Marshman, Blythe C

The Rickettsiales-like prokaryote - Candidatus Xenohaliotis californiensis (Ca. Xc) – has decimated black abalone populations along the Pacific coast of North America. White abalone, – Haliotis sorenseni – are also susceptible and nearly extinct in the wild due to overfishing in the 1970s. Candidatus Xenohaliotis californiensis proliferates in epithelial cells of the abalone gastrointestinal tract and causes clinical signs of starvation. In 2012, evidence of a putative phage associated with Ca. Xc in Haliotis rufescens was described. In this study, we investigated the virulence of Ca. Xc in red and white abalone at different environmental temperatures in the presence of phage. Using a comparative experimental design, we observed differences over time between the two abalone species in mortality, body condition, and bacterial load by quantitative real time PCR (qPCR). By day 251, all white abalone exposed to the Ca. Xc and its phage in the warm water (18.5ºC) treatment died, while red abalone exposed to the same conditions had a mortality rate of 10% despite a relatively heavy bacterial burden as determined by qPCR of posterior esophagus tissue and histological assessment at the termination of the experiment. These data support the phage as a protective and potentially therapeutic agent for withering syndrome in red abalone, while white abalone appear to remain susceptible to this disease even in phage presence. These findings have important implications for implementation of a white abalone recovery program, particularly with respect to the thermal regimes of locations where captively-reared individuals will be outplanted.

The Rickettsiales-like prokaryote - Candidatus Xenohaliotis californiensis (Ca. Xc) – has decimated black abalone populations along the Pacific coast of North America. White abalone, – Haliotis sorenseni – are also susceptible and nearly extinct in the wild due to overfishing in the 1970s. Candidatus Xenohaliotis californiensis proliferates in epithelial cells of the abalone gastrointestinal tract and causes clinical signs of starvation. In 2012, evidence of a putative phage associated with Ca. Xc in Haliotis rufescens was described. In this study, we investigated the virulence of Ca. Xc in red and white abalone at different environmental temperatures in the presence of phage. Using a comparative experimental design, we observed differences over time between the two abalone species in mortality, body condition, and bacterial load by quantitative real time PCR (qPCR). By day 251, all white abalone exposed to the Ca. Xc and its phage in the warm water (18.5ºC) treatment died, while red abalone exposed to the same conditions had a mortality rate of 10% despite a relatively heavy bacterial burden as determined by qPCR of posterior esophagus tissue and histological assessment at the termination of the experiment. These data support the phage as a protective and potentially therapeutic agent for withering syndrome in red abalone, while white abalone appear to remain susceptible to this disease even in phage presence. These findings have important implications for implementation of a white abalone recovery program, particularly with respect to the thermal regimes of locations where captively-reared individuals will be outplanted.