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. 2022 Aug 23;8(9):894.
doi: 10.3390/jof8090894.

Challenges in Diagnosing COVID-19-Associated Pulmonary Aspergillosis in Critically Ill Patients: The Relationship between Case Definitions and Autoptic Data

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Challenges in Diagnosing COVID-19-Associated Pulmonary Aspergillosis in Critically Ill Patients: The Relationship between Case Definitions and Autoptic Data

Giacomo Casalini et al. J Fungi (Basel). .

Abstract

Critically ill COVID-19 patients can develop invasive pulmonary aspergillosis (CAPA). Considering the weaknesses of diagnostic tests/case definitions, as well as the results from autoptic studies, there is a debate on the real burden of aspergillosis in COVID-19 patients. We performed a retrospective observational study on mechanically ventilated critically ill COVID-19 patients in an intensive care unit (ICU). The primary objective was to determine the burden of CAPA by comparing clinical diagnosis (through case definitions/diagnostic algorithms) with autopsy results. Twenty patients out of 168 (11.9%) developed probable CAPA. Seven (35%) were females, and the median age was 66 [IQR 59-72] years. Thirteen CAPA patients (65%) died and, for six, an autopsy was performed providing a proven diagnosis in four cases. Histopathology findings suggest a focal pattern, rather than invasive and diffuse fungal disease, in the context of prominent viral pneumonia. In a cohort of mechanically ventilated patients with probable CAPA, by performing a high rate of complete autopsies, invasive aspergillosis was not always proven. It is still not clear whether aspergillosis is the major driver of mortality in patients with CAPA.

Keywords: CAPA; COVID-19; aspergillosis; autopsy; histopathology; invasive fungal infections.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Hematoxylin and eosin-stained sections from representative areas of lung parenchyma with diffuse alveolar damage, characterized by plurifocal hyaline membranes (panel A, *), prominent type II pneumocyte hyperplasia and atypia (panel B, **) and chronic inflammatory infiltrate (lymphocytes and macrophages) (Panel C, black arrows). OM panels (A) and (B) 10×, panel (C) 20×.
Figure 2
Figure 2
Hematoxylin and eosin-stained sections from large necrotic area of the lung with exudative inflammatory and necrotic lesions (Panels A and B, *) and acute inflammation and necrosis of the bronchial wall (panels C and D, **); numerous typical fungal hyphae of Aspergillus are present (black arrows). OM panels (A) and (C) 10×, panels (B) and (D) 40×.

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