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Ecol Evol. 2018 Dec 6;8(24):12712-12726. doi: 10.1002/ece3.4699. eCollection 2018 Dec.

Context-dependent costs and benefits of tuberculosis resistance traits in a wild mammalian host.

Author information

1
Department of Integrative Biology Oregon State University Corvallis Oregon.
2
The Institute of Ecology and Evolution University of Oregon Eugene Oregon.
3
Present address: Prevention Science Institute University of Oregon Eugene Oregon.
4
Present address: Institute of Ecology and Evolution University of Oregon Eugene Oregon.
5
College of Veterinary Medicine Oregon State University Corvallis Oregon.
6
SANPARKS Skukuza South Africa.
7
Present address: Erin E. Gorsich, Zeeman Institute: Systems Biology and Infectious Disease Epidemiology Research (SBIDER) University of Warwick Coventry UK.
8
Present address: School of Life Sciences University of Warwick Coventry UK.
9
South African Medical Research Council, DST/NRF Centre of Excellence for Biomedical TB Research, Division of Molecular Biology and Human Genetics, Faculty of Health Sciences Stellenbosch University Tygerberg South Africa.
10
Department of Fisheries and Wildlife Oregon State University Corvallis Oregon.
11
Odum School of Ecology and Department of Infectious Diseases, College of Veterinary Medicine University of Georgia Athens Georgia.

Abstract

Disease acts as a powerful driver of evolution in natural host populations, yet individuals in a population often vary in their susceptibility to infection. Energetic trade-offs between immune and reproductive investment lead to the evolution of distinct life history strategies, driven by the relative fitness costs and benefits of resisting infection. However, examples quantifying the cost of resistance outside of the laboratory are rare. Here, we observe two distinct forms of resistance to bovine tuberculosis (bTB), an important zoonotic pathogen, in a free-ranging African buffalo (Syncerus caffer) population. We characterize these phenotypes as "infection resistance," in which hosts delay or prevent infection, and "proliferation resistance," in which the host limits the spread of lesions caused by the pathogen after infection has occurred. We found weak evidence that infection resistance to bTB may be heritable in this buffalo population (h 2 = 0.10) and comes at the cost of reduced body condition and marginally reduced survival once infected, but also associates with an overall higher reproductive rate. Infection-resistant animals thus appear to follow a "fast" pace-of-life syndrome, in that they reproduce more quickly but die upon infection. In contrast, proliferation resistance had no apparent costs and was associated with measures of positive host health-such as having a higher body condition and reproductive rate. This study quantifies striking phenotypic variation in pathogen resistance and provides evidence for a link between life history variation and a disease resistance trait in a wild mammalian host population.

KEYWORDS:

African buffalo; coevolution; heritability; host‐pathogen; pace‐of‐life

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