MRIMS Journal of Health Sciences

: 2021  |  Volume : 9  |  Issue : 2  |  Page : 85--87

Allergic bronchopulmonary aspergillosis misdiagnosed as pneumonia

Tarun Kumar Suvvari1, Haider Shaik2, Bhargav Prasad Bathula2, Lakshmi Venkata Simhachalam Kutikuppala3, Sumanth Tangudu4,  
1 Dr. NTR University of Health Sciences, Vijayawada, Andhra Pradesh, India
2 Departments of Pulmonology, Konaseema Institute of Medical Sciences and Research Foundation, Amalapuram, Andhra Pradesh, India
3 Konaseema Institute of Medical Sciences and Research Foundation, Amalapuram, Andhra Pradesh, India
4 NRI Academy of Sciences, Guntur, Andhra Pradesh, India

Correspondence Address:
Dr. Tarun Kumar Suvvari
Dr. NTR University of Health Sciences, Vijayawada, Andhra Pradesh


Allergic bronchopulmonary aspergillosis (ABPA) is a fungal infection of lung predisposing in long-standing bronchial asthma and cystic fibrosis patients. Due to its similar clinical and radiological findings of other pulmonary diseases such as pulmonary tuberculosis and pneumonia, ABPA is commonly misdiagnosed. The usage of anti-tubercular drugs for ABPA is exploited due to misdiagnosis. We illustrate a case of ABPA, which was misdiagnosed to be pneumonia.

How to cite this article:
Suvvari TK, Shaik H, Bathula BP, Simhachalam Kutikuppala LV, Tangudu S. Allergic bronchopulmonary aspergillosis misdiagnosed as pneumonia.MRIMS J Health Sci 2021;9:85-87

How to cite this URL:
Suvvari TK, Shaik H, Bathula BP, Simhachalam Kutikuppala LV, Tangudu S. Allergic bronchopulmonary aspergillosis misdiagnosed as pneumonia. MRIMS J Health Sci [serial online] 2021 [cited 2021 Oct 25 ];9:85-87
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Full Text


Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction due to the colonization of the airway by Aspergillus fumigatus. Mostly, bronchial asthma and cystic fibrosis (CF) are commonly associated with ABPA. The exact prevalence of ABPA is still unknown, but according to previous research works, the prevalence of ABPA is 1%–27.5% in asthma[1] and 5%–10% in CF.[2] ABPA is characterized by increased serum IgE in type 1, increased serum IgG in Type 3 hypersensitivity along with eosinophilia, central bronchiectasis, pulmonary infiltrates, and rarely with upper lobe fibrosis.[3]

 Case Report

A 25-year-old female patient had presented with cough, breathlessness, right chest pain, loss of weight, and fatigue. She has a history of bronchial asthma since childhood with intermittent usage of the metered-dose inhaler. On general examination, clubbing was seen, and all vitals are normal. On lung auscultation, wheeze and crackles were heard, and a chest X-ray revealed periocular opacities and consolidation patches.

Noncontrast computed tomography (CT) of the chest revealed cavitating consolidation in the upper lobe of the right lung with an adjacent ground-glass opacity [Figure 1]. Centrilobular opacities [Figure 2], right lower lobe opacities [Figure 3], and central bronchiectasis [Figure 4] were seen. Bronchoceles were present in the superior and posterior basal segments of the left lower lobe along with mediastinal lymphadenopathy. The finger in the glove appearance was seen due to mucoid impactions as tubular opacities [Figure 5].{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}

Laboratory tests showed erythrocyte sedimentation rate 40 mm fall at the end of 1 h, polymorphs 24%, lymphocytes 64%, eosinophils 12%, and occasionally activated lymphocytes were seen. Tridot test, Mantoux test results were negative, and sputum was sent for Ziehl–Neelsen staining, and no acid-fast bacilli were seen indicating a negative result. She was primarily diagnosed with bilateral pneumonia, and treatment was given.

After 2 months with no subsiding of symptoms, Gene Xpert MTB-RIF Assay and MTB culture was done, but the results for both were negative. Bronchoalveolar lavage showed inflammatory cytology, and no significant change in radiographs was observed when compared with a previous chest X-ray and CT scan. Fiberoptic bronchoscopy showed secretions in the upper and lower lobes of both lungs. Pathological findings showed microscopic hypochromic anemia.

In the view of previous clinical and radiological findings, the following investigations were done. Total leukocyte count 12,000 cells/mm3, absolute eosinophil count 2400/mm3, spirometry showed moderate obstruction with significant reversibility, and total serum IgE >1000 IU/ml. The skin prick test showed positive for Aspergillus. Finally, she was diagnosed with ABPA Stage 1, and treatment was given with steroids methylprednisolone (75 mg b. d) and itraconazole, nasal spray fluticasone propionate and Symbicort (budesonide and formoterol) Turbuhaler and the patient was under medication for 6 months after the diagnosis. The methylprednisolone was tapered gradually based on the response of the patient to the therapy. The patient was followed for every 3 months, and after the 1st follow-up, there was a significant improvement in the clinical conditions of the patient and completely recovered after 6 months of medication course. Even after completely recovery, the patient was followed up further 6 months and the patient was not under any medication related to ABPA but have certain food restriction which are allergic in nature and there was no recurrence of ABPA in the patient.


ABPA is also called asthmatic pulmonary eosinophilia. Other types of bronchopulmonary aspergillosis are extrinsic allergic alveolitis, intracavitary aspergilloma, invasive pulmonary aspergillosis, chronic, and subacute pulmonary aspergillosis. A. fumigatus is the main causative organism of ABPA. With the colonization of the airway by A. fumigatus hyphae, type 1 hypersensitivity is produced with predominant T-helper cell (Th)-2 type response leading to higher serum IgE, eosinophilia, and infiltrates. In some patients, type 3 hypersensitivity is produced with increased IgG, antibiotics, and precipitin production. Blocking of bronchi with mucus plugs contains hyphae leads to inflammation of bronchial wall and thereby leads to bronchiectasis and rarely upper lobe fibrosis.[4],[5]

ABPA is clinically divided into five stages: stage 1 (acute), Stage 2 (remission), Stage 3 (reoccurrence/exacerbation), Stage 4 (steroid dependent), and Stage 5 (fibrotic lung disease).[1] ABPA patient usually presents with fever, cough, weight loss, and hemoptysis. The diagnosis of ABPA is made by Rosenberg-Patterson criteria[3] (8 major and 3 minor criteria), criteria proposed by the ISHAM working group.

The current diagnostic criteria for ABPA are as follows:

Predisposing asthma or CFObligatory criteria – IgE >1000 IU/L, immediate skin test-positive IgE antibody for AspergillusSupportive criteria – eosinophils >500, increased IgG, and fleeting opacities on chest X-ray.

The treatment given for ABPA was corticosteroids, anti-fungal drugs, anti-IgE therapy, antibiotics, along with nebulization and inhalers. The prognosis, recurrence is not well known, and more research works are to be done on this. Long-term treatment had shown a good prognosis in some of the cases.[6]


ABPA still remains unknown to most people, and the symptoms of the ABPA are similar to pneumonia and tuberculosis, so there are high chances of misdiagnosis during their 1st visit to the clinical out-patient-department. Careful history taking, high awareness, sharp clinical examination is required for the correct diagnosis of ABPA.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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