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.

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Coral reefs rival rainforest in biodiversity, but are declining in part because of disease. Tissue loss lesions, a manifestation of disease, are present in dominant Pocillopora along the Pacific coast of Mexico. We characterized tissue loss in 7 species of Pocillopora from 9 locations (44 sites) spanning southern to northern Mexico. Corals were identified to species, and tissue loss lesions were photographed and classified as those explainable by predation and those that were unexplained. A focal predation study was done concurrently at 3 locations to confirm origin of explained lesions. Of 1054 cases of tissue loss in 7 species of corals, 84% were associated with predation (fish, snails, or seastar) and the remainder were unexplained. Types of tissue loss were not related to coral density; however there was significant geographic heterogeneity in type of lesion; one site in particular (Cabo Pulmo) had the highest prevalence of predator-induced tissue loss (mainly pufferfish predation). Crown-of-thorns starfish, pufferfish, and snails were the most common predators and preferred P. verrucosa, P. meandrina, and P. capitata, respectively. Of the 9 locations, 4 had unexplained tissue loss with prevalence ranging from 1 to 3% with no species predilection. Unexplained tissue loss was similar to white syndrome (WS) in morphology, indicating additional study is necessary to clarify the cause(s) of the lesions and the potential impacts to dominant corals along the Pacific coast of Mexico.

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