| Email |
ambinri@jhmi.edu |
| Phone |
(410) 955-8839 |
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Richard F. Ambinder, M.D., Ph.D.
Primary Appointment in Oncology; Secondary Appointments in Pathology, Pharmacology and Molecular Sciences
Member, Graduate Program in Biochemistry, Cellular and Molecular Biology; Member, Graduate Program in Pharmacology and Molecular Sciences
Epstein-Barr virus is consistently found in association with a variety of tumors including African Burkitt's lymphoma, nasopharyngeal carcinoma, mixed cellularity Hodgkin's disease, post-transplant lymphoma, and AIDS central nervous system lymphoma. Our laboratory studies are aimed at better defining the role(s) of the virus in the pathogenesis of these diseases and the development of strategies to diagnose and treat those malignancies. For example, is there a way to utilize the presence of the virus to specifically target therapy? In patients with EBV-associated Hodgkin's disease, every tumor cell (identified morphologically or by double labeling with CD30) carries the viral genome and expresses the latency membrane protein-1(LMP-1). In non-malignant tissues (including lymph nodes and spleen), there are very few EBV-infected cells and none express LMP-1. In approximately 1/3 of normal volunteers, cytotoxic T cell activity directed against LMP-1 can be detected. Cytotoxic T cells against other EBV antigens are much more common. Cytotoxic T cells directed against EB nuclear antigens (EBNA's)-3A, -3B and -3C can be detected in virtually all normal volunteers. However, these antigens are not expressed in EBV-associated Hodgkin's disease. Can cytotoxic T cells which specifically recognize viral antigens expressed in tumor cells be induced with a therapeutic vaccine, or expanded in vitro from an HLA-matched allogeneic donor and infused in the setting of bone marrow transplantation? Can highly immunogenic viral genes that are not expressed in tumors be induced pharmacologically so as to lead to expression and consequent immune destruction of tumorous cells? Can immuno-suppressive viral gene products such as viral IL-10 be turned off with inhibitors of viral late gene expression and thus render patients more immune competent?
Publications
Moore SM, Cannon JS, Tanhehco YC, Hamzeh FM, Ambinder RF. Induction of Epstein-Barr Virus Kinases to Sensitize Tumor Cells to Nucleoside Analogues. Antimicrob Agents Chemother. 45:2082-2091, 2001.
Murray PG, Swinnen LJ, Flavell JR, Ragni MV, Baumforth KRN, Toomey SM, Filipovich AH, Lowe D, Schnell CS, Young LS, Ambinder RF. Frequent Expression of the Tumor Necrosis Factor Receptor-Associated Factor 1 in Latent Membrane Protein 1-Positive Posttransplant Lymphoproliferative Diseaseand HIV-Associated Lymphomas. Hum Path, 32:963-969, 2001.
Gulley ML, Glaser SL, Craig FE, Borowitz M, Mann RB, Shema SJ, AmbinderRF. Guidelines for interpreting EBER in situ hybridization and LMP1 immunohistochemical tests for detecting Epstein-Barr virus in Hodgkin Lymphoma. Am J Clin Path, 117:259-267, 2002.
Tao Q, Yang J, Swinnen LJ, Ambinder RF. Conservation of Epstein-Barr VirusCytotoxic T Cell Epitopes in Post transplant Lymphomas: Implications for Immune Therapy. Am J Pathol 160:1839-45, 2002. |
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| Email |
wbishai1@jhmi.edu |
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(410) 955-3507 |
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William R. Bishai, M.D., Ph.D.
Primary Appointment in Medicine - Division of Infectious Diseases; Joint Appointments in Pathology and International Health (BSPH), and Molecular Microbiology & Immunology (BSPH)
Member, Graduate Program in Cellular and Molecular Medicine; Member, Graduate Program in Pathobiology
Transcription factors regulate bacterial adaptive response for switching from rapid growth leading to overt disease and stationary phase survival during which the host is colonized and at risk for disease. We study the role of stationary phase-specific transcription factors in disease caused by Mycobacterium tuberculosis and Staphylococcus aureus. Latent tuberculosis is a colonization state which affects one-third of the world's population and carries a significant risk for active TB. An M. tuberculosis RNA polymerase sigma factor known as SigF is both essential for full virulence in animal models and for survival in vitro under stationary phase and stress conditions. Similarly, the S. aureus SigB transcription factor is associated with virulence, stress survival, and antimicrobial resistance. We are using molecular genetic strategies along with mouse model evaluations of knockout strains to characterize the roles of these transcription factors in disease caused by M. tuberculosis and S. aureus.
