Increased Prevalence of Ubiquitous Ascomycetes in an Acropoid Coral (Acropora formosa) Exhibiting Symptoms of Brown Band Syndrome and Skeletal Eroding Band Disease

The prevalence of coral-associated fungi was four times higher in diseased Acropora formosa colonies than in healthy colonies. Since taxonomically related fungal species were isolated from diseased and healthy colonies, we suggest that their association with coral may be constitutive but that their abundance is dependent on coral health.     

Does Dark-Spot Syndrome Experimentally Transmit among Caribbean Corals?

Over the last half-century, coral diseases have contributed to the rapid decline of coral populations throughout the Caribbean region. Some coral diseases appear to be potentially infectious, yet little is known about their modes of transmission. This study experimentally tested whether dark-spot syndrome on Siderastrea siderea was directly or indirectly transmissible to neighboring coral colonies. We also tested whether open wounds were necessary to facilitate disease transmission. At the completion of the experiments, we sampled bacterial communities on diseased, exposed, and healthy coral colonies to determine whether bacterial pathogens had transmitted to the susceptible colonies. We saw no evidence of either direct or waterborne transmission of dark-spot syndrome, and corals that received lesions by direct contact with diseased tissue, healed and showed no signs of infection. There were no significant differences among bacterial communities on healthy, exposed, and diseased colonies, although nine individual ribotypes were significantly higher in diseased corals compared with healthy and exposed corals, indicating a lack of transmission. Although our experiments do not fully refute the possibility that dark-spot syndrome is infectious and transmissible, our results suggest that in situ macroscopic signs of dark-spot syndrome are not always contagious.     

<Emphasis Type="Italic">Symbiodinium</Emphasis> associations with diseased and healthy scleractinian corals

Despite recent advances in identifying the causative agents of disease in corals and understanding the impact of epizootics on reef communities, little is known regarding the interactions among diseases, corals, and their dinoflagellate endosymbionts (Symbiodinium spp.). Since the genotypes of both corals and their resident Symbiodinium contribute to colony-level phenotypes, such as thermotolerance, symbiont genotypes might also contribute to the resistance or susceptibility of coral colonies to disease. To explore this, Symbiodinium were identified using the internal transcribed spacer-2 region of ribosomal DNA from diseased and healthy tissues within individual coral colonies infected with black band disease (BB), dark spot syndrome (DSS), white plague disease (WP), or yellow blotch disease (YB) in the Florida Keys (USA) and the US Virgin Islands. Most of the diseased colonies sampled contained B1, B5a, or C1 (depending on host species), while apparently healthy colonies of the same coral species frequently hosted these types and/or additional symbiont diversity. No potentially “parasitic” Symbiodinium types, uniquely associated with diseased coral tissue, were detected. Within most individual colonies, the same dominant Symbiodinium type was detected in diseased and visually healthy tissues. These data indicate that specific Symbiodinium types are not correlated with the infected tissues of diseased colonies and that DSS and WP onset do not trigger symbiont shuffling within infected tissues. However, few diseased colonies contained clade D symbionts suggesting a negative correlation between hosting Symbiodinium clade D and disease incidence in scleractinian corals. Understanding the influence of Symbiodinium diversity on colony phenotypes may play a critical role in predicting disease resistance and susceptibility in scleractinian corals.     

Fungi in Porites lutea: association with healthy and diseased corals.

Healthy and diseased scleractinian corals have been reported to harbour fungi. However, the species of fungi occurring in them and their prevalence in terms of biomass have not been determined and their role in coral diseases is not clear. We have found fungi to occur regularly in healthy, partially dead, bleached and pink-line syndrome (PLS)-affected scleractinian coral, Porites lutea, in the reefs of Lakshadweep Islands in the Arabian Sea. Mostly terrestrial species of fungi were isolated in culture from these corals. Hyaline and dark, non-sporulating fungi were the most dominant forms. Fungal hyphae extended up to 3 cm within the corals. Immunofluorescence detection using polyclonal immunological probes for a dark, initially non-sporulating isolate (isolate # 98-N28) and for a hyaline, non-sporulating fungus (isolate # 98-N18) revealed high frequencies of these in PLS-affected, dead and healthy colonies of P. lutea. Total fungal biomass accounted for 0.04 to 0.05% of the weight of corals in bleached corals and was higher than in PLS-affected and healthy colonies. Scanning electron microscopy revealed the presence of fungi within the carbonate skeleton and around polyps. Fungi appear to be a regular component of healthy, partially dead and diseased coral skeleton.     

