocardiosis on high-resolution computed tomography (HRCT) can mimic tuberculosis, chronic pneumonia and even malignancies. Disseminated form of this condition can affect virtually any organ making the diagnosis often difficult. Early suspicion of imaging dramatically improves the prognosis considering the effectiveness of treatment. Here, we present a case of biopsy-proven nocardiosis with esophageal and nodal involvement with emphasis on imaging.
A 67-year-old female presented to the pulmonology outpatient department with complaints of a worsening cough with whitish expectoration for 1 month. She had dyspnea progressing from grades I to III over the past month. She also gave a history of hoarseness of voice and dysphagia over the past 2 weeks along with fatigue and facial swelling. She was a known case of systemic hypertension, dyslipidemia, bronchial asthma, and type 2 diabetes mellitus and was recently diagnosed with interstitial lung disease. She had been on corticosteroids for interstitial lung disease for the past 3–4 months. On examination, she was conscious, oriented, and febrile. There was pallor and bilateral pedal edema. Her vitals were normal with saturation of peripheral oxygen of 94% on room air. Auscultation was suggestive of fine crackles bilaterally.
Routine investigations were sent and total differential counts and C-reactive peptide were elevated. Hemoglobin levels were low at the time of admission. She was started on intravenous (IV) antibiotics empirically and radiological investigations were commenced.
The frontal chest radiograph (Fig. 1) showed a widened superior mediastinum. A homogeneous retrocardiac opacity was noted on the left lower zone with ill-defined margins and few tubular lucencies suggestive of an air bronchogram. There was another small irregular air space opacity in the right lung midzone. Both costophrenic angles were obliterated, suggestive of pleural effusion.
Considering the symptoms, she was further evaluated with contrast-enhanced computed tomography (CECT) thorax to rule out any mediastinal mass lesion or other pathology. The CECT showed consolidation with cavitation in the left lung lateral basal segment (Fig. 2A). Another nodule with spiculated margins and cavitation was seen in the superior segment of the right lung lower lobe (Fig. 2B). The consolidation showed ill-defined hypoenhancing areas in the center on postcontrast images (Fig. 2C). A conglomerate nodal mass with low-density areas, suggesting necrosis was seen in the lower paraesophageal region extending into the subcarinal region (Fig. 3). The subcarinal nodal mass was adherent to the adjacent thoracic esophagus, inseparable from its wall. Other discrete enlarged mediastinal lymph nodes were seen in the lower paratracheal region. In addition, there was asymmetric low-density wall thickening in the thoracic esophagus from the level of the inferior pulmonary vein extending up to esophageal hiatus (Fig. 4). There were also subpleural areas of ground glassing with interlobular septal thickening in bilateral lower lobe lung segments, suspicious of interstitial lung disease. Based on the above findings, the first consideration was tuberculosis with pulmonary parenchymal and mediastinal involvement. Since necrotic nodal masses in tuberculosis can erode into the esophagus, esophageal thickening was suspected to be due to periadenitis and esophagitis. The possibility of a primary esophageal carcinoma with mediastinal adenopathy and lung parenchymal deposits was also considered in view of the esophageal wall thickening and enlarged mediastinal nodes. Primary bronchogenic carcinoma was considered a remote possibility since esophageal wall thickening was less likely to be associated with it.
Nocardiosis is an uncommon infection that mainly affects immunocompromised individuals and rarely the healthy population. It is caused by Nocardia, a ubiquitous, gram-positive, weakly acid-fast bacteria with a characteristic filamentous branching morphology.1 Immune response to Nocardia is mainly T-cell mediated, and hence, any condition that suppresses cell-mediated immunity can make the individual susceptible to nocardiosis. Owing to the increasing numbers of organ transplants, autoimmune diseases, and widespread use of immunosuppressants like corticosteroids as well as due to increasing awareness about this condition, nocardiosis is gaining significance in day-to-day medical practice.2-4 Around >50 species of Nocardia are known to cause human infection of which Nocardia asteroides account for about 70% of the cases.5,6
Localized as well as disseminated forms of nocardiosis are known which are transmitted by inhalation or through cutaneous spread. Pulmonary nocardiosis is the most common type, with others being central nervous system and cutaneous nocardiosis. Apart from these, nocardiosis can spread to virtually any other site from a primary focus.1,7,8
Pulmonary nocardiosis can be an acute, subacute, or chronic infection with the chronic form being a great mimic of granulomatous infections like tuberculosis or malignancies.6 Clinical symptoms of pulmonary nocardiosis are often nonspecific and may include cough, fever, dyspnea, fatigue, chest pain, and hemoptysis.9
Like the clinical findings, radiological features may also overlap with tuberculosis, chronic pneumonia, and malignancy. Common radiographic findings are nodules or masses, cavities (with or without air-fluid level), air bronchogram, and pleural effusion. Bronchiectasis, lymphadenopathy, and interlobular septal thickening may also be encountered but are nonspecific.7,9
