Black abalone, Haliotis cracherodii, populations along the NE Pacific ocean have declined due to the rickettsial disease withering syndrome (WS). Natural recovery on San Nicolas Island (SNI) of Southern California suggested the development of resistance in island populations. Experimental challenges in one treatment demonstrated that progeny of disease-selected black abalone from SNI survived better than did those from naïve black abalone from Carmel Point in mainland coastal central California. Unexpectedly, the presence of a newly observed bacteriophage infecting the WS rickettsia (WS-RLO) had strong effects on the survival of infected abalone. Specifically, presence of phage-infected RLO (RLOv) reduced the host response to infection, RLO infection loads, and associated mortality. These data suggest that the black abalone: WS-RLO relationship is evolving through dual host mechanisms of resistance to RLO infection in the digestive gland via tolerance to infection in the primary target tissue (the post-esophagus) coupled with reduced pathogenicity of the WS-RLO by phage infection, which effectively reduces the infection load in the primary target tissue by half. Sea surface temperature patterns off southern California, associated with a recent hiatus in global-scale ocean warming, do not appear to be a sufficient explanation for survival patterns in SNI black abalone. These data highlight the potential for natural recovery of abalone populations over time and that further understanding of mechanisms governing host–parasite relationships will better enable us to manage declining populations.

Abalone aquaculture is a small but growing industry in Thailand and is based on both the exotic Haliotis diversicolor supertexta and the native H. asinina. Withering syndrome (WS) in abalone is caused by an infection with the Rickettsia-like organism (RLO) 'Candidatus Xenohaliotis californiensis' and has been spread to many countries globally. The present study reports the first observation of the WS-RLO agent in the small abalone, H. diversicolor supertexta in Thailand, Taiwan (ROC) and the People's Republic of China (PRC). Under light microscopy, the RLO was observed as intracytoplasmic inclusions within epithelial cells lining the post-esophagus and, to a minor extent, the intestine of H. diversicolor. Under transmission electron microscopy, inclusions were characterized as colonies of rod-shaped bacteria, 200 × 1800 nm in size, within a vesicle in the cytoplasm of the infected cell. The RLO from the small abalone bound with WS-RLO-specific in situ hybridization probes and was amplified by polymerase chain reaction (PCR), using primers designed from the 16S rDNA sequence of the original WS-RLO from California, USA. The PCR product of RLO samples from both the PRC and Thailand showed extremely high identity with the California WS-RLO (100 and 99%, respectively). These data combined with the history of abalone movements for aquaculture purposes indicate that RLOs observed in Thailand, Taiwan and the PRC are the WS-RLO that originated from California.KEY WORDS: Haliotis diversicolor · 'Candidatus Xenohaliotis californiensis' · 16S rDNA · Abalone · Withering syndrome · Thailand · Taiwan · People's Republic of China · California Resale or republication not permitted without written consent of the publisherDis Aquat Org 90: [69][70][71][72][73][74][75][76] 2010 rickettsial agent of withering syndrome (WS) are present in abalone under culture. Prior to the present study, the infection of Asian abalone species by Rickettsia-like organisms (RLOs) had not been observed or described; however, such knowledge is needed for the successful development and expansion of abalone aquaculture in Asia.WS is a catastrophic disease, caused by the intracellular RLO 'Candidatus Xenohaliotis californiensis . WS affects a variety of abalone species and was first observed in populations of wild black abalone Haliotis cracherodii in the mid-1980s (Haaker et al. 1992). Affected black abalone had an atrophied foot muscle and high mortality rates, especially in populations off southern California, USA (Haaker et al. 1992). The disease progressively spread throughout southern and central California (Haaker et al. 1992, Altstatt et al. 1996, Friedman & Finley 2003, Miner et al. 2006. By 1992, WS was associated with population declines on 6 of the 8 Channel Islands, with losses of up to 99% of H. cracherodii (VanBlaricom et al. 1993, Tissot 1995. These losses led, in part, to an initial closure of the California black abalone fishery in 1993, followed by total closure in 1997 (Haaker et al. 2001). Losses due to WS vary among host ...

No abstract