A juvenile COT Sea Star grazing among corals: not a threat to reefs in small numbers, but a significant threat when populations explode. Image by Stephani Holzwarth.

One of the most-dreaded biological threats to tropical coral reefscan be a population outbreak of Crown-of-Thorns (COT) Sea Stars (Acanthaster planci). Growing to a diameter of 30 to 60 cm (12 to 24 inches), these large echinoderms can have population explosions and form masses gliding over tropical reefs, feeding on coral polyps by everting their stomachs through their mouths and digesting the coral tissue. Although they can opportunistically feed on a variety of prey items, COT Sea Stars are notorious for eating the tissues from all types of stony corals, leaving only skeletal remains.

Outbreaks can consume live corals over large areas, leaving large swaths of white skeletons that offer a perfect substrate for algal growth. This chain of events alter reef fish populations and reduce the aesthetic value of coral reefs, which negatively affects both fishing and tourism.

Despite more than 30 years of research, the triggers and spread of COT outbreaks are not fully understood. Early researchers attributed COT plagues to “natural facets of the life-history ofAcanthaster” (Peter Vine, 1973). About a decade later, a researcher in Guam theorized that sudden population explosions of A. planci were followed periods of heavy rainfall and terrestrial runoff from ountainous islands that caused plankton blooms. With more available plankton, more larval sea stars were able to reach maturity (Charles Birkeland, 1982). (See notes below.)

Human impacts such as urbanization, runoff, and fishing have also been correlated with outbreaks, but some outbreaks continue to occur in the absence of known anthropogenic triggers. Waves of a spreading outbreak that moves southerly along the Great Barrier Reef are termed secondary outbreaks because they are thought to be seeded from dispersing larvae of a primary outbreak upstream. With a single large female capable of producing 100 million eggs per spawning season, the threat of massive numbers of pelagic larvae drifting onto a reef from afar is something of great concern to those charged with protecting reef areas.

Long-distance larval drift?

This secondary outbreak hypothesis has been widely accepted as the mechanism by which COT outbreaks spread across broad regions of the Pacific Ocean and impact remote locations such as Hawaii, Guam, or French Polynesia—until now.

A team of scientists from the Hawai‘i Institute of Marine Biology and the Joint Institute for Marine and Atmospheric Research at the University of Hawai‘i and Rutgers University have recently used genetic techniques to evaluate the spatial scale at which COT outbreaks can occur via larval dispersal across the central Pacific Ocean. Above: researchers collecting COT specimen for genetic testing. Image by Derek Smith.

The results of this work have demonstrated that, unlike on the Great Barrier Reef, COT larvae are not moving en masse among central Pacific archipelagos. In fact, contrary to expectations under the secondary outbreak hypothesis, all COT outbreaks in the study came from local populations.

On a finer scale, genetic differences were detected among reefs around islands and even between lagoon and forereef habitats of the same island, indicating that the larvae of this species are not routinely reaching their full dispersal potential, and are certainly not fueling outbreaks at distant sites.

This research has proved that outbreaks are not some rogue population that expands and ravages across central Pacific reefs. Instead, the authors hypothesize that nutrient inputs from humans and favorable climatic and ecological conditions likely create conditions that can trigger explosions of local populations. 
Large COT: a mature female can produce up to 100 million eggs in one spawning season. Image by Molly Timmers.

This work is particularly important because most current management strategies are focused on stopping secondary spread rather than preventing human activities that can start an outbreak. This study is the first genetic survey of COT populations in which both outbreak and non-outbreak populations are surveyed across a broad region of the Pacific and the results are pretty clear that outbreaks are not jumping across large expanses of open ocean.

Dr. Rob Toonen, one of the researchers involved in this project, explains “the genetic differences found among COT populations clearly indicate that outbreaks are not spreading from the Hawaiian Archipelago to elsewhere. Furthermore, the similarity between outbreak and non-outbreak COT populations within each archipelago indicates that outbreaks are a local phenomenon.

“Our recommendation to managers is to seriously consider the role that environmental conditions and local nutrient inputs play in driving COT outbreaks, Toonen said.”

The full paper will be available free online on February 17, 2012, at 5 PM:
http://dx.plos.org/10.1371/journal.pone.0031159

NOTES: from Dr. Rob Toonen (pers. comm. to CORAL):

Eating habits of A. planci: “In the couple of studies I have seen, the adults prey preferentially on specific corals but it is all corals that are observed being eaten in the field.  For example, a study at Sulawesi found that A. planci consumed a total of 70 different species of corals, but that massive species (particularly of Faviidae) were more frequently consumed than would be expected based on their abundance in the population. In my experience, though, echinoderms in general will eat damn near anything when they are starving, so I wouldn’t be surprised if they became opportunistic omnivores when there is no coral left to eat… “

Dr. Charles Birkeland: “Chuck is a great colleague and collaborator of mine, so I am more than happy to acknowledge him for the original idea. We cite his prior work in Guam in the article itself (ref 13 in our manuscript):

“Birkeland [13] correlated outbreak prevalence among high islands across the central and western Pacific with heavy rainfall and typhoon induced terrestrial runoff.  He hypothesized that the heightened nutrients in the water column from these large-scale storm events triggered phytoplankton blooms that independently increased A. planci larval survivorship, settlement, and A. planci densities around high islands. This ‘terrestrial run-off hypothesis’ was further supported by the rare occurrence of documented outbreaks on nearby nutrient poor atoll and low island systems.

“Similarly, Fabricius et al. [12] argued that the onset of outbreaks on the GBR is predominantly controlled by phytoplankton availability, which is governed by flooding rivers and elevated nutrient inputs. Our findings support that hypothesis; with the exception of Kingman Reef, outbreak locations in this study were found at high islands and of the high islands, the outbreaks were generally in the vicinity of rivers and watersheds (with the exception of Mo‘orea and Asuncion). If higher nutrient loads do drive outbreaks [as suggested by 11-13, 20, 21], then mitigating land-based sources of nutrients would be a far more effective management strategy than physically eradicating this corallivore, with the hope of precluding outbreak propagation in distant archipelagos.”