Population Dynamics of Bank Voles Predicts Human Puumala Hantavirus Risk

Hussein Khalil,Birger Hörnfeldt,Frauke Ecke,Göran Bucht,Magnus Evander

doi:10.1007/s10393-019-01424-4

Hussein Khalil, Birger Hörnfeldt + Show 3 more

Open Access

https://doi.org/10.1007/s10393-019-01424-4

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Abstract

Predicting risk of zoonotic diseases, i.e., diseases shared by humans and animals, is often complicated by the population ecology of wildlife host(s). We here demonstrate how ecological knowledge of a disease system can be used for early prediction of human risk using Puumala hantavirus (PUUV) in bank voles (Myodes glareolus), which causes Nephropathia epidemica (NE) in humans, as a model system. Bank vole populations at northern latitudes exhibit multiannual fluctuations in density and spatial distribution, a phenomenon that has been studied extensively. Nevertheless, existing studies predict NE incidence only a few months before an outbreak. We used a time series on cyclic bank vole population density (1972–2013), their PUUV infection rates (1979–1986; 2003–2013), and NE incidence in Sweden (1990–2013). Depending on the relationship between vole density and infection prevalence (proportion of infected animals), either overall density of bank voles or the density of infected bank voles may be used to predict seasonal NE incidence. The density and spatial distribution of voles at density minima of a population cycle contribute to the early warning of NE risk later at its cyclic peak. When bank voles remain relatively widespread in the landscape during cyclic minima, PUUV can spread from a high baseline during a cycle, culminating in high prevalence in bank voles and potentially high NE risk during peak densities.

Highlights

The emergence and re-emergence of virulent human pathogens over the past two decades (Kilpatrick and Randolph 2012) increased alertness to the global burden of infectious diseases originating in wildlife
For many vector-borne and zoonotic diseases, multiple species with different life histories and population dynamics are involved in the sequence of transmission events that lead to human infections
Spring Puumala hantavirus (PUUV) prevalence in bank voles was dependent on bank vole density during current spring and previous autumn in the five cycles between 1980 and 1986 (III and IV) and 2004–2013 (X, XI, XII)

Summary

Introduction

The emergence and re-emergence of virulent human pathogens over the past two decades (Kilpatrick and Randolph 2012) increased alertness to the global burden of infectious diseases originating in wildlife. Many rodent populations exhibit great spatial and temporal fluctuations in density (Krebs and Myers 1974; Davis et al 2005). These fluctuations include annual (Singleton et al 2001) and multiannual population cycles, the latter typical of northern latitudes (Krebs 1996). Fluctuations in abundance are often accompanied by changes in spatial distribution (e.g., Khalil et al 2014b; Hornfeldt et al 2006; Carver et al 2015), leading to pronounced changes in zoonotic risk over local spatial and short temporal scales (Ostfeld et al 2005)

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