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.