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Disease is an emerging threat to coral reef ecosystems worldwide, highlighting the need to understand how environmental conditions interact with coral immune function and associated microbial communities to affect holobiont health. Increased coral disease incidence on reefs adjacent to permanently moored platforms on Australia's Great Barrier Reef provided a unique case study to investigate environment-host-microbe interactions in situ. Here, we evaluate coral-associated bacterial community (16S rRNA amplicon sequencing), immune function (protein-based prophenoloxidase-activating system), and water quality parameters before, during and after a disease event. Over the course of the study, 31% of tagged colonies adjacent to platforms developed signs of white syndrome (WS), while all control colonies on a platform-free reef remained visually healthy. Corals adjacent to platforms experienced significant reductions in coral immune function. Additionally, the corals at platform sites that remained visually healthy throughout the study had reduced bacterial diversity compared to healthy colonies at the platform-free site. Interestingly, prior to the observation of macroscopic disease, corals that would develop WS had reduced bacterial diversity and significantly greater community heterogeneity between colonies compared to healthy corals at the same location. These results suggest that activities associated with offshore marine infrastructure impacts coral immunocompetence and associated bacterial community, which affects the susceptibility of corals to disease.

Photographic evidence of some important coral diseases (black band disease, black disease/Terpios hoshinota, white syndrome, pink line syndrome, pink spots, invertebrate galls, skeletal growth anomalies, tissue loss), coral competing sponges, and coral–algal phase shifts (competitive overgrowth of the seaweed Caulerpa spp. over corals and competitive scleractinian interactions such as with Halimeda spp.) have been collected during field observations in a few atolls within the Lakshadweep archipelago, Arabian Sea. Further, earlier reports of similar diseases and other stressors within the Indian Exclusive Economic Zone (EEZ) and its contiguous international waters, including the reefs of the Maldives and Sri Lanka, are highlighted and their distributional ranges are shown. [ABSTRACT FROM AUTHOR]

Coral diseases are an increasing threat to continuously degrading reefs as disease abundance and virulence are expected to increase in the future. Active conservation measures, specifically coral restoration projects, are increasingly being implemented worldwide. Yet little is known about the implications of disease occurrence in a restoration context. This study describes white syndrome pathogenesis in 2 coral genera, farmed in 2 mid-water rope nurseries located in a reef and a lagoon habitat in the Maldives. Over a 112 d monitoring period, disease metrics were obtained from 336 Pocillopora and 96 Acropora fragments to assess the impacts of unmitigated disease progression in coral nurseries. Disease had low prevalence (2.2%) and incidence (0.007) in reef-farmed Pocillopora, but survival (91%) was significantly reduced in comparison with the unaffected lagoon-farmed Pocillopora (99%). In contrast, lagoon-farmed Acropora showed high disease prevalence (78.5%) and incidence (0.064), and a lower survival (79%) than disease-unaffected reef-farmed Acropora (98%). These findings had distinct implications for coral gardening success. While Pocillopora was considered suitable for outplanting, especially since subsequent mitigation interventions were successful, the diseased, lagoon-reared Acropora posed a potential risk to the restoration site and was unsuitable for outplanting following 1 yr of farming effort. Our findings demonstrate that unmitigated diseases can cause major setbacks to restoration success. Coral gardening projects are likely to be particularly susceptible; therefore, disease monitoring and risk management are imperative. Since there is currently a lack of available diagnostic and mitigative tools, this study aims to provide case study data for restoration practitioners.

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.

Coral diseases have increased in frequency and intensity around the tropics worldwide. However, in many cases, little is known about their etiology. Montipora white syndrome (MWS) is a common disease affecting the coral Montipora capitata, a major reef builder in Hawai'i. Chronic Montipora white syndrome (cMWS) is a slow‐moving form of the disease that affects M. capitata throughout the year. The effects of this chronic disease on coral immunology and microbiology are currently unknown. In this study, we use prophenoloxidase immune assays and 16S rRNA gene amplicon sequencing to characterize the microbiome and immunological response associated with cMWS. Our results show that immunological and microbiological responses are highly localized. Relative to diseased samples, apparently healthy portions of cMWS corals differed in immune activity and in the relative abundance of microbial taxa. Coral tissues with cMWS showed decreased tyrosinase‐type catecholase and tyrosinase‐type cresolase activity and increased laccase‐type activity. Catecholase and cresolase activity were negatively correlated across all tissue types with microbiome richness. The localized effect of cMWS on coral microbiology and immunology is probably an important reason for the slow progression of the disease. This local confinement may facilitate interventions that focus on localized treatments on tissue types. This study provides an important baseline to understand the interplay between the microbiome and immune system and the mechanisms used by corals to manage chronic microbial perturbations associated with white syndrome. [ABSTRACT FROM AUTHOR]

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 cm2, s.d. = 7.8 cm2) 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.

