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Review
. 2024 Feb;45(1):21-31.
doi: 10.1055/s-0043-1776777. Epub 2024 Jan 16.

Microbiological Diagnosis of Pulmonary Aspergillus Infections

Affiliations
Review

Microbiological Diagnosis of Pulmonary Aspergillus Infections

Robina Aerts et al. Semin Respir Crit Care Med. 2024 Feb.

Abstract

As microbiological tests play an important role in our diagnostic algorithms and clinical approach towards patients at-risk for pulmonary aspergillosis, a good knowledge of the diagnostic possibilities and especially their limitations is extremely important. In this review, we aim to reflect critically on the available microbiological diagnostic modalities for diagnosis of pulmonary aspergillosis and formulate some future prospects. Timely start of adequate antifungal treatment leads to a better patient outcome, but overuse of antifungals should be avoided. Current diagnostic possibilities are expanding, and are mainly driven by enzyme immunoassays and lateral flow device tests for the detection of Aspergillus antigens. Most of these tests are directed towards similar antigens, but new antibodies towards different targets are under development. For chronic forms of pulmonary aspergillosis, anti-Aspergillus IgG antibodies and precipitins remain the cornerstone. More studies on the possibilities and limitations of molecular testing including targeting resistance markers are ongoing. Also, metagenomic next-generation sequencing is expanding our future possibilities. It remains important to combine different test results and interpret them in the appropriate clinical context to improve performance. Test performances may differ according to the patient population and test results may be influenced by timing, the tested matrix, and prophylactic and empiric antifungal therapy. Despite the increasing armamentarium, a simple blood or urine test for the diagnosis of aspergillosis in all patient populations at-risk is still lacking. Research on diagnostic tools is broadening from a pathogen focus on biomarkers related to the patient and its immune system.

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Conflict of interest statement

R.A. has received PhD funding from the Flemish Cancer Society (Kom op Tegen Kanker) and a research grant and travel support from Gilead Sciences. S.F. reports PhD funding from Research Foundation Flanders (FWO, grant number 11M6922N) and reports receiving travel grants from Pfizer and Gilead, and speaker fees from Healthbook Company Ltd. T.M. has received consultancy fees from Gilead Sciences, Pfizer, and AstraZeneca, research grants from Gilead Sciences, and travel support from AstraZeneca. K.L. received consultancy fees from MRM Health, MSD, and Mundipharma, speaker fees from Pfizer and Gilead, and a service fee from Thermo Fisher Scientific and TECOmedical.

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