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Cassiopea xamachana is a model system for studies in animal symbiosis with algal symbionts. This medusa is also associated with a microbial community that can impact its health, but this community has not been thoroughly studied. Shifts in the bacterial community following the loss of symbionts involving stress, environmental changes, or seasonal fluctuations can be complex, as the role of symbionts in structuring this community is not well established. To understand the interplay among microbial associates with this host, we explored the experimental diminishing of algal symbionts, and the influence of seasonal fluctuations over the structure of the bacterial community, through 16S rRNA gene high-throughput sequencing. Results showed that Gammaproteobacteria, Bacteroidia, and Alphaproteobacteria were dominant in all the mucus samples at the beginning of the experiments. However, after 28 days, bleached medusas showed a marked increase in Gammaproteobacteria, specifically in the genus Vibrio, as evidenced by Linear Discriminant Analysis of Effect Size (LEfSe). Seasons also resulted in shifts of the bacterial community, although bacterial genera were distinct from those found in bleached medusas, suggesting temporal associations with the host. According to PERMANOVA analysis, seasonal fluctuations affected the dominant bacterial members (p = 0.07), but symbiont presence was a more significant driver (p=0.001). We found the bacterial community of C. xamachana is like that of other jellyfish and corals, which furthers the interest in this animal as a study model. Defining relevant bacterial genera can help us understand the functional role of the holobiont members that assemble and maintain a healthy microbial community. Also, studies in other regions where C. xamachana distributes can help us define a core bacterial community for this medusa.

Reef corals in the Mexican Reef System have been severely affected by the emergence of a white syndrome that resembles both White Plague II and SCTLD descriptions. Meandroid scleractinian coral species are among the most severely affected. To gain insight into this affliction we conducted a broad study in the brain coral Pseudodiploria strigosa at a rear reef site in the NE Mexican Caribbean. We describe macro and microscopical signals of the disease, characterize the outbreak dynamics, the tissue histopathology, explore immunological responses in the individuals, and compare microbial assemblages associated with the surface mucus layer of healthy and unhealthy colonies. At the study site, the white syndrome outbreak on P. strigosa showed a high incidence rate in summer-fall and a low one in winter, as well as low survival expectation of diseased colonies at the end of the study. After 306 days of observation, out of 96 tracked colonies, eight remained apparently healthy and seven were diseased. No effective resistance to colony disease progression was observed once white syndrome signs developed. Tissue loss rate during the study varied among colonies (mean = 10.8 cm2, s.d. = 7.8 cm2) suggesting a complex relation between causal agents and colony resistance. The deterioration of tissues was evidenced from the basal to the surface body wall of polyps (up to 66% hypertrophy and liquefactive necrosis in unhealthy colonies), implying that microscopic alterations begin before macroscopic signals develop, suggesting this may be a systemic disease. We measured high levels of phenoloxidase (two orders of magnitude higher PO activity than P. strigosa affected by BBD) and antibacterial activity without significant reduction in unhealthy samples from the mucus layer, indicative of an enhanced immunological response. Results showed that opportunistic bacteria dominated damaged colonies, where six genera of the Bacteroidia class were found with significant changes in unhealthy colonies after DeSeq2 analysis. Nevertheless, histological observations did not support infection of the tissues. The opportunistic overload seems to be contained within the mucus layer but may be associated with the mortality of tissues in a yet unclear way. Future research should focus on experimental infections, the tracking of natural infections, and the immunocompetence of corals in the face of environmental pressures due to local, regional, and global impacts. If environmental deterioration is the primary cause of the continuing emergence and re-emergence of lethal coral diseases, as has been proposed by many authors, the only true option to effectively help preserve the coral reef biodiversity and services, is to restore the environmental quality of reef waters at the local scale and reduce greenhouse gases at the global scale.