Open Access Research article

Presence of qnr gene in Escherichia coli and Klebsiella pneumoniae resistant to ciprofloxacin isolated from pediatric patients in China

Aihua Wang1, Yonghong Yang1, Quan Lu2, Yi Wang3, Yuan Chen4, Li Deng5, Hui Ding1, Qiulian Deng5, Hong Zhang2, Chuanqing Wang3, Lan Liu4, Xiwei Xu1, Li Wang1 and Xuzhuang Shen1*

Author Affiliations

1 Beijing Children's Hospital, Affiliated to Capital Medical University, Beijing, PRoC

2 Shanghai Children's Hospital, Affiliated to Shanghai Jiao Tong University, Shanghai, PRoC

3 The Children's Hospital of Fudan University, Shanghai, PRoC

4 Chongqing Children's Hospital Affiliated to Chongqing Medical University, Chongqing, PRoC

5 Guangzhou Children's Hospital, Affiliated to Guangzhou Medical College, Guangzhou, PRoC

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BMC Infectious Diseases 2008, 8:68  doi:10.1186/1471-2334-8-68

Published: 22 May 2008



Quinolone resistance in Enterobacteriaceae results mainly from mutations in type II DNA topoisomerase genes and/or changes in the expression of outer membrane and efflux pumps. Several recent studies have indicated that plasmid-mediated resistance mechanisms also play a significant role in fluoroquinolone resistance, and its prevalence is increasing worldwide. In China, the presence of the qnr gene in the clinical isolates of Enterobacteriaceae has been reported, but this transmissible quinolone resistance gene has not been detected in strains isolated singly from pediatric patients. Because quinolones associated with a variety of adverse side effects on children, they are not authorized for pediatric use. This study therefore aimed to investigate the presence of the qnr gene in clinical isolates of E. coli and K. pneumoniae from pediatric patients in China.


A total 213 of non-repetitive clinical isolates resistant to ciprofloxacin from E. coli and K. pneumoniae were collected from hospitalized patients at five children's hospital in Beijing, Shanghai, Guangzhou, and Chongqing. The isolates were screened for the plasmid-mediated quinolone resistance genes of qnrA, qnrB, and qnrS by PCR. Transferability was examined by conjugation with the sodium azide-resistant E. coli J53. All qnr-positive were analyzed for clonality by enterobacterial repetitive intergenic consensus (ERIC)-PCR.


The study found that 19 ciprofloxacin-resistant clinical isolates of E. coli and K. pneumoniae were positive for the qnr gene, and most of the qnr positive strains were ESBL producers. Conjugation experiments showed that quinolone resitance could be transferred to recipients. Apart from this, different DNA banding patterns were obtained by ERIC-PCR from positive strains, which means that most of them were not clonally related.


This report on transferable fluoroquinolone resistance due to the qnr gene among E. coli and K. pneumoniae strains indicated that plasmid-mediated quinolone resistance has emerged in pediatric patients in China.