Karen Lynn Neely

Coral bleaching is an increasingly common and severe stressor to reefs that can result in mortality of wild and restoration colonies. One potential mitigation effort is the installation of shade structures that can minimize the synergistic UV stressor contributing to bleaching-related tissue loss. We tested the effect of temporarily installed in situ shade structures over wild colonies of two Caribbean species ( Pseudodiploria clivosa and Colpophyllia natans ) to determine whether they could mitigate bleaching, affect symbiont to host ratios, and alter symbiont community structure. Despite 2024 having the second highest cumulative heat stress on record at the study site, corals exhibited only moderate paling/bleaching. This is likely due to symbiont communities consisting almost exclusively of the heat-tolerant Durusdinium , a probable result of the unprecedented thermal stress the prior summer. However, even the moderate loss of color was remedied by the shade structures, preventing further paling/bleaching of experimental colonies after installation. The symbiont:host ratios exhibited moderate change through the thermal stress and recovery event, but the change was not affected by the presence of shades. We suggest that shading could be a relatively low-cost option for minimizing bleaching of high priority corals through a hyperthermal event.

Coral mortality resulting from hyperthermal bleaching events has and continues to be a major source of reef decline. Susceptibility to bleaching and associated coral death depends on abiotic as well as biotic variables and as such is known to vary widely both among reefs and within coral colonies. However, susceptibility to bleaching within individual reefs is poorly documented. Spatial variation in susceptibility could indicate abiotic variability within small spatial areas. It could also inform management actions such as likelihood of restoration outplant survival and where to focus bleaching mitigation strategies. We analyzed spatial patterns of bleaching-related mortality at two highly impacted Florida Keys patch reefs during the 2023 marine heatwave. We found significant spatial patterns and hot spots of mortality of Colpophyllia natans colonies at Cheeca Rocks and Pseudodiploria clivosa colonies at Newfound Harbor. We also found strong spatial patterning of black band disease within the same colonies at Cheeca Rocks that overlaid significantly on the bleaching-related mortality hot spots. Though fine-scale abiotic data from the 2023 event are absent, we deployed temperature logger arrays at Newfound Harbor in 2024 and 2025 and found large variation in temperature metrics throughout the site. Maximum degree heating weeks in 2025 ranged from 11.4 – 13.4, and the number of hours over 33.5 °C ranged from 19 to 50 depending on location within the site. These temperature metrics did not correlate well with whether individual colonies exhibited bleaching-related mortality in 2023. However, they were highly correlative with neighborhood means and hot/cold spot locations. This indicates that temperature may have driven neighborhood patterns of mortality, but also that individual colonies within those neighborhoods had varying susceptibilities. We suggest that reefs are likely to have much greater variability in temperature metrics than previously expected, and that this variability may influence the likelihood of bleaching-related mortality. Fate-tracking of individual corals through these events, including species-specific comparisons, can identify these spatial variations and provide valuable information for reef management during bleaching events.

The decimation of reefs from stony coral tissue loss disease prompted the use of a topical amoxicillin treatment to prevent coral mortality. Application of this treatment led to concerns about unintentional impacts such as potential alteration of the coral microbiome and possible spread of antibiotic resistance. We used three different methodologies—microbial RNA sequencing, 16S rRNA amplicon surveys, and microbial qPCR array—to assess these concerns and to establish a baseline of antibiotic resistance genes (ARGs) in untreated coral microbes. We conducted microbial RNA sequencing on wild Montastraea cavernosa coral mucus samples collected before and 24 h after amoxicillin application. While diverse antibiotic resistance genes (ARGs) were expressed, no differences in ARG expression were detected after amoxicillin treatment. Additionally, there were no notable changes in the microbial communities between the before and after samples. In a separate experiment, a microbial qPCR array was used to assess differences in ARGs over longer timescales using cores from wild Colpophyllia natans , comparing never-treated corals with ones treated a single time seven months prior and with those treated multiple times seven months and more prior. No clinically relevant ARGs were detected across any samples. A small number of above-detection reads (4 in the never-treated corals, 2 in the once-treated corals, and 0 in the multi-treated corals) may indicate weak amplification of similar environmental (non-anthropogenic) ARGs in the corals. Results indicate that the localized topical application of amoxicillin to prevent mortality of SCTLD-affected corals does not: (1) significantly disrupt microbiomes, (2) increase ARG expression in adjacent tissues of these species within 24 h, nor (3) increase abundance of clinically relevant ARGs over a 7 month time period.

