Pyrosequencing of the bacteria associated with Platygyra carnosus corals with skeletal growth anomalies reveals differences in bacterial community composition in apparently healthy and diseased tissues

• Published in: Frontiers in microbiology 2015, Vol.6, p.1142-1142
• Main Authors: Ng, Jenny C Y, Chan, Yuki, Tun, Hein M, Leung, Frederick C C, Shin, Paul K S, Chiu, Jill M Y
• Format: Article
• Language: English
• Subjects: coral disease; Metagenomics; microbial communities; Microbiology; Platygyra carnosus; skeletal growth anomalies
• ISSN: 1664-302X; 1664-302X
• DOI: 10.3389/fmicb.2015.01142

Corals are rapidly declining globally due to coral diseases. Skeletal growth anomalies (SGA) or "coral tumors" are a group of coral diseases that affect coral reefs worldwide, including Hong Kong waters in the Indo-Pacific region. To better understand how bacterial communities may vary in corals with SGA, for the first time, we examined the bacterial composition associated with the apparently healthy and the diseased tissues of SGA-affected Platgyra carnosus using 16S ribosomal rRNA gene pyrosequencing. Taxonomic analysis revealed Proteobacteria, Bacteroidetes, Cyanobacteria, and Actinobacteria as the main phyla in both the apparently healthy and the diseased tissues. A significant difference in the bacterial community composition was observed between the two conditions at the OTU level. Diseased tissues were associated with higher abundances of Acidobacteria and Gemmatimonadetes, and a lower abundance of Spirochaetes. Several OTUs belonging to Rhodobacteraceae, Rhizobiales, Gammaproteobacteria, and Cytophaga-Flavobacterium-Bacteroidetes (CFB) were strongly associated with the diseased tissues. These groups of bacteria may contain potential pathogens involved with the development of SGA or opportunistic secondary or tertiary colonizers that proliferated upon the health-compromised coral host. We suggest that these bacterial groups to be further studied based on inoculation experiments and testing of Koch's postulates in efforts to understand the etiology and progression of SGA.