Heat-evolved microalgal symbionts increase coral bleaching tolerance.

Coral reefs worldwide are suffering mass mortalities from marine heat waves. With the aim of enhancing coral bleaching tolerance, we evolved 10 clonal strains of a common coral microalgal endosymbiont at elevated temperatures (31°C) for 4 years in the laboratory. All 10 heat-evolved strains had expanded their thermal tolerance in vitro following laboratory evolution. After reintroduction into coral host larvae, 3 of the 10 heat-evolved endosymbionts also increased the holobionts' bleaching tolerance. Although lower levels of secreted reactive oxygen species (ROS) accompanied thermal tolerance of the heat-evolved algae, reduced ROS secretion alone did not predict thermal tolerance in symbiosis. The more tolerant symbiosis exhibited additional higher constitutive expression of algal carbon fixation genes and coral heat tolerance genes. These findings demonstrate that coral stock with enhanced climate resilience can be developed through ex hospite laboratory evolution of their microalgal endosymbionts.

Novel T4 bacteriophages associated with black band disease in corals.

Research into causative agents underlying coral disease have focused primarily on bacteria, whereas potential roles of viruses have been largely unaddressed. Bacteriophages may contribute to diseases through the lysogenic introduction of virulence genes into bacteria, or prevent diseases through lysis of bacterial pathogens. To identify candidate phages that may influence the pathogenicity of black band disease (BBD), communities of bacteria (16S rRNA) and T4-bacteriophages (gp23) were simultaneously profiled with amplicon sequencing among BBD-lesions and healthy-coral-tissue of Montipora hispida, as well as seawater (study site: the central Great Barrier Reef). Bacterial community compositions were distinct among BBD-lesions, healthy coral tissue and seawater samples, as observed in previous studies. Surprisingly, however, viral beta diversities based on both operational taxonomic unit (OTU)-compositions and overall viral community compositions of assigned taxa did not differ statistically between the BBD-lesions and healthy coral tissue. Nonetheless, relative abundances of three bacteriophage OTUs, affiliated to Cyanophage PRSM6 and Prochlorococcus phages P-SSM2, were significantly higher in BBD-lesions than in healthy tissue. These OTUs associated with BBD samples suggest the presence of bacteriophages that infect members of the cyanobacteria-dominated BBD community, and thus have potential roles in BBD pathogenicity.

Risk of pulmonary emboli in patients with pelvic fractures.

Multiply-injured patients with pelvic fractures are recognized to have an increased risk of deep venous thrombosis. The incidence of pulmonary emboli in patients with this injury has been reported to range from 0.5 to 8.3 per cent in several recent reviews. One hundred ninety-eight patients with pelvic fractures treated at a regional trauma center over a 3-year period were reviewed to evaluate the factors associated with an increased risk of clinically evident pulmonary embolism. The mean age SD was 44 24 years; 51 per cent were male, and mean Injury Severity Score (ISS) was 19 15. Eighteen patients (9%) died. Mortality was significantly correlated with ISS (P < 0.05), male sex, and type and severity of fracture but not with age, mechanism of injury, or operative fixation. Four patients (2.0%) had pulmonary emboli. The occurrence of clinically apparent pulmonary emboli correlated only with ISS (ISS < 15 = 0% vs ISS > 15 = 4%, P < 0.05). During the same time period, there were eight (0.2%) pulmonary emboli in 3337 trauma patients without pelvic fracture. This difference is highly significant (P < 0.0001). Pelvic fracture is indicative of severe injury and denotes a population at higher risk for pulmonary emboli than other trauma patients. Intensive screening and prophylactic measures to prevent deep venous thrombosis and subsequent pulmonary emboli should be intensively directed at this population.