Present state of diseases and other signs of reef deterioration at seven coral reefs at Los Roques Archipelago National Park, Venezuela

This work was aimed to determine the incidence of coral diseases in six different reef sites at the Parque Nacional Archipiélago de Los Roques, Venezuela: Arrecife de herradura, Arrecife costanero, both at Dos Mosquises Sur Key, Boca de Cote, Carenero, Crasquí and Pelona de Rabusquí. Each reef was surveyed by using ten 10 m2-band transects (10 x 1 m), placed parallel to the long axis of the reef within a depth gradient ranging from 1 to 9 m depth. All healthy and injured corals, along each band transect, were counted and identified to species level. Additionally, all diseases and recent mortality that were still identifiable on each colony were also recorded. The occurrence of diseased colonies and other signs of reef decline between localities were compared by means of a Chi2 test. The absolute, relative and mean incidence was estimated for each disease and other signs of damage observed for all coral species surveyed at each site. The overall incidence of coral diseases was low for all the localities surveyed, only 6.04% of the 3 344 colonies observed, showed signs of diseases. The most important diseases recorded were the Yellow-Blotch Disease (YBD) and Dark Spots Disease (DSD) with 2.1% +/- 1.52 y 2.1% +/- 2.54, respectively. Significant differences were found in the incidence of coral diseases between reef sites (Chi2 p < 0.05). Finally, the occurrence of colonies injured by parrotfish bites and pomacentrids was higher compared with the incidence of coral diseases for all the reefs surveyed. In conclusion, currently the proportion of healthy colonies at Los Roques coral reefs is higher than the percentage of both diseased and injured colonies.     

Diseases affect cold-water corals too: Eunicella verrucosa (Cnidaria: Gorgonacea) necrosis in SW England

The first recorded incidence of cold-water coral disease was noted in Eunicella verrucosa, a coral on the international 'red list' of threatened species, at a marine protected area in SW England in 2002. Video surveys of 634 separate colonies at 13 sites revealed that disease outbreaks were widespread in SW England from 2003 to 2006. Coenchyme became necrotic in diseased specimens, leading to tissue sloughing and exposing skeletal gorgonin to settlement by fouling organisms. Sites where necrosis was found had significantly higher incidences of fouling. No fungi were isolated from diseased or healthy tissue, but significantly higher concentrations of bacteria occurred in diseased specimens. Of 21 distinct bacteria isolated from diseased tissues, 19 were Vibrionaceae, 15 were strains of Vibrio splendidus and 2 others closely matched Vibrio tasmaniensis. Vibrios isolated from E. verrucosa did not induce disease at 15 degrees C, but, at 20 degrees C, controls remained healthy and test gorgonians became diseased, regardless of whether vibrios were isolated from diseased or healthy colonies. Bacteria associated with diseased tissue produced proteolytic and cytolytic enzymes that damaged E. verrucosa tissue and may be responsible for the necrosis observed. Monitoring at the site where the disease was first noted showed new gorgonian recruitment from 2003 to 2006; some individuals had died and become completely overgrown, whereas others had continued to grow around a dead central area.     

