Sm
            <i>qnr</i>
            , a New Chromosome-Carried Quinolone Resistance Gene in
            <i>Stenotrophomonas maltophilia</i>

Shimizu, Kenichiro; Kikuchi, Ken; Sasaki, Takashi; Takahashi, Namiko; Ohtsuka, Masayuki; Ono, Yuka; Hiramatsu, Kazumasa

doi:10.1128/aac.00026-08

Cited by 60 publications

(46 citation statements)

References 13 publications

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“…It has been confirmed that the Smqnr gene is capable of decreasing quinolone and fluoroquinolone susceptibilities, similar to other qnr determinants (Shimizu et al, 2008). Later, a publication from Spain demonstrated the role of the Table 2.…”

Section: Discussionmentioning

confidence: 99%

“…For example, Smqnr28-30 were variants of Smqnr2 with identities of 96-99 %, Smqnr31-34, Smqnr40 and Smqnr47 were variants of Smqnr4 with identities of 94-99 %, and Smqnr35-38 and Smqnr41-45 were variants of Smqnr6-11 with identities of 92-99 %. The Smqnr1-11 genes were initially detected in Japan and have 2-6 amino acid residue differences in the encoded proteins compared with the qnrB gene (Shimizu et al, 2008). The Smqnr12-18 genes prevail mainly in the UK and have different amino acid residue alterations in the encoded proteins from the Smqnr1-11 genes.…”

Section: Strainmentioning

confidence: 99%

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Detection of the Smqnr quinolone protection gene and its prevalence in clinical isolates of Stenotrophomonas maltophilia in China

Zhang

Sun

et al. 2012

Journal of Medical Microbiology

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The aim of this study was to detect novel variants of the Stenotrophomonas maltophilia Smqnr gene family and analyse the prevalence of Smqnr genes in clinical isolates of S. maltophilia in China. In total, 442 clinical isolates of S. maltophilia were collected from nine hospitals in four provinces in China. Antimicrobial susceptibility testing against six commonly used antibiotics was performed on these isolates. The sequences of the Smqnr genes amplified by PCR were aligned with those of known Smqnr genes in GenBank and an Smqnr database. The resistance rate against co-trimoxazole was highest at 48.6 %, followed by resistance rates against ceftazidime, chloramphenicol, ticarcillin/clavulanate and tigecycline at 28.7, 21.3, 19.0 and 16.1 %, respectively. The highest susceptibility was shown to levofloxacin, with a resistance rate of just 6.1 %. Smqnr genes were detected in 114 isolates, and comprised 11 previously identified genes and 20 new variants, bringing the total number of known Smqnr genes to 47. The 20 novel Smqnr genes were designated Smqnr28-47 and the encoded proteins showed only 1-12 amino acid differences among each other. The most common Smqnr genes in China were Smqnr8 and its variant Smqnr35 with prevalences of 17.5 % (20/114) and 13.2 % (15/114), respectively. Both the known and the novel Smqnr genes were discovered in both quinolone non-sensitive and sensitive isolates with similar frequency, suggesting that the Smqnr gene makes little contribution to quinolone resistance in this organism.

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Section: Discussionmentioning

confidence: 99%

Section: Strainmentioning

confidence: 99%

Detection of the Smqnr quinolone protection gene and its prevalence in clinical isolates of Stenotrophomonas maltophilia in China

Zhang

Sun

et al. 2012

Journal of Medical Microbiology

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“…A gene dosage effect of SmQnr was observed when the gene was plasmid borne, in contrast to the relatively low-level expression of chromosomally carried Smqnr. The expression of the Smqnr gene has been reported to result in low-level resistance to quinolones in a heterologous host (299,313). Resistance to quinolones in S. maltophilia can occur as a result of mutations of the bacterial topoisomerase and gyrase genes (126,339) and may also arise due to the overexpression of the efflux pump SmeDEF (11,12).…”

Section: ])mentioning

confidence: 99%

Stenotrophomonas maltophilia: an Emerging Global Opportunistic Pathogen

2012

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SUMMARY Stenotrophomonas maltophilia is an emerging multidrug-resistant global opportunistic pathogen. The increasing incidence of nosocomial and community-acquired S. maltophilia infections is of particular concern for immunocompromised individuals, as this bacterial pathogen is associated with a significant fatality/case ratio. S. maltophilia is an environmental bacterium found in aqueous habitats, including plant rhizospheres, animals, foods, and water sources. Infections of S. maltophilia can occur in a range of organs and tissues; the organism is commonly found in respiratory tract infections. This review summarizes the current literature and presents S. maltophilia as an organism with various molecular mechanisms used for colonization and infection. S. maltophilia can be recovered from polymicrobial infections, most notably from the respiratory tract of cystic fibrosis patients, as a cocolonizer with Pseudomonas aeruginosa . Recent evidence of cell-cell communication between these pathogens has implications for the development of novel pharmacological therapies. Animal models of S. maltophilia infection have provided useful information about the type of host immune response induced by this opportunistic pathogen. Current and emerging treatments for patients infected with S. maltophilia are discussed.

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“…SmQnr has two domains of 5 and 28 pentapeptide repeats separated by a glycine (179,182). An even closer homologue of qnrB has been found in DNA sequences in a marine metagenome, but its location on a bacterial chromosome or on a mobile genetic element is unknown (179).…”

Section: Chromosomal Qnr Genesmentioning

confidence: 99%

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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Sm qnr , a New Chromosome-Carried Quinolone Resistance Gene in Stenotrophomonas maltophilia

Cited by 60 publications

References 13 publications

Detection of the Smqnr quinolone protection gene and its prevalence in clinical isolates of Stenotrophomonas maltophilia in China

Detection of the Smqnr quinolone protection gene and its prevalence in clinical isolates of Stenotrophomonas maltophilia in China

Stenotrophomonas maltophilia: an Emerging Global Opportunistic Pathogen

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

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