Melody N. Neely, Ph.D.
Postdoctoral Washington University School of Medicine 1999 – 2001
Ph.D. University of Michigan School of Medicine, Microbiology & Immunology 1998
B.S. Eastern Michigan University, Biology 1994
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Location: Hitchner Hall, Office: 360, Laboratory: 371
Mailing Address: 5735 Hitchner Hall Orono, ME 04469-5706
The more I learn about the multitude of mechanisms for causing disease that pathogens have acquired during their co-evolution with humans, the more fascinated I become with infectious disease research. What has become increasingly clear in working with my own pathogen of choice, streptococcus, is that the bacteria have not only adapted to the human immune system, but found ways in which to both circumvent and exploit our defense mechanisms to secure their own survival. Because of this dynamic interplay between the human immune system and the infecting organism, infectious disease research requires that you not only have a good understanding of the invading pathogen, but that you also have a thorough knowledge of how the immune system responds to and defends itself from such an attack.
The long-range goal of the Neely laboratory is to identify key factors of both the host and the pathogen that lead to activation of virulence mechanisms and contribute to specific disease states during streptococcal infection. We accomplish this using a zebrafish (Danio rerio) infectious disease model. Using Streptococcus iniae and Streptococcus agalactiae, natural pathogens of both fish and humans, we analyze specific virulence mechanisms used by systemic streptococcal pathogens to cause disease. Using Streptococcus pyogenes we model the infection dynamics that occur during the necrotic invasive infections of cellulitis, streptococcal toxic shock syndrome and necrotizing fasciitis that occur in humans. The clinical pathologies that we observe in the zebrafish infections are identical to those reported in human disease. Zebrafish have both an innate and adaptive immune system with the full repertoire of immune and inflammatory cells found in mammalian systems. Because of the immunological similarities of the zebrafish model to mammalian systems, we can address questions directly related to host-pathogen interactions during streptococcal infection and the influence on infection dynamics. Furthermore, identifying the underlying virulence mechanisms used by a pathogen that has the same modus operandi as other potent human pathogens, (i.e. invasion, sepsis, and evasion of the host immune system) provides valuable insight into how other pathogens cause disease by identifying common virulence strategies. Through collaborations we have expanded our pathogen analysis in the zebrafish model using P. aeruginosa, S. aureus, V. cholera and S. mutans to name a few.