Stuart B. Price, PhD
Department of Pathobiology
College of Veterinary Medicine
1130 Wire Road
Auburn, AL 36849
PhD, University of Oklahoma, Microbiology and Immunology, 1984
BS, Oklahoma State University, Microbiology, 1980
Dr. Stuart B. Price is an associate professor in the Department of Pathobiology. Before arriving at Auburn in 1990, he earned his B.S. degree in microbiology in 1980 from Oklahoma State University. That same year he was awarded a Colin Munro MacLeod Pre-doctoral Fellowship at the University of Oklahoma Health Sciences Center, where in 1984 he received the Ph.D. degree in microbiology and immunology. He received postdoctoral training in microbial pathogenesis at Virginia Polytechnic Institute and State University (1984-1986) and at the University of Kentucky Chandler Medical Center (1986-1989).
My laboratory studies bacterial pathogens which cause animal and food-borne human disease, with the current focus being on Salmonella. The large number of serotypes of Salmonella enterica subsp. enterica infect a variety of animal species, including cattle, chickens, pigs, and horses. Human salmonellosis often results from exposure to contaminated food products, making Salmonella spp. one of the most important bacterial food safety pathogens. Therefore, the long-term goal of my research program is to develop strategies to reduce or remove Salmonella from food animals. An S. Newport experimental infection model in calves has been developed to test the effectiveness of bacteriophage treatment in reducing disease signs and fecal shedding of the pathogen. A set of lytic bacteriophages that target S. Newport has been isolated and characterized for this purpose. Results to date show that administration of S. Newport-targeted bacteriophages to experimentally infected calves does reduce disease signs and pathogen shedding in our calf model of infection. Current work is focused on determining the minimum bacteriophage dose needed to reduce shedding and disease. Successful application of this approach to animal production would reduce the losses due to Salmonella disease, and concomitantly reduce the number of human cases of salmonellosis acquired from contaminated food.
Following a human outbreak of S. Enteritidis disease linked to ground beef, we began to examine the proximal movement of Salmonella between mixed food animal species. We hypothesized that this serotype, which is transmitted to humans primarily through contaminated poultry meat and eggs, may have moved from chickens into cattle being raised in close proximity, where it caused systemic infection resulting in contaminated ground beef. Therefore, we are developing an S. Enteritidis experimental disease model in calves in order to determine if this serotype can be isolated from the peripheral lymph nodes of infected animals. And we are performing environmental sampling for Salmonella at sites where multiple animal species are present to examine the extent of pathogen movement between them. Once routes of transmission have been established, intervention strategies will be explored to slow or prevent on-farm transmission.
I am the course coordinator of a team-taught second year veterinary student class entitled “Bacteriology & Mycology.” I also coordinate and teach a graduate course entitled “Bacterial Pathogenesis” to graduate students interested in learning about the molecular basis of virulence of major bacterial pathogens.
Paiva, D.M., K.S. Macklin, S.B. Price, J.B. Hess, D.E. Conner, and M. Singh. 2010. Efficacy of a commercial concrete sealant against Listeria spp: A model for poultry processing facilities. J. Appl. Poultry Res. 19:146-151.
Paiva, D.M., M. Singh, K.S. Macklin, S.B. Price, J.B. Hess, and D.E. Conner. 2009. Antimicrobial activity of commercial concrete sealant against Salmonella spp: A model for poultry processing plants. International J. Poultry Science 8:939-945.
Toro, H., S.B. Price, S. McKee, F.J. Hoerr, J. Krehling, M. Perdue, and L. Bauermeister. 2005. Use of bacteriophage in combination with competitive exclusion to reduce Salmonella from infected chickens. Avian Dis. 49:118-124.
Price, S.B., J.C. Wright, F.J. DeGraves, M.-P. Castanie-Cornet, and J.W. Foster. 2004. Acid resistance systems required for survival of Escherichia coli O157:H7 in the bovine gastrointestinal tract and in apple cider are different. Appl. Environ. Microbiol. 70:4792-4799.
Price, S.B., C.-M. Cheng, C.W. Kaspar, J.C. Wright, F.J. DeGraves, T.A. Penfound, M.-P. C. Coronet, and J.W. Foster. 2000. Role of rpoS in acid resistance and fecal shedding of Escherichia coli O157:H7. Appl. Environ. Microbiol. 66:632-637.