Invasive pulmonary aspergillosis is a complication in critically ill patients with acute respiratory distress syndrome, especially those with severe coronavirus disease-associated pneumonia. In this study, five cases of presumed invasive pulmonary aspergillosis in one immunocompromised and four immunocompetent patients with COVID-19 in Buenos Aires are described. In all cases, the underlying conditions, clinical presentation, fungal diagnostic tests used and their results, features of the chest scan images, antifungals used and clinical outcomes are detailed.

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Summary Background Triazole resistance in Aspergillus fumigatus sensu stricto due to mutations in the cyp51A gene has been widely reported. Data from Argentina, and particularly from cystic fibrosis (CF) patients, are limited. Objectives To investigate the prevalence and molecular mechanisms of azole resistance in A. fumigatus sensu stricto recovered from this population. Methods Ninety‐three A. fumigatus isolates from 50 CF patients were retrospectively analysed for azole resistance using the standard microbroth dilution method according to CLSI M38‐A2 guidelines. Sequencing analysis of the cyp51A gene and its promoter region was conducted in those isolates displaying high MIC values to itraconazole, voriconazole and/or posaconazole. Results Overall, 14% of isolates displayed high MIC values to at least one azole. Of them, 30.7% had the mutation TR34‐L98H. No mutations in the cyp51A gene or its promoter were found in the remaining non–wild‐type strains. Therefore, other mechanisms associated with azole resistance can be highly prevalent in these isolates. Conclusions To the best of our knowledge, this is the first study in Latin America reporting azole‐resistant A. fumigatus strains recovered from respiratory secretions of CF patients. Noteworthy, the prevalence of azole resistance in A. fumigatus sensu stricto in the studied Argentinean CF population is alarmingly high.

Patients with severe COVID-19 are at increased risk for invasive fungal infections, such as invasive pulmonary aspergillosis and candidiasis, which increase morbidity and mortality. However, clinicians should also consider the possibility of reactivating latent Histoplasma capsulatum in patients with severe COVID-19 living within areas of endemicity who have worsening respiratory function or sepsis, even if they do not have classical risk factors for histoplasmosis (e.g., HIV/AIDS). Bearing in mind this scenario, serum samples of 39 non-HIV/AIDS patients from Buenos Aires hospitalized due to severe COVID-19 pneumonia were analyzed for anti-H. capsulatum-specific IgG antibodies by an in-house ELISA. Antibodies against H. capsulatum were detected in the sera of 8/39 patients (20.51%). To exclude the possibility that these antibodies arose from past exposure of these patients to the fungus, paired serum samples obtained after an interval of at least 10 days were evaluated. Of them, 5 patients (62.5%) with negative anti-H. capsulatum antibodies at baseline became seropositive 7–10 days later. Three patients (37.5%) had positive anti-H. capsulatum antibodies at baseline, but at time point 2, one of them became seronegative and the other one diminished the antibody titers (4 000 vs 16 000 at baseline). The remaining patient displayed higher antibody titers at time point 2 (4 000 vs 1 000 at baseline) and died immediately thereafter. In conclusion, awareness of the possibility of fungal co-infections is essential to reduce delays in diagnosis and treatment in order to help prevent severe illness and death from these infections.

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