Pisciricketssia salmonis is the causal agent of Salmon Rickettsial Syndrome (SRS), which affects salmon species and causes severe economic losses. Selective breeding for disease resistance represents one approach for controlling SRS in farmed Atlantic salmon. Knowledge concerning the architecture of the resistance trait is needed before deciding on the most appropriate approach to enhance artificial selection for P. salmonis resistance in Atlantic salmon. The purpose of the study was to dissect the genetic variation in the resistance to this pathogen in Atlantic salmon. 2,601 Atlantic salmon smolts were experimentally challenged against P. salmonis by means of intra-peritoneal injection. These smolts were the progeny of 40 sires and 118 dams from a Chilean breeding population. Mortalities were recorded daily and the experiment ended at day 40 post-inoculation. Fish were genotyped using a 50K Affymetrix® Axiom® myDesignTM Single Nucleotide Polymorphism (SNP) Genotyping Array. A Genome Wide Association Analysis was performed on data from the challenged fish. Linear regression and logistic regression models were tested. Genome Wide Association Analysis indicated that resistance to P. salmonis is a moderately polygenic trait. There were five SNPs in chromosomes Ssa01 and Ssa17 significantly associated with the traits analysed. The proportion of the phenotypic variance explained by each marker is small, ranging from 0.007 to 0.045. Candidate genes including interleukin receptors and fucosyltransferase have been found to be physically linked with these genetic markers and may play an important role in the differential immune response against this pathogen. Due to the small amount of variance explained by each significant marker we conclude that genetic resistance to this pathogen can be more efficiently improved with the implementation of genetic evaluations incorporating genotype information from a dense SNP array.

One of the main pathogens affecting rainbow trout (Oncorhynchus mykiss) farming is the facultative intracellular bacteria Piscirickettsia salmonis. Current treatments, such as antibiotics and vaccines, have not had the expected effectiveness in field conditions. Genetic improvement by means of selection for resistance is proposed as a viable alternative for control. Genomic information can be used to identify the genomic regions associated with resistance and enhance the genetic evaluation methods to speed up the genetic improvement for the trait. The objectives of this study were to i) identify the genomic regions associated with resistance to P. salmonis; and ii) identify candidate genes associated with the trait in rainbow trout. We experimentally challenged 2,130 rainbow trout with P. salmonis and genotyped them with a 57 K single nucleotide polymorphism (SNP) array. Resistance to P. salmonis was defined as time to death (TD) and as binary survival (BS). Significant heritabilities were estimated for TD and BS (0.48 ± 0.04 and 0.34 ± 0.04, respectively). A total of 2,047 fish and 26,068 SNPs passed quality control for samples and genotypes. Using a single-step genome wide association analysis (ssGWAS) we identified four genomic regions explaining over 1% of the genetic variance for TD and three for BS. Interestingly, the same genomic region located on Omy27 was found to explain the highest proportion of genetic variance for both traits (2.4 and 1.5% for TD and BS, respectively). The identified SNP in this region is located within an exon of a gene related with actin cytoskeletal organization, a protein exploited by P. salmonis during infection. Other important candidate genes identified are related with innate immune response and oxidative stress. The moderate heritability values estimated in the present study show it is possible to improve resistance to P. salmonis through artificial selection in the rainbow trout population studied here. Furthermore, our results suggest a polygenic genetic architecture for the trait and provide novel insights into the candidate genes underpinning resistance to P. salmonis in O. mykiss.