Stony coral tissue loss disease (SCTLD) was initially documented in Florida in 2014 and outbreaks with similar characteristics have since appeared in disparate areas throughout the northern Caribbean, causing significant declines in coral communities. SCTLD is characterized by focal or multifocal lesions of denuded skeleton caused by rapid tissue loss and affects at least 22 reef-building species of Caribbean corals. A tissue-loss disease consistent with the case definition of SCTLD was first observed in the U.S. Virgin Islands (USVI) in January of 2019 off the south shore of St. Thomas at Flat Cay. The objective of the present study was to characterize species susceptibility to the disease present in St. Thomas in a controlled laboratory transmission experiment. Fragments of six species of corals (Colpophyllia natans, Montastraea cavernosa, Orbicella annularis, Porites astreoides, Pseudodiploria strigosa, and Siderastrea siderea) were simultaneously incubated with (but did not physically contact) SCTLD-affected colonies of Diploria labyrinthiformis and monitored for lesion appearance over an 8 day experimental period. Paired fragments from each corresponding coral genotype were equivalently exposed to apparently healthy colonies of D. labyrinthiformis to serve as controls; none of these fragments developed lesions throughout the experiment. When tissue-loss lesions appeared and progressed in a disease treatment, the affected coral fragment, and its corresponding control genet, were removed and preserved for future analysis. Based on measures including disease prevalence and incidence, relative risk of lesion development, and lesion progression rates, O. annularis, C. natans, and S. siderea showed the greatest susceptibility to SCTLD in the USVI. These species exhibited earlier average development of lesions, higher relative risk of lesion development, greater lesion prevalence, and faster lesion progression rates compared with the other species, some of which are considered to be more susceptible based on field observations (e.g., P. strigosa). The average transmission rate in the present study was comparable to tank studies in Florida, even though disease donor species differed. Our findings suggest that the tissue loss disease affecting reefs of the USVI has a similar epizootiology to that observed in other regions, particularly Florida.

Disease outbreaks have caused significant declines of keystone coral species. While forecasting disease outbreaks based on environmental factors has progressed, we still lack a comparative understanding of susceptibility among coral species that would help predict disease impacts on coral communities. The present study compared the phenotypic and microbial responses of seven Caribbean coral species with diverse life-history strategies after exposure to white plague disease. Disease incidence and lesion progression rates were evaluated over a seven-day exposure. Coral microbiomes were sampled after lesion appearance or at the end of the experiment if no disease signs appeared. A spectrum of disease susceptibility was observed among the coral species that corresponded to microbial dysbiosis. This dysbiosis promotes greater disease susceptiblity in coral perhaps through different tolerant thresholds for change in the microbiome. The different disease susceptibility can affect coral’s ecological function and ultimately shape reef ecosystems.

Stony coral tissue loss disease (SCTLD), one of the most pervasive and virulent coral diseases on record, affects over 22 species of reef-building coral and is decimating reefs throughout the Caribbean. To understand how different coral species and their algal symbionts (family Symbiodiniaceae) respond to this disease, we examine the gene expression profiles of colonies of five species of coral from a SCTLD transmission experiment. The included species vary in their purported susceptibilities to SCTLD, and we use this to inform gene expression analyses of both the coral animal and their Symbiodiniaceae. We identify orthologous coral genes exhibiting lineage-specific differences in expression that correlate to disease susceptibility, as well as genes that are differentially expressed in all coral species in response to SCTLD infection. We find that SCTLD infection induces increased expression of rab7, an established marker of in situ degradation of dysfunctional Symbiodiniaceae, in all coral species accompanied by genus-level shifts in Symbiodiniaceae photosystem and metabolism gene expression. Overall, our results indicate that SCTLD infection induces symbiophagy across coral species and that the severity of disease is influenced by Symbiodiniaceae identity.

Infectious diseases are an increasing threat to coral reefs, resulting in altered community structure and hindering the functional contributions of disease-susceptible species. We exposed seven reef-building coral species from the Caribbean to white plague disease and determined processes involved in (i) lesion progression, (ii) within-species gene expression plasticity, and (iii) expression-level adaptation among species that lead to differences in disease risk. Gene expression networks enriched in immune genes and cytoskeletal arrangement processes were correlated to lesion progression rates. Whether or not a coral developed a lesion was mediated by plasticity in genes involved in extracellular matrix maintenance, autophagy, and apoptosis, while resistant coral species had constitutively higher expression of intracellular protein trafficking. This study offers insight into the process involved in lesion progression and within- and between-species dynamics that lead to differences in disease risk that is evident on current Caribbean reefs.

Coral disease has progressively become one of the most pressing issues affecting coral reef survival. In the last 50 years, several reefs throughout the Caribbean have been severely impacted by increased frequency and intensity of disease outbreaks leading to coral death. A recent example of this is stony coral tissue loss disease which has quickly spread throughout the Caribbean, devastating coral reef ecosystems. Emerging from these disease outbreaks has been a coordinated research response that often integrates ‘omics techniques to better understand the coral immune system. ‘Omics techniques encompass a wide range of technologies used to identify large scale gene, DNA, metabolite, and protein expression. In this review, we discuss what is known about coral immunity and coral disease from an ‘omics perspective. We reflect on the development of biomarkers and discuss ways in which coral disease experiments to test immunity can be improved. Lastly, we consider how existing data can be better leveraged to combat future coral disease outbreaks.