Articles
 
 

Columbia University
Lyme & Tick-borne Diseases Center

Jorge L. Benach, Ph.D., is Chairman of the Department of Molecular Genetics and Microbiology at SUNY at Stonybrook.  He is also director of the Infectious Diseases Institute of the Center for Molecular Medicine.  A Fellow of the Infectious Diseases Society of America and a former Fullbright Research Fellow, he serves on the editorial boards of Infection and Immunity and of the Infectious Diseases Society of America.  A co-discoverer of the etiologic agent of Lyme disease, his research interests have centered on the pathogenesis of spirochetal and other tick-borne infections. Dr. Benach has served on Public Health Service advisory committees and on two NIH study sections.  His current grants focus on the mechanism of action of bactericidal, complement independent antibodies that react with outer surface lipoproteins of Borrelia and on the functional relevance of host plasmin and other host proteases in bacterial invasiveness and as a bacterial defense mechanism.

Carolyn Britton, MD is Professor of Clinical Neurology at Columbia University.  She completed her MD at NYU and residency and fellowship at Columbia University. On the board of delegates of the National Medical Association, she has also been very active in clinical research related to neurologic Lyme disease and neuro-AIDS.  Particular areas of clinical expertise relate to infectious and inflammatory conditions of the CNS, including neuro-AIDS, neuro-Lyme, meningitis, encephalitis, sarcoidosis, collagen vascular disorders, and multiple sclerosis.

Diego Cadavid, MD.  Dr. Cadavid is currently Associate Professor of Neurology and Neuroscience at New Jersey Medical School in Newark, NJ.  He completed medical training at Pontificia Universidad Javeriana in Bogotá, Colombia and won the Merck-Sharpe-Dohme Award by the Colombian Association of Medical Schools as the Best Medical Graduate in the Country.  Since 1991 when he moved to the United States he has been studying the neurological complications of spirochetal infections, first as a postdoctoral appointee in Alan G. Barbour's laboratory at The University of Texas Health Science Center in San Antonio, Texas and later as a neurology resident with Andrew R. Pachner at Georgetown University in Washington, DC.  In 1998 he was awarded the Méndez Fellowship for Clinicians for training in neuropathology at the prestigious Armed Forces Institute of Pathology in Washington, DC.  Since 1999 he has been a faculty member of New Jersey Medical School where he has a laboratory for research on spirochetal infections at the Center for the Study of Emerging Pathogens.  His research has been funded as primary investigator by the American Heart Association, the Foundation of UMDNJ, and the National Institutes of Health. He was also a collaborator on a large NIH contract to study the neurological complications of Lyme disease in non-human primates.  Dr. Cadavid is an active clinician in the field of multiple sclerosis and has published extensively on relapsing fever borreliosis, Lyme borreliosis, cerebrovascular disease, and multiple sclerosis.  He has currently 30 publications in major biomedical journals and 9 book chapters.  He is an active member of the American Academy of Neurology and the American Society of Microbiology.

Andrew Dwork, MD.  Co-director, division of neuropathology, Department of Psychiatry, Columbia University.  His research has focused on neuropathologic changes associated with a variety of diseases, including schizophrenia and mood disorders. He has used animal models as well to study the impact of ECT and transcranial magnetic stimulation. In 1995, he published a post-mortem case of rapid front-lobe dementia associated with Borrelia burgdorferi infection that was associated pathologically with severe subcortical degeneration (J Clin Neuropsychiatry). He will be heading up the brain bank for patients who had well-diagnosed Lyme disease affecting the central nervous system.

Gerald Fischbach, MD, Professor of Pharmacology in the Center for Neurobiology and Behavior at Columbia University, former  Dean of the Columbia College of Physicians & Surgeons and former Director of NINDS at NIH (Ex-officio board member) .   Dr. Fischbach is interested in the formation and maintenance of synapses, the junctions between nerve cells and their targets through which information is transferred. He is particularly interested in the neuromuscular junction, a synapse that is easily accessible to experimental manipulation and has used cultured neurons and muscle cells to characterize the biochemical, cellular, and electrophysiological mechanisms underlying development and function of the neuromuscular junction. Beginning in the 1970's, Dr. Fischbach embarked on a search for molecules released by motor neurons that regulate the number of acetylcholine receptors on muscle cells. This work culminated in 1993 with the purification and cloning of a protein called ARIA (for acetylcholine receptor-inducing activity) that stimulates synthesis of acetylcholine receptors by skeletal muscle cells. This molecule is now known to be a member of a family of trophic factors called neuregulins that are thought to be involved in a variety of important developmental processes in the nervous system. Because ARIA and other neuregulins act by binding to tyrosine kinase receptors on target cells, Dr. Fischbach's work was key in demonstrating that synaptic development relies upon biochemical mechanisms that are broadly similar to those that underlie the action of nerve growth factor and other well known trophic molecules. His current focus is on trophic factors that influence synaptic efficacy and nerve cell survival.

