Algae as reservoirs for coral pathogens.
Benthic algae are associated with coral death in the form of stress and disease. It's been proposed that they release exudates, which facilitate invasion of potentially pathogenic microbes at the coral-algal interface, resulting in coral disease. However, the original source of these pathogens remains unknown. This study examined the ability of benthic algae to act as reservoirs of coral pathogens by characterizing surface associated microbes associated with major Caribbean and Indo-Pacific algal species/types and by comparing them to potential pathogens of two dominant coral diseases: White Syndrome (WS) in the Indo-Pacific and Yellow Band Disease (YBD) in the Caribbean. Coral and algal sampling was conducted simultaneously at the same sites to avoid spatial effects. Potential pathogens were defined as those absent or rare in healthy corals, increasing in abundance in healthy tissues adjacent to a disease lesion, and dominant in disease lesions. Potentially pathogenic bacteria were detected in both WS and YBD and were also present within the majority of algal species/types (54 and 100% for WS and YBD respectively). Pathogenic ciliates were associated only with WS and not YBD lesions and these were also present in 36% of the Indo-Pacific algal species. Although potential pathogens were associated with many algal species, their presence was inconsistent among replicate algal samples and detection rates were relatively low, suggestive of low density and occurrence. At the community level, coral-associated microbes irrespective of the health of their host differed from algal-associated microbes, supporting that algae and corals have distinctive microbial communities associated with their tissue. We conclude that benthic algae are common reservoirs for a variety of different potential coral pathogens. However, algal-associated microbes alone are unlikely to cause coral death. Initial damage or stress to the coral via other competitive mechanisms is most likely a prerequisite to potential transmission of these pathogens.
School of Biology, Ridley Building, Newcastle University, Newcastle upon Tyne, United Kingdom. m.j.sweet@ncl.ac.uk
Michael J
MJ
Sweet
John C
JC
Bythell
Maggy M
MM
Nugues
D000818:Animals; D037421:Anthozoa / Q000382:microbiology* / Q000469:parasitology; D001419:Bacteria / Q000145:classification / Q000235:genetics / Q000254:growth & development*; D018407:Bacterial Physiological Phenomena; D017691:Caribbean Region; D016798:Ciliophora / Q000145:classification / Q000235:genetics / Q000502:physiology*; D017753:Ecosystem; D054884:Host-Pathogen Interactions; D058086:Microalgae / Q000382:microbiology / Q000469:parasitology; D010140:Pacific Ocean; D012329:RNA, Bacterial / Q000235:genetics; D016053:RNA, Protozoan / Q000235:genetics; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D012337:RNA, Ribosomal, 18S / Q000235:genetics; D012623:Seawater / Q000382:microbiology / Q000469:parasitology; D012624:Seaweed / Q000382:microbiology* / Q000469:parasitology; D017422:Sequence Analysis, DNA; D013045:Species Specificity
D012329:RNA, Bacterial; D016053:RNA, Protozoan; D012336:RNA, Ribosomal, 16S; D012337:RNA, Ribosomal, 18S