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JAC Advance Access originally published online on October 21, 2005
Journal of Antimicrobial Chemotherapy 2005 56(6):1111-1114; doi:10.1093/jac/dki369
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Increasing incidence of quinolone resistance in human non-typhoid Salmonella enterica isolates in Korea and mechanisms involved in quinolone resistance

Sang-Ho Choi1–3,, Jun Hee Woo1,2, Jung Eun Lee1,2, Su Jin Park1,2, Eun Ju Choo1,2, Yee Gyung Kwak1,2, Mi-Na Kim4, Myung-Sik Choi3, Nam Yong Lee5, Bok Kwon Lee6, Nam Joong Kim1,2, Jin-Yong Jeong1,2, Jiso Ryu1,2 and Yang Soo Kim1,2,*

1 Division of Infectious Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; 2 Center for Antimicrobial Resistance and Microbial Genetics, University of Ulsan, Seoul, Republic of Korea; 3 Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul, Republic of Korea; 4 Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; 5 Department of Laboratory Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; 6 Department of Microbiology, Korea Center for Disease Control and Prevention, Seoul, Republic of Korea

Received 16 May 2005; returned 25 June 2005; revised 14 September 2005; accepted 15 September 2005

* Correspondence address. Division of Infectious Diseases, Asan Medical Center, 388-1 Pungnap-dong, Songpa-gu, Seoul, 138-736, Korea. Tel: +82-2-3010-3303; Fax: +82-2-3010-6970; E-mail: yskim{at}amc.seoul.kr

Objectives: We investigated the trends of nalidixic acid resistance in human non-typhoid Salmonella enterica in a Korean population, and examined some possible mechanisms involved in this resistance.

Methods: A total of 261 clinical strains were tested. For all strains, the MICs of nalidixic acid were determined. Nalidixic acid-resistant strains underwent further analysis, including determination of MICs of other antibiotics, mutation analysis within the topoisomerase genes, organic solvent tolerance test, western blotting for AcrA, marOR mutation analysis, ciprofloxacin accumulation test, and PCR for the qnr gene. The clonal relationships of Salmonella strains were examined by random amplified polymorphic DNA analysis.

Results: The incidence of nalidixic acid resistance increased from 1.8% in 1995–96 to 21.8% in 2000–02. The resistance rate was higher in S. enterica serotype Enteritidis (21.6%) than in serotype Typhimurium (12.1%). The nalidixic acid resistance rates in Salmonella Enteritidis varied according to the phage type (PT) and Salmonella Enteritidis PT 1 was most commonly associated with resistance to nalidixic acid. Several cases of clonal spread, especially by Salmonella Enteritidis PT 1, were identified. Of the 46 nalidixic acid-resistant strains, 43 had single mutations in the gyrA gene. Four strains were organic solvent-tolerant and were associated with decreased ciprofloxacin accumulation; three of these showed increased expression of AcrA and had novel mutations in marOR (84L). The qnr gene was not identified.

Conclusions: Recently, the rate of nalidixic acid resistance in Korean clinical Salmonella strains markedly increased and it was partly due to the clonal spread of Salmonella Enteritidis, especially PT 1. The main mechanism of nalidixic acid resistance was a mutation in the gyrA region.

Keywords: S. enterica , nalidixic acid , drug resistance


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