Host manipulation by parasites : adaptation to enhance transmission?

Abstract

Otto Seppälä tutki väitöskirjassaan loisten kykyä manipuloida isäntiään mahdollisena strategiana tehostaa loisten siirtymistä uusiin isäntäyksilöihin. Monien loisten on havaittu vaikuttavan mm. isäntiensä käyttäytymiseen ja ulkonäköön. Erityisesti ravintoketjuissa saaliseläimistä saalistajiin kulkeutuvilla loisilla isännän manipulointia on yleisesti pidetty loisten evolutiivisena sopeumana altistaa isännät saalistajille ja täten tehostaa loisten siirtymistä elinkierrossa eteenpäin. Manipulaatioteoriaa on kuitenkin vain harvoin testattu kriittisesti selvittämällä saalistuskokein loisten aiheuttamien käyttäytymismuutosten vaikutusta isäntien saalistusalttiuteen.Seppälä selvitti useiden eri kalalajien silmissä yleisen Diplostomum spathaceum -loisen vaikutusta kalojen käyttäytymiseen, värinsäätelyyn ja saalistusalttiuteen.

Trophically-transmitted parasites may predispose infected hosts to predation by altering their phenotype. This can be either an adaptation of the parasites to enhance their transmission to the next hosts in the life cycle or a non-adaptive side-effect of infection. In this thesis, I examined whether the Diplostomum spathaceum (Trematoda) eye fluke can manipulate the phenotype of its fish intermediate hosts to increase their susceptibility to predation, and if this could be an adaptation of the parasite to enhance its onward transmission to the bird definitive hosts. In laboratory experiments, I found that anti-predator behaviour of infected fish was reduced compared to uninfected fish. Parasitized fish did not prefer the surface layers of the water column more than control fish, but did show a weaker reaction to an approaching simulated avian predator. Furthermore, their ability to adjust to the environment using cryptic coloration and cryptic behaviour was reduced. These changes led to an increase in the susceptibility of fish to simulated avian predation (capture by dip-net). This result was not reproduced when fish were exposed to predation by wild birds in a field experiment, possibly because the experimental set-up allowed birds to feed on fish in an easy, unnatural manner. Catchability of fish in the laboratory increased with the coverage of parasite-induced cataracts, which suggests that impaired vision may be the definitive mechanism leading to manipulation. Moreover, cataract formation was most intensive after parasites had completed their development, resulting in host manipulation only after parasites had reached infectivity to bird hosts. Furthermore, manipulation was not observed to be costly for the parasite, because it did not predispose fish to predation by non-host piscivorous fish. These findings suggest that manipulation of the fish host may increase the probability of parasite transmission to bird hosts, and thus be a parasite strategy evolved to enhance transmission.