Abstract

Withering syndrome (WS) is a chronic wasting disease responsible for mass mortality in wild populations of black abalone Haliotis cracherodii. The etiology of WS is uncertain with limited evidence for the role of a gastrointestinal Rickettsiales-like prokaryote (RLP). We documented for the first time the occurrence of animals with clinical signs of WS and associated morphological changes in another haliotid species, the red abalone H. rufescens. In this study, 60 juvenile red abalone (8 cm) were randomly selected from a farmed population raised at 14 degree C that was known to have low-intensity RLP infections but lacked clinical signs of WS. The abalone were held in triplicate containers receiving water of approximately 14.7 degree C (Control, Co) or 18.5 degree C (elevated temperature, ET) and were fed equally for 220 d. Survival was 100% (30/30) for the Co group and 67% (20/30) for the ET group. The ET group animals had higher RLP infection intensities and showed more clinical signs (mantle retraction, lower weight gain, lower condition index) and morphological changes (digestive gland degeneration) associated with WS. In trials conducted immediately before termination of the experiment, ET group animals fed at half the rate of Co group animals. Among ET group animals, the intensity of RLP infections in the posterior portion of the esophagus was positively correlated with WS clinical signs and morphological changes, whereas no correlations were present among Co group animals. During 1997-1998 and in conjunction with elevated seawater temperatures associated with El Nino, several abalone farms in California experienced a dramatic increase in the proportion of red abalone showing signs of WS. Examination of 66 red abalone from five commercial farms revealed that animals with more advanced RLP infections had more severe WS clinical signs and associated morphological changes. Collectively, these data demonstrate that RLP infection plays a key role in the etiology of WS in red abalone and that warm water enhances the severity of the pathogenic effects of RLP infection.