By Janet Raloff
To sea lions, an anchovy represents little more than a bite of dinner. In a strange turn of events, microscopic algae have enabled some anchovies to bite back—albeit posthumously.
A new study establishes for the first time that fish that dine on a particular plantlike floating diatom, an alga, can become a dietary time bomb for mammals higher up the food chain.
Scientists had considered diatoms benign until a 1987 bloom of Pseudo-nitzschia australis off Canada’s Prince Edward Island. Some 140 people who ate mussels that had accumulated these algae from the water fell victim to a strange neurotoxicity. Three died. Many who survived still suffer from an Alzheimer’s-like loss of short-term memory.
Pathologists quickly linked this shellfish poisoning to domoic acid, an amino acid produced by the algae. Pseudo-nitzschia blooms were later tied to several suspicious wildlife events—from marine mammal strandings and deaths to seemingly drunk pelicans falling from the sky. No one, however, proved the alga’s toxin was to blame.
Now in the Jan. 6 Nature, Christopher A. Scholin of the Monterey Bay Aquarium Research Institute in Moss Landing, Calif., and his colleagues offer unambiguous evidence tying the toxic diatom to the deaths of more than 400 sea lions during May and June of 1998.
When the animals’ initial seizures suggested a neurotoxin, Scholin’s team homed in on the sea lions’ diet—anchovies—and found the fish loaded with toxin-producing Pseudo-nitzschia.
Autopsies showed the dead sea lions had brain lesions characteristic of mice and monkeys poisoned by
domoic acid. The final link, Scholin says, was his team’s documentation of the silicon-based skeletons of Pseudo-nitzschia in feces of affected sea lions and domoic acid in the animals’ urine, feces, and serum.
This “is a beautiful sleuthing job,” observes Pat Tester of the U.S. National Ocean Service in Beaufort, N.C. Though many studies pointed to a wildlife threat from Pseudo-nitzschia, she says, this study offers “the smoking gun.”
It’s also disturbing, maintains Paul R. Epstein of Harvard Medical School in Boston, because “it shows that the harmful alga can sneak up on us in a new way.” Many organizations currently screen shellfish to monitor for domoic acid risks to people, he notes. The poisoning of sea lions by apparently healthy fish, he says, suggests that health authorities need to look beyond shellfish.
Scholin agrees, noting that the 1998 Pseudo-nitzschia bloom that led to the sea lion kill reached only 100,000 cells per liter of seawater—one-tenth the density associated with shell-fish risks to people. To detect algae in water before the diatom gets into shellfish, his lab has been working with Saigene Corp. of Bothell, Wash., to test for algal DNA.
When blooms of Pseudo-nitzschia or any of two other classes of harmful algae are present, a test chemical turns blue. An experimental remote-sampling system that relies on this assay is set to undergo tests this summer.
With a coastal network of such sensors deployed on buoys, Scholin says, scientists could scout for potentially dangerous blooms by querying instruments from shore. His goal is to adapt these systems so that, on command, they can assay and report back concentrations of algal toxins rather than of algae.
That’s important, notes JoAnn M. Burkholder of North Carolina State University in Raleigh, because algae—including Pseudo-nitzschia—can be quite variable in their production of toxin.
For reasons that are not well understood, she observes, “they appear to make more toxin at some points in their life cycle. And sometimes they just turn toxin production off.”