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
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
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 cm
, s.d. = 7.8 cm
) 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
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.
We analyzed the spatial distribution patterns of a white syndrome (WS) outbreak affecting
Pseudodiploria strigosa
colonies in the northern Mexican Caribbean during 2018–2019. The purpose of the study ...was to describe the outbreak progression in a single species and determine if this WS incidence is related to the nearest diseased neighbor distance. Two separated sites with different
P. strigosa
colonial densities (Bocana: 0.08 col/m
2
; Picudas: 0.2 col/m
2
) were selected in similar habitats of the same reef complex.
P. strigosa
colonies within the survey sites were mapped, and their status was recorded (healthy, diseased, or dead) in sequential surveys until colonies died or the study terminated (306 days). Spatial distribution modes were assessed using Ripley’s K function. The spatial colony distribution was random in one site (Bocana) and clustered in the other (Picudas). However, the WS disease incidence per survey was randomly distributed in both sites throughout the observation period of the outbreak, suggesting that WS transmission at small spatial scales was independent of the colony distribution pattern and from the nearest diseased colonies. Survival probability since WS onset in surveyed colonies was different: 0% at Bocana and 14% at Picudas by April 2019. But, eventually, all diseased colonies died in both sites. WS outbreak timing was different at the two sites: Initial prevalence 8% at the Bocana site vs. 44% at Picudas site. Distribution of time to disease onset shown multimodality, with modes varying from 17 to 184 days and wide main modes amplitude suggest a highly variable resistance to the WS. Disease incidence was not abated during winter surveys. Differences between sites in the WS disease outbreak distribution and progression suggest that colony condition, environmental quality, and perhaps several transmission events played an essential role in the complex outbreak dynamics at the local spatial scale of our study.
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