11th ICRS Abstract book - Nova Southeastern University

7.207
Ecological Immunity Of Diseased And Healthy Montastrea Faveolata Through The
2005 Bleaching Event
Laura D. MYDLARZ* 1 , Ernesto WEIL 2 , Courtney S. COUCH 3 , Nancy L. DOUGLAS 3 ,
C. Drew HARVELL 3
1 Department of Biology, University of Texas at Arlington, Arlington, TX, 2 Marine
Science, University of Puerto Rico, Mayagüez, Puerto Rico, 3 Ecology and Evolutionary
Biology, Cornell University, Ithaca, NY
One prominent hypothesis regarding climate stress and scleractinian corals is that thermal
stress will compromise immunity. The ultimate test of this hypothesis is to track how
immunity of both healthy and diseased colonies varies with massive thermal stress in
nature. Bleached, healthy and Yellow Band Diseased (YBD) colonies of Montastrea
faveolata were marked and followed in the field through the 2005 bleaching event and
activities of known immune proteins such as prophenoloxidase, lysozyme, chitinase and
anti-bacterial activity were monitored. Mortality and infection rate was high: all
colonies except one either died or became infected by the end of the two year
observation. Tissue with YBD did not expel all their zooxanthellae, even when healthy
parts of these colonies bleached. Interestingly, the levels of all the immune proteins in
diseased tissue were statistically the same during the 2005 bleaching event and in the
subsequent year. Some immune proteins were induced systemically throughout infected
colonies, like lysozyme and antibacterial activity which was systemically higher in
diseased corals in both healthy and diseased tissue of YBD corals, compared to healthy
coral colonies. Both lysozyme and antibacterial activity showed a trend for suppression
of activity in bleached corals, while prophenoloxidase showed an opposite trend with
highly elevated levels in the bleached corals collected in 2005. These results demonstrate
that some components of immunity respond to natural temperature stress as predicted and
are suppressed, while others are actually activated by elevated temperatures, suggesting a
general stress response or resilience to a changing environment.
7.208
On The White Plague Disease in Corals, With Remarks On The Interactions
Between Disease, Environment And Host
Santiago HERRERA* 1 , Juan SANCHEZ 1
1 Ciencias Biologicas, Universidad de los Andes, Bogota, Colombia
Coral Reefs are one of the most important ecosystems in the ocean and therefore in the
planet. However a highly significant decline during the past decades is threatening their
survival. Infectious diseases are one of the biggest factors that contribute to this
phenomenon. Among the most common, widespread and virulent coral diseases is the
White Plague Disease. Here I review the literature available to date about (i) the history
and status of WPD, (ii) the factors that might account for WP epizootic events, and (iii)
immunologic interactions between the pathogen and the coral. The WPD is caused by the
bacterial pathogen Auratimonas coralicida and has the widest host range of all coral
diseases that had been detected so far in the Caribbean, with 43 scleractinian species from
24 genera and two hydrocoral species. Three different types of the disease have been
described to date, but it seems like they all are produced by the same pathogen. The
differences in the rate of the coral tissue destruction, which are the basis to distinguish the
three types of WPD, are likely the product of heterogeneous local environmental
conditions that trigger the pathogenesis. Some of the best studied factors that promote the
disease development, by producing stress in the coral and enhancing the virulence of the
pathogen, are: the increasing seawater temperature, human and terrestrial contaminants,
and the spatial distribution of the coral populations. Corals do not posses an adaptiveimmune
system, as mammals do, but they do posses other defence mechanisms against
pathogens. Primitive, but efficient cellular and humoral immune response mechanisms,
accompanied by a microbial-flora, are their main ways of protection. The future of the
coral reefs is unknown. Several measures, including reducing contaminants production,
anti-global-warming actions and more research in marine diseases, are fundamental in
order to preserve these important ecosystems.
Poster Mini-Symposium 7: Diseases on Coral Reefs
7.209
Phage Therapy Of Coral Disease
Ilil ATAD* 1 , Rotem EFRONY 1 , Eugene ROSENBERG 1
1 Department of Molecular Microbiology and Biotechnology, Faculty of Life Sciences, Tel Aviv
University, Tel Aviv, Israel
At present there are no known procedures for preventing or treating infectious diseases of
corals. In this study, the use of phage therapy of coral disease has been investigated. A lytic
bacteriophage (phage BA3) was isolated for the bacterial pathogen, Thalosomonas loyaeana
that is the causative agent of the white plague-like disease of Favia favus on the Eilat coral reef.
Phage BA3 was characterized as dsDNA lytic phage belonging to the Podoviridea family. The
genome of phage BA3 was sequenced and it contains 37,313 bp (40.9% G+C content) with 47
ORFs.
By using this pathogen-specific phage in controlled aquaria experiments, it was demonstrated
that the disease could be controlled by addition of the phage. The data indicate that initially the
phages bind to the pathogen in seawater and are then brought to the coral surface where they
multiply and lyse the pathogen. The phages remained associated with the coral and could
prevent subsequent infections. Additionally, it was shown that addition of the phages one day
after the infection also prevented the disease, whereas applying the phage 2 or 3 days after
infection failed. Phages also prevented the transmission of the disease from sick coral to healthy
corals. Subsequent infection of healthy phage-treated corals (37d after initial phage therapy)
did not cause the disease, even though no additional phages were added. Corals treated with
phage retained the phages for weeks after they were inoculated. The data presented suggest that
phage therapy has the potential to control the spread of infectious coral diseases.
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