Fatal clonal outbreak of KPC-2-producing Enterobacter roggenkampii in Pediatric patients: Cefiderocol resistance and a novel IncU plasmid.

OBJECTIVES

To investigate a clonal outbreak of carbapenemase-producing Enterobacter roggenkampii bloodstream infections in a Brazilian paediatric unit, focusing on resistance mechanisms, clonality, and clinical impact.

METHODS

A retrospective case series was conducted on six critically ill paediatric patients. Identification was confirmed via MALDI-TOF MS. Susceptibility was determined by broth microdilution. WGS was employed for phylogenomic analysis and plasmid characterisation.

RESULTS

Septic shock and multi-organ dysfunction affected 67% of patients, with a 50% case mortality rate. Standard automated platforms misidentified all isolates as Enterobacter cloacae complex, obscuring the outbreak. All strains were clonal blaKPC-2-producing E. roggenkampii ST516. The blaKPC-2 gene was situated on a novel, streamlined ∼30 kb IncU plasmid lacking conventional conjugative machinery. Isolates were extensively drug-resistant (XDR), including resistance to cefiderocol (MICs 4-8 µg/mL), which is currently unavailable in Brazil. Genomic analysis suggested that this phenotype was potentially mediated by mutations in the iron-uptake transporter (CirA) and penicillin-binding proteins (PBP2 and PBP3).

CONCLUSION

E. roggenkampii is an emerging pathogen causing fatal outbreaks in paediatric critical care. The diagnostic "blind spot" in automated systems facilitates silent transmission and compromises therapy. Cefiderocol resistance in clones harbouring atypical blaKPC-2 plasmids necessitates precise species-level identification and robust molecular surveillance to mitigate the spread of these highly resistant pathogens.