Molecular Mechanisms underlying the Interaction of Salmonella Enteritidis with the Hen Oviduct and Survival in Eggs

Please see main proposal from the University of Bristol - Reference No. G501001

The proposed work will; identify the molecular bases for the tropism of Salmonella Enteritidis (SE) for hen reproductive tissues; determine the molecular bases underlying the survival of SE in avian macrophages; determine which components of LPS regulate SE persistence in reproductive tissues and survival in forming eggs in vivo and identify the genetic determinants that permit certain SE isolates, which contain an 83 kb plasmid, to grow rapidly in fresh eggs, undermining current shelf life-based control measures. The work will explore the hypothesis that SE has cell surface determinants, unique amongst non-host-adapted salmonellae that ideally suit it to contaminate eggs, in vivo and that subtle differences in LPS structure differentiate it from STm and other poultry-associated salmonellae in this respect. In particular, we will identify the major SE genes, including 5 genomic islands, which are different from STm, that regulate infection of the hen oviduct and survival and growth in the forming and laid egg. It is difficult to exaggerate the importance of SE as a zoonotic pathogen and a better understanding of the interaction between this bacterium and its avian host could eventually enhance animal welfare and improve food safety by improving the already quite successful vaccines. Improved component vaccines, which take account of the key behaviours of SE in the avian reproductive tract, are sorely needed. In addition, current vaccines are based on SE phage type (PT) 4 and the continued evolution of SE has meant that other PTs are more common in human cases. These strains could undermine the current vaccine-based control measures in the UK and elsewhere, if they become established in the food chain.