Stony coral tissue loss disease (SCTLD) is widespread within the Caribbean and affects at least 22 species of reef-building coral. Bacteria have been implicated in the etiology of SCTLD, but the community of bacteria and archaea may also contribute to SCTLD resistance. To identify potential mechanisms through which microbes contribute to SCTLD resistance, we sequenced metagenomes from 41 colonies of the threatened coral, Orbicella faveolata, in the lower Florida Keys. All colonies were fate-tracked for 4 to 5 years, treated with amoxicillin if needed to prevent SCTLD-related mortality, and categorized into 4 health status categories following the monitoring period: never diseased (20%), diseased before sampling but recovered (10%), apparently healthy during sampling but eventually diseased (22%), and diseased (49%). Within the coral microbiome, diseased and yet-to-be diseased colonies exhibited higher variability in functional genes. In contrast, corals that remained unaffected or recovered had less variable microbiomes with greater abundances of vitamin and antibiotic biosynthesis, secretion system, and quorum-sensing genes that may support host health and resilience to pathogens. Despite repeated antibiotic treatments on some colonies, there was no effect on the diversity of beta-lactamases, antibiotic resistance genes that may confer amoxicillin resistance. Additional potentially probiotic gene clusters for the production of antimicrobial and bioactive compounds were present in many colonies regardless of fate. Taken together, we find significant putative probiotic functions in the coral microbiome to armor host O. faveolata corals against SCTLD infection, which may underpin intraspecific variation in stony coral tissue loss disease resilience and susceptibility.

Stony coral tissue loss disease (SCTLD) is widespread within the Caribbean and affects at least 22 species of reef-building coral. Bacteria have been implicated in the etiology of SCTLD, but the community of bacteria and archaea may also contribute to SCTLD resistance. To identify potential mechanisms through which microbes contribute to SCTLD resistance, we sequenced metagenomes from 41 colonies of the threatened coral, Orbicella faveolata, in the lower Florida Keys. All colonies were fate-tracked for three to five years and disease lesions were treated with amoxicillin. By 2024, 20% were never diseased, 10% had lesions before sampling but recovered, 22% were apparently healthy but were eventually susceptible to infection, and 49% had regular repeated infections. Within the coral microbiome, diseased and yet-to-be diseased colonies exhibited higher variability in functional genes. In contrast, corals that remained unaffected or recovered had less variable microbiomes with greater abundances of vitamin and antibiotic biosynthesis, secretion system, and quorum sensing genes that may support host health and resilience to pathogens. Though on some colonies antibiotic treatments were applied repeatedly, there was no effect on the diversity of beta-lactamases, antibiotic resistance genes that may confer amoxicillin resistance. Additional potentially probiotic gene clusters for the production of antimicrobial and bioactive compounds were present in many colonies regardless of fate. Taken together, we find significant probiotic potential in the coral microbiome to armor host O. faveolata corals against SCTLD infection, which may underpin intraspecific variation in stony coral tissue loss disease resilience and susceptibility.

Coral disease outbreaks are an increasingly common threat to reefs. While coral disease research is expanding rapidly, there are still monumental challenges in diagnosing and differentiating among the different diseases on a reef. We used a collaborative multidisciplinary approach to characterize a potentially novel disease affecting Orbicella faveolata colonies in the Florida Keys. We tagged and fate-tracked individual lesions for progression and cessation rates, reanalyzed in situ photographs of previously monitored corals to determine prevalence and seasonality, and assessed the efficacy of amoxicillin treatments. Samples collected from lesions as well as unaffected and healthy controls were used to examine microbiomes, assess nine coral pathological parameters via histology, and measure 19 symbiont-specific physiological metrics using transmission electron microscopy (TEM). Across all analyses, we concluded that the observed disease is unlikely to be SCTLD. Many, but not all, metrics had similarities to previous descriptions of white plague, and so we additionally conducted preliminary histology on presumed white plague samples of O. franksi for comparison. However, the dearth of quantifiable histology and TEM studies on white plague did not allow us to conclusively confirm or refute comparisons to white plague. Using the recommended coral disease nomenclature, we define this specific outbreak as "Orbicella acute tissue loss disease" (OATLD). We provide unprecedented, quantified descriptions across numerous metrics of both diseased and control colonies. We suggest that these data lay the groundwork for future efforts on this disease as well as a comprehensive set of parameters against which other diseases can be compared.

The unprecedented mortality to Caribbean corals caused by stony coral tissue loss disease (SCTLD) led to the use of an in-water medicine applied directly to disease lesions. This topical amoxicillin paste is highly effective in halting lesions and has been used on tens of thousands of wild corals since 2019, but long-term survival rates of treated corals as well as the frequency of potential reinfections remained speculative. We fate-tracked thousands of corals treated for SCTLD in the Florida Keys across numerous species and two habitats (inshore patch reefs and offshore spur and groove) every two months, assessing health condition and providing additional treatments if necessary. After three years, 84% of corals remained alive. Inshore corals had higher survival rates than offshore corals, and there were species-specific differences in survival, with the boulder corals Montastraea cavernosa and Orbicella faveolata having higher survivorship than brain coral species. Across all treated corals, 36% remained disease-free for at least one year after the initial treatment, and an additional 18% remained disease-free if any new lesions were treated within three months after the initial treatment. Reinfection rates were influenced by both habitat and species, with inshore corals more likely to remain disease-free than offshore corals. Among the species assessed, Montastraea cavernosa was the most likely to remain disease free, while the brain corals Diploria labyrinthiformis and Colpophyllia natans were the most prone to reinfection. These measurements can help guide expectations for disease intervention projects, including survival estimates if corals are regularly visited, as well as predictions of survivorship if diseased corals are visited only once or twice.