Bacterial profiling of White Plague Disease across corals and oceans indicates a conserved and distinct disease microbiome

Coral diseases are characterized by microbial community shifts in coral mucus and tissue, but causes and consequences of these changes are vaguely understood due to the complexity and dynamics of coral‐associated bacteria. We used 16S rRNA gene microarrays to assay differences in bacterial assemblages of healthy and diseased colonies displaying White Plague Disease (WPD) signs from two closely related Caribbean coral species, Orbicella faveolata and Orbicella franksi. Analysis of differentially abundant operational taxonomic units (OTUs) revealed strong differences between healthy and diseased specimens, but not between coral species. A subsequent comparison to data from two Indo‐Pacific coral species (Pavona duerdeni and Porites lutea) revealed distinct microbial community patterns associated with ocean basin, coral species and health state. Coral species were clearly separated by site, but also, the relatedness of the underlying bacterial community structures resembled the phylogenetic relationship of the coral hosts. In diseased samples, bacterial richness increased and putatively opportunistic bacteria were consistently more abundant highlighting the role of opportunistic conditions in structuring microbial community patterns during disease. Our comparative analysis shows that it is possible to derive conserved bacterial footprints of diseased coral holobionts that might help in identifying key bacterial species related to the underlying etiopathology. Furthermore, our data demonstrate that similar‐appearing disease phenotypes produce microbial community patterns that are consistent over coral species and oceans, irrespective of the putative underlying pathogen. Consequently, profiling coral diseases by microbial community structure over multiple coral species might allow the development of a comparative disease framework that can inform on cause and relatedness of coral diseases.     

Fungi in healthy and diseased sea fans (<Emphasis Type="Italic">Gorgonia ventalina)</Emphasis>: is <Emphasis Type="Italic">Aspergillus sydowii</Emphasis> always the pathogen?

Caribbean corals, including sea fans (Gorgonia spp.), are being affected by severe and apparently new diseases. In the case of sea fans, the pathogen is reported to be the fungus Aspergillus sydowii, and the disease is named aspergillosis. In order to understand coral diseases and pathogens, knowledge of the microbes associated with healthy corals is also necessary. In this study the fungal community of healthy Gorgonia ventalina colonies was contrasted with that of diseased colonies. In addition, the fungal community of healthy and diseased tissue within colonies with aspergillosis was contrasted. Fungi were isolated from healthy and diseased fans from 15 reefs around Puerto Rico, and identified by sequencing the nuclear ribosomal ITS region and by morphology. Thirty fungal species belonging to 15 genera were isolated from 203 G. ventalina colonies. Penicillum and Aspergillus were the most common genera isolated from both healthy and diseased fans. However, the fungal community of healthy fans was distinct and more diverse than that of diseased ones. Within diseased fans, fungal communities from diseased tissues were distinct and more diverse than from healthy tissue. The reduction of fungi in diseased colonies may occur prior to infection due to environmental changes affecting the host, or after infection due to increase in dominance of the pathogen, or because of host responses to infection. Data also indicate that the fungal community of an entire sea fan colony is affected even when only a small portion of the colony suffers from aspergillosis. An unexpected result was that A. sydowii was found in healthy sea fans but never in diseased ones. This result suggests that A. sydowii is not the pathogen causing aspergillosis in the studied colonies, and suggests several fungi common to healthy and diseased colonies as opportunistic pathogens. Given that it is not clear that Aspergillus is the sole pathogen, calling this disease aspergillosis is an oversimplification at best. Communicated by Biology Editor Dr Michael Lesser     

Gene expression associated with white syndromes in a reef building coral,Acropora hyacinthus

Background

Corals are capable of launching diverse immune defenses at the site of direct contact with pathogens, but the molecular mechanisms of this activity and the colony-wide effects of such stressors remain poorly understood. Here we compared gene expression profiles in eight healthy Acropora hyacinthus colonies against eight colonies exhibiting tissue loss commonly associated with white syndromes, all collected from a natural reef environment near Palau. Two types of tissues were sampled from diseased corals: visibly affected and apparently healthy.

Results

Tag-based RNA-Seq followed by weighted gene co-expression network analysis identified groups of co-regulated differentially expressed genes between all health states (disease lesion, apparently healthy tissues of diseased colonies, and fully healthy). Differences between healthy and diseased tissues indicate activation of several innate immunity and tissue repair pathways accompanied by reduced calcification and the switch towards metabolic reliance on stored lipids. Unaffected parts of diseased colonies, although displaying a trend towards these changes, were not significantly different from fully healthy samples. Still, network analysis identified a group of genes, suggestive of altered immunity state, that were specifically up-regulated in unaffected parts of diseased colonies.

