scholarly journals Reef Sediments Can Act As a Stony Coral Tissue Loss Disease Vector

2022 ◽  
Vol 8 ◽  
Author(s):  
Michael S. Studivan ◽  
Ashley M. Rossin ◽  
Ewelina Rubin ◽  
Nash Soderberg ◽  
Daniel M. Holstein ◽  
...  
Keyword(s):  
Infectious Agent ◽  
Coastal Development ◽  
Ex Situ ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Conservation Strategies ◽  
Dade County ◽  
Tissue Samples ◽  
Stony Coral ◽  
The Individual

Stony coral tissue loss disease (SCTLD) was first observed in 2014 near Virginia Key in Miami-Dade County, Florida. Field sampling, lab experiments, and modeling approaches have suggested that reef sediments may play a role in SCTLD transmission, though a positive link has not been tested experimentally. We conducted an ex situ transmission assay using a statistically-independent disease apparatus to test whether reef sediments can transmit SCTLD in the absence of direct contact between diseased and healthy coral tissue. We evaluated two methods of sediment inoculation: batch inoculation of sediments collected from southeast Florida using whole colonies of diseased Montastraea cavernosa, and individual inoculations of sediments following independent, secondary infections of ∼5 cm2 coral fragments. Healthy fragments of the coral species Orbicella faveolata and M. cavernosa were exposed to these diseased sediment treatments, as well as direct disease contact and healthy sediment controls. SCTLD transmission was observed for both batch and individual diseased sediment inoculation treatments, albeit with lower proportions of infected individuals as compared to disease contact controls. The time to onset of lesions was significantly different between species and among disease treatments, with the most striking infections occurring in the individual diseased sediment treatment in under 24 h. Following infection, tissue samples were confirmed for the presence of SCTLD signs via histological examination, and sediment subsamples were analyzed for microbial community variation between treatments, identifying 16 SCTLD indicator taxa in sediments associated with corals experiencing tissue loss. This study demonstrated that reef sediments can indeed transmit SCTLD through indirect exposure between diseased and healthy corals, and adds credence to the assertion that SCTLD transmission occurs via an infectious agent or agents. This study emphasizes the critical need to understand the roles that sediment microbial communities and coastal development activities may have on the persistence of SCTLD throughout the endemic zone, especially in the context of management and conservation strategies in Florida and the wider Caribbean.

scholarly journals Effects of the Stony Coral Tissue Loss Disease Outbreak on Coral Communities and the Benthic Composition of Cozumel Reefs

2021 ◽  
Vol 8 ◽  
Author(s):  
Nuria Estrada-Saldívar ◽  
Blanca A. Quiroga-García ◽  
Esmeralda Pérez-Cervantes ◽  
Omar O. Rivera-Garibay ◽  
Lorenzo Alvarez-Filip
Keyword(s):  
Coral Cover ◽  
Coastal Development ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Coral Mortality ◽  
Benthic Assemblages ◽  
Stony Coral ◽  
Coral Communities ◽  
The Caribbean ◽  
Benthic Composition

In the Caribbean, disease outbreaks have emerged as significant drivers of coral mortality. Stony Coral Tissue Loss Disease (SCTLD) is a novel white plague-type disease that was first reported off the Florida coast in 2014. This disease affects >20 coral species and is spreading rapidly throughout the Caribbean. In December 2018, SCTLD reached southwestern (SW) Cozumel, one of the healthiest reef systems in the Caribbean. In this study, we integrate data from multiple survey protocols conducted between July 2018 and April 2020 to track the progression of the outbreak in SW Cozumel and to quantify the impacts of SCTLD on coral communities and the benthic composition of reefs. Given that the SCTLD outbreak coincided with a period of prolonged thermal stress that concluded in widespread coral bleaching in autumn 2019, we also investigated whether this event further exacerbated coral mortality. Our findings show that SCTLD spread throughout SW Cozumel in only 2 months and reached a peak after only 5 months. By the summer of 2019, most of the afflicted corals were already dead. Species of the families Meandrinidae, Faviinae, and Montastraeidae showed 33–95% mortality. The widespread coral die-off caused an overall loss of 46% in coral cover followed by a rapid increase of algae cover across all surveyed reefs that persisted until at least April 2020. In November 2019, more than 15% of surveyed coral colonies were bleached. However, we did not find that bleaching further increased coral mortality at either the colony or the community level, which suggests that the coral communities were able to recover from this event despite still being affected by the disease. In conclusion, SCTLD is radically changing the ecology of coral reefs by decimating the populations of several key reef-builders and reconfiguring the benthic assemblages. The actions needed to restore coral populations have to be accompanied by stringent controls related to the effects of climate change, coastal development, and wastewater treatment to improve coral conditions and ecosystem resilience.

