Stony coral tissue loss disease decimated Caribbean coral populations and reshaped reef functionality

The study investigates the ecological impacts of the emergent stony coral tissue loss disease (SCTLD) on Caribbean coral reefs. Disease outbreaks have historically caused mass mortalities of foundation species on reefs, notably the late-1970s white-band disease that reduced Acropora populations by ~80% and diminished reef functionality. SCTLD emerged in Florida in 2014 and rapidly spread throughout the Caribbean, affecting nearly 30 coral species with high virulence. Although its etiology is not fully resolved, evidence suggests a multifactorial origin involving environmental conditions and pathogen-induced dysbiosis. The authors ask whether post-SCTLD coral assemblages can maintain key ecological functions, particularly reef physical functionality (three-dimensional structure and calcium carbonate production), given the Caribbean’s inherently low functional redundancy. Using pre- and post-outbreak data along a 450-km stretch of the Mexican Caribbean, they evaluate disease prevalence, environmental and anthropogenic correlates, and consequences for community composition, functional diversity, and community calcification.

Prior work documents that Caribbean reefs are disease hotspots where outbreaks (e.g., white-band, white plague, Caribbean yellow band) have driven severe declines of primary reef-builders, reshaping habitat complexity and ecosystem services. The 1970s white-band disease caused region-wide losses of Acropora palmata and A. cervicornis (~80%), leading to reduced reef functionality. Disease frequency and severity are linked to human-driven stressors, including nutrient enrichment, reduced water quality, and other local impacts, while the direct role of high temperatures in SCTLD prevalence appears limited. SCTLD has been reported across the Western Caribbean, Bahamas, Puerto Rico, and the US Virgin Islands, affecting ~30 species and progressing rapidly. Previous studies highlight low functional diversity and redundancy in the Caribbean, meaning a few species disproportionately support physical functionality. This context frames concerns that SCTLD-induced losses of key massive and brain corals could further erode functional diversity and carbonate production.

Study design and surveys: The authors assessed SCTLD impacts in the Mexican Caribbean using extensive pre- (2016) and post-outbreak (July 2018–January 2020) field surveys along a ~450-km reef tract. They surveyed 27 locations comprising 82 reef sites during the post-outbreak period; 35 sites had been surveyed pre-outbreak and were resampled to allow before–after comparisons. Surveys were conducted in back-reef and fore-reef zones from ~1 to 24 m depth using 10 × 1 m haphazardly placed belt transects. For each living colony within transects, they recorded species identity, colony size metrics (maximum size, mean height), percent cover, bleaching, mortality (new/transition/old), and signs consistent with SCTLD. Colonies with recent mortality attributable to SCTLD were counted as affected; bleaching was distinguished from SCTLD by the presence/absence of living but pale tissue. Only 241 of ~29,955 post-outbreak colonies showed other diseases; no other outbreak was detected, so mortality was attributed to SCTLD. Disease prevalence and predictors: SCTLD prevalence was calculated as the proportion of diseased plus recently dead colonies. Analyses emphasized highly susceptible species (those with >10% disease prevalence). To identify correlates of disease prevalence, the authors modeled the percentage of affected colonies as a function of colony density, reef structural complexity, zonation, depth, wind exposure (leeward/windward), coastal development intensity, coastal water quality proxies (land-based nutrient inputs), and marine protected area (MPA) age. Site and reef sector were treated as random effects to account for spatial structure and repeated sampling; species identity and sampling size were included to account for species-level responses and effort. Logistic mixed models (glmer, merTools in R) with standardized predictors (z-scores) were used; significance was evaluated at α = 0.05 with 95% confidence intervals. Community composition and functional diversity: The functional diversity of coral communities was characterized using six traits: skeletal density, growth rate, rugosity index, colony size, reproduction strategy, and corallite width (or closely related morphological/functional descriptors per their trait database). Traits were categorized (1–5) to build a multidimensional functional space. Hierarchical clustering based on Gower dissimilarities (average linkage) defined morpho-functional groups. A SIMPER analysis quantified species’ contributions to within-period similarities and between-period dissimilarities. Principal component analyses (PCA) evaluated shifts in assemblages at family and species levels, and community-weighted means (CWM) of traits assessed functional trait shifts. Functional indices included functional richness (FRic; convex hull volume) and functional evenness (FEve). Paired Welch’s t-tests compared pre- and post-outbreak values across the 35 resampled sites. Community calcification: To estimate changes in reef physical functionality, the authors calculated coral community calcification (kg or g CaCO3 m−2 y−1) by combining species’ colony size, morphological growth form, mean linear extension (growth rate), and skeletal density following established approaches (e.g., González et al.). Site-level community calcification was computed for pre- and post-outbreak periods, and differences were tested statistically (t-tests). All analyses were conducted in R (v4.1.0) with ggplot2 for visualization; data and code are available in Supplementary Data and GitHub.