Conclusions

Similarity of fully healthy samples to apparently healthy parts of diseased colonies indicates that systemic effects of white syndromes on A. hyacinthus are weak, which implies that the coral colony is largely able to sustain its physiological performance despite disease. The genes specifically up-regulated in unaffected parts of diseased colonies, instead of being the consequence of disease, might be related to the originally higher susceptibility of these colonies to naturally occurring white syndromes.

Electronic supplementary material

The online version of this article (doi:10.1186/s12864-015-1540-2) contains supplementary material, which is available to authorized users.     

The cellular stress response of the scleractinian coral <Emphasis Type="Italic">Goniopora columna</Emphasis> during the progression of the black band disease

Black band disease (BBD) is a widespread coral pathology caused by a microbial consortium dominated by cyanobacteria, which is significantly contributing to the loss of coral cover and diversity worldwide. Since the effects of the BBD pathogens on the physiology and cellular stress response of coral polyps appear almost unknown, the expression of some molecular biomarkers, such as Hsp70, Hsp60, HO-1, and MnSOD, was analyzed in the apparently healthy tissues of Goniopora columna located at different distances from the infection and during two disease development stages. All the biomarkers displayed different levels of expression between healthy and diseased colonies. In the healthy corals, low basal levels were found stable over time in different parts of the same colony. On the contrary, in the diseased colonies, a strong up-regulation of all the biomarkers was observed in all the tissues surrounding the infection, which suffered an oxidative stress probably generated by the alternation, at the progression front of the disease, of conditions of oxygen supersaturation and hypoxia/anoxia, and by the production of the cyanotoxin microcystin by the BBD cyanobacteria. Furthermore, in the infected colonies, the expression of all the biomarkers appeared significantly affected by the development stage of the disease. In conclusion, our approach may constitute a useful diagnostic tool, since the cellular stress response of corals is activated before the pathogens colonize the tissues, and expands the current knowledge of the mechanisms controlling the host responses to infection in corals.     

Bacterial community structure associated with white band disease in the elkhorn coral Acropora palmata determined using culture-independent 16S rRNA techniques

Culture-independent molecular (16S ribosomal RNA) techniques showed distinct differences in bacterial communities associated with white band disease (WBD) Type I and healthy elkhorn coral Acropora palmata. Differences were apparent at all levels, with a greater diversity present in tissues of diseased colonies. The bacterial community associated with remote, non-diseased coral was distinct from the apparently healthy tissues of infected corals several cm from the disease lesion. This demonstrates a whole-organism effect from what appears to be a localised disease lesion, an effect that has also been recently demonstrated in white plague-like disease in star coral Montastraea annularis. The pattern of bacterial community structure changes was similar to that recently demonstrated for white plague-like disease and black band disease. Some of the changes are likely to be explained by the colonisation of dead and degrading tissues by a micro-heterotroph community adapted to the decomposition of coral tissues. However, specific ribosomal types that are absent from healthy tissues appear consistently in all samples of each of the diseases. These ribotypes are closely related members of a group of alpha-proteobacteria that cause disease, notably juvenile oyster disease, in other marine organisms. It is clearly important that members of this group are isolated for challenge experiments to determine their role in the diseases.     

