scholarly journals Tissue mortality by Caribbean ciliate infection and white band disease in three reef-building coral species

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2196 ◽  
Author(s):  
Alejandra Verde ◽  
Carolina Bastidas ◽  
Aldo Croquer

Caribbean ciliate infection (CCI) and white band disease (WBD) are diseases that affect a multitude of coral hosts and are associated with rapid rates of tissue losses, thus contributing to declining coral cover in Caribbean reefs. In this study we compared tissue mortality rates associated to CCI in three species of corals with different growth forms:Orbicella faveolata(massive-boulder),O. annularis(massive-columnar) andAcropora cervicornis(branching). We also compared mortality rates in colonies ofA. cervicornisbearing WBD and CCI. The study was conducted at two locations in Los Roques Archipelago National Park between April 2012 and March 2013. InA. cervicornis, the rate of tissue loss was similar between WBD (0.8 ± 1 mm/day, mean ± SD) and CCI (0.7 ± 0.9 mm/day). However, mortality rate by CCI inA. cervicorniswas faster than in the massive speciesO. faveolata(0.5 ± 0.6 mm/day) andO. annularis(0.3 ± 0.3 mm/day). Tissue regeneration was at least fifteen times slower than the mortality rates for both diseases regardless of coral species. This is the first study providing coral tissue mortality and regeneration rates associated to CCI in colonies with massive morphologies, and it highlights the risks of further cover losses of the three most important reef-building species in the Caribbean.

2021 ◽  
Author(s):  
Ana M. Palacio-Castro ◽  
Caroline E. Dennison ◽  
Stephanie M. Rosales ◽  
Andrew C. Baker

Coral cover is declining worldwide due to multiple interacting threats. We compared the effects of elevated nutrients and temperature on three Caribbean corals: Acropora cervicornis, Orbicella faveolata, and Siderastrea siderea. Colonies hosting different algal types were exposed to either ambient nutrients (A), elevated NH4 (N), or elevated NH4 + PO4 (N+P) at control temperatures (26 °C) for > 2 months, followed by a 3-week thermal challenge (31.5 °C). A. cervicornis hosted Symbiodinium (S. fitti) and was highly susceptible to the combination of elevated nutrients and temperature. During heat stress, A. cervicornis pre-exposed to elevated nutrients experienced 84%-100% mortality and photochemical efficiency (Fv/Fm) declines of 41-50%. In comparison, no mortality and lower Fv/Fm declines (11-20%) occurred in A. cervicornis that were heat-stressed but not pre-exposed to nutrients. O. faveolata and S. siderea response to heat stress was determined by their algal symbiont community and was not affected by nutrients. O. faveolata predominantly hosted Durusdinium trenchii or Breviolum, but only corals hosting Breviolum were susceptible to heat, experiencing 100% mortality, regardless of nutrient treatment. S. siderea colonies predominantly hosted Cladocopium C1 (C. goreaui), Cladocopium C3, D. trenchii, or variable proportions of Cladocopium C1 and D. trenchii. This species was resilient to elevated nutrients and temperature, with no significant mortality in any of the treatments. However, during heat stress, S. siderea hosting Cladocopium C3 suffered higher reductions in Fv/Fm (41-56%) compared to S. siderea hosting Cladocopium C1 and D. trenchii (17-26% and 10-16%, respectively). These differences in holobiont susceptibility to elevated nutrients and heat may help explain historical declines in A. cervicornis starting decades earlier than other Caribbean corals. Our results suggest that tackling only warming temperatures may be insufficient to ensure the continued persistence of Caribbean corals, especially A. cervicornis. Reducing nutrient inputs to reefs may also be necessary for these iconic coral species to survive.


