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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.

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.

Anthropogenic and natural disturbances have modified coral reef ecosystems over the last decades, ultimately, exerting negative impacts on the persistence of the carbonated matrix and the physical function. In 2014, the Caribbean region saw the onset of a new deadly coral disease, often known as the stony coral tissue loss disease. In summer of 2018, the outbreak was first reported in the Mexican Caribbean in a diving site named ‘Fish Market’. From July 2018 to March 2019, surveys were made to assess the impacts of this new outbreak in the stony coral community in terms of composition and the effect on the coral community calcification. This disease outbreak had severe consequences for this site. Several colonies of susceptible species were lost, which resulted in significant changes in the coral community composition and reductions in the gross carbonate production in a period of only 8 months.

Infectious diseases are one of the major drivers of coral reef decline worldwide. White plague-like disease (WPL) is a widespread disease with a complex etiology that infects several coral species, including the Brazilian endemic species Mussismilia braziliensis. Gene expression profiles of healthy and WPL-affected M. braziliensis were analyzed in winter and summer seasons. The de novo assembly of the M. braziliensis transcriptome from healthy and white plague samples produced a reference transcriptome containing 119,088 transcripts. WPL-diseased samples were characterized by repression of immune system and cellular defense processes. Autophagy and cellular adhesion transcripts were also repressed in WPL samples, suggesting exhaustion of the coral host defenses. Seasonal variation leads to plasticity in transcription with upregulation of intracellular signal transduction, apoptosis regulation, and oocyte development in the summer. Analysis of the active bacterial rRNA indicated that Pantoea bacteria were more abundant in WPL corals, while Tistlia, Fulvivirga, and Gammaproteobacteria Ga0077536 were more abundant in healthy samples. Cyanobacteria proliferation was also observed in WPL, mostly in the winter. These results indicate a scenario of dysbiosis in WPL-affected M. braziliensis, with the loss of potentially symbiotic bacteria and proliferation of opportunistic microbes after the start of the infection process.

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.

Outbreaks of coral white plague (WP) disease have caused significant regional declines of reef‐building Caribbean corals. Due to a greater availability of epidemiological data, studies have primarily focused on shallow coral reefs (< 30 m). In the U.S. Virgin Islands, however, WP disease prevalence appears to be higher on upper mesophotic (30–40 m) coral reefs when compared with shallow reefs and may be inhibiting coral recovery after environmental disturbances. The aim of this study was to investigate the relationship of environmental drivers with spatio‐temporal patterns of WP prevalence across shallow and mesophotic coral reefs in the U.S. Virgin Islands. We recorded WP prevalence at 13 reef sites (five shallow, three mid‐depth and five upper‐mesophotic reefs) across the south shelf of St. Thomas approximately monthly between 2012 and 2015 using a drop camera method. The influence of environmental factors on disease prevalence was investigated using Bayesian inference with generalized linear mixed‐effect models. We found that WP tended to increase during the beginning of the rainy season (June), and when levels of water turbidity and temperature were higher, and levels of oxygen and salinity lower. The disease prevalence was higher on mesophotic than on shallow or mid‐depth reefs, probably due to higher availability of corals (host), and a possible temperature threshold for WP occurrence that allows long‐term persistence (year‐round) of the disease on upper‐mesophotic reefs. This is the first study to implement the drop camera method to survey a coral disease over several reef sites and depths. This method can be applied on surveys of other rapid tissue loss diseases, such as the newly emergent stony‐coral‐tissue‐loss‐disease (SCTLD).

Coral reefs are threatened throughout the world. A major factor contributing to their decline is outbreaks and propagation of coral diseases. Due to the complexity of coral-associated microbe communities, little is understood in terms of disease agents, hosts and vectors. It is known that compromised health in corals is correlated with shifts in bacterial assemblages colonizing coral mucus and tissue. However, general disease patterns remain, to a large extent, ambiguous as comparative studies over species, regions, or diseases are scarce. Here, we compare bacterial assemblages of samples from healthy (HH) colonies and such displaying signs of White Plague Disease (WPD) of two different coral species ( Pavona duerdeni and Porites lutea ) from the same reef in Koh Tao, Thailand, using 16S rRNA gene microarrays. In line with other studies, we found an increase of bacterial diversity in diseased (DD) corals, and a higher abundance of taxa from the families that include known coral pathogens (Alteromonadaceae, Rhodobacteraceae, Vibrionaceae). In our comparative framework analysis, we found differences in microbial assemblages between coral species and coral health states. Notably, patterns of bacterial community structures from HH and DD corals were maintained over species boundaries. Moreover, microbes that differentiated the two coral species did not overlap with microbes that were indicative of HH and DD corals. This suggests that while corals harbor distinct species-specific microbial assemblages, disease-specific bacterial abundance patterns exist that are maintained over coral species boundaries.