Coral diseases contribute to the decline of reef communities, but factors that lead to disease are difficult to detect. In the present study, we develop a multi-species model of colony-scale risk for the class of coral diseases referred to as White Syndromes, investigating the role of current or past conditions, including both environmental stressors and biological drivers at the colony and community scales. Investigating 7 years of coral survey data at five sites in Guam we identify multiple environmental and ecological associations with White Syndrome, including a negative relationship between short-term heat stress and White Syndrome occurrence, and strong evidence of increasing size-dependent White Syndrome risk across coral species. Our findings result in a generalized model used to predict colony-scale White Syndrome risk for multiple species, highlighting the value of long-term monitoring efforts to detect drivers of coral disease.

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 D 10.8 cm², s.d. D 7.8 cm²) 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. [ABSTRACT FROM AUTHOR]

Aims: Coral diseases have emerged over the last several decades, causing a loss of live coral cover in the Caribbean and Indo-Pacific reefs. Hence, microbiological and disease cultural techniques are commonly used to investigate their causative microbial agents. This is the first study to identify the potential of pathogenic Vibrio spp. isolated from apparently white syndrome (WS) coral disease in Tioman Island Marine Park using biochemical and molecular techniques. Methodology and results: The Vibrio colonies were isolated from 108 samples of WS infected corals (Acropora cytherea and Montipora aequituberculata) including seawater, sediment and algae found adjacent to infected coral colonies. A total of one hundred representative Vibrio isolates were characterized and most of them (n=50) were identified as V. vulnificus, V. alginolyticus and Photobacterium damselae following biochemical analysis. The molecular analysis revealed six Vibrio spp. (V. coralliilyticus, V. hepatarius, V. brasiliensis, V. tubiashi, V. campbellii, V. ishigakensis) and one Photobacterium rosenbergii. Vibrio coralliilyticus isolated from all infected coral samples may be highly responsible for the sign of WS disease. Conclusion, significance and impact of study: The findings of this study provide baseline data and information on potential coral pathogens identified in the coastal waters of Tioman Island. Etiological disease study is suggested to validate their severity and virulence factors in the future. [ABSTRACT FROM AUTHOR]

Reef-building corals living in extreme environments can provide insight into the negative effects of future climate scenarios. In hot environments, coral communities experience disproportionate thermal stress as they live very near or at their upper thermal limits. This results in a high frequency of bleaching episodes, but it is unknown whether temperature-driven outbreaks of coral disease follow a similar trajectory. Here we tracked outbreaks of a white-syndrome (WS) disease over three years in the hottest region inhabited by reef-building corals, the southern Persian Gulf. From 2014 to 2016, WS affected 10 of the 16 scleractinian genera recorded at inshore and offshore sites. Intra- and inter-specific transmission of lesions was frequently observed, indicative of a single contagious disease infecting multiple coral taxa. Colonies of Acropora were the most susceptible to WS disease and were more than twice as likely to experience lesions than any other genera. Prevalence reached 42% of Acropora colonies and lesions progressed at an average rate of 1 mm day−1. Platygyra colonies were the second most susceptible to WS disease, where prevalence reached 33% and lesions progressed at 0.3 mm day−1. Affected colonies of both of these genera suffered considerable partial mortality that was not recovered between years, promoting the fragmentation of larger colonies into smaller size classes. Across the 3 years of our study, the onset of WS outbreaks occurred early in summer and prevalence increased exponentially with cumulative heat exposure (coral community r2 = 0.55, Acropora r2 = 0.72, Platygyra r2 = 0.75). Peak levels of community-wide prevalence occurred in August (10% of all coral colonies) to September (14%) when preceding 4-week and 8-week average temperatures exceeded 34.5 °C and 34 °C, respectively. Outbreaks ceased following the return of cooler temperatures with prevalence remaining below 0.5% between December and June. Levels of bleaching remained relatively low (< 5% prevalence), despite exposure to daily temperatures ≥ 35 °C each summer. These findings demonstrate that thermal stress on coral reefs does not always manifest as coral bleaching and diseases can present as a primary sign of thermal stress. Consequently, temperature-driven outbreaks of coral disease are expected to become more widespread as climate warming pushes corals to be living increasingly closer to their upper thermal limits. [ABSTRACT FROM AUTHOR]

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.

