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In this paper we derive from first principles the expected body sizes of the parasite communities that can coexist in a mammal of given body size. We use a mixture of mathematical models and known allometric relationships to examine whether host and parasite life histories constrain the diversity of parasite species that can coexist in the population of any host species. The model consists of one differential equation for each parasite species and a single density-dependent nonlinear equation for the affected host under the assumption of exploitation competition. We derive threshold conditions for the coexistence and competitive exclusion of parasite species using invasion criteria and stability analysis of the resulting equilibria. These results are then used to evaluate the range of parasites species that can invade and establish in a target host and identify the ‘optimal’ size of a parasite species for a host of a given body size; ‘optimal’ is defined as the body size of a parasite species that cannot be outcompeted by any other parasite species. The expected distributions of parasites body sizes in hosts of different sizes are then compared with those observed in empirical studies. Our analysis predicts the relative abundance of parasites of different size that establish in the host and suggests that increasing the ratio of parasite body size to host body size above a minimum threshold increases the persistence of the parasite population.
This chapter contributes to the current debate regarding environmental attitudes and behaviour, and how to change them by employing systems of governance. It is also, I believe, a contribution to citizenship theory and practice, in that my enquiry into environmental attitudes and behaviour leads me to develop a notion of ecological citizenship which I take to differ in significant ways from the citizenship traditions which history has bequeathed us. Finally, to the extent that citizenship can be sensibly talked of as a potential governance tool for achieving sustainability, my argument bears directly on the two main themes of this book: governance and sustainability. Any move to enlist citizenship for the policy toolbox looks like a move towards governance rather than government – i.e. society self-steering rather than being steered by some hierarchically superior body – and I shall come back to this toward the end of the chapter.
As far as changing environmental attitudes and behaviour using different policy instruments is concerned, in the UK, at least, there is a very obvious front-runner: fiscal incentives. This is not a new idea, of course, and any primer on environmental economics will contain a description and assessment of them (e.g. Turner et al., 1994). The idea, as we know, is that people are encouraged into environmentally beneficial behaviour through offering them financial advantages and penalties, to which they respond appropriately. The idea of fiscal incentives is a useful foil for the subsequent discussion here of environmental citizenship.
Fragmentation of natural habitats has important effects on the viability and persistence of most free-living animal and plant species; the other chapters in this volume outline many of these effects in eloquent detail. In this chapter we focus our attention on the parasitic half of biodiversity and examine how the viability and persistence of pathogens and parasitic species are modified by fragmentation and reconnection of the patchy habitats in which their host species live. The problem can be addressed at a hierarchy of different scales, as almost by definition, parasites and pathogens are canonically “adapted” to live in the patchy environment defined by the individual hosts they live in (Dobson 2003). Life-history evolution in parasites is sharply defined by the twin processes of exploiting the patch of habitat in which you live (your host) and producing infective stages (your offspring), which have to then find new patches (hosts) to exploit. Movement between hosts for pathogens is similar in many ways to dispersal between patches for free-living organisms. The key difference is that all of the dispersal in pathogens is undertaken by transmission stages that are the effective offspring of the parasites that currently infect the host. So transmission between host patches is for parasites both birth and dispersal. Fragmentation of the host's habitat increases the average distances the parasites have to move between birth and successful colonization.
A long-term objective of population biology is to explain the spatiotemporal variations in abundance of organisms by understanding the factors that limit both distribution and changes in abundance. In general, theory predicts that a major determinant of distribution and dynamics is the instantaneous population growth rate, presented as r (where r = ln(λ) = ln(Nt+1/Nt). Some models reveal the obvious, such that species will tend not to exist where their population growth is consistently negative and there is no immigration (see Chapter 2). But the models also expose intriguing dynamics; for example, simple single-species nonlinear models reveal that dynamics can vary from stability through oscillatory to chaotic behaviour simply by subtle changes in the population growth rate (May 1976). As such, it is not surprising that when we incorporate interspecific interactions, the stochastic vagaries of environmental conditions and dispersal, we reveal a Pandora's box of dynamical behaviours.