Microbial functional structure of Montastraea faveolata,an important Caribbean reef‐building coral,differs between healthy and yellow‐band diseased colonies

A functional gene array (FGA), GeoChip 2.0, was used to assess the biogeochemical cycling potential of microbial communities associated with healthy and Caribbean yellow band diseased (YBD) Montastraea faveolata. Over 6700 genes were detected, providing evidence that the coral microbiome contains a diverse community of archaea, bacteria and fungi capable of fulfilling numerous functional niches. These included carbon, nitrogen and sulfur cycling, metal homeostasis and resistance, and xenobiotic contaminant degradation. A significant difference in functional structure was found between healthy and YBD M. faveolata colonies and those differences were specific to the physical niche examined. In the surface mucopolysaccharide layer (SML), only two of 31 functional categories investigated, cellulose degradation and nitrification, revealed significant differences, implying a very specific change in microbial functional potential. Coral tissue slurry, on the other hand, revealed significant changes in 10 of the 31 categories, suggesting a more generalized shift in functional potential involving various aspects of nutrient cycling, metal transformations and contaminant degradation. This study is the first broad screening of functional genes in coral‐associated microbial communities and provides insights regarding their biogeochemical cycling capacity in healthy and diseased states.     

Bacterial Communities of Two Ubiquitous Great Barrier Reef Corals Reveals Both Site- and Species-Specificity of Common Bacterial Associates

Background

Coral-associated bacteria are increasingly considered to be important in coral health, and altered bacterial community structures have been linked to both coral disease and bleaching. Despite this, assessments of bacterial communities on corals rarely apply sufficient replication to adequately describe the natural variability. Replicated data such as these are crucial in determining potential roles of bacteria on coral.

Methodology/Principal Findings

Denaturing Gradient Gel Electrophoresis (DGGE) of the V3 region of the 16S ribosomal DNA was used in a highly replicated approach to analyse bacterial communities on both healthy and diseased corals. Although site-specific variations in the bacterial communities of healthy corals were present, host species-specific bacterial associates within a distinct cluster of gamma-proteobacteria could be identified, which are potentially linked to coral health. Corals affected by “White Syndrome” (WS) underwent pronounced changes in their bacterial communities in comparison to healthy colonies. However, the community structure and bacterial ribotypes identified in diseased corals did not support the previously suggested theory of a bacterial pathogen as the causative agent of the syndrome.

Conclusions/Significance

This is the first study to employ large numbers of replicated samples to assess the bacterial communities of healthy and diseased corals, and the first culture-independent assessment of bacterial communities on WS affected Acroporid corals on the GBR. Results indicate that a minimum of 6 replicate samples are required in order to draw inferences on species, spatial or health-related changes in community composition, as a set of clearly distinct bacterial community profiles exist in healthy corals. Coral bacterial communities may be both site and species specific. Furthermore, a cluster of gamma-proteobacterial ribotypes may represent a group of specific common coral and marine invertebrate associates. Finally, the results did not support the contention that a single bacterial pathogen may be the causative agent of WS Acroporids on the GBR.     

Disturbance Driven Colony Fragmentation as a Driver of a Coral Disease Outbreak

In September of 2010, Brewer''s Bay reef, located in St. Thomas (U.S. Virgin Islands), was simultaneously affected by abnormally high temperatures and the passage of a hurricane that resulted in the mass bleaching and fragmentation of its coral community. An outbreak of a rapid tissue loss disease among coral colonies was associated with these two disturbances. Gross lesion signs and lesion progression rates indicated that the disease was most similar to the Caribbean coral disease white plague type 1. Experiments indicated that the disease was transmissible through direct contact between colonies, and five-meter radial transects showed a clustered spatial distribution of disease, with diseased colonies being concentrated within the first meter of other diseased colonies. Disease prevalence and the extent to which colonies were bleached were both significantly higher on unattached colony fragments than on attached colonies, and disease occurred primarily on fragments found in direct contact with sediment. In contrast to other recent studies, disease presence was not related to the extent of bleaching on colonies. The results of this study suggest that colony fragmentation and contact with sediment played primary roles in the initial appearance of disease, but that the disease was capable of spreading among colonies, which suggests secondary transmission is possible through some other, unidentified mechanism.     