As many as 22 of the 45 coral species on the Florida Reef Tract are currently affected by stony coral tissue loss disease (SCTLD). The ongoing disease outbreak was first observed in 2014 in Southeast Florida near Miami and as of early 2019 has been documented from the northernmost reaches of the reef tract in Martin County down to Key West. We examined the microbiota associated with disease lesions and apparently healthy tissue on diseased colonies of Montastraea cavernosa, Orbicella faveolata, Diploria labyrinthiformis, and Dichocoenia stokesii. Analysis of differentially abundant taxa between disease lesions and apparently healthy tissue identified five unique amplicon sequence variants enriched in the diseased tissue in three of the coral species (all except O. faveolata), namely an unclassified genus of Flavobacteriales and sequences identified as Fusibacter (Clostridiales), Planktotalea (Rhodobacterales), Algicola (Alteromonadales), and Vibrio (Vibrionales). In addition, several groups of likely opportunistic or saprophytic colonizers such as Epsilonbacteraeota, Patescibacteria, Clostridiales, Bacteroidetes, and Rhodobacterales were also enriched in SCTLD disease lesions. This work represents the first microbiological characterization of SCTLD, as an initial step toward identifying the potential pathogen(s) responsible for SCTLD.

Disease is an emerging threat to coral reef ecosystems worldwide, highlighting the need to understand how environmental conditions interact with coral immune function and associated microbial communities to affect holobiont health. Increased coral disease incidence on reefs adjacent to permanently moored platforms on Australia's Great Barrier Reef provided a unique case study to investigate environment–host–microbe interactions in situ. Here, we evaluate coral-associated bacterial community (16S rRNA amplicon sequencing), immune function (protein-based prophenoloxidase-activating system), and water quality parameters before, during and after a disease event. Over the course of the study, 31% of tagged colonies adjacent to platforms developed signs of white syndrome (WS), while all control colonies on a platform-free reef remained visually healthy. Corals adjacent to platforms experienced significant reductions in coral immune function. Additionally, the corals at platform sites that remained visually healthy throughout the study had reduced bacterial diversity compared to healthy colonies at the platform-free site. Interestingly, prior to the observation of macroscopic disease, corals that would develop WS had reduced bacterial diversity and significantly greater community heterogeneity between colonies compared to healthy corals at the same location. These results suggest that activities associated with offshore marine infrastructure impacts coral immunocompetence and associated bacterial community, which affects the susceptibility of corals to disease.

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. [ABSTRACT FROM AUTHOR]

As many as 22 of the 45 coral species on the Florida Reef Tract are currently affected by stony coral tissue loss disease (SCTLD). The ongoing disease outbreak was first observed in 2014 in Southeast Florida near Miami and as of early 2019 has been documented from the northernmost reaches of the reef tract in Martin County down to Key West. We examined the microbiota associated with disease lesions and apparently healthy tissue on diseased colonies of Montastraea cavernosa , Orbicella faveolata , Diploria labyrinthiformis , and Dichocoenia stokesii. Analysis of differentially abundant taxa between disease lesions and apparently healthy tissue identified five unique amplicon sequence variants enriched in the diseased tissue in three of the coral species (all except O. faveolata) , namely an unclassified genus of Flavobacteriales and sequences identified as Fusibacter (Clostridiales) , Planktotalea (Rhodobacterales) , Algicola (Alteromonadales) , and Vibrio (Vibrionales). In addition, several groups of likely opportunistic or saprophytic colonizers such as Epsilonbacteraeota, Patescibacteria, Clostridiales, Bacteroidetes, and Rhodobacterales were also enriched in SCTLD disease lesions. This work represents the first microbiological characterization of SCTLD, as an initial step toward identifying the potential pathogen(s) responsible for SCTLD. [ABSTRACT FROM AUTHOR]

Globally coral reefs have been declining at alarming rates as a result of anthropogenic stressors, leading to increased frequency and severity of widespread bleaching and disease events. These events are often associated with increased water temperatures due to climate change as well as regional and local stress from nutrient enrichment through runoff and sedimentation from coastal development. In late 2014, a white syndrome disease outbreak was reported off the coast of southeast Florida and was subsequently documented spreading throughout the region. This study examined the regional impacts of the disease event on the southeast Florida stony coral population utilizing stony coral demographic data from the Southeast Florida Coral Reef Evaluation and Monitoring Project (SECREMP). SECREMP is a long-term monitoring project examining 22 sites distributed from Miami-Dade County north to Martin County, Florida. The results revealed significant region-wide declines in stony coral diversity, density, and live tissue area corresponding with increased disease prevalence, which reached its maximum for the study period in 2016. Regional declines in coral density approached 30% loss and live tissue was upward of 60% as a result of the disease outbreak. Additionally, multiple species were severely impacted, especially the reef building, complexity-contributing species Montastraea cavernosa, Meandrina meandrites, and Siderastrea siderea. The disease outbreak resulted in acute mortality and altered the ecosystem function to a point such that recovery is uncertain. This multiyear, region-wide disease outbreak has been indiscriminate relative to coral species impacted and was arguably the most devastating disturbance event documented on the Southeast Florida Reef Tract.

