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 Table of Contents  
Year : 2021  |  Volume : 4  |  Issue : 1  |  Page : 46-50

Pleuropulmonary aspergillosis in an immunocompetent patient presenting as pleural-based peripheral lung mass: A sporadic occurrence

1 Department of Respiratory Medicine, Apollo Hospitals, Greams Road, Chennai, Tamil Nadu, India
2 Department of Cardiothoracic Surgery, Apollo Hospitals, Greams Road, Chennai, Tamil Nadu, India

Date of Submission11-Jul-2021
Date of Acceptance20-Jul-2021
Date of Web Publication22-Sep-2021

Correspondence Address:
P Amal Johnson
Department of Respiratory Medicine, Apollo Hospitals, Chennai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/japt.japt_32_21

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The importance of knowledge about pulmonary aspergillosis has increased immensely in the era of COVID-19 as a significant number of post-COVID patients develop lung infection with aspergillosis, an entity called COVID-associated pulmonary aspergillosis producing increasing morbidity and mortality. In this case report, we describe an immunocompetent elderly man presenting with a peripheral lung mass, suspected to have lung malignancy which turned out later to be pleuropulmonary aspergillosis.

Keywords: Aspergillosis, invasive, pulmonary

How to cite this article:
Johnson P A, Narasimhan R, Narasimhan A. Pleuropulmonary aspergillosis in an immunocompetent patient presenting as pleural-based peripheral lung mass: A sporadic occurrence. J Assoc Pulmonologist Tamilnadu 2021;4:46-50

How to cite this URL:
Johnson P A, Narasimhan R, Narasimhan A. Pleuropulmonary aspergillosis in an immunocompetent patient presenting as pleural-based peripheral lung mass: A sporadic occurrence. J Assoc Pulmonologist Tamilnadu [serial online] 2021 [cited 2022 Jan 28];4:46-50. Available from: http://www.japt.com/text.asp?2021/4/1/46/326414

  Introduction Top

Aspergillosis is a spectrum of diseases caused by Aspergillus , an ubiquitous mold. The disease caused primarily is dependent on the immunity of the patient. Invasive Aspergillosis usually affects people with immunodeficiency. This case is an exception in this regard.

  Case Top

A 67-year-old gentleman from West Bengal was admitted with complaints of dry cough, streaky hemoptysis, pleuritic-type left-sided chest pain, and hoarseness of voice for the past 4 months. No history of fever/breathing difficulty/loss of weight and loss of appetite was noted. He is a nonsmoker with no history of asthma/tuberculosis (TB)/diabetes in the past. He is hypertensive for 10 years – on enalapril. Respiratory examination was unremarkable. Hemogram was normal. Blood sugar levels and HbA1c were within normal limits.

There is no past history of COVID. COVID reverse transcription polymerase chain reaction (PCR) was negative, but severe acute respiratory syndrome coronavirus 2 antibody was positive. The patient did not take vaccine, and therefore, it was considered as post-COVID status.

HIV/hepatitis B and C serology was negative.

Chest X-ray showed a left upper zone peripheral opacity [Figure 1].
Figure 1: Chest X-ray showing left upper zone peripheral opacity

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Computed tomography (CT) chest showed a 2 cm × 2 cm pleural-based peripheral lung mass [Figure 2]. Bronchoscopy was done for further evaluation of hemoptysis and hoarseness of voice. Vocal cord movements were normal. No active bleeding was noted. All endobronchial orifices were free. Bronchoalveolar lavage (BAL)/bronchial brush from Left upper lobe (LUL) was negative for bacteriology, GeneXpert MTB, fungal stain, and cytology [Figure 3]. CT-guided biopsy was done from LUL peripheral mass [Figure 4]. CT-guided biopsy histopathological examination showed fibroblastic proliferation with plasma cell-rich inflammatory cellular infiltrates and patchy xanthogranulomatous reaction. CT-guided biopsy material was negative for bacteriology and GeneXpert MTB.
Figure 2: Compute tomography chest showing LUL pleural-based mass

