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Dumler, J. Stephen, M.D.

J. Stephen Dumler, M.D.

Professor, Department of Pathology, Division of Medical Microbiology 

The Johns Hopkins Hospital 
Department of Pathology
Division of Microbiology
Ross
624
720 Rutland Avenue 
Baltimore, MD 21205 
Phone: (410) 614?4862
Lab: (410) 955?8654
Fax: (443) 287?3665
Email: sdumler@jhmi.edu

Education and Training:

  • B.S., Medical Technology, University of Maryland at Baltimore School of Medicine
  • M.D., University of Maryland at Baltimore School of Medicine
  • Residencies: 
      Anatomic Pathology: Johns Hopkins University School of Medicine
      Laboratory Medicine: Johns Hopkins University School of Medicine
     
      Pathology: University of Texas Medical Branch, Galveston
  • Postdoctoral Fellowship, Infectious Diseases: University of Texas Medical Branch, Galveston

Professional Interests:

  • Vector-borne pathogens and tick-borne bacterial diseases
    • Anaplasma (human granulocytic anaplasmosis)
    • Borrelia (Lyme disease and relapsing fever)
    • Ehrlichia (human monocytic ehrlichiosis and ewingii ehrlichiosis)
    • Rickettsia (Rocky Mountain spotted fever, typhus)
  • Medical parasitology, especially hemoparasites
    • Plasmodium species (malaria)
    • Babesia species (babesiosis)
    • Trypanosoma brucei gambiense and rhodesiense (African sleeping sickness)
  • Medical entomology (ticks, lice, fleas, mites)
  • Molecular diagnostics of non-viral infectious diseases

Research:
Current research focuses upon the host-pathogen interactions of obligate intracellular tick-borne rickettsial bacteria of the genus Ehrlichia and Anaplasma, and interactions with the spirochete Borrelia burgdorferi that causes Lyme disease.  Most work focuses on Anaplasma phagocytophilum that causes human granulocytic anaplasmosis (HGA).  The bacterium that causes this increasingly recognized disease has successfully adapted to an endosomal compartment of neutrophils.  The bacterial cellular and molecular mechanisms of adherence and entry, and the mechanisms by which the bacteria manipulate the host cell are major areas of study.  One significant focus is on AnkA, a protein injected into host cells that is transported to the neutrophil nucleus where is binds to DNA and proteins and may directly influence eukaryotic gene transcription.  AnkA appears to act predominantly as a matrix attachment region binding protein and may be an important epigenetic factor in altering the host neutrophil’s transcriptional program conditioning the cell as a more hospitable environment for the intracellular infection. In addition, we have developed a murine model of granulocytic anaplasmosis that has allowed us to show that most histopathologic changes characteristic of human and mammalian disease caused by this bacterium are mediated by host inflammatory and immune responses rather than by direct pathogen effects, for which the underlying mechanisms of tissue injury are major areas of interest. The laboratory uses a multidisciplinary approach to investigation, melding new molecular and cellular biology tools with standard microbiologic, histopathologic, and immunologic studies to discern mechanisms of disease by these unique bacterial pathogens.

Recent Publications: 

Scorpio DG, von Loewenich FD, Göbel H, Bogdan C, Dumler JS. Innate immune response to Anaplasma phagocytophilum contributes to hepatic injury. Clin Vaccine Immunol. 2006; 13:806-809.

Dierberg KL, Dumler JS. Lymph node hemophagocytosis in rickettsial diseases: a pathogenetic role for CD8 T lymphocytes in human monocytic ehrlichiosis (HME)? BMC Infect Dis. 2006 21; 6:121

Wormser GP, Dattwyler RJ, Shapiro ED, Halperin JJ, Steere AC, Klempner MS, Krause PJ, Bakken JS, Strle F, Stanek G, Bockenstedt L, Fish D, Dumler JS, Nadelman RB. Infectious Diseases Society of America Practice Guidelines for Clinical Assessment, Treatment and Prevention of Lyme Disease, Human Granulocytic Anaplasmosis, and Babesiosis. Clin Infect Dis 2006; 43:1089-1134.

Choi KS, Scorpio DG, Barat NC, Dumler JS.  Msp2 variation in Anaplasma phagocytophilum in vivo does not stimulate T cell immune responses or interferon-gamma production.  FEMS Immunol Microbiol 2007; 49:374-386.

Choi KS, Webb T, Oelke M, Scorpio DG, Dumler JS. Differential innate immune cell activation and proinflammatory response in A. phagocytophilum infection. Infect Immun 2007; 75:3124-30.

Dumler JS, Barat NC, Barat CE, Bakken JS. Human granulocytic anaplasmosis and macrophage activation. Clin Infect Dis 2007; 45: 199-204.

Choi K-S, Dumler JS. A mitogenic component in polar lipid-enriched A. phagocytophilum membranes. Clin Vaccine Immunol [in press].

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