Disease can affect top predators. For instance, a Scandinavian outbreak of sarcoptic mange (caused by mites) in the late 1970s through the 1980s reduced the density of red fox. Prey (rodents, rabbits, ground birds, deer) increased as a result and then declined after the epidemic waned and fox populations recovered.
The fate of most parasites is tied to that of their hosts. If their hosts die, this is usually a bad thing for host and parasite alike. In nature, parasites are part ofnearly every meal. This puts tremendous evolutionary pressure on parasites to survive the ingestion process, particularly if they can relocate in the predator. Perhaps as a result, many parasitic species have complex life cycles where an intermediate host must be eaten by a final host. In such life cycles, the parasite must wait for the consumption of the intermediate host by an appropriate final host. However, not all parasites are patient. Some parasites manipulate the behavior or appearance ofthe intermediate host to increase the rate at which a predator host will catch and eat it. For instance, in southern California estuaries, the most common trematode, Euhaplorchis cali-forniensis, encysts on the brain of killifish; the worms alter the fish's behavior, making it shimmy and swim to the surface. These fish are 10-30 times more likely to be eaten by birds, the final host of the worm. In this system, the worms essentially dictate which fish live and die. They also provide an easy snack for egrets and herons that otherwise might have to work harder for a living. Some mathematical models indicate that such parasite-increased trophic transmission can reduce prey density; it can also increase predator density so long as the energetic costs of parasitism for the predator are not too severe. Other mathematical models suggest that some predators may depend on parasites to supply them with easy prey.
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