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1. Genotype and sex-based host variation in behaviour and susceptibility drives population disease dynamics

   https://doi.org/10.1098/rspb.2020.1653  

   White, Lauren A.; Siva-Jothy, Jonathon A.; Craft, Meggan E.; Vale, Pedro F. (November 2020, Proceedings of the Royal Society B: Biological Sciences)

   null (Ed.)

   Host heterogeneity in pathogen transmission is widespread and presents a major hurdle to predicting and minimizing disease outbreaks. Using Drosophila melanogaster infected with Drosophila C virus as a model system, we integrated experimental measurements of social aggregation, virus shedding, and disease-induced mortality from different genetic lines and sexes into a disease modelling framework. The experimentally measured host heterogeneity produced substantial differences in simulated disease outbreaks, providing evidence for genetic and sex-specific effects on disease dynamics at a population level. While this was true for homogeneous populations of single sex/genetic line, the genetic background or sex of the index case did not alter outbreak dynamics in simulated, heterogeneous populations. Finally, to explore the relative effects of social aggregation, viral shedding and mortality, we compared simulations where we allowed these traits to vary, as measured experimentally, to simulations where we constrained variation in these traits to the population mean. In this context, variation in infectiousness, followed by social aggregation, was the most influential component of transmission. Overall, we show that host heterogeneity in three host traits dramatically affects population-level transmission, but the relative impact of this variation depends on both the susceptible population diversity and the distribution of population-level variation. 

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2. Season of death, pathogen persistence and wildlife behaviour alter number of anthrax secondary infections from environmental reservoirs

   https://doi.org/10.1098/rspb.2023.2568  

   Dolfi, Amélie C; Kausrud, Kyrre; Rysava, Kristyna; Champagne, Celeste; Huang, Yen-Hua; Barandongo, Zoe R; Turner, Wendy C (February 2024, Proceedings of the Royal Society B: Biological Sciences)

   An important part of infectious disease management is predicting factors that influence disease outbreaks, such asR, the number of secondary infections arising from an infected individual. EstimatingRis particularly challenging for environmentally transmitted pathogens given time lags between cases and subsequent infections. Here, we calculatedRforBacillus anthracisinfections arising from anthrax carcass sites in Etosha National Park, Namibia. Combining host behavioural data, pathogen concentrations and simulation models, we show thatRis spatially and temporally variable, driven by spore concentrations at death, host visitation rates and early preference for foraging at infectious sites. While spores were detected up to a decade after death, most secondary infections occurred within 2 years. Transmission simulations under scenarios combining site infectiousness and host exposure risk under different environmental conditions led to dramatically different outbreak dynamics, from pathogen extinction (R< 1) to explosive outbreaks (R> 10). These transmission heterogeneities may explain variation in anthrax outbreak dynamics observed globally, and more generally, the critical importance of environmental variation underlying host–pathogen interactions. Notably, our approach allowed us to estimate the lethal dose of a highly virulent pathogen non-invasively from observational studies and epidemiological data, useful when experiments on wildlife are undesirable or impractical. 

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3. The influence of social and spatial processes on the epidemiology of environmentally transmitted pathogens in wildlife: implications for management

   https://doi.org/10.1098/rstb.2022.0532  

   Pandey, Aakash; Wojan, Chris; Feuka, Abigail; Craft, Meggan E; Manlove, Kezia; Pepin, Kim M (October 2024, Philosophical Transactions of the Royal Society B: Biological Sciences)

   Social and spatial structures of host populations play important roles in pathogen transmission. For environmentally transmitted pathogens, the host space use interacts with both the host social structure and the pathogen’s environmental persistence (which determines the time-lag across which two hosts can transmit). Together, these factors shape the epidemiological dynamics of environmentally transmitted pathogens. While the importance of both social and spatial structures and environmental pathogen persistence has long been recognized in epidemiology, they are often considered separately. A better understanding of how these factors interact to determine disease dynamics is required for developing robust surveillance and management strategies. Here, we use a simple agent-based model where we vary host mobility (spatial), host gregariousness (social) and pathogen decay (environmental persistence), each from low to high levels to uncover how they affect epidemiological dynamics. By comparing epidemic peak, time to epidemic peak and final epidemic size, we show that longer infectious periods, higher group mobility, larger group size and longer pathogen persistence lead to larger, faster growing outbreaks, and explore how these processes interact to determine epidemiological outcomes such as the epidemic peak and the final epidemic size. We identify general principles that can be used for planning surveillance and control for wildlife host–pathogen systems with environmental transmission across a range of spatial behaviour, social structure and pathogen decay rates. This article is part of the theme issue ‘The spatial–social interface: a theoretical and empirical integration’. 

