Healthy Coral Tissue Research Articles

Red Fluorescent Protein Responsible for Pigmentation in Trematode-Infected Porites compressa Tissues

Reports of coral disease have increased dramatically over the last decade; however, the biological mechanisms that corals utilize to limit infection and resist disease remain poorly understood. Compromised coral tissues often display non-normal pigmentation that potentially represents an inflammation-like response, although these pigments remain uncharacterized. Using spectral emission analysis and cryo-histological and electrophoretic techniques, we investigated the pink pigmentation associated with trematodiasis, infection with Podocotyloides stenometre larval trematode, in Porites compressa. Spectral emission analysis reveals that macroscopic areas of pink pigmentation fluoresce under blue light excitation (450 nm) and produce a broad emission peak at 590 nm (+/-6) with a 60-nm full width at half maximum. Electrophoretic protein separation of pigmented tissue extract confirms the red fluorescence to be a protein rather than a low-molecular-weight compound. Histological sections demonstrate green fluorescence in healthy coral tissue and red fluorescence in the trematodiasis-compromised tissue. The red fluorescent protein (FP) is limited to the epidermis, is not associated with cells or granules, and appears unstructured. These data collectively suggest that the red FP is produced and localized in tissue infected by larval trematodes and plays a role in the immune response in corals.

Bleached, But Not by the Sun: Sunscreen Linked to Coral Damage

Warm, shallow, sun-drenched seas sparkling with brilliantly colored fish and coral species—we’ve all seen dazzling images of tropical reefs. Coral reefs are among the most biologically productive and diverse ecosystems in the world, providing food protein for half a billion people. But tropical reefs have begun dying from bleaching, with the frequency and spatial extent of such bleaching increasing dramatically over the past 20 years. Now a study finds that chemical compounds in sunscreen products can cause abrupt and complete bleaching of hard corals, even at extremely low concentrations [EHP 116:441–447; Danovaro et al.]. Zooxanthellae, symbiotic algae that live in healthy coral tissue, provide nutrients to corals through photosynthesis. The algae also help make the spectacular colors for which corals are known. The corals lose their color when zooxanthellae die or leave the reef; the protective skeletons of the corals are thus exposed, and the corals die. Rising seawater temperatures, bacterial and viral diseases, ultraviolet light or other radiation, and pollution have been blamed for coral bleaching. Scientists at the Polytechnic University of the Marche Region in Ancona, Italy, studied the effects of sunscreen exposure on samples from tropical reefs. The researchers collected branches of hard coral from sites in the Red Sea, the Caribbean Sea, the Indian Ocean off Thailand, and the Pacific Ocean near Indonesia. Coral branches were immersed in bags of virus-free seawater supplemented with various quantities of sunscreen, then incubated in situ. These samples were compared with controls also incubated in situ in virus-free seawater. The researchers found that among the several brands of sunscreen tested, four commonly found ingredients—paraben, cinnamate, benzophenone, and camphor derivatives—can stimulate dormant viral infections in zooxanthellae. The sunscreen chemicals caused viruses within zooxanthellae to replicate until their algal hosts exploded, spilling viruses into the surrounding seawater, which could then spread infection to nearby coral communities. Coral bleaching occurred, often within a few hours, but always within 4 days, at sunscreen quantities as small as 10 μL/L. Controls remained healthy. The researchers estimate that approximately 10% of the world’s coral reefs are potentially threatened by sunscreen that washes off swimmers in reef waters. The study suggests that, as tourism continues to increase in tropical reef areas, the impact of sunscreens on coral bleaching could rise significantly in the future.

Defences against oxidative stress in vibrios associated with corals

Bacteria colonizing healthy coral tissue may produce enzymes capable of overcoming the toxic effects of reactive oxygen species, including superoxide dismutase (SOD) and catalase. Significant differences in the activities of these enzymes were observed in cultures of Vibrio campbellii, Vibrio coralliilyticus, Vibrio harveyi, Vibrio mediterranei, Vibrio pelagius, Vibrio rotiferanus, Vibrio tasmaniensis, and Photobacterium eurosenbergii isolated from healthy, bleached or necrotic tropical and cold water corals. Levels of SOD in exponential phase cultures of V. coralliilyticus grown at 28 degrees C were only slightly higher than those grown at 16 degrees C whereas the levels in stationary phase cultures at 28 degrees C were 7.3 x higher than those at 16 degrees C. The increase in catalase activity of V. coralliilyticus and V. harveyi upon entry to stationary phase conferred protection against killing by oxidative stress. Increased temperature affected up-regulation of enzymes in stationary phase cultures, but pretreatment of cultures with hydrogen peroxide had no significant effect on induction of catalase or SOD. The increased activities appear to be due to up-regulation of gene expression rather than induction of different forms of the enzymes. We suggest that SOD and catalase are unlikely to be major factors in the virulence of these bacteria for corals and that their main function may be to protect against endogenous superoxide.

