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Marilyn E. Brandt

Publications and source records attributed to Marilyn E. Brandt.

6 recordsLinked to original sources

Investigating the influence of Diadematidae scuticociliatosis on host microbiome composition

Mass mortality of Diadematidae urchins, caused by the Diadema antillarum scuticociliatosis Philaster clade (DScPc) , affected the Caribbean in spring 2022 and subsequently spread to the eastern Mediterranean, Red Sea, and western Indian Ocean. A key question around Diadematidae scuticociliatosis (DSc), the disease caused by the scuticociliate, is whether the urchin microbiome varies between scuticociliatosis-affected and grossly normal urchins. Tissue samples from both grossly normal and abnormal Diadema antillarum were collected in the field during the initial assessment of the DSc causative agent and from an experimental challenge of DScPc culture on aquacultured D. antillarum . Specimens were analyzed using 16S rRNA gene amplicon sequencing. Additional abnormal urchin samples were collected from the most recent outbreak site in the western Indian Ocean (Réunion Island). At reference (i.e., unaffected by DSc) sites, Kistimonas spp. , Propionigenium spp., and Endozoicomonas spp. were highly represented in amplicon libraries. DSc-affected urchin amplicon libraries had lower taxonomic richness and a greater representation of taxa related to Fangia hongkongensis and Psychrobium spp. Amplicon libraries of urchins experimentally challenged with the DSc pathogen had some shifts in microbial composition, but F. hongkongensis was not a part of the core bacteria in DSc-challenged specimens. DSc-affected Echinothrix diadema from Réunion Island showed a similar high representation of F. hongkongensis as that seen on Caribbean D. antillarum . Our results suggest that DSc alters Diadematidae microbiomes and that F. hongkongensis may be a candidate bacterial biomarker for DSc in environmental samples. The mechanism driving microbiome variation in host–pathogen interactions remains to be explored.

mSystems

Detection of the Diadema antillarum scuticociliatosis Philaster clade on sympatric metazoa, plankton, and abiotic surfaces and assessment for its potential reemergence

A ciliate belonging to the Diadema antillarum scuticociliatosis (DaSc)-associated Philaster clade (DaScPc) caused catastrophic long-spined urchin mass mortality in spring and summer of 2022. The ciliate can be grown in culture in both the presence and absence of D. antillarum tissues, suggesting that it may persist outside its host by consuming microorganisms or dissolved organic nutrients. We hypothesized that DaScPc was present outside its host during and after mass mortality and absent prior to 2022. We examined DaScPc in DNA extracted from 500 swabs of sym- patric metazoa and abiotic surfaces, and plankton samples, collected at 35 sites in the Caribbean in 2022 and 2023. DaScPc was detected on corals, turf algae, and a sponge, predominantly at sites with active or prior DaSc. We examined whether it was present prior to 2022 by surveying extracted DNA from Caribbean corals and water collected near corals by PCR and by mining publicly available transcriptomes and metagenomes for DaScPc rRNAs. These efforts yielded no DaScPc genes. We further hypothesized that DaScPc may recruit to the specific corals detected in field surveys, and that these may then infect naïve hosts. A mesocosm experiment to test DaScPc recruitment suggested that, while it recruited to corals, it did so inconsistently between coral species. Incubation of corals that recruited DaScPc with naïve urchins yielded inconclusive results since urchins died without characteristic DaSc signs. Overall, our results suggest that DaScPc may occur outside its urchin host, and that it may have been absent in the region prior to 2022.

Florida

A meta-analysis of the stony coral tissue loss disease microbiome finds key bacteria in unaffected and lesion tissue in diseased colonies

Stony coral tissue loss disease (SCTLD) has been causing significant whole colony mortality on reefs in Florida and the Caribbean. The cause of SCTLD remains unknown, with the limited concurrence of SCTLD-associated bacteria among studies. We conducted a meta-analysis of 16S ribosomal RNA gene datasets generated by 16 field and laboratory SCTLD studies to find consistent bacteria associated with SCTLD across disease zones (vulnerable, endemic, and epidemic), coral species, coral compartments (mucus, tissue, and skeleton), and colony health states (apparently healthy colony tissue (AH), and unaffected (DU) and lesion (DL) tissue from diseased colonies). We also evaluated bacteria in seawater and sediment, which may be sources of SCTLD transmission. Although AH colonies in endemic and epidemic zones harbor bacteria associated with SCTLD lesions, and aquaria and field samples had distinct microbial compositions, there were still clear differences in the microbial composition among AH, DU, and DL in the combined dataset. Alpha-diversity between AH and DL was not different; however, DU showed increased alpha-diversity compared to AH, indicating that, prior to lesion formation, corals may undergo a disturbance to the microbiome. This disturbance may be driven by Flavobacteriales, which were especially enriched in DU. In DL, Rhodobacterales and Peptostreptococcales–Tissierellales were prominent in structuring microbial interactions. We also predict an enrichment of an alpha-toxin in DL samples which is typically found in Clostridia. We provide a consensus of SCTLD-associated bacteria prior to and during lesion formation and identify how these taxa vary across studies, coral species, coral compartments, seawater, and sediment.