Additionally the molecular epidemiology of TB has been an active interest in the laboratory, and we have ongoing projects to track TB by DNA fingerprinting both in Baltimore City and in several foreign settings.
Publications
DeMaio J, Zhang Y, Ko C, Young DB, Bishai WR. A stationary phase, stress response sigma factor from Mycobacterium tuberculosis. Proc Natl Acad Sci USA 93:2790-2794, 1996.
Miyazaki E, Chen JM, Ko C, Bishai WR. The Staphylococcus aureus rsbW (orf159) gene encodes an anti-sigma factor of SigB. J Bacteriol 181(9):2846-2851, 1999.
Parrish N, Dick J, Bishai WR. Mechanisms of latency in Mycobacterium tuberculosis. Trends Microbiol 6:107-112, 1998.
Bishai WR, Graham NMH, Harrington S, Pope D, Hooper N, Astemborski J, Sheely L, Vlahov D, Glass GE, Chaisson RE. Molecular and geographic pattern of tuberculosis transmission after 15 years of directly observed therapy. JAMA 280:1679-1684, 1998. |
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| Email |
pcharach@jhmi.edu |
| Phone |
(410) 955-5775 |
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Patricia Charache, M.D.
Director, Performance Improvement Programs, Department of Pathology
Primary Appointment in Pathology; Secondary Appointments in Medicine, Oncology; Joint Appointment in Molecular Microbiology and Immunology (BSPH)
Member, Graduate Program in Molecular Microbiology and Immunology (BSPH)
My research interests emphasize detection of microbial pathogens in clinical material, and the application of such technologies, especially new molecular biologic approaches, to the diagnosis of infection, and the definition of the pathophysiologic role of the pathogens detected. Other areas of interest include the assessing and improving application of laboratory diagnostic information in clinical research programs, and for patient care, an interest that is national as well as international in scope.
Publications
Echavarria MS, Ray SC, Ambinder R, Dumler JS, Charache P. PCR Detection of Adenovirus in a Bone Marrow Transplant Recipient: Hemorrhagic Cystitis as a Presenting Manifestation of Disseminated Disease. J Clin Microbiol. 37:686-689, 1999.
Arav-Boger R, Echavarria M, Forman M, Charache P, Persaud D. Clearance of adenoviral hepatitis with ribavirin therapy in a pediatric liver transplant recipient. Pediatr Infect Dis J. 19:1097-100, 2000.
Echavarria M, Forman M, Van Tol Maarten JD, Vossen JM, Charache P, Kroes ACM. Prediction of severe disseminated adenovirus infection by serum PCR. Lancet. 358:384-85, 2001. |
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artdann@jhsph.edu |
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(410) 955-3062 |
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Arthur M. Dannenberg, M.D., Ph.D.
Primary Appointment in Environmental Health Sciences (BSPH); Joint Appointment in Pathology. Joint Appointment in Molecular Microbiology and Immunoloy (BSPH)
Member, Graduate Program in Environmental Health Sciences (BSPH); Member, Graduate Program in Epidemiology (BSPH); Member, Graduate Program in Molecular Microbiology and Immunology (BSPH)
We are evaluating old and new and existing vaccines for their efficacy in preventing tuberculosis (TB) or in reducing the severity of TB (immunotherapy). Our most definitive assay is the vaccine's ability to prevent primary (grossly visible) tubercles in lungs of rabbits, following the inhalation of aerosols of virulent tubercle bacilli. A reduction in the number of such primary tubercles is a measure of the vaccine's ability to prevent clinical TB. We also perform in-depth histological/histochemical analyses of the lesions produced by various vaccines and analyses of TB pulmonary lesions in vaccinated and control animals.
