Vibrio coralliilyticus as an agent of red spotting disease in the sea urchin Strongylocentrotus intermedius

Li, Ruijun; Dang, Huifeng; Huang, Yuxi; Quan, Zijiao; Jiang, Huijie; Zhang, Weijie; Ding, Jun

doi:10.1016/j.aqrep.2019.100244

Cited by 13 publications

(5 citation statements)

References 15 publications

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“…1 ) and documented as a novel member of the Splendidus clade 24 . The lesion syndrome observed in S. droebachiensis in Norway, demonstrates similar symptoms as bald sea urchin disease, but differs mainly from other diseases, for example, red spot disease show presence of purple-red viscous spots in the denuded area 7 , 23 . The lesion syndrome was observed under low temperature condition, hence, the involvement of pathogens speculated could be somewhat different than other sea urchin diseases.…”

Section: Introductionmentioning

confidence: 80%

“…Consequently, a direct or indirect association of Vibrio species with bald sea urchin disease would not be surprising. Until now, the Vibrio species that have been identified as opportunistic pathogens for diseased sea urchins, are Vibrio anguillarum 11 , Vibrio shilonii, Vibrio splendidus, Vibrio harveyi, Vibrio fortis 22 , Vibrio alginolyticus 13 , Vibrio coralliilyticus 23 . It is unclear whether these Vibrio species act as primary causative agents or secondary opportunistic colonizers 7 and the virulence features of the opportunistic Vibrios remain elusive.…”

Section: Introductionmentioning

confidence: 99%

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Evidence for association of Vibrio echinoideorum with tissue necrosis on test of the green sea urchin Strongylocentrotus droebachiensis

Hira

Stensvåg

2022

Sci Rep

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Abstract“Sea urchin lesion syndrome” is known as sea urchin disease with the progressive development of necrotic epidermal tissue and loss of external organs, including appendages on the outer body surface. Recently, a novel strain, Vibrio echinoideorum has been isolated from the lesion of green sea urchin (Strongylocentrotus droebachiensis), an economically important mariculture species in Norway. V. echinoideorum has not been reported elsewhere in association with green sea urchin lesion syndrome. Therefore, in this study, an immersion based bacterial challenge experiment was performed to expose sea urchins (wounded and non-wounded) to V. echinoideorum, thereby mimicking a nearly natural host–pathogen interaction under controlled conditions. This infection experiment demonstrated that only the injured sea urchins developed the lesion to a significant degree when exposed to V. echinoideorum. Pure cultures of the employed bacterial strain were recovered from the infected animals and its identity was confirmed by the MALDI-TOF MS spectra profiling. Additionally, the hemolytic phenotype of V. echinoideorum substantiated its virulence potential towards the host, and this was also supported by the cytolytic effect on red spherule cells of sea urchin. Furthermore, the genome sequence of V. echinoideorum was assumed to encode potential virulence genes and were subjected to in silico comparison with the established virulence factors of Vibrio vulnificus and Vibrio tasmaniensis. This comparative virulence profile provided novel insights about virulence genes and their putative functions related to chemotaxis, adherence, invasion, evasion of the host immune system, and damage of host tissue and cells. Thus, it supports the pathogenicity of V. echinoideorum. In conclusion, the interaction of V. echinoideorum with injured sea urchin facilitates the development of lesion syndrome and therefore, revealing its potentiality as an opportunistic pathogen.

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Section: Introductionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Evidence for association of Vibrio echinoideorum with tissue necrosis on test of the green sea urchin Strongylocentrotus droebachiensis

Hira

Stensvåg

2022

Sci Rep

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“…In the presence of PAMPs or danger-associated molecular patterns (DAMPs), RSCs exocytose the contents of their vesicles that includes echinochrome A (38), which may reduce the viability of microbes and yeast based on iron chelation (70, 71). RSCs accumulate around bacteria in vitro (72) and surround the edges of surface injuries or infections that appear as dark red or black bands in vivo (73)(74)(75)(76) including injuries from tissue grafting (77).…”

Section: Discussionmentioning

confidence: 99%

Coelomocyte populations in the sea urchin, Strongylocentrotus purpuratus, undergo dynamic changes in response to immune challenge