Claire M. Fraser-Liggett is the director of the new Institute of Genome Sciences at the University of Maryland.  She has left her role as President and Director of The Institute for Genomic Research in Rockville, MD, where she led the team of scientists who sequenced the genomes of several microbial organisms (including Borrelia burgdorferi).  Perhaps the most-cited authority in genomics of the last decade, Fraser has helped initiate the era of comparative genomics. Her research interests include whole genome sequence analysis of microbial genomes, and the use of genomic-based approaches to elucidate differences in gene expression. She earned her B.S. from Rensselaer Polytechnic Institute and Ph.D. from State University of New York at Buffalo.

Pamela Gallin, MD is director of Pediatric Ophthalmology and Associate Professor of both Ophthalmology and Pediatrics at the Children's Hospital of New York Presbyterian Medical Center, where she is on the faculty of the Columbia University College of Physicians and Surgeons. Dr. Gallin has an international clinical surgical practice. She has recently become interested in the central nervous system effects of Lyme disease. Dr. Gallin served on Hilary Clinton's White House Health Task Force, authored numerous scientific papers, and has been in Best Doctors in America for many years. In addition, Dr. Gallin orchestrated the air lift and medical care for many Bosnian Children treated through Columbia Presbyterian.  Dr. Gallin recent book, "How to Survive Your Doctor's Care" (LifeLine Press), was featured on the Today Show series "Second Opinions" and recommended by Forbes and The Wall Street Journal.    Dr. Gallin graduated from Washington University in St. Louis, Summa Cum Laude, Phi Beta Kappa, Tau Beta Pi and was at the top of her class in their medical school.

Scott Hammer, MD.  Dr Hammer is the Harold C. Neu Professor of Medicine, Professor of Epidemiology and Chief of the Division of Infectious Diseases at the Columbia University Medical Center (CUMC). Dr. Hammer's major investigative interest is the treatment and prevention of HIV disease. He is an investigator in the National Institutes of Health sponsored AIDS Clinical Trials Group (ACTG), a multicentre organisation which performs clinical trials designed to improve the understanding and treatment of HIV infection and its complications. As an ACTG investigator, Dr Hammer chaired the two largest national trials of antiretroviral therapy carried out by that group in the 1990s, studies which contributed to the current standard of care of HIV infection. In addition to his interest in the treatment of persons with established HIV infection, Dr Hammer is an investigator in the National Institutes of Health sponsored HIV Vaccine Trials Network (HVTN), a multicentre organisation whose mission is to develop an effective preventive HIV vaccine. He is Chair of the AIDS Vaccine Research Working Group, an advisory committee to the Division of AIDS, NIAID. He is a former Chair of the Antiviral Products Advisory Committee of the Food and Drug Administration and the HIV Disease Research Agenda Committee of the ACTG, and currently serves on the Editorial Board of the New England Journal of Medicine. At the international level, Dr. Hammer is a member of the Governing Council of the International AIDS Society, a member of the World Health Organization's Strategic and Technical Advisory Committee for HIV/AIDS, serves as Co-Chair of the Steering Committee of the WHO's Global HIV Drug Resistance Surveillance Program, and continues in his role as Editor-in-Chief of the WHO's Antiretroviral Guidelines for Resource Limited Settings.

