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.
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.
Authors: Jean Guard-Bouldin; Cesar A Morales; Jonathan G Frye; Richard K Gast; Michael Musgrove Journal: Appl Environ Microbiol Date: 2007-10-26 Impact factor: 4.792
Authors: Nabin Rayamajhi; Byeong Yeal Jung; Seung Bin Cha; Min Kyung Shin; Aeran Kim; Min Su Kang; Kang Mu Lee; Han Sang Yoo Journal: Appl Environ Microbiol Date: 2010-06-04 Impact factor: 4.792
Authors: Frank M Aarestrup; Rene S Hendriksen; Jana Lockett; Katie Gay; Kathryn Teates; Patrick F McDermott; David G White; Henrik Hasman; Gitte Sørensen; Aroon Bangtrakulnonth; Srirat Pornreongwong; Chaiwat Pulsrikarn; Frederick J Angulo; Peter Gerner-Smidt Journal: Emerg Infect Dis Date: 2007-05 Impact factor: 6.883