Abstract
COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has infected over 200 million people, causing over 4 million deaths. COVID-19 infection has been shown to lead to hypoxia, immunosuppression, host iron depletion, hyperglycemia secondary to diabetes mellitus, as well as prolonged hospitalizations. These clinical manifestations provide favorable conditions for opportunistic fungal pathogens to infect hosts with COVID-19. Interventions such as treatment with corticosteroids and mechanical ventilation may further predispose COVID-19 patients to acquiring fungal coinfections. Our literature review found that fungal coinfections in COVID-19 infected patients were most commonly caused by Aspergillus, Candida species, Cryptococcus neoformans, and fungi of the Mucorales order. The distribution of these infections, particularly Mucormycosis, was found to be markedly skewed towards low- and middle-income countries. The purpose of this review is to identify possible explanations for the increase in fungal coinfections seen in COVID-19 infected patients so that physicians and healthcare providers can be conscious of factors that may predispose these patients to fungal coinfections in order to provide more favorable patient outcomes. After identifying risk factors for coinfections, measures should be taken to minimize the dosage and duration of drugs such as corticosteroids, immunosuppressants, and antibiotics.
Highlights
Published: 4 December 2021The winter of 2019 marked the initial spread of the COVID-19 outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]
Researchers and physicians alike believe that fungi can infect and germinate indiResearchers and physicians alike believe that fungi can infect and germinate viduals with COVID-19 due to the ideal environment they present, which include: low individuals with COVID-19 due to the ideal environment they present, which include: oxygen states secondary to the patients’ hypoxemia, high glucose presence secondary low oxygen states secondary to the patients’ hypoxemia, high glucose presence secondary to diabetes and/or steroid-induced hyperglycemia, decreased to diabetes and/or steroid-induced hyperglycemia, decreased phagocytic action of white blood cells secondary to the immunosuppression from the virus phagocytic action of white blood cells secondary to the immunosuppression from the and/or steroid treatment, acidic environment from possible diabetic ketoacidosis (DKA)
COVID-19 is associated with a high number of secondary infections of both fungal and bacterial origin
Summary
The winter of 2019 marked the initial spread of the COVID-19 outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]. The presenting cytokine storm and immune dysregulation of COVID-19 may develop acute respiratory distress syndrome, organ failure, coagulation, and more [9] This cytokine storm response can lead to T-cell exhaustion, seen often in chronic infectious states. Superinfection, occurring subsequently, and coinfection, occurring concomitantly, cause greater difficulty and complication in diagnosis due to an overlap of symptoms and complicate the treatment of COVID-19 [Table 1] Such multi-infectious states often rtesult in a worse outcome than either infection alone [18,19]. For instance, often have similar symptoms to COVID-19, such as cough, shortness of breath, and fever, making it difficult to distinguish between the two diseased states [20,21]. Unilateral facial swelling, HA, nasal congestion, fever, black lesions on nasal bridge cough, chest pain, SOB, or inside the mouth, nausea, vomiting gastrointestinal (GI) bleeding
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