Coral diseases have contributed significantly to the decline of coral populations at both local and global scales. The Karimunjawa Archipelago, located off the coast of Java in Indonesia, is a marine national park with a zonation-based approach, designated by the local government due to its rich coral reef biodiversity. Unfortunately, there is a limited amount of research regarding the prevalence of coral diseases in coral reefs located on the islands. We analyzed the coral reef lesion assemblages at 6 sites within 3 designated zones, namely Tourism, Aquaculture, and Core zones. Our investigation aimed to determine (1) the types, prevalence, and patterns of coral lesions, (2) the correlation between coral cover and lesion prevalence, and (3) the susceptibility of coral taxa to lesions. A significant difference of 80.54% in the total number of coral lesions was observed between the tourism zone (24.34%) and the core zone (10.36%). Fourteen different lesion types were identified; among the non-disease lesions, sediment damage was the most prevalent (9.95%), followed by disease lesions caused by white syndrome (3.7%). A correlation was found between the cover of dominant coral taxa and the prevalence of lesions (disease and non-disease) at all sites. Mean lesion prevalence across all zones ranged from moderate to high categories. These findings present current data on the distribution of coral lesions and their patterns across zones around Karimunjawa Island. Research on the etiology and epidemiology of coral lesions should be promoted to identify ways to prevent the spread of coral diseases in Karimunjawa.

Coral diseases that have emerged since the early 1970s have caused significant regional ecological impacts. However, there has been a paucity of research into coral disease in South-East Asia, including Indonesia. This study provides baseline coral disease data in the Kepulauan Seribu Marine National Park. In this study we show a positive correlation between overall coral cover and the dominant reef building coral Montipora spp. and found two main diseases, black band disease (BBD) and WS, were highly prevalent throughout all reefs. Based on spatial location, the highest abundance of BBD (0.08 col./m2) was found at sites nearer (zone 1) to the mainland, whilst for WS (0.05 col./m2) highest abundance was found at middle sites (zone 2). According to the temporal data, the highest abundance of BBD (0.77 col./m2) was found during the transition period (between wet and dry seasons), whereas for WS higher abundance occurred within the dry season (0.07 col./m2). There was a significant difference in disease abundance among seasons which was correlated with increasing temperature and light intensity along with variations in total organic matters, nitrite and phosphate levels. Moreover, the middle sites experienced additional stress from the waste material originating from the mainland.

Abstract Impacts from human-induced direct-use perturbations on coral colonies are on the rise. Despite significant incidences of coral disease on a global-wide basis, too few studies have verified the sources of diseases affecting coral colonies. To determine if branching coral communities are prone to infection with black band disease, brown band disease, and white syndrome, this study compared the prevalence of coral disease between Great Barrier Reef Marine Park Zones in the Great Barrier Reef Marine Park, Australia. We found evidence for coral disease on 9.06% of sites, with white syndrome being the most prevalent, found on 5.46% of sites, brown band found on 2.90% of sites, and black band found on 1.45% of sites. Coral disease of any kind, specifically black band and white syndrome, were significantly less abundant in areas where line fishing was permitted than where it was prohibited. Moreover, there was an interaction between fishing regulations and location, such that fishing regulations did not predict the presence of disease offshore, but inshore coral disease was significantly more prevalent where line fishing was prohibited than where line fishing was permitted. Coral disease was most frequently found in General Use, Scientific Research Open to the Public, and Marine National Park Zones; and reliably least commonly found in Habitat Protection, Conservation Park, and Preservation Zones. There were also differences among Marine Park Management Zones with coral disease most prevalent in the Cairns/Cooktown (Offshore) zone and least prevalent in the Mackay/Capricorn (Offshore) zone. Cairns/Cooktown (Offshore and Inshore) were the highest zones for black band and brown band, and Mackay/Capricorn (Inshore) was the highest management zone for white syndrome. [ABSTRACT FROM AUTHOR]

Two of the most significant threats to coral reefs worldwide are bleaching and disease. However, there has been a scarcity of research on coral disease in South-East Asia, despite the high biodiversity and the strong dependence of local communities on the reefs in the region. This study provides baseline data on coral disease frequencies within three national parks in Sabah, Borneo, which exhibit different levels of human impacts and management histories. High mean coral cover (55%) and variable disease frequency (mean 0.25 diseased colonies m−2) were found across the three sites. Highest disease frequency (0.44 diseased colonies per m2) was seen at the site closest to coastal population centres. Bleaching and pigmentation responses were actually higher at Sipadan, the more remote, offshore site, whereas none of the other coral diseases detected in the other two parks were detected in Sipadan. Results of this study offer a baseline dataset of disease in these parks and indicate the need for continued monitoring, and suggest that coral colonies in parks under higher anthropogenic stressors and with lower coral cover may be more susceptible to contracting disease.

