Several other colonies on the reef were also losing tissue at the same time and were sampled concurrently and submitted together. This group consisted of three other boulder brain coral, a symmetrical brain coral (Pseudodiploria strigosa), three mustard hill coral (Porites asteroides), and a colony of staghorn coral (Acropora cervicornis), which all had a history of pre-existing tissue loss of between 10% and 95% of the colony size that had been static prior to this event. This boulder brain coral had lost 45% of tissue coverage to a prior mortality event that had stabilized and had recently lost an additional 30% tissue coverage (Fig 1A). It is not possible to determine at this stage whether the previous tissue loss was due to the same cause or to a different disease. Samples were taken from the disease margin and from within the apparently healthy portion of the colony.

Gross Findings: An approximately 3 x 4 x 2 cm zinc formalin fixed sample of boulder brain coral from the tissue loss margin was submitted for microscopic evaluation. The sample included a region of intact tissue, an area of newly exposed white skeleton and an unbleached necrotic tissue margin composed of fragmented greenish-brown tissue interspersed with newly exposed skeletal septae. (Fig. 1B). The skeleton was sampled at sufficient depth to collect and support the overlying tissue. A similarly sized biopsy of apparently healthy tissue was sampled distant from the lesion on the same colony.

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Histopathological Findings: There are multifocal areas of lytic necrosis within the gastrodermis and extending through mesoglea and epidermis of the surface and basal body walls. Mucocytes are multifocally hypertrophic and sometimes ruptured. Endosymbionts within these areas are often pale and vacuolated, ghosts, or hypereosinophilic and condensed (necrotic). Mucus, cellular debris, and free Symbiodinium are within the gastrovascular cavity.

Coral microscopic anatomy

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Morphologic Diagnosis/es:

1. Basal and surface body wall: Lytic necrosis, acute, multifocal, severe, with endosymbiont necrosis.
2. Mucocyte hyperplasia and rupture, acute, multifocal, marked.

Disease: Stony coral tissue loss disease

Etiology: Unknown

Distribution: Southeastern Atlantic, including the Florida Reef Tract and wider Caribbean.

Seasonality: There is no clear seasonal pattern, but lesions may stop or slow progressions after thermal bleaching. Some reefs show improvement in summer with relapse in winter, but others do not, and seasonal changes are speculated to be influenced by multiple environmental factors including rainfall, nutrient load, agricultural and urban runoff, turbidity, pH, and salinity, which vary significantly by locality.

Host range: Over 24 species of scleractinian (reef-building and stony) coral, including many massive and encrusting or plate-forming species. Boulder brain coral, pillar coral (Dendrogyra cylindrus), elliptical star coral (Dichocoenia stokesii), grooved brain coral (Diploria labyrinthiformis), smooth flower coral (Eusmilia fastigiata), knobby brain coral (Pseudodiploria clivosa), symmetrical brain coral (P. strigosa) Maze coral (Meandrina spp.), and massive starlet coral (Siderastrea siderea) are all highly susceptible. Other co-occurring species including star corals (Orbicella, Montastraea, Stephanocoenia, and Madracis spp.), and lettuce, plate, and saucer corals (Agaricia spp.) are of intermediate susceptibility. Staghorn coral (Acropora spp.) have not been affected, and finger and mustard hill coral (Porites spp.) also appear resistant or unaffected. In this case, the submitted Staghorn coral (Acropora palmata) was losing tissue to a ciliate infection, and the mustard hill coral (Porites asteroides) was suffering from tissue invasive endolithic fungal overgrowth. It is possible that an environmental stressor triggered different diseases in these colonies concurrently. This illustrates the utility of histopathology in differentiating at least some coral diseases, as tissue loss is a nonspecific gross finding.

Transmission: The disease is transmitted through the water column, via bottom sediments, or through coral-to-coral contact (in aquarium-based laboratory experiments). Laboratory studies support ballast water and ship-associated biofilms as a possible means of transmission from location to location.

Clinical signs: Rapid tissue loss that may be focal or multifocal, sometimes beginning with a bleached spot or with a ring of bleached tissue around bare skeleton.

