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Withering Syndrome Disease Dynamics in Wild and Cultured Northeastern Pacific Abalones.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Withering Syndrome Disease Dynamics in Wild and Cultured Northeastern Pacific Abalones./
作者:	Crosson, Lisa M.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
面頁冊數:	118 p.
附註:	Source: Dissertations Abstracts International, Volume: 82-03, Section: B.
Contained By:	Dissertations Abstracts International82-03B.
標題:	Aquatic sciences. -
電子資源:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28000329
ISBN:	9798662578104

Withering Syndrome Disease Dynamics in Wild and Cultured Northeastern Pacific Abalones.
Crosson, Lisa M.

Withering Syndrome Disease Dynamics in Wild and Cultured Northeastern Pacific Abalones. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 118 p.

Source: Dissertations Abstracts International, Volume: 82-03, Section: B.

Thesis (Ph.D.)--University of Washington, 2020.

This item must not be sold to any third party vendors.

Withering syndrome (WS) is a chronic bacterial disease of abalones, Haliotis spp., caused by a Rickettsia-like organism (WS-RLO). The etiological agent, Candidatus Xenohaliotis californiensis, occurs along the eastern Pacific margin of North America in California, US and Baja California, Mexico. However, as infected abalones have been transported to Chile, China, Taiwan, Iceland, Ireland, Israel, Spain, Thailand, and Japan, the geographic range of the bacterium is likely broad especially where California red abalone (Haliotis rufescens) are cultured or in areas where native species have been exposed to red abalone. Disease susceptibility varies among abalones with up to 99% losses of black abalone (H. cracherodii) in lab and field studies in the US, to no losses among the small abalone (H. diversicolor supertexta) in Thailand. Some abalone populations that have suffered severe WS mortality events have developed resistance to the disease. In addition, a newly identified phage hyperparasite of the WS-RLO may reduce pathogenicity and dampen associated losses. Proper diagnosis of WS requires the identification of infection with the pathogen (WS-RLO detected via in situ hybridization or histology coupled with PCR and sequence analysis) accompanied by morphological changes that characterize this disease (e.g. digestive gland metaplasia and pedal atrophy). A quantitative PCR (qPCR) assay was recently developed and validated for the detection of WS-RLO DNA in abalone tissues, feces, and seawater. While confirmation of infection cannot be done by PCR-based assays alone, they can be used as proxies for infection in areas where the WS-RLO is established and are recommended for inclusion in all abalone health examinations. Avoidance of WS is best accomplished by the establishment of a health history, good husbandry practices, and multiple health examinations prior to the movement of animals.Population declines in wild and cultured abalones due to WS have been well documented along the northeastern Pacific Ocean. However, observed differences in species susceptibility to the disease are not well understood. The first objective of my dissertation was to examine the susceptibility of three temperate abalone species, the cool water (4-14°C) pinto or northern abalone (H. kamtschatkana), the intermediate water (8-18°C) red abalone, 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.My second dissertation objective was to elucidate important epidemiological information on the WS-RLO. The bacterium remains unculturable thereby limiting our understanding of WS disease dynamics. My goals were to: (1) determine the temporal stability of WS-RLO DNA outside of its abalone host in 14°C and 18°C seawater, (2) develop a standardized protocol for exposing abalones to known concentrations of WS-RLO DNA and (3) calculate the dose of WS-RLO DNA required to generate 50% infection prevalence (ID50) in the highly cultured red abalone. WS-RLO stability trials were conducted in October 2016, February 2017, and June 2017 during which qPCR analysis was used to quantify bacterial DNA for 7 days in seawater collected at an abalone farm in southern California where the pathogen is endemic. For all trials and temperature treatments, WS-RLO DNA was not stable in seawater longer than 2 days. To determine an ID50, groups of uninfected juvenile red abalone were subjected to 3-hour bath exposures of WS-RLO at four concentrations: 0, 103, 104, and 105 DNA copies/mL. Abalone feces were monitored bi-weekly for the presence of WS-RLO DNA and abalone tissues were sampled 9 weeks after dosing for histology and qPCR examination. Results from the ID50 indicated that our protocol was successful in generating WS-RLO infections and a pathogen dose of 2.3 x 103 DNA copies/mL was required to generate 50% infection prevalence in the tissue of red abalone as assessed by qPCR.The WS-RLO is considered an established bacterial pathogen in coastal CA seawaters and is of great concern to coastal managers and local abalone aquaculture facilities (AFs) conducting open or flow-through seawater culture methods. California AFs are at high risk for spillback (wild to farm) and spillover (farm to wild) disease transmission due to high abalone host densities and the use and release of coastal seawater that may contain the WS-RLO and its associated novel phage. To address these concerns, my third and final dissertation objective was to sample nearshore surface seawater from nine established wild black abalone sites and four red abalone AFs from Bodega Bay, Sonoma County, CA, US to Ventura County, CA, US including the Channel Islands over two consecutive summers to determine the presence and amount of WS-RLO and phage DNA via qPCR. In July 2010, WS-RLO DNA was detected as far north as Andrew Molera State Park, Big Sur, CA and as far south as San Nicolas Island (SNI). Phage DNA was detected from Monterey Bay, CA to SNI. In July 2011, WS-RLO DNA was detected as far north as Davenport, CA and as far south as SNI. The phage DNA detection range remained the same as the 2010 survey. Phage DNA loads did not vary by year at AF or wild sites. However, WS-RLO DNA loads were greater in 2011 than 2010 at wild sites, while those at AFs did not vary by year. In October 2013, surface seawater surveys were conducted at the two southern-most AFs in Cayucos and Goleta, CA to assess fine-scale WS-RLO DNA dilution potential from a point-source discharge. In the 2013 samples, WS-RLO DNA loads in seawater directly adjacent to the AFs were less than the mean levels detected at all wild black abalone sites previously surveyed within 50 to 500 m of the AFs effluent outfalls. While these findings present management concerns for both wild and cultured California abalones, it is important to acknowledge that PCR-based assays do not indicate the presence of viable pathogen or active infection and serve as a proxy for WS exposure. In order to fully assess the potential for wild and cultured abalone disease interactions, additional experiments should be conducted to determine the longevity and infectivity of the WS-RLO and novel phage in seawater.

