Environmental parasitology of trematodes, snails and larval amphibians.

摘要

Environmental influences on trematode parasite infection in larval frogs may be mediated through effects on the frog hosts, other hosts in the parasite life cycle, or on the various life history stages of the parasites. Herein, I investigated effects of corn agriculture and landscape characteristics on trematode infection in both snails and tadpoles, and report that both affect infection patterns seen in these first and second intermediate hosts. Tadpoles from ponds adjacent to corn fields exhibit a higher prevalence of infection, whereas snails from such ponds show the opposite pattern. Landscape features likely exert an influence via habitat suitability for the definitive hosts. I also examined the impact of the herbicide atrazine (commonly used on corn crops) on the free-living cercarial infective stage of trematodes. Mortality, activity and infectivity are reduced in some species; however, when tadpoles and cercariae are exposed to the same concentration of atrazine, increased host susceptibility can be countered by detrimental effects on cercariae. This demonstrates the importance of examining the effects of an environmental factor on all aspects of a parasite life cycle. In addition to physiological or immunological effects, environmental perturbations may affect host susceptibility to trematode infection through behavioural alterations. I demonstrate that tadpoles exhibit an effective anti-parasite behaviour and that suppression of this activity results in an increase in trematode parasitism. The impact of trematode parasitism for natural frog populations was examined by investigating the interaction of infection with competition with conspecifics, a common stressor for tadpoles. Trematode infection and high rearing density had an additive negative effect on tadpole growth and development; effects were likely mediated by parasite-induced changes in resource allocation. The pattern of trematode infection observed in natural tadpole populations is thus the result of many factors, including those affecting host susceptibility (behavioural and immunological), cercarial infectivity, and abundance of definite hosts.