Diagnostic performance of Aspergillus-specific immunoglobulin G immunochromatographic and enzyme-linked immunosorbent assay testing in chronic pulmonary aspergillosis: comparative analysis across subtypes and influencing factors

Introduction

Chronic pulmonary aspergillosis (CPA), caused by various pathogenic species of the filamentous fungal genus Aspergillus, is a slowly progressive syndrome characterised by cavitating pulmonary consolidation, fibrosis, and the destruction of normal lung parenchymal tissues (1,2). CPA is usually diagnosed in individuals with chronic lung disease, particularly those with a history of pulmonary Mycobacterium tuberculosis (MTB) infection (3-5). Unlike invasive aspergillosis (IA) which predominantly affects immunocompromised individuals (e.g., those with neutropenia or chronic granulomatous disease), CPA patients are typically immunocompetent (6). CPA encompasses several distinct radiological and clinical forms: Aspergilloma (fungal ball), sub-acute (or chronic) necrotising pulmonary aspergillosis, Aspergillus nodule(s) (AN) often co-existing with rheumatoid lung disease, chronic cavitary pulmonary aspergillosis (CCPA), and chronic fibrosing pulmonary aspergillosis (CFPA) (7). While specific risk factors exist for subtypes [e.g., residual MTB cavitation for aspergilloma; hyper-immunoglobulin E (IgE) syndrome for CCPA], overlapping presentations with more than one form of the disease within patients are common (8-10).

CPA diagnosis relies on a composite of clinical symptoms, thoracic radiology, and laboratory findings, including mycological culture, fungal biomarkers, and serum Aspergillus-specific immunoglobulin G (IgG) (1,2,11). However, mycological culture exhibits low sensitivity, and specialized serological assays can be cost-prohibitive (12). This underscores the critical role of fungal biomarkers in CPA, especially in resource-limited settings with constrained access to mycological expertise and laboratory infrastructure (8). Consequently, point-of-care tests (POCTs) for CPA diagnosis are gaining significant interest. While studies have explored Aspergillus-specific IgG for CPA diagnosis (13-17), their impact is limited by small cohorts and inadequate analysis across subtypes/disease severity. Crucially, no study has directly compared the diagnostic performance of the Aspergillus-specific IgG immunochromatographic POCT (ICT-POCT) and enzyme-linked immunosorbent assay (ELISA) within the context of CPA disease characteristics. In this study, we outline the diagnostic performance of Aspergillus-specific IgG ICT vs. laboratory ELISA for diagnosing CPA within the context of disease severity and subtype. We present this article in accordance with the STARD reporting checklist (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-110/rc).

Methods

Study population

The retrospective study recruited patients with CPA from the clinics of the Respiratory Department of The First Affiliated Hospital of Guangzhou Medical University between December 2021 and November 2022. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China (Medical Ethics Approval 2021 [No. 51]). All patients were recruited with written informed consent. Age- and sex-matched patients with non-CPA pulmonary disease were co-recruited as controls. CPA cases diagnosis according to the European Society of Clinical Microbiology and Infectious Diseases (ESCMID)/European Respiratory Society (ERS) guidelines (18). In brief, CPA was defined in accordance with the composite case-definition (incorporating symptomatic, radiological and microbiological features) and exclusion of alternative diagnoses [such as lung cancer, MTB and nontuberculous mycobacteria (NTM)], reflecting the current consensus guidelines (8,18,19): (I) persistent thoracic radiographic abnormalities consistent with CPA, including consolidation, nodules (with or without cavitation) or the presence of a fungal ball; (II) at least 3 months of pulmonary symptoms (e.g., cough, sputum, hemoptysis, dyspnea); (III) mycological evidence including sputum, lung biopsy or bronchoalveolar lavage (BAL) fluid culture yielding Aspergillus spp and/or a positive BAL galactomannan (GM) index by competitive ELISA (Dynamiker Biotechnology Co., Ltd., Tianjin, China) greater than or equal to 1.0 and/or positive serum Aspergillus-specific IgG (Phadia, ImmunoCAP, Thermo Fisher Scientific, Waltham, MA, USA); and (IV) histological or cytopathological evidence, including the presence of Aspergillus-like hyphae in lesions identified in lung biopsy or lobectomy specimens. CPA diagnosis was confirmed in each patient following review by two experienced specialist clinicians independently.

