Proliferative kidney disease (PKD) of salmonids, caused by Tetracapsuloides bryosalmonae may lead to high mortalities at elevated water temperatures. However, it has not yet been investigated how temperature affects the fish host immune response to T. bryosalmonae. We exposed YOY (young of the year) rainbow trout (Oncorhynchus mykiss) to T. bryosalmonae at two temperatures (12 °C and 15 °C) that reflect a realistic environmental scenario and could occur in the natural habitat of salmonids. We followed the development of the parasite, host pathology and immune response over seven weeks. We evaluated the composition and kinetics of the leukocytes and their major subgroups in the anterior and posterior kidney. We measured immune gene expression profiles associated with cell lineages and functional pathways in the anterior and posterior kidney. At 12 °C, both infection prevalence and pathogen load were markedly lower. While the immune response was characterized by subtle changes, mainly an increased amount of lymphocytes present in the kidney, elevated expression of Th1-like signature cytokines and strong upregulation of the natural killer cell enhancement factor, NKEF at week 6 P.E. At 15 °C the infection prevalence and pathogen burden were ominously greater. While the immune response as the disease progressed was associated with a Th2-like switch at week 6 P.E and a prominent B cell response, evidenced at the tissue, cell and transcript level. Our results highlight how a subtle, environmentally relevant difference in temperature resulted in diverse outcomes in terms of the immune response strategy, altering the type of interaction between a host and a parasite.

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Numerous environmental chemicals, both long-known toxicants such as persistent organic pollutants as well as emerging contaminants such as pharmaceuticals, are known to modulate immune parameters of wildlife species, what can have adverse consequences for the fitness of individuals including their capability to resist pathogen infections. Despite frequent field observations of impaired immunocompetence and increased disease incidence in contaminant-exposed wildlife populations, the potential relevance of immunotoxic effects for the ecological impact of chemicals is rarely considered in ecotoxicological risk assessment. A limiting factor in the assessment of immunotoxic effects might be the complexity of the immune system what makes it difficult (1) to select appropriate exposure and effect parameters out of the many immune parameters which could be measured, and (2) to evaluate the significance of the selected parameters for the overall fitness and immunocompetence of the organism. Here, we present - on the example of teleost fishes - a brief discussion of how to assess chemical impact on the immune system using parameters at different levels of complexity and integration: immune mediators, humoral immune effectors, cellular immune defenses, macroscopical and microscopical responses of lymphoid tissues and organs, and host resistance to pathogens. Importantly, adverse effects of chemicals on immunocompetence may be detectable only after immune system activation, e.g., after pathogen challenge, but not in the resting immune system of non-infected fish. Current limitations to further development and implementation of immunotoxicity assays and parameters in ecotoxicological risk assessment are not primarily due to technological constraints, but are related from insufficient knowledge of (1) possible modes of action in the immune system, (2) the importance of intra- and inter-species immune system variability for the response against chemical stressors, and (3) deficits in conceptual and mechanistic assessment of combination effects of chemicals and pathogens.