Staphylococcus aureus (SA) is a pathogenic bacterium which affecting humans, primarily affecting the blood, lungs, and soft tissues. There is no vaccine available for SA and it has already developed antibiotic resistance (AR) to many antibiotics, making it extremely deadly. SA can gain AR by obtaining a resistance gene from another organism, however, the process of such is not well understood. The purpose of this project is to elucidate the process of gaining AR genes in SA strains. We hypothesize that AR is conferred through horizontal gene transfer (HGT) because of the exchange of eDNA in the biofilm, an exterior film protecting the cell. We propose that by adding antibiotics (AB) to biofilms, it will provide insight into the mechanisms of transformation HGT in SA. While AB can increase eDNA concentration in a biofilm, they can also cause more pores in the cell wall; either or both scenarios can increase the probability of transformation. We expect only cell wall synthesis inhibitors (oxacillin and vancomycin) to increase HGT via increasing the permeability of the cell while any AB causing cell lysis (erythromycin and tetracycline) could increasing HGT via increasing the eDNA concentration. In our project, we will control for the addition of eDNA due to either AB and/or the creation of porous cells which naturally take up eDNA more easily by adding DNase to AB-treated biofilms. Using this method, eDNA concentration does not increase but cell retain the ability to create pores. This project will use pre-existing protocol to co-culture P12 (meat isolate) and USA400 (human isolate) which have complementary AB profiles in AR profiles between the two strains. After co-culturing the isolates in a single biofilm, adding the treatment antibiotics and DNase, and select for double-AB resistant colonies by plating them on AB plates, we expect to see HGT.
University / Institution: Brigham Young University
Format: In Person
SESSION D (3:30-5:00PM)
Area of Research: Health & Medicine
Faculty Mentor: Bradford Berges