Aspergillus-specific IgG testing

Whole-blood samples were transferred to the laboratory immediately after venipuncture. Following refrigerated centrifugation (1,000 to 2,000 g for ten minutes), serum was aliquoted manually for immediate testing. Where immediate testing was not possible, serum aliquots were frozen immediately to −80 ℃ after centrifugation for later testing.

All serum samples were assayed for Aspergillus-specific IgG by ImmunoCAP (Phadia ImmunoCAP™ system, Thermo Fisher Scientific), quantitative ELISA (Dynamiker Biotechnology Co., Ltd.), and by an ICT-POCT (Aspergillus ICT IgG-IgM Lateral Flow Assay, LDBio Diagnostics, Lyon, France), all performed according to the manufacturer’s instructions.

Serum levels of Aspergillus fumigatus-specific IgG antibodies were quantified for all samples using the Dynamiker Aspergillus fumigatus IgG assay, following the manufacturer’s protocol. Briefly, serum samples were incubated in antigen-precoated microplate wells, allowing specific antibodies to bind. After washing to remove unbound antibodies, bound IgG was detected using a protein A-alkaline phosphatase conjugate. Following a second wash to remove unbound conjugate, optical density (OD) was measured with a microplate reader. An Aspergillus IgG concentration of ≥120 arbitrary units per milliliter (AU/mL) was designated positive; <80 AU/mL as negative; and between 80 and 120 AU/mL as intermediate—in keeping with other published data (20).

ICT-POCT was performed per manufacturer’s instructions. Following cartridge acclimation to room temperature, 15 µL of serum was applied to the sample port, followed immediately by four drops of elution buffer. Results were interpreted visually after a 30-minute incubation period. Test positivity was defined by the presence of both a blue control line and a black test line (any intensity), while a single blue control line indicated a negative result (21,22).

BAL fluid (BALF) was also assayed for Aspergillus GM by sandwich ELISA (Dynamiker Biotechnology Co., Ltd.), using an index value of 1.0 as the negative cut-off (23).

Statistical analysis

Data analysis was undertaken using R (v4.2.1). For the comparisons between the CPA group and the disease control group, the Wilcoxon rank sum test was applied in the continuous variable of age, Chi-squared test or Fisher’s exact test was applied in categorical variables. For the accuracy of diagnosis, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were computed by the R package epiR (v2.0.75), and their 95% confidence intervals (CIs) were estimated by Wilson’s confidence limits. The analysis of receiver operating characteristic (ROC) curve was performed by the R package pROC (v1.18.0) (24), and 95% CI of the area under the curve (AUC) was estimated by the DeLong method.

Results

Study profile and patient characteristics

A total of 112 patients with a CPA diagnosis (cases) and 61 controls were included in the final analysis. The characteristics and co-morbidities within the study population are outlined in Table 1. A breakdown of the CPA subtypes diagnosed among the cases is outlined in Table 2.

In 7 (6%) cases, all four diagnostic criteria for CPA were met. In the remaining cases, the 4^th criterion could not be analyzed in the absence of histological samples. Regarding the 3^rd criterion of mycological evidence, 16 (14%) grew Aspergillus by culture, 19 (19/94, 20%) had a positive respiratory sample GM, and 112 (100%) had either the ICT (99, 88%) or the ELISA (66, 59%) for Aspergillus IgG positive.

The diagnostic performance of the Aspergillus-specific IgG assays for CPA patients

Of the 112 cases, 101 (90%) had elevated Aspergillus antibody levels by ImmunoCAP in contrast to 3 (5%) of the controls. Of the 112 cases, 66 (59%) were positive by ELISA, 99 (88%) by ICT, and 53 (47%) by both. Of the 61 controls, 11 (18%) were positive by ELISA, 3 (5%) by ICT, and 1 (2%) by both.

