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Stony coral tissue loss disease (SCTLD) is destructive and poses a significant threat to Caribbean coral reef ecosystems. Characterized by the acute loss of coral tissue, SCTLD has impacted over 22 stony coral species across the Caribbean region, leading to visible declines in reef health. Based on the duration, lethality, host range, and spread of this disease, SCTLD is considered the most devastating coral disease outbreak ever recorded. Researchers are actively investigating the cause and transmission of SCTLD, but the exact mechanisms, triggers, and etiological agent(s) remain elusive. If left unchecked, SCTLD could have profound implications for the health and resilience of coral reefs worldwide. To summarize what is known about this disease and identify potential knowledge gaps, this review provides a holistic overview of SCTLD research, including species susceptibility, disease transmission, ecological impacts, etiology, diagnostic tools, host defense mechanisms, and treatments. Additionally, future research avenues are highlighted, which are also relevant for other coral diseases. As SCTLD continues to spread, collaborative efforts are necessary to develop effective strategies for mitigating its impacts on critical coral reef ecosystems. These collaborative efforts need to include researchers from diverse backgrounds and underrepresented groups to provide additional perspectives for a disease that requires creative and urgent solutions. 

East and West Flower Garden Bank (FGB) are part of Flower Garden Banks National Marine Sanctuary (FGBNMS) in the northwest Gulf of Mexico. This geographically-isolated reef system contains extensive coral communities with the highest coral cover (>50%) in the continental United States due, in part, to their remoteness and depth, and have historically exhibited low incidence of coral disease and bleaching despite ocean warming. Yet in late August 2022, disease-like lesions on seven coral species were reported during routine monitoring surveys on East and West FGB (2.1–2.6% prevalence). A series of rapid response cruises were conducted in September and October 2022 focused on 1) characterizing signs and epidemiological aspects of the disease across FGB and within long-term monitoring sites, 2) treating affected coral colonies with Base 2B plus amoxicillin, and 3) collecting baseline images through photostations and photomosaics. Marginal and/or multi-focal lesions and tissue loss were observed, often associated with substantial fish and invertebrate predation, affecting the dominant coral species Pseudodiploria strigosa (7–8% lesion prevalence), Colpophyllia natans (11–18%), and Orbicella spp. (1%). Characterizing this disease event during its early epidemic phase at East and West FGB provides a critical opportunity to observe how coral disease functions in a relatively healthy coral ecosystem versus on reefs chronically affected by various stressors (e.g., Caribbean reefs adjacent to urban centers). Insights into the etiology, spread, and impacts of the disease can ultimately inform efforts to mitigate its effects on coral communities. 

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. 

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.