Abstract

Cyanobacteria, or "blue-green algae," thrive in warm, nutrient-enriched, anthropogenically degraded watersheds worldwide. Under optimal conditions, these primitive bacteria can form super-blooms with release of potent cyanotoxins into lakes, rivers and estuaries. Over the past 20 to 30 years, an exponential increase in the distribution, severity and duration of these blooms has been noted concurrent with anthropogenic development, increased water impoundment and withdrawal form watersheds, global climate change and nutrient saturation of freshwater lakes, rivers and streams worldwide. Once formed, these environmentally persistent toxins can biomagnify through food webs and spread from their point of origin, killing downstream animals and posing human health risks. One of the most common and concerning cyanotoxins is the potent hepatotoxin, microcystin. Until recently, this toxin was widely considered to be a problem of freshwater systems, affecting primarily domestic livestock, pets, and occasionally, humans. However, increasing evidence points to terrestrial-to-marine flow of these pollutants from impaired watersheds. In 2007, deaths of 12 Southern sea otters, a state and federally protected threatened marine mammal, were linked to microcystin intoxication, and this toxin was identified in several nutrient-impaired watersheds flowing into the Monterey Bay National Marine Sanctuary where these deaths occurred. Lesions in affected animals included icterus, swollen and friable livers, severe hepatocellular cytoplasmic vacuolation, necrosis and apoptosis, and massive hemorrhage, however, a broad range of lesions were also identified in other tissues. At present, 33 stranded Southern sea otters have tested positive for microcystin via liquid chromatography-mass spectrophotometry. Review of all biochemically-confirmed cases to date has revised our understanding of the "typical" case presentation and lesion spectrum, providing information that could help optimize case recognition by clinicians. In addition, clinical treatment appears to be possible for affected animals. Another required step will be mitigation of impaired waterways to protect both human and animal health. At present, no marine sources of microcystin have been identified locally, and strong spatial associations have been identified between microcystin-positive sea otters and numerous contaminated river outflows along the central California coast. Sea otters appear to have been poisoned through contact with microcystin-contaminated freshwater runoff, or via consumption of marine filter-feeders that can bioconcentrate and retain microcystin. Because humans consume many of the same prey items, our preliminary findings raise concern regarding potential unrecognized human health risks. We will review the environmental and demographical patterns for microcystin-positive sea otters, as well as the gross and microscopic lesions associated with microcystin intoxication in this species.

Acknowledgements

This work was performed with support from the California Department of Fish and Wildlife, the California State Water Quality Control Board, the Central Coast Water Quality Control Board and the University of California, Santa Cruz. Sincere thanks go to Dominic Gregorio, Kim Ward, Karen Worcester, Dave Paradies, Abdu Mekebri and Robert Ketley for their outstanding assistance and insight. We acknowledge the Monterey Bay Aquarium, the Marine Mammal Center, USGS-BRD, the United States Fish and Wildlife Service and CDFW for their efforts to recover and care for sick, stranded marine animals in California.

*Presenting author