Article

Plasmid-mediated Quinolone Resistance among Non-TyphiSalmonella enterica Isolates, USA

Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Emerging Infectious Diseases (Impact Factor: 6.75). 11/2010; 16(11):1789-91. DOI: 10.3201/eid1611.100464
Source: PubMed

ABSTRACT

We determined the prevalence of plasmid-mediated quinolone resistance mechanisms among non-Typhi Salmonella spp. isolated from humans, food animals, and retail meat in the United States in 2007. Six isolates collected from humans harbored aac(6')Ib-cr or a qnr gene. Most prevalent was qnrS1. No animal or retail meat isolates harbored a plasmid-mediated mechanism.

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Available from: Rebecca L Howie
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    • "Notably, it was also found in 32% of screened individuals living in a remote village in the Amazonas (Pallecchi et al., 2011). In contrast, a recent study conducted on Salmonella isolates from humans, retail meat and animals in the USA detected qnr genes in only 0.3% of human isolates, and none from animal sources (Sjolund-Karlsson et al., 2010). qnr genes are also reportedly low in China, Korea, and India (on the order of 0–3%), where aac(6 )-lb-cr is more commonly present (Menezes et al., 2010; Tamang et al., 2011b; Yu et al., 2011b; Chen et al., 2012; Kim et al., 2013). "
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    Full-text · Article · Oct 2013 · Frontiers in Microbiology
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    • "Because cluster G displayed relatively diverse resistance patterns, the resistance genes for ACSSuT, trimethoprim , gentamicin, cefotaxime, ceftazidime, and ciprofloxacin were likely carried on plasmids. Many studies have indicated that extendedspectrum beta-lactamases, which confer resistance to cefotaxime and ceftazidime, and Qnr proteins, which confer ciprofloxacin resistance at low MIC, are frequently plasmid encoded (Sjolund-Karlsson et al., 2010; Yan et al., 2005). In a previous study, we characterized a multidrug-resistant S. Braenderup clone that carried resistance genes for ampicillin, chloramphenicol, trimethoprim, sulfamethoxazole and tetracycline on a variety of R plasmids (Chiou et al., 2009 ). "
    [Show abstract] [Hide abstract] ABSTRACT: Salmonella enterica serovar Typhimurium is a major zoonotic pathogen with a high prevalence of antimicrobial resistance. This pathogen can disseminate across borders and spread far distances via the food trade and international travel. In this study, we compared the genotypes and antimicrobial resistance of 378 S. Typhimurium isolates collected in Taiwan and Denmark between 2009 and 2010. Genotyping revealed that many S. Typhimurium strains were concurrently circulating in Taiwan, Denmark and other countries in 2009 and 2010. When compared to the isolates collected from Denmark, the isolates from Taiwan displayed a significantly higher level of resistance to 11 of the 12 tested antimicrobials. Seven genetic clusters (A-G) were designated for the isolates. A high percentage of the isolates in genetic clusters C, F and G were multidrug-resistant. Of the isolates in cluster C, 79.2% were ASSuT-resistant, characterized by resistance to ampicillin, streptomycin, sulfamethoxazole, and tetracycline. In cluster F, 84.1% of the isolates were ACSSuT-resistant (resistant to ASSuT and chloramphenicol). Cluster G was unique to Taiwan and characterized in most isolates by the absence of three VNTRs (ST20, ST30 and STTR6) as well as a variety of multidrug resistance profiles. This cluster exhibited very high to extremely high levels of resistance to several first-line drugs, and among the seven clusters, it displayed the highest levels of resistance to cefotaxime and ceftazidime, ciprofloxacin and gentamicin. The high prevalence of antimicrobial resistance in S. Typhimurium from Taiwan highlights the necessity to strictly regulate the use of antimicrobials in the agriculture and human health care sectors.
    Full-text · Article · Dec 2012 · International journal of food microbiology
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    [Show abstract] [Hide abstract] ABSTRACT: We report Salmonella enterica serotype Typhi strains with a nonclassical quinolone resistance phenotype (i.e., decreased susceptibility to ciprofloxacin but with susceptibility to nalidixic acid) associated with a nonsynonymous mutation at codon 464 of the gyrB gene. These strains, not detected by the nalidixic acid disk screening test, can result in fluoroquinolone treatment failure.
    Full-text · Article · Jun 2011 · Emerging Infectious Diseases
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