Campylobacter jejuni is the most common cause of foodborne illness in the UK, responsible for an estimated 400,000 cases each year. Although deaths from Campylobacter infection are rare, the annual cost to the UK economy is over £500M. The main source of the Campylobacter is poultry meat. Although this bacterium does not cause disease in poultry, it does contaminate the carcass and so can enter the human body as a result of poor kitchen hygiene and improper cooking.
Campylobacter cells dividing. Image: Mary Parker, IFR
Reducing the levels of Campylobacter in the food chain, and ultimately the incidence of Campylobacter infection in humans, is an aim of the Biotechnology and Biological Sciences Research Council, Defra and the Food Standards Agency, and to help achieve this, it is essential that we understand the biology of Campylobacter, and how it survives in the guts of both birds and mammals.
The guts of both birds and humans contain large populations of bacteria that are essential to digestion and wellbeing. There is keen competition between different bacterial species for available nutrients. Within this, Campylobacter occupies a specific niche that allows it to thrive. While some bacteria produce lactate as a result of their own metabolism, Campylobacter can use this lactate as a source of carbon and energy.
This was opposite to what was predicted based on the gene content of the bacterium, and could point to a way of controlling Campylobacter. Publishing in the journal Environmental Microbiology, the IFR and University of Sheffield have shown that Campylobacter has two new enzyme pathways for the metabolism of lactate. The presence of these novel pathways may allow for designing targeted approaches to eliminate Campylobacter from poultry, without affecting the beneficial microflora in the poultry gut.
Notes to editors
Reference: Thomas, M. T., Shepherd, M., Poole, R. K., van Vliet, A. H. M., Kelly, D. J. and Pearson, B. M. (2011), Two respiratory enzyme systems in Campylobacter jejuni NCTC 11168 contribute to growth on L-lactate. Environmental Microbiology, 13: 48-61. doi: 10.1111/j.1462-2920.2010.02307.x
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