Mady Hornig, MD, MA, is Associate Professor of Epidemiology and Director of Translational Research in the Jerome L. and Dawn Greene Infectious Disease Laboratory at the Mailman School of Public Health, Columbia University. A physician-scientist, she is widely recognized for her animal model and clinical research on the role of microbial, immune, and toxicologic factors in neuropsychiatric disorders, including autism, schizophrenia, attention-deficit/hyperactivity disorder, obsessive-compulsive disorder, and mood disorders. Her work integrates data from animal models and epidemiologic studies to understand the mechanisms by which environmental factors, including viruses, bacteria, and toxins, or common host responses to these agents during brain maturation, may act as triggers or amplifying factors in the pathogenesis of some neuropsychiatric conditions. Findings from animal models of immune-mediated neurodevelopmental damage are employed to sharpen the focus of investigations in human cohorts, creating the basis for translation into novel biomarkers and intervention strategies; and hypotheses generated from epidemiologic studies are rigorously tested in animal models. In 2004, Dr. Hornig presented to the Institute of Medicine Immunization Safety Review Committee and testified twice before congressional subcommittees regarding the role of infections and toxins in autism pathogenesis. She leads a project on immune and neuroendocrine factors in West Nile virus encephalitis within the Northeast Biodefense Center, an NIAID regional center of excellence in biodefense and emerging infectious diseases, where she is a member of the Core Oversight Committee and the Governing Council. She was recently elected to the President's Council of Cornell Women.

John Keilp, PhD.  Dr. John Keilp, Research Scientist at Columbia University and NYSPI, is a neuropsychologist with research interests in the assessment of cognitive impairment in psychiatric and neurological disease. His major focus has been on depression and the association of cognitive impairment to suicidal behavior. He heads the neuropsychology laboratory in the division of Neuroscience at the New York State Psychiatric Institute, and has major collaborations on studies of Lyme disease, genetics of working memory, and brain imaging.  He recently published "WAIS-III and WMS-III performance in Chronic Lyme Disease" in the Journal of the International Neuropsychological Society (2006) in which he reported that Lyme patients have mild to moderate deficits in processing speed and in memory (auditory immediate and delayed, visual delayed).

Ian Lipkin, MD, Professor of Neurology, Anatomy, & Neurobiology, and  Epidemiology, Director, Jerome L. and Dawn Greene Infectious Disease Laboratory, Mailman School of Public Health,  Professor of School of Basic Medical Sciences, Beijing University.  The Greene Infectious Disease Laboratory is a premier facility for emerging infectious diseases research and treatment. This lab is at the vanguard for studying the infectious disease outbreaks in the U.S. and globally.
W. Ian Lipkin, MD, is internationally recognized as an authority on the use of molecular biological methods for pathogen discovery and the role of immune and microbial factors in neurologic and neuropsychiatric diseases. His early observation that cryptic infection can influence brain function is increasingly recognized as important in the context of neuropsychiatric diseases such as autism and schizophrenia; and it may also play a role in neurodegenerative disorders. To address such questions, Dr. Lipkin created molecular methods for rapidly detecting unknown viruses in clinical materials. The first application of these methods resulted in identification of Borna disease virus, a new type of virus that had eluded classical methods for virus purification. Since isolating the first genes of this virus in 1990, Dr. Lipkin cloned its genome and defined its replication strategy and the molecular basis for neurotropism and behavioral syndromes associated with acute and persistent brain infection. An international multi-center program coordinated by Dr. Lipkin is assessing the role of Borna disease virus in human neuropsychiatric diseases using methods patented by Lipkin, Briese and colleagues. Dr. Lipkin is the leader of the team that established the method of domain specific differential display and subsequently identified the West Nile virus in the brains of encephalitis victims in New York State in the fall of 1999. Dr. Lipkin's group  contributed to the control of SARS in China, by creating the first rapid diagnostic test in the context of his role as Special Advisor to Minister Xu in directing basic and translational research May through July 2003.  Most recently (April 2007), Dr. Lipkin's team identified a mystery pathogen associated with organ transplant deaths in Australia and made another breakthrough relating to colony collapse disorder in bees (see NYTimes, Science Times, 4/24/07).