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Figure 3: Bronchoscopy showing LUL bronchus brushing

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Figure 4: Computed tomography guided lung biopsy from LUL mass

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In view of persisting hemoptysis and inconclusive diagnosis so far, we went ahead and performed video-assisted thoracic surgery excision of mass along with wedge resection of LUL, which was adherent to the mass. Postoperative was uneventful and implantable cardioverter defibrillators removed on day 3 [Figure 5].
Figure 5: Postvideo-assisted thoracic surgery wedge resection from

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Open lung biopsy histopathological examination

At the interface of lung and pleura, there is an area of necrosis and suppuration within which are seen several branching septate forms of fungus, consistent with the morphology of Aspergillus surrounded by inflammation. Periodic acid–Schiff stain confirms the presence of fungal organisms [Figure 6].
Figure 6: HPE showing septate fungus with necrotising inflammation

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  • Pleuropulmonary aspergillosis.


  • After discussion with infectious diseases specialist, he was started on oral voriconazole 400 mg twice daily on day 1 followed by 200 mg twice daily for 6 weeks
  • We could not process the sample for fungal stain and fungal culture later as the surgical team sent the complete sample in a formalin container for processing. This is a take home message for us to intimate the surgical staff preprocedure for preserving part of sample in normal saline for bacteriology and fungal testing in cases of inconclusive diagnosis
  • ENT opinion was obtained for hoarseness of voice, and angiotensin-converting enzyme inhibitors were attributed as the cause. After change of antihypertensives, the symptom resolved.

  Discussion Top

The spectrum of pulmonary aspergillosis depends upon the immune status and underlying lung architecture [Table 1].
Table 1: EORTC/MSG criteria

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Aspergillus is one of the most common causes of infectious death in immunocompromised patients. Following inhalation of the Aspergillus conidia, invasive pulmonary aspergillosis (IPA) pathogenesis begins. Damage to the respiratory epithelium because of radiation therapy, chemotherapy, graft versus host disease, or infection facilitates attachment of Aspergillus conidia to the respiratory epithelium. Once invaded, Aspergillus progressively produces disease due to lymphopenia and dysregulated Th1 response.[1]

Clinical features

The symptoms include fever, cough with or without sputum, pleuritic chest pain, hemoptysis in patients having cavity and angioinvasive disease. IPA should be suspected in immunocompromised patients having clinically nonresponding pneumonia with broad-spectrum antibiotics. Extrapulmonary sites may also be involved in severe forms such as mucormycosis.[2]

Pleuropulmonary aspergillosis was first mentioned in Cleland in 1924, and it is still an uncommon presentation. The possible pathophysiology is through damage of pulmonary immunity by chronic infections such as TB. It usually presents as pleural effusion/empyema. It is not more common in immunocompromised patients unlike pulmonary form.[3]


Classical radiological finding would be a nodule surrounded by ground-glass opacity called “halo sign.” This sign correlates with early infection where the hemorrhage and edema surround an infarct caused by thrombosis.

The air crescent sign seen in angioinvasive aspergillosis is usually seen during the period of convalescence 2–3 weeks after the initiation of treatment.[4]


Respiratory cultures of Aspergillus from expectorated sputum, bronchial washings, or BAL specimens have low sensitivity (<30%) for diagnosing IA but a high positive predictive value (>60%) in heavily immunocompromised patients. Blood cultures have little diagnostic value.[5]

