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The Hantavirus epidemic in the Southwest:Rodent population dynamics and the implications for transmission ofHantavirus-associated adult respiratory distress syndrome (HARDS) in the Four Corners Region: Report to the Federal Centers for Disease Control and Prevention, Atlanta, Georgia
... Predicting outbreaks of these infections is particularly challenging because reservoir abundance can consequently be extremely variable in space and time. Sin Nombre virus (SNV) circulates in wild deer mice (Peromyscus maniculatus; see Plate 1), causes hantavirus pulmonary syndrome (HPS) with 30–40% case fatality in humans, and is a classic illustration of the complexity of the interaction among climate, animal host ecology, and zoonoses (Parmenter et al. 1993, Yates et al. 2002). SNV was first recognized in 1993 after it caused an outbreak of HPS in the southwestern United States (CDC 1993). ...
... SNV was first recognized in 1993 after it caused an outbreak of HPS in the southwestern United States (CDC 1993). Human-to-human transmission is extremely rare, and this deadly outbreak was linked to increased primary productivity , high mouse density, and zoonotic transmission after an El Ninõ event brought increased precipitation to this usually arid region (Parmenter et al. 1993, Yates et al. 2002). This highlights the importance of understanding the reservoir host and pathogen dynamics, which can be key in controlling and preventing HPS and other zoonoses. ...
Predicting outbreaks of zoonotic infections in reservoir hosts that live in highly fluctuating environments, such as Sin Nombre virus (SNV) in deer mice, is particularly challenging because host populations vary widely in response to environmental conditions and the relationship between field infection rates and abundance often appears to contradict conventional theory. Using a stage-structured host-pathogen model parameterized and cross-validated from a unique 15-year data set, we show how stochastic population fluctuations can lead to predictable dynamics of SNV in deer mice. Significant variation in host abundance and the basic reproductive number of the virus results in intermittent crossing of the critical host population density necessary for SNV endemicity and frequent local extinctions. When environmental conditions favor growth of the host population above the threshold, host– pathogen interactions lead to delayed density dependence in reservoir prevalence. The resultant ecological delay may provide a neglected opportunity for outbreak prediction in zoonoses.
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.
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