Coral microbial communities, zooxanthellae and mucus along gradients of seawater depth and coastal pollution

The high incidence of coral disease in shallow coastal marine environments suggests seawater depth and coastal pollution have an impact on the microbial communities inhabiting healthy coral tissues. A study was undertaken to determine how bacterial communities inhabiting tissues of the coral Montastraea annularis change at 5 m, 10 m and 20 m water depth in varying proximity to the urban centre and seaport of Willemstad, Curaçao, Netherlands Antilles. Analyses of terminal restriction fragment length polymorphisms (TRFLP) of 16S rRNA gene sequences show significant differences in bacterial communities of polluted and control localities only at the shallowest seawater depth. Furthermore, distinct differences in bacterial communities were found with increasing water depth. Comparisons of TRFLP peaks with sequenced clone libraries indicate the black band disease cyanobacterium clone CD1C11 is common and most abundant on healthy corals in less than 10 m water depth. Similarly, sequences belonging to a previously unrecognized group of likely phototrophic bacteria, herein referred to as CAB-I, were also more common in shallow water. To assess the influence of environmental and physiologic factors on bacterial community structure, canonical correspondence analysis was performed using explanatory variables associated with: (i) light availability; (ii) seawater pollution; (iii) coral mucus composition; (iv) the community structure of symbiotic algae; and (v) the photosynthetic activity of symbiotic algae. Eleven per cent of the variation in bacterial communities was accounted for by covariation with these variables; the most important being photosynthetically active radiation (sunlight) and the coral uptake of sewage-derived compounds as recorded by the delta(15)N of coral tissue.

Zooxanthellae Harvested by Ciliates Associated with Brown Band Syndrome of Corals Remain Photosynthetically Competent

Brown band syndrome is a new coral affliction characterized by a local accumulation of yet-unidentified ciliates migrating as a band along the branches of coral colonies. In the current study, morphologically intact zooxanthellae (= Symbiodinium) were observed in great numbers inside the ciliates (>50 dinoflagellates per ciliate). Microscale oxygen measurements and variable chlorophyll a fluorescence analysis along with microscopic observations demonstrated that zooxanthellae within the ciliates are photosynthetically competent and do not become compromised during the progression of the brown band zone. Zooxanthellae showed similar trends in light acclimation in a comparison of rapid light curve and steady-state light curve measures of variable chlorophyll a fluorescence. Extended light exposure of steady-state light curves resulted in higher quantum yields of photosystem II. The brown band tissue exhibited higher photosynthetically active radiation absorptivity, indicating more efficient light absorption due to a higher density of zooxanthellae in the ciliate-dominated zone. This caused relatively higher gross photosynthesis rates in the zone with zooxanthella-containing ciliates compared to healthy coral tissue. The observation of photosynthetically active intracellular zooxanthellae in the ciliates suggests that the latter can benefit from photosynthates produced by ingested zooxanthellae and from photosynthetic oxygen production that alleviates diffusion limitation of oxic respiration in the densely populated brown band tissue. It remains to be shown whether the zooxanthellae form a stable symbiotic association with the ciliate or are engulfed incidentally during grazing on coral tissue and then maintained as active inside the ciliate for a period before being digested and replaced by new zooxanthellae.

