Bacteremia and Liver Failure Due to Non-K1 Escherichia coli With iss Gene in Two Full-Term Infants

BACKGROUND Escherichia coli is a major pathogen causing sepsis in neonates and young infants. Although the K1 capsule is a well-established virulence factor in invasive infections, the clinical relevance of non-K1 strains and alternative virulence factors remains insufficiently characterized, particularly in cases of pediatric liver failure. The increased serum survival (iss) gene confers resistance to complement-mediated killing; however, its clinical relevance in infants has not been clarified. CASE REPORT Two full-term infants developed acute liver failure complicated by septic shock within the first month of life. Blood cultures in both cases yielded non-K1 E. coli strains harboring the iss gene. Both patients required intensive care, including plasma exchange and continuous renal replacement therapy; they ultimately underwent liver transplantation. Detailed microbiological and molecular analyses confirmed the absence of the K1 capsule and identified iss-associated virulence profiles across distinct phylogenetic backgrounds, suggesting a shared mechanism of serum resistance distinct from classical neonatal-meningitis-associated pathogenicity. CONCLUSIONS These cases underscore an important clinical insight: acute liver failure in infants can unmask invasive infection, even when classical virulence markers such as the K1 capsule are absent. Host-related impairment of complement production and innate immunity may reveal the pathogenic potential of iss-positive non-K1 strains. Awareness of such host-pathogen interactions may improve diagnostic evaluation and risk stratification in this vulnerable population.