Publications
Dannenberg AM Jr. Macrophage turnover, division and activation within developing, peak and "healed" tuberculous lesions produced in rabbits by BCG. Tuberculosis 83: 251-260, 2003.
Dannenberg AM Jr. Pathogenesis of pulmonary Mycobacterium bovis infection: Basic principles established by the rabbit model. Tuberculosis 81: 87-96, 2001.
Shiginaga T, Dannenberg AM Jr, Lowrie DB, et al. Immune responses in tuberculosis: Antibodies and CD4-CD8 lymphocytes with vascular adhesion molecules and cytokines (chemokines) cause a rapid antigen-specific infiltration at sites of bacillus Calmette-Guerin reinfection. Immunology 102: 466-479, 2001.
Dannenberg AM Jr, Tomashefski JF Jr. Pathogenesis of pulmonarytuberculosis. In Fishman's Pulmonary Diseases & Disorders, 3rd edit.,Vol 2. AP Fishman, Editor-in-Chief. McGraw-Hill Book Co., New York, p.2447-2471,1998.
Dannenberg AM Jr. Lurie's tubercle-count method to test TB vaccine efficacy in rabbits. Frontiers in Bioscience 3: c27-33, 1998. |
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| Email |
sdumler@jhmi.edu |
| Phone |
(410) 955-8654 |
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J. Stephen Dumler, M.D.
Primary Appointment in Pathology; Joint Appointment in Molecular Microbiology & Immunology (BSPH)
Member, Graduate Program in Cellular and Molecular Medicine; Member, Graduate Program in Molecular Microbiology and Immunology (BSPH); Member, Graduate Program in Pathobiology
Molecular microbiology has been incredibly successful identifying novel and emerging infectious agents and in elucidating their pathogenetic mechanisms. We have used a multi-disciplinary approach with molecular, immunologic, pathologic, genomic, and microbiologic methods to study tick-borne diseases and obligate intracellular bacteria. As a result, we discovered a previously unknown human tick-borne infection, now called human granulocytic anaplasmosis (HGA), which is caused by Anaplasma phagocytophilum, an obligate intracellular rickettsia-like bacterium that infects neutrophils. My laboratory's current research centers upon dissecting the molecular and host immunologic mechanisms and ecologic conditions that lead to significant human morbidity with infection by these agents and concurrently transmitted tick-borne pathogens such as Borrelia burgdorferi. There are three major avenues of research in my laboratory: i) inflammatory and immunopathological mechanisms in human anaplasmosis - how does A. phagocytohilum induce inflammation and immune reactions that are the principle basis of disease? ii) interactions of A. phagocytohilum with neutrophils - how does this micro-organism change normal neutrophil function to allow pathogen survival, and what are the effects of neutrophil changes in pathogenesis at the cellular and molecular levels? iii) how do changes in A. phagocytophilum-infected neutrophils affect the ability of co-transmitted pathogens, such as Borrelia burgdorferi to cause disease? We are studying the fundamental effects of A. phagocytophilum gene products on neutrophils, with particular attention to major surface protein (Msp)-2 family that appear to be adhesions, and to AnkA, that apparently is secreted from the bacterium and transported into the host nucleus to interact with the heterochromatin at matrix attachment regions, perhaps influencing global gene transcription. We also developed animal models of human anaplasmosis that mimic disease in an effort to study our in vitro correlates of pathogenesis in an in vivo situation. The Medical Microbiology Laboratory is also interested in the application of molecular microbiologic methods as new approaches to diagnose infectious diseases. This is accomplished by identification of fastidious, slow growing, and non-cultivable agents or identification of important virulence factor genes by a variety of molecular methods, including direct nucleic acid amplification and sequencing followed by phylogenetic comparisons or by the molecular identification of genes that directly account for the pathogenesis of the infectious process. A strong area of interest is the application of new microbial genome-based techniques such as microarray applications for identification of pathogenic traits and features. As such, we hope to enter a new age in microbial disease diagnosis where disease is identified not based solely upon correlation with the presence of a potential pathogen, but based upon the identification of specific factors of the pathogen and host that result in the diseased state.
