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Stony Coral Tissue Loss Disease (SCTLD) impacts are unprecedented concerning the level of devastation they have imposed on Caribbean coral assemblages. Although SCTLD affects nearly 30 different coral species, it has been particularly lethal for Pseudodiploria strigosa. Mortality rates for this species are estimated to be between 60 and 100% in the Caribbean; however, tissue-loss rates have been shown to differ among colonies, which suggests that colony health, environmental conditions, and concurrent transmission events are crucial to the development of the disease at reef scale. To gain insight into the colony-level dynamics of SCTLD, we used a simplified photogrammetry and 3D modeling approach to quantify and compare SCTLD-related tissue-loss rates among 20 colonies of P. strigosa on a shallow back-reef in the Mexican Caribbean. Over a six-month period, SCTLD resulted in the full mortality of 70% of the colonies that were tagged shortly after infection. Although disease progression followed a multifocal-type infection in most cases, tissue-loss rates significantly differed among colonies. Some colonies died within the first 20 days of observation, while others died towards the end of the study period. We found a significant positive effect of colony size on rates of tissue loss disease, as well as evidence suggesting that elongated and vertically compressed colonies have a greater probability of experiencing higher tissue-loss rates than colonies with more spherical shapes. The observed relationship between colony morphology and tissue-loss rates is likely a result of elongated colonies having more flat surface area at the top of the colonies which facilitates accumulation of sediments, which have been shown to be a source of SCTLD transmission.

Although knowledge on the diseases affecting corals has been accumulating exponentially since the 2000s, even more effort is required to summarize and guide further investigation. Here, we used the Web of Science database to review 226 studies published, between 2000 and 2020, to identify the major geographic and taxonomic gaps in the literature, and propose future directions for the study of coral diseases. We classified the studies according to the ocean, ecoregion, coral species, disease types, approach (e.g., observational or experimental), and depth. In total, 22 types of diseases were reported for 165 coral species. Acropora spp. was the most studied taxa with 12 types of diseases and 8.2% of the records. Black band, white plague, white syndromes, skeletal eroding, dark spot, and yellow band were the six most common diseases, accounting together for 76.8% of the records. As expected, most studies were conducted in the Caribbean and Indo-Pacific (34.0% and 28.7%, respectively), but only in 44 of the 141 global ecoregions that harbour corals. Observational approaches were the most frequent (75.6% of the records), while experimental approaches accounted for 19.9% and were mainly done on Acropora. The vast majority of studies (∼98%) were performed in shallow waters (

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.

We analyzed the spatial distribution patterns of a white syndrome (WS) outbreak affecting Pseudodiploria strigosa colonies in the northern Mexican Caribbean during 2018–2019. The purpose of the study was to describe the outbreak progression in a single species and determine if this WS incidence is related to the nearest diseased neighbor distance. Two separated sites with different P. strigosa colonial densities (Bocana: 0.08 col/m2; Picudas: 0.2 col/m2) were selected in similar habitats of the same reef complex. P. strigosa colonies within the survey sites were mapped, and their status was recorded (healthy, diseased, or dead) in sequential surveys until colonies died or the study terminated (306 days). Spatial distribution modes were assessed using Ripley’s K function. The spatial colony distribution was random in one site (Bocana) and clustered in the other (Picudas). However, the WS disease incidence per survey was randomly distributed in both sites throughout the observation period of the outbreak, suggesting that WS transmission at small spatial scales was independent of the colony distribution pattern and from the nearest diseased colonies. Survival probability since WS onset in surveyed colonies was different: 0% at Bocana and 14% at Picudas by April 2019. But, eventually, all diseased colonies died in both sites. WS outbreak timing was different at the two sites: Initial prevalence 8% at the Bocana site vs. 44% at Picudas site. Distribution of time to disease onset shown multimodality, with modes varying from 17 to 184 days and wide main modes amplitude suggest a highly variable resistance to the WS. Disease incidence was not abated during winter surveys. Differences between sites in the WS disease outbreak distribution and progression suggest that colony condition, environmental quality, and perhaps several transmission events played an essential role in the complex outbreak dynamics at the local spatial scale of our study.

