Abstract
The transmission of wildlife zoonoses to humans depends, amongst others, on complex interactions of host population ecology and pathogen dynamics within host populations. In Europe, the Puumala virus (PUUV) causes nephropathia epidemica in humans. In this study we investigated complex interrelations within the epidemic system of PUUV and its rodent host, the bank vole (Myodes glareolus). We suggest that beech fructification and bank vole abundance are both decisive factors affecting human PUUV infections. While rodent host dynamics are expected to be directly linked to human PUUV infections, beech fructification is a rather indirect predictor by serving as food source for PUUV rodent hosts. Furthermore, we examined the dependence of bank vole abundance on beech fructification. We analysed a 12-year (2001-2012) time series of the parameters: beech fructification (as food resource for the PUUV host), bank vole abundance and human incidences from 7 Federal States of Germany. For the first time, we could show the direct interrelation between these three parameters involved in human PUUV epidemics and we were able to demonstrate on a large scale that human PUUV infections are highly correlated with bank vole abundance in the present year, as well as beech fructification in the previous year. By using beech fructification and bank vole abundance as predictors in one model we significantly improved the degree of explanation of human PUUV incidence. Federal State was included as random factor because human PUUV incidence varies considerably among states. Surprisingly, the effect of rodent abundance on human PUUV infections is less strong compared to the indirect effect of beech fructification. Our findings are useful to facilitate the development of predictive models for host population dynamics and the related PUUV infection risk for humans and can be used for plant protection and human health protection purposes.
Highlights
Numerous wildlife zoonoses are transmitted to humans by rodents, because rodents are an abundant and species-rich group of mammals that carry a wide variety of pathogens [2], such as leptospirosis, murine typhus, influenza, plague, trypanosomiasis, salmonellosis and toxoplasmosis [2, 3]
By using beech fructification and bank vole abundance as predictors in one model we significantly improved the degree of explanation of human Puumala virus (PUUV) incidence
We showed that masting of common beech occurred prior to years with high human PUUV incidence and that these incidence peaks were regularly accompanied by increased bank vole population densities
Summary
Numerous wildlife zoonoses (majority of emerging pathogens; [1]) are transmitted to humans by rodents, because rodents are an abundant and species-rich group of mammals that carry a wide variety of pathogens [2], such as leptospirosis, murine typhus, influenza, plague, trypanosomiasis, salmonellosis and toxoplasmosis [2, 3]. Rodents have a quick alternation of generations and if environmental conditions are favourable a high reproductive success. They can reach high densities quickly, which faciliates the transmission of pathogens [4, 5]. Habitat structure and food availability have an impact on host population dynamics, which in turn are linked to human infection risk with zoonotic pathogens. There are several factors affecting population dynamics of rodents (reviewed in [9]) and subsequently the transmission of zoonoses to humans [10, 11], including hantavirus infections
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