The Ecology of Rabies: Evidence of Co-Adaptation

Abstract

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. British Ecological Society is collaborating with JSTOR to digitize, preserve and extend access to Journal of Applied Ecology. SUMMARY(1) Currently accepted rabies lore suggests that: (a) rabies is a uniformly fatal disease that causes decimating epizootics; (b) the existence of immune subpopulations of hosts and the immunological nature of rabies-virus-inhibiting substances in the blood of wild vertebrates is questionable; and (c) models can explain observed patterns of incidence without consideration of immune subpopulations or co-adaptations between the virus and its hosts.(2) The objective of this paper is to explore the idea that rabies virus does persist in traditional host-parasite relationships that exhibit varying degrees of co-adaptation.(3) Review of the literature is used to summarize current knowledge of the ecology of infectious diseases, the genetics and pathogenesis of rabies virus, the nature of vertebrate immune response to rabies virus under experimental conditions, and the nature of persistent rabies virus-host associations.(4) Unpublished data on rabies virus and immune responses in wild populations of mustelids, canids, marsupials, and bats is presented.(5) It is well documented that: (a) vertebrates can become immune through laboratory exposure to rabies; (b) natural infections can also induce immune responses; (c) rabies-neutralizing substances in some wild vertebrates confer significant resistance to infection.(6) It is shown that rabies virus persists in diverse ecological communities and that patterns of diseases differ among these communities.(7) Differences in patterns include mode of transmission, prevalence of infection, and the proportion of the host population that is immune.(8) Differences in patterns can be related to differences in the host populations, especially differences in population density and life history traits.(9) There is suggestive evidence that: (a) landscape effects (habitat quality and habitat pattern) are important in maintaining persistent virus-host associations; and that (b) rabies is opportunistic, forming dynamic host associations that may change rapidly through time.(10) Consideration of immune subpopulations does not invalidate, but can enhance, mathematical models of patterns of rabies incidence.(11) Improved virological and immunological techniques are now sufficient to permit effective investigation of some heretofore unaddressable aspects of rabies ecology.(12) It is emphasized that current knowledge of rabies ecology is based to a large extent on unverified or anecdotal data and is fragmentary; caution should be used in making assumptions in planning research, choosing control strategies, or formulating models.

Habitat use of Medium-Sized Carnivores in Southeast Finland — Key Habitats for Rabies Spread?

“…Other studies have indicated that habitat types have infl uenced the spread (speed and intensity) of rabies (e.g. Steck & Wandeler 1980, Pool & Hacker 1982, Carey & McLean 1983, Sanson & Pearson 1997in Gylys et al 1998. It is also known that the spatial spread of rabies occurs either within territory, through neighbour-to-neighbour infection or inter-territorial movements (temporary and permanent dispersal) of infected animals.…”

Innate immune responses in raccoons after raccoon rabies virus infection

“…High densities of raccoons in urban and suburban areas (Totton et al, 2002) and the concomitant increase in potential human and pet exposures present a serious threat to human health. Contrary to the common belief that exposure to RV is always lethal, empirical studies have suggested that raccoon exposure to RRV does not always result in clinical disease, perhaps due to interindividual differences in innate immune responses (Carey & Mclean, 1983;Szanto, 2009). For example, 5-40 % of raccoons survive RRV challenge (K. Knowles, personal communication; Carey & Mclean, 1983), and the incubation period can vary among raccoons and vaccinated animals that have not demonstrated seroconversion (Rupprecht et al, 1988).…”

“…Contrary to the common belief that exposure to RV is always lethal, empirical studies have suggested that raccoon exposure to RRV does not always result in clinical disease, perhaps due to interindividual differences in innate immune responses (Carey & Mclean, 1983;Szanto, 2009). For example, 5-40 % of raccoons survive RRV challenge (K. Knowles, personal communication; Carey & Mclean, 1983), and the incubation period can vary among raccoons and vaccinated animals that have not demonstrated seroconversion (Rupprecht et al, 1988). The culmination of these factors illustrates that there is variability in the immune response of raccoons to RRV exposure that may result in abortive infections.…”

Rabies: Epidemiology, Prevention, and Future Research

“…The existence, among wildlife, of individuals that survive infection and become chronic carriers, as has been demonstrated for dogs (Fekadu et al, 1992), is undocumented and, presumably, extremely rare. However, evidence suggests that not all infected raccoons die of rabies, a phenomenon that could have a major impact on populationlevel processes (Bigler et al, 1973;Brown et al, 1990;Carey and McLean, 1983). Natural herd immunity would rise, and previously-infected immune survivors could lower the rate of transmission.…”