J. John Mann, MD, PhD. J. John Mann M.D., is The Paul Janssen Professor of Translational Neuroscience (in Psychiatry and in Radiology) at Columbia University and Chief of the Department of Neuroscience at the New York State Psychiatric Institute.
Dr. Mann is trained in Psychiatry and Internal Medicine and has also obtained a doctorate in Neurochemistry. His research employs functional brain imaging, neurochemistry and molecular genetics to probe the causes of depression and suicide. Dr. Mann is the Director of the NIMH Conte Center for the Neuroscience of Mental Disorders, Director of the Stanley Center for Applied Neuroscience of Bipolar Disorders, and President of the International Academy of Suicide Research. He has published 401 papers and edited 10 books on the subjects of the biology and treatment of mood disorders, suicidal behavior and other psychiatric disorders. In private practice he specializes in the treatment of mood disorders.

Aaron P. Mitchell, PhD, Chairman of Microbiology,  Professor of Molecular Pathogenesis, at Columbia University.  Dr. Mitchell's lab focuses on understanding the genes, pathways, and mechanisms that govern virulence and drug resistance of Candida albicans. Our studies have utilized both C. albicans itself and its relative, S cerevisiae, which is seldom a pathogen but is an outstanding model for molecular genetic analysis. We identified putative Rim101p pathway genes in C. albicans through searches of the genomic sequence and created insertion-deletion mutants through a rapid method worked out in this lab. Characterization of these strains showed that the Rim101p pathway is required for filamentation at alkaline pH and for virulence in a mouse bloodstream infection model. S. cerevisiae and C. albicans proteins Rim20p and Snf7p form a scaffold that places the protease and substrate into close proximity. Rim20p has homologs in all eukaryotes, and one (mouse Alix) has been implicated in apoptotic proteolysis. Thus our model for the Rim101p pathway may be broadly applicable to other systems.  Analysis of the S. cerevisiae MDS3 homologs indicated that their role in pH responses may be conserved. Studies of growth and virulence of C. albicans rim101-/- mds3-/- double mutants argue that Mds3p acts in a Rim101p-independent pathway (8). This analysis serves to define a new pH response pathway, whose mechanism is under study in S. cerevisiae. Perhaps more importantly, it serves as proof of principle that our mutagenesis strategy can be applied on a large scale: we have used the insertion mutant collection to identify new C. albicans genes that govern drug resistance, host-cell damage, chlamydospore formation, and biofilm formation.

Steven E. Schutzer, MD, Professor of Medicine, University of Medicine and Dentistry of New Jersey.  Dr. Steven E. Schutzer received his MD from Cornell University Medical College. He is Board Certified in Internal Medicine, Allergy and Immunology, and Diagnostic Laboratory Immunology. He is a physician-scientist, He joined New Jersey Medical School after additional research training at The Rockefeller University in immunology and microbiology. His research involves the interface of the immune system and microbes. This includes clinical and research aspects of Lyme disease.   Dr. Schutzer, continues to be a Principal Investigator of NIH grants and other funding. Many of his past and current achievements in the area of Lyme disease focus on the human immune response to the pathogen, the whole genomic sequence of Lyme agent strains, and diagnostics. His work has been published in well known journals such as Science, New England Journal of Medicine, Lancet, Journal of Clinical Investigation, and JAMA.

Brian E Scully, MD.  Dr. Scully is a graduate of University College of Dublin and is board certified in internal medicine and infectious disease.  Currently Associate Professor of Clinical Medicine in Infectious Disease at Columbia University, he is also director of the Division of Hospital Epidemiology.  Particular area of expertise includes hospital acquired infections.  In 2003, he was the senior author on a paper in Emerging Infectious Diseases reporting transfusion-associated Babesiosis after heart transplant which led to ARDS and mechanical ventilation. He serves as consultant to the Lyme and Tick-borne Diseases Clinical Research projects.

Ronald L. Van Heertum, M.D., is Professor of Radiology at Columbia University, Vice Chairman - Administration, Director of the Division of Nuclear Medicine and Director of the Morton A. Kreitchman PET Center. Dr. Van Heertum is internationally known for his work with applications of SPECT and PET brain imaging. He currently has several national roles in the American College of Radiology including Chairman of the Nuclear Medicine & PET Accreditation Committee, Chairman of the Accreditation Chief's Committee and Vice Chairman (Accreditation) of the Commission on Quality & Safety: He is also a life-member and past Chairman of the American Board of Nuclear Medicine.  Research papers from his group in the late 90's documented findings of heterogeneous hypoperfusion as seen on the brain SPECT scans of patients with neurocognitive Lyme disease, a pattern also consistent with what would expect to see among patients with encephalitis, vasculitis or with certain substance abuse (cocaine).  Dr. Van Heertum is currently collaborating with Dr. Fallon on a masked study to determine the degree to which brain SPECT imaging can be used reliably as a clinical tool to help in the differentiation of patients with Lyme Disease from other disorders.

