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 Table of Contents  
Year : 2020  |  Volume : 8  |  Issue : 2  |  Page : 106-109

A case of chronic cavitory pulmonary aspergillosis, a rare entity

Department of Pulmonary Medicine, Medical College, Kolkata, India

Date of Submission11-Jan-2020
Date of Acceptance10-Jun-2020
Date of Web Publication10-Sep-2020

Correspondence Address:
Dr. Sibes Kumar Das
MD (Pulmonary Medicine), Professor, Souhardya Appartment, West Bankim Pally, Madhyamgram, Kolkata-700129
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jacp.jacp_2_20

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Aspergillus species cause a wide spectrum of pulmonary disease including allergic, saprophytic, semi-invasive and invasive aspergillosis. Host immune system is the major determinant of the pattern of illness in human beings. Several chronic forms of Aspergillus infections have been described which include chronic cavitary pulmonary aspergillosis (CCPA), chronic fibrotic pulmonary aspergillosis (CFPA) and chronic necrotizing pulmonary aspergillosis (CNPA). Chronic cavitary pulmonary aspergillosis usually runs a progressive course, affects apparently immunocompetent individuals with a pre-existing lung disease. Diagnosis depends on presence of constitutional and pulmonary symptoms, suggestive radiological changes and microbiological or serological evidence of Aspergillus infection. We hereby present a case of 28 years immunocompetent male who had prior history of pulmonary tuberculosis and was subsequently diagnosed as chronic cavitary pulmonary aspergillosis.

Keywords: Aspergillus, chronic cavitary pulmonary aspergillosis, itraconazole

How to cite this article:
Das SK, Ghosh S, Sasmal G. A case of chronic cavitory pulmonary aspergillosis, a rare entity. J Assoc Chest Physicians 2020;8:106-9

How to cite this URL:
Das SK, Ghosh S, Sasmal G. A case of chronic cavitory pulmonary aspergillosis, a rare entity. J Assoc Chest Physicians [serial online] 2020 [cited 2023 Jan 27];8:106-9. Available from: https://www.jacpjournal.org/text.asp?2020/8/2/106/294583

  Introduction Top

Among the different species of Aspergillus, Aspergillus fumigatus is the most common and most pathogenic due to its ubiquitous nature and residence in the environment. Chronic pulmonary aspergillosis (CPA) is uncommon but problematic pulmonary disease. The uncommon form of CPA is CCPA which is characterised by formation and expansion of multiple cavities with or without fungal ball within the cavities.[1] Pulmonary TB, non tuberculous mycobacterial infection, chronic obstructive pulmonary disease and previous thoracic surgery are the common underlying diseases.[2] Few cases of CCPA progress to marked pulmonary fibrosis which is termed as chronic fibrosing pulmonary aspergillosis (CFPA). A third subtype is progressive enlargement of a single cavity, mostly with a thin wall, occurring relatively rapidly within 3 months. This group probably has a slowly progressive invasive disease and is called CNPA or subacute invasive aspergillosis (SAIA) or semi-invasive pulmonary aspergillosis. It resembles CCPA but is characterised by rapid progression (<3 months) and presence of mild to moderate degree of immunosuppression like diabetes mellitus or prolonged corticosteroid use.

  Case report Top

A 28 years old non smoker, non diabetic male was admitted with complaints of persistent dry cough and intermittent mild haemoptysis for last 1 year. He also had leftsided chest pain referred to back of left chest wall along with significant weight loss (12 kg) in last 3 months. He had history of hospitalisation for massive hemoptysis six months ago. He had no history of fever, shortness of breath, wheezing or bleeding from any other site. He had past history of microbiologically confirmed pulmonary tuberculosis 5 years back, for which he had taken full course of antituberculous drug for 6 months and was declared cured at the end of treatment. On general examination, he had digital clubbing and vitals were normal. Respiratory system examination revealed cavernous bronchial breath sound, increased vocal resonance and coarse crackles in right and left upper interscapular areas. Examination of the other systems revealed no abnormality. Routine blood examination revealed presence of anaemia (Hb=8 g/dl) with normal total and differential leucocytic count with normal liver function tests and electrolytes. Fasting plasma glucose was 94 mg/dl. Blood for HIV 1 and 2 antibody was nonreactive. Urinalysis was normal. Chest X-ray PA view done at the end of anti-tuberculosis therapy showed presence of a residual cavity in left mid zone [Figure 1]. Recent chest X-Ray PA view revealed presence of thick-walled cavities in right and left middle zones [Figure 2]. Contrast-enhanced CT scan of thorax revealed presence of thick-walled cavities in right middle lobe (5 × 3 cm2) and left lingular lobe (6 × 5 cm2) without any fluid or fungal ball within the cavities [Figure 3]. Induced sputum was negative for acid fast bacilli. Fibre optic bronchoscopy revealed frothy secretion coming out from medial segment of right upper lobe. Bronchoalveolar lavage fluid for gram stain and culture, Zeihl Neelsen stain and fungal stain did not reveal any organism. Blood for total serum IgE was 140 UI/ml and absolute eosinophil count were within normal limit 102 cells/microliter. Serum Aspergillus fumigatus specific IgE antibody was within normal limit (0.25 kUA/L) and Aspergillus fumigatus specific IgG antibody was high(38 mgA/L). SerumGalactomannan assay was within normal limit (0.45 index). Thus he was diagnosed as a case of CCPA with background of healed pulmonary tuberculosis. He was put on tablet itraconazole 200mg twice daily. Follow up visit after one month showed symptomatic improvement.
Figure 1 Chest X-ray PA view done at the end of anti tuberculosis therapy showed presence of a residual cavity in left mid zone

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Figure 2 Recent chest X-Ray PA view revealed presence of cavities in right and left middle zones

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Figure 3 Contrast-enhanced CT scan of thorax revealed presence of thick-walled cavities in right middle lobe(5 cm × 3 cm) and left lingular lobe(6 cm × 5 cm) without any fluid or fungal ball within the cavities

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  Discussion Top

The diagnostic criteria for CCPA includes[1]:
  1. One or more pulmonary cavities with this a thick wall, sometimes containing aspergilloma or irregular intramural material.
  2. Serological or microbiological evidence implicating Aspergillus species.
  3. Significant systemic and/or pulmonary symptoms.
  4. Overt radiological progression like new cavities, increasing pericavitary infiltrates.
  5. Present for at least 3 months of observation.

