Coral reefs are in a tight spot these days. Increasing CO2 levels and rising ocean temperatures aren’t doing them much good, but their biggest problems are more direct. Overfishing is wiping out important predators, the aquarium trade picks off whatever looks pretty, agricultural and other runoff is clogging the filter-feeders, and some folks are even blowing them apart with dynamite.
Places with strict environmental regulations and protected marine preserves are generally doing a better job protecting their reefs, but even there we may be doing damage without realizing it. For example, what if coral reefs are catching human diseases?
That seems to be exactly what’s happening in Caribbean elkhorn coral (Acropora palmata), an iconic and structurally crucial reef species that’s been dying from a mysterious condition called white pox, or acropora serratiosis. The disease has been so deadly that the US EPA declared A. palmata an endangered species in 2006. Now, scientists have fingered human sewage as the source of the pathogen causing white pox.
Researchers at Rollins College and the University of Georgia described the finding yesterday in PLoS ONE:
Here we hypothesize that [Serratia marcescens] strain PDR60 isolated from two distinct environments, one terrestrial (human wastewater) and one marine (APS-affected A. palmata, apparently healthy Siderastrea siderea and Coralliophila abbreviata) causes APS [acroporid serratiosis] in A. palmata. To examine this hypothesis we conducted challenge experiments by inoculating eight isolates of Serratia marcescens representing three strains onto A. palmata fragments maintained in closed seawater aquaria. Our results confirm strain PDR60 as a coral pathogen through fulfillment of Koch’s postulates. These results are also consistent with the hypothesis that non-host corals and predatory snails may function as interepizootic reservoirs or vectors of the APS pathogen. Furthermore, we show that S. marcescens isolated from human wastewater causes APS in as little as four days, unequivocally verifying humans as a source of a marine invertebrate disease.
S. marcescens is a ubiquitous gram-negative bacterium. It’s in dirt, sewage, and probably your shower. If you haven’t noticed it, it’s because you have a working immune system. People who aren’t so fortunate – especially in hospitals – can get serious opportunistic S. marcescens infections. When this bug first turned up as a possible culprit in white pox, I figured it was probably an opportunist in the elkhorn corals as well. Perhaps the coral somehow got the anthozoan equivalent of a suppressed immune system, and Serratia took advantage of the situation.
The new work suggests otherwise, though I’m not sure it quite seals the case. The investigators experimentally infected elkhorn corals growing in tanks of purified saltwater, and found that a single inoculation with a pure S. marcescens strain cultured from sewage effluent was enough to give the corals a virulent case of white pox. This is called fulfilling Koch’s postulates, and it’s the Holy Grail of epidemiology. We can now say for sure that S. marcescens from human sewage causes white pox.
Or can we? I’m certainly convinced that the bacterial strain in sewage is capable of causing the distinctive pathogenesis of this disease, consisting of bleached white zones that spread across the coral colony. But we need to read the fine print.
The coral colonies these researchers used were harvested from “healthy” wild corals. That’s the only practical way to get experimentally useful amounts of this slow-growing creature. Unlike mice or guinea pigs, we can’t just breed up a bunch of stock from a well-characterized lab strain. However, picking apparently healthy corals from the wild doesn’t prove that they really are healthy. They’re presumably exposed to the same stresses and insults that afflict their white pox-infected neighbors, and could very well be on the brink of contracting the disease themselves. Maybe they’re already infected with the real underlying cause of the disease, and are just one wound or stressor away from getting the S. marcescens component that will finish them off. Because it’s currently impossible to characterize all aspects of the immunological and infectious status of a coral sample, we can’t know whether the bacterium alone is enough to cause disease.
Worse, we can state with certainty that the corals in these experiments were exposed to unusual stress. The scientists chipped off a piece of the colony (traumatic injury), sampled its mucoid coating (open wound), then carried it by boat to a laboratory tank (physiological stress).
That’s not to say I don’t believe the conclusions or the authors’ recommendations. Indeed, the measures they suggest include improved sewage treatment plants throughout the Caribbean, a step that’s clearly a good idea for a long list of reasons, whether or not it will save the elkhorn coral. Humans already get well-documented cases of sewage-borne diseases, and many Caribbean towns use inadequate treatment systems that raise the risk of these infections. That’s why Florida is already in the process of upgrading the treatment plants throughout the Keys. Of course, someone should also take a long, hard look at the waste treatment (or lack thereof) on cruise ships in international waters.
In the meantime, I hope researchers will continue studying white pox, with an eye toward preventing and perhaps treating it. As one of the authors points out in an accompanying press release, the stakes are high, even if the metaphors are a bit mixed:
“These bacteria do not come from the ocean, they come from us,” said Porter. Water-related activities in the Florida Keys generate more than $3 billion a year for Florida and the local economy. “We are killing the goose that lays the golden egg, and we’ve got the smoking gun to prove it,” [University of Georgia Ecology Professor James] Porter said.
1. Sutherland, K., Shaban, S., Joyner, J., Porter, J., & Lipp, E. (2011). Human Pathogen Shown to Cause Disease in the Threatened Eklhorn Coral Acropora palmata PLoS ONE, 6 (8) DOI: 10.1371/journal.pone.0023468