Significance Sea stars inhabiting the Northeast Pacific Coast have recently experienced an extensive outbreak of wasting disease, leading to their degradation and disappearance from many coastal areas. In this paper, we present evidence that the cause of the disease is transmissible from disease-affected animals to apparently healthy individuals, that the disease-causing agent is a virus-sized microorganism, and that the best candidate viral taxon, the sea star-associated densovirus (SSaDV), is in greater abundance in diseased than in healthy sea stars.

Lead poisoning is a primary factor impeding the survival and recovery of the critically endangered California Condor (Gymnogyps californianus). However, the frequency and magnitude of lead exposure in condors is not well-known in part because most blood lead monitoring occurs biannually, and biannual blood samples capture only ∼10% of a bird’s annual exposure history. We investigated the use of growing feathers from free-flying condors in California to establish a bird’s lead exposure history. We show that lead concentration and stable lead isotopic composition analyses of sequential feather sections and concurrently collected blood samples provided a comprehensive history of lead exposure over the 2−4 month period of feather growth. Feather analyses identified exposure events not evident from blood monitoring efforts, and by fitting an empirically derived timeline to actively growing feathers, we were able to estimate the time frame for specific lead exposure events. Our results demonstrate the utility of using sequentially sampled feathers to reconstruct lead exposure history. Since exposure risk in individuals is one determinant of population health, our findings should increase the understanding of population-level effects from lead poisoning in condors; this information may also be helpful for other avian species potentially impacted by lead poisoning.

Throughout the world, populations of scavenger birds are declining rapidly with some populations already on the brink of extinction. Much of the current research into the factors contributing to these declines has focused on exposure to drug residues, lead, and other toxins. Despite increased monitoring of these declining populations, little is known about infectious diseases affecting scavenger bird species. To assess potential infectious disease risks to both obligate and facultative scavenger bird species, we performed a serosurvey for eleven potential pathogens in three species of scavenging birds in California: the California condor (Gymnogyps californianus), turkey vulture (Cathartes aura) and golden eagle (Aquila chrysaetos). California condors were seropositive for avian adenovirus, infectious bronchitis virus, Mycoplasma gallisepticum, avian paramyxovirus-2, West Nile virus (WNV) and Toxoplasma gondii. Golden eagles were seropositive for avian adenovirus, Chlamydophila psittaci and Toxoplasma gondii, and turkey vultures were seropositive for avian adenovirus, Chlamydophila psittaci, avian paramyxovirus-1, Toxoplasma gondii and WNV. Risk factor analyses indicated that rearing site and original release location were significantly associated with a positive serologic titer to WNV among free-flying condors. This study provides preliminary baseline data on infectious disease exposure in these populations for aiding in early disease detection and provides potentially critical information for conservation of the endangered California condor as it continues to expand its range and encounter new infectious disease threats.

A mixed group of 441 marine invertebrates was collected in Southern California. After a large mortality event, numerous water quality parameters were evaluated. Copper was present at 33 μg/L, which is below the documented toxic level. No other toxins were identified. To investigate whether copper was the etiology for the mass mortality, purple sea urchins, Strongylocentrotus purpuratus , were used as sentinel species, as they were the most severely affected during the mortality event. Purple sea urchins were placed in multiple test systems of varying copper concentrations and died in periods of time proportionate to copper concentrations. Clinical signs, disease progression, and pathologic lesions were similar between test systems and the original mortality event. Copper caused disease and death in purple sea urchins at concentrations from 15 to 50 μg/L. The source of the copper toxicity was identified as sand filters contaminated by brass pump components.