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AHPND disease: An investigation of the pVA1-type plasmid characteristics of pathogenic agents
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M.K. Pazir *   , A.H. Ahmadi , M.A. Nazari , Kh. Aein Jamshid , M. Sharifinia , O. Jafari , S. Pourmozaffar |
| Iranian Fisheries Sciences Research Institute, Agricultural Research, Education and Extension Organization (AREEO), Bushehr, 75169-89177, Iran. |
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Abstract: (240 Views) |
Acute Hepatopancreatic Necrosis Disease (AHPND), caused by pathogenic strains of Vibrio parahaemolyticus and other Vibrio species carrying the pVA1-type plasmid, has emerged as a significant threat to global shrimp aquaculture since its first outbreak in 2009. Characterized by severe hepatopancreatic necrosis and high mortality rates, the disease has spread rapidly across Asia, the Americas, and other regions, resulting in catastrophic economic losses exceeding $43 billion. The pVA1-type plasmid, which harbors the pirAB toxin genes, is central to the virulence of AHPND, enabling the production of binary toxins that disrupt shrimp cellular processes and lead to tissue damage. The plasmid's conjugative transfer capability facilitates its spread among Vibrio species and even to non-Vibrio bacteria, increasing the diversity of AHPND-causing pathogens. Environmental factors, such as poor water quality and high stocking densities, exacerbate disease outbreaks, while the shrimp's innate immune response often fails to combat the infection effectively. Despite advancements in understanding the pathogenesis of AHPND, including toxin mechanisms and plasmid dynamics, the disease remains a major challenge for the aquaculture industry. Effective control measures, including improved biosecurity, disease monitoring, and research into novel treatments, are urgently needed to mitigate its impact and ensure the sustainability of global shrimp production.
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| Keywords: AHPND, pVA1-type plasmid, Vibrio parahaemolyticus, pirAB toxins, shrimp aquaculture. |
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Full-Text [PDF 1210 kb]
(138 Downloads)
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Type of Study: Applicable |
Subject:
Special
Received: 2025/01/5 | Published: 2025/04/9
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