Assessment of the microbial communities associated with white syndrome and brown jelly syndrome in aquarium corals

Bacterial and ciliate assemblages associated with aquarium corals displaying white syndrome (WS) and brown jelly syndrome (BJS) were investigated. Healthy (n = 10) and diseased corals (WS n = 18; BJS n = 3) were analysed for 16S rRNA gene bacterial diversity, total bacterial abundance and vibrio-specific 16S rRNA gene abundance. This was conducted alongside analysis of 18S rRNA gene sequenc-ing targeting ciliates, a group of organisms largely overlooked for their potential as causal agents of coral disease. Despite significant differences between healthy and diseased corals in their 16S rRNA gene bacterial diversity, total bacterial abundance and vibrio-specific rRNA gene abundance, no domi-nant bacterial ribotypes were found consistently within the diseased samples. In contrast, one ciliate morphotype, named Morph 3 in this study (GenBank Accession Numbers JF831358 for the ciliate isolated from WS and JF831359 for the ciliate isolated from BJS) was observed to burrow into and underneath the coral tissues at the disease lesion in both disease types and contained algal endosym-bionts indicative of coral tissue ingestion. This ciliate was observed in larger numbers in BJS compared to WS, giving rise to the characteristic jelly like substance in BJS. Morph 3 varied by only 1 bp over 549 bp from the recently described Morph 1 ciliate (GenBank Accession No. JN626268), which has been shown to be present in field samples of WS and Brown Band Disease (BrB) in the Indo-Pacific. This result indicates a close relationship between these aquarium diseases and those observed in the wild

Coral diseases in aquaria and in nature

Many reef coral diseases have been described affecting corals in the wild, several of which have been associated with causal agents based on experimental inoculation and testing of Koch’s postulates. In the aquarium industry, many coral diseases and pathologies are known from the grey literature but as yet these have not been systematically described and the relationship to known diseases in the wild is difficult to determine. There is therefore scope to aid the maintenance and husbandry of corals in aquaria by informing the field of the scientifically described wild diseases, if these can be reliably related. Conversely, since the main driver to identifying coral diseases in aquaria is to select an effective treatment, the lessons learnt by aquarists on which treatments work with particular syndromes provides invaluable evidence for determining the causal agents. Such treatments are not commonly sought by scientists working in the natural environment due the cost and potential environmental impacts of the treatments. Here we review both wild and aquarium diseases and attempt to relate the two. Many important aquarium diseases could not be reconciled to those in the wild. In one case, however, namely that of the ciliate Helicostoma sp. as a causal agent of brown jelly syndrome in aquarium corals, there may be similarities with pathogenic agents of the wild coral diseases, such as white syndrome and brown band syndrome. We propose that Helicostoma is actually a misnomer, but improved understanding of this pathogen and others could benefit both fields. Improved practices in aquarium maintenance and husbandry would also benefit natural environments by reducing the scale of wild harvest and improving the potential for coral culture, both for the aquarium industry and for rehabilitation programmes

Corals Use Similar Immune Cells and Wound-Healing Processes as Those of Higher Organisms

Sessile animals, like corals, frequently suffer physical injury from a variety of sources, thus wound-healing mechanisms that restore tissue integrity and prevent infection are vitally important for defence. Despite the ecological importance of reef-building corals, little is known about the cells and processes involved in wound healing in this group or in phylogenetically basal metazoans in general

Fine-Tuning Heat Stress Algorithms to Optimise Global Predictions of Mass Coral Bleaching

