Presented at the 30th Annual Eastern Fish Health Workshop, June 13 - 17, 2005, Shepherdstown, West Virginia

Geoffrey Cook, Dept. of Envr. Sci. and Policy, George Mason Univ., Fairfax, VA, USA,
gcook3@gmu.edu
 
Patrick Gillevet, Dept. of Envr. Sci. and Policy, George Mason Univ., Fairfax, VA, USA,
pgilleve@gmu.edu

Esther Peters, Tetra Tech, Inc., and George Mason Univ., Fairfax, VA, USA,
esther.peters@tetratech-ffx.com

J. Paige Rothenberger, Dept. of Envr. Sci. and Policy, George Mason Univ., Fairfax, VA, USA, jrothenb@gmu.edu

Masi Sikaroodi, Dept. of Envr. Sci. and Policy, George Mason Univ., Fairfax, VA, USA,
msikaroo@gmu.edu

Robert B. Jonas, Dept. of Envr. Sci. and Policy, George Mason Univ., Fairfax, VA, USA,
rjonas@gmu.edu

Comparison of bacterial communities between geographically separated corals infected with white plague type II

Abstract:                (Presentation)
White plague type II (WPII) is a disease of scleractinian corals which characteristically destroys tissue beginning at the edge of the colony.  This investigation probed fundamental questions about the bacterial community associated with WPII and the tissue/cell responses by comparing WPII-diseased corals with apparently healthy controls.  We collected tissue cores from healthy and diseased Montastraea annularis (complex) from the U.S. Virgin Islands and the Bahamas.  The tissues were analyzed using a combination of molecular (amplicon length heterogeneity – LH-PCR) fingerprinting, microbial culturing, 16S rRNA gene sequencing, and histological examination. We hypothesized (1) that the causative agent(s) is/are opportunistic pathogen(s) normally present in the host or its environs rather than a novel, obligate pathogen; (2) that corals exhibiting WPII disease signs from different geographical regions harbor differing microbial communities in healthy and diseased tissue; and (3) the WPII disease process is the result of a broad shift in the microbial community (dysbiosis).  The LH-PCR fingerprints indicate that the bacterial diversity in healthy M. annularis tissue from the Bahamas was significantly greater than in samples from the USVI.  In the Bahamas bacterial diversity was lower in the diseased tissue compared to healthy tissue, but that was not true for the USVI.  Principal component analysis of LH-PCR data from pairs of corals suggest that the microbial community on control corals and apparently healthy areas of diseased corals were similar at each geographical location, but the microflora on the Bahamian corals differed markedly from that on the USVI corals. Similarly, the fingerprints of the active diseased samples from each geographic location clustered together, but there was little clustering between the different locations.  An amplicon corresponding to that of the bacterium Aurantimonas coralicida was found in tissue from diseased and healthy coral from the Bahamas but not from the USVI.