Invasive Pulmonary Aspergillosis Due to Aspergillus Niger and COVID-19 Pneumonia

Abstract

INTRODUCTION: Aspergillus, a hyaline mold, causes invasive pulmonary aspergillosis (IPA), a severe systemic infection in immunocompromised patients. IPA has a high mortality rate and is a well-documented complication of severe influenza pneumonia. Emerging studies in Europe have identified secondary IPA cases with coronavirus disease 2019 (COVID-19), known as CAPA. With over 72.8 million confirmed cases of patients with COVID-19 infection worldwide as of December 2020, CAPA is a significant complication. Here, we report an immunocompromised female patient with IPA likely due to the adverse effects of COVID-19 therapy. CASE: A 58-year-old Caucasian woman with a history of chronic obstructive pulmonary disease (COPD), type 2 diabetes mellitus, obstructive sleep apnea, and hypertension was admitted for COVID-19 pneumonia with elevated inflammatory markers. She was started on dexamethasone, remdesivir and received convalescent plasma. She was ventilated and pronated. Bronchoscopy on day 5 showed multiple white plaques and a single black plaque of 1 cm diameter on the left bronchial wall. Bronchoalveolar lavage (BAL) fungal stain revealed acute-angled septate hyphae and culture yielded Aspergillus. niger. BAL and serum galactomannan (GM) levels returned elevated at ≥ 3.750 index with a negative serum beta-D glucan assay. A diagnosis of IPA was made, and voriconazole was initiated. Due to refractory hypoxia, extracorporeal membrane oxygenation was started. Her stay was further complicated by a Dieulafoy's lesion, bronchial bleeding, and E. coli pneumonia. On day 31, care was withdrawn, and she passed away. DISCUSSION: IPA is a well-known complication in immunocompromised patients, with known risk factors including COPD, diabetes mellitus, and severe influenza infection. The hypothesized CAPA mechanisms include damaged respiratory epithelium, dysfunctional mucociliary clearance, and local immune paralysis facilitating fungal invasion. COVID-19 pneumonia therapy with experimental use of dexamethasone and tocilizumab may alter local and systemic immunity, increasing IPA's risk. While no diagnostic criteria exist for CAPA, our patient met diagnostic criteria for IPA with her elevated BAL and serum GM levels >3.750 and positive BAL fungal stain with culture. Recommended treatment for IPA is voriconazole, which is superior to amphotericin in reducing mortality. CONCLUSION: Here, we report a rare case of CAPA by A. niger in an immunocompromised patient with severe COVID- 19 pneumonia. Further studies must consider the regular screening of IPA in critically ill patients, determine the performance of serum and BAL GM in COVID-19 patients, and if COVID-19 pneumonia or its treatments are independent risk factors for CAPA.