Post COVID-19 MSSA pneumonia.

Coronavirus disease 2019 (COVID-19) was first identified at the end of 2019 as a cluster of pneumonia cases in Wuhan, China. By February 2020, this virus quickly spread, becoming a global pandemic. The spectrum of symptomatic infection severity can range from mild, severe, and critical disease. Many correlated comorbidities were established, including smoking, socioeconomic background, gender (male prevalence), hypertension, obesity, cardiovascular disease, chronic lung disease, diabetes mellitus, cancer, and chronic kidney disease. In an extensive literature search, post-COVID-19 necrotizing Staphylococcus aureus pneumonia with pneumothorax has not been recorded. We present a case about a 62-year-old male who presented with symptoms of COVID-19 with many underlying comorbidities, including hypertension and hyperlipidemia. He was on ventilatory support during his first week in the hospital and then received supplemental oxygenation as he recovered from his COVID-19 pneumonia. Nearly a month and a half after his initial presentation, he quickly decompensated and was started on supplemental oxygen and the necessary treatments. It was then, with the aid of lab work and imaging, that we determined that he had developed necrotizing Staphylococcus aureus pneumonia with pneumothorax. He was adequately treated, and once he was stable, he was discharged home and was told to continue his therapy.

Collective epithelial migration drives kidney repair after acute injury.

Acute kidney injury (AKI) is a common and significant medical problem. Despite the kidney's remarkable regenerative capacity, the mortality rate for the AKI patients is high. Thus, there remains a need to better understand the cellular mechanisms of nephron repair in order to develop new strategies that would enhance the intrinsic ability of kidney tissue to regenerate. Here, using a novel, laser ablation-based, zebrafish model of AKI, we show that collective migration of kidney epithelial cells is a primary early response to acute injury. We also show that cell proliferation is a late response of regenerating kidney epithelia that follows cell migration during kidney repair. We propose a computational model that predicts this temporal relationship and suggests that cell stretch is a mechanical link between migration and proliferation, and present experimental evidence in support of this hypothesis. Overall, this study advances our understanding of kidney repair mechanisms by highlighting a primary role for collective cell migration, laying a foundation for new approaches to treatment of AKI.