In the empirical literature, the population growth rate parameter does not enjoy the same importance as it does in the theoretical literature. Rarely do workers make an estimate of the intrinsic growth rate parameter (r) or its empirical equivalent, the maximum growth rate (rmax) which is simply the maximum rate of growth observed within a time-series. Changes in the observed growth rate at a specific time (rt) may be recorded along with the factors associated with the reproductive output of individuals, but studies tend not to estimate the extent to which the growth rate is reduced by density dependent regulatory factors.
Historically, control of virulence in wild animals has only been attempted when the disease threatened humans or their livestock. However, as populations of some wild animals have become increasingly rare, public demand to protect endangered species has lead to an increasing effort to control disease in wildlife. Habitat fragmentation and the ensuing edge effects have further exposed wildlife populations to exotic species and livestock that may act as vectors for infectious and parasitic diseases to which the wildlife population has not been exposed previously. Small populations are at greater risk, because the loss of individuals can reduce genetic diversity, make the population more sensitive to the natural fluctuations of the environment, and trigger a population crash as a consequence of high predation pressure or the disruption of social structure (May 1988; Hutchins et al. 1991). Moreover, these negative effects may be enhanced by the loss of immunity through the natural elimination of the disease at low population densities. If the disease is then accidentally reintroduced into the now immunologically naive population, hosts may suffer a higher level of mortality with respect to epidemics of previously endemic diseases (Cunningham 1996).
In this chapter, we first present a simple formula to estimate the time for virulence or resistance to evolve. Then, after a brief consideration of the potential consequences of vaccination programs on the evolution of resistance, we briefly review some of the reasons why wildlife virulence management is still a science in its infancy.
The interaction between pathogens and their hosts is the most intimate of interspecific interactions. The pathogen is entirely dependent upon the host for resources and transmission to the next susceptible host in its life cycle. In contrast, the presence of pathogens usually leads to a reduction in host fitness through reductions in survival, fecundity, or opportunities to locate a mate. However, only a proportion of the host population is ever exposed to any particular parasite species, while all parasite populations are exposed to their hosts. These asymmetries in association and in the costs and benefits accrued to parasites and hosts are further compounded by asymmetries in the generation time of the two species: the generation time of the host often exceeds that of the parasite by several orders of magnitude. Consequently, when we examine the evolution of virulence and other components of parasite fitness, we usually focus on changes in parasite phenotype in response to constraints placed by the host's life history.
In this chapter, we analyze different aspects of the evolution of virulence in systems of free-living hosts and their parasites. First we establish the difference between micro- and macroparasite dynamics. Several documented population dynamic studies in which parasites have been shown to dramatically affect the abundance of host populations and the structure of biological communities are then discussed.
These papers deal with different aspects of understanding how hosts cope with the diversity of antigenic challenges that pathogens provide. These comments examine common threads underlying three of the presentations and describe some recent work on the more general problem of the diversity of pathogens that any host population can sustain.
The work of Martin Nowak and his colleagues at Oxford, Imperial College and Amsterdam University epitomizes the challenges that mathematical models present to empirical epidemiologists. As with other recent work on the mathematics of the immune system and infection with HIV (McLean 1993), the work suggests alternative interpretations of epidemiological data and has stimulated the collection (and analysis) of data not normally collected by immunologists and clinicians. At the heart of the Nowak model is the interaction between the diversity of HIV quasi-species in individual patients and the ability of the host to produce a sufficient diversity of antigens to cope with this. At a crucial level of quasi-species diversity, the diversity threshold, the immune system is overwhelmed, CD4 counts decline precipitously and the patient succumbs to full-blown AIDS. The length of time until this occurs is dependent upon a variety of factors, but most importantly upon the replication and mutation rate of the virus, and upon the host's ability to mount an efficient and diverse immune response. My main questions are about this diversity threshold; the diversity levels presented in the model seem much higher than the diversity levels observed in individually infected HIV/AIDS patients.
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