Fungal infection profile in critically ill COVID-19 patients: a prospective study at a large teaching hospital in a middle-income country.

BACKGROUND: Critically ill COVID-19 patients are highly susceptible to opportunistic fungal infection due to many factors, including virus-induced immune dysregulation, host-related comorbidities, overuse and misuse of antibiotics or corticosteroids, immune modulator drugs, and the emergencies caused by the pandemic. This study aimed to assess the incidence, identify the potential risk factors, and examine the impact of fungal coinfection on the outcomes of COVID-19 patients admitted to the intensive care unit (ICU). METHODS: A prospective cohort study including 253 critically ill COVID-19 patients aged 18 years or older admitted to the isolation ICU of Zagazig University Hospitals over a 4-month period from May 2021 to August 2021 was conducted. The detection of a fungal infection was carried out. RESULTS: Eighty-three (83) patients (32.8%) were diagnosed with a fungal coinfection. Candida was the most frequently isolated fungus in 61 (24.1%) of 253 critically ill COVID-19 patients, followed by molds, which included Aspergillus 11 (4.3%) and mucormycosis in five patients (1.97%), and six patients (2.4%) diagnosed with other rare fungi. Poor diabetic control, prolonged or high-dose steroids, and multiple comorbidities were all possible risk factors for fungal coinfection [OR (95% CI) = 10.21 (3.43-30.39), 14.1 (5.67-35.10), 14.57 (5.83-33.78), and 4.57 (1.83-14.88), respectively]. CONCLUSION: Fungal coinfection is a common complication of critically ill COVID-19 patients admitted to the ICU. Candidiasis, aspergillosis, and mucormycosis are the most common COVID-19-associated fungal infections and have a great impact on mortality rates.

Does mass management of chronic hepatitis C protect the Egyptian population against fulminant coronavirus disease-2019? “Postulating a hypothesis”

Coronavirus disease (COVID-19) is caused by the pathogenic virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Egypt has launched a national treatment program to provide a cure for Egyptian patients infected with hepatitis C virus (HCV). A common mechanism is shared between both the anticipated and unexpected aspects of COVID-19. The activity of the renin-angiotensin system (RAS) is intrinsically high in the lungs, which is a major source of ACE and hence a significant site of systemic synthesis of Ang II. Angiotensin-converting enzyme 2 (ACE2) is the cellular receptor for SARS-CoV-2, the etiological agent of the COVID-19 disease. ACE-2 and its angiotensin 1–7 (Ang 1–7) product, which acts on the Mas oncogene receptor, have been shown to play a protective role in fibrogenesis and inflammation of many organs, including the liver and lung. Antiviral treatment with interferon (IFN) in conjunction with ribavirin in patients with chronic hepatitis C reduces serum ACE activity and indirectly affects liver parenchyma fibrogenesis. The antifibrotic activity of sofosbuvir plus daclatasvir (SOF/DAC) is independent of its antiviral action. Elimination of HCV infection by DAA therapy in patients with chronic hepatitis C could improve natural killer (NK) activity by increasing the frequency of CD 16+ CD 56+ NK cells. COVID-19 individuals exhibit enhanced platelet activation and aggregation, as well as platelet-monocyte aggregation, which is linked to coagulative disorders. Lower systemic inflammation and enhanced hepatic synthesis of both pro- and anti-coagulant factors were noticed soon after antiviral therapy. In order to protect against the severity of COVID-19, treatment of chronic hepatitis C has been observed as a possible key as a prophylaxis beside the vaccine and should be tested for evidence or rejection of observation.