# Genomic Insights into the Pathogenicity of Hypervirulent Aeromonas hydrophila Strain D4 Isolated from Diseased Blunt Snout Bream with the Epidemic Sequence Type 251 Clones

## TL;DR

This study explores the genomic features of a highly virulent strain of Aeromonas hydrophila, revealing genetic elements linked to its pathogenicity and adaptability in aquaculture.

## Contribution

The study identifies unique genomic islands and plasmids in ST251 strains that contribute to hypervirulence and environmental adaptability.

## Key findings

- ST251 strain D4 shows enhanced motility, hemolytic activity, and protease production compared to ATCC 7966T.
- Genomic islands in ST251 strains include pathways for nutrient acquisition and flagellar assembly.
- Distinct plasmids and prophages in ST251 strains may regulate stress responses and virulence genes.

## Abstract

Aeromonas hydrophila ST251 is a crucial pathogen responsible for the outbreaks of Motile Aeromonas Septicemia (MAS) in global aquaculture. To elucidate the genetic basis underlying its hypervirulence, we investigated strain D4, an ST251 isolate recovered from diseased blunt snout bream. Phenotypic assays revealed that, compared to the environmental strain ATCC 7966T, D4 exhibited enhanced motility, hemolytic activity, and protease production. Average nucleotide identity (ANI) analysis demonstrated that D4 clustered within a distinct ST251 clade, with ANI values ≥ 99.74%. Comparative genomic analysis of D4, nine additional ST251 strains, and ATCC 7966T identified multiple unique genomic islands in ST251 strains, including pathways for myo-inositol and L-fucose utilization and a pseudaminic acid biosynthesis gene cluster. These genetic elements are associated with nutrient acquisition and flagellar assembly, potentially enhancing colonization and environmental adaptability. In addition, distinct plasmids and prophages in ST251 strains may contribute to host adaptation and virulence by regulating stress responses and virulence-associated genes. These findings offer new insights into the molecular mechanisms driving the pathogenicity and adaptability of hypervirulent A. hydrophila ST251 strains.