Disease-driven mass mortality event leads to widespread extirpation and variable recovery potential of a marine predator across the eastern Pacific.

The prevalence of disease-driven mass mortality events is increasing, but our understanding of spatial variation in their magnitude, timing and triggers are often poorly resolved. Here, we use a novel range-wide dataset comprised 48 810 surveys to quantify how sea star wasting disease affected Pycnopodia helianthoides, the sunflower sea star, across its range from Baja California, Mexico to the Aleutian Islands, USA. We found that the outbreak occurred more rapidly, killed a greater percentage of the population and left fewer survivors in the southern half of the species's range. Pycnopodia now appears to be functionally extinct (greater than 99.2% declines) from Baja California, Mexico to Cape Flattery, Washington, USA and exhibited severe declines (greater than 87.8%) from the Salish Sea to the Gulf of Alaska. The importance of temperature in predicting Pycnopodia distribution rose more than fourfold after the outbreak, suggesting latitudinal variation in outbreak severity may stem from an interaction between disease severity and warmer waters. We found no evidence of population recovery in the years since the outbreak. Natural recovery in the southern half of the range is unlikely over the short term. Thus, assisted recovery will probably be required to restore the functional role of this predator on ecologically relevant time scales.

Interaction of dantrolene with the hepatic mixed function oxidase system.

Dantrolene pretreatment of rats (100 mg/kg/day for five days) causes a fifty percent decrease in hepatic mixed function oxidase (MFO) system activity and a fifty percent decrease in cytochrome P450 content. Recovery of hepatic MFO system activity after discontinuing dantrolene therapy is slow (only sixty-three percent recovery in ten days) and greatly exceeds the half-life of dantrolene in rats (thirty-one minutes). The inactivation of the hepatic MFO system and the slow-recovery of its activity is apparently caused by dantrolene binding and forming a stable complex with hepatic proteins. 14C-dantrolene (1.0 mg/kg) administered i.v. eighteen hours before sacrificing the rats forms a stable complex with hepatic microsomal and soluble proteins. The dantrolene binding to hepatic proteins is decreased by phenobarbital pretreatment and is enhanced by diethylmaleate pretreatment.