Stony coral tissue loss disease (SCTLD) has persisted since 2014 in the Southeast Florida Coral Reef Ecosystem Conservation Area (Coral ECA) where it was first discovered. Most of the highly susceptible corals have perished, leaving Montastraea cavernosa as the most abundant reef-building species with high SCTLD prevalence. Disease interventions (DI) have been conducted throughout Florida’s Coral Reef to save the remaining corals and reduce the disease prevalence with varying degrees of success. The two main treatments were chlorinated (Chl) epoxy and an antibiotic paste. The antibiotic paste was highly effective in the Florida Keys, but its effectiveness in the Coral ECA was questionable. Therefore, we compared the effectiveness of the antibiotic paste and Chl epoxy treatments on M. cavernosa to optimize DI efforts on this species in the Coral ECA. Significant differences were found between the treatment materials and applications related to the proportion of quiesced lesions and corals where antibiotic paste (91.2% success) outperformed Chl epoxy (20% success). By day 351, 50.6% of the antibiotic paste disease-break tissue was fully healed compared to 2.2% of the total Chl epoxy-filled disease-break area. During the study, new lesions occurred on previously treated colonies, as well as colonies not previously treated and new lesion rates varied through time, indicating revisitation is necessary to eliminate disease. Most margin treatments failed within the first 9 days, however, most disease-breaks failed before 44 days. Considering the high treatment success of the antibiotic paste and the conditional variation of new lesion rates, about 1 month is a good practical re-visitation time for retreating failures and any new lesions. DI using antibiotic paste is currently the most effective way to intervene the SCTLD epidemic, but this is only effective as a stopgap measure while the larger causative agents are identified and remediated. Conducting DI at a reef-scape scale is time consuming and requires extensive person-power and resources, making it very expensive. But this expense pales in comparison to the current cost to restore the diversity and live tissue saved with DI. This method also comes with the risk of introducing antibiotics into coral reef environments, which may have unintended outcomes.

In the Caribbean, disease outbreaks have emerged as significant drivers of coral mortality. Stony Coral Tissue Loss Disease (SCTLD) is a novel white plague-type disease that was first reported off the Florida coast in 2014. This disease affects >20 coral species and is spreading rapidly throughout the Caribbean. In December 2018, SCTLD reached southwestern (SW) Cozumel, one of the healthiest reef systems in the Caribbean. In this study, we integrate data from multiple survey protocols conducted between July 2018 and April 2020 to track the progression of the outbreak in SW Cozumel and to quantify the impacts of SCTLD on coral communities and the benthic composition of reefs. Given that the SCTLD outbreak coincided with a period of prolonged thermal stress that concluded in widespread coral bleaching in autumn 2019, we also investigated whether this event further exacerbated coral mortality. Our findings show that SCTLD spread throughout SW Cozumel in only 2 months and reached a peak after only 5 months. By the summer of 2019, most of the afflicted corals were already dead. Species of the families Meandrinidae, Faviinae, and Montastraeidae showed 33–95% mortality. The widespread coral die-off caused an overall loss of 46% in coral cover followed by a rapid increase of algae cover across all surveyed reefs that persisted until at least April 2020. In November 2019, more than 15% of surveyed coral colonies were bleached. However, we did not find that bleaching further increased coral mortality at either the colony or the community level, which suggests that the coral communities were able to recover from this event despite still being affected by the disease. In conclusion, SCTLD is radically changing the ecology of coral reefs by decimating the populations of several key reef-builders and reconfiguring the benthic assemblages. The actions needed to restore coral populations have to be accompanied by stringent controls related to the effects of climate change, coastal development, and wastewater treatment to improve coral conditions and ecosystem resilience.

Caribbean reef corals have experienced unprecedented declines from climate change, anthropogenic stressors and infectious diseases in recent decades. Since 2014, a highly lethal, new disease, called stony coral tissue loss disease, has impacted many reef-coral species in Florida. During the summer of 2018, we noticed an anomalously high disease prevalence affecting different coral species in the northern portion of the Mexican Caribbean. We assessed the severity of this outbreak in 2018/2019 using the AGRRA coral protocol to survey 82 reef sites across the Mexican Caribbean. Then, using a subset of 14 sites, we detailed information from before the outbreak (2016/2017) to explore the consequences of the disease on the condition and composition of coral communities. Our findings show that the disease outbreak has already spread across the entire region by affecting similar species (with similar disease patterns) to those previously described for Florida. However, we observed a great variability in prevalence and tissue mortality that was not attributable to any geographical gradient. Using long-term data, we determined that there is no evidence of such high coral disease prevalence anywhere in the region before 2018, which suggests that the entire Mexican Caribbean was afflicted by the disease within a few months. The analysis of sites that contained pre-outbreak information showed that this event considerably increased coral mortality and severely changed the structure of coral communities in the region. Given the high prevalence and lethality of this disease, and the high number of susceptible species, we encourage reef researchers, managers and stakeholders across the Western Atlantic to accord it the highest priority for the near future.

