Genomic epidemiology and mechanisms of antibiotic resistance in Pseudomonas aeruginosa isolated from children’s hospital in Shenzhen, China

Background: The emergence of multi-drug-resistant Pseudomonas aeruginosa poses a global threat worldwide. We studied the molecular epidemiology and antibiotic resistance mechanisms in 294 clinical isolates of P. aeruginosa from a paediatric hospital. Methods Isolates were identified using an API-20 kit and antimicrobial susceptibility testing was performed using the VITEK ® 2 compact. β-lactamases, plasmid types and sequence types were determined by PCR and sequencing. The double-disc diffusion method for ESBL was performed. Results 56% (n = 164) isolates were resistant to piperacillin-tazobactam followed by cefepime 40% (n = 117), ceftazidime 39% (n = 115), imipenem 36% (n = 106), meropenem 33% (n = 97), ciprofloxacin 32% (n = 94). 42% (n = 126) isolates were positive for ESBL by double-disc diffusion. The bla CTX-M-15 cephalosporinase was observed in 32% (n = 40/126) while 26% (n = 33/126) were positive for bla NDM-1 carbapenemase. Aminoglycoside resistance gene aac(3)IIIa was observed in 16% (n = 20/126) and glycylcycline resistance gene tetA(Aa) in 12% (n = 15/126) of the isolates. A total of 23 sequence types were detected, ST1963, 12% (n = 16) followed by ST381, 11% (n = 14); ST234, 10% (n = 13; ST145, 58% (n = 10); ST304, 57% (n = 9); ST663 5% (n = 7) and a novel strain. In ESBL-producing P. aeruginosa , 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. Conclusion The spread of antibiotic resistance is likely due to clonal spread and circulation of different plasmids in clinical strains of P. aeruginosa .