Staphylococcus epidermidis is more often known as a human skin commensal, serving as a primary protective bacterium on the skin’s surface. However, more recent literature highlights the role of S. epidermidis as a nosocomial pathogen and a multidrug-resistant organism that poses a global threat. The evolution of S. epidermidis can be owed to its accumulation of resistance mechanisms, including adhesion, biofilm formation, genomic islands, phage elements, integrated plasmids, and quorum sensing. It is suspected that through gene transfer, S. epidermidis is partially responsible for the feared multidrug-resistant Staphylococcus aureus through the mecA gene and many other genomic island transfers. Overall, prolonged nosocomial exposure and misuse of antibiotics have driven dramatic genomic remodeling in S. epidermidis, characterized by many methods of genetic recombination, SCCmec and insertion sequence acquisition, and accumulation of multiple resistance genes. Our review reviews the role of S. epidermidis as both a commensal and a pathogenic bacterium, summarizes the genes responsible for its multidrug resistance, and describes methods of combatting its invasion.

Acute Respiratory Distress Syndrome (ARDS) is a severe and life-threatening form of acute lung injury with high mortality. It affects approximately 150,000–190,000 patients annually in the United States, and a substantial proportion of patients require invasive mechanical ventilation for respiratory support. The progression of ARDS involves thrombo-inflammation, the disruption of the alveolar–capillary barrier, and oxidative injury within pulmonary tissues. Across diverse ARDS etiologies such as sepsis, aspiration, trauma, and COVID-19, the excessive production of reactive oxygen species (ROS) is a central mediator of lung injury. Central to the neutralization of oxidative stress is glutathione (GSH), a key intracellular antioxidant responsible for neutralizing ROS. Decreased levels of GSH have been associated with increased cytokine levels and thrombosis, but the full extent of GSH’s role in these processes remains unclear. This review provides an overview of the role of glutathione in the pathophysiological sequelae of ARDS, highlights its relevance in COVID-19-related lung injury, and explores its potential as a clinical marker to predict the need for mechanical ventilation.