Alumni

Michelle Su

TRAINEE:
Michelle Su
Graduate Student
michelle.su@emory.edu

I am interested in how the Gram-positive pathogen Staphylococcus aureus develops intermediate resistance to vancomycin; these strains are called VISA. My project tests the hypothesis that different VISA mutations have different fitness in two clinically important genetic backgrounds and are compensated by different mutations. Aim 1. Interaction of genetic background, mutation and fitness costs for vancomycin resistance level. I will determine how single nucleotide polymorphisms (SNPs) in candidate genes modulate vancomycin resistance to characterize mutations found in VISA strains by using isogenic USA100 and USA300 mutants and testing for a phenotypic effect on vancomycin resistance. Validated VISA determinants will be introduced into USA100 and USA300 MRSA lineages to investigate how vancomycin resistance alters the fitness and virulence of strains and ultimately the fitness landscape between lineages. Aim 2. Parallel evolution of vancomycin resistance and subsequent divergence. I will determine the convergent mutation in candidate genes of USA100 and USA300 by generating and sequencing laboratory VISA strains at different bottlenecking pressures. Maintenance of these VISA strains at sub-MIC antibiotic concentrations will allow for the study of divergence in evolution that will occur after selection pressures have decreased and more evolutionary pathways have opened. Together, these two approaches will be a comprehensive study of the evolution of vancomycin intermediate resistance in S. aureus and its effects on the fitness landscape.

Timothy Read

MENTOR:
Timothy Read, PhD

Professor
tread@emory.edu

Dr. Read is Professor of Infectious Diseases with Secondary Appointment in Human Genetics. Dr. Read's research interests center around the application of genomics technologies to understanding infectious diseases. In particular, he is interested in trying to frame the questions that only become possible to answer as new and even better instruments for generating DNA sequence information come online. Genomics for infectious disease detection and clinical diagnosis. The rapidly decreasing cost of sequencing offers the opportunity in the near future to rapidly acquire large portions of the genome sequence of pathogens, either from DNA extracted from pure cultures or directly from clinical samples (metagenomics).

Dr. Read is interested in applying new technologies to determine their limits of sensitivity and to develop software to extract clinically useful information from the sequence data. Bacterial Pathogen Genome Evolution. The availability of multiple high quality genomes of pathogens such as Bacillus anthracis (etiologic agent of anthrax) and its less pathogenic close relatives affords the opportunity to ask questions about the evolution of virulence in these lineages. His particular interest is the extrachromosomal elements such as plasmids and bacteriophage, and intergenic repeat sequences. These extraneous genetic entities often carry vital virulence genes (like the anthrax toxin and plague virulence genes). They are also potent factors for short term genome change, through insertion, expansion and movement in the genomes and through the selection pressure they presumably exert on the genome for resistance.

Dr. Read seeks to find out how (and why) pathogens evolve to infect humans. What are the species that recent ancestors of B. anthracis were infecting before they developed virulence for mammals? What are the danger signs to look for in predicting the source of new emerging diseases? A genome based understanding of pathogen evolution will be vital for interpreting genetic variation in clinical sequence data (see above). The same knowledge can also be applied to vaccine and drug target selection.

Dr. Read received a BSc in Biological Sciences from the University of London and then studied Microbial Genetics at the University of Leicester with Prof Brian Wilkins. 

Jessica Trost

TRAINEE:
Jessica Trost, BS
Graduate Student
jessica.trost@emory.edu

Jessica Trost received her BS in Biology from the University of Wisconsin-Madison in 2007.  After graduation, she pursued work in pediatric respiratory virus research and clinical diagnostic development at the Medical College of Wisconsin.  Following the 2009 influenza pandemic, and inspired by the importance of preparedness, she applied and was awarded the APHL/CDC Emerging Infectious Disease (EID) fellowship at CDC and joined the Influenza Division.  At CDC, her work included detecting and evaluating potentially broadly neutralizing antibodies in influenza, vaccine strain selection, and the first evidence of influenza infection in sea otters.  Her current research at Emory University as a student in the Microbiology and Molecular Genetics (MMG) program in Dr. David Steinhauer’s lab focuses on understanding the relationship and balance of the two major surface glycoproteins of influenza, HA and NA.  Her aim is to understand the impact of these two proteins in the reassortment and emergence of novel and pandemic influenza viruses from natural avian reservoirs.  With the support of the Antimicrobial Resistance and Therapeutic Discovery Training Program, she hopes to evaluate the potential for novel influenza subtypes to emerge in naive human populations, or reassort with current influenza strains in humans, to highlight and improve vaccine and antiviral targets in advance of emerging epidemics and pandemics.  

Dr. David Steinhauer

MENTOR:
David Steinhauer, PhD
Associate Professor
steinh@emory.edu

The Steinhauer laboratory is primarily interested in influenza virus entry into host cells and the role of the hemagglutinin glycoprotein (HA) in this process. The work has a strong focus on the structure-function relationships of HA with regard to its receptor binding and membrane fusion properties. The work combines protein structure analysis and molecular virology techniques to address specific questions on how influenza viruses attach to cells, deliver their genomes, assemble at the end of the replication cycle, and evolve to evade host immune responses and the action of antiviral drugs. We are also attempting to exploit our knowledge of high resolution HA structures to design novel vaccines for influenza, and for other pathogens using influenza as a vector.