Porites ulcerative white spot disease: description, prevalence, and host range of a new coral disease affecting Indo-Pacific reefs

The results of an investigation of a new coral disease affecting Indo-Pacific reefs are presented. Porites ulcerative white spot disease (PUWS) is characterized by discrete, bleached, round foci, 3 to 5 mm in diameter, that may either regress or progress to full tissue-thickness ulcerations that coalesce, occasionally resulting in colony mortality. Monitoring of 25 diseased and 5 healthy reference colonies for 17 mo revealed that advanced stages of the disease were characterized by lesion coalescence, partial colony death (i.e. portions of the colony still alive; n = 17) and total colony death (n = 2). Field transmission experiments revealed that 95% of healthy colonies developed lesions within 5 wk after continual exposure to diseased branches, while 60% of the reference colonies remained healthy. The host range of PUWS includes branching and massive Porites spp., and prevalence per species was positively correlated with species density. On 10 reefs surveyed in the Central Philippines, 22 +/- 7% (mean +/- SE) of poritid colonies were infected, and the disease was present on 80% of the surveyed reefs. Poritids are dominant Indo-Pacific reef builders; a disease targeting this genus could cause major shifts in community structure over time. This report contributes to the limited knowledge of PUWS impacts in this region.     

PhyloChip™ microarray comparison of sampling methods used for coral microbial ecology

Interest in coral microbial ecology has been increasing steadily over the last decade, yet standardized methods of sample collection still have not been defined. Two methods were compared for their ability to sample coral-associated microbial communities: tissue punches and foam swabs, the latter being less invasive and preferred by reef managers. Four colonies of star coral, Montastraea annularis, were sampled in the Dry Tortugas National Park (two healthy and two with white plague disease). The PhyloChip™ G3 microarray was used to assess microbial community structure of amplified 16S rRNA gene sequences. Samples clustered based on methodology rather than coral colony. Punch samples from healthy and diseased corals were distinct. All swab samples clustered closely together with the seawater control and did not group according to the health state of the corals. Although more microbial taxa were detected by the swab method, there is a much larger overlap between the water control and swab samples than punch samples, suggesting some of the additional diversity is due to contamination from water absorbed by the swab. While swabs are useful for noninvasive studies of the coral surface mucus layer, these results show that they are not optimal for studies of coral disease.     

Selective feeding by coral reef fishes on coral lesions associated with brown band and black band disease

Recent studies have suggested that corallivorous fishes may be vectors for coral disease, but the extent to which fishes actually feed on and thereby potentially transmit coral pathogens is largely unknown. For this study, in situ video observations were used to assess the level to which fishes fed on diseased coral tissues at Lizard Island, northern Great Barrier Reef. Surveys conducted at multiple locations around Lizard Island revealed that coral disease prevalence, especially of brown band disease (BrB), was higher in lagoon and backreef locations than in exposed reef crests. Accordingly, video cameras were deployed in lagoon and backreef habitats to record feeding by fishes during 1-h periods on diseased sections of each of 44 different coral colonies. Twenty-five species from five fish families (Blennidae, Chaetodontidae, Gobiidae, Labridae and Pomacentridae) were observed to feed on infected coral tissues of staghorn species of Acropora that were naturally infected with black band disease (BBD) or brown band disease (BrB). Collectively, these fishes took an average of 18.6 (±5.6 SE) and 14.3 (±6.1 SE) bites per hour from BBD and BrB lesions, respectively. More than 40% (408/948 bites) and nearly 25% (314/1319 bites) of bites were observed on lesions associated with BBD and BrB, respectively, despite these bands each representing only about 1% of the substratum available. Moreover, many corallivorous fishes (Labrichthys unilineatus, Chaetodon aureofasciatus, C. baronessa, C. lunulatus, C. trifascialis, Cheiloprion labiatus) selectively targeted disease lesions over adjacent healthy coral tissues. These findings highlight the important role that reef fishes may play in the dynamics of coral diseases, either as vectors for the spread of coral disease or in reducing coral disease progression through intensive and selective consumption of diseased coral tissues.     