The population of pillar coral, Dendrogyra cylindrus, in Florida was decimated from 2013 to 2020, primarily by the emergence of stony coral tissue loss disease (SCTLD). Monitoring of survivors from 2021 to early 2025 showed that the population underwent an additional 96% decline in live tissue, a 78% loss in living colonies, and a 55% loss of genotypes. SCTLD continued to be the primary cause of these losses. Although some surviving tissue isolates exhibited small amounts of growth, the population remains extremely small, with only an estimated 9.6 m² of tissue remaining on 23 colonies (15 genotypes). Additionally, the colonies are far too dispersed to successfully fertilize spawned gametes. Further declines in the population since 2020 highlight the instability of the remnant population and underscore the value of the pillar coral rescue program and ongoing propagation efforts. As of February 2025, eight different in situ and ex situ facilities were caring for rescued D. cylindrus. Experimental fragmentation at one in situ nursery identified variable, but continually improving, growth rates across multiple fragmentation events. Sexual propagation efforts at an ex situ nursery documented 105 different rescue fragments spawning over 5 years. The smallest fragment was 9 cm × 7 cm × 9 cm, suggesting a potential “minimum colony size” for this species to have reproductive capacity. During these spawning events, 82 juveniles were being raised ex situ in early 2025. Two of these sexually propagated juveniles spawned 6 years after settlement, thus establishing a potential minimum age for reproduction.

The population of the pillar coral, Dendrogyra cylindrus , in Florida was decimated from 2013-2020, primarily by the emergence of stony coral tissue loss disease (SCTLD). Monitoring of survivors from 2021 – early 2025 showed that the population underwent an additional 96% decline in live tissue, 78% loss in living colonies, and 57% loss of genotypes. SCTLD continued to be the primary cause of these losses. Though some surviving tissue isolates exhibited small amounts of growth, the population remains extremely small, with only an estimated 9.6 square meters of tissue remaining on 23 colonies (15 genotypes). Additionally, colonies are far too dispersed to successfully fertilize spawned gametes. The further declines in the population since 2020 highlight the instability of the remnant population, as well as the value of the pillar coral rescue program and ongoing propagation efforts. As of February 2025, eight different in situ and ex situ facilities were caring for rescued D. cylindrus . Experimental fragmentation at one in situ nursery identified variable, but continually increasing, growth rates across multiple fragmentation events. Sexual propagation efforts at an ex situ nursery documented 105 different rescue fragments spawning across five years. The smallest fragment was 9 × 7 × 9 cm, establishing a potential “minimum colony size” for reproductive capacity for this species. From these spawning events, 82 juveniles were being raised ex situ in early 2025. Two of these sexually propagated juveniles spawned six years after settlement, thus establishing a potential minimum age for reproduction.

The unprecedented mortality to Caribbean corals caused by stony coral tissue loss disease (SCTLD) led to the use of an in-water medicine applied directly to disease lesions. This topical amoxicillin paste is highly effective in halting lesions and has been used on tens of thousands of wild corals since 2019, but long-term survival rates of treated corals as well as the frequency of potential reinfections remained speculative. We fate-tracked thousands of corals treated for SCTLD in the Florida Keys across numerous species and two habitats (inshore patch reefs and offshore spur and groove) every two months, assessing health condition and providing additional treatments if necessary. After three years, 84% of corals remained alive. Inshore corals had higher survival rates than offshore corals, and there were species-specific differences in survival, with the boulder corals Montastraea cavernosa and Orbicella faveolata having higher survivorship than brain coral species. Across all treated corals, 36% remained disease-free for at least one year after the initial treatment, and an additional 18% remained disease-free if any new lesions were treated within three months after the initial treatment. Reinfection rates were influenced by both habitat and species, with inshore corals more likely to remain disease-free than offshore corals. Among the species assessed, Montastraea cavernosa was the most likely to remain disease free, while the brain corals Diploria labyrinthiformis and Colpophyllia natans were the most prone to reinfection. These measurements can help guide expectations for disease intervention projects, including survival estimates if corals are regularly visited, as well as predictions of survivorship if diseased corals are visited only once or twice.