2021 ◽  
Vol 8 ◽  
Author(s):  
Aldo Cróquer ◽  
Ernesto Weil ◽  
Caroline S. Rogers

For several decades, white plagues (WPDs: WPD-I, II and III) and more recently, stony coral tissue loss disease (SCTLD) have significantly impacted Caribbean corals. These diseases are often difficult to separate in the field as they produce similar gross signs. Here we aimed to compare what we know about WPD and SCTLD in terms of: (1) pathology, (2) etiology, and (3) epizootiology. We reviewed over 114 peer-reviewed publications from 1973 to 2021. Overall, WPD and SCTLD resemble each other macroscopically, mainly due to the rapid tissue loss they produce in their hosts, however, SCTLD has a more concise case definition. Multiple-coalescent lesions are often observed in colonies with SCTLD and rarely in WPD. A unique diagnostic sign of SCTLD is the presence of bleached circular areas when SCTLD lesions are first appearing in the colony. The paucity of histopathologic archives for WPDs for multiple species across geographies makes it impossible to tell if WPD is the same as SCTLD. Both diseases alter the coral microbiome. WPD is controversially regarded as a bacterial infection and more recently a viral infection, whereas for SCTLD the etiology has not been identified, but the putative pathogen, likely to be a virus, has not been confirmed yet. Most striking differences between WPD and SCTLD have been related to duration and phases of epizootic events and mortality rates. While both diseases may become highly prevalent on reefs, SCTLD seems to be more persistent even throughout years. Both transmit directly (contact) and horizontally (waterborne), but organism-mediated transmission is only proven for WPD-II. Given the differences and similarities between these diseases, more detailed information is needed for a better comparison. Specifically, it is important to focus on: (1) tagging colonies to look at disease progression and tissue mortality rates, (2) tracking the fate of the epizootic event by looking at initial coral species affected, the features of lesions and how they spread over colonies and to a wider range of hosts, (3) persistence across years, and (4) repetitive sampling to look at changes in the microbiome as the disease progresses. Our review shows that WPDs and SCTLD are the major causes of coral tissue loss recorded in the Caribbean.


PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9289 ◽  
Author(s):  
Karen L. Neely ◽  
Kevin A. Macaulay ◽  
Emily K. Hower ◽  
Michelle A. Dobler

Since 2014, Stony Coral Tissue Loss Disease (SCTLD) has led to mass mortality of the majority of hard coral species on the Florida Reef Tract. Following the successful treatment of SCTLD lesions on laboratory corals using water dosed with antibiotics, two topical pastes were developed as vehicles to directly apply antibiotic treatments to wild corals. These pastes were tested as placebos and with additions of amoxicillin on active SCTLD lesions on multiple coral species. The effectiveness of the pastes without antibiotics (placebo treatments) was 4% and 9%, no different from untreated controls. Adding amoxicillin to both pastes significantly increased effectiveness to 70% and 84%. Effectiveness with this method was seen across five different coral species, with success rates of the more effective paste ranging from 67% (Colpophyllia natans) to 90% (Orbicella faveolata and Montastraea cavernosa). Topical antibiotic application is a viable and effective tool for halting disease lesions on corals affected by SCTLD.


2021 ◽  
Vol 8 ◽  
Author(s):  
Nuria Estrada-Saldívar ◽  
Blanca A. Quiroga-García ◽  
Esmeralda Pérez-Cervantes ◽  
Omar O. Rivera-Garibay ◽  
Lorenzo Alvarez-Filip

In the Caribbean, disease outbreaks have emerged as significant drivers of coral mortality. Stony Coral Tissue Loss Disease (SCTLD) is a novel white plague-type disease that was first reported off the Florida coast in 2014. This disease affects >20 coral species and is spreading rapidly throughout the Caribbean. In December 2018, SCTLD reached southwestern (SW) Cozumel, one of the healthiest reef systems in the Caribbean. In this study, we integrate data from multiple survey protocols conducted between July 2018 and April 2020 to track the progression of the outbreak in SW Cozumel and to quantify the impacts of SCTLD on coral communities and the benthic composition of reefs. Given that the SCTLD outbreak coincided with a period of prolonged thermal stress that concluded in widespread coral bleaching in autumn 2019, we also investigated whether this event further exacerbated coral mortality. Our findings show that SCTLD spread throughout SW Cozumel in only 2 months and reached a peak after only 5 months. By the summer of 2019, most of the afflicted corals were already dead. Species of the families Meandrinidae, Faviinae, and Montastraeidae showed 33–95% mortality. The widespread coral die-off caused an overall loss of 46% in coral cover followed by a rapid increase of algae cover across all surveyed reefs that persisted until at least April 2020. In November 2019, more than 15% of surveyed coral colonies were bleached. However, we did not find that bleaching further increased coral mortality at either the colony or the community level, which suggests that the coral communities were able to recover from this event despite still being affected by the disease. In conclusion, SCTLD is radically changing the ecology of coral reefs by decimating the populations of several key reef-builders and reconfiguring the benthic assemblages. The actions needed to restore coral populations have to be accompanied by stringent controls related to the effects of climate change, coastal development, and wastewater treatment to improve coral conditions and ecosystem resilience.


PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252593
Author(s):  
Ian R. Combs ◽  
Michael S. Studivan ◽  
Ryan J. Eckert ◽  
Joshua D. Voss

Since 2014, stony coral tissue loss disease (SCTLD) has contributed to substantial declines of reef-building corals in Florida. The emergence of this disease, which impacts over 20 scleractinian coral species, has generated a need for widespread reef monitoring and the implementation of novel survey and disease mitigation strategies. This study paired SCTLD prevalence assessments with colony-level monitoring to help improve understanding of disease dynamics on both individual coral colonies and at reef-wide scales. Benthic surveys were conducted throughout the northern Florida Reef Tract to monitor the presence/absence of disease, disease prevalence, and coral species affected by SCTLD. Observed SCTLD prevalence was lower in Jupiter and Palm Beach than in Lauderdale-by-the-Sea or St. Lucie Reef, but there were no significant changes in prevalence over time. To assess colony-level impacts of the disease, we optimized a low-cost, rapid 3D photogrammetry technique to fate-track infected Montastraea cavernosa coral colonies over four time points spanning nearly four months. Total colony area and healthy tissue area on fate-tracked colonies decreased significantly over time. However disease lesion area did not decrease over time and was not correlated with total colony area. Taken together these results suggest that targeted intervention efforts on larger colonies may maximize preservation of coral cover. Traditional coral surveys combined with 3D photogrammetry can provide greater insights into the spatiotemporal dynamics and impacts of coral diseases on individual colonies and coral communities than surveys or visual estimates of disease progression alone.


2021 ◽  
Vol 8 ◽  
Author(s):  
Katherine R. Eaton ◽  
Jan H. Landsberg ◽  
Yasunari Kiryu ◽  
Esther C. Peters ◽  
Erinn M. Muller

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.


2014 ◽  
Vol 281 (1788) ◽  
pp. 20140094 ◽  
Author(s):  
M. J. Sweet ◽  
A. Croquer ◽  
J. C. Bythell

Coral diseases have been increasingly reported over the past few decades and are a major contributor to coral decline worldwide. The Caribbean, in particular, has been noted as a hotspot for coral disease, and the aptly named white syndromes have caused the decline of the dominant reef building corals throughout their range. White band disease (WBD) has been implicated in the dramatic loss of Acropora cervicornis and Acropora palmata since the 1970s, resulting in both species being listed as critically endangered on the International Union for Conservation of Nature Red list. The causal agent of WBD remains unknown, although recent studies based on challenge experiments with filtrate from infected hosts concluded that the disease is probably caused by bacteria. Here, we report an experiment using four different antibiotic treatments, targeting different members of the disease-associated microbial community. Two antibiotics, ampicillin and paromomycin, arrested the disease completely, and by comparing with community shifts brought about by treatments that did not arrest the disease, we have identified the likely candidate causal agent or agents of WBD. Our interpretation of the experimental treatments is that one or a combination of up to three specific bacterial types, detected consistently in diseased corals but not detectable in healthy corals, are likely causal agents of WBD. In addition, a histophagous ciliate ( Philaster lucinda ) identical to that found consistently in association with white syndrome in Indo-Pacific acroporas was also consistently detected in all WBD samples and absent in healthy coral. Treatment with metronidazole reduced it to below detection limits, but did not arrest the disease. However, the microscopic disease signs changed, suggesting a secondary role in disease causation for this ciliate. In future studies to identify a causal agent of WBD via tests of Henle–Koch's postulates, it will be vital to experimentally control for populations of the other potential pathogens identified in this study.


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