Susceptibility of broiler chickens to Campylobacter: impacts of the gut environment and immune status on colonisation

Campylobacter spp. are very important food borne bacteria and the most common cause of bacterial diarrhoea in the EU. Campylobacter caused an estimated 700,000 cases of infection in the UK in 2010. Each year there are around 100 deaths as a result of this infection. It is estimated that Campylobacter infections cost the UK economy over £1 billion per year. Infection is characterised by acute and sometimes bloody diarrhoea, particularly in children. The last few years have seen a marked rise in cases in elderly populations and in such people, particularly those with bowel cancer, infection can be fatal. Chicken meat is the most important source and vehicle for human Campylobacter infections and around 80% of chickens on sale in the UK are Campylobacter-positive. Campylobacter are commonly found in the intestinal tract of chickens and other food animals. Contamination of chicken meat takes two forms. Carcass surfaces can carry high levels of Campylobacter and this leads to cross-contamination in both domestic and commercial catering. This is an important risk factor for infection. However, and perhaps more importantly, Campylobacter have been recovered from deep leg and breast muscle tissues of up to 27% of chickens tested. Furthermore, liver tissues are also commonly contaminated. In these tissues the bacteria will be better protected from the effects of cooking. Undercooked chicken meat and chicken liver are internationally important vehicles of Campylobacter infection.

To improve public health in the UK it is essential that the number of contaminated chickens on sale is reduced. The ultimate aim of the proposed research in working with the UK chicken industry is to identify cost-effective control measures, which can be implemented across the poultry industry. One common feature of Campylobacter in chicken production is that there is a delay before flocks become colonised by the bacteria. The length of the delay varies between flocks and has not been accurately characterised. The reasons for the delay have not been clearly identified and the proposed project seeks to address this important data gap and thereby identify mitigation strategies to prevent colonisation. If the mechanisms that appear to give young chickens enhanced resistance to Campylobacter can be identified it may be possible to extend the Campylobacter-free phase until the animals are sent for slaughter. Past research suggests that one mechanism is the transfer of anti-Campylobacter antibodies to the yolk of eggs laid by infected hens. If this is so, it will have implications for vaccination for Campylobacter in both broiler birds and breeders. However, past work has only examined this in isolation and our work has shown that young chickens can have a population of gut bacteria that inhibit Campylobacter. It may be that both play a part in this process. Again, this may highlight new novel ways in which to prevent Campylobacter colonisation of chickens, either directly or through dietary manipulation.

Our work will focus on chickens reared intensively in housed systems as these comprise ~90% of the UK market. The work will be in direct collaboration with one of the three biggest poultry producers in the UK, with other producers and all the major UK food retailers supporting the work. We will conduct studies on housed flocks to determine when birds first become Campylobacter-infected and relate this to changes in the bird gut, where Campylobacter colonises, and changes in levels of maternal antibodies. We will use modelling to investigate direct and indirect drivers of colonisation and to identify possible targets for mitigation against colonisation.

Our aim is to provide the UK poultry industry with science-based and cost-effective control options, which will help it meet customer demands and comply with forthcoming EU legislation aimed at reducing the number of chickens that are Campylobacter-positive

Chicken is the main source of human Campylobacter and this threat must be reduced. The proposed work will determine mechanisms behind the delay before broiler chickens become Campylobacter-positive in housed flocks. The project is in partnership with poultry producers to identify cost-effective control measures to protect chickens against Campylobacter.

Past work suggested that maternal antibodies provide chicks with some protection against Campylobacter in early life. However, this was done in isolation and other protective factors were not studied. Campylobacter-negative chicks can have gut bacteria that inhibit C. jejuni. In most flocks, the 'protective bacteria' were not present when birds reached 3-4 weeks of age and flocks rapidly became Campylobacter-positive.

We will determine whether maternally-derived antibodies and/or gut microbiota and/or gut architecture is the most important in determining broiler susceptibility to Campylobacter. We will study Ross 308 birds, the most common type in the UK. The field studies will relate changes in naturally acquired maternal anti-Campylobacter antibodies and gut microbiota with events in flock management, like diet change and with the presence of Campylobacter. State of the art techniques will be used to determine microbiota.

Laboratory experiments will test field-generated hypotheses in a controlled manner. B-cell deficient breeders will be produced by surgical bursectomy. This creates B-cell- and thus antibody-deficient hens. These will be used to form breeding flocks producing progeny deficient in maternal antibodies. We can then determine definitively the role of maternal antibodies in the resistance of chicks to Campylobacter. We will use modelling to investigate dynamics of chicken gut microbiota and its impact and maternal antibodies as direct and proximal drivers of colonisation in commercial chicken production. These models will be used to identify targets for mitigating Campylobacter colonisation.

Campylobacter is the most important food borne zoonosis in the UK and the wider EU. In the UK it is estimated that there are 700000 cases of infection each year and that chicken-associated Campylobacter infection costs the UK economy ~£1 billion per year. Chicken is overwhelmingly the most important vehicle for human infection and is believed to be responsible for up to 80% of infections. ~80% of chickens on sale in the UK are Campylobacter-positive. Contaminated chicken presents two health threats. Surface contamination levels can be very high and contamination of deep muscle and liver tissues has been reported in up to 27 and 60% of samples tested respectively. The project seeks to better understand the processes that occur during the early development of chickens that leads them to become colonised by Campylobacter.
We seek to accurately determine when broiler flocks first become Campylobacter-positive, as there is a delay before this happens, and will be investigating the roles in this process of maternally acquired anti-Campylobacter antibodies and changes in gut microbiota and gut architecture for the first time all together. Such processes that are driven by bird age and/or diet and this project proposes to study these by laboratory studies, but also importantly in the field on commercial farms. By determining the reasons for changes to susceptibility to this major zoonotic pathogen, we will be able to identify farm-based control measures that will reduce levels of Campylobacter in UK poultry and not rely on biosecurity alone. In particular, our work will importantly inform studies on the use of vaccines and the use of pre- and/or probiotics. The project is in partnership with the UK poultry industry and all major UK retailers. Thus the beneficial impacts of our work can quickly be transferred to stakeholders.