Measuring Stony Coral Tissue Loss Disease Induction and Lesion Progression Within Two Intermediately Susceptible Species, Montastraea cavernosa and Orbicella faveolata

Abstract

During the last several decades, Florida’s Coral Reef (FCR) has been impacted by both global and local stressors that have devastated much of its living coral cover. Additionally, since 2014 FCR has experienced a lethal disease outbreak termed stony coral tissue loss disease (SCTLD). Here, we examined SCTLD spreading dynamics within and among fragmented coral colonies and quantified lesion progression rate of two intermediately susceptible species—Montastraea cavernosa and Orbicella faveolata—through induction experiments conducted in laboratory aquaria. M. cavernosa colonies showing subacute tissue loss were sequentially fragmented parallel to the lesion edge to determine whether isolated tissue that showed no tissue-loss signs, referred to as isolated apparently healthy (AH) donor fragments, would subsequently exhibit tissue loss. Additionally, AH M. cavernosa and O. faveolata fragments, referred to as recipient fragments, were placed in direct contact with the M. cavernosa donor fragments to assess incidence of new tissue-loss lesions. Finally, AH M. cavernosa donor fragments were placed in direct contact with recipient M. cavernosa and O. faveolata fragments to account for aggression from direct contact. Samples were collected for histopathology of the corals through time. Many isolated AH donor fragments developed tissue-loss lesions during the 60-day study, suggesting SCTLD may be systemic within small-sized colonies. Our results confirmed that physical contact between recipient fragments and subacute SCTLD-lesioned tissue often led to tissue loss in recipient fragments. None of the control recipient or donor fragments experienced tissue loss. Grossly, multifocal lesions started on or adjacent to the septal and costal basal body walls with tissue loss progressing across the polyp septa and coenenchyme, respectively, in both species. Histologically, initial tissue-loss lesions in both species exhibited characteristic lytic necrosis (LN) at the basal body wall of the gastrodermis. O. faveolata exhibited higher rates of lesion appearance and subsequent mortality compared to M. cavernosa, but once a lesion appeared, M. cavernosa lost tissue faster than O. faveolata. This work contributes to the growing knowledge of SCTLD dynamics and highlights the differences in lesion progression within susceptible species.

Effect of species, size, and chimerism on the susceptibility of Caribbean brain coral recruits to stony coral tissue loss disease (SCTLD)

“…Lesion appearance and progression in C. natans and D. labyrinthiformis recruits largely matched similar descriptions for adult colonies (FKNMS, 2018;Landsberg et al, 2020;Eaton et al, 2021). Beginning in some recruits of both species after just 48 h of exposure, lesions continued to present in new, previously healthy recruits over time.…”

“…Although the causative pathogen(s) for SCTLD remain unidentified, enrichment of disease-associated bacteria in lesions, along with the efficacy of antibiotics, suggests that bacteria play a role in disease progression (Meyer et al, 2019; Neely et al, 2020; Rosales et al, 2020; Neely et al, 2021b; Clark et al, 2021). Transmission has been shown to occur through direct contact as well as through the water column in neutrally buoyant particles (Aeby et al, 2019; Dobbelaere et al, 2020; Eaton et al, 2021). Williams et al (2021) found that in the Florida Keys, SCTLD disproportionately affected large corals and areas with high species diversity and colony density.…”

Characterization of the Microbiome of Corals with Stony Coral Tissue Loss Disease along Florida’s Coral Reef

“…Similarly, in the present study, there were no significant differences between the DL tissue and the DU tissue of C. natans. Therefore, colonies showing signs of SCTLD may have a disrupted microbiome even far away from the lesion, suggesting a systemic effect [55]. It has been reported in other studies that stress, such as heat stress, often has a stochastic effect on the microbial community composition that can result in an increase in the beta diversity [56].…”

“…In Rosales et al [57], for example, Acropora cervicornis exposed to diseased ramets had a higher beta diversity compared to control corals not exposed to disease. Eaton et al [55] also showed that visibly unaffected areas (DU tissue) on diseased corals later showed signs of tissue loss after coral fragments were separated and isolated from the active disease border on the parent colony, and Landsberg et al [30] found lytic necrosis characteristic of SCTLD lesions within some samples of DU tissue, again suggesting that SCTLD may be systemic within coral colonies.…”

Viral-Like Particles Are Associated With Endosymbiont Pathology in Florida Corals Affected by Stony Coral Tissue Loss Disease

“…Supporting this hypothesis is a spatial epidemiology suggestive of a contagion (Muller et al, 2020), corals affected by SCTLD have specific groups of bacteria associated with lesions as detected by molecular assays (Meyer et al, 2019;Rosales et al, 2020;Ushijima et al, 2020), and multiple species of affected corals respond positively to treatments with antibiotics (Neely et al, 2020(Neely et al, , 2021, although this practice does not prevent genesis of additional lesions (Shilling et al, 2021;Walker et al, 2021). Finally, experimental mesocosm studies suggest SCTLD is transmissible (Aeby et al, 2019;Eaton et al, 2021;Meiling et al, 2021).…”