Tuesday, August 7, 2007

PS 25-35: Landscape rodent dispersal as a triggering mechanism for rodent-borne disease outbreaks

Robert R. Parmenter, Valles Caldera Trust and Terry L. Yates, University of New Mexico.

Climate variability is thought to affect a number of rodent-borne zoonotic diseases such as plague, vector-borne zoonotic bartonellosis and hantaviral diseases.  Our project team is evaluating the Trophic Cascade Hypothesis (TCH), an hypothesis that was developed to explain changing levels of human risk for zoonotic diseases associated with climate variability in the American Southwest.  When applied to rodent-borne zoonotic diseases, the TCH predicts that:  1. Local unseasonable precipitation in the late winter and early spring is the ultimate mechanism triggering increased zoonotic disease risk.  2. Precipitation acts to increase vegetation growth, that provides increased food and shelter for the rodent reservoirs and vectors of disease, whose population densities then increase.  3. Transmission of pathogens within the reservoir populations then occurs at an increased rate.   4. As rodent populations build, and/or climatic conditions return to normal, the rodent populations will disperse and expand into “suboptimal” habitats (dispersal wave). 5. Pathogen infection wave follows rodent population dispersal wave.  6. Expanded distribution of infected rodents increases the probability of contact with humans, eventually resulting in regional outbreaks of disease in humans.  We report here that two components of the TCH have been confirmed in New Mexico:  landscape level dispersal waves of rodents occur from montane “refugia” and that a hantavirus wave follows the rodent wave.  Data are presented for several genera of rodents, and Sin Nombre Hantavirus data are shown for the deer mouse (Peromyscus maniculatus) from different mountains ranges in New Mexico.
 
 
 

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