Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/49959
Title: Resistance to ceftazidime in Escherichia coli associated with AcrR, MarR and PBP3 mutations and overexpression of sdiA
Authors: Tavío, María M. 
Aquili, Virginia D.
Vila, Jordi
Poveda, Jose B. 
Keywords: Ampc Beta-Lactamase
Multiple Antibiotic-Resistance
Penicillin-Binding Proteins
Organic-Solvent Tolerance
Clinical Isolate, et al
Issue Date: 2014
Publisher: 0022-2615
Journal: Journal of Medical Microbiology 
Abstract: The mechanisms responsible for the increase in ceftazidime MIC in two Escherichia coli in vitro selected mutants, Caz/20-1 and Caz/20-2, were studied. OmpF loss and overexpression of acrB, acrD and acrF that were associated with acrR and marR mutations and sdiA 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 beta-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 ampC promoter, whereas beta-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 acrB derived from acrR mutation. The two Caz mutants and PS/20 showed the same mutations in AmpG and ParE.
URI: http://hdl.handle.net/10553/49959
ISSN: 0022-2615
DOI: 10.1099/jmm.0.063727-0
Source: Journal Of Medical Microbiology[ISSN 0022-2615],v. 63, p. 56-65
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