Increasing global temperatures due to climate change have resulted in respective increases in the severity and frequency of epizootics around the globe. Corals in particular have faced rapid declines due to disease outbreaks. Understanding immune responses and associated potential life-history trade-offs is therefore a priority. In the autumn of 2011, a novel disease of octocorals of the genus Eunicea was first documented in the Florida Keys. Termed Eunicea Black Disease (EBD), the disease is easily identified by the dark appearance of affected tissue, caused by a strong melanization response on the part of the host. In order to better understand the response of corals to EBD, we conducted full transcriptome analysis of 3 healthy and 3 diseased specimens of Eunicea calyculata collected from offshore southeast Florida. Differential expression and protein analyses revealed a strong, diverse immune response to EBD characterized by phagocytosis, adhesion and melanization on the part of the host. Furthermore, coexpression network analyses suggested this might come at the cost of reduced cell cycle progression and growth. This is in accordance with past histological studies of naturally infected hard corals, suggesting that potential trade-offs during infection may affect post-outbreak recovery of reef ecosystems by reducing both organismal growth and fecundity. Our findings highlight the importance of considering factors beyond mortality when estimating effects of disease outbreaks on ecosystems.

As scleractinian coral cover declines in the face of increased frequency in disease outbreaks, future reefs may become dominated by octocorals. Understanding octocoral disease responses and consequences is therefore necessary if we are to gain insight into the future of ecosystem services provided by coral reefs. In Florida, populations of the octocoral Eunicea calyculata infected with Eunicea black disease (EBD) were observed in the field in the fall of 2011. This disease was recognized by a stark, black pigmentation caused by heavy melanization. Histological preparations of E. calyculata infected with EBD demonstrated granular amoebocyte (GA) mobilization, melanin granules in much of the GA population, and the presence of fungal hyphae penetrating coral tissue. Previous transcriptomic analysis also identified immune trade-offs evidenced by increased immune investment at the expense of growth. Our investigation utilized proteogenomic techniques to reveal decreased investment in general cell signaling while increasing energy production for immune responses. Inflammation was also prominent in diseased E. calyculata and sheds light on factors driving the extreme phenotype observed with EBD. With disease outbreaks continuing to increase in frequency, our results highlight new targets within the cnidarian immune system and provide a framework for understanding transcriptomics in the context of an organismal disease phenotype and its protein expression.

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