Drug-resistant Mechanisms and Prevalence of Enterobacter cloacae Resistant to Multi-antibiotics

OBJECTIVE To investigate the main drug resistant mechanisms of Enterobacter cloacae and to make clear the prevalence of E. cloacae resistant to multi antibiotics. METHODS Standard agar dilution method, phenotype screening test, PCR amplification, gene clone and DNA sequencings were performed in the 58 strains of E. cloacae resistant to the third generation cephalosporins. RESULTS From the 58 strains of E. cloacae, AmpC beta lactamase producers were 65.52%; ESBLs producers were 13.79%, ESBLs plus AmpC beta lactamase producers were 20.69%, respectively. Fifty eight clinical isolates of E. cloacae were multi drug resistant. The susceptible ratio to cefotaxime+sulbactam was 55.3% for AmpC beta lactamase producers, 87.5% for ESBLs producers and 16.7% for ESBLs plus AmpC beta lactamase producers, respectively. The susceptible ratio to piperacillin+tazobactam was 28.9% for AmpC beta lactamase producers, 50% for ESBLs producers and 8.3% for ESBLs plus AmpC beta lactamase producers, respectively. The susceptible ratio to cefepime was 97.4% for AmpC beta lactamase producers, 37.5% for ESBLs producers and 16.7% for ESBLs plus AmpC beta lactamase producers, respectively. All of strains were susceptible to imipenem. DNA sequences of the strains revealed ESBLs of SHV 2, SHV 2a, SHV 12, CTX M 14 and CTX M 3, respectively. Forty nine of 58 strains harbored ampD gene. The ampD gene sequencing results of 8 strains highly producing AmpC beta lactamase showed that there were amino acid substitutions or deletion in the carboxy terminal of ampD. CONCLUSIONS The main drug resistant mechanisms of E. cloacae are producing ESBLs and the derepressed AmpC beta lactamase.