The direct impacts of coral diseases on coral populations have been assessed by quantifying coral tissue loss and colony mortality, but the determination of the indirect effects of diseases, such as disruptions in life history functions (e.g. reproduction, growth and maintenance), are more difficult to ascertain and have been scant. This study involved a comparison of various measures of reproductive output from histological slides of healthy tissue samples of Montastraea faveolata and tissue samples from colonies with white plague (WP) infections in Dominica (West Indies). Although the variability in the reproductive data was high, WP had significant negative impacts on the percentage of reproductive polyps per cm2, the percentage of reproductive mesenteries within a polyp, oocyte quantity per polyp, mean oocyte volume (mm3), and fecundity (oocyte volume per cm2 of tissue). However, these effects were only observed in the tissue directly impacted by the WP disease "band" and were not observed in tissue samples taken 20 cm away from the lesion. Therefore, the effects of a coral disease (WP) on reproductive output are localized and not expressed colony-wide. Rev. Biol. Trop. 58 (Suppl. 3): 99-110. Epub 2010 October 01.

The direct impacts of coral diseases on coral populations have been assessed by quantifying coral tissue loss and colony mortality, but the determination of the indirect effects of diseases, such as disruptions in life history functions (e.g. reproduction, growth and maintenance), are more difficult to ascertain and have been scant. This study involved a comparison of various measures of reproductive output from histological slides of healthy tissue samples of Montastraea faveolata and tissue samples from colonies with white plague (WP) infections in Dominica (West Indies). Although the variability in the reproductive data was high, WP had significant negative impacts on the percentage of reproductive polyps per cm2, the percentage of reproductive mesenteries within a polyp, oocyte quantity per polyp, mean oocyte volume (mm3), and fecundity (oocyte volume per cm2 of tissue). However, these effects were only observed in the tissue directly impacted by the WP disease "band" and were not observed in tissue samples taken 20 cm away from the lesion. Therefore, the effects of a coral disease (WP) on reproductive output are localized and not expressed colony-wide. Rev. Biol. Trop. 58 (Suppl. 3): 99-110. Epub 2010 October 01.

Shallow leeward reefs off the western end of Curaçao are dominated by extensive populations of M. annularis (complex). These species are larger in size (mean= 66 cm diameter) than all other species, with few small colonies (10 cm observed within transects, and most exhibited low levels of partial mortality (mean= 22.5%). These species were less abundant (38% of all colonies) in 2005. Partial mortality among live colonies of M. annularis and M. faveolata increased by 85% (mean = 42% partial mortality) and numerous dead colonies of M. faveolata and M. annularis were observed; M. franksi colonies were generally in excellent condition (14% partial tissue mortality). A high prevalence of coral diseases (3-30%) was documented among M. annularis and M. faveolata, while all other species were less frequently affected. Yellow band disease (YBD) emerged shortly after the 1995 bleaching event, and rapidly spread throughout all depths, with the highest prevalence between 1997-1999. YBD caused slow rates of mortality (=1 cm/month), but multiple focal lesions appeared on individual colonies, and these progressively radiated outward as they killed the colonies. By 2005, 44% of the tagged corals were dead; the remainder exhibited active YBD infections (21%) or were in remission (31.6%) but were missing on average >90% of their tissue. Although the incidence of YBD has declined since 2000, white plague (WP) prevalence was unusually high (4-12%) in 2001 and 2005, with affected colonies exhibiting recent mortality of up to 70%. Dead Montastraea spp. surfaces are being colonized by other corals, including poritids, agaricids, and other faviids, while recruits of M. annularis (complex) are absent. If diseases and other biotic stressors persist on these reefs, M. annularis and M. faveolata populations may undergo a decline similar to that observed in the 1980s among Caribbean acroporids. Rev. Biol. Trop. 54 (Suppl. 3): 45- 58. Epub 2007 Jan. 15.Los arrecifes someros a sotavento del oeste de Curaçao están dominados por extensas poblaciones de Montastraea annularis (complejo). Estas especies son mayores en tamaño (promedio= 66 cm de diámetro) que las otras especies, con algunas colonias pequeñas (10 cm observadas en transectos y la mayoría exhibió bajos niveles de mortalidad parcial (prom= 22.5%). En el 2005, fueron menos abundantes (38% de las colonias). La mortalidad parcial en colonias vivas de M. annularis y M. faveolata se incrementó en un 85% (promedio= 42% de mortalidad parcial) y se observaron numerosas colonias de M. annularis y M. faveolata muertas; las colonias de M. franski generalmente se encontraron en excelentes condiciones (14% de mortalidad parcial). Se documentó una alta prevalencia de enfermedades de coral (3-30%) en M. annularis y M. faveolata, mientras que las otras especies se vieron afectadas con menor frecuencia. La enfermedad de banda amarilla (BA) emergió poco después del blanqueamiento de 1995 y se dispersó rápidamente en todas las profundidades, alcanzando su mayor prevalencia entre 1997-1999. La BA causó mortalidades lentas (= 1cm/mes), con aparición de múltiples lesiones focales en colonias individuales; estas lesiones fueron creciendo progresivamente al tiempo que mataban las colonias. Para el año 2005, el 44% de los corales que se etiquetaron habían muerto; los restantes exhibían infecciones activas de BA (21%), o estaban en remisión (31.6%) pero habían perdido un promedio de >90% de su tejido. Aunque la incidencia de BA disminuyó a partir del 2000, la prevalencia de la plaga blanca (PB) fue inusualmente alta (4-12%) en el 2001 y 2005, provocando mortalidades recientes de hasta un 70% en las colonias afectadas. Las superficies muertas de Montastraea spp. han sido colonizadas por otros corales, incluyendo porítidos, agarícidos y otros fávidos, mientras que continúa la ausencia de reclutas de M. annularis (complejo). Si las enfermedades y otros estresores bióticos persisten en estos arrecifes, las poblaciones de M. annularis y M. faveolata podrían decaer de forma similar a como lo hicieron los acropóridos del Caribe durante la década de 1980.