Publications
Choi K-s, Scorpio DG, Dumler JS. Anaplasma phagocytophilum ligation to TLR2 but not TLR4 activates macrophages for NF-kB nuclear translocation. J Infect Dis 2004 189:1921-1925.
Scorpio DG, Caspersen K, Ogata H, Park JH, Dumler JS. Restricted changes in major surface protein-2 (msp2) transcription after prolonged in vitro passage of Anaplasma phagocytophilum. BMC Microbiology 2004; 4:1.
Choi K-s, Grab DJ, Dumler JS. Anaplasma phagocytophilum infection induces protracted neutrophil degranulation. Infect Immun 2004; 72:3680-3.
Park J, Kim KJ, Choi K-s, Grab DJ, Dumler JS. Anaplasma phagocytophilum AnkA binds to granulocyte DNA and nuclear proteins. Cell Microbiol 2004; 6:743-751.
Scorpio DG, Akkoyunlu M, Fikrig E, Dumler JS. CXCR2 blockade influences Anaplasma phagocytophilum propagation but not histopathology in the mouse HGA model. Clin Diagn Lab Immunol 2004; 11:963-968.
Stone JH, Dierberg K, Aram G, Dumler JS. Human monocytic ehrlichiosis. JAMA. 2004; 292:2263-2270. |
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| Email |
mfowler5@jhmi.edu |
| Phone |
(410) 502-0684 |
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Mary G. Fowler, M.D., M.P.H.
Primary Appointment in Pathology
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Publications
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| Email |
jgarci17@jhmi.edu |
| Phone |
(410) 955-8654 |
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Jose C. Garcia-Garcia, Ph.D.
Primary Appointment in Pathology
My main research interest is to understand the molecular basis of the pathogenic mechanisms that allow intracellular bacterial pathogens to subvert the host defense and cause disease. Host phenotypic and functional alterations that occur upon intracellular bacterial infection can often be explained by global transcriptional changes induced in host cells by: i) interactions of bacterial components with host signaling pathways, ii) bacterial effectors translocated into the host cells and iii) host epigenetic alterations triggered by the intracellular infection. Our current research targets these three pathogenetic mechanisms, using as a model extreme examples of host-pathogen interactions in which intracellular bacteria propagate within host defense cells, particularly neutrophils and monocytes. Although our previous work focused mostly on rickettsial and ehrlichial pathogens, we hypothesize that these pathogenic mechanisms are conserved among intracellular bacteria, and we are starting preliminary work to extend our observations to include other medically important intracellular pathogens such as Chlamydia trachomatis and Mycobacterium tuberculosis.
Publications
Epigenetic silencing of host cell defense genes enhances intracellular survival of the rickettsial pathogen Anaplasma phagocytophilum. Garcia-Garcia JC, Barat NC, Trembley SJ, Dumler JS. PLoS Pathog. 2009 Jun;5(6):e1000488. Epub 2009 Jun 19.
Differential impairment of neutrophil function by strains of Anaplasma phagocytophilum. Grzeszczuk A, Milstone A, Choi KS, Barat N, Garcia-Garcia JC, Petrovec M, Dumler JS. Clin Microbiol Infect. 2009 Apr 3.
Silencing of host cell CYBB gene expression by the nuclear effector AnkA of the intracellular pathogen Anaplasma phagocytophilum. Garcia-Garcia JC, Rennoll-Bankert KE, Pelly S, Milstone AM, Dumler JS. Infect Immun. 2009 Jun;77(6):2385-91.
Anaplasma marginale (Rickettsiales: Anaplasmataceae): recent advances in defining host-pathogen adaptations of a tick-borne rickettsia. Kocan KM, de la Fuente J, Blouin EF, Garcia-Garcia JC. Parasitology. 2004;129 Suppl:S285-300.
Differential expression of the msp1alpha gene of Anaplasma marginale occurs in bovine erythrocytes and tick cells. Garcia-Garcia JC, de la Fuente J, Blouin EF, Johnson TJ, Halbur T, Onet VC, Saliki JT, Kocan KM. Vet Microbiol. 2004 Mar 5;98(3-4):261-72.
