Publication: A natural Vibrio parahaemolyticus ΔpirAVp pirBVp+ mutant kills shrimp but produces neither PirVp toxins nor acute hepatopancreatic necrosis disease lesions
0
0
Issued Date
2017
Resource Type
File Type
application/pdf
ISSN
992240
Other identifier(s)
2-s2.0-85026555961
Rights Holder(s)
Scopus
Bibliographic Citation
Applied and Environmental Microbiology. Vol 83, No.16 (2017), p.-
Suggested Citation
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. A natural Vibrio parahaemolyticus ΔpirAVp pirBVp+ mutant kills shrimp but produces neither PirVp toxins nor acute hepatopancreatic necrosis disease lesions. Applied and Environmental Microbiology. Vol 83, No.16 (2017), p.-. doi:10.1128/AEM.00680-17 Retrieved from: https://hdl.handle.net/20.500.14740/4115
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.
Subject(s)
DNA
Electrophoresis
Metabolites
Shellfish
Toxic materials
Transcription
AHPND
Penaeus vannamei
Pir toxin
Shrimp
Vibrio parahaemolyticus
Genes
Bacterial disease
Bacterium
Cells and cell components
Crustacean
Disease incidence
Gene
Gene expression
Genetic analysis
Mortality
Plasmid
Protein
RNA
Stomach content
Toxin
Virulence
Decapoda (Crustacea)
Litopenaeus vannamei
Vibrio parahaemolyticus
Electrophoresis
Metabolites
Shellfish
Toxic materials
Transcription
AHPND
Penaeus vannamei
Pir toxin
Shrimp
Vibrio parahaemolyticus
Genes
Bacterial disease
Bacterium
Cells and cell components
Crustacean
Disease incidence
Gene
Gene expression
Genetic analysis
Mortality
Plasmid
Protein
RNA
Stomach content
Toxin
Virulence
Decapoda (Crustacea)
Litopenaeus vannamei
Vibrio parahaemolyticus