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Parasites are frequently associated with odd host behaviors such as unusual levels of activity, increased conspicuousness, disorientation, and altered responses to stimuli (Holmes and Bethel 1972). For the many life cycles where transmission depends on predation, it is often suggested that parasites alter host behavior and increase the susceptibility of intermediate hosts to predation by final hosts (e.g., Rothschild 1962, Holmes and Bethel 1972). Three main lines of evidence currently support the hypothesis that behavior modification is a parasite strategy evolved to increase transmission: hosts infected by transmissible stages of parasites often behave differently (Holmes and Bethel 1972, Dobson 1988, Curio 1988, Moore and Gotelli 1990 and Poulin 1994a discuss several examples); are eaten more readily by predators in the laboratory than are unparasitized hosts (Holmes and Bethel 1972, Kennedy et al. 1978, Camp and Huizinga 1979, Brassard et al. 1982, Moore 1983, Helluy 1984, Webber et al. 1987, Poulin et al. 1992); and are taken more frequently by predators than expected in the wild (VanDobben 1952, Feare 1971, Rau and Caron 1979, Moore 1983, Hoogenboom and Dijkstra 1987). As a whole, this evidence is quite convincing and, because the ingestion of larval parasites during predation is a frequent occurrence, helps us to better understand foraging dynamics and food webs.

Several studies have used a combination of approaches, helping to expand the base of evidence used to support the behavior modification hypothesis. For example, Moore (1983) found that terrestrial isopods infected with a larval acanthocephalan were more active and spent more time in dry areas, on contrasting backgrounds, and away from shelter than did unparasitized isopods. In aviary predation trials, 59% of isopods eaten by Starlings were parasitized, compared with an initial 47% prevalence of infection among the isopods available in the cage (Margolis et al. [1982] define "prevalence" as the proportion of hosts in a sample that are parasitized). There was indirect evidence that transmission was not random in nature because the prevalence of adult acanthocephalans in wild Starling nestlings (13%) was higher than expected, given the rates at which parents fed isopods to their young multiplied over the age of nestlings and the very low prevalence of parasitized isopods nearby (0.2%).

Although the link between conspicuous behaviors induced by parasites and increased parasite transmission is logical and well supported, Moore and Gotelli (1990) discuss alternative explanations. Pathology can affect host behavior in ways that do not necessarily increase transmission. For example, hosts may alter their behaviors to help rid themselves of parasites (Hart 1990) or compensate for metabolic drains of parasitism (Milinski 1985). Thus, it is important to also assess how predation risk varies with parasitism. From studies of predator gut contents, it might appear that parasites make prey more susceptible to predation if predators prefer larger, older prey that have had a longer time to accumulate parasites. Also, if the dispersal of hosts and parasites is limited, areas where predators abound will have higher rates of parasite transmission to nearby prey, leading to more parasitized prey in the predator's diet compared with the prevalence of parasitism seen in the prey population on a broader spatial scale. Another potential limitation of gut-content studies is the difficulty of accurately determining the prevalence of the parasite in the prey population. As an example, the relatively high proportion of Sarcocystis-infected voles in the diet of Kestrels could reflect either increased predation or decreased trapping success for parasitized voles (Hoogenboom and Dijkstra 1987).

In combination with evaluations of host behavior, predation experiments can best test the link between behavior and increased transmission (Bethel and Holmes 1977). Unfortunately, results from laboratory predation experiments may only allow limited inference about events in nature. Although field experiments with natural final hosts can effectively determine whether behavior modification increases parasite transmission in the wild, few have been conducted. A notable exception is the work by Aeby (1991, 1992). Aeby found coral polyps (Porites spp.) become distended following infection with metacercariae (Plagioporous sp.), causing colonies to suffer reduced growth. The metacercariae appear as bright pink nodules and hinder the ability of parasitized polyps to retract into the calyx. Using manipulative field and laboratory experiments, Aeby demonstrated that butterfly fish, the appropriate definitive host, forage more frequently on parasitized coral polyps. Ironically, due to the regenerative capabilities of the colony, parasitized corals did better in treatments that allowed butterfly fish to feed on them, suggesting that the parasite-induced alteration of the parasitized polyp is beneficial to the coral, the trematode, and, perhaps, the fish.

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