Global biodiversity loss, habitat fragmentation, and climate change are significantly reshaping the landscape of public health in Europe through the disruption of the natural transmission cycles of rodent-borne zoonotic pathogens, including tick-borne encephalitis virus (TBEV), hantaviruses, and arenaviruses. A multi-scale One Health approach integrates individual host traits with predictions of human risk, from local to broad European spatial patterns. A key role in these complex dynamics is played by rodent populations, largely governed by bottom-up fac tors such as climate and food availability. Resilient generalist species such as the bank vole (Cle thrionomys glareolus) and the yellow-necked mouse (Apodemus flavicollis) play pivotal roles in driving these dynamics across latitudes. While northern rodent populations follow multiannual cycles, southern European populations exhibit dramatic, mast-driven outbreaks linked to tree seed production and resource availability [1]. These population fluctuations are also statistically predictable using specific climatic drivers. For instance, warmer summers occurring two years prior correlate with population peaks, whereas autumnal precipitations in the preceding year serve as a limiting factor [2]. At the local level, the transmission of tick- and rodent-borne pathogens is often regulated through specific interactions among key hosts. In the case of TBE, the virus spreads effectively through non-viraemic co-feeding [3]central and eastern Europe, Russia and the Far East, with considerable altitudinal and latitudinal shifts described during recent decades. The reported routes of transmission for TBE virus include the saliva-activated non-viraemic transmission between co-feeding ticks taking place on rodent hosts. During the period 2001–2014, a popu lation of the yellow-necked mouse (Apodemus flavicollis, a mechanism where infected and uninfected ticks exchange the pathogen while simultaneously feeding on the same rodent host. The presence of larger animals, such as deer, introduces a further layer of complexity. Ungulates act as tick amplifiers by providing necessary blood meals for reproduction, yet they simultane ously serve as pathogen dilution hosts, as they are incompetent to transmit the virus back to the ticks. This effect is highly scale-dependent, meaning that the local density of deer can either exacerbate or mitigate the risk of infection [4]. Directly transmitted viruses, such as arenavi ruses (e.g., lymphocytic choriomeningitis virus) and hantaviruses, spread horizontally through density-dependent mechanisms. The transmission is primarily driven by aggressive encounters between older males, making these pathogens highly susceptible to stochastic fadeouts if host density thresholds are not maintained. This vulnerability highlights the fragility of viral persis tence during low phases of rodent population [5]. At regional and continental scales, pathogen risk can be forecasted by integrating vari ous ecological and environmental indicators. Factors such as habitat richness indices, host community composition (specifically deer and rodents), and specific climatic variables serve as robust predictors for TBE occurrence [6–7]. Furthermore, a biological indicator for tree masting, the airborne pollen abundance, acts as a particularly innovative proxy for TBE risk. Monitoring of pollen levels enables the prediction of human TBE risk with a significant two year lag time [8]. An effective One Health strategy must harness together these multiscale ecological complex threads, from individual scale events to continental climatic trends. Transitioning from reactive monitoring to proactive early warning systems allows for effective anticipation of zoonotic spill over events before they impact human populations.
Tagliapietra, V.; Arnoldi, D.; Dagostin, F.; Ferrari, G.; Marini, G.; Rosso, F.; Rizzoli, A. (2026). From rodent population dynamics to zoonotic risk: a multi-scale ecoepidemiological approach in Europe. Biologija, 72 (1): 42-43. handle: https://hdl.handle.net/10449/96695
From rodent population dynamics to zoonotic risk: a multi-scale ecoepidemiological approach in Europe
Tagliapietra, V.
Primo
;Arnoldi, D.;Dagostin, F.;Ferrari, G.;Marini, G.;Rosso, F.;Rizzoli, A.Ultimo
2026-01-01
Abstract
Global biodiversity loss, habitat fragmentation, and climate change are significantly reshaping the landscape of public health in Europe through the disruption of the natural transmission cycles of rodent-borne zoonotic pathogens, including tick-borne encephalitis virus (TBEV), hantaviruses, and arenaviruses. A multi-scale One Health approach integrates individual host traits with predictions of human risk, from local to broad European spatial patterns. A key role in these complex dynamics is played by rodent populations, largely governed by bottom-up fac tors such as climate and food availability. Resilient generalist species such as the bank vole (Cle thrionomys glareolus) and the yellow-necked mouse (Apodemus flavicollis) play pivotal roles in driving these dynamics across latitudes. While northern rodent populations follow multiannual cycles, southern European populations exhibit dramatic, mast-driven outbreaks linked to tree seed production and resource availability [1]. These population fluctuations are also statistically predictable using specific climatic drivers. For instance, warmer summers occurring two years prior correlate with population peaks, whereas autumnal precipitations in the preceding year serve as a limiting factor [2]. At the local level, the transmission of tick- and rodent-borne pathogens is often regulated through specific interactions among key hosts. In the case of TBE, the virus spreads effectively through non-viraemic co-feeding [3]central and eastern Europe, Russia and the Far East, with considerable altitudinal and latitudinal shifts described during recent decades. The reported routes of transmission for TBE virus include the saliva-activated non-viraemic transmission between co-feeding ticks taking place on rodent hosts. During the period 2001–2014, a popu lation of the yellow-necked mouse (Apodemus flavicollis, a mechanism where infected and uninfected ticks exchange the pathogen while simultaneously feeding on the same rodent host. The presence of larger animals, such as deer, introduces a further layer of complexity. Ungulates act as tick amplifiers by providing necessary blood meals for reproduction, yet they simultane ously serve as pathogen dilution hosts, as they are incompetent to transmit the virus back to the ticks. This effect is highly scale-dependent, meaning that the local density of deer can either exacerbate or mitigate the risk of infection [4]. Directly transmitted viruses, such as arenavi ruses (e.g., lymphocytic choriomeningitis virus) and hantaviruses, spread horizontally through density-dependent mechanisms. The transmission is primarily driven by aggressive encounters between older males, making these pathogens highly susceptible to stochastic fadeouts if host density thresholds are not maintained. This vulnerability highlights the fragility of viral persis tence during low phases of rodent population [5]. At regional and continental scales, pathogen risk can be forecasted by integrating vari ous ecological and environmental indicators. Factors such as habitat richness indices, host community composition (specifically deer and rodents), and specific climatic variables serve as robust predictors for TBE occurrence [6–7]. Furthermore, a biological indicator for tree masting, the airborne pollen abundance, acts as a particularly innovative proxy for TBE risk. Monitoring of pollen levels enables the prediction of human TBE risk with a significant two year lag time [8]. An effective One Health strategy must harness together these multiscale ecological complex threads, from individual scale events to continental climatic trends. Transitioning from reactive monitoring to proactive early warning systems allows for effective anticipation of zoonotic spill over events before they impact human populations.| File | Dimensione | Formato | |
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