Recent Alumni of the Adult Infectious Disease & Basic Microbiologic Mechanisms Training Program

Jonathan Abraham, MD, PhD, 2016 Trainee
Dr. Abraham transitioned to an NIH Director's Early Independence (DP5) award and a Burroughs-Wellcome Fund Career Award for Medical Scientists. He is currently a faculty member in the Department of Microbiology at Harvard Medical School. His work focuses on profiling the human antibody response in survivors of viral hemorrhagic fevers, the development of antibody therapies for human viral hemorrhagic fevers, and the prevention of late neurological complications of these infections.

Kelly Bachta, MD, PhD, 2014-2016 Trainee
Under the mentorship of Dr. John Mekalanos, Dr. Bachta’s project focused on the mechanisms of multi-drug resistance in Pseudomonas aeruginosa. Pseudomonas aeruginosa is an opportunistic pathogen that commonly affects immunocompromised hosts, including those with cystic fibrosis or neutropenia, who frequently receive multiple courses of antibiotics. As a result, P. aeruginosa is serially exposed to selective pressure to develop and maintain mechanisms of antibiotic resistance. One such mechanism involves the coordination of drug-efflux pumps. P. aeruginosa has several known multi-drug efflux pumps which efflux a variety of antibiotics including beta-lactams, fluoroquinolones and aminoglycosides. Dr. Bachta’s project characterized these efflux pumps with the hope of developing novel inhibitors to expand the array of clinically useful anti-pseudomonal therapies. Dr. Bachta is currently conducting additional mentored postdoctoral training at Northwestern Memorial Hospital.

Roby Bhattacharyya, MD, PhD, 2012-2013 Trainee
Dr. Bhattacharyya transitioned to a Foundation for Medical Discovery individual fellowship from the Mass General Executive Committee on Research and an NIH K08. He is currently an Instructor in Medicine in the Division of Infectious Diseases at Massachusetts General Hospital. Dr. Bhattacharyya is working with Dr. Deborah Hung to develop rapid, non-culture based diagnostics for a variety of pathogens and from a range of human samples. This group showed that RNA expression signatures can be used to identify a variety of common pathogens rapidly and specifically using RNA probes that target sequences highly conserved within but not shared between pathogenic species. Targeting RNA expression signatures of stress response pathways that respond early to antibiotic therapy enables discrimination of susceptible strains from resistant ones. The development of rapid diagnostic methods for important human pathogens has the potential to revolutionize early diagnosis and treatment, particularly in resource-poor settings, with enormous impact on the control and prevention of transmission of infectious diseases.

Tyler Bold, MD, PhD, 2017-2018 Trainee
Dr. Bold is currently an Assistant Professor at University of Minnesota Medical School. A hallmark of Mycobacterium tuberculosis infection is bacterial persistence, which may cause chronic T cell antigenic stimulation that results in the development of T cell exhaustion phenotypes, which limit the efficacy of effector and memory immune responses. Under the mentorship of Dr. Eric Rubin, Dr. Bold investigated the hypothesis that T cell exhaustion contributes to the inability of endogenous adaptive immunity to eradicate M. tuberculosis and prevent future infection.

Daniel Bourque, MD, 2014-2016 Trainee
Under the mentorship of Dr. Jason Harris, Dr. Bourque investigated the mechanisms that promote long-term immunity from natural infection to Vibrio cholerae. The aims of his research were to identify mucosal innate immune pathways and early B cell responses, which lead to the development of long lasting B cell memory after natural infection as compared to oral vaccination.

Thea Brennan-Krohn, MD, Trainee 2017-2018
Dr. Brennan-Krohn transitioned to an NIH K08 award under the mentorship of James Kirby, MD, at Beth Israel-Deaconess Medical Center. Dr. Brennan-Krohn is working to develop new antimicrobial strategies for treatment of carbapenem resistant Enterobacteriacae (CRE), which are among the most drug-resistant bacteria known. Her work is based on the observation that treatment with more than one antibiotic in combination is associated with better patient outcomes. Dr. Brennan-Krohn's project involves the development of new methods to test for synergy and investigation of the impact of drug combinations in a mouse model of CRE infection.

Allison Carey, MD, 2015-2017 Trainee
Dr. Carey transitioned to an NIH K08 award. Under the mentorship of Sarah Fortune, MD, Dr. Carey is investigating the modulating features and genetic determinants of tuberculosis infection. Tuberculosis, the disease caused by the pathogen Mycobacterium tuberculosis, is a global health crisis, with over 9 million new cases of active disease and more than a million deaths annually. Tuberculosis was long thought to be a genetically monomorphic pathogen, but recent work uncovered substantial genetic diversity among circulating clinical strains. Dr. Carey uses genome-wide genetic screening and quantitative molecular tools to explore the impact of genetic diversity among clinical strains in the settings of reinfection and vaccination.

Heather Eshleman, PhD, 2016-2017 Trainee
Under the mentorship of Marcia Goldberg, MD, at Massachusetts General Hospital, Dr. Eshleman investigated the mechanism of action of the Shigella flexneri effector protein OspB. Shigella spp. deliver into host cells effector proteins that alter the function of host cell pathways in ways that promote infection. OspB induces cell proliferation of host cells. Dr. Eshleman worked on defining the pathway that is impacted by OspB and the mechanism by which OspB manipulates it.

