OHEJP Lead Institute: University of Surrey (UoS)

OHEJP Collaborators:

Public Health England (PHE), UK.

Non-OHEJP Collaborators:

Department for Environment Food & Rural Affairs (DEFRA), UK

Zoetis

Three years

Title

Environment and Foodborne Zoonosis: Linking Mechanism and Phenomenology

Summary

Foodborne diseases remain an important cause of morbidity, mortality, and healthcare costs worldwide. For instance,  in 2015 diarrhea alone caused more than 1.3 million deaths and 71·59 million DALY globally (1). The problem is expected to be exacerbated by population growth and the rising of resistance to antibiotics (2). Furthermore, anthropogenic activities are constantly changing the environment (here and throughout we refer to weather, climate, land use and also socio-economics factors as ‘environment’ or ‘environmental factors’) which is a well-recognized driver of diseases (see (3–5) and references therein). The environment can affect pathogen abundance, survival, and virulence, host susceptibility to infection  as well as human behaviour (6). It is thought that the accelerating rate of global climate and other environmental change will impact the distribution, frequency and patterns of established diseases as well as the emergence and re-emergence of new and old ones. As a society, it is our duty to be prepared.

Our ultimate goal is to develop a tool to assess the public health risk of foodborne zoonosis based on information of relevant environmental factors. Accordingly, we are interested in the following over-arching questions:

• Can we identify the key environmental processes triggering and propagating foodborne zoonoses?
• Can we disentangle the role of animal, human (including socio-economic factors) and environmental factors in foodborne zoonoses?
• Can we identify the delay between variations in the environment (e.g. increase in the temperature or behavioural change) and the occurrence of a foodborne outbreak?
• How can we quantify their impact on Public Health?

We will focus on Salmonella, for which the mechanism of transmission is relatively well known (e.g. effects of temperature and water activity (7)), which will help in validating our approach.

References

1. C. Troeger et al., Lancet Infect. Dis. 17, 909–948 (2017).
2. C. Dye, Philos. Trans. R. Soc. Lond. B. Biol. Sci. 369, 20130426 (2014).
3. J. G. Ayres, R. M. Harrison, R. L. Maynard, R. P. McClellan, G. L. Nichols, in Environmental Medicine, J. G. Ayres, R. M. Harrison, G. L. Nichols, R. L. Maynard, Eds. (Edward Arnold & Co., 2010).
4. G. Lo Iacono et al., PLoS Negl. Trop. Dis. 11, e0005659 (2017).
5. G. Lo Iacono, G. L. Nichols, Modeling the Impact of Environment on Infectious Diseases (Oxford University Press, 2017; https://environmentalscience.oxfordre.com/view/10.1093/acrefore/9780199389414.001.0001/acrefore-9780199389414-e-339), vol. 1.
6. D. N. Fisman, Annu. Rev. Public Health. 28, 127–43 (2007).
7. S. M. Santillana Farakos, J. F. Frank, D. W. Schaffner, Int. J. Food Microbiol. 166, 280–293 (2013).
8. MEDMI – Connecting health and environment data (2017), (available at https://www.ecehh.org/research-projects/medmi/).

Recruitment will be advertised soon. More information to follow.