While there is good evidence linking animal introductions to impacts on native communities via disease emergence, our understanding of how such impacts occur is incomplete. Invasion ecologists have focused on the disease risks to native communities through "spillover" of infectious agents introduced with nonindigenous hosts, while overlooking a potentially more common mechanism of impact, that of "parasite spillback." We hypothesize that parasite spillback could occur when a nonindigenous species is a competent host for a native parasite, with the presence of the additional host increasing disease impacts in native species. Despite its lack of formalization in all recent reviews of the role of parasites in species introductions, aspects of the invasion process actually favor parasite spillback over spillover. We specifically review the animal-parasite literature and show that native species (arthropods, parasitoids, protozoa, and helminths) account for 67% of the parasite fauna of nonindigenous animals from a range of taxonomic groups. We show that nonindigenous species can be highly competent hosts for such parasites and provide evidence that infection by native parasites does spillback from nonindigenous species to native host species, with effects at both the host individual and population scale. We conclude by calling for greater recognition of parasite spillback as a potential threat to native species, discuss possible reasons for its neglect by invasion ecologists, and identify future research directions.

Summary1. We review our ecological understanding of wildlife infectious diseases from the individual host to the ecosystem scale, highlighting where conceptual thinking lacks verification, discussing difficulties and challenges, and offering potential future research directions. 2. New molecular approaches hold potential to increase our understanding of parasite interactions within hosts. Also, advances in our knowledge of immune systems makes immunological parameters viable measures of parasite exposure, and useful tools for improving our understanding of causal mechanisms. 3. Studies of transmission dynamics have revealed the importance of heterogeneity in host behaviour and physiology, and of contact processes operating at different spatial and temporal scales. An important future challenge is to determine the key transmission mechanisms maintaining the persistence of different types of diseases in the wild. 4. Regulation of host populations is too complex to consider parasite effects in isolation from other factors. One solution is to seek a unified understanding of the conditions under which (and the ecological rules determining when) population scale impacts of parasites can occur. 5. Good evidence now shows that both direct effects of parasites, and trait mediated indirect effects, frequently mediate the success of invasive species and their impacts on recipient communities. A wider exploration of these effects is now needed. 6. At the ecosystem scale, research is needed to characterize the circumstances and conditions under which both fluxes in parasite biomass, and trait mediated effects, are significant in ecosystem processes, and to demonstrate that parasites do indeed increase 'ecosystem health'. 7. There is a general need for more empirical testing of predictions and subsequent development of theory in the classic research cycle. Experimental field studies, meta-analyses, the collection and analysis of long-term data sets, and data constrained modelling, will all be key to advancing our understanding. 8. Finally, we are only now beginning to understand the importance of cross-scale interactions associated with parasitism. Such interactions may offer key insights into bigger picture questions such as when and how different regulatory factors are important, when disease can cause species extinctions, and what characteristics are indicative of functionally resilient ecosystems.

Although a parapoxvirus harmful to red squirrels is present in UK squirrel populations it has not been considered a major cause of red squirrel decline, and replacement by the introduced grey squirrel, mainly because diseased individuals are rarely observed. By developing a generic model we show that parapoxvirus is likely to have played a crucial role in the red squirrel decline even though the prevalence of infection is low. Conservationists are quite rightly concerned with the invasion of exotic organisms such as the grey squirrel. Our work emphasizes that they, along with other ecologists, should pay particular attention to pathogens, even when they occur at low prevalence.

The Tasmanian devil, Sarcophilus harrisii, is the largest extant marsupial carnivore. In 1996, a debilitating facial tumor was reported. It is now clear that this is an invariably lethal infectious cancer. The disease has now spread across the majority of the range of the species and is likely to occur across the entire range within 5 to 10 years. The disease has lead to continuing declines of up to 90% and virtual disappearance of older age classes. Mark-recapture analysis and a preliminary epidemiological model developed for the population with the best longitudinal data both project local extinction in that area over a timeframe of 10 to 15 years from disease emergence. However, the prediction of extinction from the model is sensitive to the estimate of the latent period, which is poorly known. As transmission appears to occur by biting, much of which happens during sexual encounters, the dynamics of the disease may be typical of sexually transmitted diseases. This means that transmission is likely to be frequency-dependent with no threshold density for disease maintenance. Extinction over the entire current range of the devil is therefore a real possibility and an unacceptable risk.

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