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Integrating immune mechanisms to model nematode worm burden: an example in sheep

Published online by Cambridge University Press:  18 August 2015

ROMAIN GARNIER*
Affiliation:
Department of Ecology and Evolutionary Biology, Princeton University, Princeton, New Jersey, USA
BRYAN T. GRENFELL
Affiliation:
Department of Ecology and Evolutionary Biology, Princeton University, Princeton, New Jersey, USA Fogarty International Center, National Institutes of Health, Bethesda, Maryland, USA
ALASDAIR J. NISBET
Affiliation:
Moredun Research Institute, Pentlands Science Park, Edinburgh, Scotland, UK
JACQUELINE B. MATTHEWS
Affiliation:
Moredun Research Institute, Pentlands Science Park, Edinburgh, Scotland, UK
ANDREA L. GRAHAM
Affiliation:
Department of Ecology and Evolutionary Biology, Princeton University, Princeton, New Jersey, USA Fogarty International Center, National Institutes of Health, Bethesda, Maryland, USA
*
*Corresponding author. Department of Ecology and Evolutionary Biology, 106A Guyot Hall, Princeton University, Princeton, New Jersey 08544, USA. E-mail: [email protected]

Summary

Gastrointestinal nematodes represent important sources of economic losses in farmed ruminants, and the increasing frequency of anthelmintic resistance requires an increased ability to explore alternative strategies. Theoretical approaches at the crossroads of immunology and epidemiology are valuable tools in that context. In the case of Teladorsagia circumcincta in sheep, the immunological mechanisms important for resistance are increasingly well-characterized. However, despite the existence of a wide range of theoretical models, there is no framework integrating the characteristic features of this immune response into a tractable phenomenological model. Here, we propose to bridge that gap by developing a flexible modelling framework that allows for variability in nematode larval intake which can be used to track the variations in worm burdens. We parameterize this model using data from trickle infection of sheep and show that using simple immunological assumptions, our model can capture the dynamics of both adult worm burdens and nematode fecal egg counts. In addition, our analysis reveals interesting dose-dependent effects on the immune response. Finally, we discuss potential developments of this model and highlight how an improved cross-talk between empiricists and theoreticians would facilitate important advances in the study of infectious diseases.

Type
Special Issue Article
Copyright
Copyright © Cambridge University Press 2015 

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References

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