Search for: All records

ABSTRACT To explain patterns between anthropogenic loss of species diversity and the rise in the number of novel zoonotic diseases, the “dilution effect” hypothesis predicts that with lower species diversity, infection risk will increase. The underlying mechanisms have been largely investigated in systems where pathogen transmission is vector‐borne or environmental. Relatively less research has been conducted in systems where transmission is direct, such as with orthohantaviruses (hereafter hantaviruses) and their rodent reservoir hosts. These systems are commonly cited as supporting a negative diversity‐disease pattern. To motivate empirical research on underlying mechanisms driving this pattern, we extend a mechanistic framework that links species diversity and infection prevalence of directly transmitted zoonotic pathogens by using rodent‐hantavirus systems in the Americas as models. Additionally, we summarize empirical studies, synthesize mechanistic evidence, and identify knowledge gaps. Our findings suggest that host regulation is a key mechanism likely to drive diversity‐disease patterns in rodent‐hantavirus systems of the Americas. Other mechanisms have received less empirical support but also less attention. Although host regulation likely functions via density‐dependent transmission, and can thus change contact rates among hosts, consequences to other mechanisms have been neglected. As observed in rodent‐hantavirus systems in the Americas, we propose that for a negative diversity‐disease pattern to manifest, the primary reservoir host species should be resilient to anthropogenic disturbance but also vulnerable to competition, predation, or both, and the “diversity” measure should be associated with host density. 

Abstract Ecological and environmental factors can influence the transmission of infectious diseases. They can accomplish this via effects on host susceptibility and exposure to infection, which are governed by host physiology and behavior, respectively. To better inform disease control, more information is needed about how extrinsic factors affect physiological and behavioral processes that determine transmission. We investigated how heterospecific competitors and seasonality may influence host susceptibility and intraspecific contact rates using a directly transmitted disease system, the North American deer mouse (Peromyscus maniculatus)—Sin Nombre hantavirus (SNV) system. In grasslands of western Montana, USA, deer mice compete with dominant voles (Microtusspp.) and shrews (Sorexspp.) and experience a seasonal temperate climate. Higher SNV transmission occurs primarily during spring/summer, when changes in physiology and behavior may serve as influential contributors. We hypothesized that (1) voles, and to a lesser extent shrews, will induce chronic stress, suppress immunity, and may change contact rates of deer mice; and (2) during spring/summer, deer mice may experience chronic stress, suppressed immunity, and higher contact rates, which may help explain the reported seasonality in SNV transmission. Over two years, we trapped small mammals at four grids in western Montana. Deer mice were sampled for feces and blood and evaluated for scar numbers, demography, and body condition scores (BCSs). We evaluated stress physiology with fecal corticosterone metabolites (FCMs), neutrophil/lymphocyte (N/L) ratios and BCSs, immunity with white blood cell (WBC) counts, and contact rates with scar numbers. We found that shrew density was negatively associated with stress response FCMs, suggestive of chronic stress. Additionally, although complex interactions existed, shrew and vole densities were negatively associated with BCSs, but differentially with scar numbers. N/L ratios were higher in spring/summer, whereas WBC counts were lower in summer, suggestive of chronic stress and suppressed immunity, respectively. Our results suggest that (1) heterospecific competitors may differentially influence disease transmission via stress physiology and contact rates, and that (2) chronic stress, suppressed immunity, and higher contact rates may help explain why higher SNV transmission has been previously reported during spring/summer in Montana. Our findings may extend to other directly transmitted disease systems.