Abstract

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) can result in life threatening skin and soft tissue infections (SSTIs) in healthy individuals. SSTIs can lead to deeper bloodstream infections resulting in bacteremia, which is responsible for high mortality rates ranging from 20-50%. In response to infections, phagocytes from the host immune system produce radical nitric oxide (NO࢈) to limit bacterial proliferation. The complex biomechanisms of S. aureus enable it to evade NO࢈ immune defenses. With the rising occurrence of S. aureus bacteremia in developing countries and MRSA resisting host defenses and prescribed antibiotics, it is important to identify new targets for developing novel antibiotics. A previous student created a deletion mutant in the yqeK gene and characterized the phenotype of the yqeK mutant in NO࢈ stress and on sheep’s blood agar plates. This resulted in delayed growth, dysregulated expression of genes in stress response, decreased hemolytic toxin production, and a decrease in virulence gene expression. The aim of this study is to investigate the virulence phenotypes of the yqeK deletion mutant in S. aureus, using a quantitative hemolysis assay and Caenorhabditis elegans as whole animal models. A liquid hemolysis assay in sheep blood was performed and showed a decreased production of hemolytic toxins in the yqeK mutant, thus suggesting a decrease in virulence gene expression. C. elegans represent an established model to study S. aureus infections since they are infected and killed by the same S. aureus virulence factors involved in human SSTIs. Therefore, we are currently performing C. elegans infection assays and nematode gut proliferation assays. Current and future work will focus on increasing replications and optimizing the nematode assays. Expected outcomes for the yqeK mutant include increased survival rates in the animal model assay, decreased bacterial gut proliferation, and decreased hemolytic activity.

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