Length of intervals between epidemics: evaluating the influence of maternal transfer of immunity

Garnier, Romain; Gandon, Sylvain; Hårding, Karin C.; Boulinier, Thierry

doi:10.1002/ece3.955

Cited by 11 publications

(10 citation statements)

References 56 publications

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“…Several empirical studies have demonstrated individual variation in susceptibility, immune response and sickness behaviours across populations from different geographical locations (Adelman, Bentley, Wingfield, Martin, & Hau, ; Adelman, Kirkpatrick, Grodio, & Hawley, ; Gibson, Jokela, & Lively, ). Waning immunity from maternal antibodies or prior exposure to an infectious agent may also contribute to temporal lags in the availability of susceptible individuals on different host patches depending on the local history of exposure (Fouchet et al., ; Garnier, Gandon, Harding, & Boulinier, ; Garnier et al., ; Plowright et al., ). Importantly, behavioural and physiological processes may be linked through host–parasite feedbacks (Ezenwa et al., ; Gudelj & White, ; VanderWaal & Ezenwa, ).…”

Section: Future Directions: Addressing Global Challengesmentioning

confidence: 99%

“…Waning immunity from maternal antibodies or prior exposure to an infectious agent may also contribute to temporal lags in the availability of susceptible individuals on different host patches depending on the local history of exposure Garnier, Gandon, Harding, & Boulinier, 2014;Garnier et al, 2012;. Importantly, behavioural and physiological processes may be linked through host-parasite feedbacks VanderWaal & Ezenwa, 2016).…”

Section: Accounting For Host Heterogeneitymentioning

confidence: 99%

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Dynamic, spatial models of parasite transmission in wildlife: Their structure, applications and remaining challenges

White

Forester

Craft

2017

Journal of Animal Ecology

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Individual differences in contact rate can arise from host, group and landscape heterogeneity and can result in different patterns of spatial spread for diseases in wildlife populations with concomitant implications for disease control in wildlife of conservation concern, livestock and humans. While dynamic disease models can provide a better understanding of the drivers of spatial spread, the effects of landscape heterogeneity have only been modelled in a few well-studied wildlife systems such as rabies and bovine tuberculosis. Such spatial models tend to be either purely theoretical with intrinsic limiting assumptions or individual-based models that are often highly species- and system-specific, limiting the breadth of their utility. Our goal was to review studies that have utilized dynamic, spatial models to answer questions about pathogen transmission in wildlife and identify key gaps in the literature. We begin by providing an overview of the main types of dynamic, spatial models (e.g., metapopulation, network, lattice, cellular automata, individual-based and continuous-space) and their relation to each other. We investigate different types of ecological questions that these models have been used to explore: pathogen invasion dynamics and range expansion, spatial heterogeneity and pathogen persistence, the implications of management and intervention strategies and the role of evolution in host-pathogen dynamics. We reviewed 168 studies that consider pathogen transmission in free-ranging wildlife and classify them by the model type employed, the focal host-pathogen system, and their overall research themes and motivation. We observed a significant focus on mammalian hosts, a few well-studied or purely theoretical pathogen systems, and a lack of studies occurring at the wildlife-public health or wildlife-livestock interfaces. Finally, we discuss challenges and future directions in the context of unprecedented human-mediated environmental change. Spatial models may provide new insights into understanding, for example, how global warming and habitat disturbance contribute to disease maintenance and emergence. Moving forward, better integration of dynamic, spatial disease models with approaches from movement ecology, landscape genetics/genomics and ecoimmunology may provide new avenues for investigation and aid in the control of zoonotic and emerging infectious diseases.

