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Posted by NiyazAhmed on 26 Feb 2008 at 04:14 GMT

The general topic of coral reef decline is of major interest. The microbial communities involved and their precise activity in coral decline and the mechanisms thereof have so far been elusive. This paper majorly describes a high-tech approach to oceanic microbial metagenomics as juxtaposed to coral health. It is indeed a large scale attempt to understand how microbes play an important role in declining reefs, and is of broad interest. The authors do report significant observation. The paper shows that, with the increasing human inhabitation/activity in the Line Islands, there exists a chain of events: more human activity  more microbes  more heterotrophs  more microbes classified as opportunistic pathogens  more inorganic nutrients  lower coral cover  higher incidence of unhealthy corals.

The observed increase in the abundance of microbes, in both the direct counts and by culturing, and assignments of such microbes to potential pathogenic groups as shown in this work has the very real potential for coral reef degradation. The authors have assigned such microbial communities to ‘pathogenic’ guilds based on robust metagenomics based inputs. The data generated in the form of metagenomes and viromes from sea microbial communities is in fact an invaluable resource.

However, one substantive criticism could be due to referring to sets of organisms associated with degraded reefs as ‘opportunistic pathogens’. Such an assignment must not mean that these organisms are classical pathogens themselves. For example, commensal E. coli might share sequence homologies with E. coli or Shigella or Helicobacters. Another example could be from the hundreds of saprophytic mycobacteria who might have a highly conserved genomic overlaps with extremely dreaded pathogens such as M. tuberculosis and M. leprae, but, the former group does not represent seasoned pathogens. The major problem to blame for this is the rampant genomic fluidity expressing as phenotypic versatility of the microbial players. Some coral reef ecologists may be hesitant to accept an ‘infectious’ cause of coral degradation. I have read through some of the arguments on the issue; to address these it will be necessary to embark upon a direct ‘cause and effect’ study (prove Koch’s postulates for corals!) to show that coral reefs ‘bounce back’ and recover when the ‘infectious causes’ are removed/treated. This is what we see in case of animal infectious diseases.

Another of the most vocal criticism of the paper is its being mostly correlative rather than experimental. But thanks to this fact that correlational studies are often the only option when trying to collate bio-geo-climatic patterns, so the basic approach is not the issue. Also, since the four reefs studied vary in many different parameters, it sounds difficult to provide evidence of a direct link between human activity and coral disease.

I believe this dataset although not an ultimate decree on the causes of coral degradation, should serve as an important foundation stone for future studies of coral reef microbes.

I hope this will be a good feast for interested readers together with one more paper related from the same group of authors (http://www.plosone.org/do...) and an accompanying commentary in PLoS Biology (http://dx.doi.org/10.1371...). The authors are indeed wise to have chosen the interactive platform of PLoS ONE. I am sure this approach will promote lively debate on the issues linked to coral reef health.

Niyaz Ahmed
Section Editor, PLoS ONE

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