Invasive Fungal Rhinosinusitis in the Era of COVID-19: Is It an Emerging Association?

Invasive fungal rhinosinusitis (IFRS) typically affects immunocompromised patients. The coronavirus disease 2019 (COVID-19) pandemic may be associated with rare opportunistic fungal infections, probably as a result of immune dysregulation. The COVID-19 infection is characterized by low levels of CD4+T and CD8+T cells which could increase the risk of co-infections from Mucor or Aspergillus species. An invasive fungal infection should be suspected in patients who have recently recovered from COVID-19 pneumonia and present with acute destructive rhinosinusitis. There are few cases of IFRS reported in Europe during the pandemic of COVID-19. We describe the case of a 67-year-old patient with diabetes who received corticosteroids during the treatment for COVID-19 infection and was readmitted a few days later for radiologically and clinically suggested IFRS. Aspergillus niger was identified, and the patient received pharmacological and surgical treatment.

Suppression of cytokine release by fluticasone furoate vs. mometasone furoate in human nasal tissue ex-vivo.

BACKGROUND: Topical glucocorticosteroids are the first line therapy for airway inflammation. Modern compounds with higher efficacy have been developed, but head-to-head comparison studies are sparse. OBJECTIVE: To compare the activity of two intranasal glucocorticoids, fluticasone furoate (FF) and mometasone furoate (MF) with respect to the inhibition of T helper (Th)1, Th2 and Th17 cytokine release in airway mucosa. METHODS: We used an ex-vivo human nasal mucosal tissue model and employed pre- and post- Staphylococcus aureus enterotoxin B (SEB)-challenge incubations with various time intervals and drug concentrations to mimic typical clinical situations of preventive or therapeutic use. RESULTS: At a fixed concentration of 10-10 M, FF had significantly higher suppressive effects on interferon (IFN)-γ, interleukin (IL)-2 and IL-17 release, but not IL-5 or tumor necrosis factor (TNF)-α, vs. MF. While the maximal suppressive activity was maintained when FF was added before or after tissue stimulation, the cytokine suppression capacity of MF appeared to be compromised when SEB-induced cell activation preceded the addition of the drug. In a pre-challenge incubation setting with removal of excess drug concentrations, MF approached inhibition of IL-5 and TNF-α after 6 and 24 hours while FF maximally blocked the release of these cytokines right after pre-incubation. Furthermore, FF suppressed a wider range of T helper cytokines compared to MF. CONCLUSION: The study demonstrates the potential of our human mucosal model and shows marked differences in the ability to suppress the release of various cytokines in pre- and post-challenge settings between FF and MF mimicking typical clinical situations of preventive or therapeutic use.