Pathology: There is lytic necrosis within the gastrodermis, moist often of basal and surface body walls, that may extend through the body wall or across gastrovascular canals into apposing gastrodermis. Necrosis, degeneration, and loss of dinoflagellate endosymbionts is typical. On transmission electron microscopy, filamentous viral-like particles have been observed within degenerate or necrotic endosymbionts but their role in disease is not known.

Pathogenesis: Lesions typically begin in the basal and surface gastrodermis with swelling, vacuolation and necrosis of the dinoflagellate endosymbionts and hypertrophy and lysis of gastrodermal mucocytes followed by loss of gastrodermal and body wall integrity. Mesoglea becomes locally pale (edematous) and eroded, and the lesion may extend through mesoglea to epidermis with rupture of the body wall. Grossly visible tissue loss follows sufficiently severe loss of polyp integrity, and tissue may peel away from the colony demonstrating a “bottom up” progression of necrosis. Healthy-appearing tissue from colonies of susceptible species in affected reefs may have microscopic lesions even if not actively losing tissue.

Diagnosis: A history of acute, rapid tissue loss with other susceptible species affected on the same reef, with consistent histological lesions is consistent with a diagnosis of stony coral tissue loss disease. No etiological test exists.

Public health concerns: Not transmissible to humans. Loss of reefs can increase coastal flood risks.

Wildlife population impacts: Stony coral tissue loss disease was first observed off the coast of Miami in 2014 and since then has spread to the entire Florida Reef Tract and into the Caribbean. In parts of the Florida Reef Tract, some susceptible species have experienced up to 97% mortality, resulting in local extirpation of some species. Loss of reef-building coral also threatens other species that rely on coral for habitat, food, and as a nursery to rear young.

Management: Trenching of a ‘firebreak’ around lesions and filling this with amoxicillin paste is the most effective treatment to date in halting lesions but does not prevent formation of new lesions and raises concern for antibiotic resistance. Probiotic treatments show promise as a potential non-antibiotic treatment and are under investigation. Efforts to avoid spread from reef to reef, such as appropriate ballast handling and dive gear decontamination, are important to help slow progression across the Caribbean.

References:

• Evans JS, Paul VJ, Kellogg, CA. 2022. Biofilms as potential reservoirs of stony coral tissue loss disease. Front Mar Sci 2022;9.
• Florida Coral Disease Response & Epidemiology Team. SCTLD Case Definition. 2018. Florida DEP. https://floridadep.gov/rcp/coral/documents/stony-coral-tissue-loss-disease-sctld-case-definition. Acessed July 2023.
• Gulf and Carribean Fisheries Institute. 2022. Stony coral tissue loss disease. https://www.gcfi.org/emerging-issues-florida-coral-disease-outbreak/. Accessed July, 2023.
• Landsberg JH, Kiryu Y, Peters EC, et al. 2020. Stony coral tissue loss disease in Florida is associated with disruption of host–zooxanthellae physiology. Front Mar Sci 2020;7. https://doi.org/10.3389/fmars.2020.576013
• Precht WF, Gintert BE, Robbart ML, Fura R, van Woesik R. 2016. Unprecedented disease-related coral mortality in southeastern Florida. Sci Rep 6, 31374. https://doi.org/10.1038/srep31374
• Studivan MS, Baptist M, Molina V. Riley S, First M, Soderberg N, Rubin E, Rossin A, Holstein D, Enochs IC. 2022. Transmission of stony coral tissue loss disease (SCTLD) in simulated ballast water confirms the potential for ship-born spread. Sci Rep 12, 19248. https://doi.org/10.1038/s41598-022-21868-z
• Ushijima B, Gunasekera SP, Meyer JL. Tittl J, Potts KA, Thompson S, Sneed J, Ding Y, Chen M, Houk JL, Aeby G, Hase C, Paul VJ. 2032. Chemical and genomic characterization of a potential probiotic treatment for stony coral tissue loss disease. Commun Biol 6, 248 https://doi.org/10.1038/s42003-023-04590-y
• Work TM, Weatherby TM, Landsberg JH, Kiryu Y, Cook SM, Peters EC. 2021. Viral-like particles are associated with endosymbiont pathology in Florida corals affected by stony coral tissue loss disease. Front Mar Sci 2021;8. https://doi.org/10.3389/fmars.2021.750658