The Rickettsiales-like prokaryote and causative agent of Withering Syndrome (WS)- Xenohaliotis californiensis ( Xc)-decimated black abalone populations along the Pacific coast of North America. White abalone--are also susceptible to WS and have become nearly extinct in the wild due to overfishing in the 1970s. Xenohaliotis californiensis proliferates within epithelial cells of the abalone gastrointestinal tract and causes clinical signs of starvation. In 2012, evidence of a putative bacteriophage associated with Xc in red abalone--was described. Recently, histologic examination of animals with Xc infection in California abalone populations universally appear to have the phage-containing inclusions. In this study, we investigated the current virulence of Xc in red abalone and white abalone at different environmental temperatures. 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 current variant of Xc held in the warm water (18.5 °C) treatment died, while red abalone exposed to the same conditions had a mortality rate of only 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 current status of . Xc as less virulent in red abalone, and may provide correlative evidence of a protective phage interaction. However, white abalone appear to remain highly susceptible to this disease. 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.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6022723 | PMC |
http://dx.doi.org/10.7717/peerj.5104 | DOI Listing |
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