No abstract

Stony coral tissue loss disease (SCTLD) has persisted since 2014 in the Southeast Florida Coral Reef Ecosystem Conservation Area (Coral ECA) where it was first discovered. Most of the highly susceptible corals have perished, leaving Montastraea cavernosa as the most abundant reef-building species with high SCTLD prevalence. Disease interventions (DI) have been conducted throughout Florida’s Coral Reef to save the remaining corals and reduce the disease prevalence with varying degrees of success. The two main treatments were chlorinated (Chl) epoxy and an antibiotic paste. The antibiotic paste was highly effective in the Florida Keys, but its effectiveness in the Coral ECA was questionable. Therefore, we compared the effectiveness of the antibiotic paste and Chl epoxy treatments on M. cavernosa to optimize DI efforts on this species in the Coral ECA. Significant differences were found between the treatment materials and applications related to the proportion of quiesced lesions and corals where antibiotic paste (91.2% success) outperformed Chl epoxy (20% success). By day 351, 50.6% of the antibiotic paste disease-break tissue was fully healed compared to 2.2% of the total Chl epoxy-filled disease-break area. During the study, new lesions occurred on previously treated colonies, as well as colonies not previously treated and new lesion rates varied through time, indicating revisitation is necessary to eliminate disease. Most margin treatments failed within the first 9 days, however, most disease-breaks failed before 44 days. Considering the high treatment success of the antibiotic paste and the conditional variation of new lesion rates, about 1 month is a good practical re-visitation time for retreating failures and any new lesions. DI using antibiotic paste is currently the most effective way to intervene the SCTLD epidemic, but this is only effective as a stopgap measure while the larger causative agents are identified and remediated. Conducting DI at a reef-scape scale is time consuming and requires extensive person-power and resources, making it very expensive. But this expense pales in comparison to the current cost to restore the diversity and live tissue saved with DI. This method also comes with the risk of introducing antibiotics into coral reef environments, which may have unintended outcomes.

Previous research evaluating hydrocarbon toxicity to corals and coral reefs has generally focused on community-level effects, and results often are not comparable between studies because of variability in hydrocarbon exposure characterization and evaluation of coral health and mortality during exposure. Toxicity of the polycyclic aromatic hydrocarbon 1-methylnaphthalene to the coral Porites divaricata was assessed in a constant exposure toxicity test utilizing a novel toxicity testing protocol uniquely applicable to shallow-water corals, which considered multiple assessment metrics and evaluated the potential for post-exposure mortality and/or recovery. Acute and subacute effects (gross morphological changes, photosynthetic efficiency, mortality, and histologic cellular changes) were evaluated during pre-exposure (4 wk), exposure (48 h), and post-exposure recovery (4 wk) periods. Coral condition scores were used to determine a 48-h median effective concentration of 7442 μg/L. Significant physical and histological changes resulted from exposure to 640 μg/L and 5427 μg/L 1-methylnaphthalene, with a 1-d to 3-d delay in photosynthetic efficiency effects (ΔF/Fm). Pigmented granular amoebocyte area was found to be a potentially useful sublethal endpoint for this species. Coral mortality was used to estimate a 48-h median lethal concentration of 12 123 μg/L. Environ Toxicol Chem 2017;36:212-219. © 2016 SETAC.

The Chemical Response to Oil Spill: Ecological Effects Research Forum's water accommodated fraction procedure was compared with 2 alternative techniques in which crude oil was passively dosed from silicone tubing or O-rings. Fresh Macondo oil (MC252) was dosed at 30 mg/L using each approach to investigate oil dissolution kinetics, which was monitored by fluorometry as estimated oil equivalents (EOEs). Subsequent experiments with each dosing method were then conducted at multiple oil loadings. Following equilibration, test media were analytically characterized for polyaromatic hydrocarbons (PAHs) using gas chromatography (GC)-mass spectrometry and dissolved oil using biomimetic solid-phase microextraction (SPME). The results showed that equilibrium was achieved within 72 h for all methods. Measured PAH concentrations were compared with oil solubility model predictions of dissolved exposures. The concentration and composition of measured and predicted dissolved PAHs varied with oil loading and were consistent between dosing methods. Two-dimensional GC compositional data for this oil were then used to calculate dissolved toxic units for predicting MC252 oil acute toxicity across the expected range of species sensitivities. Predicted toxic units were nonlinear with loading and correlated to both EOE and biomimetic SPME. Passive dosing methods provide a practical strategy to deliver and maintain dissolved oil concentrations while avoiding the complicating role that droplets can introduce in exposure characterization and test interpretation. Environ Toxicol Chem 2018;37:2810-2819. © 2018 SETAC.

There are few studies that have evaluated hydrocarbon toxicity to vertically migrating deep-sea micronekton. Crustaceans were collected alive using a 9-m 2 Tucker trawl with a thermally insulated cod end and returned to the laboratory in 10 8C seawater. Toxicity of the polycyclic aromatic hydrocarbon 1-methylnaphthalene to Americamysis bahia, Janicella spinacauda, Systellaspis debilis, Sergestes sp., Sergia sp., and a euphausiid species was assessed in a constant exposure toxicity test utilizing a novel passive dosing toxicity testing protocol. The endpoint of the median lethal concentration tests was mortality, and the results revealed high sensitivity of the deep-sea micronekton compared with other species for which these data are available. Threshold concentrations were also used to calculate critical target lipid body burdens using the target lipid model.