ANÁLISE DA RESISTÊNCIA A QUINOLONAS EM ESCHERICHIA COLI UROPATOGÊNICA COM FENÓTIPO LACTOSE NEGATIVO

• Autor(a) principal: Gomig, Franciane
• Data de Publicação: 2013
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UEPG
• Texto Completo: http://tede2.uepg.br/jspui/handle/prefix/977
• topic: resistência; quinolonas; Escherichia coli; lactose negativo; biótipo; bacterial resistance; quinolones; Escherichia coli; lactose negative; biotype; CNPQ::CIENCIAS BIOLOGICAS::BIOQUIMICA::BIOLOGIA MOLECULAR

Urinary tract infections show a high incidence in the population, mainly in women, the elderly and pregnant women. The main etiological agent is E. coli, especially in Community infections. Antimicrobial therapy is performed extensively with the Quinolones and resistance emergence is striking and upward. It is known E. coli resistance mechanisms are related with QRDR (Quinolone Resistance Region Determining) mutations in gyrA and parC genes that are the drug targets. These genes encode respectively DNA Girase and Topoisomerase IV subunits responsible for DNA supercoiling and DNA decatenating. Another resistance mechanism that come from plasmids is qnr genes encoding a protein that can protect DNA girase and Topoisomerase IV. Another plasmidial gene is aac(6´)-Ib-cr encoding an aminoglycoside acetyltransferase that can inactivate ciprofloxacin and norfloxacin. This study analyzed 58 E. coli lactose negative samples from urine, in order to draw a profile of resistance in this population from the region of Ponta Grossa and analyze the resistance mechanisms involved. There was a high resistance rate of 48%, among which 79% were resistant to all quinolones tested: nalidixic acid, ciprofloxacin, norfloxacin and ofloxacin. There was also a direct relationship between the biotypes 971 and resistance in contrast to biotype 981 and sensitivity. Therefor Quinolones are not recommended in infection due to E. coli biotype 971. On molecular analysis on the multiresistant samples mutations with aminoacid substitution were found in three positions: the gyrA gene at codons 83 and 87 and in the parC gene at codon 80 in three strains and at codon 84 on a single strain. Mutations only at gyrA gene appeared for a sample resistant just to nalidixic acid. These facts are according to the theory of mutations accumulation causing increased resistance to quinolones. Plasmidial genes qnr and aac(6´)-Ib-cr were not found in these strains.