John Szumowski, MD, MPH, an infectious diseases fellow at the University of Washington, is the 2012 recipient of the Merle A. Sande/Pfizer Fellowship Award in International Infectious Diseases. This award is intended to encourage young physicians who are interested in international medicine, and is given for important clinical research conducted in a resource-limited setting and relating to infectious complications of HIV.
Dr. Szumowski received his medical and public health degrees from Harvard Medical School and the Harvard School of Public Health in 2007. He completed residency in internal medicine at Beth Israel Deaconess Medical Center in 2010. As a third year infectious diseases fellow at the University of Washington, he has completed his clinical training and continues to maintain an HIV clinic, while doing research with Drs. Lalita Ramakrishnan at the University of Washington and William Bishai at Kwazulu-Natal Research Institute for Tuberculosis and HIV.
His proposed research project will be based in Durban, South Africa and builds upon recent insights from the Ramakrishnan laboratory that have the potential to dramatically alter the clinical management of tuberculosis meningitis (TBM). Outcomes with current therapies for TBM remain poor; mortality has ranged from 20 to 50 percent, with a high prevalence of disability in survivors. The prognosis is even worse for HIV co-infected patients.
Although tuberculosis (TB) has been traditionally viewed as a disease of failed immunity, these new data indicate that an excessive inflammatory response is also associated with worse outcomes. Studies from a well-characterized Vietnamese TBM cohort found that a common genetic variant in leukotriene A4 hydrolase (LTA4H) modulates tumor necrosis factor (TNF) levels, thereby setting the host inflammatory response. Moreover, the benefit of adjunctive corticosteroids was confined to persons of the high-inflammatory genotype. Dr. Szumowski proposes to extend this work by identifying genetic variants in LTA4H and other key components of eicosanoid and TNF pathways in Durban via gene sequencing. He will subsequently correlate these genotypes to key clinical outcomes in a Durban-based TBM cohort. This work will lay the foundation for future study of a genotype-based approach to anti-inflammatory therapy in TB. His findings may be applicable to the pathogenesis and treatment responsiveness of other forms of TB as well as other bacterial infections that take a severe toll on HIV-positive patients.
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