Even though parasitic infections are often costly or deadly for the host, we know
very little which genes influence parasite susceptibility and disease severity. Proliferative
kidney disease is an emerging and, at elevated water temperatures, potentially deadly
disease of salmonid fishes that is caused by the myxozoan parasite Tetracapsuloides bryosalmonae. By screening >7.6 K SNPs in 255 wild brown trout (Salmo trutta) and combining association mapping and Random Forest approaches, we identified several
candidate genes for both the parasite resistance (inverse of relative parasite load;
RPL) and the severe anaemic response to the parasite. The strongest RPL‐associated
SNP mapped to a noncoding region of the congeneric Atlantic salmon (S. salar) chromosome 10, whereas the second strongest RPL‐associated SNP mapped to an intronic
region of PRICKLE2 gene, which is a part of the planar cell polarity signalling pathway involved in
kidney development. The top SNP associated with anaemia mapped to the intron of the
putative PRKAG2 gene. The human ortholog of this gene has been associated with haematocrit and other
blood‐related traits, making it a prime candidate influencing parasite‐triggered anaemia
in brown trout. Our findings demonstrate the power of association mapping to pinpoint
genomic regions and potential causative genes underlying climate change‐driven parasitic
disease resistance and severity. Furthermore, this work illustrates the first steps
towards dissecting genotype–phenotype links in a wild fish population using closely
related genome information.