Increasingly intense marine heatwaves threaten the persistence of many marine ecosystems. Heat stress-mediated episodes of mass coral bleaching have led to catastrophic coral mortality globally. Remotely monitoring and forecasting such biotic responses to heat stress is key for effective marine ecosystem management. The Degree Heating Week (DHW) metric, designed to monitor coral bleaching risk, reflects the duration and intensity of heat stress events and is computed by accumulating SST anomalies (HotSpot) relative to a stress threshold over a 12-week moving window. Despite significant improvements in the underlying SST datasets, corresponding revisions of the HotSpot threshold and accumulation window are still lacking. Here, we fine-tune the operational DHW algorithm to optimise coral bleaching predictions using the 5 km satellite-based SSTs (CoralTemp v3.1) and a global coral bleaching dataset (37,871 observations, National Oceanic and Atmospheric Administration). After developing 234 test DHW algorithms with different combinations of the HotSpot threshold and accumulation window, we compared their bleaching prediction ability using spatiotemporal Bayesian hierarchical models and sensitivity–specificity analyses. Peak DHW performance was reached using HotSpot thresholds less than or equal to the maximum of monthly means SST climatology (MMM) and accumulation windows of 4–8 weeks. This new configuration correctly predicted up to an additional 310 bleaching observations globally compared to the operational DHW algorithm, an improved hit rate of 7.9%. Given the detrimental impacts of marine heatwaves across ecosystems, heat stress algorithms could also be fine-tuned for other biological systems, improving scientific accuracy, and enabling ecosystem governance

Incidence, prevalence, and survival in patients with Langerhans cell histiocytosis: a national registry study from England, 2013-2019

This analysis is the largest population-based study to date to provide contemporary and comprehensive epidemiological estimates of all third edition of the International Classification of Diseases for Oncology (ICD-O-3) coded Langerhans cell histiocytosis (LCH) from England. People of all ages were identified from the National Cancer Registration Dataset using ICD-O-3 morphologies 9751–9754 for neoplasms diagnosed in 2013–2019. A total of 658 patients were identified, of whom 324 (49%) were children aged <15 years. The age-standardised incidence rate was 4.46 (95% confidence interval [CI] 3.99–4.98) per million children and 1.06 (95% CI 0.94–1.18) per million adults aged ≥15 years. Prevalence of LCH was 9.95 (95% CI 9.14–10.81) per million persons at the end of 2019. The 1-year overall survival (OS) was 99% (95% CI 97%–100%) for children and 90% (95% CI 87%–93%) for adults. Those aged ≥60 years had poorer OS than those aged <15 years (hazard ratio [HR] 22.12, 95% CI 7.10–68.94; p < 0.001). People in deprived areas had lower OS than those in the least deprived areas (HR 5.36, 95% CI 1.16–24.87; p = 0.03). There will inevitably be other environmental factors and associations yet to be identified, and the continued standardised data collection will allow further evaluation of data over time. This will be increasingly important with developments in LCH management following the large collaborative international trials such as LCH IV

Development of Bacterial Biofilms on Artificial Corals in Comparison to Surface-Associated Microbes of Hard Corals

Numerous studies have demonstrated the differences in bacterial communities associated with corals versus those in their surrounding environment. However, these environmental samples often represent vastly different microbial micro-environments with few studies having looked at the settlement and growth of bacteria on surfaces similar to corals. As a result, it is difficult to determine which bacteria are associated specifically with coral tissue surfaces. In this study, early stages of passive settlement from the water column to artificial coral surfaces (formation of a biofilm) were assessed. Changes in bacterial diversity (16S rRNA gene), were studied on artificially created resin nubbins that were modelled from the skeleton of the reef building coral Acropora muricata. These models were dip-coated in sterile agar, mounted in situ on the reef and followed over time to monitor bacterial community succession. The bacterial community forming the biofilms remained significantly different (R = 0.864 p<0.05) from that of the water column and from the surface mucus layer (SML) of the coral at all times from 30 min to 96 h. The water column was dominated by members of the α-proteobacteria, the developed community on the biofilms dominated by γ-proteobacteria, whereas that within the SML was composed of a more diverse array of groups. Bacterial communities present within the SML do not appear to arise from passive settlement from the water column, but instead appear to have become established through a selection process. This selection process was shown to be dependent on some aspects of the physico-chemical structure of the settlement surface, since agar-coated slides showed distinct communities to coral-shaped surfaces. However, no significant differences were found between different surface coatings, including plain agar and agar enhanced with coral mucus exudates. Therefore future work should consider physico-chemical surface properties as factors governing change in microbial diversity