Effects of novel bacteriophage on red abalone (Haliotis rufescens) and white abalone (H. sorenseni) exposed to Candidatus Xenohaliotis californiensis – the causative agent of abalone withering syndrome
- Published
- Accepted
- Subject Areas
- Aquaculture, Fisheries and Fish Science, Conservation Biology, Microbiology, Virology, Natural Resource Management
- Keywords
- Bacteriophage, Abalone, Candidatus Xenohaliotis californiensis, withering syndrome, Phage therapy, Ocean warming, White abalone, Haliotis rufescens, Haliotis sorenseni, Rickettsia
- Copyright
- © 2017 Vater et al.
- Licence
- This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.
- Cite this article
- 2017. Effects of novel bacteriophage on red abalone (Haliotis rufescens) and white abalone (H. sorenseni) exposed to Candidatus Xenohaliotis californiensis – the causative agent of abalone withering syndrome. PeerJ Preprints 5:e3351v1 https://doi.org/10.7287/peerj.preprints.3351v1
Abstract
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.
Author Comment
This is a preprint submission to PeerJ Preprints.
Supplemental Information
Figure 2: Animal survival, Figure 3: Condition Index over time, Figure 4: pathogen gene copy numbers
Figure 2. Percent survival of experimental red and white abalone held in ambient water (13.6 °C) or at elevated temperature (18.5°C) with and without Candidatus Xenohaliotis californiensis (Ca. Xc) exposure for 343 d; N = 64 for each group at day 0. Each curve represents one of the six treatment groups, with variables: Ca. Xc exposure, seawater temperature, and species. We observe a significant difference between survival curves of red and white abalone held under elevated seawater temperature and Ca. Xc exposure conditions.
Figure 3. Longitudinal plot of mean (+/- standard error) values in condition index (calculated by total abalone weight divided by shell length cubed) over time of experimental groups. Error bars represent standard error of the mean.
Figure 4. Log transformed qPCR-derived Candidatus Xenohaliotis californiensis gene copy numbers from PE tissue at days 161 and 343.