ISBN: 9798662578104Subjects--Topical Terms:

3174300
Aquatic sciences.
Subjects--Index Terms:

Abalone

Withering Syndrome Disease Dynamics in Wild and Cultured Northeastern Pacific Abalones.
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300 $a 118 p.
500 $a Source: Dissertations Abstracts International, Volume: 82-03, Section: B.
500 $a Advisor: Friedman, Carolyn.
502 $a Thesis (Ph.D.)--University of Washington, 2020.
506 $a This item must not be sold to any third party vendors.
520 $a Withering syndrome (WS) is a chronic bacterial disease of abalones, Haliotis spp., caused by a Rickettsia-like organism (WS-RLO). The etiological agent, Candidatus Xenohaliotis californiensis, occurs along the eastern Pacific margin of North America in California, US and Baja California, Mexico. However, as infected abalones have been transported to Chile, China, Taiwan, Iceland, Ireland, Israel, Spain, Thailand, and Japan, the geographic range of the bacterium is likely broad especially where California red abalone (Haliotis rufescens) are cultured or in areas where native species have been exposed to red abalone. Disease susceptibility varies among abalones with up to 99% losses of black abalone (H. cracherodii) in lab and field studies in the US, to no losses among the small abalone (H. diversicolor supertexta) in Thailand. Some abalone populations that have suffered severe WS mortality events have developed resistance to the disease. In addition, a newly identified phage hyperparasite of the WS-RLO may reduce pathogenicity and dampen associated losses. Proper diagnosis of WS requires the identification of infection with the pathogen (WS-RLO detected via in situ hybridization or histology coupled with PCR and sequence analysis) accompanied by morphological changes that characterize this disease (e.g. digestive gland metaplasia and pedal atrophy). A quantitative PCR (qPCR) assay was recently developed and validated for the detection of WS-RLO DNA in abalone tissues, feces, and seawater. While confirmation of infection cannot be done by PCR-based assays alone, they can be used as proxies for infection in areas where the WS-RLO is established and are recommended for inclusion in all abalone health examinations. Avoidance of WS is best accomplished by the establishment of a health history, good husbandry practices, and multiple health examinations prior to the movement of animals.Population declines in wild and cultured abalones due to WS have been well documented along the northeastern Pacific Ocean. However, observed differences in species susceptibility to the disease are not well understood. The first objective of my dissertation was to examine the susceptibility of three temperate abalone species, the cool water (4-14°C) pinto or northern abalone (H. kamtschatkana), the intermediate water (8-18°C) red abalone, 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.My second dissertation objective was to elucidate important epidemiological information on the WS-RLO. The bacterium remains unculturable thereby limiting our understanding of WS disease dynamics. My goals were to: (1) determine the temporal stability of WS-RLO DNA outside of its abalone host in 14°C and 18°C seawater, (2) develop a standardized protocol for exposing abalones to known concentrations of WS-RLO DNA and (3) calculate the dose of WS-RLO DNA required to generate 50% infection prevalence (ID50) in the highly cultured red abalone. WS-RLO stability trials were conducted in October 2016, February 2017, and June 2017 during which qPCR analysis was used to quantify bacterial DNA for 7 days in seawater collected at an abalone farm in southern California where the pathogen is