First Report of Potential Coral Disease in the Coral Hatchery of Thailand

In this study, coral disease was first reported in the coral hatchery in Thailand. Disease were usually found on corals aged two to five years old during the months of November to December of each year. To identify bacterial strains, culture-based methods for strain isolation and molecular techniques of the 16S rRNA gene analysis were used. The resuts showed that the dominant genera of bacteria in diseased corals were Vibrio spp. (comprising 41.01% of the isolates). The occurrence of the disease in the coral hatchery can have a significant effect on the health and survival of juvenile corals before being transplanted to natural reefs for restoration.

Coral diseases of mushroom coral (Fungiidae) in Pari Island, Kepulauan Seribu, Jakarta

Coral disease is one of the causes of the decline in the condition of coral reef ecosystems. This study aims to measure coral health based on the abundance and prevalence of coral health categories. The research was conducted in the Pari Island Cluster, Seribu Islands at four stations. The Belt Transect method with 2 × 100 meters was used to calculate coral health and a 30 m Line Intercept Transect (LIT) with three replications to determine substrate cover. The condition of coral reefs can be categorized as moderate to good based on this percentage value. The study results found five genera from the Fungiidae, namely Fungia, Ctenactis, Herpolitha, Heliofungia, and Sandalolitha. The most commonly found genus is the genus Fungia. The health condition of Fungiidae corals in Pari Island is divided into two categories, namely 35% healthy and 65% unhealthy, consisting of changes in tissue color - white (coral bleaching), changes in tissue color - not white (yellow band disease), and compromised health (damage by sedimentation). Yellow band disease is only found in the genus ˆ and is not found in other genera.

Characterization of the Coral Disease 'Porites Bleaching with Tissue Loss' (PBTL) From Hawaii

<p>Coral reefs around the world are facing many threats and have sustained severe losses in coral cover over the past few decades. Coral bleaching and disease outbreaks have contributed substantially to this reef decline, however our understanding of factors contributing to the increase in coral disease prevalence are poorly understood. Information on the disease dynamics of different diseases affecting a reef system is essential for the development of effective management strategies. The aim of this research was to characterise and build a case study of a bleaching response affecting Porites compressa in Kaneohoe Bay, Oahu, Hawaii. It manifests as a localised, discrete area on the coral colony with a bleached coenenchyme and pigmented polyps, giving the affected area a “speckled” appearance. A disease by definition is any interruption, cessation or disorder of body functions, systems or organs. Results of this study showed that this localised bleaching causes tissue loss and a reduction in the number of gametes, and hence harm to the host. It was therefore classified as a disease and named Porites bleaching with tissue loss (PBTL). In addition, PBTL does not appear to represent a common thermal bleaching response as it was present throughout the year during times when seawater temperature was well within the coral’s thermal threshold. Symbiodinium cell density in PBTL-affected areas of the coral colony was reduced by 65%, and examination of affected host tissue using light microscopy showed fragmentation and necrosis. However, no potential pathogen was observed. Transmission electron microscopy (TEM) revealed a high occurrence of potential apoptotic Symbiodinium cells and a potential increase in the abundance of virus-like particles (VLPs) in PBTL-affected tissue. However a causal relationship remains to be established. Long-term monitoring showed spatio-temporal variations in PBTL prevalence. Temporal variations in prevalence reflected a seasonal trend with a peak during the summer months, linked to increasing seawater temperature. Spatial variations in disease prevalence were correlated with parrotfish density, turbidity and water motion. Of these, a negative correlation with variability (SD) in turbidity explained most of the variability in PBTL prevalence (12.8%). A positive correlation with water motion explained 9% and a positive correlation with the variability in parrotfish density explained 4.4%. Overall, only a relatively small proportion of variability in PBTL prevalence could be explained by these three factors (26.2%), suggesting that other factors, not investigated in this study, play a more important role in explaining PBTL patterns or that temporal variation in temperature is the overall major driving force. Monitoring of individually tagged P. compressa colonies showed that >80% of affected colonies sustained partial colony mortality (tissue loss) within two months; on average, one third of the colony is lost. The amount of tissue loss sustained was correlated to lesion size but not colony size. Case fatality (total mortality) was low (2.6%), however this disease can affect the same colonies repeatedly, suggesting a potential for progressive damage which could cause increased tissue loss over time. PBTL was not transmissible through direct contact or the water column in controlled aquaria experiments, suggesting that this disease might not be caused by a pathogen, is not highly infectious, or perhaps requires a vector for transmission. At present, PBTL has only been observed within Kaneohe Bay. An investigation of the potential role of host and Symbiodinium genetics in disease susceptibility revealed the same Symbiodinium sub-clade (C15) in healthy and PBTL-affected colonies, suggesting no involvement of Symbiodinium type in disease etiology. Results regarding host genetics remained inconclusive; however a difference in allele frequency at one microsatellite locus was observed between healthy and diseased samples. This difference could, however, be due to a lower amplification of PBTL-affected samples at this locus and needs to be regarded with some caution. The results of this study provide a case definition of PBTL which can be used as a baseline in further studies. P. compressa is the main framework building species in Kaneohe Bay, and the information gathered here on disease dynamics and virulence suggests that PBTL has the potential to negatively impact the resilience of reefs within the bay. Further research into the etiology of PBTL is necessary to fully understand the impact that this disease could have on coral reefs in Hawaii.</p>