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Section: Future Directions: Addressing Global Challengesmentioning

confidence: 99%

Section: Accounting For Host Heterogeneitymentioning

confidence: 99%

Dynamic, spatial models of parasite transmission in wildlife: Their structure, applications and remaining challenges

White

Forester

Craft

2017

Journal of Animal Ecology

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“…Consequently local population abundance, haul-out density, animal movement and the seasonal timing of any future outbreak could all affect contact rate. In addition, a recent study investigated the effect of maternal immunity on estimating the inter-epidemic interval for PDV in Europe [ 225 ]. Depending on the model assumptions, this could range from 6 to 12 years.…”

Section: Epidemiologymentioning

confidence: 99%

Phocine Distemper Virus: Current Knowledge and Future Directions

Duignan

Bressem

Baker

et al. 2014

Viruses

137

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Phocine distemper virus (PDV) was first recognized in 1988 following a massive epidemic in harbor and grey seals in north-western Europe. Since then, the epidemiology of infection in North Atlantic and Arctic pinnipeds has been investigated. In the western North Atlantic endemic infection in harp and grey seals predates the European epidemic, with relatively small, localized mortality events occurring primarily in harbor seals. By contrast, PDV seems not to have become established in European harbor seals following the 1988 epidemic and a second event of similar magnitude and extent occurred in 2002. PDV is a distinct species within the Morbillivirus genus with minor sequence variation between outbreaks over time. There is now mounting evidence of PDV-like viruses in the North Pacific/Western Arctic with serological and molecular evidence of infection in pinnipeds and sea otters. However, despite the absence of associated mortality in the region, there is concern that the virus may infect the large Pacific harbor seal and northern elephant seal populations or the endangered Hawaiian monk seals. Here, we review the current state of knowledge on PDV with particular focus on developments in diagnostics, pathogenesis, immune response, vaccine development, phylogenetics and modeling over the past 20 years.

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“…In a peak year following an increase year, the seroprevalence in overwintered voles in spring approaches 100% (see Supplementary Material ), and consequently most of the young born to these females should have maternal antibodies. This influx of maternally protected newborns may delay transmission beyond the abundance peak, hence reducing the infection prevalence (Garnier et al, 2014 ). The existence of MatAb immunity in juveniles has been described in multiple hantavirus studies in both US and Europe (for an overview see Kallio et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Why Hantavirus Prevalence Does Not Always Increase With Host Density: Modeling the Role of Host Spatial Behavior and Maternal Antibodies

Reijniers

Tersago²,

Borremans

et al. 2020

Front. Cell. Infect. Microbiol.

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For wildlife diseases, one often relies on host density to predict host infection prevalence and the subsequent force of infection to humans in the case of zoonoses. Indeed, if transmission is mainly indirect, i.e., by way of the environment, the force of infection is expected to increase with host density, yet the laborious field data supporting this theoretical claim are often absent. Hantaviruses are among those zoonoses that have been studied extensively over the past decades, as they pose a significant threat to humans. In Europe, the most widespread hantavirus is the Puumala virus (PUUV), which is carried by the bank vole and causes nephropathia epidemica (NE) in humans. Extensive field campaigns have been carried out in Central Finland to shed light on this supposed relationship between bank vole density and PUUV prevalence and to identify other drivers for the infection dynamics. This resulted in the surprising observation that the relationship between bank vole density and PUUV prevalence is not purely monotonic on an annual basis, contrary to what previous models predicted: a higher vole density does not necessary result in a higher infection prevalence, nor in an increased number of humans reported having NE. Here, we advance a novel individual-based spatially-explicit model which takes into account the immunity provided by maternal antibodies and which simulates the spatial behavior of the host, both possible causes for this discrepancy that were not accounted for in previous models. We show that the reduced prevalence in peak years can be attributed to transient immunity, and that the density-dependent spatial vole behavior, i.e., the fact that home ranges are smaller in high density years, plays only a minor role. The applicability of the model is not limited to the study and prediction of PUUV (and NE) occurrence in Europe, as it could be easily adapted to model other rodent-borne diseases, either with indirect or direct transmission.

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Length of intervals between epidemics: evaluating the influence of maternal transfer of immunity

Cited by 11 publications

References 56 publications

Dynamic, spatial models of parasite transmission in wildlife: Their structure, applications and remaining challenges

Dynamic, spatial models of parasite transmission in wildlife: Their structure, applications and remaining challenges

Phocine Distemper Virus: Current Knowledge and Future Directions

Why Hantavirus Prevalence Does Not Always Increase With Host Density: Modeling the Role of Host Spatial Behavior and Maternal Antibodies

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