endemic. For all trials and temperature treatments, WS-RLO DNA was not stable in seawater longer than 2 days. To determine an ID50, groups of uninfected juvenile red abalone were subjected to 3-hour bath exposures of WS-RLO at four concentrations: 0, 103, 104, and 105 DNA copies/mL. Abalone feces were monitored bi-weekly for the presence of WS-RLO DNA and abalone tissues were sampled 9 weeks after dosing for histology and qPCR examination. Results from the ID50 indicated that our protocol was successful in generating WS-RLO infections and a pathogen dose of 2.3 x 103 DNA copies/mL was required to generate 50% infection prevalence in the tissue of red abalone as assessed by qPCR.The WS-RLO is considered an established bacterial pathogen in coastal CA seawaters and is of great concern to coastal managers and local abalone aquaculture facilities (AFs) conducting open or flow-through seawater culture methods. California AFs are at high risk for spillback (wild to farm) and spillover (farm to wild) disease transmission due to high abalone host densities and the use and release of coastal seawater that may contain the WS-RLO and its associated novel phage. To address these concerns, my third and final dissertation objective was to sample nearshore surface seawater from nine established wild black abalone sites and four red abalone AFs from Bodega Bay, Sonoma County, CA, US to Ventura County, CA, US including the Channel Islands over two consecutive summers to determine the presence and amount of WS-RLO and phage DNA via qPCR. In July 2010, WS-RLO DNA was detected as far north as Andrew Molera State Park, Big Sur, CA and as far south as San Nicolas Island (SNI). Phage DNA was detected from Monterey Bay, CA to SNI. In July 2011, WS-RLO DNA was detected as far north as Davenport, CA and as far south as SNI. The phage DNA detection range remained the same as the 2010 survey. Phage DNA loads did not vary by year at AF or wild sites. However, WS-RLO DNA loads were greater in 2011 than 2010 at wild sites, while those at AFs did not vary by year. In October 2013, surface seawater surveys were conducted at the two southern-most AFs in Cayucos and Goleta, CA to assess fine-scale WS-RLO DNA dilution potential from a point-source discharge. In the 2013 samples, WS-RLO DNA loads in seawater directly adjacent to the AFs were less than the mean levels detected at all wild black abalone sites previously surveyed within 50 to 500 m of the AFs effluent outfalls. While these findings present management concerns for both wild and cultured California abalones, it is important to acknowledge that PCR-based assays do not indicate the presence of viable pathogen or active infection and serve as a proxy for WS exposure. In order to fully assess the potential for wild and cultured abalone disease interactions, additional experiments should be conducted to determine the longevity and infectivity of the WS-RLO and novel phage in seawater.
520 $a Collectively, these findings are critical components of disease dynamics that will help assess WS transmission risk within and among abalone populations and facilitate appropriate management and restoration strategies for both wild and cultured abalone species in WS-endemic areas.
590 $a School code: 0250.
650 4 $a Aquatic sciences. $3 3174300
650 4 $a Animal diseases. $3 3181862
650 4 $a Molecular biology. $3 517296
653 $a Abalone
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653 $a Quantitative PCR
653 $a Rickettsia
653 $a Withering syndrome
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710 2 $a University of Washington. $b Aquatic and Fishery Sciences. $3 2093042
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