One of the current problems in the field of coral disease research is that of tracking coral pathogens in the natural environment.A promising method to do this is by use of pathogen-specific molecular probes. However,this approach has been little used to date.We constructed,and validated in the laboratory,a fluoro-chrome-labeled molecular probe specific to Aurantimonas coralicida ,the bacterial pathogen of the Caribbean coral disease white plague type II (WPII).We then used the probe to test field samples of diseased coral tissue for the presence of this pathogen.Probe design was based on a unique subset (25 nucleotides)of the complete16S rRNA gene sequence derived from a pure culture of the pathogen.The pathogen-specific probe was labeled with the fluorochrome GreenStar*™FITC (fluorescein isothiocyanate,GeneDetect Ltd,New Zealand).As a control, we used the universal eubacterial probe EUB 338,labeled with a different fluorochrome (TRITC,tetra-methyl-rhodamine isothiocyanate).Both probes were applied to laboratory samples of pure cultures of bacteria, and field samples collected from the surface of the disease line of corals exhibiting signs of white plague (types I and II),healthy controls,and corals with an uncharacterized disease ("patchy necrosis ").All samples were analyzed using fluorescence in situ hybridization (FISH).We have determined that the probe is specific to our laboratory culture of the coral pathogen,and does not react with other bacterial species (the eubacterial probe does).The WPII pathogen was detected in association with diseased coral samples collected from coral colonies on reefs of the Bahamas (n=9 samples)exhibiting signs of both WPI and WPII.Diseased (and healthy)tissue samples (n=4)from corals exhibiting signs of "patchy necrosis "were also assayed.In this case the results were negative, indicating that the same pathogen is not involved in the two diseases.Incorporation and use of pathogen-specific probes can significantly expand our knowledge of the etiology of coral diseases.Uno de los problemas actuales en el campo de la investigación sobre las enfermedades de corales es el de poder seguir a los patógenos en el ambiente natural.Un método prometedor para lograrlo es el uso de sondas moleculares específicas para el patógeno.Sin embargo,esta técnica ha sido poco usada hasta la fecha.Construimos y validamos en el laboratorio una sonda molecular de fluorocromo marcado específicamente para Aurantimonas coralicida ,la bacteria responsable de la enfermedad de corales del Caribe,plaga blanca Tipo II (PBII).Después usamos la sonda con muestras de campo de tejidos de corales enfermos para detectar la presencia del patógeno.La sonda se diseñó usando un sub-grupo único de 25 nucleótidos del gen 16S del rARN derivado de cultivos puros del patógeno.La sonda específica para el patógeno se marcó con fluorocromo GreenStar*™ FITC (fluorescein isotiocianato,GeneDetect Ltd,New Zealand).Como testigo usamos la sonda universal de eubacterias EUB 338,marcada con un fluorocromo diferente (TRITC,tetra-metil-rodamina isotiocianato).Ambas sondas fueron usadas con muestras de laboratorio de cultivos puros de bacterias,y muestras de campo recolectadas de la superficie de la línea de la enfermedad en corales con signos de plaga blanca (tipos I y II),de corales sanos y de corales con enfermedades no características (parches de tejido necrótico).Todas las muestras fueron analizadas usando hibridización fluorescente in situ .Determinamos que la sonda es específica para el patógeno cultivado en nuestro laboratorio y no reacciona con otras especies de bacterias (la sonda para eubacterias sí).El patógeno de PBII fue detectado en muestras de corales enfermos (exhibían signos de PBI y PBII)recolectadas en arrecifes de Bahamas (n=9 muestras).Muestras de tejidos enfermos (y sanos)(n=4)de corales con parches necróticos fueron probados.En este caso los resultados fueron negativos,indicando que el mismo patógeno no es responsable de las dos enfermedades.El desarrollo y uso de sondas específicas para cierto patógeno puede ampliar significativamente nuestro conocimiento de la etiología de enfermedades de corales.