scholarly journals Exploring the Stony Coral Tissue Loss Disease Bacterial Pathobiome

2020 ◽  
Author(s):  
D.D. Iwanowicz ◽  
W.B. Schill ◽  
C. M. Woodley ◽  
A. Bruckner ◽  
K. Neely ◽  
...  
Keyword(s):  
Direct Sequencing ◽  
Bacterial Species ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Coral Host ◽  
Dade County ◽  
Sequencing Data ◽  
Stony Coral ◽  
Clinically Normal ◽  
Diseased Coral

ABSTRACTA devastating novel coral disease outbreak, referred to as Stony Coral Tissue Loss Disease (SCTLD), was first described in 2014. It is thought to have originated offshore of Miami-Dade County, FL, but has persisted and spread, affecting new reefs along the Florida Reef Tract and reefs of at least 8 other Caribbean jurisdictions. We investigated the microbial communities of clinically normal and diseased specimens of five species of affected corals using targeted 16S ribosomal DNA sequencing (Illumina MiSeq). Fifty-nine bacterial sequences were identified using contrast analysis that had enriched abundance in diseased coral host microbiomes relative to the microbiomes of clinically normal hosts. Several sequences from known bacterial pathogens were identified in this group. Additionally, we identified fifty-three bacterial species that had differentially elevated numbers in clinically normal coral host samples relative to samples from diseased host corals. The bacterial consortia composing the clinically normal and diseased coral microbiomes were clearly distinct taxonomically. Predicted functional profiles based on taxonomy, however, were found to be quite similar. This indicates a high level of functional redundancy among diseased and clinically normal microbiome members. Further examination of the direct sequencing data revealed that while some bacteria were differentially distributed according to disease status, others were not. Fifty-one bacterial species were found in both diseased and clinically normal coral host samples and not differentially abundant in either disease state. These still may be important in explaining the presentation of disease.IMPORTANCEDetermining causation is a management top priority to guide control and intervention strategies for the SCTLD outbreak. Towards this goal we examined bacterial taxa that were differentially elevated in numbers in diseased corals as compared to clinically normal corals at Looe Key, FL in August 2018. Many of the bacterial species we detected are known to be pathogenic to humans, animals, and (or) plants, and some of these have been found associated with diseased corals in other studies. Microbes that were present (or conspicuous by their absence) in both diseased as well as clinically normal corals were also examined because “healthy” corals from a diseased location such as Looe Key may have been exposed but may not have been showing overt disease at the time of sampling. Although untangling of causation is not possible currently, certain bacterial cliques and excess nutrients appear to be potential risk factors in SCTLD pathology.

scholarly journals Multi-Variate Analyses of Coral Mortality From the 2014–2015 Stony Coral Tissue Loss Disease Outbreak Off Miami-Dade County, Florida

2021 ◽  
Vol 8 ◽  
Author(s):  
Rachele Spadafore ◽  
Ryan Fura ◽  
William F. Precht ◽  
Steven V. Vollmer
Keyword(s):  
Coral Disease ◽  
Disease Outbreak ◽  
Coral Community ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Dade County ◽  
Coral Mortality ◽  
Monitoring Period ◽  
Stony Coral ◽  
The Impact

