Abstract

Among the major threats to endangered species are habitat alteration and destruction, overharvesting, and the biotic effects of introduced competitors and predators. In recent years, it has become widely recognized that endangered species may be also threatened by exposure to pathogens, many of them exotic and novel to the endangered species.⁵ Disease resistance often has a significant genetic component. In particular, genes in the major histocompatibility complex (MHC) play an important role in pathogen resistance in vertebrates.^2,3 In endangered species, the level of genetic variation in the MHC, and other genes that may influence host resistance, may be lower because of past or present small population size, than more common species. Further, in the small populations of endangered species, there may also be a higher frequency of inbreeding, a factor that results in an increase in homozygosity for all loci. There is evidence that inbred animals within a population may have higher susceptibility to pathogens than outbred individuals.^1,4 Pathogens introduced from more common species, then, may result in final decline to extinction in an already imperiled species.

We have carried out the first major infectivity trial to examine differential genetic resistance in fish for pathogens. We used captive-bred, endangered winter-run chinook salmon Oncorhynchus tshawytscha to determine resistance to three pathogens: the bacterium, Listonella (Vibrio) anguillarum, infectious hematopoietic necrosis virus (IHNV), and Myxobolus cerebralis, the causative agent of whirling disease. We compared resistance to these three pathogens between inbred and outbred salmon and between siblings that were heterozygous or homozygous for a MHC class II gene. In two of these six different comparisons, we found significant genetic effects on disease resistance. First, MHC heterozygotes had a higher survival than MHC homozygotes when exposed to IHNV. Second, outbred fish had a higher resistance (or lower infection severity) than inbred fish when exposed to M. cerebralis. Overall, our study suggests that pathogen susceptibility in the winter-run chinook salmon will increase if further genetic variation is lost in this endangered species.

Acknowledgements

This research was conducted under a permit from the National Marine Fisheries Service and was funded in part by grants from the United States Fish and Wildlife Service. Further support for this work was provided by funds from the California Department of Water Resources Contract #4600000804.

References

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