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논문 기본 정보

자료유형
학술저널
저자정보
(Keimyung University School of Medicine) (Keimyung University School of Medicine)
저널정보
대한바이러스학회 JOURNAL OF BACTERIOLOGY AND VIROLOGY JOURNAL OF BACTERIOLOGY AND VIROLOGY Vol.49 No.3
발행연도
수록면
95 - 114 (20page)

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초록· 키워드

Increasing resistance due to the production of extended-spectrum β-lactamase (ESBL) in Escherichia coli is a major problem to public health and CTX-M enzymes have become the most prevalent ESBL worldwide. In this study, resistance profiles of E. coli isolated in Korea and the genetic environments of blaCTX-M genes were analyzed by PCR and direct sequencing to clarify the mechanisms of spread of CTX-M. Resistance rates of CTX-M-producing E. coli, including β-lactams, fluoroquinolones and aminoglycosides, were significantly higher than that of CTX-M-non-producers (p<0.01). Of 41 tested, 39 (95.1%) isolates of CTX-M-producing E. coli showed resistance transfer by conjugation. All the transconjugants harboured large plasmids of 118~172 megadalton. Insertion sequence ISEcp1B was detected in the upstream of the blaCTX-M in 38 (92.7%) isolates with blaCTX-M. ISEcp1B was disrupted by IS26 in 16 (39.0%) isolates with blaCTX-M. ISEcp1B carried -35 and -10 promoter components between right inverted repeat (IRR) and the start codon of blaCTX-M. orf477 or IS903D was observed in the downstream of the blaCTX-M in all the isolates with blaCTX-M-3/15/55 or with blaCTX-M-14/27, respectively. Sequence similar to IRR of ISEcp1B was located downstream of orf477. Target duplication sequences were detected both upstream of IRL and downstream of IRR. These results showed the involvement of ISEcp1B in the mobilization of the resistance genes. In conclusion, the surrounding DNAs of blaCTX-M genes were very diverse, and the spread and the expression of CTX-M may be deeply related with ISEcp1B. These informations will provide important knowledge to control the increase in CTX-M-ESBLs.
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목차

  1. INTRODUCTION
  2. MATERIALS AND METHODS
  3. RESULTS
  4. DISCUSSION
  5. REFERENCES

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UCI(KEPA) : I410-ECN-0101-2019-475-001282453