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CASE REPORT  
Year : 2017  |  Volume : 60  |  Issue : 2  |  Page : 285-287
A case of Aspergillus tracheobronchitis in a patient with chronic obstructive pulmonary disease


Department of Respiratory Medicine, Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Jiang'an, Wuhan, China

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Date of Web Publication19-Jun-2017
 

   Abstract 

Aspergillus tracheobronchitis (AT) is a unique form of invasive pulmonary aspergillosis, which is commonly found in patients with impaired immunity. Early-stage AT presents in a nonspecific way, both clinically and radiographically, thereby delaying diagnosis and resulting in a high mortality. Owing to impaired mucociliary clearance, previous nonfungal infections, and administration of corticosteroids, among other aspects, patients with chronic obstructive pulmonary disease (COPD) are predisposed to AT, although they are mostly immunocompetent. AT in COPD patients has not been well recognized and the condition is often misdiagnosed or missed. We herein report a case of AT diagnosed in a male with past COPD, with the features of pseudomembranous AT upon bronchoscopy. This contradicts the opinion that pseudomembranous AT is found in severely immunocompromised hosts with hematologic malignancies.

Keywords: Dyspnea, aspergillosis, Aspergillus tracheobronchitis, chronic obstructive pulmonary disease

How to cite this article:
Yuan ML, Yang G, Hu HL, Yin W, Tan WJ, Zhao S. A case of Aspergillus tracheobronchitis in a patient with chronic obstructive pulmonary disease. Indian J Pathol Microbiol 2017;60:285-7

How to cite this URL:
Yuan ML, Yang G, Hu HL, Yin W, Tan WJ, Zhao S. A case of Aspergillus tracheobronchitis in a patient with chronic obstructive pulmonary disease. Indian J Pathol Microbiol [serial online] 2017 [cited 2020 Feb 21];60:285-7. Available from: http://www.ijpmonline.org/text.asp?2017/60/2/285/208384



   Introduction Top


Aspergillus tracheobronchitis (AT) accounts for ≤5% of cases of invasive pulmonary aspergillosis (IPA), mainly involves the trachea and bronchi, and is commonly seen in patients with impaired immunity,[1],[2] while seldom seen in immunocompetent populations. The diagnosis of AT is usually delayed because of its nonspecific clinical presentation and the lack of radiographic findings in the early stages, which results in a high mortality rate.[3] Reports on this condition have gradually accumulated, revealing the characteristics of AT in immunocompromised patients, but few studies have focused on patients without markedly impaired immunity. We herein report a case of AT in an immunocompetent male with a history of chronic obstructive pulmonary disease (COPD).


   Case Report Top


A 68-year-old male smoker with a 5-year history of COPD and a 3-year history of coronary heart disease was admitted to our department because of exacerbation of dyspnea for 2 days. The patient had regularly inhaled salmeterol (50 μg) and fluticasone (500 μg) for 2 years, and over the past 1 year frequently received intravenous corticosteroids and antibiotics for the “exacerbation of COPD” in a community hospital. Vital signs on admission were as follows: temperature, 37.1°C; heart rate, 113 beats/min (regular); blood pressure, 137/85 mm Hg; respiratory rate, 24 breaths/min; and oxygen saturation, 90% while on 40% oxygen. Wheezing and moist rales were heard bilaterally upon physical examination. Laboratory tests showed a white blood cell count of 8530/mL (86% neutrophils and 8.6% lymphocytes); hemoglobin level of 14.3 g/dL; platelet count of 242,000/mL; C-reactive protein level of 10.4 mg/dL; and negative sputum culture. The results for serum (1 → 3)-β-D-glucan, renal function, electrolytes, liver enzymes, and coagulation studies were within normal limits. Chest computed tomography (CT) revealed thickening and stenosis of the right main bronchus [Figure 1]a, right intermediate bronchus [Figure 1]b, and right lower bronchus [Figure 1]c.
Figure 1: Computed tomography of the chest revealing thickening and stenosis of the right main bronchi (a), the right intermediate bronchus (b), and the right lower bronchus (c)

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Bronchoscopy was subsequently performed which revealed severe inflammation, ulceration, necrosis, and pseudomembranous lesions of the bronchial mucosa, and particularly the right bronchus: white necrotic pseudomembranes partly obstructed the right main bronchus [Figure 2]a and the lower bronchus. Therapeutic bronchoscopy was performed with aspiration of the necrotic mass and balloon dilation of the narrowed lumen. Hematoxylin and eosin staining of bronchial biopsy specimens revealed diffuse ulcerative inflammatory tracheobronchitis associated with fungal hyphae with superficial mucosal invasion, and the septate and branching fungal hyphae were consistent with the features of Aspergillus [Figure 2]b. Thus, voriconazole was used, with 6 mg/kg intravenously for every 12 h as a loading dose on the 1st day, and 400 mg/day as a maintenance dose; in the meantime, voriconazole (200 mg dissolved in 20 mL saline, twice a week, for 1 week) was administrated through local intraluminal instillation. After treatment with voriconazole for 2 weeks, the respiratory symptoms of the patient gradually improved, moreover bronchoscopy showed that the necrotic pseudomembranes in the right bronchus were reduced and that stenosis was relieved [Figure 2]c. The patient was discharged at his request and was instructed to take oral voriconazole sequentially at home.
Figure 2: A mass of white pseudomembranes consisting of necrotic epithelium and endobronchial mucus adhered on the right main bronchus, partly blocking the right bronchus, moreover the mucosa appeared was swollen, reddened, ulcerative, and even bleeding (a). Hematoxylin and eosin staining of bronchial biopsy specimens revealing diffuse ulcerative inflammatory tracheobronchitis associated with fungal hyphae with superficial mucosal invasion (b) (×100), and inset showing septate and branching fungal hyphae consistent with the features of Aspergillus (×400). Compared with those observed in Figure 2a, white pseudomembranes were obviously reduced in the right main bronchus (c) accompanied with enlargement of the lumen

