Summary
Few studies have examined vertebrate models of invasive species to explore parasite release as a proposed mechanism through which host species might become invasive. In this study, we examined evidence for parasite release in invasive American bullfrogs (Rana catesbeiana/Lithobates catesbeianus) from five sites in Victoria, British Columbia, Canada. We examined helminth species richness, as well as the prevalence, intensity and abundance of lung and kidney fluke infections. These flukes are expected to impose costs on host survival, growth and reproductive output. We compared measures of these parasite taxa with bullfrogs from Ontario and New Brunswick where they are endemic. Helminth species richness in bullfrogs from the Victoria sites was lower than in Ontario bullfrogs, but comparable to reported indices for other endemic populations. The prevalence of lung flukes (Haematoloechus spp.) in bullfrogs from Victoria was twice as high as was observed in the Ontario bullfrogs, and higher than has been reported from other endemic locations. In four of the five study sites in Victoria, numbers of Echinostoma spp. kidney cysts were lower than observed in endemic populations; however, the fifth site had uncharacteristically high numbers of cysts. In this study, there did not appear to be clear evidence to support parasite release using either parasite species numbers, or infection by specific parasite taxa. Instead, the invasive bullfrogs demonstrated high parasite species richness and high levels of infection for parasites known to be harmful to their hosts.
Methodology
We sampled a total of 76 bullfrogs from across all native (N ¼ 26) and introduced sites (N ¼ 50). Adult (.3 years old) and juvenile (1–2 years post-metamorphosis) bullfrogs were collected with dip and seine nets from five sites in the greater Victoria area, Vancouver Island, British Columbia, in the summer and autumn of 2003. They were euthanized with MS-222 and frozen for future necropsy. We also collected bullfrogs from a site in Ontario in the summer and autumn of 2007.
The five sites around Victoria were 2.5–7 km apart from one another. Trevlac pond was a peat bog/wetland that was mined and converted into a permanent lake. Bullfrogs colonized Trevlac (48 29 44.6N; 123 26 37.6W) in the 1990s and are the most recent introduction of host species among our samples. Better approximations of dates for introductions to the other four lakes are not available. Florence Lake (48 27 31.8N; 123 30 43.9W) and Eagle Lake (48 30 32.2N; 123 27 40.4W) are natural lakes. Wade pond is a man-made agricultural pond (48 33 13N; 123 26 58.0W). The Interurban pond (48 31 11.87N; 123 25 34.45W) is a dugout pond located near a highway.
We collected road-killed bullfrogs from Bishops Mills, Kemptville, Ontario (44 52 60.0N; 75 40 0.0W). The sample site is an extensive wetland area sectioned by roads, but not fragmented by large bodies of land. High vehicle-induced mortality occurs in this area, indicating significant movement of frogs across roads that divide the body of water. Consequently, we expect that our samples were from a large population of bullfrogs in the area that provided a broader parasite profile than would be observed from a single isolated lake or smaller pond population. The ample information available from other studies on the richness, prevalence and intensity of helminth parasites in bullfrogs in native habitats, made it possible to compare our observations with others, in particular, New Brunswick (McAlpine, 1997). We collected adult and juvenile frogs over the summer and autumn to coincide with seasonal times of collection of bullfrogs from the Victoria sites, although collections were performed 4 years later. Collections were made within minutes of mortality, before any desiccation of the carcass occurred.
We examined lungs and kidneys of all frogs from Bishops Mills and Victoria sites for trematodes. However, one road-killed frog from Bishops Mills did not have kidneys present upon collection, and thus our sample size when enumerating kidney cysts was 25.