Spread and prevalence: SCTLD spread across hundreds of kilometers in months. Across 29,095 colonies surveyed (Jul 2018–Jan 2020), 17% were already dead with recent signs and an additional 10% were diseased. Twenty-five of 48 recorded species were impacted. Mortality among 21 afflicted species ranged from <10% to 94%; most Meandrinidae and Faviinae sustained >50% losses. Highly susceptible species such as Dendrogyra cylindrus and Meandrina meandrites exhibited high prevalence and severe population declines; many colonies of highly susceptible species likely died and were rapidly overgrown by algae/sediment, underestimating post-outbreak detection. Environmental and anthropogenic drivers: Disease prevalence in highly susceptible species did not differ significantly by depth, zonation, structural complexity, or coral density, suggesting waterborne transmission within and among reefs. Prevalence was significantly higher at sites near coastal development; windward exposure and MPA age were also associated with higher prevalence. Banco Chinchorro, an isolated offshore bank with minimal human infrastructure and strong current separation, remained unaffected at least until December 2021; removing these reefs from analyses retained coastal development as a significant predictor. Community composition: Reefs were already dominated pre-outbreak by encrusting/submassive agaricids and Porites astreoides. Post-outbreak, these groups increased further, accounting for 63.33% and 71.81% of within-period similarity before and after, respectively. Their relative increases explained 50.42% of the dissimilarity between periods, while decreases of highly susceptible (often rarer) species explained 13.06%. Functional diversity and traits: Trait-based analyses revealed a contraction in functional space and homogenization of assemblages. Functional richness declined (t = 2.67, d.f. = 46.04, p = 0.01) and functional evenness declined (t = 3.81, d.f. = 65.54, reported p > 0.01 in text). Apparent species richness increased (t = 2.36, d.f. = 65.19, p = 0.21), likely reflecting increased sampling effort rather than true recovery. Despite low absolute abundance, acroporids emerged as notable functional elements in the post-outbreak trait space due to the reduced contributions of many other species. Community calcification and functionality: Coral community calcification declined markedly, from 4.60 ± 0.77 g CaCO3 m−2 y−1 pre-outbreak to 3.27 ± 0.53 g post-outbreak (t = −3.40, d.f. = 34, p = 0.004), approximately a 30% reduction. Losses were largely driven by declines in highly susceptible species (from 3.04 ± 0.62 to 1.91 ± 0.34). The shift toward weedy, stress-tolerant taxa with simpler morphologies and slower growth further reduced physical functionality.

The findings demonstrate that SCTLD precipitated rapid, widespread mortality across the Mexican Caribbean, disproportionately affecting functionally important massive and brain corals. This non-random loss compressed functional trait space, reduced functional richness and evenness, and substantially lowered coral community calcification. Consequently, key ecological functions reliant on live reef builders—including three-dimensional habitat maintenance, sediment generation, and carbonate production needed to keep pace with sea-level rise—are compromised. The absence of strong effects of depth, zonation, structural complexity, or coral density on prevalence supports a waterborne, rapidly transmissible agent, while higher prevalence near developed coasts implicates anthropogenic stressors (e.g., nutrient enrichment, poorer water quality) in modulating vulnerability and progression. Although acroporids appear as prominent functional vectors in post-outbreak ordinations, their absolute populations remain depressed relative to historical baselines, limiting their capacity to restore functionality. Without recovery, bioerosion and skeletal dissolution could outpace carbonate production, pushing reefs toward net framework loss. Regionally, overlapping species distributions suggest similar consequences across the Caribbean, elevating extinction risk for highly susceptible taxa and genetic bottlenecks for families such as Meandrinidae and the Faviinae. Management will need to address both disease dynamics and chronic local stressors to preserve or restore reef functionality.

SCTLD has rapidly decimated key Caribbean reef-building corals, reshaping assemblages toward weedy, stress-tolerant taxa and triggering substantial losses in functional diversity and coral community calcification. The outbreak, likely to become the most lethal disturbance recorded in the Caribbean, is driving a shift to a new functional regime with diminished physical functionality, even as acroporids reappear as notable functional elements at low abundance. To safeguard reef ecosystem services, actions should prioritize reducing land-based stressors (e.g., improving coastal water quality), targeted conservation of vulnerable species (e.g., rescue and ex situ preservation of genetic material), and facilitating recovery processes (e.g., enhancing recruitment and reducing macroalgal dominance). Future research should clarify SCTLD etiology and transmission pathways, quantify the role of anthropogenic drivers in disease dynamics, refine estimates of carbonate budget changes under ongoing bioerosion and warming, and evaluate the efficacy of intervention strategies to restore functional reef frameworks.

The study is observational and region-specific to the Mexican Caribbean, which may limit direct generalization across the entire Caribbean despite similar species ranges. Mortality was attributed to SCTLD given the absence of other detected outbreaks; however, some misattribution cannot be completely excluded. Rapid algal/sediment overgrowth of dead colonies likely led to underestimation of total mortality and prevalence, especially for highly susceptible species. Sampling effort differed between periods (greater post-outbreak), potentially inflating apparent species richness. Some reported statistics (e.g., p-value for functional evenness) appear inconsistent in the text. Environmental covariates such as nutrient inputs and coastal development were represented by proxies and may not capture all relevant local-scale variability. Banco Chinchorro’s lack of disease through 2021 affected model inferences; removing these sites changed some effect sizes. The temporal window (pre-2016 vs. 2018–2020) may not fully capture longer-term dynamics, recruitment, or delayed disease effects.