Plasmid-mediated Quinolone Resistance in<i>Salmonella enterica</i>, United Kingdom

Hopkins, Katie L.; Day, Martin; Threlfall, E. John

doi:10.3201/eid1402.070573

Cited by 52 publications

(39 citation statements)

References 10 publications

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“…The agent for which the loss of activity was least pronounced was nalidixic acid (twofold to eightfold increases in MIC) (211). Illustrating this phenomenon, Hopkins et al found that in non-Typhi Salmonella isolates, a phenotype of reduced susceptibility to ciprofloxacin (MIC Ͼ 0.06 g/ml) but preserved susceptibility to nalidixic acid (MIC Յ 16 g/ml) identified qnr-positive strains (82,83). Also noteworthy is the finding that some qnrA-carrying plasmids from U.S. K. pneumoniae isolates yielded transconjugants with very similar quinolone susceptibilities (211), whereas other qnrA-carrying plasmids from U.S. and Chinese isolates of Enterobacteriaceae varied in ciprofloxacin susceptibilities by 16-fold (212).…”

Section: Effect On Micmentioning

confidence: 98%

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

et al. 2009

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SUMMARY Although plasmid-mediated quinolone resistance (PMQR) was thought not to exist before its discovery in 1998, the past decade has seen an explosion of research characterizing this phenomenon. The best-described form of PMQR is determined by the qnr group of genes. These genes, likely originating in aquatic organisms, code for pentapeptide repeat proteins. These proteins reduce susceptibility to quinolones by protecting the complex of DNA and DNA gyrase or topoisomerase IV enzymes from the inhibitory effect of quinolones. Two additional PMQR mechanisms were recently described. aac(6′)-Ib-cr encodes a variant aminoglycoside acetyltransferase with two amino acid alterations allowing it to inactivate ciprofloxacin through the acetylation of its piperazinyl substituent. oqxAB and qepA encode efflux pumps that extrude quinolones. All of these genes determine relatively small increases in the MICs of quinolones, but these changes are sufficient to facilitate the selection of mutants with higher levels of resistance. The contribution of these genes to the emergence of quinolone resistance is being actively investigated. Several factors suggest their importance in this process, including their increasing ubiquity, their association with other resistance elements, and their emergence simultaneous with the expansion of clinical quinolone resistance. Of concern, these genes are not yet being taken into account in resistance screening by clinical microbiology laboratories.

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Section: Effect On Micmentioning

confidence: 98%

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

et al. 2009

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“…Isolates collected from travelers returning from Thailand or Malaysia should especially be examined for fl uoroquinolone susceptibility because nalidixic acid screening test results may no longer be predictive of fl uoroquinolone resistance. At the present time, the nonclassical phenotype appears to be mainly confi ned to Thailand and Malaysia (10,11), but given the continuous increase in global travel, these isolates may emerge in other parts of the world.…”

Section: Discussionmentioning

confidence: 99%

“…It is to be expected that this screening approach may fail due to susceptibility or only low-level resistance to nalidixic acid in these isolates (10)(11)(12). Isolates collected from travelers returning from Thailand or Malaysia should especially be examined for fl uoroquinolone susceptibility because nalidixic acid screening test results may no longer be predictive of fl uoroquinolone resistance.…”

Section: Discussionmentioning

confidence: 99%

Reduced Fluoroquinolone Susceptibility inSalmonella entericaIsolates from Travelers, Finland

Lindgren

Kotilainen²,

Huovinen³

et al. 2009

Emerg. Infect. Dis.

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“…A study from the United States (51) reported that among NTS isolates with decreased susceptibility to ciprofloxacin (referring to ciprofloxacin MIC AE0.25 mg/L) collected in 2004-2006, 17 (9.8z) had qnr genes, of which 11 had qnrS1. The qnrS gene was also the commonest qnr gene detected among selected Salmonella isolates tested for qnr genes in reports from the United Kingdom (qnrS1) (45) and Denmark (mainly qnrS1) (48,53) and in another report involving selected Salmonella enterica Corvallis isolated in Denmark and Thailand (qnrS1) (36).…”

Section: Discussionmentioning

confidence: 99%

“…There have been numerous reports of plasmidmediated qnr genes detected in Salmonella with decreased/reduced susceptibility to ciprofloxacin from around the world (31,(33)(34)(35)(45)(46)(47)(48)(49)(50)(51)(52). Studies have reported that since 2003 in Finland, NTS isolates with reduced susceptibility to fluoroquinolone (referring to ciprofloxacin MIC AE0.125 mg/mL), which were either susceptible or had only low-level resistance to nalidixic acid, had been isolated from Finnish travelers returning from Thailand or Malaysia (30,32,33).…”

Section: Discussionmentioning

confidence: 99%

Molecular Analysis of Ciprofloxacin Resistance among Non-Typhoidal <i>Salmonella</i> with Reduced Susceptibility to Ciprofloxacin Isolated from Patients at a Tertiary Care Hospital in Kuala Lumpur, Malaysia

et al. 2014

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SUMMARY:We investigated the prevalence of non-typhoidal Salmonella (NTS) with``reduced susceptibility to ciprofloxacin'' (RS-Cip) (minimum inhibitory concentration [MIC], 0.12-1.0 mg/mL) as well as their resistance genes in 75 NTS isolates (53 from stool, 21 from blood, and 1 from urine) from patients at a tertiary care Malaysian hospital between January and December 2009. RS-Cip was detected in 24/75 (32.0z) isolates. Using the ciprofloxacin MIC interpretive criteria for Salmonella in the Clinical and Laboratory Standards Institute 2013 guidelines, 51/75 (68.0z) isolates were found to be sensitive, 22/75 (29.3z) were intermediate, and 2/75 (2.7z) were resistant to ciprofloxacin. The 24 isolates that were intermediate or resistant to ciprofloxacin were the same isolates categorized as having RS-Cip. Among the 23 tested isolates with RS-Cip, the qnrS gene was detected in 17/23 (73.9z) and single gyrA mutations were detected in 6/23 (26.1z) (Asp87Tyr [n ＝ 3], Asp87Asn [n ＝ 2], and Ser83Phe [n ＝ 1]). A parC (Thr57Ser) mutation was detected in 13/23 (56.5z) isolates, coexisting with either a qnrS gene or a gyrA mutation. The high incidence of the qnrS gene among isolates with RS-Cip needs to be monitored because qnr genes can spread via plasmids and aid in the emergence of increased resistance levels.

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Plasmid-mediated Quinolone Resistance inSalmonella enterica, United Kingdom

Cited by 52 publications

References 10 publications

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

Reduced Fluoroquinolone Susceptibility inSalmonella entericaIsolates from Travelers, Finland

Molecular Analysis of Ciprofloxacin Resistance among Non-Typhoidal <i>Salmonella</i> with Reduced Susceptibility to Ciprofloxacin Isolated from Patients at a Tertiary Care Hospital in Kuala Lumpur, Malaysia

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