Erinn M. Muller

Bleaching increases likelihood of disease on Acropora palmata (Lamarck) in Hawksnest Bay, St John, US Virgin Islands

Anomalously high water temperatures may enhance the likelihood of coral disease outbreaks by increasing the abundance or virulence of pathogens, or by increasing host susceptibility. This study tested the compromised-host hypothesis, and documented the relationship between disease and temperature, through monthly monitoring of Acropora palmata colonies from May 2004 to December 2006, in Hawksnest Bay, St John, US Virgin Islands (USVI). Disease prevalence and the rate of change in prevalence showed a positive linear relationship with water temperature and rate of change in water temperature, respectively, but only in 2005 during prolonged periods of elevated temperature. Both bleached and unbleached colonies showed a positive relationship between disease prevalence and temperature in 2005, but the average area of disease-associated mortality increased only for bleached corals, indicating host susceptibility, rather than temperature per se, influenced disease severity on A. palmata.

Shading reduces coral-disease progression

The growing incidence of tropical-marine diseases is attributed to increases in pathogen prevalence and virulence associated with global warming. Additionally, the compromised-host hypothesis suggests that rising ocean temperatures may increase disease activity by making the corals more susceptible to ubiquitous pathogens. We tested the effects of reducing irradiance stress on coral-disease progression rates by shading corals showing signs consistent with white-plague disease. Our results showed that white-plague disease on shaded corals progressed significantly more slowly than on controls. Although the mechanisms are unknown, this study suggests that light intensity influences the rate of coral-disease progression.

Extensive coral mortality in the US Virgin Islands in 2005/2006: A review of the evidence for synergy among thermal stress, coral bleaching and disease

Abstract. In the summer/fall of 2005, extensive coral bleaching on reefs in the US Virgin Islands (USVI) was associated with sea water temperatures exceeding 30°C. Almost all coral species bleached, including Acropora palmata, which bleached for the first time on record in the USVI. As water temperatures cooled, corals began to regain their normal coloration. However, a severe disease outbreak then occurred on deeper, non-acroporid reefs. The disease demonstrated signs consistent with white plague. Monitoring of coral cover along previously established long-term transects on several reefs in St. John and St. Croix was intensified. Data on bleaching and disease were collected before, during and after this bleaching/disease episode. Average coral cover declined by over 50%, from 21.4% to 10.3% at the long-term study sites, within one year of the onset of bleaching, declining further to 8.3% after two years. This loss of coral cover was greater than from all other stressors affecting the USVI reefs in preceding years, and no significant recovery is evident. Disease prevalence increased on bleached A. palmata colonies that were being monitored as well as on the colonies of other species on the deeper reefs. Bleached A. palmata colonies had more disease (primarily white pox and other un-described diseases) than unbleached colonies. The non-acroporid corals that bleached most severely suffered the highest mortality from disease. Although the research summarized in this paper is not conclusive, the results suggest that high water temperatures lead to bleaching, which weakens corals and makes them more vulnerable to diseases.

Relationships between the history of thermal stress and the relative risk of diseases of Caribbean corals

The putative increase in coral diseases in the Caribbean has led to extensive declines in coral populations. Coral diseases are a consequence of the complex interactions among the coral hosts, the pathogens, and the environment. Yet, the relative influence that each of these components has on the prevalence of coral diseases is unclear. Also unknown is the extent to which historical thermal-stress events have influenced the prevalence of contemporary coral diseases and the potential adjustment of coral populations to thermal stress. We used a Bayesian approach to test the hypothesis that in 2012 the relative risk of four signs of coral disease (white signs, dark spots, black bands, and yellow signs) differed at reef locations with different thermal histories. We undertook an extensive spatial study of coral diseases at four locations in the Caribbean region (10(3) km), two with and two without a history of frequent thermal anomalies (approximately 4-6 years) over the last 143 years (1870-2012). Locations that historically experienced frequent thermal anomalies had a significantly higher risk of corals displaying white signs, and had a lower risk of corals displaying dark spots, than locations that did not historically experience frequent thermal anomalies. By contrast, there was no relationship between the history of thermal stress and the relative risk of corals displaying black bands and yellow signs, at least at the spatial scale of our observations.

Genetic Susceptibility, Colony Size, and Water Temperature Drive White-Pox Disease on the Coral Acropora palmata

Outbreaks of coral diseases are one of the greatest threats to reef corals in the Caribbean, yet the mechanisms that lead to coral diseases are still largely unknown. Here we examined the spatial-temporal dynamics of white-pox disease on Acropora palmata coral colonies of known genotypes. We took a Bayesian approach, using Integrated Nested Laplace Approximation algorithms, to examine which covariates influenced the presence of white-pox disease over seven years. We showed that colony size, genetic susceptibility of the coral host, and high-water temperatures were the primary tested variables that were positively associated with the presence of white-pox disease on A. palmata colonies. Our study also showed that neither distance from previously diseased individuals, nor colony location, influenced the dynamics of white-pox disease. These results suggest that white-pox disease was most likely a consequence of anomalously high water temperatures that selectively compromised the oldest colonies and the most susceptible coral genotypes.

