Abstract
Stony coral tissue loss disease (SCTLD) was first documented in 2014 near the Port of Miami, Florida, and has since spread north and south along Florida’s Coral Reef, killing large numbers of more than 20 species of coral and leading to the functional extinction of at least one species, Dendrogyra cylindrus. SCTLD is assumed to be caused by bacteria based on presence of different molecular assemblages of bacteria in lesioned compared to apparently healthy tissues, its apparent spread among colonies, and cessation of spread of lesions in individual colonies treated with antibiotics. However, light microscopic examination of tissues of corals affected with SCTLD has not shown bacteria associated with tissue death. Rather, microscopy shows dead and dying coral cells and symbiotic dinoflagellates (endosymbionts) indicating a breakdown of host cell and endosymbiont symbiosis. It is unclear whether host cells die first leading to death of endosymbionts or vice versa. Based on microscopy, hypotheses as to possible causes of SCTLD include infectious agents not visible at the light microscopy level or toxicosis, perhaps originating from endosymbionts. To clarify this, we examined corals affected with SCTLD and apparently healthy corals using transmission electron microscopy. Endosymbionts in SCTLD-affected and apparently healthy corals consistently had varying degrees of pathology associated with elongated particles compatible in morphology with filamentous positive single-stranded RNA viruses of plants termed anisometric viral-like particles (AVLP). There was apparent progression from early to late replication of AVLP in the cytoplasm of endosymbionts adjacent to or at times within chloroplasts, with morphologic changes in chloroplasts consistent with those seen in plant cells infected by viruses. Coral host cell pathology appeared limited to massive proliferation and lysis of mucus cells. Based on these findings, we hypothesize that SCTLD is a viral disease of endosymbionts leading to coral host death. Efforts to confirm the presence of a virus associated with SCTLD through other means would be appropriate. These include showing the presence of a virus through molecular assays such as deep sequencing, attempts to grow this virus in the laboratory through culture of endosymbionts, localization of virus in tissue sections using immunohistochemistry or in situ hybridization, and experimental infection of known-virus-negative corals to replicate disease at the gross and microscopic level.
Highlights
Stony coral tissue loss disease (SCTLD) was first identified in 2014 near Virginia Key off Miami, Florida (Precht et al, 2016; Aeby et al, 2019), and has spread to the northernmost extent of Florida’s Coral Reef (FCR), south through the Florida Keys and multiple distant sites
Putative late-stage infections were characterized by large cavities replete with coarse anisometric viral-like particles (AVLP) (Figures 2E,F) that occasionally appeared to originate from electron-dense viroplasms (Figures 3E,F); AVLP ranged in diameter from 15–20 nm
Terminal infections were characterized by endosymbionts distorted with large cavities replete with stacks of coarse AVLP mixed with membranes (Figures 4A,B) or clusters of AVLP that appeared to be emerging from host cells associated with lysed cell membrane (Figures 4C–F)
Summary
Stony coral tissue loss disease (SCTLD) was first identified in 2014 near Virginia Key off Miami, Florida (Precht et al, 2016; Aeby et al, 2019), and has spread to the northernmost extent of Florida’s Coral Reef (FCR), south through the Florida Keys and multiple distant sites. SCTLD presents as varying degrees of acute to subacute tissue loss, variably bordered by focal bleaching, affecting more than 20 species of corals (Florida Coral Disease Response Research and Epidemiology Team, 2018; Aeby et al, 2019) and is assumed by some to be caused by an infectious agent (Muller et al, 2020). Studies exist documenting production of toxins in endosymbiotic dinoflagellates from corals (Nakamura et al, 1993) some of which are implicated in pathogenesis of coral bleaching (McConnaughey, 2012)
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