Overall, the ICT assay had a sensitivity of 88.4% and a specificity of 95.1% (Table 3). The Aspergillus IgG ELISA assay, on the other hand, showed a sensitivity of 58.9% and a specificity of 82.0% for all CPA patients when the diagnostic cut-off value was set at 80 AU/mL (Table 3). ROC curve analysis for ELISA assay showed that the AUC was 0.720 (95% CI: 0.643–0.798) for differentiating CPA vs. non-CPA (Figure 1). Furthermore, the combination of the ICT and ELISA assays on serum achieved the highest specificity (98.4%), while the use of either the ICT or ELISA assay alone resulted in the highest sensitivity (93.8%) for CPA diagnosis (Table 4). For CCPA, the Aspergillus-specific IgG ICT assay achieved 89.1% sensitivity. Similarly, for simple aspergilloma (SA), the assay demonstrated a sensitivity of 88.9% (Table 5).

Figure 1 ROC curve of aspergillus IgG ELISA assay in serum for CPA cases vs. pulmonary disease controls. AUC, area under the curve; CI, confidence interval; CPA, chronic pulmonary aspergillosis; ELISA, enzyme-linked immunosorbent assay; IgG, immunoglobulin G; ROC, receiver operating characteristic.

Effect of prior antifungal therapy on sensitivity of Aspergillus-specific IgG

Of all CPA patients, 43 (38%) had been started on mould-active antifungal therapy prior to enrollment and sampling [5 (range, 1–12) days prior]. Of these, 12 (28%) had a negative ICT result and 20 (47%) had a negative ELISA result compared to 1 (1%) and 26 (38%), respectively, of those not on antifungal therapy. Antifungal therapy decreased the sensitivity and specificity of both ICT and ELISA assays for all CPA subtypes (Table 5).

Impact of underlying disease on performance of Aspergillus-specific IgG

The sensitivity and specificity of the Aspergillus-specific IgG ICT assay on serum were significantly higher in CPA patients with previous cavitary tuberculosis, chronic obstructive pulmonary disease (COPD), and bronchiectasis compared to those obtained with the ELISA assay. Notably, CPA patients with COPD who were not receiving steroid therapy exhibited significantly better sensitivity of Aspergillus-specific IgG testing than those receiving any form of steroid therapy, including intravenous or oral administration (Table 6).

Discussion

This is the first study to compare the performance of Aspergillus-specific IgG ICT and ELISA assays in a large population of CPA patients with different subtypes. In our clinically and microbiologically validated cohort, Aspergillus-specific IgG ICT assay was shown to have better sensitivity than the Aspergillus-specific IgG ELISA assay (88.4% vs. 25.9% at 120 AU/mL cut-off) and comparable performance to ImmunoCAP used for the diagnosis of CPA. However, the specificity of ICT assay was marginally lower compared to the ELISA (cut-off =120 AU/mL) (95.1% vs. 96.7%). These findings contrast with a recent Nigerian study by Balogun et al. reporting higher sensitivity for Bordier ELISA than ICT (100% vs. 69.4%) (21). We propose several explanations for this discrepancy: (I) geographic variation in Aspergillus species distribution due to Aspergillus fumigatus accounting for only 50–60% of cases in Nigeria; and (II) distinct CPA subtypes distribution and prior treatment exposure between cohorts.

To date, multiple serum and BALF biomarkers have been evaluated for CPA diagnosis. Although serum GM testing is the most widely utilized Aspergillus biomarker clinically, its well-documented low sensitivity in immunocompetent/non-neutropenic patients renders it unsuitable for CPA detection. Of note, BALF GM demonstrates significant diagnostic value for early-stage CPA identification (25). In this study, we found that the sensitivity of the Aspergillus-specific IgG ICT assay was superior to BALF GM test (cut-off =1.0) (88.4% vs. 20.2%). We speculate the better sensitivity of Aspergillus-specific IgG ICT assay stems from sustained IgG immune response and resilience to antifungal treatment. Aspergillus-specific IgG remain detectable for extended periods (weeks to months) after antigen clearance, whereas GM antigen is rapidly cleared from circulation during effective treatment or immune reconstitution (26,27).

