Many fishes possess specialized epidermal cells that are ruptured by the teeth of predators, thus reliably indicating the presence of an actively foraging predator. Understanding the evolution of these cells has intrigued evolutionary ecologists because the release of these alarm chemicals is not voluntary. Here, we show that predation pressure does not influence alarm cell production in fishes. Alarm cell production is stimulated by exposure to skin-penetrating pathogens (water moulds: Saprolegnia ferax and Saprolegnia parasitica), skin-penetrating parasites (larval trematodes: Teleorchis sp. and Uvulifer sp.) and correlated with exposure to UV radiation. Suppression of the immune system with environmentally relevant levels of Cd inhibits alarm cell production of fishes challenged with Saprolegnia. These data are the first evidence that alarm substance cells have an immune function against ubiquitous environmental challenges to epidermal integrity. Our results indicate that these specialized cells arose and are maintained by natural selection owing to selfish benefits unrelated to predator-prey interactions. Cell contents released when these cells are damaged in predator attacks have secondarily acquired an ecological role as alarm cues because selection favours receivers to detect and respond adaptively to public information about predation.

I examined growth and survival of the European toad, Bufo bufo, from hatching to the approximate time of first hibernation. I varied tadpole density in experimental ponds such that individuals from low—density ponds emerged 48.5% larger than those from high—density ponds. In the laboratory, metamorphs from both pond densities were maintained in containers at densities of one or six. Nine weeks after metamorphosis they were exposed to 0 or 80 larvae of the lungworm, Rhabdias bufonis. A factorial experiment aimed to determine (1) the extent to which conditions experienced by larvae carried over to the terrestrial stage (2) the effects of resource limitation and past history on a host's response to a potential pathogen. The density of metamorphs had the strongest effect on growth and survival: 18 wk after metamorphosis, those raised alone were °80% heavier than those in groups and they had 31% higher survival. However, larval history also affected growth and survival and affected how metamorphs responded to density. First, single toads emerging from low—density ponds were 14.5% larger at the time of hibernation than those from high—density ponds. The mechanism for this growth advantage probably lies in the consistently higher growth rates of single toads from low—density ponds, especially during the first 3 wk after metamorphosis. Second, survival in group containers was higher for toads from low—density ponds, especially during the first few weeks after metamorphosis when most deaths involved toads from high—density ponds. These results support a carry—over effect between larval history and subsequent performance in an organism with a complex life cycle. Infection with lungworms had no detectable effect on metamorph growth or survival. This result contrasts earlier studies on this system, possibly due to the relatively low worm burdens or low statistical power. Yet, the results may also indicate that the predicted impact of infection on hosts, especially those limited by resources, is not as straightforward as theoretical studies suggest.

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The growth and survival of juvenile toads, Bufo bufo, infected with a common lung nematode, Rhabdias bufonis, were studied. Toads were raised from tadpoles in the laboratory and infected 2 months after metamorphosis. Individual toads were exposed to doses of 10, 40, 80 or 160 larvae, which enabled examination of the hypothesis that parasite-induced mortality is affected by worm numbers. Growth of infected toads began to diverge from that of uninfected controls at 6 weeks post infection (WPI) and by 12 WPI the most heavily infected toads were approximately half the mass of controls. No controls died throughout the experiment; however, mortality of infected toads was strongly affected by parasite density. A mechanism for mortality is suggested by the significant negative relationship between parasite density and dietary intake. This parasite-induced anorexia was detected at 3 WPI and persisted up to 9 WPI. Patterns of reduced host growth, survival and dietary intake provide experimental evidence of the negative consequences of parasitic infection in a natural parasite-host system which may also be present under natural conditions.