Abstract
We use data collected on 18,1-ha live trapping grids monitored from 1994 through 2005 and on five of those grids through 2013 in the mesic northwestern US to illustrate the complexity of the deer mouse (Peromyscus maniculatus)/Sin Nombre virus (SNV) host-pathogen system. Important factors necessary to understand zoonotic disease ecology include those associated with distribution and population dynamics of reservoir species as well as infection dynamics. Results are based on more than 851,000 trap nights, 16,608 individual deer mice and 10,572 collected blood samples. Deer mice were distributed throughout every habitat we sampled and were present during every sampling period in all habitats except high altitude habitats over1900 m. Abundance varied greatly among locations with peak numbers occurring mostly during fall. However, peak rodent abundance occurred during fall, winter and spring during various years on three grids trapped 12 mo/yr. Prevalence of antibodies to SNV averaged 3.9% to 22.1% but no grids had mice with antibodies during every month. The maximum period without antibody-positive mice ranged from one month to 52 months, or even more at high altitude grids where deer mice were not always present. Months without antibody-positive mice were more prevalent during fall than spring. Population fluctuations were not synchronous over broad geographic areas and antibody prevalences were not well spatially consistent, differing greatly over short distances. We observed an apparently negative, but non-statistically significant relationship between average antibody prevalence and average deer mouse population abundance and a statistically significant positive relationship between the average number of antibody positive mice and average population abundance. We present data from which potential researchers can estimate the effort required to adequately describe the ecology of a rodent-borne viral system. We address different factors affecting population dynamics and hantavirus antibody prevalence and discuss the path to understanding a complex rodent-borne disease system as well as the obstacles in that path.
Highlights
We investigated the possibilities of a widespread synchrony among populations by comparing population trends in abundance and antibody prevalence in a pairwise fashion
Deer mice were captured in all locations and habitats across Central and Western Montana (Table 1, Figs. 2 and 3)
Unlike deer mouse populations in the southwestern US (Yates et al 2002, Mills et al 2010), the only place deer mice were not continuously present in Montana was in high altitude (>2440 m) subalpine forests (Wisdom)
Summary
The study of hantaviruses has attracted increasing attention from ecologists in the last two decades (Schmaljohn and Hjelle 1997, Mills and Childs 1998, Singleton et al 1999, Escutenaire et al 2000, Calisher et al 2002, Murua et al 2003, Piudo et al 2005, Jonsson et al 2010, Mills et al 2010, Zhang et al 2010, Vadell et al 2011), resulting in a proliferation of scientific articles addressing population dynamics of the rodent hosts, the prevalence of infection in their populations and rodent-pathogen dynamics. In 1993, a cluster of a human disease, later named Hantavirus Pulmonary Syndrome (HPS), occurred in the southwestern United States. Because the cluster occurred following an El Niño event, it has been hypothesized that, in at least areas of the arid southwestern United States where deer mice are not always persistent, human risk may be related to a bottom up trophic cascade (Parmenter et al 1993, Yates et al 2002). In the trophic cascade hypothesis, increased precipitation results in improved plant productivity, and deer mouse abundance and distribution increases, increasing the number of infected deer mice and prevalence of infection in deer mice, translating to greater disease risk to humans. Though not usually stated as such, this hypothesis has been assumed to be true for other areas within the distribution of deer mice and in other rodent/hantavirus systems throughout the world
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