Aspergillus has a cell wall component called “galactomannan” which is released into the blood during fungal growth in tissues. A sandwich enzyme-linked immunosorbent assay capable of detecting galactomannan at concentrations as low as 0.5 ng/ml has been developed recently. The sensitivity of the test ranges from 67% to 100% and specificity ranges from 86% to 99%. False-positive results have been described in patients receiving β-lactam antibiotics, particularly piperacillin-tazobactam. A colorimetric assay for the detection of 1,3-β-D-glucan, an integral cell-wall component in a number of pathogenic yeasts and filamentous fungi, is commercially available. The sensitivity and specificity rates for this test range from 67% to 100% and from 84% to 100%, respectively. False-positive test results have been reported in patients with cirrhosis, those undergoing hemodialysis, receiving chemotherapy with particular agents, and patients following abdominal surgery.[1]

Treatment options

Until recently, amphotericin B (AMB-D) was the only drug available for the treatment of aspergillosis. A major obstacle to evaluating the merit of antifungal therapy for IPA was the difficulty in establishing the diagnosis; hence, most patients received empirical treatment. The recent introduction of uniform diagnostic criteria for proven, probable, and possible IA by the European Organization for Research and Treatment of Cancer/Mycoses Study Group[5] [Table 2] consortium has been a major advance. These criteria are practical, validated, standardized, and reproducible and consist of host-risk, microbiological, clinical/radiological, PCR, and/or galactomannan antigen criteria.
Table 2: Clinical manifestations of Aspergillosis

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Recently, the broad-spectrum triazole voriconazole was introduced for therapy for aspergillosis. It is available in both intravenous and oral preparations and is much better tolerated than AMB-D [Table 3]. Caspofungin is one of a new class of antifungal agents (echinocandins) that inhibit the synthesis of 1,3-β-D-glucan, an essential component of the cell wall of many fungi. It is available only in an intravenous preparation. The lack of an effective treatment modality for aspergillosis has made the concept of combination therapy theoretically appealing. To date, no clinical studies have convincingly determined whether antifungal combinations are more beneficial than monotherapy for aspergillosis.[6],[7]
Table 3: Formulations, dosage and adverse effects of drugs for Aspergillosis

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  Conclusion Top

Invasive pulmonary fungal infection has varied presentation, and though quite rare in immunocompetent individuals, it should be always in the possibility when sequestered infection is suspected.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

  Acknowledgment Top

Thanks to the Department of Respiratory Medicine, Apollo Hospitals, Chennai.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Grippi MA, Elias JA, Fishman JA, Kotloff RM, Pack AI, Senior RM, et al. Fishman's Pulmonary Diseases and Disorders. 5th ed. New York: McGraw-Hill Medical; 2015.  Back to cited text no. 1
Brandt ME, Warnock DW. Epidemiology, clinical manifestations and therapy of infections caused by dematiaceous fungi. J Chemother 2003;15:S36-47.  Back to cited text no. 2
Bhatnagar T, Bhatnagar A. Pleural aspergillosis in an otherwise healthy individual. Lung India 2014;31:155.  Back to cited text no. 3
[PUBMED]  [Full text]  
Blot SI, Taccone FS, Van den Abeele AM, Bulpa P, Meersseman W, Brusselaers N, et al. AspICU Study Investigators. A clinical algorithm to diagnose invasive pulmonary aspergillosis in critically ill patients. Am J Respir Crit Care Med 2012;186:56-64.  Back to cited text no. 4
De Pauw B, Walsh TJ, Donnelly JP, Stevens DA, Edwards JE, Calandra T, et al. Revised definitions of invasive fungal disease from the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group (EORTC/MSG) Consensus Group. Clin Infect Dis 2008;46:1813-21.  Back to cited text no. 5
Herbrecht R, Denning DW, Patterson TF, Bennett JE, Greene RE, Oestmann JW, et al. Voriconazole versus amphotericin B for primary therapy of invasive aspergillosis. N Engl J Med 2002;347:408-15.  Back to cited text no. 6
Kontoyiannis DP, Bodey GP. Invasive aspergillosis in 2002: An update. Eur J Clin Microbiol Infect Dis 2002;21:161-72.  Back to cited text no. 7


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]

  [Table 1], [Table 2], [Table 3]


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