Disease Prevalence and Snail Predation Associated with Swell-Generated Damage on the Threatened Coral, Acropora palmata (Lamarck)

Disturbances such as tropical storms cause coral mortality and reduce coral cover as a direct result of physical damage. Storms can be one of the most important disturbances in coral reef ecosystems, and it is crucial to understand their long-term impacts on coral populations. The primary objective of this study was to determine trends in disease prevalence and snail predation on damaged and undamaged colonies of the threatened coral species, Acropora palmata, following an episode of heavy ocean swells in the US Virgin Islands (USVI). At three sites on St. Thomas and St. John, colonies of A. palmata were surveyed monthly over one year following a series of large swells in March 2008 that fragmented 30 to 93% of colonies on monitored reefs. Post-disturbance surveys conducted from April 2008 through March 2009 showed that swell-generated damage to A. palmata caused negative indirect effects that compounded the initial direct effects of physical disturbance. During the 12 months after the swell event, white pox disease prevalence was 41% higher for colonies that sustained damage from the swells than for undamaged colonies (df = 207, p = 0.01) with greatest differences in disease prevalence occurring during warm water months. In addition, the corallivorous snail, Coralliophila abbreviata, was 46% more abundant on damaged corals than undamaged corals during the 12 months after the swell event (df = 207, p = 0.006).

Does Dark-Spot Syndrome Experimentally Transmit among Caribbean Corals?

Over the last half-century, coral diseases have contributed to the rapid decline of coral populations throughout the Caribbean region. Some coral diseases appear to be potentially infectious, yet little is known about their modes of transmission. This study experimentally tested whether dark-spot syndrome on Siderastrea siderea was directly or indirectly transmissible to neighboring coral colonies. We also tested whether open wounds were necessary to facilitate disease transmission. At the completion of the experiments, we sampled bacterial communities on diseased, exposed, and healthy coral colonies to determine whether bacterial pathogens had transmitted to the susceptible colonies. We saw no evidence of either direct or waterborne transmission of dark-spot syndrome, and corals that received lesions by direct contact with diseased tissue, healed and showed no signs of infection. There were no significant differences among bacterial communities on healthy, exposed, and diseased colonies, although nine individual ribotypes were significantly higher in diseased corals compared with healthy and exposed corals, indicating a lack of transmission. Although our experiments do not fully refute the possibility that dark-spot syndrome is infectious and transmissible, our results suggest that in situ macroscopic signs of dark-spot syndrome are not always contagious.

The stable microbiome of inter and sub-tidal anemone species under increasing p CO 2

Increasing levels of pCO2 within the oceans will select for resistant organisms such as anemones, which may thrive under ocean acidification conditions. However, increasing pCO2 may alter the bacterial community of marine organisms, significantly affecting the health status of the host. A pH gradient associated with a natural volcanic vent system within Levante Bay, Vulcano Island, Italy, was used to test the effects of ocean acidification on the bacterial community of two anemone species in situ, Anemonia viridis and Actinia equina using 16 S rDNA pyrosequencing. Results showed the bacterial community of the two anemone species differed significantly from each other primarily because of differences in the Gammaproteobacteria and Epsilonproteobacteria abundances. The bacterial communities did not differ within species among sites with decreasing pH except for A. viridis at the vent site (pH = 6.05). In addition to low pH, the vent site contains trace metals and sulfide that may have influenced the bacteria community of A. viridis. The stability of the bacterial community from pH 8.1 to pH 7.4, coupled with previous experiments showing the lack of, or beneficial changes within anemones living under low pH conditions indicates that A. viridis and A. equina will be winners under future ocean acidification scenarios.

Low pH reduces the virulence of black band disease on Orbicella faveolata

Black band is a deadly coral disease found worldwide, which may become more virulent as oceanic conditions continue to change. To determine the effects of climate change and ocean acidification on black band disease virulence, Orbicella faveolata corals with black band were exposed to different temperature and pH conditions. Results showed a significant decrease in disease progression under low pH (7.7) conditions. Low pH also altered the relative abundance of the bacterial community of the black band disease consortium. Here, there was a significant decrease in Roseofilum, the cyanobacterium that typically dominates the black band mat. These results indicate that as oceanic pH decreases so may the virulence of a worldwide coral disease.

Susceptibility of coral-disease models

The scarcity of empirical data on marine diseases highlights the need for epidemiological models that explain patterns and processes. Yakob and Mumby (1) used a generic susceptible-infected model to describe the prevalence of white plague type II disease on a coral population ( Dichocoenia stokesii ). They compared their model with the metapopulation model of Sokolow et al. (2). Yakob and Mumby (1) stated that rapid population turnover explained the observed oscillations in disease prevalence. Previous marine-disease models have largely ignored life-history traits. Indeed, systems subjected to high return periods of stress can be dominated by weedy species with rapid turnover rates. Although the Yakob and Mumby (1) model incorporated life-history traits and fits the data better than the model of Sokolow et al. (2), we find four conceptual inconsistencies within their model. First, Yakob and Mumby (1) indicated that recruitment increased with the availability of settlement space. The loss of coral colonies usually has the opposite effect, reducing recruitment (3). Similarly, D. stokesii most likely suffered recruitment reduction after the initial disease outbreak, because … [↵][1]2To whom correspondence should be addressed. E-mail: rvw{at}fit.edu. [1]: #xref-corresp-1-1