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Parasitism and phenotypic change in colonial hosts.
Hanna Hartikainen1, Inês Fontes, Beth Okamura
1Department of Aquatic Ecology, EAWAG, Überlandstrasse 133, Dübendorf 8600, Switzerland. h.hartikainen@nhm.ac.uk
Parasitology
|August 23, 2013
Summary
Parasites alter host phenotypes, causing colony size reduction but module gigantism in bryozoans. This study reveals complex host-parasite interactions without trophic transmission, impacting reproduction and survival.
Area of Science:
- Ecology
- Parasitology
- Evolutionary Biology
Background:
- Host phenotype changes are often linked to parasite transmission strategies.
- Trophic transmission is a common parasite manipulation mechanism.
- Understanding non-trophic transmission systems is crucial for parasite ecology.
Purpose of the Study:
- To characterize host phenotype changes in a colonial bryozoan-myxozoan system lacking trophic transmission.
- To investigate the effects of the parasite Tetracapsuloides bryosalmonae on Fredericella sultana colonies and modules.
- To explore the mechanisms driving altered host phenotypes and transmission dynamics.
Main Methods:
- Comparative analysis of infected and uninfected Fredericella sultana colonies.
- Phenotypic measurements including colony size, growth rate, and module morphology.
- Assessment of host metabolic rates and offspring (statoblast) quality and hatching success.
Main Results:
- Parasitism reduced overall colony size and growth but induced gigantism in individual modules.
- Overtly infected hosts exhibited lower metabolic rates, suggesting resource competition and parasite-induced castration.
- Malformed statoblasts showed reduced production and hatching success, limiting vertical transmission.
Conclusions:
- Parasitism in F. sultana and T. bryosalmonae leads to opposing phenotypic effects at colony and module levels.
- Resource competition and parasite manipulation (castration) are key drivers of the infected phenotype.
- Overt infections trade off horizontal transmission potential with rare vertical transmission due to impaired offspring viability.
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