Campylobacter: a hidden threat in our food chain
Unknown risks: Campylobacter versus Salmonella
Everyone is familiar with Salmonella as a significant foodborne pathogen in chicken meat. However, consumers and veterinarians are often less aware of its distant relative, Campylobacter. Surprisingly, the prevalence of registered human campylobacteriosis cases is more than double that of human salmonellosis cases.
Extent of the threat
In 2022, EFSA recorded 137,107 cases, making Campylobacter the leading cause of human gastroenteritis and one of the most significant zoonoses. The actual number is likely much higher. For every registered case, there are an estimated 46.6 unregistered cases (Havelaar et al., 2013), bringing the true number in the EU to over 6.4 million per year!
The symptoms are similar to salmonellosis, namely diarrhea, abdominal cramps, nausea, and vomiting. Usually, these symptoms are self-limiting and resolve within 7 days, but in rare cases, campylobacteriosis can lead to severe complications such as the autoimmune disease Guillain-Barré syndrome. This imposes significant societal costs, estimated at €2.4 billion per year (EFSA, 2014).
Sources of contamination
These numbers are staggering; but where do all these cases come from? The primary source is the consumption of poultry meat, responsible for 50-70% of all human infections (Seliwiorstow et al., 2015). The two main culprits are Campylobacter jejuni and Campylobacter coli, accounting for 88% and 10% of cases, respectively (ECDC, 2022).
One reason Campylobacter is less known to the general public than, for example, Salmonella, is that it requires very specific conditions to grow. Therefore, Campylobacter does not multiply on chicken meat. This makes Campylobacter less associated with outbreaks and more with isolated cases, contributing to its lower public profile.
Routes of infection and spread
According to EFSA, in 2022 18.1% of the samples in chickens were positive for Campylobacter, although numbers are very varying across the different member states, going from 10% in Bulgaria to 80.5% in Cyprus. The bacterium is part of the normal gut microflora and behaves as a commensal, primarily residing in the cecum. Generally, it is assumed that this bacterium is not harmful to chickens, although recent studies show that Campylobacter can lead to increased feed conversion, wetter litter, and pododermatitis (Humphrey et al., 2014).
Chickens can be infected in various ways (e.g., flies, contaminated water near the barns, and other farm animals), almost exclusively through oral intake. In the cecum, Campylobacter can reach enormous numbers within 24 hours, from 107 to 109 per gram, and is then excreted into the environment via cecal droppings. At such high levels, Campylobacter spreads rapidly in the flock, and within 6 days, an entire barn of 30,000 broilers can be colonized (van Gerwe et al., 2005).
Interestingly, Campylobacter seems to occur scarcely in broiler chickens during the first two weeks (Newell and Fearnley, 2003). This is due to reasons such as increased biosecurity for younger chicks, an unstable gut microflora, and the presence of maternal antibodies passed from hen to chick (Sahin et al., 2003; Cawthraw and Newell, 2010; Haems et al., 2024).
Most infections appear to occur primarily towards the end of the production cycle, especially after partial depopulation (Hertogs et al., 2021): a few days before most birds go to slaughter, some are collected to create more space and use the area more efficiently. Crates from the slaughterhouse used to transport the animals are often not sufficiently disinfected and still contain significant amounts of Campylobacter from the previous cycle. Bringing these crates into the barn can infect a large portion of the remaining birds.
Once at the slaughterhouse, tearing of the cecum (e.g., due to improperly adjusted equipment) during evisceration can massively contaminate the carcass, which can in turn contaminate other carcasses through cross-contamination.
How can this be prevented?
Research on preventing Campylobacter-colonization has been ongoing for decades, but with limited success so far. Tested control measures include organic acids, bacteriophages, probiotics, prebiotics, and vaccinations. These have proven insufficient in various experimental studies or were not applicable in practice. Antibiotic treatment is also not an option due to high antimicrobial resistance, such as to ciprofloxacin, which is reserved for treating human campylobacteriosis cases.