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| Email |
ghayward@jhmi.edu |
| Phone |
(410) 955-8686 |
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Gary S. Hayward, Ph.D.
Primary Appointment in Oncology and in Pharmacology and Molecular Sciences; Secondary Appointment in Pathology
Member, Graduate Program in Biochemistry, Cellular and Molecular Biology; Member, Graduate Program in Cellular and Molecular Medicine; Member, Graduate Programin Pathobiology; Member, Graduate Program in Pharmacology and Molecular Sciences
Herpes viruses have developed successful genetic strategies that allow them to target to specific cell types or tissues where they can reside temporarily in a quiescent or latent state without damaging the host cell. However, immuno suppression, allograft transplantation and other stress conditions often lead to accelerated reactivation and disseminated spread of lytic or abortive infection with associated serious pathology and disease. The molecular mechanisms used by herpes simplex virus and Epstein Barr virus to establish and reactivate from latency in sensory neurons and immortalized B lymphocytes are now relatively well understood. However, in recent years it has also become apparent that cytomegalovirus (CMV), HHV 6/7 and Kaposi's sarcoma herpes virus (HHV 8) are harbored as widespread latent infections in monocytes, T cells and vascular endothelial cells and can be associated with or causative agents of chronic disease after immunosuppression and organ transplantation. Our group is especially interested in molecular mechanisms involved in herpes virus host cell interactions in vascular tissue and myeloid cells in the settings of cardiac, lung and renal transplants and AIDS. This includes study of the roles of viral encoded angiogenic cytokines and chemokine receptors, effects of viral immediate-early genes on cell cycle regulation and very early events in the nucleus including alterations in subnuclear compartments involving PML and SUMO-modification mechanisms. Potential pathogenic variants of specific viral genes are also being evaluated.
Publications
Wu F., Ahn J-H, Alcendor D, Jang W-J, Xiao J, Hayward SD, Hayward GS. OriginIndependent Assembly of Kaposi's Sarcoma-associated Herpesvirus DNAReplication Compartments in Transient Cotransfection Assays and Association with the ORF-K8 Protein and Cellular PML. J. Virol. 75:1487-1506, 2001.
Ciufo DM, Cannon JS, Poole LJ, Wu F, Murray P, Ambinder RF, Hayward GS. Spindle Cell Conversion by Kaposi's Sarcoma-Associated Herpesvirus: Formation of Colonies and Plaques with Mixed Lytic and Latent Gene Expression in Infected Primary Dermal Microvascular Endothelial Cell Cultures. J. Virol.75:5614-5626, 2001.
Poole L., Yu Y, Kim P, Zheng QZ, Pevsner J, Hayward GS. Altered Patternsof Cellular Gene Expression in Dermal Microvascular Endothelial Cells Infected with the Kaposi's Sarcoma Associated Herpesvirus. J. Virol.76:3395-3420, 2002.
Chiou C-J, Poole L, Kim P, Ciufo DM, Cannon JS, ap Rhys CM, Alcendor DJ,Zong J-C, Ambinder RF, Hayward GS. Patterns of Gene Expression and a Transactivation Function Exhibited by the vGCR (ORF 74) Chemokine Receptor Protein of Kaposi's Sarcoma-Associated Herpesvirus. J. Virol. 76:3421-3439,2002. |
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| Email |
smagill2@jhmi.edu |
| Phone |
(410) 614-9690 |
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Shelley S. Magill, M.D.
Primary Appointment in Medicine - Division of Infectious Diseases; Secondary Appointment in Pathology
Invasive fungal infections are increasingly common causes of morbidity and mortality in critically ill and immunocompromised patient populations. My research currently focuses on the epidemiology of Candida colonization and infection in critically ill patients, and the impact of prophylactic/preemptive antifungal therapy on this epidemiology. Other studies explore the relationship between Candida colonization and invasive infection, and the emergence of breakthrough/refractory mould infections during the era of second-generation triazoles.
