Metabolomics of Healthy and Stony Coral Tissue Loss Disease Affected Montastraea cavernosa Corals

Stony coral tissue loss disease, first observed in Florida in 2014, has now spread along the entire Florida Reef Tract and on reefs in many Caribbean countries. The disease affects a variety of coral species with differential outcomes, and in many instances results in whole-colony mortality. We employed untargeted metabolomic profiling of Montastraea cavernosa corals affected by stony coral tissue loss disease to identify metabolic markers of disease. Herein, extracts from apparently healthy, diseased, and recovered Montastraea cavernosa collected at a reef site near Ft. Lauderdale, Florida were subjected to liquid-chromatography mass spectrometry-based metabolomics. Unsupervised principal component analysis reveals wide variation in metabolomic profiles of healthy corals of the same species, which differ from diseased corals. Using a combination of supervised and unsupervised data analyses tools, we describe metabolite features that explain variation between the apparently healthy corals, between diseased corals, and between the healthy and the diseased corals. By employing a culture-based approach, we assign sources of a subset of these molecules to the endosymbiotic dinoflagellates, Symbiodiniaceae. Specifically, we identify various endosymbiont- specific lipid classes, such as betaine lipids, glycolipids, and tocopherols, which differentiate samples taken from apparently healthy corals and diseased corals. Given the variation observed in metabolite fingerprints of corals, our data suggests that metabolomics is a viable approach to link metabolite profiles of different coral species with their susceptibility and resilience to numerous coral diseases spreading through reefs worldwide.

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

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.

Measuring Stony Coral Tissue Loss Disease Induction and Lesion Progression Within Two Intermediately Susceptible Species, Montastraea cavernosa and Orbicella faveolata

During the last several decades, Florida’s Coral Reef (FCR) has been impacted by both global and local stressors that have devastated much of its living coral cover. Additionally, since 2014 FCR has experienced a lethal disease outbreak termed stony coral tissue loss disease (SCTLD). Here, we examined SCTLD spreading dynamics within and among fragmented coral colonies and quantified lesion progression rate of two intermediately susceptible species—Montastraea cavernosa and Orbicella faveolata—through induction experiments conducted in laboratory aquaria. M. cavernosa colonies showing subacute tissue loss were sequentially fragmented parallel to the lesion edge to determine whether isolated tissue that showed no tissue-loss signs, referred to as isolated apparently healthy (AH) donor fragments, would subsequently exhibit tissue loss. Additionally, AH M. cavernosa and O. faveolata fragments, referred to as recipient fragments, were placed in direct contact with the M. cavernosa donor fragments to assess incidence of new tissue-loss lesions. Finally, AH M. cavernosa donor fragments were placed in direct contact with recipient M. cavernosa and O. faveolata fragments to account for aggression from direct contact. Samples were collected for histopathology of the corals through time. Many isolated AH donor fragments developed tissue-loss lesions during the 60-day study, suggesting SCTLD may be systemic within small-sized colonies. Our results confirmed that physical contact between recipient fragments and subacute SCTLD-lesioned tissue often led to tissue loss in recipient fragments. None of the control recipient or donor fragments experienced tissue loss. Grossly, multifocal lesions started on or adjacent to the septal and costal basal body walls with tissue loss progressing across the polyp septa and coenenchyme, respectively, in both species. Histologically, initial tissue-loss lesions in both species exhibited characteristic lytic necrosis (LN) at the basal body wall of the gastrodermis. O. faveolata exhibited higher rates of lesion appearance and subsequent mortality compared to M. cavernosa, but once a lesion appeared, M. cavernosa lost tissue faster than O. faveolata. This work contributes to the growing knowledge of SCTLD dynamics and highlights the differences in lesion progression within susceptible species.

Metabolomics of healthy and stony coral tissue loss disease affected Montastraea cavernosa corals

Stony coral tissue loss disease, first observed in Florida in 2014, has now spread along the entire Florida Reef Tract and on reefs in many Caribbean countries. The disease affects a variety of coral species with differential outcomes, and in many instances results in whole-colony mortality. We employed untargeted metabolomic profiling of Montastraea cavernosa corals affected by stony coral tissue loss disease to identify metabolic markers of disease. Herein, extracts from apparently healthy, diseased, and recovered corals, Montastraea cavernosa, collected at a reef site near Ft. Lauderdale, Florida were subjected to liquid-chromatography mass spectrometry-based metabolomics. Unsupervised principal component analysis reveals wide variation in metabolomic profiles of healthy corals of the same species, which differ from diseased corals. Using a combination of supervised and unsupervised data analyses tools, we describe metabolite features that explain variation between the apparently healthy corals, between diseased corals, and between the healthy and the diseased corals. By employing a culture-based approach, we assign sources of a subset of these molecules to the endosymbiotic dinoflagellates, Symbiodiniaceae. Specifically, we identify various endosymbiont- specific lipid classes, such as betaine lipids, glycolipids, and tocopherols, which differentiate samples taken from apparently healthy corals and diseased corals. Given the variation observed in metabolite fingerprints of corals, our data suggests that metabolomics is a viable approach to link metabolite profiles of different coral species with their susceptibility and resilience to numerous coral diseases spreading through reefs worldwide.

