Identification and pathogenicity of Vibrio parahaemolyticus isolates and immune responses of Penaeus (Litopenaeus) vannamei (Boone)

Abstract

Five different Vibrio parahaemolyticus strains (SH8, SH108, SH58, AH5 and GD10) isolated from the hepatopancreas of moribund shrimp in farms of mainland China were identified and capable of inducing massive mortality of Penaeus (Litopenaeus) vannamei. The immersion challenge results with five isolates indicated variance of virulence, while only GD10 caused massive sloughing of tubule epithelial cells which was recognized as the most significant symptom of AHPND. Differences in immune responses were detected of P. vannamei during 48 h post-infection (p.i.) by injection or immersion challenge with V. parahaemolyticus (SH8, SH108 and GD10) isolates. When injected SH8 and SH108 isolates, the expression of lysozyme (LSZ) showing statistically significant upregulation at 16 and 48 h p.i. and that of Toll-like receptors (TLR) showed statistically significant upregulation at 48 h p.i. When immersion challenge with the GD10 isolate, TLR were upregulated after 8 h p.i. challenge with 10(4) cfu mL(-1) ; however, LSZ was downregulated when challenged with 10(3) cfu mL(-1) . The results suggested that LSZ and TLR serve as crucial molecular markers of innate immunity in shrimp against V. parahaemolyticus infection. LSZ is a vital marker for acute bacterial infection, while TLR serves as a crucial marker for chronic infection.

Recombinant PirA‐like toxin protects shrimp against challenge with Vibrio parahaemolyticus, the aetiological agent of acute hepatopancreatic necrosis disease

“…; Hong et al . ). This effect is related to the level of secreted V. parahaemolyticus PirAB‐like binary toxin but not with the gene copy number (Tinwongger et al .…”

“…No mortality was found in the control group. In this regard, several reports have highlighted that V. parahaemolyticus AHPND strains vary in virulence and cause mortalities near to 100% at 7, 24 or 96 h post-infection by the immersion route (Joshi et al 2014;Soto-Rodr ıguez et al 2015;Hong et al 2016). This effect is related to the level of secreted V. parahaemolyticus PirAB-like binary toxin but not with the gene copy number (Tinwongger et al 2016) and might be also related with differences in transposons and small sequence repeats in the acquired plasmid (Han, Tang & Lightner 2015b).…”

Characterization and growth conditions of Vibrio parahaemolyticus strains with different virulence degrees that cause acute hepatopancreatic necrosis disease in Litopenaeus vannamei

“…There are major differences among Vp strains with respect to pathogenicity—human pathogenic Vp strains are different from Vp AHPND+ strains because they involve specific virulence factors. Virulent strains cause mass mortalities of cultivated shrimp, Penaeus ( Litopenaeus ) vannamei (Boone) and Penaeus monodon (Hong, Xu, Zhuo, Liu, & Lu, ). The disease typically affects juvenile shrimp within 20–35 days of stocking.…”

Isolation of Bdellovibrio and like organisms and potential to reduce acute hepatopancreatic necrosis disease caused by Vibrio parahaemolyticus

“…PirA is only present at the later stage, whereas PirB is detected in the hepatopancreas at the early stage of infection but is sufficient to cause cellular damage (Lai et al 2015). This bacterium has been disastrous for the shrimp industry and has reduced shrimp production worldwide by up to 20% (Hong et al 2016). Strenuous efforts to solve this problem have included cessation of shrimp cultivation and drying out of shrimp ponds for a period of time.…”

“…AHPND V. parahaemolyticus (AHPND Vp) harbors a unique large plasmid containing genes encoded for toxin homologs to the Photorhabdus insectrelated toxins PirA and PirB (Yang et al 2014). The bacterium affects post-larvae approximately 30 to 35 d after stocking the shrimp pond, causing massive rounding and sloughing of hepatopancreatic tubule epithelial cells in the early to mid stages of the disease (Hong et al 2016). PirA is only present at the later stage, whereas PirB is detected in the hepatopancreas at the early stage of infection but is sufficient to cause cellular damage (Lai et al 2015).…”