The withering syndrome bacterium Candidatus Xenohaliotis californiensis was believed to be confined to warmer ocean waters south of San Francisco. A survey of abalone beds, conducted by fish pathologist Dr. Carolyn Friedman, however, has revealed that the bacterium has spread to two isolated locations in colder northern waters. Her work suggests that human activity—aquaculture practices or abalone “outplantings”—may have contributed to the spread of the bacterium.

Hypothesis: Quantitative real-time PCR can be used to quantify loads of the WS rickettsial bacterium (infection intensity) in abalone.

Hypothesis: Juvenile black abalone recruiting on the California Channel Islands are more resistant to WS than are black abalone in northern Central California that have not experienced high disease (WS) selection pressure.

NOTE: only abstract of study available at this time pending publication of papers. For further information, please contact Carolyn S. Friedman (carolynf@u.washington.edu) or Glenn VanBlaricom (glennvb@u.washington.edu ).

The focus is on research conducted and the progress made toward the achievement of all specific aims outlined in the original proposal. Three abstracts describing aspects of our work in oysters were presented at national and international meetings. Specific Aim: Test methods of introducing pantropic vectors into C. virginica embryos to create transgenic oysters

Withering syndrome (WS) is a disease of wild and cultured abalone, caused by aRickettsiales-like prokaryote (WS-RLP). While WS has decimated black abalone populationsthroughout most of California, both wild and cultured red abalone have shown resilience incertain environmental conditions. The changes in seawater temperature and food availabilityassociated with El Niño events may, however, stimulate the pathogenesis of WS in WS-RLP-infected red abalone. This study sought to examine the relative contributions and synergisticeffects of multiple stressors on development of WS, and establish sensitive and robust markersfor characterizing the sequential pathological changes associated with disease progression. This information is critical for the proper management of WS by both private aquaculturists and stateresource managers.

Sea Grant research has led to the development of a cure for an abalone wasting disease that destroyed about $1.5-million worth of farmed abalone product at two California farms during the1997–98 El Niño. The antibiotic therapy is now being used to help in the restoration of endangered wild white abalone on the U.S. West Coast.

Withering syndrome is a chronic, often fatal disease of multiple species of California abalone. It was first observed in the mid-1980s at the Channel Islands off Southern California and has since spread along the main coastline as far north as the San Francisco bay area. Recent research has demonstrated that the causative agent is a Rickettsiales-like prokaryote (WS-RLP, Friedman et al. 2000), and that WS expression is much more rapid and severe at elevated water temperatures (Moore et al. 2000). Aside from impacts on wild populations, WS has resulted in substantial losses in red abalone farms. As a result of these losses and our observation that the WS-RLP is sensitive to tetracyclines, we developed and oral administration of oxytetracycline in conjunction with researchers at The Abalone Farm, Inc.

The white abalone , Haliotis sorenseni, supported valuable commercial fisheries only 30 years ago. In 2002, this species became the first marine invertebrate in the United States to achieve federal endangered species status. The overall goal of this project was to collect life history, genetic and disease susceptibility data that to support recovery.

Withering syndrome (WS) is a catastrophic disease of both wild and cultured abalone caused by “Candidatus Xenohaliotis californiensis”, a Rickettsia-like procaryote (WS-RLP). Losses from this disease have severely hampered the abalone aquaculture industry and abalone restoration efforts in California. Oxytetracycline (OTC) was recently demonstrated to be an effective therapeutant for WS-RLP infections and associated losses due to WS. In addition, a long duration of protection (approximately one year) was noted anecdotally. Part one of this study examined the efficacy and pharmacokinetics of OTC treatment in red abalone, Haliotis rufescens, held at 13.4oC. Medication was administered orally in an artificial diet containing 1.85% active OTC at a rate of 103.4 mg/kg abalone for 10, 20 and 30 days. Control abalone were fed the same diet lacking OTC. Significant differences in prevalence and intensity of infection in both the post-esophagus and digestive gland were observed. Although the digestive gland from abalone medicated for 10 days and foot muscle from those medicated for 30 days was best described with a two-compartment model, pharmacokinetic trends were adequately described by a one-compartment model. Significant differences in OTC accumulation and depletion were observed among treatments. Animals medicated for 10 days accumulated significantly less than those medicated for 20 or 30 days. Despite this, terminal elimination rate constants were similar. Significantly less OTC was present in foot muscle samples relative to corresponding digestive gland samples. Estimated half-life values were similar among treatments for both foot muscle (10.7-13.4 d) and digestive gland (23.8-27.5 d) samples.

Once harvested commercially, the white abalone (Haliotis sorenseni) is in danger of extinction and since 2002 has been under the protection of the federal Endangered Species Act. Recent failed efforts to find remnant populations in the species’ historical deep-seafloor habitats underscore the animal’s scarcity. In the time between when the grant for the project was written and funded, NOAA Fisheries halted the collection of wild white abalone for research. It now appears that species recovery is either going to happen on its own over the course of several or more decades, or captive-bred white abalone will have to be outplanted in the wild. Outplanting is not without its own set of risks, as it may erode genetic diversity or introduce the withering syndrome pathogen into previously uninfected deep-water refuges. Just as worrisome is the potential to unknowingly introduce previously unknown pathogens.