High genomic diversity of Vibrio parahaemolyticus from underexplored tropical northern Australia: a baseline for future surveillance

<i>Vibrio parahaemolyticus</i> is an autochthonous marine bacterium that causes gastroenteritis after ingestion of raw or undercooked seafood and, less frequently, wound and tissue infections. Genomic information from northern Australia is scarce, and most sequences to date stem from foodborne outbreaks in southern states. We analysed 24 environmental and 5 clinical isolates (4 wound and 1 gastrointestinal case) collected in the wet-dry tropics from northern Australia and placed them alongside 48 representative public genomes. Core-genome phylogeny showed that the northern Australian strains sit within the broad VppAsia lineage and intermix with Asian and South American isolates, reflecting the limited geographic structuring in the marine environment. A gastrointestinal isolate (RDH3, ST-2901) harboured the <i>trh2</i>-positive VPaI-β pathogenicity island (including <i>vtrAB</i> and <i>hlyDBAC</i> genes) and displayed an A187S change in the TRH2 toxin which was absent in the other TRH-1/-2 sequences of the isolates analysed in this study. Wound isolates lacked <i>tdh</i> and <i>trh</i> genes, suggesting that the species' intrinsic virulome may suffice for tissue colonization; notably, one wound strain carried a plasmid with a <i>Vibrio alginolyticus pilT</i> copy linked to twitching motility which has been associated with wound infections. It remains to be determined whether this additional <i>pilT</i> copy, beyond the core genome copies, confers a selective advantage for tissue colonization. Plasmid diversity amongst clinical isolates and a diseased aquaculture fish, including a putative chimaera plasmid in the gastrointestinal isolate, underscores the role of mobile elements as reservoirs allowing adaptability to changing environments. Our findings expand the Australian genomic catalogue beyond outbreak strains, reveal extensive accessory-genome variability in tropical waters and underscore the need for One-Health surveillance frameworks that monitor virulence and resistance markers beyond the canonical hemolysin genes.