Master of Science (MS)


Veterinary Medical Sciences - Pathobiological Sciences

Document Type



Although the biochemical characterization of E. ictaluri, the subsequent disease progression of enteric septicemia of catfish (ESC), and the associated pathologic lesions are well characterized, the mechanism of invasion of E. ictaluri into a susceptible host is poorly understood. Identification and confirmation of virulence factors and associated genes of E. ictaluri is crucial to elucidating the pathogenesis of this important disease. A signature tagged mutagenesis (STM) study conducted by Thune et al. (2006) identified 50 E. ictaluri clones with transposon insertions in genes potentially involved in pathogenesis. A specific STM mutant, 233PR, carrying a transposon insertion in a gene encoding a hypothetical adhesin protein, was selected for further characterization. In addition, an isogenic mutant was created by inserting a kanamycin resistance cassette 222 bp downstream from the site of the transposon insertion in 233PR in order to examine the effects of differential protein truncation on function. Bioinformatic analysis of the E. ictaluri genome revealed a pathogenicity island encoding genes with similarity to a gene cluster encoding putative adhesin/hemolysin genes in E. coli CL3 (Shen et al. 2004). In vivo results demonstrated the importance of the putative adhesin’s role in E. ictaluri pathogenesis and that protein length correlated to the level of attenuation. In vitro data did not support a role in adhesion, invasion, or intracellular replication in cell culture. The E. ictaluri PAI genes were designated eacA-H for Edwardsiella attenuation complex Results demonstrate that EacF, the putative adhesin, is a virulence factor, but further investigation is required to determine its specific role in E. ictaluri pathogenesis.



Document Availability at the Time of Submission

Release the entire work immediately for access worldwide.

Committee Chair

Ronald L. Thune