We begin by defining parasite, infection, pathogen and disease. The diversity of animal and plant parasites is then outlined, based on the distinctions between micro- and macroparasites and between those with direct and those with indirect (vectored) life cycles. The particular case of social and brood parasites (e.g. cuckoos) is also described.
We explain the difference between biotrophic and necro-trophic parasites (pioneer saprotrophs), and we use a discussion of zoonoses (wildlife infections transmissible to man) to illustrate the nature of host specificity amongst parasites.
Hosts are reactive environments: they may resist, or recover, or (in vertebrates) acquire immunity. We describe the contrasting responses in vertebrates to micro- and macroparasites and contrast these in turn with the responses of plants to infection. The costliness of host defense against attack is emphasized. Parasites may also induce profound changes in host growth and behavior.
We explain why it may be difficult to distinguish the effects of intraspecific competition amongst parasites from parasite density-dependent host immune responses, and that patterns associated with interspecific competition are as observable amongst parasites as they are in other organisms.
The distinctions between different types of parasite transmission are outlined and a formal description of transmission dynamics is developed, using the form of the contact rate to distinguish between density- and frequency-dependent transmission, though it is emphasized that these may merely be ends of a spectrum. There may also be great spatial variation in the speed with which infection spreads, either as a result of infectious foci or because of spatial mixtures of susceptible and resistant species or varieties.
The distribution of parasites within host populations is usually aggregated. This makes it especially important to understand the distinctions between prevalence, intensity and mean intensity.
We discuss the effects of parasites on the survivorship, growth and fecundity of hosts. The effects are often subtle, affecting, for example, interactions of hosts with other species.
We then examine the dynamics of infection within host populations. Key concepts here are the basic reproductive rate, R0, the transmission threshold (R0 = 1) and the critical population size. These form a framework for directly transmitted microparasites that sheds light on the kinds of population in which we might expect to find different sorts of infection, on the nature of the epidemic curve of an infection, on the dynamic patterns of different types of parasite, and on the planning of immunization programs based on the principle of 'herd immunity'.
The dynamics are also outlined of pathogens attacking crops, of vector-borne infections and macroparasites, and of parasites infecting metapopulations of hosts.
We examine the role that parasites and pathogens play in the dynamics of their hosts. We address first the question of whether host and parasite dynamics are coupled, or whether the parasite simply modifies the underlying dynamics of the host, without there being any detectable feedback. A series of case studies then emphasizes that data supporting a role for parasites in the dynamics of their hosts are sparse and often liable to alternative interpretations.
Finally, we consider the coevolution of parasites and their hosts, stressing the absence of any 'cosy accommodation', but rather that the selective pressures in both cases - parasite and host - favor maximizing individual fitness.
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