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A natural Vibrio parahaemolyticus ΔpirAVp pirBVp+ mutant kills shrimp but produces neither PirVp toxins nor acute hepatopancreatic necrosis disease lesions
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Metadata
Document Title
A natural Vibrio parahaemolyticus ΔpirAVp pirBVp+ mutant kills shrimp but produces neither PirVp toxins nor acute hepatopancreatic necrosis disease lesions
Author
Phiwsaiya K.,Charoensapsri W.,Taengphu S.,Dong H.T.,Sangsuriya P.,Nguyen G.T.T.,Pham H.Q.,Amparyup P.,Sritunyalucksana K.,Taengchaiyaphum S.,Chaivisuthangkura P.,Longyant S.,Sithigorngul P.,Senapin S.
Name from Authors Collection
Affiliations
National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, Thailand; Center of Excellence for Shrimp Molecular Biology and Biotechnology (Centex Shrimp), Faculty of Science, Mahidol University, Bangkok, Thailand; Department Microbiology, Faculty of Science, King Mongkut's University of Technology Thonburi (KMUTT), Bangkok, Thailand; Aquatic Molecular Genetics and Biotechnology Laboratory, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, Thailand; Institute of Aquaculture, Nha Trang University, Nha Trang, Viet Nam; Shrimp-Virus Interaction Laboratory, National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, Thailand; Department of Biology, Faculty of Science, Srinakharinwirot University, Bangkok, Thailand
Type
Article
Source Title
Applied and Environmental Microbiology
ISSN
00992240
Year
2017
Volume
83
Issue
16
Open Access
All Open Access, Hybrid Gold, Green
Publisher
American Society for Microbiology
DOI
10.1128/AEM.00680-17
Abstract
Acute hepatopancreatic necrosis disease (AHPND) of shrimp is caused by Vibrio parahaemolyticus isolates (VPAHPND isolates) that harbor a pVA plasmid encoding toxins PirAVp and PirBVp. These are released from VPAHPND isolates that colonize the shrimp stomach and produce pathognomonic AHPND lesions (massive sloughing of hepatopancreatic tubule epithelial cells). PCR results indicated that V. parahaemolyticus isolate XN87 lacked pirAVp but carried pirBVp. Unexpectedly, Western blot analysis of proteins from the culture broth of XN87 revealed the absence of both toxins, and the lack of PirBVp was further confirmed by enzyme-linked immunosorbent assay. However, shrimp immersion challenge with XN87 resulted in 47% mortality without AHPND lesions. Instead, lesions consisted of collapsed hepatopancreatic tubule epithelia. In contrast, control shrimp challenged with typical VPAHPND isolate 5HP gave 90% mortality, accompanied by AHPND lesions. Sequence analysis revealed that the pVA plasmid of XN87 contained a mutated pirAVp gene interrupted by the out-of-frame insertion of a transposon gene fragment. The upstream region and the beginning of the original pirAVp gene remained intact, but the insertion caused a 2-base reading frameshift in the remainder of the pirAVp gene sequence and in the downstream pirBVp gene sequence. Reverse transcription-PCR and sequencing of 5HP revealed a bicistronic pirABVp mRNA transcript that was not produced by XN87, explaining the absence of both toxins in its culture broth. However, the virulence of XN87 revealed that some V. parahaemolyticus isolates carrying mutant pVA plasmids that produce no PirVp toxins can cause mortality in shrimp in ponds experiencing an outbreak of early mortality syndrome (EMS) but may not have been previously recognized to be AHPND related because they did not cause pathognomonic AHPND lesions. © 2017 American Society for Microbiology.
Keyword
AHPND | EMS | Penaeus vannamei | Pir toxin | Shrimp | Vibrio parahaemolyticus
Industrial Classification
Knowledge Taxonomy Level 1
Knowledge Taxonomy Level 2
Knowledge Taxonomy Level 3
Funding Sponsor
Mahidol University
License
CC BY
Rights
Author
Publication Source
Scopus