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We read with interest the article by Elamin et al. published recently in Clinical and Experimental Dermatology. 1 The authors described a 66-year-old woman who developed new-onset generalized pustular psoriasis (GPP) 3 weeks after receiving her first dose of the Oxford-AstraZeneca COVID-19 vaccine. 1 The authors then contemplated the possible underlying immunopathological mechanisms. We would like to highlight the Type I interferons (IFN-I) and their chief cellular source, the plasmacytoid dendritic cell (pDC), as possible connections that may explain the development of GPP after COVID-19 vaccine.In psoriasis, the role of the innate immune system, especially IFN-I and pDCs, in driving the autoimmune Tcell cascade is well known. 2,3 Characterized by their unique surface phenotype and plasma cell-like morphology, pDCs are distinctive DCs that are key effectors in innate antiviral immunity because of their potent ability to secrete large IFN-Is. 2 This is achieved by their ability to sense nucleic acids via their endosomally located Tolllike receptor (TLRs), TLR-9 and TLR-7, which upon activation, lead to massive production of IFN-I, which are crucial cytokines functioning in controlling viral replication by inducing gene expression. 2 In addition, pDCs link the innate and adaptive immunity by their ability to regulate the function of other immune cells. In normal conditions, pDCs are usually present in the blood and lymphoid organs; however, active pDC recruitment occurs from the blood into peripheral sites of infection or inflammation. In psoriasis, pDCs infiltrate lesional skin, where they contribute to the early disease processes mainly through pDC-derived IFN-I production. 2 In particular, GPP, which is a clinical psoriasis variant characterized by recessive mutations of the interleukin (IL)-36 receptor antagonist gene (IL36RN), has recently been shown to demonstrate a prominent systemic IFN-I signature that correlates with the known abnormal upregulated IL-36 activity. 3 The underlying immune mechanism leading to this effect in GPP, which also applies to psoriasis vulgaris, has been shown to be mediated by the direct action of IL-36 on pDCs, potentiating TLR-9 activation and production of IFN-a. 3 These findings thus reveal the IL-36/IFN-I axis as a major contributor to inflammation in psoriasis. 3 Additional evidence of a significant role of IFN-I and pDCs in psoriasis/GPP originates from clinical observations such as reports describing psoriasis/GPP induction in patients treated with recombinant IFN-a, and the frequently reported association of psoriasis/GPP with

Introduction Critically ill COVID-19 patients are at high risk for nosocomial bacterial and fungal infections due to several predisposing factors such as intensive care unit stay, mechanical ventilation, and broad-spectrum antibiotics. Data regarding multidrug resistant (MDR) Candida species in COVID-19 patients is scarce, and nonexistent regarding Candida duobushaemulonii superinfections. Case description A 34-year-old male presented to our institution with acute respiratory distress syndrome (ARDS) due to COVID-19 infection and developed Candida duobushaemulonii fungemia after multiple courses of antibiotics and prolonged mechanical ventilation. He died after recurrent pneumothorax led to respiratory failure and cardiac arrest. Discussion Bacterial and fungal infections are common complications of viral pneumonia in critically ill patients. Data regarding these infections in COVID-19 patients has been poorly studied with only a few cases reporting secondary infection, mostly without identifying specific pathogens. Prolonged hospital stays, invasive interventions (central venous catheter, mechanical ventilation), and the use of broad-spectrum antibiotics in COVID-19 infections could carry a high risk of bacterial and/or fungal superinfections. Conclusion Strategies to improve outcome in COVID-19 ICU patients should include early recognition of candidemia and appropriate antifungal therapy.

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