A 6-month voriconazole therapy is recommended for the treatment of CPA, but monitoring the course of disease is difficult. In this study, we found that antifungal therapy decreased the sensitivity and specificity of Aspergillus-specific IgG ICT and ELISA assays. This suggests that the Aspergillus-specific IgG levels in serum may decrease in CPA patients relatively quickly after commencing antifungal therapy. As radiological changes alone may not be sufficient to accurately assess the progression of the disease, quantitative Aspergillus IgG assays, along with clinical and other microbiological markers, may be valuable tools for evaluating disease progression and therapeutic response (8,28).

Most CPA cases are predicted to occur as a complication of pulmonary tuberculosis (29). A study has demonstrated that the incidence rate of CPA in post-tuberculosis therapy populations varies between 4.9% and 14.3% (30). In our study, 53.6% patients had a pulmonary tuberculosis history. However, the Aspergillus-specific IgG ICT assay shows higher sensitivity and specificity in CPA patients with previous cavitary tuberculosis, COPD, and bronchiectasis. This further supports its potential for clinical use in CPA diagnosis.

A history of steroid use was also found as a common associated condition, and an association between corticosteroid use and the development of pulmonary aspergillosis has been observed in previous studies (31,32). In our study, we found that steroid treatment decreased the sensitivity and specificity of the Aspergillus-specific IgG ICT assay in CPA patients with COPD. A previous study has shown that steroid treatment could inhibit the host’s inflammatory immune response and affect immune cell function (33). If host’s immune responses to Aspergillus antigens are inhibited, this is likely to decrease the production of Aspergillus-specific IgG.

While ImmunoCAP exhibits excellent diagnostic accuracy and remains widely adopted for CPA detection, its dependence on specialized laboratory infrastructure and high cost substantially restrict accessibility in resource-limited regions, where CPA burden is disproportionately high. Our study demonstrates that the LDBio ICT-POCT achieves comparable diagnostic performance to ImmunoCAP while outperforming both the Dynamika ELISA and BALF GM testing for Aspergillus-specific IgG detection in CPA. These findings position ICT as a clinically viable, cost-effective alternative to ImmunoCAP, particularly in resource-constrained settings. Furthermore, in treatment response monitoring, Aspergillus-specific IgG serology provides distinct advantages over serial radiological assessment, particularly by eliminating repeated radiation exposure. Our data confirm the dual utility of the LDBio Aspergillus IgG ICT assay in both diagnosing CPA and tracking therapeutic outcomes.

Conclusions

Aspergillus-specific IgG testing provides significant diagnostic value for CPA, particularly in the CCPA subtype. The ICT assay demonstrates superior sensitivity over ELISA, positioning it as a valuable point-of-care tool for rapid CPA diagnosis in resource-limited settings. However, prior antifungal and glucocorticoid therapy reduces the diagnostic accuracy of both assays.

Acknowledgments

We would like to thank the patients for participating in this study and donating their biological samples.

Footnote

Reporting Checklist: The authors have completed the STARD reporting checklist. Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-110/rc

Data Sharing Statement: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-110/dss

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-110/prf

Funding: This study was supported by the National Natural Science Foundation of China (No. 82170003 to Dr. L.L.C. and No. 82201929 to Dr. J.L.D.), the NIHR Manchester Biomedical Research Centre (No. NIHR203308 to Dr. R.R.R.), the Talent Development Foundation of the First Dongguan Affiliated Hospital of Guangdong Medical University (No. GCC2025008 to Dr. J.L.D.), and the Guangdong Medical Scientific Research Found (No. A2025060 to Dr. J.L.D.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-110/coif). W.J.G. serves as an unpaid editorial board member of Journal of Thoracic Disease. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China (Medical Ethics Approval 2021 [No. 51]). All patients were recruited with written informed consent.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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