The present study reports the results of the first quantitative survey of lesions on coral and crustose coralline algae (CCA) on reefs in the lagoon of New Caledonia. Surveys on inshore and offshore reefs were conducted at 13 sites in 2010, with 12 sites resurveyed in 2013. Thirty coral diseases affecting 15 coral genera were found, with low overall disease prevalence (<1%). This study extends the known distribution of growth anomalies to the coral genera Platygyra and Hydnophora, endolithic hypermycosis to Platygyra, Leptoria and Goniastrea and extends the geographic range of three CCA diseases. We found the first trematode infection in Porites outside of Hawaii. Disease prevalence differed among coral genera, with Porites having more lesions, and Acropora and Montipora fewer lesions, than expected on the basis of field abundance. Inshore reefs had a lower coral-colony density, species diversity and reduced CCA cover than did the offshore reefs. Disease prevalence was significantly higher on inshore reefs in 2013 than in 2010, but did not change on offshore reefs. The potential ecological impact of individual coral diseases was assessed using an integrative-scoring and relative-ranking scheme based on average frequency of occurrence, prevalence and estimated degree of virulence. The top-five ranked diseases were all tissue-loss diseases. [ABSTRACT FROM AUTHOR]

Coral reefs are constantly subjected to multiple stresses like diseases and fish predation, which can profoundly influence the coral microbiome. This study investigated the differences in bacterial community structure of healthy, white syndrome affected and blenny nipped coral colonies of Porites lutea, collected from the coral reefs of Gulf of Kachchh, north-west coast of India. Present study observed that the stressed coral colonies harbored more OTUs and contained higher diversity values compared to healthy corals colonies. Similarly, beta diversity analysis indicated the dissimilarities among the three coral samples analyzed. Though the taxonomy analysis indicated bacterial phyla like Proteobacteria, Firmicutes, Bacteroidetes, and Actinobacteria among the entire coral samples studied, there was a variation in their relative abundances. Huge variations were observed in the relative dominance at the bacterial genera level. About 13phyla and 11 genera was identified in healthy coral. The PBN sample was found to contain Proteobacteria, Cyanobacteria, Verrucomicrobia, and Lentisphaerae as dominant phyla and Endozoicomonas, Dyella, Woeseia, and Winogradskyella as dominant genera. The PWS sample contained Proteobacteria, Lentisphaerae, Spirochaetes, and Tenericutes as dominant phyla and Endozoicomonas, Arcobacter, Sunxiuqinia, and Carboxylicivirgia as dominant genera. Among the healthy samples, sequences belonging to Uncultured Rhodospirillaceae were dominant, while Woeseia and sequences belonging to Uncultured Rhodovibrionaceae were dominant among the blenny nipped white syndrome infected corals. Although any previously established pathogen was not identified, present study revealed the presence of a potentially pathogenic bacterium, Arcobacter, among the diseased corals. It also demonstrated a dynamic microbiome among the Porites lutea colonies on subjecting to various stresses. [ABSTRACT FROM AUTHOR]

Coral diseases that have emerged since the early 1970s have caused significant regional ecological impacts. However, there has been a paucity of research into coral disease in South-East Asia, including Indonesia. This study provides baseline coral disease data in the Kepulauan Seribu Marine National Park. In this study we show a positive correlation between overall coral cover and the dominant reef building coral Montipora spp. and found two main diseases, black band disease (BBD) and WS, were highly prevalent throughout all reefs. Based on spatial location, the highest abundance of BBD (0.08 col./m2) was found at sites nearer (zone 1) to the mainland, whilst for WS (0.05 col./m2) highest abundance was found at middle sites (zone 2). According to the temporal data, the highest abundance of BBD (0.77 col./m2) was found during the transition period (between wet and dry seasons), whereas for WS higher abundance occurred within the dry season (0.07 col./m2). There was a significant difference in disease abundance among seasons which was correlated with increasing temperature and light intensity along with variations in total organic matters, nitrite and phosphate levels. Moreover, the middle sites experienced additional stress from the waste material originating from the mainland. [ABSTRACT FROM AUTHOR]

