|Event Title||First Global Alliance for Research on Avian Diseases (GARAD) Conference|
|Event Date & Time||On Wed, 01 Jul 2015 at 09:25:00 - 09:40:00|
|Venue||Edmond J. Safra Lecture Theatre|
|Abstract Title||Infection biology of Campylobacter: not all chickens and not all Campylobacter are the same-Lizeth|
|Affiliations||Department of Infection Biology, Institute of Infection and Global Health, University of Liverpool, Leahurst Campus, Neston, UK|
Campylobacter is the most common foodborne bacterial gastrointestinal infection. Campylobacter jejuni causes around 85% of human cases. Recent surveys showed around 70% of UK retail chicken is contaminated with C. jejuni. Control of Campylobacter in poultry production is a public health priority. Here we describe recent research that has shed new light on the infection biology of C. jejuni in the broiler chicken.
Experimental infection of broiler chickens with C. jejuni M1 leads to an intestinal inflammatory response. In some breeds expression of regulatory cytokines leads to control of inflammation, accompanied by Th1, Th2 and Th17 responses restricting infection to the gut. However in certain breeds limited regulation leads to prolonged inflammation, gut damage and diarrheoa and challenges the paradigm that Campylobacter is a’ harmless commensal’.
C. jejuni isolates show markedly different infection ecologies within the chicken. M1, for example, is largely restricted to the caeca, but the ST21 isolate 13126 colonises the length of the gastrointestinal tract with high levels of extra-intestinal spread. Moreover 13126 shows increased ability to invade human epithelial cells and increased virulence in the Galleria infection model.
Understanding the basis of protective immunity is key to vaccine development for Campylobacter. Through experimental C. jejuni M1 infection in bursectomised and control broiler chickens we have shown caecal colonisation is not affected by antibody, but that there are greater levels of colonisation in ileum and jejunum of bursectomised birds. This indicates that antibody production leads to reduced colonisation of the small intestine, but has little or no impact on Campylobacter colonisation of the caeca.
In conclusion detailed studies of infection and host response in broiler chickens are providing new insight into the infection biology of C. jejuni. Campylobacter is not merely a commensal and that both host and pathogen genotype impact on the progression of infection. It would seem that the chicken responds to infection to limit infection to the gut -in effect a ‘stalemate’ between host and pathogen as there is little disease. Nevertheless certain isolates show an invasive phenotype that may impact on this balance and the potential for increased risk to animal and public health.