Presented at The Washington D.C. Branch of The American Society for Microbiology , Student Day Conference - May  05, 2005

Geoffrey Cook, Dept. of Envr. Sci. and Policy, George Mason Univ., Fairfax, VA, USA,
geoffreymcook@yahoo.com

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
This investigation probed fundamental questions about the coral disease white plague type II (WPII), a disease which characteristically destroys coral tissue at the edge of a lesion (denuded skeleton appearing from the base of the colony). We compared microbial community composition in apparently healthy and diseased corals (Montastraea annularis) from the U.S. Virgin Islands and the Bahamas using a combination of molecular fingerprinting, microbial culturing, and 16S rRNA sequencing. We hypothesize (1) that the causative agents 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 normal tissue and diseased tissue; (3) the WPII disease process is the result of a broad shift in the microbial community (dysbiosis).  Principal component analysis of LH-PCR fingerprints 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.