Phenotypic and genotypic characterization of antimicrobial resistance in Escherichia coli O111 isolates.
OBJECTIVES: The aim of this study was to generate baseline data on the prevalence and molecular basis of antimicrobial resistance in Escherichia coli O111 isolates. METHODS: A total of 105 epidemiologically unrelated E. coli O111 isolates from humans and cattle (isolated between 1983 and 2003) were tested for susceptibility to 17 antimicrobial agents by broth microdilution. Resistant isolates were screened by molecular methods for resistance genes, class 1 and 2 integrons and mutations in the quinolone-resistance determining regions. RESULTS: Resistance was found in 76% of the isolates, with a prevalence of 72% for multiresistance. The most prevalent resistances were to streptomycin, sulfamethoxazole and tetracycline (72-68%), followed by spectinomycin, ampicillin and kanamycin/neomycin (39-25%). For each antimicrobial agent, the predominant resistance genes were ampicillin, bla(TEM) (94%); chloramphenicol, catA1 (100%); gentamicin, aac(3)-IV and aac(3)-II (50% each); kanamycin, aphA1 (100%); streptomycin, aadA1- like (66%); sulfamethoxazole, sul1 (59%); tetracycline, tet(A) (86%); and trimethoprim, dfrA1-like (83%). Class 1 integrons were found in 41% of the isolates. They carried aadA1, dfrA1-aadA1 and dfrA15-aadA1. A class 2 integron (dfrA1-sat1-aadA1) was found in one isolate. Only three isolates (3%) were resistant to nalidixic acid (reduced susceptibility to ciprofloxacin), with a single mutation in the gyrA gene. CONCLUSIONS: E. coli O111 strains exhibit a wide repertoire of genetic elements to sustain antimicrobial pressure. Two specific antimicrobial resistance pheno/genotypes, [STR-SPT]-SUL-TET/aadA1-sul1-tet(A) and STR-SUL-TET-AMP-[KAN-NEO]/strA/B-sul2-tet(A)-bla(TEM)-aphA1, are predominant.[1]References
- Phenotypic and genotypic characterization of antimicrobial resistance in Escherichia coli O111 isolates. Guerra, B., Junker, E., Schroeter, A., Helmuth, R., Guth, B.E., Beutin, L. J. Antimicrob. Chemother. (2006) [Pubmed]
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