11th ICRS Abstract book - Nova Southeastern University

7-45
The Effect Of Sediment And Heat Stress On The Initiation And Spread Of Black
Band Disease
Aaron MILLER* 1 , Laurie RICHARDSON 1
1 Biology, Florida International University, Miami, FL
Experiments were conducted to determine the effects of heat and sediment stress on the
properties of mucus from the coral Montastraea cavernosa, and how this relates to the
initiation and spread of black band disease (BBD). Three fragments of M. cavernosa
were placed into each of four treatments: a control (26°C, no sediment), heat stress
(30°C, no sediment), sediment stress (26°C, twice daily 150mg/cm 2 sediment loading),
and a combination of the two stressors (30°C, plus sediment loading). After the threeweek
experimental period, mucus was collected from each fragment to determine the
number of cyanobacterial filaments isolated from BBD (two strains) that adhere to the
mucus after one hour. At the end of the experiment, fragments were inoculated with
fresh BBD, and were observed for eight days.
There was a significantly greater number of cyanobacteria adhering to the heat stressed
mucus than to the controls, while the other treatments did not differ significantly. The
control corals showed little spread of the BBD consortium eight days after inoculation.
Those fragments exposed to heat stress had complete coverage of the fragment by a
biofilm of the BBD microbial consortium within the eight days. In the sediment stressed
corals and corals exposed to the combination of stressors there was progressive skeletal
exposure (tissue lysis) associated with a very thin line of BBD which was more
pronounced with the combination of sediment and heat stress. After the eight day
observation period, the control fragments were then placed into the 30°C treatment, and
observed for an additional six days. The consortium started to spread in 2/3 of the
fragments only after day four. These results indicate that the environmental stressors
cause the host coral M. cavernosa to be more susceptible to BBD infection.
7-46
Temporal Dynamics Of The Ongoing Caribbean Yellow Band Epizootic Event:
Potential Link To Increasing Water Temperatures.
Ernesto WEIL* 1
1 Department of Marine Sciences, University of Puerto Rico, Lajas, Puerto Rico
Geographic and local epizootic events affecting corals, octocorals, sponges and other reef
organisms have become more frequent and damaging. Two of these events affecting
acroporid corals and the urchin Diadema antillarum produced substantial ecological
changes in coral reefs throughout the Caribbean in the 1980’s. However, the ongoing
epizootic event of Caribbean Yellow Band Disease (YBD) could be the most devastating
yet. This disease is rapidly killing colonies of three of the four Montastraea species, the
most important reef building genus in the region. Eight years of data and observations
throughout the region indicate that YBD (1) is present in almost every single coral reef
throughout the region, (2) prevalence have increased significantly in most reefs with
higher numbers of infected M. faveolata (20-65%) and M. franksi (2-35%) colonies, (3)
YBD significantly decreases colony reproductive output (fecundity) and therefore, the
potential for recovery, (4) has produced significant coral cover loss (up to 45%) and
killed very old (>1000 y) colonies in a relative short time, and (5) etiology has changed
through time: a- from a seasonal, sporadic problem to a perseverant, year-long, common
affection, b- band advance rates (mortality rates) have increased significantly from 0.7 to
4 cm/month, c- increase in the number of lesions per colony (up to 36), and d- lesion
signs (bands) are wider, more white (less zooxanthellae?) with new wide yellow tissue
areas now common in most colonies. Most of these changes seem to be correlated with
increased monthly average minimum sea water temperature and/or might reflect the
disease dynamics over time or epizootic dynamics in high density populations. YBD is
today the worst threat to Caribbean coral reefs.
Keywords: Caribbean, Yellow Band Disease,threat epizootic, disease dynamics
Oral Mini-Symposium 7: Diseases on Coral Reefs
7-47
Coral Diseases After The 2005 Caribbean Bleaching Event: Did Prevalence Increased
Accordingly With Bleaching Severity?
Aldo CROQUER* 1 , Ernesto WEIL 2
1 Biologia de Organismos, Simon Bolivar University, Caracas, Venezuela, 2 Marine Sciences,
University of Puerto Rico, La Parguera, Puerto Rico
In the GBR temperature anomalies are correlated with coral diseases, but in the Caribbean, this
hypothesis remains controversial. In 2005, a bleaching event affected corals throughout the
region but mostly in the eastern and northern areas. Surveys were conducted over permanent
belt-transects along a latitudinal gradient from Bermuda to Grenada where bleaching severity
(i.e. percentage of corals affected) varied significantly. Surveys were done again in 2006 to test
the hypothesis that localities with higher bleaching prevalence in 2005 will show a significat
increase in disease prevalence. A 3-way ANOVA with site and depth as crossed and fixed
factors and time as a repeated measure, was performed for bleaching and the overall prevalence
of coral disease. To look at which specific diseases explained differences between particular
sites and depths between years, a one-way ANOSIM and SIMPER analyses were used.
Bleaching prevalence significantly decreased by the summer of 2006 at all sites and depth
intervals. There was a significant interaction between reef sites, depth and years with significant
reductions in the prevalence of coral diseases in 2006 in all sites and depths except in Flamingo
Bay (Grenada) where yellow band disease (YBD) prevalence at intermediate and deep habitats
significantly increased. All other diseases significantly decreased in 2006 at all sites and depths
that had different bleaching levels in 2005. While sites with low bleaching prevalence in 2005
(i.e. Curacao and Bermuda) had less diseases compared to sites where bleaching was more
severe (Grenada and Puerto Rico), in 2006 all sites and depths (except deeper and intermediate
habitats in Flamingo) experienced a significant reduction in the prevalence of coral diseases
regardless of bleaching severity. Thus, our results partly support the hypothesis of coral
bleaching as a factor promoting coral epizootics.
7-48
Testing the compromised-host hypothesis during the 2005 Caribbean coral-bleaching and
disease event
Erinn MULLER* 1 , Caroline ROGERS 2 , Jeff MILLER 3 , Robert VAN WOESIK 1
1 Department of Biological Sciences, Florida Institute of Technology, Melbourne, FL, 2 United
States Geological Survey, St. John, Virgin Islands (U.S.), 3 South Florida/Caribbean Network,
National Park Service, St. John, Virgin Islands (U.S.)
Anomalously high-water temperatures can increase coral-disease prevalence by either
influencing pathogen concentrations or virulence, or by increasing host susceptibility through
bleaching. The 2005 Caribbean coral-bleaching event provided the opportunity to test the
compromised-host hypothesis on two species in the US Virgin Islands. At Hawksnest Bay,
from 2004-2007, 60 randomly selected Acropora palmata colonies were examined monthly for
bleaching, disease prevalence, and disease-associated mortality. Also, the number of diseaseinduced
lesions was examined in 20, 2 m by 10 m belt transects, in five Montastraea spp.dominated
reefs, from 2005-2007. The prevalence of disease on both bleached and unbleached
A. palmata colonies was positively related with water temperature; however, bleached A.
palmata colonies suffered greater disease-associated mortality than unbleached colonies. By
November 2005, >98% of the Montastraea spp. had bleached, and within five months disease
incidence had increased 51 fold. The lack of unbleached Montastraea prohibited a comparison
between bleached and unbleached colonies, however, disease incidence returned to prebleaching
conditions once colonies partially recovered (July 2006). These studies indicate
disease prevalence and severity increases when colonies bleach, at least for A. palmata and
Montastraea spp., supporting the compromised-host hypothesis.
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