ISME Communications

Rapid prototyping for quantifying belief weights of competing hypotheses about emergent diseases

Emerging diseases can have devastating consequences for wildlife and require a rapid response. A critical first step towards developing appropriate management is identifying the etiology of the disease, which can be difficult to determine, particularly early in emergence. Gathering and synthesizing existing information about potential disease causes, by leveraging expert knowledge or relevant existing studies, provides a principled approach to quickly inform decision-making and management efforts. Additionally, updating the current state of knowledge as more information becomes available over time can reduce scientific uncertainty and lead to substantial improvement in the decision-making process and the application of management actions that incorporate and adapt to newly acquired scientific understanding. Here we present a rapid prototyping method for quantifying belief weights for competing hypotheses about the etiology of disease using a combination of formal expert elicitation and Bayesian hierarchical modeling. We illustrate the application of this approach for investigating the etiology of stony coral tissue loss disease (SCTLD) and discuss the opportunities and challenges of this approach for addressing emergent diseases. Lastly, we detail how our work may apply to other pressing management or conservation problems that require quick responses. We found the rapid prototyping methods to be an efficient and rapid means to narrow down the number of potential hypotheses, synthesize current understanding, and help prioritize future studies and experiments. This approach is rapid by providing a snapshot assessment of the current state of knowledge. It can also be updated periodically (e.g., annually) to assess changes in belief weights over time as scientific understanding increases. Synthesis and applications: The rapid prototyping approaches demonstrated here can be used to combine knowledge from multiple experts and/or studies to help with fast decision-making needed for urgent conservation issues including emerging diseases and other management problems that require rapid responses. These approaches can also be used to adjust belief weights over time as studies and expert knowledge accumulate and can be a helpful tool for adapting management decisions.

Journal of Environmental Management

A scuticociliate causes mass mortality of Diadema antillarum in the Caribbean Sea

Echinoderm mass mortality events shape marine ecosystems by altering the dynamics among major benthic groups. The sea urchin Diadema antillarum , virtually extirpated in the Caribbean in the early 1980s by an unknown cause, recently experienced another mass mortality beginning in January 2022. We investigated the cause of this mass mortality event through combined molecular biological and veterinary pathologic approaches comparing grossly normal and abnormal animals collected from 23 sites, representing locations that were either affected or unaffected at the time of sampling. Here, we report that a scuticociliate most similar to Philaster apodigitiformis was consistently associated with abnormal urchins at affected sites but was absent from unaffected sites. Experimentally challenging naïve urchins with a Philaster culture isolated from an abnormal, field-collected specimen resulted in gross signs consistent with those of the mortality event. The same ciliate was recovered from treated specimens postmortem, thus fulfilling Koch’s postulates for this microorganism. We term this condition D. antillarum scuticociliatosis.

Science Advances

Disease prevalence and snail predation associated with swell-generated damage on the threatened coral, Acropora palmata (Lamarck)

Disturbances such as tropical storms cause coral mortality and reduce coral cover as a direct result of physical damage. Storms can be one of the most important disturbances in coral reef ecosystems, and it is crucial to understand their long-term impacts on coral populations. The primary objective of this study was to determine trends in disease prevalence and snail predation on damaged and undamaged colonies of the threatened coral species, Acropora palmata, following an episode of heavy ocean swells in the US Virgin Islands (USVI). At three sites on St. Thomas and St. John, colonies of A. palmata were surveyed monthly over 1 year following a series of large swells in March 2008 that fragmented 30–93% of colonies on monitored reefs. Post-disturbance surveys conducted from April 2008 through March 2009 showed that swell-generated damage to A. palmata caused negative indirect effects that compounded the initial direct effects of physical disturbance. During the 12 months after the swell event, white pox disease prevalence was 41% higher for colonies that sustained damage from the swells than for undamaged colonies (df = 207, p = 0.01) with greatest differences in disease prevalence occurring during warm water months. In addition, the corallivorous snail, Coralliophila abbreviata, was 46% more abundant on damaged corals than undamaged corals during the 12 months after the swell event (df = 207, p = 0.006).

Frontiers in Marine Science