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Vikash Kumar
Laboratory of Aquaculture & Artemia Reference Center, Department of Animal Sciences and Aquatic Ecology, Faculty of Bioscience Engineering, Ghent University, B-9000 Ghent, Belgium

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Review
Published: 27 July 2021 in Toxins
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Shrimp, as a high-protein animal food commodity, are one of the fastest growing food producing sectors in the world. It has emerged as a highly traded seafood product, currently exceeding 8 MT of high value. However, disease outbreaks, which are considered as the primary cause of production loss in shrimp farming, have moved to the forefront in recent years and brought socio-economic and environmental unsustainability to the shrimp aquaculture industry. Acute hepatopancreatic necrosis disease (AHPND), caused by Vibrio spp., is a relatively new farmed penaeid shrimp bacterial disease. The shrimp production in AHPND affected regions has dropped to ~60%, and the disease has caused a global loss of USD 43 billion to the shrimp farming industry. The conventional approaches, such as antibiotics and disinfectants, often applied for the mitigation or cure of AHPND, have had limited success. Additionally, their usage has been associated with alteration of host gut microbiota and immunity and development of antibiotic resistance in bacterial pathogens. For example, the Mexico AHPND-causing V. parahaemolyticus strain (13-306D/4 and 13-511/A1) were reported to carry tetB gene coding for tetracycline resistance gene, and V. campbellii from China was found to carry multiple antibiotic resistance genes. As a consequence, there is an urgent need to thoroughly understand the virulence mechanism of AHPND-causing Vibrio spp. and develop novel management strategies to control AHPND in shrimp aquaculture, that will be crucially important to ensure food security in the future and offer economic stability to farmers. In this review, the most important findings of AHPND are highlighted, discussed and put in perspective, and some directions for future research are presented.

ACS Style

Vikash Kumar; Suvra Roy; Bijay Behera; Peter Bossier; Basanta Das. Acute Hepatopancreatic Necrosis Disease (AHPND): Virulence, Pathogenesis and Mitigation Strategies in Shrimp Aquaculture. Toxins 2021, 13, 524 .

AMA Style

Vikash Kumar, Suvra Roy, Bijay Behera, Peter Bossier, Basanta Das. Acute Hepatopancreatic Necrosis Disease (AHPND): Virulence, Pathogenesis and Mitigation Strategies in Shrimp Aquaculture. Toxins. 2021; 13 (8):524.

Chicago/Turabian Style

Vikash Kumar; Suvra Roy; Bijay Behera; Peter Bossier; Basanta Das. 2021. "Acute Hepatopancreatic Necrosis Disease (AHPND): Virulence, Pathogenesis and Mitigation Strategies in Shrimp Aquaculture." Toxins 13, no. 8: 524.

Original research article
Published: 24 June 2020 in Frontiers in Microbiology
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The biofloc system is a relatively new aquaculture technology that offers practical solution to maintain culture water quality by recycling nutrients and improves the health status and resistance of shrimps against microbial infection, yet the mode of action involved remains unclear. This study aimed to unravel the underlying mechanism behind the protective effect of a biofloc system using Litopenaeus vannamei and acute hepatopancreatic necrosis disease (AHPND)-causing Vibrio parahaemolyticus M0904 strain as a host-pathogen model. The results showed that a biofloc system maintained at a C/N ratio of 15, improves the water quality and contributes to the nutrition of cultured animals as bioflocs might serve as an additional protein source. Furthermore, the study demonstrated that the biofloc system enhances the survival of L. vannamei upon challenge with a V. parahaemolyticus AHPND strain. Remarkably, the results highlight that in the biofloc system, AHPND-causing V. parahaemolyticus possibly switch from free-living virulent planktonic phenotype to a non-virulent biofilm phenotype, as demonstrated by a decreased transcription of flagella-related motility genes (flaA, CheR, and fliS), Pir toxin (PirBVP), and AHPND plasmid genes (ORF14) and increased expression of the phenotype switching marker AlkPhoX gene in both in vitro and in vivo conditions. Taken together, results suggest that biofloc steer phenotype switching, contributing to the decreased virulence of V. parahaemolyticus AHPND strain toward shrimp postlarvae. This information reinforces our understanding about AHPND in a biofloc setting and opens the possibility to combat AHPND not only by trying to eliminate the AHPND-causing V. parahaemolyticus from the system but rather to steer the phenotypic switch.

