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We present a susceptibles-exposed-infectives (SEI)model to analyze the effects of seasonality on epidemics, mainly of rabies, in a wide range of wildlife species. Model parameters are cast as simple allometric functions of host body size. Via nonlinear analysis, we investigate the dynamical behavior of the disease for different levels of seasonality in the transmission rate and for different values of the pathogen basic reproduction number (R0) over a broad range of body sizes. While the unforced SEI model exhibits long-term epizootic cycles only for large values of R0, the seasonal model exhibits multiyear periodicity for small values of R0. The oscillation period predicted by the seasonal model is consistent with those observed in the field for different host species. These conclusions are not affected by alternative assumptions for the shape of seasonality or for the parameters that exhibit seasonal variations. However, the introduction of host immunity (which occurs for rabies in some species and is typical of many other wildlife diseases) significantly modifies the epidemic dynamics; in this case, multiyear cycling requires a large level of seasonal forcing. Our analysis suggests that the explicit inclusion of periodic forcing in models of wildlife disease may be crucial to correctly describe the epidemics of wildlife that live in strongly seasonal environments. [ABSTRACT FROM AUTHOR]

Pathogens that can infect multiple host species will have different dynamics than pathogens that are restricted to a single species of host. This article examines the conditions for establishment and long-term population dynamic behavior of pathogens that infect multiple species of hosts. The article attempts to address three major questions in this area: First, under which conditions will increases in the diversity of host species buffer infectious disease outbreaks, and under which conditions will host diversity amplify disease outbreaks? Second, under what conditions is it possible to control an infectious agent by focusing control against only one host species? Third, what role does host species diversity play in maintaining pathogen persistence? The answers to these questions supply some important general insights into the role that biodiversity plays in buffering humans and other species against new and emerging pathogens. [ABSTRACT FROM AUTHOR]

We derive a model that has one predator and one prey species and includes antipredator behavior. The prey are allowed to increase their investment in antipredator behavior, thereby decreasing their chance of being captured by the predator. However, they must pay for this protection by a cost exacted through decreased fecundity or increased mortality caused by factors other than predation. The population-dynamic consequences of antipredator behaviors are explored by comparing systems in which the efficiencies of the antipredator behavior differ; as the antipredator behavior becomes more efficient, the prey need to invest less in order to achieve the same level of protection from the predator. We assume that for any degree of efficiency, the prey choose their level of investment in antipredator behavior in order to optimize their expected reproductive fitness. By assuming only that the predators and prey coexist and that there is a stable equilibrium, we show that increased efficiency of antipredator behaviors increases prey densities and decreases the ratio of predator-to-prey densities. This is true even though the prey's level of investment in antipredator behavior initially increases and then decreases with increasing efficiency of the antipredator behavior. Consequently, the effect of antipredator behaviors on population densities cannot be inferred from the level of prey investment in these behaviors. A specific model is used to illustrate the second result of the paper, that antipredator behaviors tend to decrease the oscillatory dynamics inherent in model predatorprey systems. [ABSTRACT FROM AUTHOR]