Plasmid-borne florfenicol and ceftiofur resistance encoded by the floR and blaCMY-2 genes in Escherichia coli isolates from diseased cattle in France (original) (raw)
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Relationship between Phenotypic and Genotypic Florfenicol Resistance in Escherichia coli
Antimicrobial Agents and Chemotherapy, 2004
This study evaluated the relationship between florfenicol resistance and flo genotypes in 1,987 Escherichia coli isolates from cattle. The flo gene was detected in 164 isolates, all of which expressed resistance to florfenicol at MICs of >256 g/ml. The florfenicol MICs for all isolates that lacked flo were <16 g/ml.
Detection of Florfenicol Resistance Genes in Escherichia coli Isolated from Sick Chickens
Antimicrobial Agents and Chemotherapy, 2000
Florfenicol is an antibiotic approved for veterinary use in cattle in the United States in 1996. Although this drug is not used in poultry, we have detected resistance to florfenicol in clinical isolates of avian Escherichia coli. Molecular typing demonstrated that the florfenicol resistance gene, flo, was independently acquired and is plasmid encoded.
FEMS Microbiology Letters, 2004
Multidrug resistance plasmids carrying the bla CMY-2 gene have been identified in Salmonella enterica serovars Typhimurium and Newport from the United States. This gene confers decreased susceptibility to ceftriaxone, and is most often found in strains with concomitant resistance to ampicillin, chloramphenicol, streptomycin, sulfamethoxazole and tetracycline. The bla CMY-2-carrying plasmids studied here were shown to also carry the florfenicol resistance gene, floR, on a genetic structure previously identified in Escherichia coli plasmids in Europe. These data indicate that the use of different antimicrobial agents, including phenicols, may serve to maintain multidrug resistance plasmids on which extended-spectrum cephalosporin resistance determinants co-exist with other resistance genes in Salmonella.
Objective: Genomic analyses were performed on florfenicol resistant (FFNR) Campylobacter coli (C. coli) isolated from cattle and the cfr(C) gene-associated multi-drug resistance (MDR) plasmid was characterized. Methods: Sixteen FFNR C. coli isolates recovered between 2013-2018 from beef cattle were sequenced. SNPs across the genome and the structures of MDR plasmids were investigated. Conjugation was performed to determine the transferability of cfr(C) associated MDR plasmids. The spectrum of resistance encoded by the cfr(C) gene was further investigated by agar dilution. Results: All 16 FFNR isolates were MDR and exhibited co-resistance to ciprofloxacin, nalidixic acid, clindamycin and tetracycline. All isolates carried aph(3′)-III, hph, ΔaadE (truncated), blaOXA-61, cfr(C), and tet(O) genes plus a mutation of GyrA T86I. The cfr(C), aph(3′)-III, hph ΔaadE, and tet(O) genes were co-located on transferable MDR plasmids with size 48-50 kb. These plasmids showed high sequence homology ...
Journal of Clinical Microbiology, 2000
Florfenicol, a veterinary fluorinated analog of thiamphenicol, is approved for treatment of bovine respiratory pathogens in the United States. However, florfenicol resistance has recently emerged among veterinary Escherichia coli isolates incriminated in bovine diarrhea. The flo gene, which confers resistance to florfenicol and chloramphenicol, has previously been identified in Photobacterium piscicida and Salmonella enterica serovar Typhimurium DT104. The flo gene product is closely related to the CmlA protein identified in Pseudomonas aeruginosa . The cmlA gene confers nonenzymatic chloramphenicol resistance via an efflux mechanism. Forty-eight E. coli isolates recovered from calves with diarrhea, including 41 that were both chloramphenicol and florfenicol resistant, were assayed for the presence of both flo and cmlA genes. Forty-two of the 44 isolates for which florfenicol MICs were ≥16 μg/ml were positive via PCR for the flo gene. All E. coli isolates for which florfenicol MICs ...
Identification of the Multi-Resistance Gene cfr in Escherichia coli Isolates of Animal Origin
PLoS ONE, 2014
Previous study indicated that the multi-resistance gene cfr was mainly found in gram-positive bacteria, such as Staphylococcus and Enterococcus, and was sporadically detected in Escherichia coli. Little is known about the prevalence and transmission mechanism of cfr in E. coli. In this study, the presence of cfr in E. coli isolates collected during 2010-2012 from food-producing animals in Guangdong Province of China was investigated, and the cfr-positive E. coli isolates were characterized by PFGE, plasmid profiling, and genetic environment analysis. Of the 839 E. coli isolates, 10 isolates from pig were cfr positive. All the cfr-positive isolates presented a multi-resistance phenotype and were genetically divergent as determined by PFGE. In 8 out of the 10 strains, the cfr gene was located on plasmids of ,30 kb. Restriction digestion of the plasmids with EcoRI and sequence hybridization with a cfr-specific probe revealed that the cfr-harboring fragments ranged from 6 to 23 kb and a ,18 kb cfr-carrying fragment was common for the plasmids that were ,30 kb. Four different genetic environments of cfr were detected, in which cfr is flanked by two identical copies of IS26, which may loop out the intervening sequence through homologous recombination. Among the 8 plasmids of ,30 kb, 7 plasmids shared the same genetic environment. These results demonstrate plasmid-carried cfr in E. coli and suggest that transposition and homologous recombination mediated by IS26 might have played a rule in the transfer of the cfr gene in E. coli.
Journal of Antimicrobial Chemotherapy, 2012
method. 9 Interestingly, the transformed strain, R6M-2-P454S, that carried the parE mutation showed a 16-fold increase in resistance to moxifloxacin, a 2-fold increase in resistance to ciprofloxacin and a 4-fold increase in resistance to levofloxacin compared with strain R6M-2. The mutation of parE was a relatively late event, as it was detected only in the strain R6M-3; thus, this mutation may occur after other mutations in gyrA and parC. Consistent with this hypothesis, no transformants were obtained in the presence of 0.125 mg/L moxifloxacin when PCR fragments containing the parE mutation were transformed into the R6WT strain. This study has identified a novel resistance mutation in parE that confers high-level resistance to moxifloxacin in S. pneumoniae. These results advance our understanding of mutations that are required for the development of fluoroquinolone resistance.