Parasite-induced changes to host dispersal potentially influence the distribution of parasites and infection risk for hosts. Gasteromermis is a castrating endoparasitic nematode that infects both males and female mayflies (Baetis bicaudatus) but feminizes male hosts and manipulates them to disperse parasites to aquatic habitats via a mimicry of female oviposition behavior. In a stream network with high spatial heterogeneity in parasitism we used surveys and a large-scale field manipulation to 1) evaluate parasite effects on host dispersal capacity and site selection, and 2) test whether experimentally increasing host oviposition habitat would increase immigration of parasitized hosts, with subsequent increases in parasite recruitment and prevalence in the next generation. Initially assuming that manipulation benefits the parasite by increasing host encounters around oviposition sites, we predicted the parasite would not affect host dispersal capacity or site selection, and that more parasites would be dispersed to sites with abundant oviposition habitat subsequently increasing parasite transmission. In contrast to predictions, we found that parasites decreased host dispersal capacity (flight muscle ratio) and <2% of adult mayflies captured at oviposition sites were parasitized. We also observed a negative relationship between the flight muscle ratio of hosts and the percent biomass of parasite they contained, consistent with a tradeoff between parasite growth and host dispersal capacity. Furthermore, experimentally increasing oviposition habitat available for dispersal of hosts in natural streams had no effect on parasite recruitment or host infection risk. We conclude that the variability in suitable habitat that limits host recruitment does not limit its parasite and, therefore, does not contribute to observed spatial patterns of infection. Instead, life history events that occur in the months between when parasites are dispersed and when their offspring infect the next generation of hosts disconnect dispersal dynamics from recruitment and dilute colonization effects. Therefore, heterogeneity in infection rates may be shaped more strongly by post-colonization conditions within patches than by between-patch differences that influence dispersal.
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