Taura syndrome of marine penaeid shrimp: Discovery of the viral agent and disease characterization studies

Persistent Link:
http://hdl.handle.net/10150/282661
Title:
Taura syndrome of marine penaeid shrimp: Discovery of the viral agent and disease characterization studies
Author:
Hasson, Kenneth Wolf, 1956-
Issue Date:
1998
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
These studies were begun during the summer of 1994, W2 years after the recognition of Taura Syndrome (TS), a lethal disease of farm-raised Penaeus vannamei in Ecuador of then unknown etiology. Utilizing specific pathogen free (SPF) P. vannamei test shrimp, the combined results of four initial TS bioassays suggested that the disease had an infectious instead of a toxic etiology as originally reported. The hypothesis that TS was virus-caused prompted the application of a shrimp parvovirus (IHHNV) purification protocol, which resulted in the discovery of Taura Syndrome virus (TSV), a previously unrecognized virus that was isolated from TS diseased shrimp tissues. Three serial infectivity studies were performed in which purified cell-free extracts of TSV were injected into SPF P. vannamei test shrimp and the criteria of Rivers' postulates were fulfilled, establishing that TS has a viral etiology. In situ hybridization assays for the detection of TSV resulted in frequent false negative gene probe results. This problem was due to fixative-induced acid hydrolysis of the TSV RNA genome resulting from tissue fixation with Davidson's solution (pH 3.5-4). Development and use of a neutral fixative, R-F (RNA-Friendly) fixative, was shown to prevent this problem. The pathogenesis of TSV lesions was analyzed in experimentally infected, time course sampled SPF P. vannamei. The TSV disease cycle was found to consist of three clinically and histologically distinct overlapping phases; an W7 d acute phase, an W5 d transition phase and a long term cyclic chronic phase of at least 8 months duration. TSV susceptibility studies of two endemic North American (P. setiferus and P. aztecus) and one Asian penaeid species (P. chinensis) showed that P. aztecus and P. chinensis juveniles were susceptible, whereas, P. setiferus appeared refractory to TSV infection. The geographic range of TSV within the Americas was documented based on gene probe and histological findings of archived P. vannamei samples dating from 1992 to 1996. TSV was detectable within P. vannamei submitted from Ecuador when the disease was first recognized (1992) and has since spread into 12 other countries. The causes and effects of the international controversy of a viral versus a toxic etiology for TS are discussed and a solution offered to prevent similar disputes in the future.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Agriculture, Animal Pathology.; Agriculture, Fisheries and Aquaculture.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Veterinary Science and Microbiology
Degree Grantor:
University of Arizona
Advisor:
Lightner, Donald V.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleTaura syndrome of marine penaeid shrimp: Discovery of the viral agent and disease characterization studiesen_US
dc.creatorHasson, Kenneth Wolf, 1956-en_US
dc.contributor.authorHasson, Kenneth Wolf, 1956-en_US
dc.date.issued1998en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractThese studies were begun during the summer of 1994, W2 years after the recognition of Taura Syndrome (TS), a lethal disease of farm-raised Penaeus vannamei in Ecuador of then unknown etiology. Utilizing specific pathogen free (SPF) P. vannamei test shrimp, the combined results of four initial TS bioassays suggested that the disease had an infectious instead of a toxic etiology as originally reported. The hypothesis that TS was virus-caused prompted the application of a shrimp parvovirus (IHHNV) purification protocol, which resulted in the discovery of Taura Syndrome virus (TSV), a previously unrecognized virus that was isolated from TS diseased shrimp tissues. Three serial infectivity studies were performed in which purified cell-free extracts of TSV were injected into SPF P. vannamei test shrimp and the criteria of Rivers' postulates were fulfilled, establishing that TS has a viral etiology. In situ hybridization assays for the detection of TSV resulted in frequent false negative gene probe results. This problem was due to fixative-induced acid hydrolysis of the TSV RNA genome resulting from tissue fixation with Davidson's solution (pH 3.5-4). Development and use of a neutral fixative, R-F (RNA-Friendly) fixative, was shown to prevent this problem. The pathogenesis of TSV lesions was analyzed in experimentally infected, time course sampled SPF P. vannamei. The TSV disease cycle was found to consist of three clinically and histologically distinct overlapping phases; an W7 d acute phase, an W5 d transition phase and a long term cyclic chronic phase of at least 8 months duration. TSV susceptibility studies of two endemic North American (P. setiferus and P. aztecus) and one Asian penaeid species (P. chinensis) showed that P. aztecus and P. chinensis juveniles were susceptible, whereas, P. setiferus appeared refractory to TSV infection. The geographic range of TSV within the Americas was documented based on gene probe and histological findings of archived P. vannamei samples dating from 1992 to 1996. TSV was detectable within P. vannamei submitted from Ecuador when the disease was first recognized (1992) and has since spread into 12 other countries. The causes and effects of the international controversy of a viral versus a toxic etiology for TS are discussed and a solution offered to prevent similar disputes in the future.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectAgriculture, Animal Pathology.en_US
dc.subjectAgriculture, Fisheries and Aquaculture.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineVeterinary Science and Microbiologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorLightner, Donald V.en_US
dc.identifier.proquest9831832en_US
dc.identifier.bibrecord.b38635707en_US
All Items in UA Campus Repository are protected by copyright, with all rights reserved, unless otherwise indicated.