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Infectious disease dynamics depend on the speed, number and fitness of parasites transmitting from infected hosts (‘donors’) to parasite-naive ‘recipients’. Donor heterogeneity likely affects these three parameters, and may arise from variation between donors in traits including: (i) infection load, (ii) resistance, (iii) stage of infection, and (iv) previous experience of transmission. We used the Trinidadian guppy, Poecilia reticulata, and a directly transmitted monogenean ectoparasite, Gyrodactylus turnbulli, to experimentally explore how these sources of donor heterogeneity affect the three transmission parameters. We exposed parasite-naive recipients to donors (infected with a single parasite strain) differing in their infection traits, and found that donor infection traits had diverse and sometimes interactive effects on transmission. First, although transmission speed increased with donor infection load, the relationship was nonlinear. Second, while the number of parasites transmitted generally increased with donor infection load, more resistant donors transmitted more parasites, as did those with previous transmission experience. Finally, parasites transmitting from experienced donors exhibited lower population growth rates on recipients than those from inexperienced donors. Stage of infection had little effect on transmission parameters. These results suggest that a more holistic consideration of within-host processes will improve our understanding of between-host transmission and hence disease dynamics. [ABSTRACT FROM AUTHOR]

Transmission is a fundamental step in the life cycle of every parasite but it is also one of the most challenging processes to model and quantify. In most host–parasite models, the transmission process is encapsulated by a single parameter b. Many different biological processes and interactions, acting on both hosts and infectious organisms, are subsumed in this single term. There are, however, at least two undesirable consequences of this high level of abstraction. First, nonlinearities and heterogeneities that can be critical to the dynamic behaviour of infections are poorly represented; second, estimating the transmission coefficient β from field data is often very difficult. In this paper,we present a conceptual model,which breaks the transmission process into its component parts. This deconstruction enables us to identify circumstances that generate nonlinearities in transmission, with potential implications for emergent transmission behaviour at individual and population scales. Such behaviour cannot be explained by the traditional linear transmission frameworks. The deconstruction also provides a clearer link to the empirical estimation of key components of transmission and enables the construction of flexible models that produce a unified understanding of the spread of both micro- and macro-parasite infectious disease agents. [ABSTRACT FROM AUTHOR]

Invasive populations frequently harbour a reduced parasite community compared with their native counterparts. The loss of regulating enemies may result in re-allocation of resources away from costly defences, effects that may be particularly pronounced at the wave-front of the invasion during the range expansion stage. Bottlenecking and increased genetic drift is also expected to result in a loss of immunogenetic diversity. As the invasive species expands its range, selection will strongly favour increased growth and reproduction, traits that may trade-off against immune function., Relaxed parasite-mediated selection is expected to alter the trade-offs between immune response and immunopathology. Hence, we might expect that a combination of necessity (i.e. loss of specific alleles at immune loci) and natural selection away from immunity towards other fitness traits should result in invasive populations having reduced resistance to parasites but greater potential for demographic growth in the invaded range., Following this argument to its logical conclusion would suggest that invasive species could also be more vulnerable to novel parasites, or to parasites to which the invasive population has lost immunity arriving from the native range. Despite this attractive narrative, there is currently little empirical evidence on the ecoimmunology and immunogenetics of invasions., In this article, we review the evidence for changes in the immune response of invasive species. We also examine the likely effects of range expansions and population genetic processes on the immune systems of invasive species. We conclude that much more empirical research is necessary in this field before general patterns and predictions can emerge. [ABSTRACT FROM AUTHOR]

Predator-prey models are often applied to the interactions between host immunity and parasite growth. A key component of these models is the immune system's functional response, the relationship between immune activity and parasite load. Typically, models assume a simple, linear functional response. However, based on the mechanistic interactions between parasites and immunity we argue that alternative forms are more likely, resulting in very different predictions, ranging from parasite exclusion to chronic infection. By extending this framework to consider multiple infections we show that combinations of parasites eliciting different functional responses greatly affect community stability. Indeed, some parasites may stabilize other species that would be unstable if infecting alone. Therefore hosts' immune systems may have adapted to tolerate certain parasites, rather than clear them and risk erratic parasite dynamics. We urge for more detailed empirical information relating immune activity to parasite load to enable better predictions of the dynamic consequences of immunemediated interspecific interactions within parasite communities. [ABSTRACT FROM AUTHOR]