Our patient had multiple pulmonary cavities with thick walls without any intracavitary fungal ball, serological evidence of aspergillus infection (Positive Aspergillus fumigatus specific IgG), systemic and pulmonary symptoms, new cavity formation in subsequent x-rays and total duration of illness more than 3 months.

CCPA should be differentiated from other two variants of CPA. This distinction is not absolute but depends on the dominant clinical and radiological manifestations. CFPA is described as severe fibrotic destruction of two or more lobes of lung complicating CCPA leading to a major loss of lung function.[3] Absence of fibrosis in two or more lobes in CT scan thorax in our case excluded CFPA as a diagnosis in our case. SAIA is a form of invasive aspergillosis occurring in mildly immunocompromised patients (malnutrition, chronic granulomatous disease, diabetes mellitus, alcoholism or prolonged corticosteroid therapy) over 1-3 months with variable radiological features like cavitation, nodules and consolidation. Biopsy shows hyphae in invading lung tissue and microbiological investigation reveals positive aspergillus galactomannan antigen in blood or respiratory fluids. Absence of immunosupression, duration of illness more than 3 months and absence of radiological changes other than cavitation goes against the diagnosis of SAIA.

Acute invasive pulmonary aspergillosis (IPA) occurs in highly immunocompromised patients like profound neutropenia or following transplantation. Absence of gross immunosupression and duration of illness for more has 1 month excluded acute IPA.

Cavities in the lung in a patient of CCPA may have concomitant infection with Streptococcus pneumonia, Hemophilus influenza, Staphylococcus aureus etc. They should be treated along with CCPA.[1] Mycobacterial infection is an important differential diagnosis for CPA and either a pulmonary tuberculosis or nontuberculous mycobacterial infection may precede, follow or occasionally occur simultaneously with CCPA.[1] Sputum for AFB smear, nucleic acid amplification test (NAAT) or culture are important investigations in a patient of suspected CCPA. Our patient did not have any microbiological evidence of pulmonary tuberculosis. However diagnosing Mycobacterial diseases does not exclude CPA. Other possible diseases that should be excluded include cavitary lung cancer, pulmonary infarct, vasculitides and rheumatoid nodule.

Detection of aspergillus specific IgG is a key diagnostic feature of CPA, which is helpful to differentiate between infection and colonisation. It is 80–96% sensitive and about 85% specific.[4] Antibody titre has little relationship to the severity or extent of disease. The titre slowly falls with successful antifungal therapy and sharply rising titre is a sign of therapeutic failure or relapse.

Oral itraconzole therapy is now standard of care of CCPA.[5] Voriconazole can be considered as a primary therapy or following itraconazole (because of failure or side effects).[6] Response to antifungal therapy is slow but most respond by 6 months. So minimal 4-6 months therapy is recommended initially.[6] Those who respond sub optimally should have extended period of treatment for 9 months. Patient who deteriorates should be offered alternative treatment including intravenous Echinocandins orAmphotericin B.[7],[8]In conclusion, though uncommon, CCPA is serious pulmonary disease. It clinically mimics pulmonary tuberculosis. In any patient presenting with pulmonary cavities, possibilities of CCPA should be considered and thoroughly investigated, especially if other causes are excluded.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Denning DW, Cadranel J, Beigelman-Aubry C et al. Chronic pulmonaryaspergillosis: rationale and clinical guidelines for diagnosisand management. Eur Respir J 2016;47:45-68.  Back to cited text no. 1
Maghrabi F, Denning DW. The management of chronic pulmonary aspergillosis: The UK National Aspergillosis Centre Approach. Curr Fungal Infect Rep 2017;11:242-51.  Back to cited text no. 2
Kosmidis C, Newton P, Muldoon EG, Denning DW. Chronicfibrosing pulmonary aspergillosis: a cause of “destroyed lung” syndrome. Infect Dis 2017;49:296-301.  Back to cited text no. 3
Richardson MD, Page ID. Aspergillus serology: have we arrived yet? Med Mycol 2017;55:48-55.  Back to cited text no. 4
Agarwal R, Vishwanath G, Aggarwal AN, Garg M, Gupta D, Chakrabarti A. Itraconazole in chronic cavitary pulmonary aspergillosis:a randomised controlled trial and systematic review of literature. Mycoses 2013;56:559-70.  Back to cited text no. 5
Felton TW, Baxter C, Moore CB, Roberts SA, Hope WW, Denning DW. Efficacy and safety of posaconazole for chronic pulmonary aspergillosis. Clin Infect Dis 2010;51:1383-91.  Back to cited text no. 6
Newton PJ, Harris C, Denning DW. The clinical response to a short-term course of intravenous liposomalamphotericin B therapy in patients with chronic pulmonary aspergillosis. Mycosis 2013;56:164.  Back to cited text no. 7
Kohno S, Izumikawa K, Ogawa K, Kurashima A, Okimoto N, Amitani R et al. Intravenous micafungin versus voriconazole for chronic pulmonaryaspergillosis: a multicenter trial in Japan. J Infect 2010;61:410-8.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]


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