Environmental compliance monitoring associated with the Port Miami dredging project (2013–2015), designed to assess the impact of project-generated sediments on the local coral community, fortuitously captured a thermal bleaching event and the first reports of an emergent, highly contagious, white-plague-like coral disease outbreak in the fall of 2014. The disease, now termed stony coral tissue loss disease (SCTLD), has decimated reefs throughout Florida and is now spreading across the Caribbean. The high prevalence of disease, the number of affected species, and the high mortality of corals affected suggests SCTLD may be the most lethal coral disease ever recorded. Previous analyses of the dredge monitoring data have reached mixed conclusions about the relative impact of dredging on coral mortality and has often parsed out disease susceptible individuals to isolate the impacts of dredging only. We use multi-variate analyses, including time-based survival analyses, to examine the timing and impacts of dredging, coral bleaching, and disease on local coral mortality. By examining the status of corals monthly from the October 2013 to July 2015 observational period, we found that coral mortality was not significantly affected by a coral’s proximity to the dredge site or sediment burial. Instead, coral mortality was most strongly impacted by disease and the emergence of SCTLD during the monitoring period. During the 2-year monitoring period, 26.3% of the monitored corals died, but the only conditions significantly affected by the dredge were partial burial and partial mortality. The strongest link to mortality was due to disease, which impacted coral species differently depending on their susceptibility to SCTLD. The focus on disturbances associated with dredging created a circumstance where the greater impacts of this emergent disease were downplayed, leading to a false narrative of the resulting mortality on the local coral communities. The results of this study reveal that while local events such as a dredging project do have quantifiable effects and can be harmful to corals, regional and global threats that result in mass coral mortality such as thermal stress and disease represent an existential threat to coral reefs and must be urgently addressed.

scholarly journals White Syndrome-Affected Corals Have a Distinct Microbiome at Disease Lesion Fronts

2016 ◽  
Vol 83 (2) ◽  
Author(s):  
F. Joseph Pollock ◽  
Naohisa Wada ◽  
Gergely Torda ◽  
Bette L. Willis ◽  
David G. Bourne
Keyword(s):  
Disease Ecology ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Health States ◽  
Host Coral ◽  
Tissue Samples ◽  
Content Type ◽  
White Syndrome ◽  
Community Profiling

ABSTRACT Coral tissue loss diseases, collectively known as white syndromes (WSs), induce significant mortality on reefs throughout the Indo-Pacific, yet definitive confirmation of WS etiologies remains elusive. In this study, we integrated ecological disease monitoring, bacterial community profiling, in situ visualization of microbe-host interactions, and cellular responses of the host coral through an 18-month repeated-sampling regime. We assert that the observed pathogenesis of WS lesions on acroporid corals at Lizard Island (Great Barrier Reef) is not the result of apoptosis or infection by Vibrio bacteria, ciliates, fungi, cyanobacteria, or helminths. Histological analyses detected helminths, ciliates, fungi, and cyanobacteria in fewer than 25% of WS samples, and helminths and fungi were also observed in 12% of visually healthy samples. The abundances of Vibrio-affiliated sequences (assessed using 16S rRNA amplicon sequencing) did not differ significantly between health states and never exceeded 3.3% of reads in any individual sample. In situ visualization detected Vibrio bacteria only in summer WS lesion samples and revealed no signs of these bacteria in winter disease samples (or any healthy tissue samples), despite continued disease progression year round. However, a 4-fold increase in Rhodobacteraceae-affiliated bacterial sequences at WS lesion fronts suggests that this group of bacteria could play a role in WS pathogenesis and/or serve as a diagnostic criterion for disease differentiation. While the causative agent(s) underlying WSs remains elusive, the microbial and cellular processes identified in this study will help to identify and differentiate visually similar but potentially distinct WS etiologies. IMPORTANCE Over the past decade, a virulent group of coral diseases known as white syndromes have impacted coral reefs throughout the Indian and Pacific Oceans. This article provides a detailed case study of white syndromes to combine disease ecology, high-throughput microbial community profiling, and cellular-scale host-microbe visualization over seasonal time scales. We provide novel insights into the etiology of this devastating disease and reveal new diagnostic criteria that could be used to differentiate visually similar but etiologically distinct forms of white syndrome.

scholarly journals Changing Stony Coral Tissue Loss Disease Dynamics Through Time in Montastraea cavernosa

2021 ◽  
Vol 8 ◽  
Author(s):  
Greta Aeby ◽  
Blake Ushijima ◽  
Erich Bartels ◽  
Cory Walter ◽  
Joseph Kuehl ◽  
...  
Keyword(s):  
Common Species ◽  
Disease Prevalence ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Disease Dynamics ◽  
Western Atlantic ◽  
Fort Lauderdale ◽  
Stony Coral ◽  
Montastraea Cavernosa ◽  
Lesion Morphology