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4. The dynamics of evolutionary rescue from a novel pathogen threat in a host metapopulation

   https://doi.org/10.1038/s41598-021-90407-z  

   Jiao, Jing; Fefferman, Nina (December 2021, Scientific Reports)

   Abstract When a novel disease strikes a naïve host population, there is evidence that the most immediate response can involve host evolution while the pathogen remains relatively unchanged. When hosts also live in metapopulations, there may be critical differences in the dynamics that emerge from the synergy among evolutionary, ecological, and epidemiological factors. Here we used a Susceptible-Infected-Recovery model to explore how spatial and temporal ecological factors may drive the epidemiological and rapid-evolutionary dynamics of host metapopulations. For simplicity, we assumed two host genotypes: wild type, which has a positive intrinsic growth rate in the absence of disease, and robust type, which is less likely to catch the infection given exposure but has a lower intrinsic growth rate in the absence of infection. We found that the robust-type host would be strongly selected for in the presence of disease when transmission differences between the two types is large. The growth rate of the wild type had dual but opposite effects on host composition: a smaller increase in wild-type growth increased wild-type competition and lead to periodical disease outbreaks over the first generations after pathogen introduction, while larger growth increased disease by providing more susceptibles, which increased robust host density but decreased periodical outbreaks. Increased migration had a similar impact as the increased differential susceptibility, both of which led to an increase in robust hosts and a decrease in periodical outbreaks. Our study provided a comprehensive understanding of the combined effects among migration, disease epidemiology, and host demography on host evolution with an unchanging pathogen. The findings have important implications for wildlife conservation and zoonotic disease control. 

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5. Variation in herbivore space use: comparing two savanna ecosystems with different anthrax outbreak patterns in southern Africa

   Huang, Y.-H.; Owen-Smith, N.; Henley, M.D.; Kilian, J.W.; Kamath, P.L.; Ochai, S.O.; van Heerden, H.; Mfune, J.K.E.; Getz, W.M.; Turner, W.C. (January 2023, Movement ecology)

   Background The distribution of resources can affect animal range sizes, which in turn may alter infectious disease dynamics in heterogenous environments. The risk of pathogen exposure or the spatial extent of outbreaks may vary with host range size. This study examined the range sizes of herbivorous anthrax host species in two ecosystems and relationships between spatial behavior and patterns of disease outbreaks for a multi-host environmentally transmitted pathogen. Methods We examined range sizes for seven host species and the spatial extent of anthrax outbreaks in Etosha National Park, Namibia and Kruger National Park, South Africa, where the main host species and numbers of cases differ. We evaluated host range sizes using the local convex hull method at different temporal scales, within-individual temporal range overlap, and relationships between ranging behavior and species contributions to anthrax cases in each park. We estimated the spatial extent of annual anthrax mortalities and evaluated whether the extent was correlated with case numbers of a given host species. Results Range size differences among species were not linearly related to anthrax case numbers. In Kruger the main host species had small range sizes and high range overlap, which may heighten exposure when outbreaks occur within their ranges. However, different patterns were observed in Etosha, where the main host species had large range sizes and relatively little overlap. The spatial extent of anthrax mortalities was similar between parks but less variable in Etosha than Kruger. In Kruger outbreaks varied from small local clusters to large areas and the spatial extent correlated with case numbers and species affected. Case numbers of secondary host species with larger range sizes were positively correlated with the spatial extent of outbreaks in both parks. Conclusions Our results provide new information on the spatiotemporal structuring of ranging movements of anthrax host species in two ecosystems. The results linking anthrax dynamics to host space use are correlative, yet suggest that, though partial and proximate, host range size and overlap may be contributing factors in outbreak characteristics for environmentally transmitted pathogens. 

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