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Stony coral tissue loss disease (SCTLD) is a highly contagious disease, causing mass coral mortalities in the Atlantic/Caribbean since 2014. In Puerto Rico, SCTLD was first reported in 2019 off the east coast, spreading to the north-central region by early February 2021. Benthic surveys were conducted at Cueva del Indio (CI) and Peñón de Mera (PM) off Arecibo to (1) quantify coral species-specific SCTLD prevalence using four 10 × 1-m2 belt transects and (2) acquire time-series photo and video surveys to illustrate the impact of SCTLD, to evaluate coral species-specific susceptibilities, and estimate the timing of onset in Arecibo. A total of 650 corals in six species (Pseudodiploria strigosa, P. clivosa, Montastraea cavernosa, Siderastrea siderea, Orbicella annularis, Porites astreoides) were recorded inside the belt transects at both sites. SCTLD prevalence varied between 54% (P. strigosa) and 35.5% (M. cavernosa) at CI, and between 87.5% (S. siderea) and 25% (O. faveolata) at PM. Photo/video surveys revealed that SCTLD caused partial mortality in 11 species and full mortality in P. strigosa, P. clivosa, S. siderea, M. cavernosa, and Dendrogyra cylindrus. The results are discussed in view of prior research and contribute to understanding the spread and impact of SCTLD around Puerto Rico, which can be applied to predict its spread to other regions in the Caribbean. 

As coral reefs face increasing threats from a variety of stressors, coral restoration has become an important tool to aid coral populations. A novel strategy for restoring boulder corals is microfragmentation, which may enhance coral growth by at least five times, depending on species and conditions. However, mortality rates are still significant during the early weeks after transplanting microfragments to impacted areas. We examined the effects of predation after transplanting fragments by cagingOrbicella faveolatamicrofragments and testing if field survival rates would increase after an acclimation period. We tracked the health and growth of ten genotypes across different acclimation periods from a control group of no acclimation (0 months) to full acclimation (4 months). After four months, we presented a mix of acclimated and unacclimated corals to reef predators. Coral survivorship was highest in acclimation cages (near 100%) compared to the field (p < 0.001), with significant growth differences across genotypes (p < 0.001). Microfragments also grew more in acclimation cages (p < 0.001), with rates slowing down in the first two months after being planted into the substrate. Microfragments that had been acclimated for longer than one month also showed comparatively higher survival rates, further supporting the importance of acclimation during restoration. These results suggest caging fragments boost coral survival during initial stages of restoration by > 50% and increase the persistence of transplanted fragments. Results also highlight the importance of identifying and prioritizing genotypes with high survival and growth rates. Beyond coral restoration, results demonstrate the possible negative ecological effects of corallivores, particularly parrotfishes, on recent transplants of fragments. 

For several decades, white plagues (WPDs: WPD-I, II and III) and more recently, stony coral tissue loss disease (SCTLD) have significantly impacted Caribbean corals. These diseases are often difficult to separate in the field as they produce similar gross signs. Here we aimed to compare what we know about WPD and SCTLD in terms of: (1) pathology, (2) etiology, and (3) epizootiology. We reviewed over 114 peer-reviewed publications from 1973 to 2021. Overall, WPD and SCTLD resemble each other macroscopically, mainly due to the rapid tissue loss they produce in their hosts, however, SCTLD has a more concise case definition. Multiple-coalescent lesions are often observed in colonies with SCTLD and rarely in WPD. A unique diagnostic sign of SCTLD is the presence of bleached circular areas when SCTLD lesions are first appearing in the colony. The paucity of histopathologic archives for WPDs for multiple species across geographies makes it impossible to tell if WPD is the same as SCTLD. Both diseases alter the coral microbiome. WPD is controversially regarded as a bacterial infection and more recently a viral infection, whereas for SCTLD the etiology has not been identified, but the putative pathogen, likely to be a virus, has not been confirmed yet. Most striking differences between WPD and SCTLD have been related to duration and phases of epizootic events and mortality rates. While both diseases may become highly prevalent on reefs, SCTLD seems to be more persistent even throughout years. Both transmit directly (contact) and horizontally (waterborne), but organism-mediated transmission is only proven for WPD-II. Given the differences and similarities between these diseases, more detailed information is needed for a better comparison. Specifically, it is important to focus on: (1) tagging colonies to look at disease progression and tissue mortality rates, (2) tracking the fate of the epizootic event by looking at initial coral species affected, the features of lesions and how they spread over colonies and to a wider range of hosts, (3) persistence across years, and (4) repetitive sampling to look at changes in the microbiome as the disease progresses. Our review shows that WPDs and SCTLD are the major causes of coral tissue loss recorded in the Caribbean. 

Diseases of tropical reef organisms is an intensive area of study, but despite significant advances in methodology and the global knowledge base, identifying the proximate causes of disease outbreaks remains difficult. The dynamics of infectious wildlife diseases are known to be influenced by shifting interactions among the host, pathogen, and other members of the microbiome, and a collective body of work clearly demonstrates that this is also the case for the main foundation species on reefs, corals. Yet, among wildlife, outbreaks of coral diseases stand out as being driven largely by a changing environment. These outbreaks contributed not only to significant losses of coral species but also to whole ecosystem regime shifts. Here we suggest that to better decipher the disease dynamics of corals, we must integrate more holistic and modern paradigms that consider multiple and variable interactions among the three major players in epizootics: the host, its associated microbiome, and the environment. In this perspective, we discuss how expanding the pathogen component of the classic host-pathogen-environment disease triad to incorporate shifts in the microbiome leading to dysbiosis provides a better model for understanding coral disease dynamics. We outline and discuss issues arising when evaluating each component of this trio and make suggestions for bridging gaps between them. We further suggest that to best tackle these challenges, researchers must adjust standard paradigms, like the classic one pathogen-one disease model, that, to date, have been ineffectual at uncovering many of the emergent properties of coral reef disease dynamics. Lastly, we make recommendations for ways forward in the fields of marine disease ecology and the future of coral reef conservation and restoration given these observations.