Runaway coral-algal dysbiosis may be responsible for rapid coral tissue loss

Stony coral tissue loss disease (SCTLD) affects at least 22 Western Atlantic coral species and presents as focal or multifocal lesions, which swiftly expand across the colony, resulting in rapid tissue loss and mortality. Previous histopathological examinations have noted necrosis, body wall breakage, gastrodermal separation, exocytosis, and vacuolization of the symbiont as pathological signs; however, the same signs are present to some degree in otherwise apparently healthy coral tissues processed for histology. Here, we quantify the degree of symbiont vacuolization, symbiont size change, exocytosis, and gastrodermal separation in apparently healthy and diseased coral tissues of eight coral species in association with SCTLD transmission experiments in Florida (USA) and the United States Virgin Islands. We describe a characteristic progression of disease signs which support the hypothesis that coral-algal dysbiosis contributes to SCTLD-associated tissue loss. Progression begins with symbiont cell vacuolization, followed by symbiont cell exocytosis and gastrodermal cell lysis. The lysing of gastrodermal cells leads to separation of the gastrodermis from the mesoglea, and finally to liquifying necrosis. Disease signs varied by coral species and symbiont genus following known hierarchy in disease susceptibility across coral and algal genera. SCTLD histological dynamics were also associated with differential expression of genes considered indicative of stress and dysbiosis and further influenced by both coral species and algal symbiont genus.