Thayer King, BS
Thayer received her Bachelor of Science degree in Biology from the University of Georgia in 2011. During her undergraduate research career she studied the protozoan parasite Toxoplasma gondii and worked on understanding molecular mechanisms essential for parasite survival. She continued this research after graduation before entering the Immunology and Molecular Pathogenesis program at Emory University in 2013. In continuation of her interest in parasite pathogenesis and host-pathogen interactions, she joined the lab of Dr. Tracey Lamb to study the immunopathogenesis of malaria, a disease caused by infection with protozoan parasites of the genus Plasmodium. The Lamb Lab is particularly interested in understanding the immune response during Plasmodium infection and how it contributes to disease pathogenesis as well as developing novel vaccination and therapeutic targeting strategies against Plasmodium infection. Thayer’s project focuses on understanding the role of Eph receptors in the immune response during cerebral malaria and exploring targeted therapeutic approaches against Eph receptors to prevent the development of disease. Malaria remains a severe global public health issue and the Antimicrobial Resistance and Therapeutic Discovery Training Program will allow her to expand her research to address the need for new adjunct therapies for malaria.
Tracey J. Lamb, PhD
Tracey Lamb, PhD, is an assistant professor in the Department of Pediatric Infectious Diseases at Emory University School of Medicine. Dr Lamb originally trained as a parasitologist, receiving her PhD from the University of Edinburgh, UK, in the immunological factors mediating susceptibility and resistance to filarial nematodes. After postdoctoral training under the auspices of Dr Jean Langhorne at the National Institute of Medical Research in London, UK, she set up her own laboratory with a focus on understanding the immunopathogenesis of malaria. Her lab utilizes mouse models of malaria in parallel with studies of malaria in children to understand how the immune response to Plasmodium parasites contributes to malarial disease – in doing so the goal is to identify novel therapeutic targets to alleviate disease symptoms. Current research projects include work on the Eph receptor family of molecules that appear to be involved in trafficking of cells to areas of the body where Plasmodium parasites sequester, a key event in organ-specific pathologies in malaria. Her lab is also undertaking research into the role of co-infecting pathogens in shaping the pathogenesis of malaria. It is rare for children infected with Plasmodium not to be co-infected with other pathogens. In collaboration with Dr Sam Speck of the Emory Vaccine Centre and Department of Microbiology and Immunology, Dr Lamb has shown that gammaherpesvirus co-infection can lower the protective immune response to malaria. This work suggests that infection with gammaherpesviruses such as Epstein-Barr Virus may be a risk factor for developing poor immunity to Plasmodium and in turn influence the development of severe malaria. If so, targeting EBV may be an important and novel therapeutic target to boost immunity to malaria in children.
Samantha Prezioso, BS
Samantha Prezioso received her BS in microbiology from the University of Maryland in 2010. During that time she did a yearlong internship with the FDA’s Center for Food Safety and Applied Nutrition in which she improved detection methods for paralytic shellfish poisons in clams, and later E. coli O157:H7 in leafy greens. After graduation, she spent two years at the Centers for Disease Control and Prevention (CDC) in Atlanta, GA in the Department of Foodborne, Waterborne, and Environmental Diseases. There she worked on several projects with the goal of advancing bioterrorism preparedness through improved detection assays. One such project included a study of mutations in Bacillus anthracis conferring resistance to ciprofloxacin. Currently she is studying at Emory University in the lab of Dr. Joanna Goldberg, where she is investigating the regulation and cellular impact of EF-Tu trimethylation in Pseudomonas aeruginosa. Of particular interest is the emerging field of literature suggesting that modulation of cellular translation leads to persister cell formation; persister cells being those that survive antibiotic treatment without an acquisition of a resistance mechanism. She hopes to advance our understanding of this phenomenon through the completion of her graduate study, and proceed to a career investigating persisters and other timely topics in microbiology.