Characterization of the Coral Disease 'Porites Bleaching with Tissue Loss' (PBTL) From Hawaii

<p>Coral reefs around the world are facing many threats and have sustained severe losses in coral cover over the past few decades. Coral bleaching and disease outbreaks have contributed substantially to this reef decline, however our understanding of factors contributing to the increase in coral disease prevalence are poorly understood. Information on the disease dynamics of different diseases affecting a reef system is essential for the development of effective management strategies. The aim of this research was to characterise and build a case study of a bleaching response affecting Porites compressa in Kaneohoe Bay, Oahu, Hawaii. It manifests as a localised, discrete area on the coral colony with a bleached coenenchyme and pigmented polyps, giving the affected area a “speckled” appearance. A disease by definition is any interruption, cessation or disorder of body functions, systems or organs. Results of this study showed that this localised bleaching causes tissue loss and a reduction in the number of gametes, and hence harm to the host. It was therefore classified as a disease and named Porites bleaching with tissue loss (PBTL). In addition, PBTL does not appear to represent a common thermal bleaching response as it was present throughout the year during times when seawater temperature was well within the coral’s thermal threshold. Symbiodinium cell density in PBTL-affected areas of the coral colony was reduced by 65%, and examination of affected host tissue using light microscopy showed fragmentation and necrosis. However, no potential pathogen was observed. Transmission electron microscopy (TEM) revealed a high occurrence of potential apoptotic Symbiodinium cells and a potential increase in the abundance of virus-like particles (VLPs) in PBTL-affected tissue. However a causal relationship remains to be established. Long-term monitoring showed spatio-temporal variations in PBTL prevalence. Temporal variations in prevalence reflected a seasonal trend with a peak during the summer months, linked to increasing seawater temperature. Spatial variations in disease prevalence were correlated with parrotfish density, turbidity and water motion. Of these, a negative correlation with variability (SD) in turbidity explained most of the variability in PBTL prevalence (12.8%). A positive correlation with water motion explained 9% and a positive correlation with the variability in parrotfish density explained 4.4%. Overall, only a relatively small proportion of variability in PBTL prevalence could be explained by these three factors (26.2%), suggesting that other factors, not investigated in this study, play a more important role in explaining PBTL patterns or that temporal variation in temperature is the overall major driving force. Monitoring of individually tagged P. compressa colonies showed that >80% of affected colonies sustained partial colony mortality (tissue loss) within two months; on average, one third of the colony is lost. The amount of tissue loss sustained was correlated to lesion size but not colony size. Case fatality (total mortality) was low (2.6%), however this disease can affect the same colonies repeatedly, suggesting a potential for progressive damage which could cause increased tissue loss over time. PBTL was not transmissible through direct contact or the water column in controlled aquaria experiments, suggesting that this disease might not be caused by a pathogen, is not highly infectious, or perhaps requires a vector for transmission. At present, PBTL has only been observed within Kaneohe Bay. An investigation of the potential role of host and Symbiodinium genetics in disease susceptibility revealed the same Symbiodinium sub-clade (C15) in healthy and PBTL-affected colonies, suggesting no involvement of Symbiodinium type in disease etiology. Results regarding host genetics remained inconclusive; however a difference in allele frequency at one microsatellite locus was observed between healthy and diseased samples. This difference could, however, be due to a lower amplification of PBTL-affected samples at this locus and needs to be regarded with some caution. The results of this study provide a case definition of PBTL which can be used as a baseline in further studies. P. compressa is the main framework building species in Kaneohe Bay, and the information gathered here on disease dynamics and virulence suggests that PBTL has the potential to negatively impact the resilience of reefs within the bay. Further research into the etiology of PBTL is necessary to fully understand the impact that this disease could have on coral reefs in Hawaii.</p>

