EseD, a putative T3SS translocon component of Edwardsiella tarda, contributes to virulence in fish and is a candidate for vaccine development.

Edwardsiella tarda has a type III secretion system (T3SS) essential for pathogenesis. EseD, together with EseB and EseC, has been suggested to form a putative T3SS translocon complex, although its further function is unclear. To investigate the physiological role of EseD, a mutant strain of E. tarda was constructed with an in-frame deletion of the entire eseD gene. One finding was that the ∆eseD mutant decreased the secretion levels of EseC and EseB proteins. Additionally, the ∆eseD mutant showed attenuated swarming and contact-hemolysis abilities. However, the ∆eseD mutant showed increased biofilm formation. Complementation of the mutant strain with eseD restored these phenotypes to those similar to the wild-type strain. Furthermore, infection experiments in fish showed that the ∆eseD mutant exhibited slower proliferation and a tenfold decrease in virulence in fish. These results indicate a specific role of EseD in the pathogenesis of E. tarda. Finally, recombinant EseD protein elicited high antibody titers in immunized fish and various levels of protection against lethal challenge with the wild-type strain. These results indicate that EseD protein may be a candidate antigen for development of a subunit vaccine against Edwardsiellosis.