Pathogenic infection attenuates the response of the estrogenic biomarker, vitellogenin, in rainbow trout

In the environment, aquatic organisms are exposed multiple instead of single stressors. During recent years, considerable progress has been achieved in assessing combination effects of chemical mixtures. For instance, it has been demonstrated that the induction of vitellogenin (VTG) in (male) fish – an established biomarker of exposure to estrogen-active compounds – responds additively to combinations of estrogen-active compounds, while simultaneous exposure to ligands of the estrogen receptor and of the arylhydrocarbon receptor has an antagonistic effect on VTG induction. In contrast to the progress in understanding combination effects of chemical mixtures, approaches to assess the combined effects of chemical and physical and/or biological stressors are less developed. Here, we study the combined impact of a chemical and a biological stressor on the biomarker VTG in rainbow trout. To this end, juvenile fish were exposed to two doses of the prototypic estrogen-active compound, 17-beta-estradiol (E2) in combination with the fish-pathogenic parasite Tetracapsuloides bryosalmonae, the etiological agent of the proliferative kidney disease (PKD). The VTG response was assessed at the mRNA level using qRT-PCR; in parallel, the liver transcriptomic response to the single stressors and their combinations was examined. Combined chemical/biological exposure resulted in a significant inhibition of both the rate and the magnitude of the VTG response, while neither the parasite nor the fish response to the parasite was affected by the presence of E2. The observed attenuation of the VTG biomarker response in diseases may have implications for the utility of this marker in environmental scenarios with low estrogenic exposure.