Coral Disease and the Environment in the Pacific Ocean

<p>Coral diseases are a major threat to coral reef health and functioning worldwide. Little is known about how coral disease prevalence relates to multiple interacting changes in host densities, abiotic stressors, and levels of human impact. In particular, almost nothing is known about coral disease dynamics under changing abiotic conditions in the absence of direct anthropogenic stressors. Understanding how disease dynamics change relative to shifts in environmental conditions is crucial for the successful management and future survival of coral reefs. With the use of existing and novel field data and statistical modeling I examined the associations (abiotic and biotic) of multiple coral disease states across a variety of spatial scales encompassing a wide range of environmental conditions. Biomedical techniques were then used to relate these environmental associations to potential disease etiology. Study sites included areas with high levels of anthropogenic impact (e.g. Oahu, main Hawaiian Islands); to extremely remote quasi-pristine reefs removed from direct human influence (e.g. Palmyra Atoll National Wildlife Refuge). Over small spatial scales (100s m) at a marine reserve in the main Hawaiian Islands I modelled the spatial patterns of four coral diseases (Porites growth anomalies, Porites tissue loss, Porites trematodiasis and Montipora white syndrome). While Porites tissue loss and Montipora white syndrome were positively associated with poor environmental conditions (poor water quality, low coral cover), Porites growth anomalies and Porites trematodiasis were more prevalent in areas considered to be of superior quality (clearer water, increased host abundance, higher numbers of fish). At Palmyra Atoll, fatal tissue loss diseases were largely absent and although coral growth anomalies were present their prevalence was extremely low. Patterns of growth anomaly prevalence at Palmyra were positively associated with host abundance across four coral genera (Acropora, Astreopora, Montipora and Porites) and generally negatively associated with algal cover. Growth anomalies, although progressive and detrimental to the hosts, were most prevalent in the "healthiest" regions (the highest coral cover regions) of Palmyra. I hypothesised that differences seen in the types and prevalence of coral diseases between heavily populated parts of Hawaii and remote uninhabited locations such as Palmyra Atoll, could be a result of differing levels of either direct (e.g. pollution) or indirect (e.g. pollution leading to loss of key hosts) human stressors, in addition to natural changes in the environment. To begin disentangling the confounding effects of natural variability and human stressors on coral disease prevalence patterns I modelled two diseases (Acropora and Porites growth anomalies) across hundreds of sites throughout the Indo-Pacific Ocean (1000s km). Predictors included host densities, human population numbers, frequency of sea surface temperature anomalies, and input of ultra-violet radiation. Porites growth anomaly prevalence was positively associated with human population density (and to a lesser extent host density), while the prevalence of Acropora growth anomalies was strongly host density dependent. The positive association between the prevalence of Porites growth anomalies and human density suggests the presence and prevalence of the disease are related, directly or indirectly, to some environmental co-factor associated with increased human density at regional spatial scales. Although this association has been widely posited, this is one of the first wide scale studies unambiguously linking a coral disease with human population size. In summary, the types of coral diseases observed, their prevalence, and spatial patterns of distribution within reef systems are the result of multiple abiotic and biotic factors and stressors interacting, in some cases synergistically. Statistical modelling, in conjunction with biomedical techniques and field observations, proved essential to the understanding of coral disease ecology within single reefs and atolls to patterns across entire oceans.</p>

An emerging coral disease outbreak decimated Caribbean coral populations and reshaped reef functionality

Diseases are major drivers of the deterioration of coral reefs, linked to major declines in coral abundance, reef functionality, and reef-related ecosystems services1-3. An outbreak of a new disease is currently rampaging through the populations of the remaining reef-building corals across the Caribbean region. The outbreak was first reported in Florida in 2014 and reached the northern Mesoamerican reef by summer 2018, where it spread across the ~ 450-km reef system only in a few months4. Rapid infection was generalized across all sites and mortality rates ranged from 94% to < 10% among the 21 afflicted coral species. This single event further modified the coral communities across the region by increasing the relative dominance of weedy corals and reducing reef functionality, both in terms of functional diversity and calcium carbonate production. This emergent disease is likely to become the most lethal disturbance ever recorded in the Caribbean, and it will likely result in the onset of a new functional regime where key reef-building and complex branching acroporids (a genus apparently unaffected) will once again become conspicuous structural features in reef systems with yet even lower levels of physical functionality.

Ascidians Outbreak: A Threat For Coral Reefs in Panjang Island, Jepara

Eutrophication and sedimentation have become a major threat to coral reefs in nearby areas with anthropogenic activities. These threats are often accompanied by shifting ecosystems from coral-rich to fast-growing algae-dominated water, and high prevalence of coral disease. In Panjang Island, Jepara, we observed the outbreak of photosynthetic ascidians along with a high sedimentation at the eastern part of the island. The ascidians were seen overgrowing most substrates including corals, macroalgae, dead-coral-algae, and rubbles in April to May 2019. In July and August 2019, observation and data collection using quadrant transect were conducted to monitor the outbreak. The result showed that ascidians were still present in the area, despite becoming pale and smaller. This report shows that the outbreak of these photosynthetic ascidians was not persistent, however, the effect on coral reef health should not be overlooked.

