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Reduced disease in black abalone following mass mortality: phage therapy and natural selection

Black abalone, Haliotis cracherodii, populations along the NE Pacific ocean have declined due to the rickettsial disease withering syndrome (WS). Natural recovery on San Nicolas Island (SNI) of Southern California suggested the development of resistance in island populations. Experimental challenges...

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Autores principales: Friedman, Carolyn S., Wight, Nathan, Crosson, Lisa M., VanBlaricom, Glenn R., Lafferty, Kevin D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3957727/
https://www.ncbi.nlm.nih.gov/pubmed/24672512
http://dx.doi.org/10.3389/fmicb.2014.00078
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author Friedman, Carolyn S.
Wight, Nathan
Crosson, Lisa M.
VanBlaricom, Glenn R.
Lafferty, Kevin D.
author_facet Friedman, Carolyn S.
Wight, Nathan
Crosson, Lisa M.
VanBlaricom, Glenn R.
Lafferty, Kevin D.
author_sort Friedman, Carolyn S.
collection PubMed
description Black abalone, Haliotis cracherodii, populations along the NE Pacific ocean have declined due to the rickettsial disease withering syndrome (WS). Natural recovery on San Nicolas Island (SNI) of Southern California suggested the development of resistance in island populations. Experimental challenges in one treatment demonstrated that progeny of disease-selected black abalone from SNI survived better than did those from naïve black abalone from Carmel Point in mainland coastal central California. Unexpectedly, the presence of a newly observed bacteriophage infecting the WS rickettsia (WS-RLO) had strong effects on the survival of infected abalone. Specifically, presence of phage-infected RLO (RLOv) reduced the host response to infection, RLO infection loads, and associated mortality. These data suggest that the black abalone: WS-RLO relationship is evolving through dual host mechanisms of resistance to RLO infection in the digestive gland via tolerance to infection in the primary target tissue (the post-esophagus) coupled with reduced pathogenicity of the WS-RLO by phage infection, which effectively reduces the infection load in the primary target tissue by half. Sea surface temperature patterns off southern California, associated with a recent hiatus in global-scale ocean warming, do not appear to be a sufficient explanation for survival patterns in SNI black abalone. These data highlight the potential for natural recovery of abalone populations over time and that further understanding of mechanisms governing host–parasite relationships will better enable us to manage declining populations.
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spelling pubmed-39577272014-03-26 Reduced disease in black abalone following mass mortality: phage therapy and natural selection Friedman, Carolyn S. Wight, Nathan Crosson, Lisa M. VanBlaricom, Glenn R. Lafferty, Kevin D. Front Microbiol Microbiology Black abalone, Haliotis cracherodii, populations along the NE Pacific ocean have declined due to the rickettsial disease withering syndrome (WS). Natural recovery on San Nicolas Island (SNI) of Southern California suggested the development of resistance in island populations. Experimental challenges in one treatment demonstrated that progeny of disease-selected black abalone from SNI survived better than did those from naïve black abalone from Carmel Point in mainland coastal central California. Unexpectedly, the presence of a newly observed bacteriophage infecting the WS rickettsia (WS-RLO) had strong effects on the survival of infected abalone. Specifically, presence of phage-infected RLO (RLOv) reduced the host response to infection, RLO infection loads, and associated mortality. These data suggest that the black abalone: WS-RLO relationship is evolving through dual host mechanisms of resistance to RLO infection in the digestive gland via tolerance to infection in the primary target tissue (the post-esophagus) coupled with reduced pathogenicity of the WS-RLO by phage infection, which effectively reduces the infection load in the primary target tissue by half. Sea surface temperature patterns off southern California, associated with a recent hiatus in global-scale ocean warming, do not appear to be a sufficient explanation for survival patterns in SNI black abalone. These data highlight the potential for natural recovery of abalone populations over time and that further understanding of mechanisms governing host–parasite relationships will better enable us to manage declining populations. Frontiers Media S.A. 2014-03-18 /pmc/articles/PMC3957727/ /pubmed/24672512 http://dx.doi.org/10.3389/fmicb.2014.00078 Text en Copyright © 2014 Friedman, Wight, Crosson, VanBlaricom and Lafferty. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Friedman, Carolyn S.
Wight, Nathan
Crosson, Lisa M.
VanBlaricom, Glenn R.
Lafferty, Kevin D.
Reduced disease in black abalone following mass mortality: phage therapy and natural selection
title Reduced disease in black abalone following mass mortality: phage therapy and natural selection
title_full Reduced disease in black abalone following mass mortality: phage therapy and natural selection
title_fullStr Reduced disease in black abalone following mass mortality: phage therapy and natural selection
title_full_unstemmed Reduced disease in black abalone following mass mortality: phage therapy and natural selection
title_short Reduced disease in black abalone following mass mortality: phage therapy and natural selection
title_sort reduced disease in black abalone following mass mortality: phage therapy and natural selection
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3957727/
https://www.ncbi.nlm.nih.gov/pubmed/24672512
http://dx.doi.org/10.3389/fmicb.2014.00078
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