Disease and cell death in white syndrome of Acroporid corals on the Great Barrier Reef

White syndromes (WS) are among the most prevalent coral diseases, and are responsible for reef demise on the Great Barrier Reef. The disease manifests as a clear differentiation between tissue and exposed skeleton and results in rapid tissue loss. Fluorescence in situ hybridisation (FISH) was used in conjunction with histology and transmission electron microscopy (TEM) to investigate bacterial communities and cell death associated with WS. No evidence of bacterial communities or microbial association (using six bacterial probes, TEM and histopathology) was evident within the lesion or adjacent tissues, despite the presence of dense possible secondary invaders in the exposed skeletal regions. Despite widespread reference to necrosis in coral disease literature, there was no evidence of necrosis in any WS lesion or the adjacent tissues in this study. However, in situ end labelling, light microscopy and TEM of WS and healthy coral tissue sections showed evidence of extensive programmed cell death (PCD) exclusively in WS. This study provides the first evidence of intrinsic or PCD as a primary mechanism of cell death in WS, and may provide some explanation for the failure to isolate pathogens from over 80% of identified coral diseases, many of which show similar lesion patterns and WS characteristics.

The pink-blue spot syndrome in Acropora eurystoma (Eilat, Red Sea): A possible marker of stress?

The appearance of pink-blue spots (termed here as pink-blue spot syndrome – PBSS) in the branching coral Acropora eurystoma from the Gulf of Eilat, Red Sea, is described. We monitored 18 transects (10×1 m 2 each) in front of the H. Steinitz Marine Laboratory (Eilat), at 3, 6 and 9 m depth, during March and August in 2001 and 2002. Transect measurements revealed high frequencies of colonies with PBSS (up to 100% of colonies) between 3 and 9 m depth. Ten PBSS-affected colonies of A. eurystoma were labelled and monitored for the development of spots. From March to August 2001, the number of spots per colony increased and remained constantly high at both sampling dates in 2002. Spot size ranged between 7 and 149 mm 2. Spots were primarily recorded in areas where coral tissues contacted foreign biological matter, either around regenerative wounds or when surrounded by encrusting organisms, in fast-growing areas and in allogeneic interactions. A preliminary biochemical examination suggested that the pink-blue pigment in A. eurystoma is part of a family of compounds (pocilloporin) responsible for the pink-blue colours in pocilloporid and acroporid corals. Pink-blue colour could be experimentally induced in A. eurystoma by tissue-to-tissue contacts between distressed and non-distressed allogeneic branches. PBSS was also induced in healthy coral tissue by contact with inert objects, e.g., by bandaging a branch with plastic strips. Any specific pink-blue colour spots faded within 1–3 months from onset. These results suggest that PBSS in A. eurystoma may not be considered a regular coral disease, but rather a locally induced syndrome caused by restricted environmental and/or biological stress conditions.

Microbiological assessment of a disease outbreak on corals from Magnetic Island (Great Barrier Reef, Australia)

Unusual disease lesions were observed in Montipora corals on the fringing reef of Magnetic Island (Great Barrier Reef, Australia) following a period of high water temperature in early January 2002. Tissue death in Montipora spp. appeared as a black layer that spread rapidly across the colony surface, though this appeared as the final phase of disease progression (with three previous disease phases now identified, S. Anthony, unpublished). Culture and molecular-based microbial analysis of this layer did not identify a likely microbial pathogen. Despite this, DNA sequencing of microbial 16S rDNA indicated a shift in the bacterial population associated with affected coral tissue. A clone library of the healthy coral sample predominantly contained sequences within the γ-Proteobacteria. A disease coral sample representing the margin of the black lesion and healthy coral tissue was dominated by sequences, which demonstrated low sequence identity to a range of α-Proteobacteria, γ-Proteobacteria and cyanobacteria. The microbes identified in the diseased Montipora spp. samples are likely to be opportunistic rather than the causative agent of the observed lesion. Studies are in progress to further characterise the ecology of this disease and describe the potential microbial pathogen(s).

Coral disease outbreak: pattern, prevalence and transmission in Acropora cervicornis