2022

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The sea urchin, Strongylocentrotus purpuratus has seven described populations of distinct coelomocytes in the coelomic fluid that are defined by morphology, size, and for some types, by known functions. Of these subtypes, the large phagocytes are thought to be key to the sea urchin cellular innate immune response. The concentration of total coelomocytes in the coelomic fluid increases in response to pathogen challenge. However, there is no quantitative analysis of how the respective coelomocyte populations change over time in response to immune challenge. Accordingly, coelomocytes collected from immunoquiescent, healthy sea urchins were evaluated by flow cytometry for responses to injury and to challenge with either heat-killed Vibrio diazotrophicus, zymosan A, or artificial coelomic fluid, which served as the vehicle control. Responses to the initial injury of coelomic fluid collection or to injection of V. diazotrophicus show significant increases in the concentration of large phagocytes, small phagocytes, and red spherule cells after one day. Responses to zymosan A show decreases in the concentration of large phagocytes and increases in the concentration of small phagocytes. In contrast, responses to injections of vehicle result in decreased concentration of large phagocytes. When these changes in coelomocytes are evaluated based on proportions rather than concentration, the respective coelomocyte proportions are generally maintained in response to injection with V. diazotrophicus and vehicle. However, this is not observed in response to zymosan A and this lack of correspondence between proportions and concentrations may be an outcome of clearing these large particles by the large phagocytes. Variations in coelomocyte populations are also noted for individual sea urchins evaluated at different times for their responses to immune challenge compared to the vehicle. Together, these results demonstrate that the cell populations in sea urchin immune cell populations undergo dynamic changes in vivo in response to distinct immune stimuli and to injury and that these changes are driven by the responses of the large phagocyte populations.

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“…Ex situ and spatial epidemiological studies suggest SCTLD is contagious (Aeby et al, 2019;Muller et al, 2020) and hydrodynamic models predict that the spatial distribution of the disease spread through time, suggesting a waterborne pathogen (Dobbelaere et al, 2020). Additionally, co-infection with Vibrio coralliilyticus, a bacterium associated with coral diseases (Ben-Haim et al, 2003;Sussman et al, 2008;Vezzulli et al, 2010;Vidal-Dupiol et al, 2011;Aeby et al, 2019;Ushijima et al, 2016;Zhou et al, 2019), compromised coral immunity, shellfish larvae mass mortalities (Estes et al, 2004;Elston et al, 2008;Kesarcodi-Watson et al, 2009;Richards et al, 2014), and red spotting disease in sea urchins (Li et al, 2020) may increase SCTLD virulence (Ushijima et al, 2020). The causative agent for SCTLD has yet to be identified, but several bacterial orders including Rhodobacterales, Rhizobiales, Flavobacteriales, Clostridiales, Alteromonadales, and Vibrionales were enriched within SCTLD lesions compared with apparently healthy corals (Meyer et al, 2019;Rosales et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida

et al. 2021

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Since 2014, corals within Florida’s Coral Reef have been dying at an unprecedented rate due to stony coral tissue loss disease (SCTLD). Here we describe the transcriptomic outcomes of three different SCTLD transmission experiments performed at the Smithsonian Marine Station and Mote Marine Laboratory between 2019 and 2020 on the corals Orbicella faveolata and Montastraea cavernosa. Overall, diseased O. faveolata had 2194 differentially expressed genes (DEGs) compared with healthy colonies, whereas diseased M. cavernosa had 582 DEGs compared with healthy colonies. Many significant DEGs were implicated in immunity, extracellular matrix rearrangement, and apoptosis. These included, but not limited to, peroxidases, collagens, Bax-like, fibrinogen-like, protein tyrosine kinase, and transforming growth factor beta. A gene module was identified that was significantly correlated to disease transmission. This module possessed many apoptosis and immune genes with high module membership indicating that a complex apoptosis and immune response is occurring in corals during SCTLD transmission. Overall, we found that O. faveolata and M. cavernosa exhibit an immune, apoptosis, and tissue rearrangement response to SCTLD. We propose that future studies should focus on examining early time points of infection, before the presence of lesions, to understand the activating mechanisms involved in SCTLD.

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Vibrio coralliilyticus as an agent of red spotting disease in the sea urchin Strongylocentrotus intermedius

Cited by 13 publications

References 15 publications

Evidence for association of Vibrio echinoideorum with tissue necrosis on test of the green sea urchin Strongylocentrotus droebachiensis

Evidence for association of Vibrio echinoideorum with tissue necrosis on test of the green sea urchin Strongylocentrotus droebachiensis

Coelomocyte populations in the sea urchin, Strongylocentrotus purpuratus, undergo dynamic changes in response to immune challenge

Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida

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