Abstract
Elizabethkingia miricola is a multidrug-resistant pathogen that can cause life-threatening infections in immunocompromised patients and outbreaks in amphibians. However, the specific virulence factors of this microorganism have not been previously determined. In this study, we identified the polysaccharide biosynthesis protein gene capD, located in the conserved region of the Wzy-dependent capsule synthesis gene cluster in E. miricola strain FL160902, and investigated its role in the pathogenesis of E. miricola. Our results showed that the capD deletion strain (ΔcapD) lost its typical encapsulated structure with a 45% reduction in cell wall thickness. CapD affects Wza expression in the capsule polysaccharide synthesis pathway. Furthermore, the survival rates were significantly reduced in ΔcapD in response to complement-mediated killing, desiccation stress, oxidative stress, and macrophage phagocytosis, while biofilm formation, self-aggregation ability, and adherence to both endothelial and epithelial cells were enhanced. Additionally, the deletion of ΔcapD sharply attenuated the virulence of E. miricola in a frog infection model. Overall, these findings suggest that CapD contributes to polysaccharide synthesis and plays a crucial role in the pathogenesis of E. miricola.