Anthony Martini successfully defended his Ph.D. thesis, "Contribution of the S. sanguinis Type IV Pili to Infective Endocarditis Pathogenesis" on Monday, April 20, 2020. His mentor is Professor Bradley Jones.
About Tony
Tony grew up in the suburbs of Chicago and is the eldest child of Anthony and Valerie Martini. He has one sister, Cara, an architect. An avid interest in reading and technology during adolescence would prove valuable in developing the skills necessary for the road ahead, even if that road were more winding than straight.
Before developing an interest in microbiology, his interests in computers and literature took him through two majors in college: information systems and publishing. As a senior, he began undergraduate research in the laboratory of Dr. Brian J. Wilkinson at Illinois State University. The experience provided an essential window into microbiology research and spurred his decision to apply to the Master's program in biotechnology in the same laboratory. In the summer before starting graduate school, he worked as a field technician assisting research on free-living songbirds. This work provided further research experience in working with animals and instilled the importance of working within ecologically representative systems. Research for his Master's thesis focused on the physiological response of Listeria monocytogenes to membrane alterations that prevented adaptation and growth in low temperatures. This experience investigating microbial physiology provided the essential push to continue onward toward a career in microbiological research.
In joining the laboratory of Dr. Brad Jones at the University of Iowa, he worked on several projects, including virulence mechanisms of oral streptococci in infective endocarditis. The ability to work with an animal model of disease and investigate environmental conditions necessary for bacterial gene expression and virulence potential synthesized elements of both prior research experiences. It provided the opportunity to address questions related to human health and disease.
In addition to research, Tony served as the Graduate Student President for Microbiology and organized the student journal club and annual student-invited seminar.
Outside the laboratory, Tony enjoys exceptionally nerdy activities including overly-complicated board games, tabletop RPGs, and reading political science, philosophy of science, and legal literature. He also endeavors to become a connoisseur of schnapps and to win at least one battle of wills with his cat, Harley.
Research
Infective endocarditis (IE) is a serious and potentially fatal infection of the heart associated with significant morbidity and mortality. Vegetative lesions comprised of microorganisms and host factors develop on the valves and can directly impede heart function, resulting in heart failure. Treatment is effectively limited to prolonged antibiotic therapy and surgery, and little progress has been made toward prevention in at-risk individuals and populations. Predisposing conditions include congenital heart defects, rheumatic heart disease, intravenous drug use, and periodontal disease.
Streptococcus sanguinis is among the most common oral bacteria identified in IE. Although a high level of S. sanguinis colonization in the oral cavity is associated with good oral health, bacteria can gain access to the bloodstream following dental procedures and as a result of gingival or periodontal inflammation. S. sanguinis causes a subacute form of the disease which develops insidiously over several weeks or months and is often complicated by late diagnosis. Despite the long association of these bacteria with IE, the virulence mechanisms critical for disease progression are poorly understood. To address this shortcoming, we identified putative virulence genes and investigated their roles in disease-related processes. In addition to characterizing several previously unknown gene functions, we establish and validate an in vivo model for future pathogenesis research. Using this model, we also determined the contribution of type IV pili to virulence and characterized the mechanisms by which they contribute to disease pathogenesis.
Together, our work validates an in vivo model of experimental native valve IE and expands on the mechanisms used by oral streptococci to cause this disease. We expect these advances to aid further research and contribute to the development of preventative therapeutics.