Objective:Rare coexistence of disease or pathology 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 Reports: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. Conclusiosn: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.
Shikaze et al. (Tue,) studied this question.