Kara Phipps

TRAINEE:
Kara Phipps, BS
Graduate Student
k.l.phipps@emory.edu

Kara Phipps graduated in 2014 with a BS in Biology from Southwest Baptist University. While at SBU, Kara developed a strong interest in the study and control of infectious diseases and participated in undergraduate research.  Her studies focused on the relationship between DNA damage responses to fluoroquinolone treatment and biofilm formation and motility in Pseudomonas aeruginosa. Upon entering the Microbiology and Molecular Genetics program at Emory University, Kara joined the laboratory of Anice Lowen to study the factors which impact gene reassortment and diversification of influenza viruses. Kara particularly seeks to identify mechanisms which impact reassortment and viral diversification following transfer of influenza viruses to a non-native host species. With the opportunities and support provided by the Antimicrobial Resistance and Therapeutic Discovery Training Program, Kara hopes to further current knowledge of the basic mechanisms by which influenza viruses evolve to allow escape of current antiviral treatments and vaccine-induced immunity. 

Dr. Anice Lowen

MENTOR:
Anice Lowen, PhD

Assistant Professor

anice.lowen@emory.edu

Dr. Lowen is an Assistant Professor in the Department of Microbiology and Immunology, Emory University School of Medicine. She obtained her PhD from the University of Glasgow, UK, and carried out postdoctoral training at Mount Sinai School of Medicine in New York, NY. 

Despite its clear importance to the epidemiology of influenza, the process by which human influenza viruses travel from one individual to another is not well understood. Prior to the zoonotic outbreak of H5N1 influenza viruses in Southeast Asia, it was generally assumed that if an influenza virus could productively infect a given host species, that virus would also transmit among individuals of that species. The lack of transmission of H5N1 influenza viruses among humans and other mammals has shown that, on the contrary, viral growth is not the only prerequisite for transmission. Research over the past six years has revealed that viral, host and environmental factors each play a role in determining the efficiency with which an influenza virus transmits. We previously showed, for example, that ambient conditions of humidity and temperature have a strong impact on the efficiency of transmission, that host-specific adaptive changes in the viral polymerase can alter transmission efficiency, and that host immunity resulting from either vaccination or natural infection limits transmission to varying degrees. Despite such progress, an in-depth understanding of transmission remains a high priority in the influenza field. Going forward, my research will focus on the viral traits which allow transmission to proceed in guinea pigs, a mammalian model system which we have demonstrated to reflect humans well in terms of influenza virus transmissibility.

Sarah Anderson

TRAINEE:
Sarah Anderson, BS
Graduate Student
sarah.emily.anderson
@emory.edu

Sarah Anderson received her BS in 2013 from the University of North Carolina, where she double majored in biology and chemistry.  As an undergraduate, Sarah conducted research projects on gene regulation in Drosophila melanogaster, and on innate immune responses to influenza infection.  Following graduation, she was awarded an APHL/CDC Emerging Infectious Diseases (EID) Fellowship to conduct research at the Wadsworth Center in the New York State Department of Health.  There she developed a diagnostic assay to detect fluoroquinolone-resistant Mycobacterium tuberculosis, and worked on a basic research project studying conjugation in Mycobacterium smegmatis.  Sarah enrolled in the Microbiology and Molecular Genetics program at Emory University in 2014.  Her interests in antibiotic resistance, bacterial genetics, and pathogenesis led her to join the laboratory of Dr. Philip Rather.  Sarah’s current research in the Rather lab focuses on understanding the mechanisms regulating phase variation and intrinsic antimicrobial resistance in Acinetobacter baumannii.  By participating in the Antimicrobial Resistance and Therapeutic Discovery Training program, Sarah hopes to expand her training outside of the laboratory by presenting her work at conferences and networking with scientists both inside and outside academia. 

Dr. Philip N. Rather

MENTOR:
Philip N. Rather, PhD

Professor
prather@emory.edu

Philip N. Rather is a Professor in the Department of Microbiology and Immunology. His lab studies the mechanisms of virulence and intrinsic antibiotic resistance in the nosocomial pathogen Acinetobacter baumannii. A novel regulatory switch has been identified in A. baumannii that results in the interconversion between two phenotypically distinct cell types distinguished by their opaque or translucent colony opacity phenotype. The opaque variant is virulent and exhibits higher levels of resistance to cationic antimicrobials. The regulatory mechanism controlling this interconversion is under investigation as well as identifying the differentially expressed genes that confer increased virulence and resistance to cationic antimicrobials. A second area of focus is the regulation of intrinsic beta-lactam resistance in A. baumannii. For this area of study, a link between cell division and chromosomally mediated beta-lactam resistance has been identified and is being characterized. 

