Assuntos
Antibacterianos/metabolismo , Antibacterianos/farmacologia , Infecções por Campylobacter/veterinária , Campylobacter/efeitos dos fármacos , Campylobacter/metabolismo , Farmacorresistência Bacteriana , Doenças das Aves Domésticas/microbiologia , Animais , Transporte Biológico Ativo , Campylobacter/isolamento & purificação , Infecções por Campylobacter/microbiologia , Testes de Sensibilidade Microbiana , Aves Domésticas , SenegalRESUMO
In this study, topoisomerase mutations in ciprofloxacin-resistant and -susceptible Campylobacter jejuni were analysed by DNA sequencing. In certain ciprofloxacin-resistant C. jejuni, the mechanism of resistance was complex. The Thr86-Ala substitution in the GyrA protein appears to play a role in increasing the minimum inhibitory concentration of nalidixic acid only. In addition, isolates with this amino acid change and those resistant to quinolones but lacking a mutation in the GyrA quinolone resistance-determining region could be derived from two different clones. Based on gyrA and gyrB polymorphisms, C. jejuni isolates from the Dakar region of Senegal appeared to be less diverse than those from other countries. Moreover, C. jejuni isolates in Senegal appeared to differ from European isolates by lack of a silent mutation at codon 120 of the gyrA gene.
Assuntos
Campylobacter jejuni/efeitos dos fármacos , Campylobacter jejuni/genética , DNA Girase/genética , Farmacorresistência Bacteriana/genética , Fluoroquinolonas/farmacologia , Animais , Infecções por Campylobacter/tratamento farmacológico , Infecções por Campylobacter/epidemiologia , Infecções por Campylobacter/microbiologia , DNA Girase/efeitos dos fármacos , DNA Topoisomerase IV/efeitos dos fármacos , DNA Topoisomerase IV/genética , Europa (Continente) , Testes de Sensibilidade Microbiana , Mutação , Ácido Nalidíxico/farmacologia , Polimorfismo Genético , Senegal/epidemiologiaRESUMO
We used the multilocus sequence typing (MLST) method to study the genetic diversity of Campylobacter coli isolated from chickens in Senegal, and to check the presence of genetic exchange with Campylobacter jejuni. In addition, we assessed the resistance of the isolates to ciprofloxacin and nalidixic acid, and their gyrA sequences. MLST revealed a low level of diversity and the absence of lineages among C. coli isolates. In addition, an exchange of alleles with C. jejuni was found. Twenty percent of the ciprofloxacin-resistant isolates lacked mutations within the quinolone resistance-determining region (QRDR) of GyrA. There was no link between quinolone resistance and sequence type (ST).
Assuntos
Campylobacter coli/efeitos dos fármacos , Campylobacter coli/genética , Galinhas/microbiologia , Quinolonas/farmacologia , Alelos , Animais , Anti-Infecciosos/farmacologia , Campylobacter jejuni/genética , Ciprofloxacina/farmacologia , DNA Girase/genética , Farmacorresistência Bacteriana , Variação Genética , Ácido Nalidíxico/farmacologia , Reação em Cadeia da Polimerase , SenegalRESUMO
We used the multilocus sequence typing (MLST) method to evaluate the genetic diversity of 46 Campylobacter jejuni isolates from chickens and to determine the link between quinolone resistance and sequence type (ST). There were a total of 16 ST genotypes, and the majority of them belonged to seven clonal complexes previously identified by using isolates from human disease. The ST-353 complex was the most common complex, whereas the ST-21, ST-42, ST-52, and ST-257 complexes were less well represented. The resistance phenotype varied for each ST, and the Thr-86-Ile substitution in the GyrA protein was the predominant mechanism of resistance to quinolone. Nine of the 14 isolates having the Thr-86-Ile substitution belonged to the ST-353 complex. MLST showed that the emergence of quinolone resistance is not related to the diffusion of a unique clone and that there is no link between ST genotype and quinolone resistance. Based on silent mutations, different variants of the gyrA gene were shown to exist for the same ST. These data provide useful information for understanding the epidemiology of C. jejuni in Senegal.
