IgaA Mutation Enhances Extracellular Polysaccharides Production and Virulence via Rcs Phosphorelay in Enterobacter cloacae Complex
In this study, we identified a mucoid phenotype ECC isolate that emerged during bloodstream infection in a single patient and exhibited potential enhanced virulence during the treatment. To investigate the virulence profile and molecular mechanisms underlying the phenotype change, whole-genome sequencing and genome comparative study were conducted. We identified a point mutation in igaA gene which was responsible for the shift toward a mucoid phenotype. It also widely impacted other downstream exopolysaccharide biosynthesis and metabolism genes, making the mucoid strains exhibit significantly higher virulence both in vivo and in vitro. Further validation in reference strains and clinical isolates suggests that igaA associated regulation plays a broader role in ECC pathogenicity. These findings underscore the importance of igaA in controlling extracellular polysaccharides (EPSs) overproduction and suggest that targeting EPS biosynthesis may offer a promising strategy for preventing or treating ECC infections.