Overuse and misuse of antibiotics leads to antibiotic resistance which has become a significant public health concern. is the most common pathogenic bacteria underlying nosocomial infections due to the expression of virulence factors and occurrence of antibiotic resistance. Evidence indicates that β-lactamase is involved in the antibiotic resistance of to β-lactam antibiotics. The aim of the present study was to investigate the association between the molecular biological mechanisms of antibiotic resistance of and extended-spectrum β-lactamase (ESBL). In order to assess temporal trends in prevalence and antimicrobial susceptibility, bacteria were isolated and the ESBL expression level was analyzed. Susceptibility tests were performed using automated systems. The β-lactam-resistance in was assessed by the β-lactam agar screen plate and respective MIC values were evaluated using E-test strips. The confirmatory disk diffusion methods were applied for phenotypic identification of the ESBL production of . The results showed that bacteria exhibited higher ESBL production after treatment with β-lactam compared to the control. The ESBL gene expression was upregulated in after treatment with β-lactam. Results identified that penicillin-binding proteins (PBPs) were associated with the growth and resistance to β-lactams. Zinc finger nuclease markedly inhibited the antibiotic resistance of β-lactam. PBP knockdown abolished the inhibitory effects of zinc finger nuclease on the growth of induced by β-lactam antibiotic treatment. In conclusion, these results suggest that the resistance of bacteria antimicrobial drugs is through the ESBL signaling pathway, which indicates that ESBL may be a potential target for abolishing resistance to β-lactam.