The HRCT is the workhorse in the evaluation of pulmonary infections that do not respond to initial antibiotic therapy. Documented HRCT findings of pulmonary nocardiosis include consolidation, well-defined nodules or masses with or without cavitation, centrilobular nodules, pleural effusion, and bronchiectasis. Other rare features are lymph node enlargement, interlobular septal thickening, and mucoid impaction.9,10
Consolidation can be multifocal or solitary with the former being more common. These areas may show central low density on noncontrast images which are hypoenhancing postcontrast due to early abscess formation. The well-formed abscess will show central fluid density with an enhancing rim. Peribronchovascular consolidation simulating bronchopneumonia has also been reported. Nodules in nocardiosis can be indistinguishable from fungal infection and can be with or without a ground glass halo. Like consolidation, these nodules can also undergo breakdown and cavitation.8,11
Endobronchial spread is possible in pulmonary nocardiosis and can manifest as multiple centrilobular nodules as in tuberculosis. Other findings in endobronchial spread include bronchial wall thickening and intraluminal debris.12 Endobronchial mass formation has also been reported.13
Pleural involvement can be in the form of pleural effusion, empyema, or pleural thickening. Chest wall extension can also occur as in tuberculosis and actinomycosis and is usually manifested as an inflammatory mass or abscess. Bony destruction, muscle edema, and fat stranding may be demonstrated in HRCT.8,14 Chronic inflammation may show hypertrophy of the chest wall fat. Empyema necessitates another complication in which there is a dissection of the abscess into the skin of the chest wall across the soft tissue.15
Distinguishing an empyema from a lung abscess is important as the former may require a chest tube and drainage while the latter is usually treated with antibiotics and chest physiotherapy. Empyema usually has a characteristic lentiform shape with smooth walls and a split enhancing pleura as margins and the adjacent lung parenchyma may be compressed by it. There may also be features of inflammation in the adjacent chest wall. A parenchymal abscess is usually rounded and irregular with thicker enhancing walls, and there may be interruption of adjacent vessels and bronchi.16,17
Moreover, imaging findings of risk factors may also be present as in this case interstitial lung disease for which steroids were taken. Also, conditions like alveolar proteinosis are considered to be risk factors for pulmonary nocardiosis though the reasons aren’t clear.18
In this case, typical lung parenchymal findings of nocardiosis were present like consolidations with central hypoenhancing areas and nodules. However, mediastinal lymph node enlargement was a significant feature that is said to be relatively rare in pulmonary nocardiosis in the available literature.8,14 These nodes were large, discrete as well and conglomerate, with central ill-defined low-density areas similar to the necrotic mediastinal nodes encountered in tuberculosis and malignancies. Moreover, there was a long segment of significant esophageal wall thickening which, to our knowledge, has not been previously reported in nocardiosis. These findings closely mimic tuberculosis with its known sequence of caseating mediastinal nodes which may cause the spread of inflammation into the esophagus (periesophagitis) and the adjacent bronchi (peribronchitis) giving rise to bronchesophageal fistula.19,20 In such cases, mural involvement of the esophagus can present as diffuse wall thickening mimicking malignancy. Diagnosis in such cases may be made with endoscopic ultrasound-guided biopsies which paves the way for early and effective therapy.
Another entity that should be kept in mind is tuberculosis-nocardiosis coinfection which can occur especially in patients with human immunodeficiency virus. Early suspicion of imaging in such cases significantly changes the prognosis.21
The treatment of choice for nocardiosis is trimethoprim-sulfamethoxazole, though alternative antibiotics like amikacin, tetracyclines, or ceftriaxone may be required based on severity. Surgical drainage of abscesses may also be warranted. Our patient was treated with trimethoprim-sulfamethoxazole which showed good clinical response.
Nocardiosis can virtually involve any organ system. Esophageal manifestation of nocardiosis is rare with only a few cases reported. It is a great mimicker of granulomatous diseases like tuberculosis and malignancies. Nocardiosis should always be considered in the HRCT evaluation of an immunocompromised patient. Raising an early suspicion is life-saving due to the effectiveness of early antibiotic therapy.
Informed consent was obtained from the patient for publishing.
Vishnu Appukuttan Kumari https://orcid.org/0000-0001-6631-7666
Ameer K Azeez https://orcid.org/0000-0002-9353-6562
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2. Wadhwa T, Baveja U, Kumar N, et al. Clinical manifestations of nocardiosis: study of risk factors and outcomes in a tertiary care hospital. J Lab Physicians 2017;9(4):288–295. DOI: 10.4103/JLP.JLP_111_16
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6. Ajith Kumar AK, Hegde M, Padyana M, et al. Pulmonary nocardiosis: under-diagnosed respiratory opportunistic infection – a case report. Radiol Infect Dis 2017;4(4):175–178. DOI: https://doi.org/10.1016/j.jrid.2017.11.002
13. Abdel-Rahman N, Izhakian S, Wasser WG, et al. Endobronchial enigma: a clinically rare presentation of nocardia beijingensis in an immunocompetent patient. Case Rep Pulmonol 2015;2015:970548. DOI: 10.1155/2015/970548
15. Yauba MS, Ahmed H, Imoudu IA, et al. Empyema necessitans complicating pleural effusion associated with proteus species infection: a diagnostic dilemma. Case Rep Pediatr 2015;2015:108174. DOI: 10.1155/2015/108174
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