The prevalence of coral disease was previously unreported on the reefs of the Padang Shelf Reef System, West Sumatra and is relatively uncommon. The objective of this study was to get coral disease prevalence of each site which located at inshore, mid-shelf reef and off-shore reefs. The research was carried out by using belt transect method with 1 m left and right of tape as long 30 m with 3 replications. Two kinds of coral disease and two indicators of stressed coral were observed. While relatively infrequent, Black Band Disease was most common (1.3%) occurring on Pandan Island at 5m. White Syndrome occurred at Air patch reef (0.3%). A few bleached colonies of Montipora sp. and Pocillopora verrucosa were observed on Pieh Island reef (2.1%). Focal bleaching was observed on Galaxea sp. and Goniastrea sp. at Gabuo patch reefs (2.5%) and on Pocillopora verrucosa at Sipakal patch reef (3.9%). BBD infected both Montipora sp. and Porites sp. WS only infected on Montipora sp. Montipora, Pocillopora and Porites were the most common genera observed on the reefs. It suggests that coral disease infection was classified as a minor and it will not hamper coral recovery processes and coral health status in Padang Waters, West Sumatera. [ABSTRACT FROM AUTHOR]

Terrestrial runoff and sedimentation have been implicated in a variety of impacts on scleractinian corals. However, despite accumulating evidence, little work has been done to investigate their influence on coral disease development. This study examined the role that river runoff and the associated sedimentation could play in affecting the prevalence of the coral disease “white syndrome” in SW Madagascar. Corals from reefs affected by river discharge and terrestrial sediments were more affected by white syndrome than reefs located far from any source of terrestrial runoff. Terrestrial runoff-affected reefs also displayed a wider diversity of coral species affected by this disease. While much evidence has been pointing in the direction of indirect effects of such runoff on coral disease development, our data corroborates earlier suggestions that pathogens are present within the sediments. As such, sediments released on reefs through river discharge could act as reservoirs of coral pathogens. [ABSTRACT FROM AUTHOR]

Recreational diving and snorkeling on coral reefs is one of the fastest growing tourism sectors globally. Damage associated with intensive recreational tourist use has been documented extensively on coral reefs, however other impacts on coral health are unknown. Here, we compare the prevalence of 4 coral diseases and 8 other indicators of compromised coral health at high and low use dive sites around the island of Koh Tao, Thailand. Surveys of 10,499 corals reveal that the mean prevalence of healthy corals at low use sites (79%) was twice that at high use sites (45%). We also found a 3-fold increase in coral disease prevalence at high use sites, as well as significant increases in sponge overgrowth, physical injury, tissue necrosis from sediment, and non-normally pigmented coral tissues. Injured corals were more susceptible to skeletal eroding band disease only at high use sites, suggesting that additional stressors associated with use intensity facilitate disease development. Sediment necrosis of coral tissues was strongly associated with the prevalence of white syndromes, a devastating group of diseases, across all sites. We did not find significant differences in mean levels of coral growth anomalies or black band disease between high and low use sites. Our results suggest that several indicators of coral health increase understanding of impacts associated with rapid tourism development. Identifying practical management strategies, such as spatial management of multiple reef-based activities, is necessary to balance growth of tourism and maintenance of coral reefs. [ABSTRACT FROM AUTHOR]

Predation on coral tissue by the crab Cymo melanodactylus has been hypothesized to contribute to tissue loss caused by white syndromes (WS) in acroporid corals. Here, we demonstrate that transplanting C. melanodactylus crabs from WS-infected Acropora colonies onto healthy coral fragments in controlled aquarium experiments does not result in WS transmission over a 21-day experimental period. Furthermore, progression of WS lesions was three times more rapid on corals with all C. melanodactylus crabs removed than on those with crabs (2.28 ± 0.21 vs. 0.74 ± 0.22 cm/day, respectively); thus, crabs slow WS disease progression under experimental conditions. In choice experiments, C. melanodactylus crabs were strongly attracted to corals with WS lesions, with 87 % of crabs migrating to WS fragments versus 3 % to healthy fragments. The strong attraction of C. melanodactylus to WS-infected corals and their ability to significantly reduce lesion progression rates suggest a mechanism whereby these coral-dwelling crabs could mitigate the effects of WS diseases on reefs. [ABSTRACT FROM AUTHOR]

Tissue loss diseases or white syndromes (WS) are some of the most important coral diseases because they result in significant colony mortality and morbidity, threatening dominant Acroporidae in the Caribbean and Pacific. The causes of WS remain elusive in part because few have examined affected corals at the cellular level. We studied the cellular changes associated with WS over time in a dominant Hawaiian coral, Montipora capitata, and showed that: (i) WS has rapidly progressing (acute) phases mainly associated with ciliates or slowly progressing (chronic) phases mainly associated with helminths or chimeric parasites; (ii) these phases interchanged and waxed and waned; (iii) WS could be a systemic disease associated with chimeric parasitism or a localized disease associated with helminths or ciliates; (iv) corals responded to ciliates mainly with necrosis and to helminths or chimeric parasites with wound repair; (v) mixed infections were uncommon; and (vi) other than cyanobacteria, prokaryotes associated with cell death were not seen. Recognizing potential agents associated with disease at the cellular level and the host response to those agents offers a logical deductive rationale to further explore the role of such agents in the pathogenesis of WS in M. capitata and helps explain manifestation of gross lesions. This approach has broad applicability to the study of the pathogenesis of coral diseases in the field and under experimental settings. [ABSTRACT FROM AUTHOR]

