Withering syndrome susceptibility of northeastern pacific abalones: A complex relationship with phylogeny and thermal experience

Abstract Population declines in wild and cultured abalones ( Haliotis spp.) due to a bacterial disease called withering syndrome (WS) have been documented along the northeastern Pacific Ocean. However, observed differences in species susceptibility to the disease are not well understood. Here, we examined the susceptibility of three temperate abalone species, the cool water (4–14 °C) pinto or northern abalone ( Haliotis kamtschatkana ), the intermediate water (8–18 °C) red abalone ( H. rufescens ), and the warm water (12–23 °C) pink abalone ( H. corrugata ), to experimental WS infection at temperatures facilitating disease proliferation. Mortality data paired with histological and molecular detection of the WS pathogen confirmed that these abalone species exhibit different levels of susceptibility to infection and resistance to WS development ranging from high susceptibility and low resistance in pinto abalone to moderate/low susceptibility and resistance in red and pink abalones. The temperature associated with WS induced mortalities also varied among species: pinto abalone died at the lowest experimental temperature (17.32 ± 0.09 °C), while red abalone died at an intermediate temperature (17.96 ± 0.16 °C), and pink abalone required the highest temperature (18.84 ± 0.16 °C). When data from the current and previous studies were examined, susceptibility to WS was inversely related to phylogenetic distance from white abalone ( H. sorenseni ), which had the highest susceptibility and lowest resistance of all abalone species tested prior to the current study. These results provide further evidence that an abalone’s thermal optima and phylogenetic relationship can determine its susceptibility to WS; species with cool water evolutionary histories are most susceptible to WS and the most susceptible species appear to be closely related. Differences among the thermal ranges of abalone species have broad implications for WS disease dynamics and highlight the importance of understanding the mechanisms governing the abalone-WS relationship in order to properly manage declining abalone populations.