ACS Style

Vikash Kumar; Mathieu Wille; Tânia Margarida Lourenço; Peter Bossier. Biofloc-Based Enhanced Survival of Litopenaeus vannamei Upon AHPND-Causing Vibrio parahaemolyticus Challenge Is Partially Mediated by Reduced Expression of Its Virulence Genes. Frontiers in Microbiology 2020, 11, 1270 .

AMA Style

Vikash Kumar, Mathieu Wille, Tânia Margarida Lourenço, Peter Bossier. Biofloc-Based Enhanced Survival of Litopenaeus vannamei Upon AHPND-Causing Vibrio parahaemolyticus Challenge Is Partially Mediated by Reduced Expression of Its Virulence Genes. Frontiers in Microbiology. 2020; 11 ():1270.

Chicago/Turabian Style

Vikash Kumar; Mathieu Wille; Tânia Margarida Lourenço; Peter Bossier. 2020. "Biofloc-Based Enhanced Survival of Litopenaeus vannamei Upon AHPND-Causing Vibrio parahaemolyticus Challenge Is Partially Mediated by Reduced Expression of Its Virulence Genes." Frontiers in Microbiology 11, no. : 1270.

Journal article
Published: 01 January 2020 in Emerging Microbes & Infections
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Gram-negative marine bacterium Vibrio parahaemolyticus is an important aquatic pathogen and has been demonstrated to be the causative agent of acute hepatopancreatic necrotic disease (AHPND) in shrimp aquaculture. The AHPND-causing V. parahaemolyticus strains contain a pVA1 plasmid encoding the binary PirAVP and PirBVP toxins, are the primary virulence factor that mediates AHPND and mortality in shrimp. Since, PirABVP toxins are secreted extracellularly, one can hypothesize that PirABVP toxins would aggravate vibriosis in the aquatic environment. To address this, in vivo and in vitro experiments were conducted. Germ-free Artemia franciscana were co-challenged with PirABVP toxins and 10 Vibrio spp. The in vivo results showed that PirABVP toxin interact synergistically with MM30 (a quorum sensing AI-2 deficient mutant) and V. alginolyticus AQ13-91, aggravating vibriosis. However, co-challenge by PirABVP toxins and V. campbellii LMG21363, V. parahaemolyticus CAIM170, V. proteolyticus LMG10942 and V. anguillarum NB10 worked antagonistically, increasing the survival of Artemia larvae. The in vitro results showed that the addition of PirABVP toxins significantly modulated the production of the virulence factors of studied Vibrio spp. Yet these in vitro results did not help to explain the in vivo results. Hence it appears that PirABVP toxins will not always aggravate vibriosis and the dynamics of interaction is strain dependent.

ACS Style

Phuong Thi Ngoc Tran; Vikash Kumar; Peter Bossier. Do acute hepatopancreatic necrosis disease-causing PirABVP toxins aggravate vibriosis? Emerging Microbes & Infections 2020, 9, 1 -47.

AMA Style

Phuong Thi Ngoc Tran, Vikash Kumar, Peter Bossier. Do acute hepatopancreatic necrosis disease-causing PirABVP toxins aggravate vibriosis? Emerging Microbes & Infections. 2020; 9 (1):1-47.

Chicago/Turabian Style

Phuong Thi Ngoc Tran; Vikash Kumar; Peter Bossier. 2020. "Do acute hepatopancreatic necrosis disease-causing PirABVP toxins aggravate vibriosis?" Emerging Microbes & Infections 9, no. 1: 1-47.

Research article
Published: 22 December 2019 in Environmental Microbiology
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Bacteria in nature are widely exposed to differential fluid shears which are often a trigger for phenotypic switches. The latter mediates transcriptional and translation remodeling of cellular metabolism impacting among others virulence, antimicrobial resistance and stress resistance. In this study, we evaluated the role of fluid shear on phenotypic switch in an acute hepatopancreatic necrosis disease (AHPND)‐causing Vibrio parahaemolyticus M0904 strain under both in vitro and in vivo conditions. The results showed that V. parahaemolyticus M0904 grown at lower shaking speed (110 rpm constant agitation, M0904/110), causing low fluid shear, develop cellular aggregates or floccules. These cells increased levan production (as verified by concanavalin binding) and developed differentially stained colonies on Congo Red agar plates and resistance to antibiotics. In addition, the phenotypic switch causes a major shift in the protein secretome. At 120 rpm (M0904/120), PirA/B toxins are mainly produced, while at 110 rpm PirA/B toxin production is stopped and an alkaline phosphatase PhoX becomes the dominant protein in the protein secretome. These observations are matched with a very strong reduction in virulence of M0904/110 towards two crustacean larvae, namely Artemia and Macrobrachium. Taken together, our study provides substantial evidence for the existence of two phenotypic forms in AHPND Vibrio parahaemolyticus strain displaying differential phenotypes. Moreover, as aerators and pumping devices are frequently used in shrimp aquaculture facilities, they can inflict fluid shear to the standing microbial agents. Hence, our study could provide a basis to understand the behaviour of AHPND‐causing Vibrio parahaemolyticus in aquaculture settings and open the possibility to monitor and control AHPND by steering phenotypes. This article is protected by copyright. All rights reserved.

