Aliivibrio salmonicida is the cause of cold-water vibriosis, a hemorrhagic septicemia of farmed salmonids. Previous reports have shown that Al. salmonicida is able to circumvent defense systems of the fish host, and it has been suggested that the tissue damage observed in moribund fish is associated with the immune response raised towards the invading pathogen. This project was initiated to identify components of importance for virulence and immunogenicity, in order to increase the understanding of interactions between Al. salmonicida and its salmonid host. For microbial detection and induction of defense systems, the host immune system relies on microbe-associated molecular patterns (MAMPs), structures specific to microbes that serve as signatures for microbial presence. In this thesis, two well-known MAMPs have been investigated: flagellin of the flagellar motility apparatus, and lipopolysaccharide (LPS) of the outer membrane. In addition to their roles as targets for the immune system, both the flagellum and LPS serve important functions that aid bacterial survival. The results presented here demonstrate that neither flagellar motility nor LPS are required for invasion of salmon. However, both structures were shown to be involved in later stages of disease development. Results of challenge experiments demonstrated a function in virulence for the flagellar flagellins. Interestingly, bacteria cultured in implants within the peritoneal cavity of salmon showed an increase in production of flagellins, but not other components associated with motility. Combined, these results indicate a motility-independent requirement for flagellation in the cold-water vibriosis pathogenesis. However, the mechanisms involved remain unknown. In addition, the O-antigen moiety of LPS was shown to be essential for virulence. The results of this thesis indicate that O-antigen contributes to survival within the host and modulates the magnitude of the immune response raised in experimentally infected salmon. These observations may relate to the presence of LPS in VS-P1, an outer membrane complex that is shed from the bacterial surface and is hypothesized to decoy the immune response away from bacterial cells. While the findings of this thesis elucidate certain aspects of mechanisms involved in virulence in Al. salmonicida, new questions have also been raised. Knowledge about microbial pathogenesis is crucial for control of diseases, and this work may contribute to improvement of prophylactic strategies for cold-water vibriosis as well as other bacterial fish diseases.