Diagnosis of Allergic Bronchopulmonary Aspergillosis: A Case-Based Approach

Sahajal Dhooria; Ritesh Agarwal

Disclosures

Future Microbiol. 2014;9(10):1195-1208. 

In This Article

What Is the Next Step in the Protocol for the Diagnosis of ABPA?

A peripheral blood eosinophil count, serum precipitins (or IgG) against A. fumigatus and a chest radiograph along with a high-resolution computed tomogram (HRCT) of the thorax should be obtained (Box 5).

Eosinophil Count

A peripheral blood eosinophil count >1000 cells/µl has been used as a threshold in the diagnosis of ABPA. However, as many as 60% of patients with ABPA present with an eosinophil count <1000 cells/µl at diagnosis, and a quarter of ABPA patients have a count lesser than 500 cells/µl.[41] Therefore, eosinophil count should not be used as a screening test for ABPA. In a recent study, the sensitivity and specificity of eosinophil count >1000 cells/µl were found to be approximately 30 and 93%, respectively, for the diagnosis of ABPA among asthmatics.[8] Due to the poor sensitivity of this cutoff, an eosinophil count >500 cells/µl is proposed as the limit in the recent diagnostic criteria.[7] One should remember that an elevation in eosinophil count may be observed in several systemic disorders including parasitic infestations, Churg–Strauss syndrome and other eosinophilic lung diseases. Further, patients receiving oral steroids (common in asthma) can have lower or normal eosinophil levels.

Serum Precipitins or Specific IgG Against A. fumigatus

A positive precipitin reaction against A. fumigatus is found in nearly 80% of patients with ABPA.[34,39] Precipitins refer to the IgG antibodies mounted against the organism, usually detected by immunoprecipitation techniques. The double gel diffusion has been the preferred method for detection of precipitins over the years.[4,37,39] Automated commercial enzyme immunoassays are now available, which have been found to be sensitive and reproducible.[42,43] It should be borne in mind that IgG antibodies are not specific for ABPA and can be seen in semi-invasive forms of aspergillosis like chronic pulmonary aspergillosis. Chronic pulmonary aspergillosis can complicate the course of ABPA,[20] and presence of constitutional symptoms, pulmonary cavities along with positive IgG (in high titres) may point toward its occurrence.[44]

Chest Radiograph

A host of abnormalities can be seen on chest radiograph in ABPA but are generally nonspecific.[45] Chest radiograph may be normal in 50% of the cases.[46] Certain radiographic features occur during acute episodes and clear up during remission.[47] They include consolidation, lobar or segmental atelectasis, band-like or toothpaste shadows, tramline shadows and gloved-finger shadows.[47,48] Serial radiographs may reveal the transient nature of these migratory infiltrates, termed as 'fleeting shadows'.[49] Permanent changes include parallel line shadows, ring shadows, generalized overinflation and localized emphysema.[47,48] Perihilar opacities representing infiltrates that surround the dilated, secretion-filled central bronchi may be seen, which can be mistaken for hilar adenopathy.[50] Toothpaste and gloved-finger shadows represent mucus impaction, tramline shadows represent bronchial wall thickening, while parallel line and ring shadows represent dilated bronchi and/or mucoid impaction. Consolidation, considered to be the most common chest radiograph finding, most often is found to represent mucus-filled bronchiectatic cavities, when imaged with an HRCT chest.[46] Chest radiographs need to be performed in all cases as they can be done during follow-up, and thus preclude the need for repeated CT scans.

Computed Tomography

Computed tomography is more sensitive than chest radiography in identification of bronchiectasis (Figure 1), and thus allows earlier detection of the onset and progression of lung damage.[51,52] HRCT of the chest is as sensitive and more acceptable than bronchography, the earlier gold standard for discernment of bronchiectasis.[53] Bronchiectasis is the most common (73–95%) abnormality seen in ABPA on CT chest along with bronchial wall thickening (95%).[39,54] Bronchiectasis may be cylindrical (less severe), varicose or cystic (considered more severe forms).[54,55] It may be central (medial half or two-thirds of the lung field, on an imaginary line drawn from the hilum to the chest wall) or may extend to the periphery (in approximately 40% of the cases).[46,56] Because of the lack of specificity of central bronchiectasis in diagnosis of ABPA,[54] and the fact that a significant proportion of patients with ABPA have 'peripheral' bronchiectasis, the term central has been removed by the recent expert group.[7] Not specific to ABPA, bronchiectasis is also seen in patients with Aspergillus-sensitized asthma, though less commonly than ABPA.[57,58] Bronchiectasis affecting three or more lobes with mucoid impaction is suggestive but not characteristic of ABPA.[54] An important HRCT finding, considered pathognomonic for ABPA, is airway plugging with high attenuation mucus (HAM).[59–63] This term is used if the mucus plug is visually denser than the normal paraspinal skeletal muscle (Figure 2).[64] The density may range from 108 to 168 Hounsfield units (HU),[13] and is attributed to the presence of calcium salts and ions of iron and manganese[65] or desiccated mucus.[66] Approximately 20% of ABPA patients demonstrate this finding on HRCT.[13] On latent-class analysis, the specificity of HAM was found to be 100%.[8] The presence of bronchiectasis and/or HAM indicate an immunologically severe disease with predisposition to recurrent relapses.[9,13,67]

Figure 1.

High-resolution computed tomography of the thorax (lung windows) demonstrating extensive areas of bronchiectasis involving the right lung.

Figure 2.

High-resolution computed tomography of the chest (mediastinal windows) demonstrating high attenuation mucus (arrow).
*The mucoid impaction is visually denser than the paraspinal skeletal muscle.

Centrilobular nodules (32–90%), tree-in-bud and mucoid impaction (70%) are commonly seen especially in the acute stage.[47] Other parenchymal abnormalities include consolidation, segmental or lobar collapse, parenchymal scarring, cavities and bullae.[56] Pleural abnormalities include thickening/fibrosis and, rarely, pneumothorax and effusion.[56,57,68,69] Uncommon findings include pulmonary masses,[70] miliary nodules,[14] aspergilloma[71] and total lung collapse.[72] HRCT of the chest is found to be normal in a third of the patients; in that case they are labeled as ABPA-S.[39,46]

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