Dr. Seshu is a Professor of Bacterial Pathogenesis in the Department of Biology at The University of Texas at San Antonio and a full member of the South Texas Center for Emerging Infectious Diseases (STCEID). He received a degree in Veterinary Medicine from Madras Veterinary College in India and his doctorate in Microbiology at Washington State University in Pullman, Washington. He completed post-doctoral training at Texas A&M University Health Science Center in College Station, Texas, focusing on pathogenic mechanisms that lead to the establishment of Lyme disease. He developed a robust gene manipulation system for Borrelia burgdorferi. He has determined the contributions of several genes that enable Lyme disease spirochetes to establish infection.
Dr. Seshu’s lab at UTSA currently focuses on how Borrelia burgdorferi survives in both ticks and mammalian hosts. He uses a variety of cutting-edge technologies that are directed at limiting or eliminating the survival and transmission of Lyme disease pathogen between ticks and reservoir hosts such as small rodents that sustain pathogen life cycle in nature. Dr. Seshu’s laboratory has identified several enzymes in Borrelia burgdorferi that can be inhibited by drugs that are currently under clinical use for treating other diseases. However, it is unclear how effective these drugs are in limiting the survival of Borrelia burgdorferi in mammalian and tick hosts. A major focus of the current study funded by Bay Area Lyme Foundation will address the efficacy of select drugs in limiting pathogen survival by inhibiting central and intermediary metabolic pathways. In addition, Dr. Seshu’s laboratory is also focused on the response of mammalian hosts to infection and on mechanisms that can be exploited to block the spread of Lyme disease pathogen from the site of tick bite in the skin to deeper tissues such as the joints, heart and brain. Dr. Seshu has expanded his research efforts to identify how gene regulatory networks affect antibiotic resistance mechanisms in pathogens that are responsible for hospital-acquired infections.