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Resistance to ceftazidime in Escherichia coli associated with AcrR, MarR and PBP3 mutations and overexpression of sdiA
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| Zeitschriftentitel: | Journal of Medical Microbiology |
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| Personen und Körperschaften: | , , , |
| In: | Journal of Medical Microbiology, 63, 2014, 1, S. 56-65 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Microbiology Society
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| Schlagwörter: |
| Zusammenfassung: | <jats:p>The mechanisms responsible for the increase in ceftazidime MIC in two <jats:italic>Escherichia coli in vitro</jats:italic> selected mutants, Caz/20-1 and Caz/20-2, were studied. OmpF loss and overexpression of <jats:italic>acrB</jats:italic>, <jats:italic>acrD</jats:italic> and <jats:italic>acrF</jats:italic> that were associated with <jats:italic>acrR</jats:italic> and <jats:italic>marR</jats:italic> mutations and <jats:italic>sdiA</jats:italic> overexpression, together with mutations A233T and I332V in FtSI (PBP3) resulted in ceftazidime resistance in Caz/20-2, multiplying by 128-fold the ceftazidime MIC in the parental clinical isolate PS/20. Absence of detectable β-lactamase hydrolytic activity in the crude extract of Caz/20-2 was observed, and coincided with Q191K and P209S mutations in AmpC and a nucleotide substitution at −28 in the <jats:italic>ampC</jats:italic> promoter, whereas β-lactamase hydrolytic activity in crude extracts of PS/20 and Caz/20-1 strains was detected. Nevertheless, a fourfold increase in ceftazidime MIC in Caz/20-1 compared with that in PS/20 was due to the increased transcript level of <jats:italic>acrB</jats:italic> derived from <jats:italic>acrR</jats:italic> mutation. The two Caz mutants and PS/20 showed the same mutations in AmpG and ParE.</jats:p> |
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| Umfang: | 56-65 |
| ISSN: |
0022-2615
1473-5644 |
| DOI: | 10.1099/jmm.0.063727-0 |