Abstract

Loss of heterozygosity due to consanguineous matings⁵ often has negative consequences for offspring, which have long been documented for aspects of reproduction, survival and disease susceptibility.⁴ A previous study reported that individual levels of heterozygosity of California sea lions (Zalophus californianus) varied significantly among disease classes¹ and that the immune response to different pathogens appeared to be influenced by heterozygosity.² Based on these results, we tested the hypothesis that for each disease class, heterozygosity will influence duration and success of rehabilitation of stranded California sea lions. To examine this, we gathered genetic and clinical data for 1238 sea lions stranded alive and treated at The Marine Mammal Center between 2001 and 2005. For each of the seven disease classes (domoic acid intoxication, leptospirosis, malnutrition, trauma, bacterial diseases, parasite diseases and undetermined), a series of linear regressions were built to determine whether individual levels of multilocus heterozygosity (calculated as Internal Relatedness, IR,³ using a panel of 13 apparently neutral markers⁴) were related to the duration of rehabilitation, success (released vs. dead in treatment or euthanized), number of concomitant processes during rehabilitation and probability of re-stranding. We found that IR was not significantly related to the duration of rehabilitation for sea lions stranded due to domoic acid intoxication, leptospirosis, malnutrition, trauma and undetermined causes (p > 0.05 in all cases), whereas sea lions with parasitic infections tended to last less in rehabilitation when more heterozygous (r² = 0.10, n = 30, p = 0.000). Unexpectedly, rehabilitation time of sea lions afflicted with bacterial infections was significantly lower for individuals with higher levels of IR (r² = 0.17, n = 14, p = 0.001). IR values were not significantly different for animals that were released, died during treatment or were euthanized for bacterial infections, domoic acid intoxication, malnutrition, parasitic infections, trauma and undetermined causes (p > 0.05 in all cases), but differed significantly for animals afflicted with leptospirosis (ANOVA F_2,320 = 3,25, p = 0.039). IR did not appear to explain occurrence of concomitant processes or probability of restranding (p > 0.05 in all cases). The relationship between IR and the duration of rehabilitation in sea lions afflicted with bacterial and parasitic infections may reflect differences in rehabilitation protocols for each disease class. Furthermore, the results observed might suggest that the effect of inbreeding or loss of heterozygosity affects different components of the immune system in distinct ways, depending on the type of disease present. The absence of a relationship between IR and rehabilitation tenure for other clinical conditions such as malnutrition, domoic acid or trauma, may arise because the immune system is not likely to be activated in the same way as what occurs in infectious conditions, and responds to organ or tissue damage rather than to an antigen. Our results are relevant to rehabilitation programs as they suggest that heterozygosity does not play a critical role in determining the duration and success, and thus the associated cost of rehabilitation, of all clinical conditions common to California sea lions.

* Presenting author
+ Student presenter

Literature Cited

1.  Acevedo-Whitehouse K, Gulland F, Greig D, Amos W. 2003. Disease susceptibility in California sea lions: Inbreeding influences the response of these animals to different pathogens in the wild. Nature, 422: 35.

2.  Acevedo-Whitehouse K, Spraker TR, Lyons E, Melin SR, Gulland F, Delong RL, Amos W. 2006. Contrasting effects of heterozygosity on survival and hookworm resistance in California sea lion pups. Mol Ecol 15:1973–1982.

3.  Amos W, Acevedo-Whitehouse K. 2009. A new test for genotype-fitness associations reveals a single microsatellite allele that strongly predicts the nature of tuberculosis infections in wild boar. Mol Ecol 9:1102–1111.

4.  Crow JF. 1948. Alternative hypotheses of hybrid vigor. Genetics 33:477.

5.  Reed DH, Frankham R. 2003. Correlation between fitness and genetic diversity. Cons Biol 17,230–237.