Porites Ulcerative White Spot Disease (PUWSD): A New Coral Disease in the Philippines; Microbial Ecology and Histopathology
IAAAM Archive
Taylor L. Reynolds1; L.J. Raymundo2; Norman Wainwright3
1North Carolina State University, College of Veterinary Medicine, Raleigh, NC, USA; 2Silliman University Marine Laboratory, Dumaguete City, Philippines; 3Marine Biological Laboratory, Woods Hole, MA, USA


Porites Ulcerative White Spot Disease (PUWSD) is manifested as round, 3-5 mm in diameter, multi-focal to coalescing, bleached tissue or erosions. Foci of bleached, intact tissue either regress, or progress to erosions. Occasionally, discrete erosions coalesce, and after 3 to 5 months, entire coral heads die, leaving a bare skeleton for opportunistic plants and invertebrates to colonize. Discovered in the central Philippines in 1996, PUWSD has been observed on 10 of the commonest Porites coral species. From 1997-1998, an El Nino year, its severity on coral heads monitored increased dramatically.12

In 1998, 120 bacterial isolates were taken from the surface of colonies of Porites attenuata with and without characteristic lesions. Sixteen-s ribosomal DNA extracted from bacterial isolates was amplified and restriction fragment length polymorphism (RFLP) analysis performed. RFLP patterns were used to assemble similar or identical strains into 12 groups. Two of these were principally composed of isolates taken from diseased coral (18/21 and 12/16 total isolates). There is a discernable genetic distinction between the population of isolates from diseased versus clinically healthy coral.

One or 2 representative isolates from each group (15 total) were then subjected to DNA sequence analysis (850 bp). Results of a BLAST search (NCBI) revealed that the 2 representatives from the RFLP groups dominated by isolates from diseased coral (putative pathogens 1 and 2) had 89% identity with Vibrio carchiariae and 84% identity with Vibrio nereis, respectively. Sequences were aligned, and neighbor-joining trees were assembled, in order to examine the phyolgenetic relationships between the two bacterial populations.5 Due to the relatively large distance of the branches containing the putative pathogens, compared to the other Vibrio species included in the trees, the putative pathogens may represent an undescribed Vibrio species.

Both coral surface microorganisms and the coral itself were chemically extracted and assayed for antimicrobial activity against the putative pathogens and two reference strains.7,8 A chemical extract of healthy P. attenuata had antimicrobial activity against all 20 of the coral bacteria assayed, and no activity against reference strains of E. coli and B. subtillis. On average, bacterial strains isolated from diseased coral were more resistant to the antimicrobial compound than those isolated from healthy coral (P=0.006). The two putative pathogens were the most resistant of all, and putative pathogen 2 was found to be significantly more resistant than the average from the disease group (P=0.000).

When viewed with the light microscope, histologic preparations of 5 diseased Porites species contained multifocal coral tissue necrosis, paucity of symbiotic algae, and an increase in filamentous algae and bacteria.2,3,4,10,11 These changes are non-specific, and may represent a primary bacterial infection, or they may be due to effects of microbial invaders secondary to viral infection or environmental stressors. Coral bleaching, or loss of symbiotic algae, has a complex etiology, and may be related to elevated sea surface temperatures, increased UV radiation, pollutants, or primary microbial pathogens.1,6,9 It is likely that PUWSD represents a manifestation, although atypical, of the bleaching process.


The authors would like to thank the follow people for their contributions: Aileen Maypa M.S., Silliman University Marine Lab, Negros Philippines; Tom Schmidt, Ph.D., Alice Child, M.S., Marine Biological Laboratory in Woods Hole, MA; Esther Peters, Ph.D, National Tumor Registry, George Washington University; Andrew Lackner, D.V.M., Ph. D., New England Primate Center, Harvard Medical School; and Mike Waddington, Ph.D., Accugenix, Newark, DE.

This research was supported by the National Institute of Health Research Training Grant, the Geraldine R. Dodge Foundation, Tufts Institute of the Environment, and International Programs, Tufts University School of Veterinary Medicine.


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Taylor L. Reynolds

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