The gene in bacteria, which plays a key role in adaptation to various environmental stresses, is associated with pathogenicity. However, its role in conferring external environmental stress resistance in remains unclear. In this study, we used the clinically isolated serotype 5 CF7066 strain (wild type) to investigate the effects of on the external environmental stress response of by constructing mutant () and complemented strains. Our data indicated that the viable bacterial count of was significantly lower than that of the wild type under high temperature, osmotic pressure, and oxidative stress conditions. Moreover, the strain exhibited extreme sensitivity to complement-mediated killing compared with the wild-type strain, whereas its serum-resistance ability was largely restored after gene complementation. Additionally, knockdown significantly attenuated the pathogenicity of the wild-type strain, and gene complementation largely recovered its phenotype in mouse and pig models. Taken together, our findings reveal as a novel virulence gene in , contributing to a deeper understanding of the pathogenic mechanisms employed by this bacterium.The gene in bacteria is crucial for adapting to environmental stresses and is linked to pathogenicity. However, its role in conferring stress resistance in is unclear. This study investigates the impacts of on ' stress response by creating a mutant () and complemented strain. The had reduced viability under heat, osmotic pressure, and oxidative stress conditions. It was also more sensitive to complement-mediated killing but regained serum resistance with complementation. knockdown reduced the wild-type strain's pathogenicity in mice and pigs, which was largely restored by gene complementation. Thus, is identified as a novel virulence factor in , enhancing our understanding of its pathogenic mechanisms.