Sea star wasting disease (SSWD) first appeared in Oregon in April 2014, and by June had spread to most of the coast. Although delayed compared to areas to the north and south, SSWD was initially most intense in north and central Oregon and spread southward. Up to 90% of individuals showed signs of disease from June-August 2014. In rocky intertidal habitats, populations of the dominant sea star Pisaster ochraceus were rapidly depleted, with magnitudes of decline in density among sites ranging from -2x to -9x (59 to 84%) and of biomass from -2.6x to -15.8x (60 to 90%) by September 2014. The frequency of symptomatic individuals declined over winter and persisted at a low rate through the spring and summer 2015 (~5–15%, at most sites) and into fall 2015. Disease expression included six symptoms: initially with twisting arms, then deflation and/or lesions, lost arms, losing grip on substrate, and final disintegration. SSWD was disproportionally higher in orange individuals, and higher in tidepools. Although historically P. ochraceus recruitment has been low, from fall 2014 to spring 2015 an unprecedented surge of sea star recruitment occurred at all sites, ranging from ~7x to 300x greater than in 2014. The loss of adult and juvenile individuals in 2014 led to a dramatic decline in predation rate on mussels compared to the previous two decades. A proximate cause of wasting was likely the “Sea Star associated Densovirus” (SSaDV), but the ultimate factors triggering the epidemic, if any, remain unclear. Although warm temperature has been proposed as a possible trigger, SSWD in Oregon populations increased with cool temperatures. Since P. ochraceus is a keystone predator that can strongly influence the biodiversity and community structure of the intertidal community, major community-level responses to the disease are expected. However, predicting the specific impacts and time course of change across west coast meta-communities is difficult, suggesting the need for detailed coast-wide investigation of the effects of this outbreak.

The prevalence of disease-driven mass mortality events is increasing, but our understanding of spatial variation in their magnitude, timing and triggers are often poorly resolved. Here, we use a novel range-wide dataset comprised 48 810 surveys to quantify how sea star wasting disease affected Pycnopodia helianthoides , the sunflower sea star, across its range from Baja California, Mexico to the Aleutian Islands, USA. We found that the outbreak occurred more rapidly, killed a greater percentage of the population and left fewer survivors in the southern half of the species's range. Pycnopodia now appears to be functionally extinct (greater than 99.2% declines) from Baja California, Mexico to Cape Flattery, Washington, USA and exhibited severe declines (greater than 87.8%) from the Salish Sea to the Gulf of Alaska. The importance of temperature in predicting Pycnopodia distribution rose more than fourfold after the outbreak, suggesting latitudinal variation in outbreak severity may stem from an interaction between disease severity and warmer waters. We found no evidence of population recovery in the years since the outbreak. Natural recovery in the southern half of the range is unlikely over the short term. Thus, assisted recovery will probably be required to restore the functional role of this predator on ecologically relevant time scales.

Summary1. Several studies on trait-mediated indirect interactions (TMIIs) have shown that predators can initiate trophic cascades by altering prey behaviour. Although it is well recognized that individual prey state alters antipredator and foraging behaviour, few studies explore whether this state-dependent prey behaviour can alter the strength of the ensuing tritrophic cascade. Here, we link state-dependent individual behaviour to community processes by experimentally testing whether hunger level and body size of prey altered antipredator behaviour and thus changed the strength of trophic cascades between predators and primary producers. 2. In rocky intertidal tide pools on the California Coast, waterborne cues from the predatory seastar Leptasterias spp. (Stimpson) can cause the herbivorous snail Tegula (Chlorostoma) funebralis (A. Adams) to reduce grazing and flee tide pools, resulting in positive indirect effects on tide pool microalgae. 3. However, we show that the strength of this behaviourally-mediated cascade may be contingent on prey hunger level and body size. During short field experiments at low tide, mediumsized snails that were either newly collected from the field or fed for 1 week in the laboratory mediated strong TMIIs because they grazed less when seastars were present. In contrast, no TMIIs occurred when medium-sized snails had been starved for 1 week because they continued grazing regardless of seastar presence. Newly collected small snails fled from seastars but did not mediate cascades because they ate little algae. Despite reaching an apparent size refuge from predation, many newly collected large snails fled from seastars, but those individuals that remained tended to graze the algae more quickly, resulting in unexpected negative indirect effects of seastars on algae cover. The implication of this pattern for the natural system is unclear. 4. Because average hunger level and size of snails vary over time and space in nature, a mosaic of TMII strength may exist. 5. Overall, the strength of tritrophic TMIIs in tide pools depended on individual prey state, supporting model predictions and adding to sparse empirical evidence. This outcome suggests that patterns occurring system-wide over the long term may be influenced by the state-dependent decisions made by the individuals present.