Transmission of the Rickettsiales-like prokaryote "Candidatus Xenohaliotis californiensis" and its role in withering syndrome of California abalone, Haliotis spp.

James D. Moore, Thea T. Robbins, Ronald Hedrick, Carolyn S. Friedman

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Withering syndrome (WS) is a chronic, wasting disease responsible for mass mortality in southern California populations of black abalone Haliotis cracherodii and responsible for significant losses of cultured red abalone H. rufescens. Ongoing studies in our laboratory indicate that a recently described gastrointestinal Rickettsiales-like prokaryote, "Candidatus Xenohaliotis californiensis" (RLP) is the etiologic agent of WS. Here we describe attempts to experimentally transmit the RLP and demonstrate its role in WS. In two preliminary experiments, RLP-infected black abalone postesophagus homogenate (IPEH) was injected into the foot or orally administered to RLP-free black abalone. No RLPs were detected 8 wk after pedal injection. Low rates of transmission were observed 8 to 12 wk after oral inoculation, although an RLP-positive animal was also detected in a negative control group inoculated with filtered seawater. In a separate, 16-wk study, RLP infections were detected in red abalone that received effluent from a tank of infected red abalone while control animals that received direct-source seawater remained RLP-free. A fourth, long-term study delivered IPEH or seawater to RLP-free red abalone with either bath exposure or intra-digestive gland injection. An additional treatment to test a potential viral etiology for WS consisted of intra-digestive gland injection with a 0.1-0.2 μm filtrate of IPEH and subsequent treatment with antibiotics. Each treatment was administered six times over a 16-wk period. Cohabiting RLP-infected black abalone with RLP-free red abalone provided a positive control treatment. At wk 63 post-initiation, untreated, saline injected and IPEH filtrate injected groups had low cumulative mortality (0-20%), while mortality in the IPEH bath, IPEH injection and cohabitation treatment groups was 70-90%. There were statistically significant relationships between experimental treatment, RLP burdens and signs of WS. Low-level RLP infections of uncertain origin were observed in one each of the duplicate tanks of the negative control and the IPEH filtrate-injected animals. An absence of WS signs in recipients of the IPEH filtrate provides strong evidence that the agent of WS is non-viral. Collectively these studies provide solid evidence that the RLP is the etiologic agent of WS.

Original languageEnglish (US)
Pages (from-to)867-874
Number of pages8
JournalJournal of Shellfish Research
Volume20
Issue number2
StatePublished - Dec 1 2001

Fingerprint

Haliotis cracherodii
Rickettsiales
Haliotis
prokaryote
abalone
prokaryotic cells
Haliotis rufescens
seawater
animal
chronic wasting disease
cohabitation
mortality
mass mortality
etiology
filtrates
antibiotics
inoculation
effluent
injection
experiment

Keywords

  • Abalone
  • Cracherodii
  • Haliotis rufescens
  • Rickettsiales
  • Transmission
  • Withering syndrome

ASJC Scopus subject areas

  • Aquatic Science

Cite this

Transmission of the Rickettsiales-like prokaryote "Candidatus Xenohaliotis californiensis" and its role in withering syndrome of California abalone, Haliotis spp. / Moore, James D.; Robbins, Thea T.; Hedrick, Ronald; Friedman, Carolyn S.

In: Journal of Shellfish Research, Vol. 20, No. 2, 01.12.2001, p. 867-874.

Research output: Contribution to journalArticle

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abstract = "Withering syndrome (WS) is a chronic, wasting disease responsible for mass mortality in southern California populations of black abalone Haliotis cracherodii and responsible for significant losses of cultured red abalone H. rufescens. Ongoing studies in our laboratory indicate that a recently described gastrointestinal Rickettsiales-like prokaryote, {"}Candidatus Xenohaliotis californiensis{"} (RLP) is the etiologic agent of WS. Here we describe attempts to experimentally transmit the RLP and demonstrate its role in WS. In two preliminary experiments, RLP-infected black abalone postesophagus homogenate (IPEH) was injected into the foot or orally administered to RLP-free black abalone. No RLPs were detected 8 wk after pedal injection. Low rates of transmission were observed 8 to 12 wk after oral inoculation, although an RLP-positive animal was also detected in a negative control group inoculated with filtered seawater. In a separate, 16-wk study, RLP infections were detected in red abalone that received effluent from a tank of infected red abalone while control animals that received direct-source seawater remained RLP-free. A fourth, long-term study delivered IPEH or seawater to RLP-free red abalone with either bath exposure or intra-digestive gland injection. An additional treatment to test a potential viral etiology for WS consisted of intra-digestive gland injection with a 0.1-0.2 μm filtrate of IPEH and subsequent treatment with antibiotics. Each treatment was administered six times over a 16-wk period. Cohabiting RLP-infected black abalone with RLP-free red abalone provided a positive control treatment. At wk 63 post-initiation, untreated, saline injected and IPEH filtrate injected groups had low cumulative mortality (0-20{\%}), while mortality in the IPEH bath, IPEH injection and cohabitation treatment groups was 70-90{\%}. There were statistically significant relationships between experimental treatment, RLP burdens and signs of WS. Low-level RLP infections of uncertain origin were observed in one each of the duplicate tanks of the negative control and the IPEH filtrate-injected animals. An absence of WS signs in recipients of the IPEH filtrate provides strong evidence that the agent of WS is non-viral. Collectively these studies provide solid evidence that the RLP is the etiologic agent of WS.",
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