ACS Style

Vikash Kumar; Suvra Roy; Kartik Baruah; Delphi Van Haver; Francis Impens; Peter Bossier. Environmental conditions steer phenotypic switching in acute hepatopancreatic necrosis disease‐causing Vibrio parahaemolyticus , affecting PirA VP /PirB VP toxins production. Environmental Microbiology 2019, 22, 4212 -4230.

AMA Style

Vikash Kumar, Suvra Roy, Kartik Baruah, Delphi Van Haver, Francis Impens, Peter Bossier. Environmental conditions steer phenotypic switching in acute hepatopancreatic necrosis disease‐causing Vibrio parahaemolyticus , affecting PirA VP /PirB VP toxins production. Environmental Microbiology. 2019; 22 (10):4212-4230.

Chicago/Turabian Style

Vikash Kumar; Suvra Roy; Kartik Baruah; Delphi Van Haver; Francis Impens; Peter Bossier. 2019. "Environmental conditions steer phenotypic switching in acute hepatopancreatic necrosis disease‐causing Vibrio parahaemolyticus , affecting PirA VP /PirB VP toxins production." Environmental Microbiology 22, no. 10: 4212-4230.

Journal article
Published: 09 December 2019 in Toxins
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Acute hepatopancreatic necrosis disease (AHPND), a newly emergent farmed penaeid shrimp bacterial disease originally known as early mortality syndrome (EMS), is causing havoc in the shrimp industry. The causative agent of AHPND was found to be a specific strain of bacteria, e.g., Vibrio and Shewanella sps., that contains pVA1 plasmid (63–70 kb) encoding the binary PirAVP and PirBVP toxins. The PirABVP and toxins are the primary virulence factors of AHPND-causing bacteria that mediates AHPND and mortality in shrimp. Hence, in this study using a germ-free brine shrimp model system, we evaluated the PirABVP toxin-mediated infection process at cellular level, including toxin attachment and subsequent toxin-induced damage to the digestive tract. The results showed that, PirABVP toxin binds to epithelial cells of the digestive tract of brine shrimp larvae and produces characteristic symptoms of AHPND. In the PirABVP-challenged brine shrimp larvae, shedding or sloughing of enterocytes in the midgut and hindgut regions was regularly visualized, and the intestinal lumen was filled with moderately electron-dense cells of variable shapes and sizes. In addition, the observed cellular debris in the intestinal lumen of the digestive tract was found to be of epithelial cell origin. The detailed morphology of the digestive tract demonstrates further that the PirABVP toxin challenge produces focal to extensive necrosis and damages epithelial cells in the midgut and hindgut regions, resulting in pyknosis, cell vacuolisation, and mitochondrial and rough endoplasmic reticulum (RER) damage to different degrees. Taken together, our study provides substantial evidence that PirABVP toxins bind to the digestive tract of brine shrimp larvae and seem to be responsible for generating characteristic AHPND lesions and damaging enterocytes in the midgut and hindgut regions.

ACS Style

Vikash Kumar; Lobke De Bels; Liesbeth Couck; Kartik Baruah; Peter Bossier; Wim Van Den Broeck. PirABVP Toxin Binds to Epithelial Cells of the Digestive Tract and Produce Pathognomonic AHPND Lesions in Germ-Free Brine Shrimp. Toxins 2019, 11, 717 .

AMA Style

Vikash Kumar, Lobke De Bels, Liesbeth Couck, Kartik Baruah, Peter Bossier, Wim Van Den Broeck. PirABVP Toxin Binds to Epithelial Cells of the Digestive Tract and Produce Pathognomonic AHPND Lesions in Germ-Free Brine Shrimp. Toxins. 2019; 11 (12):717.

Chicago/Turabian Style

Vikash Kumar; Lobke De Bels; Liesbeth Couck; Kartik Baruah; Peter Bossier; Wim Van Den Broeck. 2019. "PirABVP Toxin Binds to Epithelial Cells of the Digestive Tract and Produce Pathognomonic AHPND Lesions in Germ-Free Brine Shrimp." Toxins 11, no. 12: 717.