Project Number: 8072-42000-082-03-R
Project Type: Reimbursable
Start Date: Sep 1, 2013
End Date: Aug 31, 2016
The long-term goal is to reduce the zoonotic transmission of food-borne pathogens. The overall research objective of this proposal is to fill a critical information gap regarding the epidemiology of Shiga toxin-producing E. coli (STEC) shedding in swine and the risk of zoonotic transmission of food-borne pathogens. The central research hypothesis is that pigs are a reservoir of STEC, particularly non-O157 STEC that pose a public health risk. The specific objectives are to: (1) Describe the epidemiology of STEC in swine. The need addressed by this objective is to generate longitudinal descriptive epidemiology of STEC in swine. (2) Identify risk factors for STEC shedding in swine. The working hypothesis is that there are risk factors that if removed or reduced, would result in a decreased risk of STEC shedding in swine; and (3) Elucidate the molecular epidemiology of STEC from cattle, swine and humans. The working hypothesis is that swine STEC will be related but genetically unique from cattle strains, though a subset will be similar to STEC strains isolated from humans with diarrheal disease. The completion of these objectives will provide the first descriptive epidemiology of STEC in swine, including molecular epidemiology, as well as an understanding of risk factors for STEC shedding in swine. This study will also lead to a more precise estimate of the frequency of STEC associated human illness attributable to pork, which could guide the development of effective and efficient intervention policies for food safety that ultimately reduce food-borne illness.
These studies will provide a description of the epidemiology of STEC in swine. A longitudinal descriptive epidemiology of STEC in swine will be generated, and the approach is to conduct a prospective cohort study of STEC shedding in swine, which includes determining their incidence by detecting and isolating STEC from swine feces, as well as the phenotypic and genotypic descriptive epidemiology. STEC strains isolated will be serotyped and characterized to determine their virulence potential. Second, risk factors for STEC shedding in swine will be determined by conducting a longitudinal prospective cohort study. Thirdly, the molecular epidemiology of STEC from cattle, swine, and humans will be determined. It will be determine if swine STEC are related but genetically unique from cattle strains and if a subset will be similar to STEC strains isolated from humans with diarrheal disease. The approach will be to compare the genetic relatedness of STEC isolated from cattle, swine, and human clinical isolates using pulsed-field gel electrophoresis (PFGE), multilocus sequence typing (MLST), and virulence gene profiling.