An integrated approach at three levels (primary production, slaughterhouse, and consumer) is necessary to minimize the risk of Campylobacter infection.
- Stricter biosecurity measures in poultry barns could reduce prevalence at slaughter age by 50% (Newell et al., 2011).
- Since 2018, a process hygiene criterion has been implemented in slaughterhouses (EU 2017/1495). This requires routine weekly sampling of five neck skin samples from each slaughterhouse. If more than 15 neck skin samples contain >1000 colony-forming units per gram of Campylobacter over a 10-week period, the slaughterhouse must take corrective measures to reduce the number of contaminated carcasses.
- Finally, when contaminated chicken meat reaches the consumer’s kitchen, hygienic measures can prevent infection, such as thoroughly cooking poultry meat. This is especially important when preparing whole poultry carcasses or minced meat, when Campylobacter presence is not only limited to the surface. It is also recommended to wash hands after handling raw poultry products. Cutting boards can serve as potential carriers for cross-contamination of pathogens from chicken to other surfaces. Therefore, it is crucial to clean or replace kitchen surfaces and utensils after the preparation of chicken meat.
References
Cawthraw, S.A., and D.G. Newell. 2010. Investigation of the presence and protective 13 effects of maternal antibodies against Campylobacter jejuni in chickens. Avian Dis. 54:86-93.
EFSA. 2014. EFSA explains zoonotic diseases: Campylobacter.
EFSA. 2023. The European Union One Health 2022 Zoonoses Report. EFSA J. 21(12):e8842.
European Centre for Disease Prevention and Control (ECDC). 2022a. Campylobacteriosis. In: ECDC. Annual Epidemiological Report for 2021. Stockholm (SE): ECDC.
Haems, K., D. Strubbe, N. Van Rysselberghe, G. Rasschaert, A. Martel, F. Pasmans, and A. Garmyn. 2024. Role of Maternal Antibodies in the Protection of Broiler Chicks against Campylobacter Colonization in the First Weeks of Life. Animals (Basel) 14(9):1291.
Havelaar, A.H., S. Ivarsson, M. Lofdahl, and M.J. Nauta. 2013. Estimating the true incidence of campylobacteriosis and salmonellosis in the European Union, Epidemiol. Infect. 141:293-302.
Hertogs, K., M. Heyndrickx, P. Gelaude, L. De Zutter, J. Dewulf, and G. Rasschaert. 2021a. The effect of partial depopulation on Campylobacter introduction in broiler houses. Poult. Sci. 100(2):1076-1082.
Humphrey S, Chaloner G, Kemmett K, Davidson N, Williams N, Kipar A, Humphrey T, Wigley P. 2014. Campylobacter jejuni is not merely a commensal in commercial broiler chickens and affects bird welfare. mBio. ;5(4):e01364-14.
Newell, D.G and C. Fearnley. 2003. Sources of campylobacter colonization in broiler chickens. Appl. Environ. Microbiol. 69:4343–4351.
Newell D.G., K.T. Elvers, D. Dopfer, I. Hansson, P. Jones, S. James, J. Gittins, N.J. Stern, R. Davies, I. Connerton, D. Pearson, G. Salvat, and V.M. Allen. 2011. Biosecurity-based interventions and strategies to reduce Campylobacter spp. on poultry farms. Appl. Environ. Microbiol. 77:8605–8614.
Sahin, O., N. Luo, S. Huang, and Q. Zhang. 2003. Effect of Campylobacter-specific maternal antibodies on Campylobacter jejuni colonization in young chickens. Appl. Environ. Microbiol. 69(9):5372-9.
Van Gerwe, T.J., A. Bouma, W.F. Jacobs-Reitsma, J. van den Broek, D. Klinkenberg, J.A. Stegeman, and J.A. Heesterbeek. 2005. Quantifying transmission of Campylobacter spp. among broilers. Appl. Environ. Microbiol. 71(10):5765-70.