Dr. Armand Brown graduated from the University of Texas at Austin with a Bachelor of Science in Microbiology in 2009. Shortly after, he attended Baylor College of Medicine for one year as a post-baccalaureate student prior to entering graduate school in the Fall of 2010 at The University of Texas Health Science Center at San Antonio. In the Fall of 2011, he joined the Department of Microbiology & Immunology where he obtained his Ph.D. in Microbiology & Immunology in December of 2014. Dr. Brown’s dissertation was focused on investigating the interactions of the Gram-positive bacterium Streptococcus pneumoniae with the heart during severe pneumonia. As a result, Dr. Brown discovered the new pathology of cardiac microlesion formation during severe pneumococcal infection, identified the mechanism, and developed a therapy to prevent its formation. Cardiac microlesions are currently thought to contribute to heart failure during severe pneumonia. Dr. Brown subsequently entered a Postdoctoral Fellowship at Columbia University where he investigated the mechanisms of persistent bone and soft tissue infections caused by antimicrobial-resistant strains of the Gram-positive bacterium Staphylococcus aureus such as Methicillin-Resistant Staphylococcus aureus (MRSA). After completing his fellowship, Dr. Brown returned to Texas where he began a second fellowship at The University of Texas Health Science Center at Houston investigating the interkingdom interactions between the Gram-positive bacterium Enterococcus faecalis and the fungus Candida albicans. This work led to the discovery of a previously uncharacterized E. faecalis thioredoxin known as DsbA that was determined to be required for the E. faecalis mediated suppression of C. albicans pathogenicity. Dr. Brown also discovered that E. faecalis is capable of forming cardiac microlesions through an alternative mechanism than was previously shown for S. pneumoniae. Moreover, he determined that DsbA is not only required for microlesion formation but contributes to the modulation of the host immune response to E. faecalis. Dr. Brown is currently investigating DsbA as a potential target for future therapeutic development against antimicrobial-resistant pathogens, such as Vancomycin Resistance Enterococcus (VRE). In addition, he is investigating the mechanism of cardiac microlesion formation during severe E. faecalis infection. Dr. Brown is currently applying for tenure-track assistant professorships.