Mucormycosis co-infection in COVID-19 patients: An update

Mucormycosis (MCM) is a rare fungal disorder that has recently been increased in parallel with novel COVID-19 infection. MCM with COVID-19 is extremely lethal, particularly in immunocompromised individuals. The collection of available scientific information helps in the management of this co-infection, but still, the main question on COVID-19, whether it is occasional, participatory, concurrent, or coincidental needs to be addressed. Several case reports of these co-infections have been explained as causal associations, but the direct contribution in immunocompromised individuals remains to be explored completely. This review aims to provide an update that serves as a guide for the diagnosis and treatment of MCM patients’ co-infection with COVID-19. The initial report has suggested that COVID-19 patients might be susceptible to developing invasive fungal infections by different species, including MCM as a co-infection. In spite of this, co-infection has been explored only in severe cases with common triangles: diabetes, diabetes ketoacidosis, and corticosteroids. Pathogenic mechanisms in the aggressiveness of MCM infection involves the reduction of phagocytic activity, attainable quantities of ferritin attributed with transferrin in diabetic ketoacidosis, and fungal heme oxygenase, which enhances iron absorption for its metabolism. Therefore, severe COVID-19 cases are associated with increased risk factors of invasive fungal co-infections. In addition, COVID-19 infection leads to reduction in cluster of differentiation, especially CD4+ and CD8+ T cell counts, which may be highly implicated in fungal co-infections. Thus, the progress in MCM management is dependent on a different strategy, including reduction or stopping of implicit predisposing factors, early intake of active antifungal drugs at appropriate doses, and complete elimination via surgical debridement of infected tissues

Cross-linked polystyrene sulfonic acid and polyethylene glycol as a low-fouling material

A negatively charged hydrophilic low fouling film was prepared by thermally cross-linking a blend consisting of polystyrene sulfonic acid (PSS) and polyethylene glycol (PEG). The film was found to be stable by dip-washing. The fouling resistance of this material towards bacterial (Escherichia coli) and colloidal (polystyrene particles) attachment, non-specific protein (fibronectin) adsorption and cell (3T3 NIH) adhesion was evaluated and was compared with glass slides modified with polyethylene glycol (PEG) brushes, oxidized 3-mercaptopropyltrimethoxysilane (sulfonic acid, SA), and n-octadecyltrichlorosilane (OTS). The extended Derjaguin-Landau- Verwey-Overbeek (XDLVO) theory and thermodynamic models based on surface energy were used to explain the interaction behaviors of E. coli/polystyrene particles–substrate and protein–substrate interactions, respectively. The cross-linked PSS-PEG film was found to be slightly better than SA and PEG towards resisting non-specific protein adsorption, and showed comparable low attachment results as those of PEG towards particle, bacterial and NIH-3T3 cells adhesion. The low-fouling performance of PSS-PEG, a cross-linked film by a simple thermal curing process, could allow this material to be used for applications in aqueous environments, where most low fouling hydrophilic polymers, such as PSS or PEG, could not be easily retained

Zosteric Acid, a Bioactive Component in Eelgrass <i>Zostera marina</i>, Reduced Collagen I Expression in a Repaired Mouse Fibroblast Scratch

Zosteric acid (ZA), a bioactive component in Zostera marina eelgrass, was applied to assess closure of normal mouse fibroblast scratch and collagen I expression. The cytotoxicity of ZA on the fibroblast at different ZA concentrations was evaluated. ZA showed low toxicity with ~80% of cell viability at a concentration of ~1600 ppm. A single scratch (~1500 μm) was made on a layer of fibroblast, and collagen expression was determined after 72 hours when the scratch fully closed for both ZA-treated and untreated samples. Compared to control, the ZA-treated cells were slightly less dense and randomly oriented in the closure region and had lower actin and vinculin expressions. The total collagen expressions were comparable to the control, whereas collagen I expression of the mouse fibroblast treated with 1600 ppm of ZA was significantly lower than untreated fibroblasts. </jats:p