Abstract
Invasive aspergillosis (IA) has been increasingly reported in populations other than the historical hematology patients and there are new questions about the performance of microbiological tools. Microscopy and culture have been completed by biomarkers, either antigens or DNA, and in blood or respiratory specimens or both. First studied in hematology, the antigen galactomannan performance in serum is low in other patient populations where the pathophysiology of the infection can be different and the prevalence of IA is much lower. DNA detection with polymerase chain reaction (PCR) in blood or serum (or both) has reached a certain level of acceptance thanks to consensus methods based on real-time quantitative PCR (qPCR). When used on respiratory specimens, galactomannan and qPCR depend on standardization of the sampling and the diverse mycological procedures. Thus, culture remains the main diagnostic criterion in critically ill patients. The current trend toward more effective anti-mold prophylaxis in hematology hampers the yield of a screening strategy, as is usually performed in hematology. Therefore, circulating biomarkers as confirmatory tests should be considered and their performance should be reappraised in each new setting. The use of azole prophylaxis also raises the issue of selecting azole-resistance Aspergillus fumigatus isolates. Ideally, the biomarkers will be more efficient when individual genetic risks of IA are defined. Culture, though not standardized, remains a key element for the diagnosis of IA and has the advantage to easily detect molds other than A. fumigatus. It is still unclear whether next-generation sequencing will replace culture in the future.
Highlights
Invasive aspergillosis (IA) is the prototype of opportunistic diseases: all of the diagnostic and therapeutics difficulties are due to the fact that only the presence of the germ cannot identify the infection
To help epidemiological studies and the evaluation of therapeutic trials, the European Organization for Research and Treatment of Cancer/Invasive Fungal Infections Cooperative Group and the National Institute of Allergy and Infectious Diseases Mycoses Study Group (EORTC/MSG) proposed criteria for defining IA, incorporating clinical, imaging, and microbiological items[1]. These definitions are suitable for hematological diseases—mainly, acute leukemia and hematopoietic stem cell transplant (HSCT) recipients—and, to a lesser extent, solid organ transplantations (SOTs)
Either because clinicians of other specialties are increasingly interested in IA or because of the improvement of diagnostic means, IA is reported in other immunocompromised patient populations, such as intensive care unit (ICU) patients, patients given anti-tumor necrosis factor therapy[2], patients with AIDS3, as well as in hematology, in patients with chronic lymphoproliferative diseases, including multiple myeloma[4] instead of acute leukemia[5]
Summary
Invasive aspergillosis (IA) is the prototype of opportunistic diseases: all of the diagnostic and therapeutics difficulties are due to the fact that only the presence of the germ cannot identify the infection. The definition of putative aspergillosis relies on four criteria: an Aspergillus-positive lower respiratory tract specimen (entry condition); abnormal medical imaging; and either other host risk factors or a semi-quantitative Aspergillus-positive culture of bronchoalveolar lavage (BAL) fluid with a positive microscopy (hyphae with morphology indicative of Aspergillus sp.) and without bacterial growth[16] This would imply that the microbiological procedures to identify, quantify, and culture molds are similar in all microbiology laboratories, which is not the case even for hematology patients at high risk of IA18. Diagnostic means Besides direct microscopy and culture, which remain important for identification and anti-fungal susceptibility testing of the fungus, several biomarkers have been evaluated: GM, 1,3-B-Dglucan (BDG), and Aspergillus DNA. These biomarkers have been tested in blood or serum (or both) and in respiratory specimens. Given the individual risk among a group of patients with similar treatments, the genetics underlying the susceptibility to IA should be further investigated to restrict the use of universal prophylaxis
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