Acropora white syndrome ( AWS) is characterized by rapid tissue loss revealing the white underlying skeleton and affects corals worldwide; however, reports of causal agents are conflicting. Samples were collected from healthy and diseased corals and seawater around American Samoa and bacteria associated with AWS characterized using both culture-dependent and culture-independent methods, from coral mucus and tissue slurries, respectively. Bacterial 16 S r RNA gene clone libraries derived from coral tissue were dominated by the Gammaproteobacteria, and Jaccard's distances calculated between the clone libraries showed that those from diseased corals were more similar to each other than to those from healthy corals. 16 S r RNA genes from 78 culturable coral mucus isolates also revealed a distinct partitioning of bacterial genera into healthy and diseased corals. Isolates identified as Vibrionaceae were further characterized by multilocus sequence typing, revealing that whilst several Vibrio spp. were found to be associated with AWS lesions, a recently described species, Vibrio owensii, was prevalent amongst cultured Vibrio isolates. Unaffected tissues from corals with AWS had a different microbiota than normal Acropora as found by others. Determining whether a microbial shift occurs prior to disease outbreaks will be a useful avenue of pursuit and could be helpful in detecting prodromal signs of coral disease prior to manifestation of lesions. [ABSTRACT FROM AUTHOR]

Abstract: We performed histological examination of 69 samples of Acropora sp. manifesting different types of tissue loss (Acropora White Syndrome-AWS) from Hawaii, Johnston Atoll and American Samoa between 2002 and 2006. Gross lesions of tissue loss were observed and classified as diffuse acute, diffuse subacute, and focal to multifocal acute to subacute. Corals with acute tissue loss manifested microscopic evidence of necrosis sometimes associated with ciliates, helminths, fungi, algae, sponges, or cyanobacteria whereas those with subacute tissue loss manifested mainly wound repair. Gross lesions of AWS have multiple different changes at the microscopic level some of which involve various microorganisms and metazoa. Elucidating this disease will require, among other things, monitoring lesions over time to determine the pathogenesis of AWS and the potential role of tissue-associated microorganisms in the genesis of tissue loss. Attempts to experimentally induce AWS should include microscopic examination of tissues to ensure that potentially causative microorganisms associated with gross lesion are not overlooked. [Copyright &y& Elsevier]

The article discusses a study on the prevalence of white syndrome (WS) in the Indian Ocean and its conformity to the patterns found for coral diseases in the Caribbean and the Pacific Ocean. The two types of coral diseases include white diseases and WS. The reason behind the decision of researchers to conduct such study was the damage caused by such diseases to coral reefs found in the Caribbean and the Pacific Ocean. The impact of WS on Acropora plate corals is also noted. It was found that the distribution WS indicates that patterns in disease prevalence and the impact on coral reefs can be location- or region-specific.

Acroporid white syndrome, a disease-like syndrome from the Great Barrier Reef, results from degenerative host tissue at lesion borders. Tissue preceding lesion borders appears visually healthy, but it is currently unclear whether the endosymbiotic zooxanthellae (Symbiodinium) are physiologically impacted. Compared to healthy colonies, this study found no significant differences in symbiont density, mitotic index or chlorophyll a content in tissue bordering (0 cm), and 8 cm away from white syndrome lesions. Using chlorophyll a fluorescence techniques, the border tissue did not appear to be photosynthetically compromised, and Symbiodinium extracted from this area were photosynthetically competent. Transmission electron microscopy revealed extensive degeneration of host tissues surrounding symbionts in affected areas, however, Symbiodinium cells were structurally intact with no sign of in situ degradation. Collectively, these results suggest that Symbiodinium at white syndrome lesion borders exist in a dynamic intra-cellular state during active host tissue loss, yet remain physiologically uncompromised. [ABSTRACT FROM AUTHOR]

