Abstract
Outbreaks in fish of motile Aeromonad septicemia (MAS) caused by Aeromonas hydrophila have caused a great concern worldwide. Here, for the first time, we provide two complete genomes of epidemic A. hydrophila strains isolated in China. To gain an insight into the pathogenicity of epidemic A. hydrophila, we performed comparative genomic analyses of five epidemic strains belonging to sequence type (ST) 251, together with the environmental strain ATCC 7966T. We found that the known virulence factors, including a type III secretion system, a type VI secretion system and lateral flagella, are not required for the high virulence of the ST251 clonal group. Additionally, our work identifies three utilization pathways for myo-inositol, sialic acid and L-fucose providing clues regarding the factors that underlie the epidemic and virulent nature of ST251 A. hydrophila. Based on the geographical distribution and biological resources of the ST251 clonal group, we conclude that ST251 is a high-risk clonal group of A. hydrophila which may be responsible for the MAS outbreaks in China and the southeastern United States.
Highlights
Outbreaks in fish of motile Aeromonad septicemia (MAS) caused by Aeromonas hydrophila have caused a great concern worldwide
Based on comparative genomic and functional analyses, we provide novel insights into the pathogenicity of epidemic A. hydrophila by identifying putative factors that may be involved in the bacterial pathogenicity, and we determined that the ST251 clonal group of A. hydrophila is likely responsible for the ongoing MAS outbreaks in China and the southeastern United States
A. hydrophila possesses a variety of virulence genes, and some of them, such as the genes in T3SS and lateral flagella, are recognized as virulence markers[13]
Summary
Maoda Pang1, *, Jingwei Jiang2, *, Xing Xie[1], Yafeng Wu1, Yuhao Dong[1], Amy H. A. hydrophila could still cause the outbreaks of motile Aeromonad septicemia (MAS) in fish. Increasing reports[5,6,7] have proposed that animal environments that pathogens colonize have likely driven the evolution of new metabolic adaptations to maximize these new nutritional opportunities, and these adaptations may link with bacterial virulence. These suggest the known virulence factors may not be the only players in the bacterial infection process.
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