Genetic Susceptibility,Colony Size,and Water Temperature Drive White-Pox Disease on the Coral Acropora palmata

Outbreaks of coral diseases are one of the greatest threats to reef corals in the Caribbean, yet the mechanisms that lead to coral diseases are still largely unknown. Here we examined the spatial-temporal dynamics of white-pox disease on Acropora palmata coral colonies of known genotypes. We took a Bayesian approach, using Integrated Nested Laplace Approximation algorithms, to examine which covariates influenced the presence of white-pox disease over seven years. We showed that colony size, genetic susceptibility of the coral host, and high-water temperatures were the primary tested variables that were positively associated with the presence of white-pox disease on A. palmata colonies. Our study also showed that neither distance from previously diseased individuals, nor colony location, influenced the dynamics of white-pox disease. These results suggest that white-pox disease was most likely a consequence of anomalously high water temperatures that selectively compromised the oldest colonies and the most susceptible coral genotypes.     

A comparison of culture-dependent and culture-independent techniques used to characterize bacterial communities on healthy and white plague-diseased corals of the Montastraea annularis species complex

Diseases of hermatypic corals pose a global threat to coral reefs, and investigations of bacterial communities associated with healthy corals and those exhibiting signs of disease are necessary for proper diagnosis. One disease, commonly called white plague (WP), is characterized by acute tissue loss. This investigation compared the bacterial communities associated with healthy coral tissue (N = 15), apparently healthy tissue on WP-diseased colonies (N = 15), and WP-diseased tissues (N = 15) from Montastraea annularis (species complex) colonies inhabiting a Bahamian reef. Aliquots of sediment (N = 15) and water (N = 15) were also obtained from the proximity of each coral colony sampled. Samples for culture-dependent analyses were inoculated onto one-half strength Marine Agar (½ MA) and Thiosulfate Citrate Bile Salts Sucrose Agar to quantify the culturable communities. Length heterogeneity PCR (LH-PCR) of the 16S rRNA gene characterized the bacterial operational taxonomic units (OTU) associated with lesions on corals exhibiting signs of a white plague-like disease as well as apparently healthy tissue from diseased and non-diseased conspecifics. Analysis of Similarity was conducted on the LH-PCR fingerprints, which indicated no significant difference in the composition of bacterial communities associated with apparently healthy and diseased corals. Comparisons of the 16S rRNA gene amplicons from cultured bacterial colonies (½ MA; N = 21) with all amplicons obtained from the whole coral-associated bacterial community indicated ≥39 % of coral-associated bacterial taxa could be cultured. Amplicons from these bacterial cultures matched amplicons from the whole coral-associated bacterial community that, when combined, accounted for >70 % total bacterial abundance. An OTU with the same amplicon length as Aurantimonas coralicida (313.1 bp), the reported etiological agent of WPII, was detected in relatively low abundance (<0.1 %) on all tissue types. These findings suggest a coral disease resembling WP may result from multiple etiologies.     

Changes in the microbial communities associated with Gorgonia ventalina during aspergillosis infection

The surface mucopolysaccharide layer (SML) secreted by corals is a rich environment where bacteria live and proliferate, with population levels often being several orders of magnitude higher than in the surrounding waters (at least for culturable microbes). Some studies have suggested that these communities play an important role in energy and nutrient flux in marine environments. We hypothesize that the microbial community structure of the SML also plays a role in protection against disease. This hypothesis is based on studies that have shown differences in the bacterial composition of the mucus of healthy and diseased corals. In this study we tested the differences in the microbial communities living in association with the SML of healthy and diseased Gorgonia ventalina by comparing their metabolic profiles using Biolog EcoPlates. Overall, metabolic profiles of the coral surface microbiota were significantly different to those in the water column based on stepwise canonical discriminant analyses (CDAs). Furthermore, differences between communities living in healthy and diseased corals were also found. Changes were observed between affected and unaffected areas of the same colony, although these changes were not as obvious as between individual healthy and diseased colonies. Results suggest that the microbial communities living in the SML of G. ventalina are affected by the presence of aspergillosis, even if the area is not in direct contact with the infection. This suggests the possibility of changes in the composition of the SML throughout the colony as a response to aspergillosis infection.