Vibrio parahaemolyticus: An Opportunistic Marine Pathogen Becomes Virulent by Acquiring a Plasmid that Expresses a Deadly Toxin

Outbreaks of acute hepatopancreatic necrosis disease (AHPND) have been causing losses to the shrimp farming industry globally since 2009. The causative agent of AHPND is a specific strain of Vibrio parahaemolyticus that has become highly virulent by acquiring a unique AHPND-associated plasmid (pVA1). This virulence plasmid is stably inherited via a postsegregational killing system and it is disseminated by conjugative transfer. The plasmid encodes a binary toxin that is formed from V. parahaemolyticus Photorhabdus insect-related toxins PirA^vp and PirB^vp. Neither PirA^vp nor PirB^vp alone are sufficient to produce the characteristic symptoms of AHPND, but the PirAB^vp complex induces cell death, and its cytotoxicity is analogous to that of the structurally similar insecticidal pore-forming Cry toxin. Further evidence of the importance of the PirAB^vp toxin in causing AHPND comes from V. parahaemolyticus strain M2-36, which was isolated from a culture pond in Vietnam after an outbreak of AHPND. Although M2-36 has acquired a pVA1-like plasmid, it fails to induce AHPND in shrimp, and we found that the reason for this was that the entire pirAB^vp operon was missing from the M2-36 pVA1-like plasmid. The gene organization of pVA1 further suggests that PirAB^vp may be lost or acquired by horizontal gene transfer via transposition or homologous recombination. Taken together, these results imply that any measures that successfully block the formation of the active PirAB^vp complex and/or its interaction with PirAB^vp receptors should greatly reduce the impact of this disease.