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Research Project: Integrated Research to Improve On-Farm Animal Health in Salmonid Aquaculture

Location: Cool and Cold Water Aquaculture Research

Title: Flagellar regulation is required for virulence in Yersinia ruckeri

item Welch, Timothy - Tim
item Jozwick, Anna - Goucher College

Submitted to: International Symposium on Aquatic Animal Health
Publication Type: Abstract Only
Publication Acceptance Date: 7/10/2018
Publication Date: 9/4/2018
Citation: Welch, T.J., Jozwick, A. 2018. Flagellar regulation is required for virulence in Yersinia ruckeri [abstract]. International Symposium on Aquatic Animal Health. P156.

Interpretive Summary:

Technical Abstract: The gram-negative Enterobacterium Yersinia ruckeri is the etiologic agent of enteric redmouth disease (ERM), a septicemia affecting primarily farmed rainbow trout (Oncorhynchus mykiss, Walbaum). Expression of the flagellin locus (fliC) is repressed during the course of infection and subsequently up-regulated upon host mortality in a motile strain of Y. ruckeri. We have recently used a selective method to identify a spontaneous Y. ruckeri mutant strain (TW32) that displays elevated and constitutive expression of the flagellar motility phenotype. Strain TW32 is non-virulent and exposure of rainbow trout to this strain induces a specific anti- Y. ruckeri IgM antibody response and non-specific anti-Flavobacterium pschrophillum immunity of unknown duration. Virulence in TW32 is restored when the flagellar secretion system is inactivated through mutation of the filR gene in the TW32 background. This demonstrates that the attenuating mutation in TW32 exerts its effect through the flagellar secretion system and is thus dependent on either a component of the system (flagellin) or a secreted factor. Genome sequencing of the TW32 strain and marker-exchange experiments revealed that a single mutation in the promoter region of the flagellar master regulator FlhDC is responsible for this phenotype. These results suggest that the inappropriate expression of flagellar secretion during infection triggers host recognition and thus immune stimulation resulting in attenuation of virulence. The repression of flagellin expression during infection likely occurs in order to evade host recognition and is critical for Y. ruckeri virulence. We also hypothesize that these unique properties of TW32 could make this strain an ideal live-attenuated vaccine.