Resistance genomics and molecular epidemiology of high-risk clones of ESBL-producing in young children.

Introduction: The emergence of multidrug-resistant poses a global threat, but the distribution and resistance profiling are unclear, especially in young children. Infections due to are common, associated with high mortality, and increasingly β-lactam drug resistant.

Methods: We studied the molecular epidemiology and antibiotic resistance mechanisms in 294 clinicalisolates of from a pediatric hospital in China. Non-duplicate isolates were recovered from clinical cases and were identified using an API-20 kit followed by antimicrobial susceptibility testing using the VITEK®2 compact system (BioMerieux, France) and also by broth dilution method. In addition, a double-disc synergy test for the ESBL/E-test for MBL was performed. The presence of beta-lactamases, plasmid types, and sequence types was determined by PCR and sequencing.

Results: Fifty-six percent ( = 164) of the isolates were resistant to piperacillin-tazobactam, followed by cefepime (40%; = 117), ceftazidime (39%; = 115), imipenem (36%; = 106), meropenem (33%; = 97), and ciprofloxacin (32%; = 94). Forty-two percent (n = 126) of the isolates were positive for ESBL according to the double-disc synergy test. The blaCTX-M-15 cephalosporinase was observed in 32% (n = 40/126), while 26% (n = 33/126) werepositive for blaNDM-1 carbapenemase. Aminoglycoside resistance gene was observed in 16% (n = 20/126), and glycylcyclines resistance gene tet(A) was observed in 12% (n = 15/126) of the isolates. A total of 23 sequence types were detected, including ST1963 (12%; n = 16), followed by ST381 (11%; = 14), ST234 (10%; = 13), ST145 (58%; = 10), ST304 (57%; = 9), ST663 (5%; n = 7), and a novel strain. In ESBL-producing , 12 different Incompatibility groups (Inc) were observed, the most common being IncFI, IncFIS, and IncA/C. The MOBP was the most common plasmid type, followed by MOBH, MOBF, and MOBQ.

Discussion: Our data suggest that the spread of antibiotic resistance is likely due toclonal spread and dissemination of different clinical strains of harbouring different plasmids. This is a growing threat in hospitals particularly in young children which needs robust prevention strategies.