Summary: | <p>Abstract</p> <p>Background</p> <p>Several studies have shown that a number of serovars of <it>Salmonella enterica </it>may be isolated from wild birds, and it has been suggested that wild birds may play a role in the epidemiology of human and livestock salmonellosis. However, little is known about the relationship between wild bird <it>S. enterica </it>strains and human- and livestock- associated strains in the United Kingdom. Given the zoonotic potential of salmonellosis, the main aim of this study was to investigate the molecular epidemiology of <it>S. enterica </it>infections in wild birds in the north of England and, in particular, to determine if wild bird isolates were similar to those associated with disease in livestock or humans.</p> <p>Results</p> <p>Thirty two <it>Salmonella enterica </it>isolates were collected from wild birds in northern England between February 2005 and October 2006, of which 29 were <it>S. enterica </it>serovar Typhimurium (<it>S</it>. Typhimurium); one <it>S</it>. Newport, one <it>S</it>. Senftenberg, and one isolate could not be classified by serotyping. Further analysis through phage typing and macro-restriction pulsed-field gel electrophoresis indicated that wild passerine deaths associated with salmonellosis were caused by closely-related <it>S</it>. Typhimurium isolates, some of which were clonal. These isolates were susceptible to all antimicrobials tested, capable of invading and persisting within avian macrophage-like HD11 cells <it>in vitro</it>, and contained a range of virulence factors associated with both systemic and enteric infections of birds and mammals. However, all the isolates lacked the <it>sopE </it>gene associated with some human and livestock disease outbreaks caused by <it>S</it>. Typhimurium.</p> <p>Conclusion</p> <p>The wild bird isolates of <it>S. enterica </it>characterised in this investigation may not represent a large zoonotic risk. Molecular characterisation of isolates suggested that <it>S</it>. Typhimurium infection in wild passerines is maintained within wild bird populations and the causative strains may be host-adapted.</p>
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