Coral reefs are deteriorating at an alarming rate mainly as a consequence of the emergence of coral diseases. The white plague disease (WPD) is the most prevalent coral disease in the southwestern Caribbean, affecting dozens of coral species. However, the identification of a single causal agent has proved problematic. This suggests more complex etiological scenarios involving alterations in the dynamic interaction between environmental factors, the coral immune system and the symbiotic microbial communities. Here we compare the microbiome of healthy and WPD-affected corals from the two reef-building species Diploria strigosa and Siderastrea siderea collected at the Tayrona National Park in the Caribbean of Colombia. Microbiomes were analyzed by combining culture-dependent methods and pyrosequencing of 16S ribosomal DNA (rDNA) V5-V6 hypervariable regions. A total of 20 410 classifiable 16S rDNA sequences reads were obtained including all samples. No significant differences in operational taxonomic unit diversity were found between healthy and affected tissues; however, a significant increase of Alphaproteobacteria and a concomitant decrease in the Beta- and Gammaproteobacteria was observed in WPD-affected corals of both species. Significant shifts were also observed in the orders Rhizobiales, Caulobacteriales, Burkholderiales, Rhodobacterales, Aleteromonadales and Xanthomonadales, although they were not consistent between the two coral species. These shifts in the microbiome structure of WPD-affected corals suggest a loss of community-mediated growth control mechanisms on bacterial populations specific for each holobiont system.

White plague disease has caused widespread coral mortality and affects over 30 Caribbean coral species, yet how different coral species respond to disease exposure has not been tested experimentally. This study quantified white plague transmission from Orbicella franksi to three susceptible and abundant coral species in the U.S. Virgin Islands: Orbicella annularis, Siderastrea siderea, and Porites astreoides. White plague was observed in 83% of tested O. annularis corals within 5.8 ± 1.1 (mean ± SE) d, 42% of S. siderea corals within 9.1 ± 1.4 d, and 17% of P. astreoides corals within 12 ± 0.87 d. Results from this study indicate that: (1) O. annularis is significantly more susceptible to white plague than S. siderea and P. astreoides, and (2) white plague infection occurs more rapidly in O. annularis than in P. astreoides. These results are important for understanding how multi-species diseases may impact coral species assemblages.

Reef corals in the Mexican Reef System have been severely affected by the emergence of a white syndrome that resembles both White Plague II and SCTLD descriptions. Meandroid scleractinian coral species are among the most severely affected. To gain insight into this affliction we conducted a broad study in the brain coral Pseudodiploria strigosa at a rear reef site in the NE Mexican Caribbean. We describe macro and microscopical signals of the disease, characterize the outbreak dynamics, the tissue histopathology, explore immunological responses in the individuals, and compare microbial assemblages associated with the surface mucus layer of healthy and unhealthy colonies. At the study site, the white syndrome outbreak on P. strigosa showed a high incidence rate in summer-fall and a low one in winter, as well as low survival expectation of diseased colonies at the end of the study. After 306 days of observation, out of 96 tracked colonies, eight remained apparently healthy and seven were diseased. No effective resistance to colony disease progression was observed once white syndrome signs developed. Tissue loss rate during the study varied among colonies (mean = 10.8 cm 2 , s.d. = 7.8 cm 2 ) suggesting a complex relation between causal agents and colony resistance. The deterioration of tissues was evidenced from the basal to the surface body wall of polyps (up to 66% hypertrophy and liquefactive necrosis in unhealthy colonies), implying that microscopic alterations begin before macroscopic signals develop, suggesting this may be a systemic disease. We measured high levels of phenoloxidase (two orders of magnitude higher PO activity than P. strigosa affected by BBD) and antibacterial activity without significant reduction in unhealthy samples from the mucus layer, indicative of an enhanced immunological response. Results showed that opportunistic bacteria dominated damaged colonies, where six genera of the Bacteroidia class were found with significant changes in unhealthy colonies after DeSeq2 analysis. Nevertheless, histological observations did not support infection of the tissues. The opportunistic overload seems to be contained within the mucus layer but may be associated with the mortality of tissues in a yet unclear way. Future research should focus on experimental infections, the tracking of natural infections, and the immunocompetence of corals in the face of environmental pressures due to local, regional, and global impacts. If environmental deterioration is the primary cause of the continuing emergence and re-emergence of lethal coral diseases, as has been proposed by many authors, the only true option to effectively help preserve the coral reef biodiversity and services, is to restore the environmental quality of reef waters at the local scale and reduce greenhouse gases at the global scale.