Feeding behavior of <i>Coralliophila</i> sp. on corals affected by Caribbean Ciliate Infection (CCI):A new possible vector?

Coral reefs in the Caribbean are known to be affected by many coral diseases, yet the ecology and etiology of most diseases remain understudied. The Caribbean ciliate infection (CCI) caused by ciliates belonging to the genus Halofolliculina is a common disease on Caribbean reefs, with direct contact considered the most likely way through which the ciliates can be transmitted between infected and healthy colonies. Here we report an observation regarding a Coralliophila sp. snail feeding in proximity to a cluster of ciliates forming the typical disease band of CCI. The result of this observation is twofold. The feeding behavior of the snail may allow the passive attachment of ciliates on the body or shell of the snail resulting in indirect transport of the ciliates among colonies, which makes it eligible as a possible disease vector. Alternatively, the lesions created from snail feeding may enhance the progression of the ciliates already present on the coral as well as promoting additional infections allowing pathogens to enter through the feeding scar

Draft Genome Sequence of Vibrio coralliilyticus strain OCN008 Isolated from Kāneʻohe Bay, Hawaiʻi.

Vibrio coralliilyticus is a Gram-negative bacterium found in seawater and is associated with diseased marine organisms. Strains of V. coralliilyticus have been shown to infect coral from multiple genera. We report the draft genome sequence of V. coralliilyticus strain OCN008, the third V. coralliilyticus genome to be sequenced

Case-control design identifies ecological drivers of endemic coral diseases

Endemic disease transmission is an important ecological process that is challenging to study because of low occurrence rates. Here, we investigate the ecological drivers of two coral diseases-growth anomalies and tissue loss-affecting five coral species. We first show that a statistical framework called the case-control study design, commonly used in epidemiology but rarely applied to ecology, provided high predictive accuracy (67-82%) and disease detection rates (60-83%) compared with a traditional statistical approach that yielded high accuracy (98-100%) but low disease detection rates (0-17%). Using this framework, we found evidence that 1) larger corals have higher disease risk; 2) shallow reefs with low herbivorous fish abundance, limited water motion, and located adjacent to watersheds with high fertilizer and pesticide runoff promote low levels of growth anomalies, a chronic coral disease; and 3) wave exposure, stream exposure, depth, and low thermal stress are associated with tissue loss disease risk during interepidemic periods. Variation in risk factors across host-disease pairs suggests that either different pathogens cause the same gross lesions in different species or that the same disease may arise in different species under different ecological conditions

Assessment of disease lesion removal as a method to control chronic Montipora white syndrome

Coral colonies in Ka–ne‘ohe Bay, Hawai‘i (USA), are afflicted with the tissue loss disease chronic Montipora white syndrome (cMWS). Here we show that removal of chronic disease lesions is a potential method to slow the progression of cMWS in M. capitata. Over the 24 wk observation period, treatment colonies lost almost half the amount of tissue that was lost by control colonies. The percentage of tissue loss at each sampling interval (mean ± SEM; treatment: 1.17 ± 0.47%, control: 2.25 ± 0.63%) and the rate of tissue loss per day (treatment: 0.13 ± 0.04%, control: 0.27 ± 0.08%) were both significantly lower on treated colonies than control colonies. While lesion removal stopped tissue loss at the initial infection site, which allowed colony healing, it did not prevent re-infection; in all but one of the treated colonies, new cMWS lesions appeared in other areas of the colony but not around the treatment margins. Additionally, the rate of new infections was similar between treatment and control colonies, indicating that physical injury from lesion removal did not appear to increase cMWS susceptibility. These results indicate that lesion removal reduced morbidity in M. capitata exhibiting cMWS but did not stop the disease

Complete Genome Sequence of Vibrio coralliilyticus Strain OCN014, Isolated from a Diseased Coral at Palmyra Atoll

Vibrio coralliilyticus is a marine gammaproteobacterium that has been implicated as an etiological agent of disease for multiple coral genera on reefs worldwide. We report the complete genome of V. coralliilyticus strain OCN014, isolated from a diseased Acropora cytherea colony off the western reef terrace of Palmyra Atoll

Complete Genome Sequence of Pseudoalteromonas sp. Strain OCN003, Isolated from Kāneʻohe Bay, Oʻahu, Hawaii

Pseudoalteromonas sp. strain OCN003 is a marine gammaproteobacterium that was isolated from a diseased colony of the common Hawaiian reef coral, Montipora capitata, found on a reef surrounding Moku o Loʻe in Kāneʻohe Bay, Hawaii. Here, we report the complete genome of Pseudoalteromonas sp. strain OCN003

Localized outbreaks of coral disease on Arabian reefs are linked to extreme temperatures and environmental stressors

The Arabian Peninsula borders the hottest reefs in the world, and corals living in these extreme environments can provide insight into the effects of warming on coral health and disease. Here, we examined coral reef health at 17 sites across three regions along the northeastern Arabian Peninsula (Persian Gulf, Strait of Hormuz and Oman Sea) representing a gradient of environmental conditions. The Persian Gulf has extreme seasonal fluctuations in temperature and chronic hypersalinity, whereas the other two regions experience more moderate conditions. Field surveys identified 13 coral diseases including tissue loss diseases of unknown etiology (white syndromes) in Porites, Platygyra, Dipsastraea, Cyphastrea, Acropora and Goniopora; growth anomalies in Porites, Platygyra and Dipsastraea; black band disease in Platygyra, Dipsastraea, Acropora, Echinopora and Pavona; bleached patches in Porites and Goniopora and a disease unique to this region, yellow-banded tissue loss in Porites. The most widespread diseases were Platygyra growth anomalies (52.9% of all surveys), Acropora white syndrome (47.1%) and Porites bleached patches (35.3%). We found a number of diseases not yet reported in this region and found differential disease susceptibility among coral taxa. Disease prevalence was higher on reefs within the Persian Gulf (avg. 2.05%) as compared to reefs within the Strait of Hormuz (0.46%) or Oman Sea (0.25%). A high number of localized disease outbreaks (8 of 17 sites) were found, especially within the Persian Gulf (5 of 8 sites). Across all regions, the majority of variation in disease prevalence (82.2%) was associated with the extreme temperature range experienced by these corals combined with measures of organic pollution and proximity to shore. Thermal stress is known to drive a number of coral diseases, and thus, this region provides a platform to study disease at the edge of corals’ thermal range

Vibrio coralliilyticus Strain OCN008 Is an Etiological Agent of Acute Montipora White Syndrome

Identification 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 107 and 108 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