MEPS Marine Ecology Progress Series Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsTheme Sections MEPS 301:119-128 (2005) - doi:10.3354/meps301119 Coral disease outbreak: pattern, prevalence and transmission in Acropora cervicornis Dana E. Williams1,2,*, Margaret W. Miller2 1Cooperative Institute of Marine and Atmospheric Science, Rosenstiel School of Marine and Atmospheric Science, University of Miami, 4600 Rickenbaker Causeway, Miami, Florida 33149, USA,2NOAA Fisheries, Southeast Science Center, 75 Virginia Beach Drive, Miami, Florida 33149, USA *Email: dana.williams@noaa.gov. Address for correspondence: NOAA Fisheries ABSTRACT: A rapidly progressing disease outbreak affecting Acropora cervicornis (staghorn coral) was recently observed over a wide geographic range (>200 km) in the Florida Keys, USA. Original observations made at White Bank Dry Rocks revealed colonies with tissue rapidly sloughing from multifocal lesions. Over the course of the epizootic at least 72% of tagged colonies were affected, live tissue cover of these colonies decreased from 96 ± 1% to 12 ± 5% (mean ± SE), and 28% of the colonies suffered complete mortality. Observed rates of tissue loss were highly variable, ranging from 2 to 43 cm2 d–1, but the mean was a rapid 13 ± 11 cm2 d–1 or about 4 cm branch length d–1. Field experiments demonstrate that this disease is transmissible not only by direct contact between affected and healthy staghorn coral tissue but also by the corallivorous snail Coralliophila abbreviata. The disease was also transmissible, although less effectively so, to the congener A. palmata (elkhorn coral). No transmission was observed in indirect contact treatments designed to simulate diver interaction. Transmissibility implies that the condition is indeed a biotic disease and the demonstration of effective vector transmission suggests that predation may exacerbate disease outbreaks in remnant Caribbean acroporid populations, further impeding their potential recovery. KEY WORDS: Coralliophila abbreviata · Predator · Transmission experiment · Vector · Whiteband disease Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in MEPS Vol. 301. Online publication date: October 11, 2005 Print ISSN: 0171-8630; Online ISSN: 1616-1599 Copyright © 2005 Inter-Research.

Effects of live coral, epilithic algal communities and substrate type on algal recruitment

The recruitment of algae is a critical process during algal colonization and invasions, including coral-to-algal phase shifts. Although algae are widely assumed to colonize and kill corals, there is very little known about the recruitment dynamics of coral reef algae. This study tested the ability of two dominant macroalgae (Fucales including Sargassum spp. and Lobophora variegata) to settle and grow on healthy coral tissue. The study also explored the effects of interactions with prior occupants, and of abiotic substrate properties (texture, and ceramic and carbonate material). The results indicate that healthy corals were able to prevent attachment or survival of recruits of these macroalgae. This is a significant point, since it suggests that the replacement of corals by algae may often require prior stress or death in the coral tissue. Pre-conditioning of plates at different sites had some effects, but these were relatively minor, whereas there was considerable variation within sites. Some of this variation appeared to be related to the amount of turf algae or crustose coralline algae on the plates. Recruitment was generally, but not always, higher on plates with rougher texture. Overall, this preliminary exploration indicates considerable potential for variability in outcomes of algal colonization, with implications for the dynamics of algal invasions. In particular, the results do not support suggestions that planktonic algal propagules can directly settle on and colonize healthy coral tissue.

A new coral disease from the southern Arabian Gulf

During an ecological survey of coral communities at Jebel Ali in Dubai, United Arab Emirates, a high incidence of coral diseases was observed. Although coral disease has been reported from the Gulf of Oman (Coles 1994), this is the first report from in the Arabian Gulf. The encountered diseases were the well described Black Band and White Band Diseases (Antonius, 1995) and a hitherto undescribed disease, which we refer to as Yellow Band Disease. It manifests itself as a broad yellow band moving across healthy coral tissue in a manner similar to the Black Band disease (Rutzler, Santavy and Antonius, 1983) insofar as where the yellow band actively moves onto healthy tissue, a band of decaying and sloughing off tissue is observed. However, the entire area denuded by the infection can retain the characteristic yellow colour. The Yellow Band Disease is not similar to the Aggressive Orange Band recently described by Littler and Littler (1994), which attacks coralline algae. Investigations into establishing the pathogen are underway. Preliminary measurements indicate that within-colony spreading rates (on Acropora clathrata) are faster in summer (x = 19.7 ± 4.9 mm per week, measured mid October), than in winter (x = 9.4 ± 3.9 mm per week, measured beginning February). Disease spread is significantly different between these seasons (Mann-Whitney U-Test, Z = 2.67, P < 0.001). Species found to be affected by Yellow Band Disease were: Acropora clathrata, A. pharaonis, A. tenuis, A. valida, A. florida, Porites lutea, P. lichen, P. nodifera, Turbinaria reniformis, Cyphastrea microphthalma. Acknowledgements. We acknowledge funding assistance by the Dubai Municipality and Charles Martin of Martin Mid East for the opportunity to work in Gulf waters, and for logistical support.