scholarly journals Effect of Biofloc on the Survival of Whiteleg Shrimp, Penaeus vannamei Boone 1931, When Challenged with a Pathogenic Strain of Vibrio parahaemolyticus, the Causative Agent of Acute Hepatopancreatic Necrosis Disease (AHPND)

2018 ◽  
Vol 31S ◽  
Author(s):  
A.P. SHINN ◽  
2017 ◽  
Vol 44 (3) ◽  
pp. 470-479
Author(s):  
Patricia López-León ◽  
Antonio Luna-González ◽  
Ruth Escamilla-Montes ◽  
María del Carmen Flores-Miranda ◽  
Jesús A. Fierro-Coronado ◽  
...  

Vibrio parahaemolyticus, the causative agent of acute hepatopancreatic necrosis disease (AHPND), was isolated from the hepatopancreas of moribund whiteleg shrimp of commercial farms from Guasave, Sinaloa, Mexico. The isolates were screened on thiosulfate citrate bile salt sucrose agar plates for the selection of green colonies and further characterized through PCR with AP3 primers, 89F/R primers, hemolysin genes, hemolytic and enzymatic activity, hydrophobicity, autoaggregation, and biofilm formation. Bioassays by immersion challenge were conducted to confirm the pathogenicity of selected bacterial strains. In addition, the LC50 was calculated for each isolate. All isolates (35) belonged to V. parahaemolyticus, but three isolates did not correspond to strains that cause AHPND since they were negative with 89F/R primers. All isolates were αhemolytic and showed biofilm formation (from moderate to strong). Isolates were hydrophobic or hydrophilic and showed high autoaggregation capacity. Eight strains did not kill shrimp and eleven were pathogenic, but differences in virulence were found among them perhaps due to α-hemolysis and differences in biofilm formation and hydrophobicity. Therefore, performed characterization may help to understand the pathogenicity of V. parahaemolyticus. Finally, results showed that smaller shrimp are less resistant to V. parahaemolyticus infection.


Biology ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 280
Author(s):  
Linh Nguyen Thi Truc ◽  
Tuu Nguyen Thanh ◽  
To Tran Thi Hong ◽  
Day Pham Van ◽  
Minh Vo Thi Tuyet ◽  
...  

This study aimed to evaluate the growth, survival rate, and resistance to acute hepatopancreatic necrosis disease (AHPND) of white leg shrimp (Penaeus vannamei) by using Lactobacillus plantarum, Lactobacillus fermentum, and Pediococcus pentosaceus mixed with feed, and at the same time supplying CNP in a ratio of 15:1:0.1 to the water. As a result, the treatments that shrimp were fed with feed containing lactic acid bacteria (LAB), especially L. plantarum, have increased shrimp growth, total hemocyte cells, granulocyte cells, and hyaline cells significantly (p < 0.05) in comparison to the control group. The supply of CNP to the water has promoted the intensity of V. parahaemolyticus effects on shrimp health and significantly decreased total hemocyte cells, granulocyte cells, and hyaline cells by 30–50% in the period after three days of the challenge, except in L. plantarum treatment, which had only a 20% decrease compared to other treatments. In CNP supplying treatments, the AHPND infected rate and mortality of shrimp were higher than those in other treatments. In summary, the supply of CNP had significantly reduced the shrimp’s immune response and promoted the susceptibility of shrimp to AHPND in both cases of use with and without LAB-containing diets.


2018 ◽  
Vol 7 (11) ◽  
Author(s):  
Sridevi Devadas ◽  
Subha Bhassu ◽  
Tze Chiew Christie Soo ◽  
Fatimah M. Yusoff ◽  
Mohamed Shariff

We sequenced the genome of Vibrio parahaemolyticus strain ST17.P5-S1, isolated from Penaeus vannamei cultured in the east coast of Peninsular Malaysia. The strain contains several antibiotic resistance genes and a plasmid encoding the Photorhabdus insect-related (Pir) toxin-like genes, pirAvp and pirBvp, associated with acute hepatopancreatic necrosis disease (AHPND).


2018 ◽  
Vol 6 (25) ◽  
Author(s):  
Siddhartha Kanrar ◽  
Arun K. Dhar

ABSTRACT Vibrio parahaemolyticus carrying the toxin genes pirA and pirB causes acute hepatopancreatic necrosis disease in shrimp. A genome sequence of V. parahaemolyticus strain R13 was determined that showed deletions of the entire pirA gene and the 5ʹ end of the pirB gene and does not cause the disease in experimental challenge.


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