Genetic variation for disease resistance in rainbow trout (Oncorhynchus mykiss)

Abstract

Proliferative Kidney Disease (PKD) caused by the Malacosporean parasite Tetracapsuloides bryosalmonae, is presently the most economically damaging disease of British rainbow trout farming, costing the industry in excess of £2.5 million per annum in the UK alone. With no vaccine or prophylactic treatment available, and only management techniques currently adopted to minimise the stress and mortality associated with the disease, alternative approaches must now be considered. This document investigates if selective breeding for PKD resistance is possible by assessing the level of additive genetic variation, and calculating the subsequent estimates of heritability, for commercial strains of rainbow trout. During a PKD outbreak on a commercial farm, 1500 communally reared juvenile rainbow trout from two strains (Houghton Spring and Isle of Man) were sampled on a single day, their body weight and fork length measured, and severity of kidney swelling scored according to the scale of Clifton-Hadley et al. (1987). Fish were assigned to individual families using microsatellite parentage assignment. Significant additive genetic variation was observed in the population, and families were ranked according to estimated breeding values. A combined estimate of heritability (h2 = 0.19 ± 0.08) for kidney score suggests the population will respond well to selective breeding for kidney score, which may be deemed a measure of resistance, whilst the favourable genetic correlations between kidney score and the production traits measured suggest simultaneous selection for kidney score and growth traits should also be effective. In order to support the findings of the initial research, controlled challenge experiments were conducted. Using the family EBV information on kidney score from the IoM strain (due to its certification as a disease-free site), four females, two with high and two with low response to PKD, were each crossed with a randomly selected neomale to produce twenty two families for PKD challenge experiments. The PKD experimental challenges showed evidence of additive genetic variation to kidney score over an eleven week period, supporting initial findings. A low score was deemed as evidence of greater resistance to the parasite in this study. Although female EBV was taken into consideration in the statistical model, there was found to be no significant difference in resistance according to family. Immunohistochemistry stained kidney sections from each individual involved in the challenges proved kidney score correlated significantly to the number of parasites in the kidney, suggesting that the scale of Clifton-Hadley et al. (1987) is a sufficient and accurate basis on which to describe the severity of PKD, and infection level in rainbow trout. Having discovered evidence that furunculosis, causative agent Aeromonas salmonicida, plays a major role in the mortality of fish suffering from PKD in the field, the bacterial disease was investigated to assess the resistance of the same families used in the PKD challenges. Twenty one of the families were used to discover that additive genetic variation for resistance to furunculosis is apparent when assessed as both a binary and longitudinal trait, suggesting significant genetic improvement can be made to increase resistance to furunculosis in the IoM stock. No significant correlation was observed between kidney score, EBV, and resistance to this bacterium, but there was a positive phenotypic correlation found between furunculosis resistance and size, suggesting simultaneous selection for performance and resistance is possible within this population.