Janis Weis, PhD, Prof of Pathology, University of  UtahDr. Weis' research has focused on the pathogenic mechanisms of Lyme arthritis. Arthritis results from bacterial invasion of joint tissue and is characterized by edema, inflammatory cell infiltration dominated by PMNs, and synovial hyperproliferation.   B. burgdorferi abundantly expresses outer surface lipoproteins that interact with Toll-like receptor 2 and activate a signaling pathway utilizing the adapter protein MyD88.   This results in induction of numerous inflammatory molecules including cytokines, chemokines, adhesion molecules, and oxidative enzymes.   Activation of inflammatory cells through toll-like receptors is an important aspect to the inflammatory response and host defense to B. burgdorferi . Unexpectedly, she found that Lyme arthritis can develop even in the absence of the Toll like receptor signaling pathway, therefore indicating that other inflammatory pathways are active in vivo .   However, host defense to this pathogen is exquisitely dependent on TLR and MyD88 signaling pathway.   Microarray analysis of severely arthritic mice has revealed MyD88 dependent and independent pathways important in arthritis development and the MyD88 dependence of host defense is an area of current investigation.  Dr. Weis' group also studies the genetic regulation of arthritis development in a murine model of disease.  Her findings are consistent with the T cell independence of Lyme arthritis development and regulation, and argue that novel genes, not involved in models of rheumatoid arthritis, are regulating murine Lyme arthritis. Dr. Weis research team is also using  a microarray approach to identify genes whose expression is differentially regulated by mice that develop mild and severe Lyme arthritis.   Differentially expressed genes encoded within arthritis regulatory QTL will be pursued as candidate genes.   Additionally, the chromosomal linkages of upstream regulatory molecules for genes that are differentially expressed will be determined, and those mapping to arthritis QTL will be pursued as candidates for regulation of arthritis severity.

Robert Winchester, MD, Chief, Rheumatology, Professor of  Medicine, Pediatrics, & Pathology at Columbia University. Dr. Winchester has had a sustained interest in autoimmunity and autoimmune diseases, with articles early in the 90s linking HLA DR markers to predisposition to chronic Lyme arthritis. His laboratory is focused on understanding the genetic basis of susceptibility to autoimmune disease and the mechanisms responsible for triggering and mediating autoimmune injury. His earlier studies defined the molecular importance of IgG rheumatoid factors in rheumatoid arthritis and other autoantibodies in various human autoimmune diseases. He also introduced the use of F(ab')2fragments into cell surface immunofluorescence. Moreover, Dr. Winchester was one of the first to identify human MHC class II molecules on B cells and monocytes and the first to show that they were expressed on human T cells as markers of activation. As importantly, his studies of the polymorphisms of MHC molecules have provided the basis of establishing the link between MHC genotype and susceptibility to multiple forms of autoimmunity. For example in the late 1980's Dr. Winchester and colleagues showed that susceptibility to rheumatoid arthritis was determined by sequences in the HLA-DR beta chain of MHC class II molecules, and formulated the shared MHC 'epitope' hypothesis. This hypothesis provides a molecular basis for susceptibility to rheumatoid arthritis, implicating a region on the MHC molecule that both binds a peptide side chain and interacts with the TCR. This key discovery has emphasized the importance of the modern means of HLA typing, which involves DNA sequencing of the MHC genes and the theoretical basis for the discovery of antigens that initiate autoimmune disease. More recently, Dr. Winchester has coupled the DNA sequencing of the MHC genes with the analysis and high throughput DNA sequencing of human T cell receptor genes to permit molecular analysis of the cognitive T cell/peptide/MHC recognition events that underlie the role of the adaptive immune system in autoimmunity. His laboratory is also interested in the role played in immunity and by the triggering of innate immune receptors present on CD8 T cells, that is relevant to entities as diverse as celiac disease, psoriatic arthritis and the maternal-infant transmission of HIV-1.

 

 

 
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