“…Although hosts can use multiple strategies to mitigate infection by parasites (e.g. avoidance behaviours to reduce infection as well as tolerance mechanisms to limit pathology) (Fantham & Porter, 1954), we focus here on the proportion of administered parasites establishing infections (i.e. infection success) as our primary measure of parasite adaptation.…”
Classical theory suggests that parasites will exhibit higher fitness in sympatric relative to allopatric host populations (local adaptation). However, evidence for local adaptation in natural host–parasite systems is often equivocal, emphasizing the need for infection experiments conducted over realistic geographic scales and comparisons among species with varied life history traits. Here, we used infection experiments to test how two trematode (flatworm) species (Paralechriorchis syntomentera and Ribeiroia ondatrae) with differing dispersal abilities varied in the strength of local adaptation to their amphibian hosts. Both parasites have complex life cycles involving sequential transmission among aquatic snails, larval amphibians and vertebrate definitive hosts that control dispersal across the landscape. By experimentally pairing 26 host‐by‐parasite population infection combinations from across the western USA with analyses of host and parasite spatial genetic structure, we found that increasing geographic distance—and corresponding increases in host population genetic distance—reduced infection success for P. syntomentera, which is dispersed by snake definitive hosts. For the avian‐dispersed R. ondatrae, in contrast, the geographic distance between the parasite and host populations had no influence on infection success. Differences in local adaptation corresponded to parasite genetic structure; although populations of P. syntomentera exhibited ~10% mtDNA sequence divergence, those of R. ondatrae were nearly identical (<0.5%), even across a 900 km range. Taken together, these results offer empirical evidence that high levels of dispersal can limit opportunities for parasites to adapt to local host populations.
“…Although hosts can use multiple strategies to mitigate infection by parasites (e.g. avoidance behaviours to reduce infection as well as tolerance mechanisms to limit pathology) (Fantham & Porter, 1954), we focus here on the proportion of administered parasites establishing infections (i.e. infection success) as our primary measure of parasite adaptation.…”
Classical theory suggests that parasites will exhibit higher fitness in sympatric relative to allopatric host populations (local adaptation). However, evidence for local adaptation in natural host–parasite systems is often equivocal, emphasizing the need for infection experiments conducted over realistic geographic scales and comparisons among species with varied life history traits. Here, we used infection experiments to test how two trematode (flatworm) species (Paralechriorchis syntomentera and Ribeiroia ondatrae) with differing dispersal abilities varied in the strength of local adaptation to their amphibian hosts. Both parasites have complex life cycles involving sequential transmission among aquatic snails, larval amphibians and vertebrate definitive hosts that control dispersal across the landscape. By experimentally pairing 26 host‐by‐parasite population infection combinations from across the western USA with analyses of host and parasite spatial genetic structure, we found that increasing geographic distance—and corresponding increases in host population genetic distance—reduced infection success for P. syntomentera, which is dispersed by snake definitive hosts. For the avian‐dispersed R. ondatrae, in contrast, the geographic distance between the parasite and host populations had no influence on infection success. Differences in local adaptation corresponded to parasite genetic structure; although populations of P. syntomentera exhibited ~10% mtDNA sequence divergence, those of R. ondatrae were nearly identical (<0.5%), even across a 900 km range. Taken together, these results offer empirical evidence that high levels of dispersal can limit opportunities for parasites to adapt to local host populations.
“…Incidental dissections of dead keelbacks suggested they often bore heavy helminth infections and thus offered an opportunity to assess the effects of parasites under a wide range of infection intensities. Among reptiles, semi‐aquatic snakes like keelbacks often bear especially high parasite burdens (Fantham & Porter ), possibly due to their diet, high population density or habitat conditions conducive to parasite transmission. Our goals in this study were to (i) document patterns of gastrointestinal nematode infections in keelbacks and their anuran prey, (ii) characterize populations of the nematodes infecting the snakes to elucidate factors affecting sex ratio and sexual size dimorphism (SSD) of the parasite, and (iii) experimentally manipulate nematode infections in captive keelbacks to assess the parasite's effect on host fitness.…”
22We investigated patterns of prevalence and intensity of gastrointestinal nematode infections in 23 a tropical natricine snake, the keelback (Tropidonophis mairii). Ninety-eight percent of 24 keelbacks were infected with Tanqua anomala (Gnathostomidae), with infection intensities of 25 up to 243 worms per snake. Infection with T. anomala caused severe inflammation of 26 stomach mucosa and submucosa at the sites of parasite attachment and encystment. 27Nonetheless, we did not detect detrimental effects of nematode infection on measures of 28 fitness among wild or captive snakes. Snakes with heavier nematode infections had higher 29 body condition scores than did less-infected individuals. De-worming captive snakes had no 30 measurable effect on their growth rate, body condition or locomotor performance. In 31 combination with an earlier study on blood-dwelling hepatozoons, our work suggests that 32 keelbacks have a high tolerance to parasites. The 'fast-pace' life history and short lifespan of 33 these snakes may make it beneficial for them to tolerate infection, rather than expend energy 34 on resisting parasite attack. 35 36
“…The first references to the occurrence of trypanosomes in snakes appeared at the beginning of the 20th century in various continents (Wenyon, 1909; Brumpt, 1914), later followed by a few papers about snake trypanosomes in Brazil (Pessôa, 1928; Arantes and Fonseca, 1931 a ; Fonseca, 1935), Africa (Fantham and Porter, 1950, 1953) and North America (Ayala et al 1983; Chia and Miller, 1984). Most papers on snake trypanosomes are only occurrence reports or morphological descriptions.…”
Blood examination by microhaematocrit and haemoculture of 459 snakes belonging to 37 species revealed 2.4% trypanosome prevalence in species of Viperidae (Crotalus durissus and Bothrops jararaca) and Colubridae (Pseudoboa nigra). Trypanosome cultures from C. durissus and P. nigra were behaviourally and morphologically indistinguishable. In addition, the growth and morphological features of a trypanosome from the sand fly Viannamyia tuberculata were similar to those of snake isolates. Cross-infection experiments revealed a lack of host restriction, as snakes of 3 species were infected with the trypanosome from C. durissus. Phylogeny based on ribosomal sequences revealed that snake trypanosomes clustered together with the sand fly trypanosome, forming a new phylogenetic lineage within Trypanosoma closest to a clade of lizard trypanosomes transmitted by sand flies. The clade of trypanosomes from snakes and lizards suggests an association between the evolutionary histories of these trypanosomes and their squamate hosts. Moreover, data strongly indicated that these trypanosomes are transmitted by sand flies. The flaws of the current taxonomy of snake trypanosomes are discussed, and the need for molecular parameters to be adopted is emphasized. To our knowledge, this is the first molecular phylogenetic study of snake trypanosomes.
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