Molecular basis of foodborne disease risk of variants of Salmonella Typhimurium DT193 and U288
Lead Research Organisation:
QUADRAM INSTITUTE BIOSCIENCE
Department Name: UNLISTED
Abstract
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Technical Summary
The overall aim of this project is to investigate the genotypic and phenotypic variation of two S. Typhimurium epidemic clones present in pig population but that differ in their ability to enter or cause disease in the human population. The central hypothesis is that genotypic differences in S. Typhimurium variants that represent different foodborne disease risk are associated with phenotypes linked to entering and surviving in the food chain or causing disease. The significance of this work is that an understanding of the molecular basis of risk to food safety posed by Salmonella Typhimurium is critical to the surveillance of high risk variants and intervention strategies aimed at avoiding their entry into the food chain. Specifically we will;
. Compare the molecular epidemiology, spread and transmission of S. Typhimurium DT193 and U288 isolates in the pig herds in the UK and into the food chain.
. Determine the phenotypic variation of representative S. Typhimurium DT193 and U288 isolates in in vivo infection models and response to environmental stress in vitro.
. Define the microevolution and gene flux and transcriptional response specific to representative isolates of S. Typhimurium DT193 and U288
. Determine lineage-specific genetic factors identified by whole genome comparison that account for lineage-specific phenotypes.
. Compare the molecular epidemiology, spread and transmission of S. Typhimurium DT193 and U288 isolates in the pig herds in the UK and into the food chain.
. Determine the phenotypic variation of representative S. Typhimurium DT193 and U288 isolates in in vivo infection models and response to environmental stress in vitro.
. Define the microevolution and gene flux and transcriptional response specific to representative isolates of S. Typhimurium DT193 and U288
. Determine lineage-specific genetic factors identified by whole genome comparison that account for lineage-specific phenotypes.
Planned Impact
unavailable
People |
ORCID iD |
| Robert Kingsley (Principal Investigator) |