Campioni Fábio, Souza Roberto Antonio, Martins Vinicius Vicente, Stehling Eliana Guedes, Bergamini Alzira Maria Morato, Falcão Juliana Pfrimer
1 Universidade de São Paulo - Faculdade de Ciências Farmacêuticas de Ribeirão Preto , Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Ribeirão Preto, Brazil .
2 Instituto Adolfo Lutz de Ribeirão Preto-Rua Minas , Ribeirão Preto, Brazil .
Microb Drug Resist. 2017 Jun;23(4):421-428. doi: 10.1089/mdr.2016.0024. Epub 2016 Aug 25.
Salmonella Enteritidis strains that are resistant to nalidixic acid and exhibit reduced susceptibility to fluoroquinolones have been increasing worldwide. In Brazil, few studies have been conducted to elucidate the quinolone resistance mechanisms of S. Enteritidis strains. This study analyzed the profile of gyrA, gyrB, parC, and parE mutations and plasmid-mediated quinolone resistance (PMQR) mechanisms in S. Enteritidis Nal strains isolated in Brazil. Moreover, the minimum inhibitory concentrations (MICs) of ciprofloxacin were evaluated in 84 Nal strains and compared with 20 Nal strains. The mutation profiles of the gyrA gene were accessed by high-resolution melting analysis and gyrB, parC, and parE by quinolone resistance-determining region sequencing. The MICs of ciprofloxacin were accessed with Etest. The strains were divided into five gyrA melting profiles. The Nal strains exhibited the following amino acid substitutions: Ser97→Pro, Ser83→Phe, Asp87→Asn, or Asp87→Tyr. The average MICs of ciprofloxacin was 0.006 μg/ml in the Nal and 0.09 μg/ml in the Nal strains. No points of mutation were observed in the genes gyrB, parC, and parE. The qnrB gene was found in two strains. In conclusion, the reduced susceptibility to ciprofloxacin observed in Nal strains may cause treatment failures once this drug is commonly used to treat Salmonella infections. Moreover, this reduced susceptibility in these Brazilian strains was provided by target alteration of gene gyrA and not by mobile elements, such as resistance plasmids.
对萘啶酸耐药且对氟喹诺酮类药物敏感性降低的肠炎沙门氏菌菌株在全球范围内不断增加。在巴西,针对肠炎沙门氏菌菌株喹诺酮耐药机制的研究较少。本研究分析了巴西分离出的肠炎沙门氏菌耐萘啶酸(Nal)菌株中gyrA、gyrB、parC和parE基因突变情况以及质粒介导的喹诺酮耐药(PMQR)机制。此外,对84株Nal菌株的环丙沙星最低抑菌浓度(MIC)进行了评估,并与20株Nal菌株进行了比较。通过高分辨率熔解分析检测gyrA基因的突变情况,通过喹诺酮耐药决定区测序检测gyrB、parC和parE基因的突变情况。用Etest测定环丙沙星的MIC。这些菌株被分为五种gyrA熔解图谱类型。Nal菌株出现了以下氨基酸替代:Ser97→Pro、Ser83→Phe、Asp87→Asn或Asp87→Tyr。Nal菌株中环丙沙星的平均MIC为0.006μg/ml,而Nal菌株为0.09μg/ml。在gyrB、parC和parE基因中未观察到突变位点。在两株菌株中发现了qnrB基因。总之,Nal菌株中观察到的对环丙沙星敏感性降低可能会导致治疗失败,因为该药物常用于治疗沙门氏菌感染。此外,这些巴西菌株中敏感性降低是由gyrA基因的靶点改变所致,而非由耐药质粒等移动元件引起。