Multi-Variate Analyses of Coral Mortality From the 2014–2015 Stony Coral Tissue Loss Disease Outbreak Off Miami-Dade County, Florida

Environmental compliance monitoring associated with the Port Miami dredging project (2013–2015), designed to assess the impact of project-generated sediments on the local coral community, fortuitously captured a thermal bleaching event and the first reports of an emergent, highly contagious, white-plague-like coral disease outbreak in the fall of 2014. The disease, now termed stony coral tissue loss disease (SCTLD), has decimated reefs throughout Florida and is now spreading across the Caribbean. The high prevalence of disease, the number of affected species, and the high mortality of corals affected suggests SCTLD may be the most lethal coral disease ever recorded. Previous analyses of the dredge monitoring data have reached mixed conclusions about the relative impact of dredging on coral mortality and has often parsed out disease susceptible individuals to isolate the impacts of dredging only. We use multi-variate analyses, including time-based survival analyses, to examine the timing and impacts of dredging, coral bleaching, and disease on local coral mortality. By examining the status of corals monthly from the October 2013 to July 2015 observational period, we found that coral mortality was not significantly affected by a coral’s proximity to the dredge site or sediment burial. Instead, coral mortality was most strongly impacted by disease and the emergence of SCTLD during the monitoring period. During the 2-year monitoring period, 26.3% of the monitored corals died, but the only conditions significantly affected by the dredge were partial burial and partial mortality. The strongest link to mortality was due to disease, which impacted coral species differently depending on their susceptibility to SCTLD. The focus on disturbances associated with dredging created a circumstance where the greater impacts of this emergent disease were downplayed, leading to a false narrative of the resulting mortality on the local coral communities. The results of this study reveal that while local events such as a dredging project do have quantifiable effects and can be harmful to corals, regional and global threats that result in mass coral mortality such as thermal stress and disease represent an existential threat to coral reefs and must be urgently addressed.

Prevalence of Stony Coral Tissue Loss Disease at El Seco, a Mesophotic Reef System off Vieques Island, Puerto Rico

Mesophotic coral ecosystems (MCEs) are ecologically and functionally vital, as they are Essential Fish Habitats that function as refugia for corals and sponges of shallow-water reefs. Stony Coral Tissue Loss Disease (SCTLD) is a relatively new lethal coral disease, first affecting coral reefs in Florida and has now spread through most of the Caribbean. SCTLD was observed in Puerto Rico in December 2019 in Culebra Island. Since then, SCTLD has appeared along the east coast of Puerto Rico, affecting primarily shallow reefs in San Juan, Culebra and Vieques Island, and Fajardo. During late June and July 2020, four mesophotic reef habitats were surveyed at El Seco (off Vieques Island), on the southeast coast of Puerto Rico. SCTLD was observed at colonized pavement (CPRT – 23–30 m), bank coral reef (BCR – 35–40 m), patch coral reef (PCR – 36–42 m), and rhodolith (Rhodo – 40–50 m) habitats. The mean percent substrate cover by sessile-benthic categories varied significantly between habitats (PERMANOVA, p &lt; 0.001), with a higher mean (± SE) coral cover at BCR (26.95 ± 5.60%), followed by PCR (12.88 ± 3.88%). SCTLD was detected in all habitats, but the disease prevalence was significantly higher at BCR, ranging from 9.70 to 21.13% of colonies infected (Kruskal-Wallis ANOVA, p &lt; 0.007). Even though PCR habitats exhibited less coral cover, SCTLD prevalence was still elevated ranging from 6.66 to 15.07%. The deepest record of SCTLD at El Seco was 40.9 m. The majority (∼98%) of the corals infected with the disease were from the Orbicella complex spp. (faveolata/franksi). However, there were other infected species, such as Agaricia grahamae, A. lamarcki, Montastraea cavernosa, and Porites astreoides. As seen in the surveys conducted in 2011 and 2020, the loss of coral cover allows for the emergence of other benthic “detractors,” such as peyssonnelids, specifically Ramicrusta spp. Ramicrusta spp., an aggressive encrusting red alga known to take over available space and overgrow corals, significantly increased its substrate cover at the impacted reefs. Therefore, the severity and virulence of SCTLD will most likely have severe and long-lasting negative impacts on the coral communities at El Seco mesophotic reef system.