Introduction
Little evidence for genetic variation associated with susceptibility to sea star wasting syndrome in the keystone species, Pisaster ochraceus, Rising sea water temperatures, due to climate change, are becoming increasingly stressful to marine ecosystems. As a result, marine diseases have become more prevalent in the last few decades (Harvell et al., 2004, 2002). Disease outbreaks can have detrimental downstream effects on marine species due to changes in community structure and age distribution (Behringer, Silliman, & Lafferty, 2018; Burge et al., 2014). Many marine taxa have suffered intense population declines as a result of the increasing prevalence of diseases (Harvell et al. 2004, Burge et al. 2013). These declines can result in reduced variation due to population bottlenecks and genetic drift, and possibly from strong directional selection associated with tolerance or resistance to disease (Nei, Maruyama, & Chakrabort, 1975; Zenger, Richardson, & Vachot-Griffin, 2003).
The Sea Star Wasting Syndrome (SSWS) epidemic event that began in 2013 is believed to be the largest marine wildlife disease on record (Gravem et al., 2021; Harvell et al., 2019). SSWS affected over 20 species of sea stars from Baja California, Mexico to the Gulf of Alaska, United States (Hewson et al., 2018, 2014), and severely reduced population sizes of several sea star species (Gravem et al., 2021; Harvell et al., 2019; Hewson et al., 2014; Menge, Cerny-Chipman, Johnson, & Sullivan, 2016; Miner et al., 2018; Montecino-Latorre et al., 2016). Similar SSWS symptoms have been observed in British Columbia in 2008 (Bates, Hilton, & Harley, 2009), along the US east coast (Bucci et al., 2017), the South Pacific (Pratchett, 1999; Zann, Brodie, & Vuki, 1990), Australia and Yellow Sea (Hewson et al., 2019). While the viral candidate sea star-associated densovirus (SSaDV) has been debunked (Jackson et al., 2020), other hypotheses of causative or exacerbating agents remains unknown, with hypotheses including pathogen(s) (Lloyd & Pespeni, 2018), inconsistent etiology stress responses between location, species, and environment (Hewson et al., 2018), microbial dysbiosis (Lloyd & Pespeni, 2018), and microbial-driven depletion of oxygen at the animal-water interface (Aquino et al., 2021). There is also mixed evidence for whether anomalously warm waters linked to global warming initiated the outbreak (Eisenlord et al., 2016; Menge, Cerny-Chipman, Johnson, Sullivan, et al., 2016b; Miner et al., 2018; Tracy, Weil, & Harvell, 2020) (Aalto et al., 2020). Regardless, it is clear that the disease is exacerbated in warmer conditions (Bates et al., 2009; Eckert, Engle, & Kushner, 1999; Eisenlord et al., 2016; Kohl, McClure, & Miner, 2016), and that severe population reductions occurred in warmer southern regions (Gravem et al., 2021; Harvell et al., 2019; Miner et al., 2018). The interplay between climate change and disease is a growing threat to wildlife species, especially when it causes rapid and extreme populations decline. What is still unclear is whether tolerance or resistance to some of these diseases has a genetic bases that may allow populations to adapt if outbreaks continue to occur.