An outbreak of stony coral tissue loss disease (SCTLD), emerged on reefs off the coast of southeast Florida in 2014 and continues to spread throughout Florida's Reef Tract. SCTLD is causing extensive mortality of multiple coral species and disease signs vary among affected coral species with differences in rates of tissue loss (acute and subacute), lesion morphology (adjacent bleached zone or not) and lesion occurrence (focal and multi-focal). We examined the virulence, transmission dynamics and response to antibiotic treatment of coral species exhibiting different types of tissue loss lesions from two regions in Florida. Montastraea cavernosa with subacute tissue loss lesions in the southeast Florida region near Fort Lauderdale was compared to corals (multiple species) with acute tissue loss lesions in the Middle Keys. Corals from both regions showed progressive tissue loss but the in situ rate of mortality was significantly higher in tagged colonies in the Keys. Aquaria studies showed disease transmission occurred through direct contact and through the water column for corals from both regions. However, transmission success was higher for corals with acute vs. subacute lesions. There was 100% transmission for both test species, M. cavernosa and Meandrina meandrites, touching acute lesions. Among the three species touching subacute lesions, the disease transmitted readily to Orbicella faveolata (100%) followed by M. cavernosa (30%) with no transmission occurring with Porites astreoides. Diseased fragments of all species tested responded to antibiotic treatment with a cessation or slowing of the disease lesions suggesting that bacteria are involved in disease progression. Mortality was higher for in situ corals with acute lesions and transmission was higher in M. cavernosa exposed to acute lesions compared to subacute lesions, suggesting that different microbes may be involved with the two lesion types. However, since in situ mortality of M. cavernosa was not measured in the Middle Keys, we cannot completely rule out that a common pathogen is involved but is less virulent within M. cavernosa.

As many as 22 of the 45 coral species on the Florida Reef Tract are currently affected by stony coral tissue loss disease (SCTLD). The ongoing disease outbreak was first observed in 2014 in Southeast Florida near Miami and as of early 2019 has been documented from the northernmost reaches of the reef tract in Martin County down to Key West. We examined the microbiota associated with disease lesions and apparently healthy tissue on diseased colonies of Montastraea cavernosa, Orbicella faveolata, Diploria labyrinthiformis, and Dichocoenia stokesii. Analysis of differentially abundant taxa between disease lesions and apparently healthy tissue identified five unique amplicon sequence variants enriched in the diseased tissue in three of the coral species (all except O. faveolata), namely an unclassified genus of Flavobacteriales and sequences identified as Fusibacter (Clostridiales), Planktotalea (Rhodobacterales), Algicola (Alteromonadales), and Vibrio (Vibrionales). In addition, several groups of likely opportunistic or saprophytic colonizers such as Epsilonbacteraeota, Patescibacteria, Clostridiales, Bacteroidetes, and Rhodobacterales were also enriched in SCTLD disease lesions. This work represents the first microbiological characterization of SCTLD, as an initial step toward identifying the potential pathogen(s) responsible for SCTLD.

dIdentification of a pathogen is a critical first step in the epidemiology and subsequent management of a disease. A limited number of pathogens have been identified for diseases contributing to the global decline of coral populations. Here we describe Vibrio coralliilyticus strain OCN008, which induces acute Montipora white syndrome (aMWS), a tissue loss disease responsible for substantial mortality of the coral Montipora capitata in Ka ne'ohe Bay, Hawai'i. OCN008 was grown in pure culture, recreated signs of disease in experimentally infected corals, and could be recovered after infection. In addition, strains similar to OCN008 were isolated from diseased coral from the field but not from healthy M. capitata. OCN008 repeatedly induced the loss of healthy M. capitata tissue from fragments under laboratory conditions with a minimum infectious dose of between 10 7 and 10 8 CFU/ml of water. In contrast, Porites compressa was not infected by OCN008, indicating the host specificity of the pathogen. A decrease in water temperature from 27 to 23°C affected the time to disease onset, but the risk of infection was not significantly reduced. Temperature-dependent bleaching, which has been observed with the V. coralliilyticus type strain BAA-450, was not observed during infection with OCN008. A comparison of the OCN008 genome to the genomes of pathogenic V. coralliilyticus strains BAA-450 and P1 revealed similar virulence-associated genes and quorum-sensing systems. Despite this genetic similarity, infections of M. capitata by OCN008 do not follow the paradigm for V. coralliilyticus infections established by the type strain.

Incidences of coral disease in the Indo-Pacific are increasing at an alarming rate. In particular, Montipora white syndrome, a tissue-loss disease found on corals throughout the Hawaiian archipelago, has the potential to degrade Hawaii’s reefs. To identify the etiologic agent of Montipora white syndrome, bacteria were isolated from a diseased fragment of Montipora capitata and used in a screen for virulent strains. A single isolate, designated strain OCN002, recreated disease signs in 53% of coral fragments in laboratory infection trials when added to a final concentration of 107 cells/ml of seawater. In addition to displaying similar signs of disease, diseased coral fragments from the field and those from infection trials both had a dramatic increase in the abundance of associated culturable bacteria, with those of the genus Vibiro well represented. Bacteria isolated from diseased fragments used in infection trails were shown to be descendants of the original OCN002 inocula based on both the presence of a plasmid introduced to genetically tag the strain and the sequence of a region of the OCN002 genome. In contrast, OCN002 was not re-isolated from fragments that were exposed to the strain but did not develop tissue loss. Sequencing of the rrsH gene, metabolic characterization, as well as multilocus sequence analysis indicated that OCN002 is a strain of the recently described species Vibrio owensii. This investigation of Montipora white syndrome recognizes V. owensii OCN002 as the first bacterial coral pathogen identified from Hawaii’s reefs and expands the range of bacteria known to cause disease in corals.