Chapter 2 : Heterogeneities in macroparasite infections : patterns and processes

Animals vary markedly in the number of parasites they harbour-most have just a few, but some have many. In this chapter, we ask why there is so much variation between individuals, how do we quantify this variation and what are the consequences of these heterogeneities for the dynamics of the host-parasite interaction? 2.1 Background Exhaustive empirical surveys have shown that, almost without exception, macroparasites (parasitic helminths and arthropods) are aggregated across their host populations, with most individuals harbouring low numbers of parasites, but a few individuals playing host to many (Shaw and Dobson 1995). Heterogeneities such as these are generated by variation between individuals in their exposure to parasite infective stages and by differences in their susceptibility once an infectious agent has been encountered. Experimental studies have shown that the extent of spatial aggregation in the infective stage distribution is reflected in the level of parasite aggregation across hosts (Keymer and Anderson 1979). Moreover, in the absence of any heterogeneity in exposure, even small differences in susceptibility between hosts can rapidly produce non-random, aggregated distributions of parasites (Anderson and May 1978). What is unclear at present, is the relative significance of these different mechanisms, and the importance of interactions between mechanisms in accentuating individual differences in parasite loads. Mathematical models that examine these problems rapidly become intractable (Grenfell et al. 1995), while experimental studies and computer simulations also become rather complex. Some of the variation in parasite loads we observe is predictable. For example, in mammals and some other taxa, males tend to be more heavily infected than females, perhaps due to differences in immune function (Poulin 1996a, Schalk and Forbes 1997, McCurdy et al. 1998). Parasite loads tend to increase with age and may plateau in older animals, though if acquired immunity is important (or there is parasite-induced host mortality) then they may ultimately decline again, so reducing the degree of parasite aggregation. Genetic differences in susceptibility to infection may also be important, though their extent and direction are much more difficult to predict. Other factors that may contribute to the observed heterogeneities in worm burdens are the condition of the host (which may be a function of parasite load), host behaviour, parasite genetics and seasonality. Comparative studies of aggregation suggest that the infection process and the habitat of the host may make significant contributions to the between-species pattern of aggregation (Shaw and Dobson 1995, Shaw et al. 1998). …