Publications
Sylvester SL, Diaz LA, Port JD, Sterling TR. Reversible posterior leukoencephalopathy in an HIV-infected patient with thrombotic thrombocytopenic purpura. Scand J Infect Dis 2002;34:706-9.
Magill SS, Puthanakit T, Swoboda SM, Carson KA, Salvatori R, Lipsett PA, Hendrix CW. Impact of fluconazole prophylaxis on cortisol levels in critically ill surgical patients. Antimicrob Agents Chemother 2004;48:2471-6
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| Email |
wmerz@jhmi.edu |
| Phone |
(410) 955-5077 |
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William G. Merz, Ph.D.
Primary Appointment in Pathology; Secondary Appointments in Dermatology, Epidemiology (BSPH) and Molecular Microbiology and Immunology (BSPH)
Member, Graduate Program in Epidemiology (BSPH); Member, Graduate Program in Molecular Microbiology and Immunology (BSPH); Co-Director, Graduate Program in Pathobiology
My research interests are focused on areas of medical mycology and molecular epidemiology. The development, validation and application of molecular genotypic methods and their application to the epidemiology and pathogenesis of important bacterial and fungal pathogens comprise one of the major thrusts of my research. Current methods include pulsed-field electrophoresis, automated ribotyping and repcPCR. Pathogens include members of the genera Staphylococcus, Pseudomonas, Aspergillus and Candida. In addition, I am conducting research on Candida species especially in relation to the molecular epidemiology and mechanisms of resistance to antifungal agents. This research focuses on methodologies, incidence and shifts in patient populations, as well as molecular mechanisms.
Publications
Jabra-Rizk MA, Falkler WA, Merz WG, Kelley JI, Baqui A and Meiller TF.1999. Candida dubliniensis and Candida albicans display surface variations consistent with observed intergeneric co-aggregation. Rev. Iber. Mycol.16:187-193.
Pelz R, Hendrix CW, Swoboda S, Diene-West M, Merz WG. 2000. A doubleblind placebo controlled trial of phophylactic fluconazole to prevent Candida infections in critically ill surgical patients. Am. Surg. 233: 542-548.
Jabra-Rizk MA, Falkler WA, Merz WG, Baqui AAMA, Kelly JL and Meiller TF.2001. Cell surface hydropholicity-associated adherence of Candida dubliniensis to human buccal epitheled cells. Rev. Iber. Mycol. 18: 17-22.
Srinivasan, A,....Merz, W.... 2003. An outbreak of Pseudomonas aeruginosa infections associated with flexible bronchoscopes. N Engl J Med 348: 191-192.
Odds,FC....W. Merz...2004. Interlaboratory comparison of results of susceptibility testing with caspofungin against Candida and Aspergillus species. J Clin Microbiol 42: 3475-82. |
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| Email |
nparrish@jhmi.edu |
| Phone |
(410) 550-3525 |
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Nicole M. Parrish, Ph.D.
Primary Appointment in Pathology
Tuberculosis continues to be the leading cause of death worldwide due to an infectious agent. Of greater concern in recent years, is the emergence of multi-drug resistance and the increasing incidence of infection with atypical mycobacteria in immunocompromised patients. These factors have highlighted the need for new antibiotics targeting these organisms. My primary research focus is aimed at characterization of the mechanism of action of a novel class of antimycobacterial compounds which have demonstrated potent in vitro efficacy against pathogenic mycobacteria, including multi-drug resistant strains. A variety of methods lead this approach including, proteomics, protein and lipid biochemistry as well as current molecular techniques.
Publications
Parrish, N.M., F.P. Kuhajda, H.S. Heine, W.R. Bishai, and J.D. Dick. 1999. Antimycobacterial activity of cerulenin and its effects on lipid biosynthesis. Journal of Antimicrobial Chemotherapy. 43: 219-226.
Jones, P.B., N.M. Parrish, T.A. Houston, A. Stapon, N.P. Bansal, J.D. Dick, and C.A.Townsend. 2000. A new class of antituberculosis agents. J. Med. Chem. 43(17): 3304-14.