Sherman

TRAINEE:
Edgar Sherman, BS
Graduate Student
edgar.sherman@emory.edu

Edgar Sherman received his BS from The University of Texas at San Antonio (UTSA) in 2014. Edgar developed a strong interest in microbial genetics following two research internships where he investigated the role of mitochondrial gene function in eukaryotic respiration at The University of Texas at Austin and studied how protein turnover affects aging in rodents at The University of Texas Health Science Center in San Antonio.  At UTSA, Edgar’s research focused on mechanisms of biofilm formation in the nosocomial pathogen Acinetobacter baumannii by targeting genes involved in bacterial cell signaling. After graduating, Edgar was accepted into the Microbiology and Molecular Genetics (MMG) program at Emory University where his research interest in antimicrobial resistance led him to join Dr. David Weiss’ lab and focus on studying antibiotic resistance mechanisms in Multi-drug resistant Gram-Negative pathogens. Specifically, Edgar’s research focuses on understanding the underlying genetic pathways facilitating resistance to aminoglycosides, an important class of antibiotics, in A. baumannii and how these mechanisms lead to treatment failure in a patient. Under the Antimicrobial Resistance and Therapeutic Discovery Training Program, Edgar seeks to characterize novel resistance mechanisms to ultimately improve patient outcome and expand our understanding on how bacteria evolve to combat our clinical therapeutics. 

Dr. Weiss

MENTOR:
David S. Weiss, PhD

Associate Professor
david.weiss@emory.edu

David S. Weiss is an Associate Professor in the Division of Infectious Diseases and Co-Director of the Emory Antibiotic Resistance Center. His lab's research is focused on understanding mechanisms of antibiotic resistance employed by Gram-negative nosocomial pathogens such as Acinetobacter baumannii and Enterobacter cloacae.

His lab has identified and mechanistically characterized several novel genes that contribute to resistance to the last-line, cationic polymyxin antibiotics in diverse bacteria. Furthermore, this research has shown that the development of polymyxin resistance in treated patients leads to cross-resistance to cationic antimicrobial peptides of the host innate immune system. Thus, polymyxin treatment may select for bacterial strains with increased virulence. In addition to how antibiotics may alter bacterial susceptibility to the immune system, his lab is very interested in exploring the causes of unexplained treatment failures in which antibiotic therapy is ineffective despite bacterial strains appearing to be susceptible to a given antibiotic.

King

TRAINEE:
Thayer King, BS
Graduate Student
thayer.king@emory.edu

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. 

Dr. Lamb

MENTOR:
Tracey J. Lamb, PhD

Assistant Professor
tracey.j.lamb@emory.edu

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.

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TRAINEE:
Samantha Prezioso, BS
Graduate Student
sprezio@emory.edu

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. 

Dr. Goldberg

MENTOR:
Joanna B. Goldberg, PhD

Professor
joanna.goldberg@emory.edu

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.  

Nawrocki

TRAINEE:
Katie Nawrocki, BS
Graduate Student
knawroc@emory.edu

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. 

Dr. McBride

MENTOR:
Shonna M. McBride, PhD
Assistant Professor
shonna.mcbride@emory.edu

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.  

Crispell

TRAINEE:
Emily Crispell, BS
Graduate Student
ecrispell@emory.edu

Emily Crispell received her BS in Chemistry from the Georgia Institute of Technology in 2009. After graduation, she switched fields to pursue an interest in microbiology, infectious diseases, and epidemiology through a four-year position with the Georgia Emerging Infections Program (GAEIP) laboratory in Atlanta, GA. Her research with the GAEIP focused primarily on antibiotic resistance trends and mechanisms in Staphylococcus aureus. Her current research at Emory University in the laboratory of Dr. David Weiss focuses on novel antibiotic resistance mechanisms in multi-drug resistant Gram-negative pathogens and the development of inhibitors to target these resistance mechanisms. Particular research interests include how bacterial signaling systems govern the regulation of antibiotic resistance and how host factors influence the development of antibiotic resistance during bacterial infection. As a trainee of the Antimicrobial Resistance and Therapeutic Discovery Training Program, she aims to develop unique insight into the problem of antibiotic resistance by connecting basic science research training with mentorship from leaders in the clinic. 

Dr. Weiss

MENTOR:
David S. Weiss, PhD

Associate Professor
david.weiss@emory.edu

David S. Weiss is an Associate Professor in the Division of Infectious Diseases and Co-Director of the Emory Antibiotic Resistance Center. His lab's research is focused on understanding mechanisms of antibiotic resistance employed by Gram-negative nosocomial pathogens such as Acinetobacter baumannii and Enterobacter cloacae. His lab has identified and mechanistically characterized several novel genes that contribute to resistance to the last-line, cationic polymyxin antibiotics in diverse bacteria. Furthermore, this research has shown that the development of polymyxin resistance in treated patients leads to cross-resistance to cationic antimicrobial peptides of the host innate immune system. Thus, polymyxin treatment may select for bacterial strains with increased virulence. In addition to how antibiotics may alter bacterial susceptibility to the immune system, his lab is very interested in exploring the causes of unexplained treatment failures in which antibiotic therapy is ineffective despite bacterial strains appearing to be susceptible to a given antibiotic.