Synergistic Effects of Thermal Stress and Estuarine Discharge on Transcriptomic Variation of Montastraea cavernosa Corals in Southeast Florida

Coral reefs at the northern extent of Florida’s coral reef tract are exposed to many localized anthropogenic influences including controlled freshwater discharges, runoff, upwelling, and seasonal environmental variability. To better understand coral responses to sublethal stressors in nearshore environments, we conducted complementary experiments to assess the impacts of estuarine runoff and temperature stress on local populations of the scleractinian coral species, Montastraea cavernosa, using Tag-Seq global gene expression profiling. In an in situ time series experiment, fate-tracked colonies were sampled during periods of relatively low and high estuarine discharge over 4 years to investigate temporal trends in transcriptional patterns and to identify if coral stress indicators were regulated through time. There was significant transcriptomic variation through time, but patterns did not appear to be attributed to distance from nearby estuarine tidal flux. In an ex situ factorial experiment, clonal replicates of coral genotypes were exposed to temperature (25°C and 30°C) and water (offshore and estuarine discharge, representing typical oceanic conditions and episodic discharge conditions, respectively) treatments to quantify the potential individual and synergistic effects of sublethal stress on coral and algal gene expression. Comparative analyses suggested that corals and their algal symbionts were more responsive to thermal stress than to estuarine discharge, although there was evidence of a synergistic relationship between the two stressors. Strong genotype effects also demonstrated that transcriptomic responses to thermal stress were largely based on coral genotype, indicating the potential for stress resilience among certain members of coral populations from southeast Florida.

Assessing the effectiveness of two intervention methods for stony coral tissue loss disease on Montastraea cavernosa

Stony coral tissue loss disease (SCTLD) was first observed in Florida in 2014 and has since spread to multiple coral reefs across the wider Caribbean. The northern section of Florida’s Coral Reef has been heavily impacted by this outbreak, with some reefs experiencing as much as a 60% loss of living coral tissue area. We experimentally assessed the effectiveness of two intervention treatments on SCTLD-affected Montastraea cavernosa colonies in situ. Colonies were tagged and divided into three treatment groups: (1) chlorinated epoxy, (2) amoxicillin combined with CoreRx/Ocean Alchemists Base 2B, and (3) untreated controls. The experimental colonies were monitored periodically over 11 months to assess treatment effectiveness by tracking lesion development and overall disease status. The Base 2B plus amoxicillin treatment had a 95% success rate at healing individual disease lesions but did not necessarily prevent treated colonies from developing new lesions over time. Chlorinated epoxy treatments were not significantly different from untreated control colonies, suggesting that chlorinated epoxy treatments are an ineffective intervention technique for SCTLD. The results of this experiment expand management options during coral disease outbreaks and contribute to overall knowledge regarding coral health and disease.

Recovery from finfish predation on newly outplanted boulder coral colonies on three reefs in the Florida Keys

Corals throughout the Caribbean have experienced major declines since the 1970s. In response, many agencies have focused their conservation and restoration efforts on outplanting nursery-grown coral fragments onto degraded reefs. Predation on newly outplanted corals can be an important but often unmonitored factor contributing to the declining health and survival of these fragments. In this study, we outplanted 360 boulder coral fragments (Montastraea cavernosa, Orbicella faveolata, Pseudodiploria clivosa), sourced from both ex situ and in situ nurseries, at three locations in the Florida Keys. Each location included one inshore and one offshore site. Ten fragments of each species and source were outplanted at each site (60 corals per site). Transplants were monitored for finfish predation, live tissue area, and survival at 1, 2, 6, and 12 wks post-outplanting. We found the highest finfish predation for all species during the first week monitoring period. Predation during this first week varied by location and reef type, with two locations showing higher predation on offshore sites and one location experiencing increased predation on the inshore site. We also found that coral fragments produced in the ex situ nursery experienced higher initial predation compared to fragments produced in the in situ nursery. However, overall coral survival at 12 wks post-outplanting was 96%, suggesting there was no effect of initial predation on survival. Our results indicate that coral restoration efforts may be affected by intense, initial predation on newly-outplanted boulder coral colonies, but this initial predation may not lead to an increase in mortality.