Campylobacter is a serious problem in the western world because it is one of the leading causes of food poisoning.

In the UK, it is responsible for an estimated 700,000 cases, over 100 deaths and costs almost £1 billion to the UK economy. Across Europe the numbers just get bigger. Thus, Campylobacter-related food poisoning results in a serious public health burden.

The majority of cases are the result of contaminated chicken meat, which has not been cooked properly. This leads to the bacterium still being in a viable state to reproduce in the human gut and make an individual ill.

The difficulty in dealing with this problem is identifying how and where do you intervene along the production and supply chain to minimise the risk of an individual contracting food poisoning?

There is no easy answer to this. Educating consumers to prepare and cook meat safely is one way to reduce Campylobacter food poisoning.

Maintaining tight biosecurity practices during production and processing to stop cross-contamination among Campylobacter positive and negative flocks is another way. However, this neglects our understanding of Campylobacter-host interactions and possible welfare considerations of the chicken.

The researchers looked at the very start of the production process by trying to understand the biological interactions between the chicken and Campylobacter. Campylobacter is closely associated with the chicken yet our understanding of infection is still poor.

Over the last few decades broiler chickens have been bred to be fast growing (i.e. marketable weight by approximately 40 days) and uniform size for processing. This has been driven in part by a demand for affordable meat, which may potentially be at the expense of other aspects of the chicken’s “biology”.

In their analysis, the team examined the broiler’s immune response to Campylobacter infection.

They looked at something called cytokines, which are messenger molecules that tell the body, which is the best way to fight an infection. The team found that the immune response is similar to other animals that are fighting a bacterial infection in the gut.

The immune response’s aim is to stop Campylobacter invading the host by containing it within the gut. However, the chicken cannot seem to get rid of Campylobacter, unlike in humans.

The immune response protects the chicken but it allows Campylobacter to persist in the gut and contaminate the production environment through the broiler’s faeces. The contaminated production house means that Campylobacter can spread quickly through a flock resulting in more chickens going for processing that are colonised by Campylobacter.

Furthermore, the team found differences in the way the cytokines were expressed in different breeds even though the overall aim of the response was similar.

The problem is longer term exposure to certain cytokines can lead to inflammation and tissue damage. The team found this interesting because along with other work undertaken by some of their collaborators on this paper, it appears that Campylobacter can no longer be described as a harmless “passenger” in the chicken gut.

The team concluded that their research will give a better understanding of the immune response of different chicken breeds to Campylobacter, which will inform the development of vaccines and possible ‘Campylobacter-resistant’ chickens and hopefully reduce the potential of Campylobacter entering the food chain.

The research project was funded by the BBSRC, involving the universities of Newcastle, Liverpool and Swansea and a resulting research paper has been published by the Royal Society Open Science journal.