Parrish, N.M, C. Townsend, P. Jones, T. Houston, and J. Dick. 2001. In vitro activity of a novel antimycobacterial compound, N-octanesulfonylacetamide, and its effects on lipid and mycolic acid synthesis. Antimicrob. Agents Chemother. 45:1143-1150.
Parrish, N.M., C.A. Townsend, C.G. Ko, and J.D. Dick. 2004. Effect of n-Octanesulfonylacetamide (OSA) on ATP and protein expression in Mycobacterium bovis BCG. J. Antimicrob. Chemother. 54(4): 722-9.
Parrish, N.M., C.A. Townsend, C.G. Ko, and J.D. Dick. 2004. Congo red agar colony morphotypes and antibiotic susceptibility testing of M. avium subspecies paratuberculosis. 2004. Clinical Medicine and Research. 2: 107-114. |
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| Email |
mreller1@jhmi.edu |
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(410) 955-5077 |
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Megan E. Reller,
Primary Appointment in Pathology
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Publications
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| Email |
sriedel2@jhmi.edu |
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(410) 550-0648 |
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Stefan Riedel, M.D., Ph.D.
Primary Appointment in Pathology
Director, Clinical Pathology Laboratories, Johns Hopkins Bayview Medical Center
My research interests are focused on the epidemiology of emerging bacterial resistance, mechanisms and laboratory detection of antimicrobial resistance, with a particular interest in gram-negative organisms (e.g. Acinetobacter baumanii and Pseudomonas aeruginosa). Additional areas of my research are focusing on the early detection of blood stream infections, the evaluation of bacteremia/sepsis and the clinical impact of laboratory testing with regard to a cost-effective and clinically relevant management of the laboratory. Recent studies include the development and evaluation of novel diagnostic methods in clinical microbiology for the evaluation of sepsis.
Publications
Riedel S, Bourbeau P, Swartz B, Brecher S, Carroll KC, Stamper PD, Dunne M Wm, McCardle T, Walk N, Fiebelkorn K, Sewell D, Richter SS, Beekmann S, and Doern GV. The Timing of Specimen Collection for Blood Cultures in Febrile Patients with Bacteremia. Journal of Clinical Microbiology; April 2008; 46 (4): 1381-1385
Lockhart S, Abramson M, Beekmann S, Gallagher G, Riedel S, Diekema D, Quinn J, Doern GV
Antimicrobial resistance among gram negative bacilli as causes of infections in intensive care unit patients in the United States between 1993 and 2004
Journal of Clinical Microbiology; 2007; 45(10): 3352-3359
Riedel S, Beekmann S, Heilmann K, Richter S, Garcia-de-Lomas J, Ferech M, Goossens H, Doern GV.
Antimicrobial Use in Europe and Antimicrobial Resistance with Streptococcus pneumoniae
European Journal of Microbiology & Infectious Diseases; 2007; 26(7): 485-490
Riedel S, Siwek G, Beekmann S, Richter S, Raife T, Doern GV.
Comparison of the BACTEC and the BacT/Alert Blood Culture System for Detection of Bacterial Contamination of Platelet Concentrates
Journal of Clinical Microbiology, 2006; 44 (6): 2262-2264
Riedel S. Edward Jenner and the history of smallpox and vaccination
Baylor University Medical Center Proceedings, 2005; 18 (1): 21-25 |
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jticehur@jhmi.edu |
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(410) 550-0648 |
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John R. Ticehurst, M.D.