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   Discussion Top


Aspergillus is typically found in immunocompromised populations, because of the impaired immune function of their polymorphonuclear neutrophils and macrophages, but it was not immediately clear why our patient with COPD was predisposed to AT. We consider that impaired mucociliary clearance, previous nonfungal infections, corticosteroid administration (either inhaled or systemic), and prolonged antibiotics use may have accounted for the invasion of bronchial mucosa by Aspergillus hyphae after spores had colonized the respiratory tract.[4],[5]

AT causes acute exacerbation and respiratory failure in up to 5% of critically ill COPD patients admitted to the intensive care unit;[6] however, AT is often misdiagnosed or missed in COPD patients owing to the following factors. The clinical presentation of AT is nonspecific and includes fever, dyspnea, cough, wheezing, or hemoptysis. The diagnostic value of serum galactomannan or (1 → 3)-β-D-glucan in AT is far from being confirmed,[7] although galactomannan measurement in bronchoalveolar lavage fluid (BALF) may slightly elevate diagnostic sensitivity.[8] Unfortunately, the restrictions of our laboratory did not allow us to evaluate galactomannan in serum or BALF. The chest radiograph and CT scan of patients with AT are commonly negative, although occasionally nonspecific findings, such as atelectasis, bronchial wall thickening, or pulmonary infiltrates may be seen on CT images. In addition, AT may be the early stage of IPA; when the invasion has progressed to the distal airway and lung parenchyma, AT may present concurrently with IPA.[6] Thus, we speculate that findings on CT scans may be dependent on the stage of AT.

Bronchoscopy remains the most important diagnostic modality for AT. It allows the direct visualization of endobronchial lesions and the collection of specimens. Based on the bronchoscopic or pathologic appearance, three different invasive forms of tracheobronchial Aspergillus have been described: AT, ulcerative AT, and pseudomembranous AT, the subtypes are characterized by evidence of bronchial and/or tracheal inflammation and excessive mucus production without invasion of the bronchial mucosa on biopsy; the presence of variable, ulcerative, or plaque-like lesions in the bronchial walls or extensive involvement of the lower airways, respectively. The latter is associated with sloughing of necrotic epithelium, which, together with endobronchial mucus, forms the pseudomembranes overlying the mucosal surface.[9] It should be noted that the morphological appearance of airway aspergillosis may easily change and that different forms of Aspergillus-related invasive airway involvement may coexist. Based on pseudomembranous AT, the other two forms concurrently present in our case, contradicting the opinion that pseudomembranous AT is typically found in severely immunocompromised hosts with hematologic malignancies.[7]

Voriconazole is recommended as the initial therapy in the treatment of AT, and local therapeutic aspiration, recanalization, or topical application of antifungal drugs through bronchoscopy also play an important role in the therapy of AT, particularly pseudomembranous AT. The prognosis seems to be largely dependent on the underlying disease: patients who had nonmalignant underlying diseases had better prognosis.

In conclusion, AT, including pseudomembranous AT, is not only confined to severely immunocompromised hosts, more attention should be paid to this diagnosis in COPD patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Fernández-Ruiz M, Silva JT, San-Juan R, de Dios B, García-Luján R, López-Medrano F, et al. Aspergillus tracheobronchitis: Report of 8 cases and review of the literature. Medicine (Baltimore) 2012;91:261-73.  Back to cited text no. 1
    
2.
Grosu HB, Bashoura L, Ost D, Ordonez NG, Faiz SA. Critical airway obstruction due to pseudomembranous Aspergillus tracheitis. Am J Respir Crit Care Med 2014;190:e65-6.  Back to cited text no. 2
    
3.
Karnak D, Avery RK, Gildea TR, Sahoo D, Mehta AC. Endobronchial fungal disease: An under-recognized entity. Respiration 2007;74:88-104.  Back to cited text no. 3
    
4.
Wu N, Huang Y, Li Q, Bai C, Huang HD, Yao XP. Isolated invasive Aspergillus tracheobronchitis: A clinical study of 19 cases. Clin Microbiol Infect 2010;16:689-95.  Back to cited text no. 4
    
5.
Putnam JB Jr., Dignani C, Mehra RC, Anaisse EJ, Morice RC, Libshitz HI. Acute airway obstruction and necrotizing tracheobronchitis from invasive mycosis. Chest 1994;106:1265-7.  Back to cited text no. 5
    
6.
He H, Jiang S, Zhang L, Sun B, Li F, Zhan Q, et al. Aspergillus tracheobronchitis in critically ill patients with chronic obstructive pulmonary diseases. Mycoses 2014;57:473-82.  Back to cited text no. 6
    
7.
Krenke R, Grabczak EM. Tracheobronchial manifestations of Aspergillus infections. ScientificWorldJournal 2011;11:2310-29.  Back to cited text no. 7
    
8.
Husain S, Paterson DL, Studer SM, Crespo M, Pilewski J, Durkin M, et al. Aspergillus galactomannan antigen in the bronchoalveolar lavage fluid for the diagnosis of invasive aspergillosis in lung transplant recipients. Transplantation 2007;83:1330-6.  Back to cited text no. 8
    
9.
Denning DW. Commentary: Unusual manifestations of aspergillosis. Thorax 1995;50:812-3.  Back to cited text no. 9
    

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Correspondence Address:
Su Zhao
Department of Respiratory Medicine, Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, 26 Shengli Street, Jiang'an, Wuhan 430014
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_248_16

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1 Antibiotics/corticosteroids/fluticasone propionate
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