Morphological diagnosis and descriptions of seven disease-like syndromes affecting scleractinian corals were characterized from the southern Great Barrier Reef (GBR). Chl a fluorescence of PSII was measured using an Imaging-PAM (pulse amplitude modulated) fluorometer, enabling visualization of the two-dimensional variability in the photophysiology of endosymbiotic dinoflagellates (zooxanthellae) by measuring rapid light curves. Three of four syndromes associated with active tissue loss (type a) were spatially homogenous (white syndrome, brown band, and skeletal eroding band), with no impact on the photochemical function of zooxanthellae populations at or behind the lesion borders. However, a decline in maximum quantum yield ( Fv/ Fm) and elevated levels of maximum nonphotochemical quenching (NPQmax) occurred in visually healthy tissue of black band disease adjacent to the lesion borders, possibly due to hypoxic conditions caused by the black band cyanobacterial mat. Two out of three syndromes associated with pathological change of intact tissue with no active tissue loss (type b) showed variable photophysiological responses (neoplasia and pigmentation response). Only the bleached foci associated with white patch syndrome appeared to impact primarily on the symbiotic dinoflagellates, as evidenced by declines in minimum fluorescence ( F0) and maximum quantum yield ( Fv/ Fm), with no indication of degeneration in the host tissues. Our results suggest that for the majority of coral syndromes from the GBR, pathogenesis occurs in the host tissue, while the impact on the zooxanthellae populations residing in affected corals is minimal. [ABSTRACT FROM AUTHOR]

Following rapid lesion progression of white syndrome in tabular Acropora spp., the white bare skeleton gradually changes to green, a result of endolithic algae blooms (primarily Ostreobium spp.). Endolithic algal biomass and chlorophyll concentration were found to be an order of magnitude higher in the green zone compared with healthy appearing parts of each colony. Chl b to Chl a ratio increased from 1:1.6 in the healthy area to 1:2 and 1:3.5 in the white exposed skeleton and green zones, respectively. These observations together with pulse amplitude modulated (PAM) fluorometry suggest photoacclimation of the endoliths in the green zone. Histopathological microscopy revealed that the endolithic algal filaments penetrate the coral tissue. This study highlights the interaction of endolithic algae with both the skeleton and host tissue. This may have a critical role in the processes that accompany the post-disease state in reef-building corals. [ABSTRACT FROM AUTHOR]

'White syndrome' is considered to be the most prevalent coral disease on the Great Barrier Reef, characterised by rapid rates of lesion progression and high levels of colony mortality. This study investigated the production and translocation of photoassimilates towards white syndrome lesions (WSLs) and artificially inflicted lesions in healthy and diseased colonies of tabular Acropora spp. to determine the intra-colonial response to white syndrome using 14C labelling. Translocation of 14C labelled photoassimilates was preferentially orientated away from active WSLs, with minimal 14C activity observed in the lesion borders, whilst artificial lesions (ALs) created directly opposite WSL borders showed significantly higher 14C activity, suggesting active translocation of photoassimilates for tissue regeneration. Transport of photoassimilates in healthy coral colonies was preferentially oriented towards ALs with a higher perimeter-area ratio, although translocation towards WSL boundaries was minimal even though the lesion perimeter was often the width of the colony (>200 cm). We suggest that the preferential orientation of photoassimilates away from WSLs may represent a deliberate strategy by the colony to induce a 'shutdown reaction' in order to preserve intra-colonial resources within areas of the colony that are more likely to survive and recover. [ABSTRACT FROM AUTHOR]

Recent observations suggest that a spreading disease is increasingly contributing to hard coral mortality in the Solitary Islands Marine Park, NSW, Australia. This study determined coral disease prevalence and rate-of-spread through individual affected colonies and investigated the effect this epizootic had on coral populations at sites adjacent to South West Solitary Island. Quantitative data were collected between 2002 and 2004 using photographic and video methods, and visual census along radial arc belt transects. Disease similar to the reported white syndrome and white plague was apparent, spreading through hard coral species from the genera Turbinaria, Acropora, Goniastrea, Pocillopora, Stylophora and Porites. Coral disease prevalence varied between survey dates with mean prevalence increasing from 8.55% during March 2003 to 13.58% in June and declining to 7.75% in September and 6.21% during March 2004. There was a significant difference in mean prevalence between the affected species (p < 0.001) and an overall difference between survey dates (p = 0.001). Additionally, the rate-of-spread of coral disease through coral colonies determined using repeated, seasonal, still photographs followed similar patterns, with disease progression differing between affected species (p = 0.004), and between survey dates (p < 0.001). Analysis of the video-transects indicated significant difference in disease prevalence over larger spatial scales (100s of m). However, disease frequency did not vary significantly between 2002 and 2003. [ABSTRACT FROM AUTHOR]

The aim of the article is to provide nurse practitioners with a basic understanding of the pathophysiology, clinical characteristics, diagnostic methods, and management of Wolff-Parkinson White (WPW) syndrome. WPW syndrome is the most common form of ventricular preexcitation, a condition in which the ventricular myocardium is activated earlier than if the impulse had traveled to the ventricles through the normal arrioventricular conduction system. Due to a defect in early cardiac development, a muscular connection permits a direct connection between the arrial and ventricular myocardium.