Joanna B. Goldberg, PhD
Joanna B. Goldberg, PhD, received her BA in Biology from Boston University and PhD in Microbiology and Immunology from University of California (UC), Berkeley. Following postdoctoral training at UC Berkeley, she took her first faculty position in Boston at the Channing Laboratory, Brigham & Women’s Hospital, Harvard Medical School. In 1996, she was recruited as an Associate Professor to the Department of Microbiology at the University of Virginia and moved up the ranks to Full Professor. Her research program in bacterial pathogenesis continues to focus on infectious diseases, particularly in cystic fibrosis (CF), with the goal of developing novel therapies to prevent or treat chronic infections. In 2012, she was recruited as a Full Professor to the Division of Pulmonary, Allergy/Immunology, Cystic Fibrosis and Sleep in Department of Pediatrics at Emory University School of Medicine. She holds a secondary appointment in the Department of Microbiology and Immunology and is the Director of Outreach and Education at the Emory+Children’s Center for CF Research.
Katie Nawrocki, BS
Katie received her B.S. in Microbiology from Michigan State University in 2011. During her undergraduate study she worked with Neisseria gonorrhoeae investigating the impact of antimicrobials on the frequency of genetic competence. In continuation of her interest in antimicrobials, she is currently studying the impact of nutrition on the process of sporulation in Clostridium difficile in the McBride lab at Emory University. The CDC has currently ranked C. difficile as a major antibiotic resistance threat due to its natural capacity for resistance to a wide variety of antimicrobials. A portion of these resistances are conferred by the spore form of C. difficile. The formation of the spore allows C. difficile to survive in the environment outside of the host and persist, especially in hospital environments. Spores are a metabolically dormant and are resistant to many antibiotics and disinfectants. The McBride lab works to understand the process of sporulation in hopes of discovering ways to limit sporulation and transmission of this antibiotic mediated disease. The Antimicrobial Resistance and Therapeutic Discovery Training Program will allow her to have the opportunity to take her research to conferences, both local and abroad. The issue of antimicrobial resistance is a global problem and at these conferences she will gain an international perspective of the issue and how others approach the problem of antimicrobial resistance. Additionally, this program will allow her to take part in a variety of experiences that will familiarize her with how the issue of antimicrobial resistance is approached in industry, academia, and the clinic.
Shonna M. McBride, PhD
Shonna McBride, PhD, is Assisant Professor in the Department of Microbiology and Immunology at Emory University School of Medicine. Her research laboratory centers on the emerging pathogen, Clostridium difficile. C. difficile causes chronic intestinal disease that is difficult and costly to treat. The focus of her laboratory is to identify mechanisms that C. difficile uses to colonize the host and disseminate in the environment, with the intent of opening new avenues for treatment of infections. These studies employ a combination of molecular genetic, genomic, biochemical and in vivo approaches to tease apart these mechanisms and their regulation in C. difficile. To colonize the intestine and cause persistent disease, the bacterium must be able to circumvent killing by host innate immune mechanisms. The production of antimicrobial peptides (AMPs) by the innate immune system represents a critical component of host defense against infections that bacteria must overcome to cause persistent disease. Resistance to these peptides is a demonstrated virulence factor for many bacterial pathogens. They hypothesize that resistance of C. difficile to antimicrobial peptides plays a major role in the ability of the bacterium to colonize the human intestine and cause disease. As such, the laboratory is focused on identifying and understanding the mechanisms that C. difficile utilizes to resist AMPs produced by the host and the indigenous microbiota of the intestine. To date, they have identified multiple AMP resistance mechanisms employed by C. difficile, including the novel bacteriocin resistance mechanism, CprABC. By uncovering the bacterial resistance mechanisms that influence disease progression, it is expected that this research will generate knowledge that can be used to manipulate the interactions between the bacteria and the host to prevent and treat infections.
Dr. McBride joined the Emory faculty in June 2012. She received her Ph.D. degree from the University of Texas Health Science Center at San Antonio in 2005 and a Bachelor of Science degree from McNeese State University in 1999. She trained as a postdoctoral fellow in the field of bacterial pathogenesis at the Schepens Eye Research Institute of Harvard Medical School from 2005 to 2008 and at the Tufts University School of Medicine from 2008 to 2012. Dr. McBride’s research is supported by a K01 Career Development Award and an R03 Research grant from the NIDDK/NIH.