Stony coral tissue loss disease (SCTLD) is affecting corals across the Western Atlantic and displays species-specific and regional differences in prevalence, incidence, degree of mortality, and lesion morphology. We examined two Florida sites with different temporal histories of disease emergence; Fort Lauderdale where SCTLD is endemic and the Lower Florida Keys where SCTLD has recently emerged. Our objectives were to (1) assess the potential impact of SCTLD on overall reef condition by surveying reefs in each region, (2) in a single common species, Montastraea cavernosa, examine differences in SCTLD prevalence, colony mortality, and lesion morphology in each region, and (3) look for differences in contagion by conducting transmission experiments using lesions from each region. Reef surveys found sites in both regions had low coral cover, high algae cover, and similar coral species composition. SCTLD prevalence was higher in the Lower Keys than at Fort Lauderdale and two of the common species, M. cavernosa and S. siderea at Fort Lauderdale were dominated by smaller colonies (<5 cm) whereas larger colonies occurred in the Lower Keys. Tagged M. cavernosa SCTLD-affected colonies were followed for 2 years at one site in each region. In both years, Fort Lauderdale colonies showed declining disease prevalence, low colony mortality, and disease lesions were mainly bleached spots lacking tissue loss. In contrast, Lower Keys colonies tagged in the first year maintained 100% disease prevalence with high mortality, and disease lesions were predominantly tissue loss with no bleached edges. However, SCTLD dynamics changed, with year two tagged colonies showing declining disease prevalence, low mortality, and lesion morphology switched to a mixture of bleached polyps and tissue loss with or without bleached edges. Lesion morphology on colonies was a significant predictor of amount of tissue loss. Aquaria studies found the rate of SCTLD transmission using lesions from the different zones (emergent and endemic) were similar. Our study highlights that differences in coral mortality from SCTLD are not necessarily linked to host species, lesion morphology is reflective of subsequent rate of mortality, and disease dynamics change through time on reefs where the disease has newly emerged.

Reef-scale impacts of the stony coral tissue loss disease outbreak

Coral Reefs ◽  
2020 ◽  
Vol 39 (4) ◽  
pp. 861-866 ◽  
Author(s):  
Nuria Estrada-Saldívar ◽  
Ana Molina-Hernández ◽  
Esmeralda Pérez-Cervantes ◽  
Francisco Medellín-Maldonado ◽  
F. Javier González-Barrios ◽  
...  
Keyword(s):  
Disease Outbreak ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Stony Coral

scholarly journals Stony Coral Tissue Loss Disease in Florida Is Associated With Disruption of Host–Zooxanthellae Physiology

2020 ◽  
Vol 7 ◽  
Author(s):  
Jan H. Landsberg ◽  
Yasunari Kiryu ◽  
Esther C. Peters ◽  
Patrick W. Wilson ◽  
Noretta Perry ◽  
...  
Keyword(s):  
Body Wall ◽  
Chromatin Condensation ◽  
Periodic Acid ◽  
Clinical Signs ◽  
Host Cells ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Crystalline Inclusion ◽  
Periodic Acid Schiff ◽  
Stony Coral

Samples from eight species of corals (Colpophyllia natans, Dendrogyra cylindrus, Diploria labyrinthiformis, Meandrina meandrites, Montastraea cavernosa, Orbicella faveolata, Pseudodiploria strigosa, and Siderastrea siderea) that exhibited gross clinical signs of acute, subacute, or chronic tissue loss attributed to stony coral tissue loss disease (SCTLD) were collected from the Florida Reef Tract during 2016–2018 and examined histopathologically. The hallmark microscopic lesion seen in all eight species was focal to multifocal lytic necrosis (LN) originating in the gastrodermis of the basal body wall (BBW) and extending to the calicodermis, with more advanced lesions involving the surface body wall. This was accompanied by other degenerative changes in host cells such as mucocyte hypertrophy, degradation and fragmentation of gastrodermal architecture, and disintegration of the mesoglea. Zooxanthellae manifested various changes including necrosis (cytoplasmic hypereosinophilia, pyknosis); peripheral nuclear chromatin condensation; cytoplasmic vacuolation accompanied by deformation, swelling, or atrophy; swollen accumulation bodies; prominent pyrenoids; and degraded chloroplasts. Polyhedral intracytoplasmic eosinophilic periodic acid–Schiff-positive crystalline inclusion bodies (∼1–10 μm in length) were seen only in M. cavernosa and P. strigosa BBW gastrodermis in or adjacent to active lesions and some unaffected areas (without surface lesions) of diseased colonies. Coccoidlike or coccobacilloidlike structures (Gram-neutral) reminiscent of microorganisms were occasionally associated with LN lesions or seen in apparently healthy tissue of diseased colonies along with various parasites and other bacteria all considered likely secondary colonizers. Of the 82 samples showing gross lesions of SCTLD, 71 (87%) were confirmed histologically to have LN. Collectively, pathology indicates that SCTLD is the result of a disruption of host–symbiont physiology with lesions originating in the BBW leading to detachment and sloughing of tissues from the skeleton. Future investigations could focus on identifying the cause and pathogenesis of this process.