Sanjat Kanjilal, MD, MPH, 2015-2017 Trainee
Under the mentorship of Marc Lipsitch, PhD, and Yonatan Grad, MD PhD, Dr. Kanjilal worked to define population dynamics and genotypic correlates of invasion and antibiotic resistance of methicillin-resistant Staphylococcus aureus (MRSA). With the goal of defining S. aureus genes and regulatory networks that underlie clinically important phenotypes and of defining patterns of transmission through human populations, Dr. Kanjilal investigated the population structure, antibiotic resistance, and virulence factors of MRSA, using phylogenetic and statistical tools to analyze a data set of over 1400 genomes from well-characterized isolates.

Jacob Lazarus, MD, PhD, 2017-2018 Trainee
Dr. Lazarus transitioned to a KL2 MeRIT fellowship. Under the mentorship of Dr. Matthew Waldor, Dr. Lazarus is working to identify host and pathogen factors that influence induction of antibiotic resistance, the switch from commensal to pathogen, and bloodstream translocation by Enterobacteriaceae, a large group of Gram-negative bacteria than can both colonize the human gut as commensals and cause life-threatening infections as invasive pathogens. Enterobacteriaceae frequently acquire resistance to multiple antibiotics, especially extended-spectrum beta-lactams and carbapenems, making them challenging and occasionally impossible to treat successfully.

Philip Lederer, MD, 2015-2016 Trainee
Under the mentorship of Dr. Edward Nardell, Dr. Lederer worked to evaluate the impact of a novel approach to identify and treat individuals with tuberculosis on ruducing delays in tuberculosis treatment and on health care worker infections in Peru.

Kelly Miller, PhD, 2014-2016 Trainee
Under the mentorship of Marcia Goldberg, MD, Dr. Miller characterized interactions of Shigella flexneriand host cells at the molecular level to better understand Shigella pathogenesis. S. flexneri is an intracellular bacterial pathogen that is the most common cause of diarrheal disease worldwide. To establish successful infection bacteria must induce uptake into human colonic epithelial cells, evade host innate immune responses, and spread into neighboring cells within the epithelium. Many steps in this process require the activity of bacterial “effector” proteins that are translocated into host cells using a conserved syringe-like secretion apparatus called a type three secretion system. Dr. Miller investigated how interaction of bacterial effector proteins and host proteins interfere with the host cell innate immune response during Shigella infection.

Anne Piantadosi, MD, PhD, 2016 Trainee
Dr. Piantadosi transitioned to a KL2 MeRIT fellowship. Under the mentorship of Dr. Pardis Sabeti, she is using next-generation sequencing to identify known and unknown viral pathogens in infectious encephalitis and is then characterizing a selected subset of these pathogens.

Jennifer Reedy, MD, PhD, 2012-2014 Trainee
Dr. Reedy transitioned to a KL2 MeRIT fellowship. Under the mentorship of Jay Vyas, MD, PhD, Dr. Reedy investigated how the innate immune system recognizes and responds to fungal pathogens. Her research focused on the dematiaceous mold Exserohilum rostratum and elucidating the mechanisms by which the innate immune system recognizes and responds to this fungus. Specifically, she analyzed the carbohydrate composition of spores and hyphae of E. rostratum and evaluated the cytokine response elicited by macrophages in response to E. rostratum.

Chanu Rhee, MD, MPH, 2014-2015 Trainee
Dr. Rhee is a faculty member in the Department of Population Medicine, Brigham and Women’s Hospital. Under the mentorship of Richard Platt, MD, MSc, Dr. Rhee focused on the epidemiology, surveillance, and prevention of healthcare-associated infections, particularly in critically ill patients. His research project, a multicenter observational study being conducted with the CDC Prevention Epicenters, used objective clinical data captured by electronic health records to improve the public health system’s capacity to accurately track the incidence and burden of severe sepsis and septic shock.

Jonathan Robbins, MD, PhD, 2014-2017 Trainee
Now a Medical Director at Merck & Co., Dr. Robbins studied malaria, a parasitic disease responsible for hundreds of thousands of deaths each year, under the mentorship of Jeffrey Drovin, MD PhD. Dr. Robbins used a combination of forward and reverse genetic approaches to better understand the cell division cycle of P. falciparum.

William Robins, PhD, 2012-2013 Trainee
Dr. Robins is working with John Mekalanos, PhD, to characterize the transcriptional regulation of V. cholerae, the agent of cholera, during its exit from the host into the environment. Where cholera is present, a substantial number of environmental V. cholerae organisms exist as clumps of metabolically-inhibited cells that persist for weeks or months. These conditionally viable environmental cells resist growth under standard conditions, but revert to an infectious and virulent form when introduced into animals. Dr. Robins’ seeks to uncover the transcriptional patterns occurring in conditionally viable environmental cholera as they form and persist in environmental water and then as they are resuscitated by exposure to autoinducers.

Brian Russo, PhD, 2014-2016 Trainee
Under the mentorship of Marcia Goldberg, MD, Dr. Russo works to define molecular mechanisms required for the virulence of the bacterium Shigella, the most common cause of diarrhea worldwide. To establish disease, Shigella infects epithelial cells lining the intestine and spreads to adjacent cells. Effector proteins, delivered into the epithelial cells by Shigella, usurp host signaling in ways that promote infection. Dr. Russo is investigating the mechanisms by which the host cell activates type 3 secretion, including the role of cellular intermediate filaments and actin polymerization.

Ana Weil, MD, 2014-2015 Trainee
Dr. Weil is currently supported on a K08 and is a junior faculty member in the Division of Infectious Diseases at Massachusetts General Hospital. Under the mentorship of Edward Ryan, MD, and Regina LaRocque, MD, Dr. Weil investigates factors that modulate the spread of cholera among humans, focusing on the human gut microbiome. Analyzing the microbial population structure of samples taken from household contacts of cholera patients, she determined specific bacterial groups associated with a higher likelihood of becoming infected with V. cholerae.