Moore Et Al.: Withering Syndrome and Restoration of Southern California Abalone Populations

Withering syndrome is a chronic wasting disease of California abalone (Haliotis spp.) first observed in the Channel Islands in the mid-1980s. This fatal disease played a significant role in the demise of southern California black abalone and may also be contributing to the lack of recovery of other species following their severe depletion by overfishing. The causative agent of withering syndrome is an intracellular Rickettsiales-like prokaryote that infects gastrointestinal epithelia. The entire southern California region is considered endemic for this pathogen, and therefore all abalone restoration plans for this area need to consider the implications of its presence. Here we review the current state of knowledge regarding withering syndrome and discuss its potential impact on species recovery programs. INTRODUCTION Before the arrival of Europeans, large abalone in southern California were preyed upon primarily by aboriginal peoples and sea otters. During the 1800s the aboriginal peoples were relocated from the Channel Islands and the sea otters were hunted to local extinction. This resulted in higher local population densities of black abalone (Haliotis cracherodii) and probably other species than previously experienced in recent history (Davis et al. 1992). Throughout the midto late-1900s various abalone species were serially depleted by commercial harvesting (Karpov et al. 2000). Withering syndrome first appeared in the mid-1980s at the Channel Islands in high-density populations of black abalone. Here we review the current state of knowledge regarding withering syndrome and the implications of this disease for abalone recovery programs. WITHERING SYNDROME In the mid-1980s large numbers of dying black abalone with severe pedal atrophy and the empty shells of recently deceased black abalone were observed in populations along the central Channel Islands. The term withering syndrome (WS) was coined to describe the phenomenon (Haaker et al. 1992). The disease spread throughout the Channel Islands (Lafferty and Kuris 1993; VanBlaricom et al. 1993) and to the mainland (Steinbeck et al. 1992; Alstatt et al. 1996) throughout the early 1990s. Although overfishing had already greatly reduced many black abalone populations in southern California, WS nearly eliminated the remaining populations throughout the Channel Islands and off central California (Haaker et al. 1992; Richards and Davis 1993; Alstatt et al. 1996). Overfishing was responsible for population declines of pink (H. corrugata), green (H. fulgens), and red abalone (H. rufescens) in southern California prior to the appearance of WS (Karpov et al. 2000). WS signs have been observed in all three species (Pete Haaker, pers. comm.), and the impact of WS on the natural recovery of their populations remains unclear. Overfishing had also depleted populations of white abalone (H. sorenseni) before the appearance of WS (Davis et al. 1998). In 2001 this species became the first marine invertebrate to be listed under the federal Endangered Species Act (Federal Register 66 (103), 29046-29055, 29 May 2001). Although two shrunken white abalone were collected from Santa Catalina Island in 1993 (cited in Hobday et al. 2001), and 20 freshly dead, undamaged shells were collected from Farnsworth Bank in 1990 (Tegner et al. 1996), shrunken animals can occur for reasons other than WS. Further studies are needed to determine the susceptibility of white abalone to WS. During the 1997–98 El Niño, red abalone farms from Mexico to central California experienced high mortality rates, and animals showed signs of WS (Moore et al. 2000). Contribution no. 2173 from the Bodega Marine Laboratory, University of California at Davis.