scholarly journals Stony Coral Tissue Loss Disease biomarker bacteria identified in corals and overlying waters using a rapid field-based sequencing approach

2021 ◽  
Author(s):  
Cynthia C. Becker ◽  
Marilyn Brandt ◽  
Carolyn A. Miller ◽  
Amy Apprill
Keyword(s):  
Coral Disease ◽  
The United States ◽  
Virgin Islands ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Rna Sequences ◽  
Disease Biomarker ◽  
Stony Coral ◽  
Ribosomal Rna Sequences ◽  
Reef Tract

AbstractStony Coral Tissue Loss Disease (SCTLD) is a devastating disease. Since 2014, it has spread along the entire Florida Reef Tract, presumably via a water-borne vector, and into the greater Caribbean. It was first detected in the United States Virgin Islands (USVI) in January 2019. To more quickly identify disease biomarker microbes, we developed a rapid pipeline for microbiome sequencing. Over a span of 10 days we collected, processed, and sequenced coral tissue and near-coral seawater microbiomes from diseased and apparently healthy Colpophyllia natans, Montastraea cavernosa, Meandrina meandrites and Orbicella franksi. Analysis of the resulting bacterial and archaeal 16S ribosomal RNA sequences revealed 25 biomarker amplicon sequence variants (ASVs) enriched in diseased tissue. These biomarker ASVs were additionally recovered in near-coral seawater (within 5 cm of coral surface), a potential recruitment zone for pathogens. Phylogenetic analysis of the biomarker ASVs belonging to Vibrio, Arcobacter, Rhizobiaceae, and Rhodobacteraceae revealed relatedness to other coral disease-associated bacteria and lineages novel to corals. Additionally, four ASVs (Algicola, Cohaesibacter, Thalassobius and Vibrio) were exact sequence matches to microbes previously associated with SCTLD. This work represents the first rapid coral disease sequencing effort and identifies biomarkers of SCTLD that could be targets for future SCTLD research.

scholarly journals Considering Commercial Vessels as Potential Vectors of Stony Coral Tissue Loss Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Nicholas A. Rosenau ◽  
Sarah Gignoux-Wolfsohn ◽  
Richard A. Everett ◽  
A. Whitman Miller ◽  
Mark S. Minton ◽  
...  
Keyword(s):  
Ballast Water ◽  
Management Strategies ◽  
Tissue Loss ◽  
Coral Tissue ◽  
Caribbean Region ◽  
Future Research ◽  
Ship Traffic ◽  
Marine Invasion ◽  
Stony Coral ◽  
Resource Managers

Stony coral tissue loss disease (SCTLD) is a troubling new disease that is spreading rapidly across the greater Caribbean region, but the etiological agent(s) and the mechanisms(s) of spread are both unknown. First detected off the coast of Miami, Florida, major ocean currents alone do not explain the pattern of spread, with outbreaks occurring across geographically disjunct and distant locations. This has raised concerns by researchers and resource managers that commercial vessels may contribute as vectors to spread of the disease. Despite existing regulatory and management strategies intended to limit coastal marine invasion risks, the efficacy of these measures is still unresolved for ship-borne microorganisms, and disease transport via ballast water and hull biofouling are under examination given the high ship traffic in the region. Here, to help inform the discussion of ships as possible vectors of SCTLD, we provide an overview of the current state of knowledge about ships and their potential to transfer organisms in the greater Caribbean, focusing in particular on ballast water, and outline a set of recommendations for future research.

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