Director, Clinical Pathology, Johns Hopkins Bayview Medical Center
Primary Appointment in Pathology; Joint Appointment in Medicine
Interest in virology and associated infectious diseases, with a particular interest in hepatitis viruses, has led me to three current areas of research effort: (1) hepatitis C viruses (HCV); (2) hepatitis E virus (HEV); and (3) enteroviruses and parechoviruses (EV and PeV; because they are distantly related to hepatitis A virus). HCV work involves collaboration with David Thomas, Stuart Ray, and Dale Netski (Division of InfectiousDiseases, Department of Medicine): we characterize virologic and host correlates of pathogenesis in a large cohort of intravenous drug users. Because HCV, EV, and PeV have long, highly conserved 5' non-translated regions that serve internal ribosomal entry site for regulating translation (and are template for PCR-based lab assays), we analyze nucleotide sequences that represent many strains of these viruses to determine if variation correlates with pathogenesis. I am also participating in studies of HEV infections in Bangladesh via collaboration with Alain Labrique and Kenrad Nelson (Department of Epidemiology, Bloomberg School of Public Health) and with the Armed Forces Research Institute of Medical Sciences in Bangkok. Recent clinical lab efforts have concentrated on developing and implementing laboratory assays, often based on polymerase chain reaction (PCR) and involving sequence analysis; e.g., assays for detecting EV, PeV, and adenoviruses. Opportunities are available or could develop in these areas of applied and basic virology or could develop in new areas of practical interest to the Clinical Laboratories at Johns Hopkins Bayview Medical Center or the Microbiology and Immunology Divisions at The Johns Hopkins Hospital.
Publications
Cohen JI, Purcell RH, Feinstone SM, Ticehurst JR. Chimeric hepatitis Avaccine. US Patent 5,837,260 issued 17 Nov 98.
Ticehurst JR. Hepatitis E virus. In: Murray PR, Barron EJ, Pfaller MA,Tenover FC, Yolken RH, eds. Manual of Clinical Microbiology, 7th ed. Washington DC: American Society for Microbiology, 1999; 1053-1069.
Mao Q, Ray S, Laeyendecker O, Ticehurst J, Strathdee S, Vlahov D, Thomas DL. HIV seroconversion and evolution of the HCV quasispecies. J Virol75:3259-3267, 2001.
Quantitative Molecular Methods for Infectious Diseases; Proposed Guideline. NCCLS document MM6-P, 2001. [Prepared by a Subcommittee of theCommittee on Molecular Methods: Madej RM, chair, Caliendo AM, Day SP,Ferreira-Gonzalez A, Krajden M, Loeffelholz M, Nolte FS, Piatak M, Pope L,Ticehurst J.] |
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Alexandra Valsamakis, M.D., Ph.D.
Primary Appointment in Pathology; Joint Appointment in Molecular Medicine and Immunology (BSPH)
Member, Graduate Program in Molecular Microbiology and Immunology (BSPH)
My research is focused on the detection, identification, and therapeutic monitoring of infectious diseases, particularly viral infections. My current work entails 1) improving molecular assays that are critical for the management of hepatitis C and hepatitis B infections, 2) devising quantitative assays for viral infections and studying their clinical utility particularly in immunocompromised patients, and 3) investigation of the performance and utility of automated nucleic acid preparation instrumentation in the clinical laboratory. We utilize a variety of conventional (cell culture, antigen detection) and molecular techniques (nucleic acid amplification, primarily PCR and real time PCR).
Publications
Forman, M.S. and A. Valsamakis. Increased sensitivity of the Roche COBAS
AMPLICOR HCV test v.2.0, using modified extraction techniques. J. Molec. Diag. 6:225-30, 2004.
Forman, M.S. and A. Valsamakis. Verification of an assay for
quantification of HCV RNA using an analyte specific reagent and two different extraction methods. J. Clin. Micro. 42:3581-8, 2004.
Elbeik T, J Surtihadi, M Destree, J Gorlin, M Holodniy, S Jortani, K Kuramoto, V Ng, R Valdes, A Valsamakis, N Terrault. Multicenter evaluation of the performance characteristics of the Bayer VERSANT‘ HCV RNA 3.0 assay (bDNA). J. Clin. Micro. 42:563-9, 2004
Knepp, J.H., M.A. Geahr, M.S. Forman, and A. Valsamakis. Comparison of Automated and Manual Nucleic Acid Extraction Methods for the Detection of Enterovirus RNA. J. Clin. Microbiol. 41: 3532-3536, 2003.
Dumler, J.S. and A. Valsamakis. Molecular diagnostics of infectious diseases: complementary tools for a new era of clinical microbiology. Am J Clin Path 112: S33-S39, 1999. |
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