Increasing incidence of quinolone resistance in human non-typhoid Salmonella enterica isolates in Korea and mechanisms involved in quinolone resistance.
OBJECTIVE
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.
Choi
Sang-Ho
SH
Division of Infectious Diseases, Asan Medical Center, University of Ulsan College of Medicine, Songpa-gu, Seoul, Republic of Korea.
Woo
Jun Hee
JH
Lee
Jung Eun
JE
Park
Su Jin
SJ
Choo
Eun Ju
EJ
Kwak
Yee Gyung
YG
Kim
Mi-Na
MN
Choi
Myung-Sik
MS
Lee
Nam Yong
NY
Lee
Bok Kwon
BK
Kim
Nam Joong
NJ
Jeong
Jin-Yong
JY
Ryu
Jiso
J
Kim
Yang Soo
YS
D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics; D001434:Bacteriophage Typing; D002939:Ciprofloxacin / Q000378:metabolism; D016172:DNA Fingerprinting; D026942:DNA Topoisomerases / Q000235:genetics; D024881:Drug Resistance, Bacterial; D005798:Genes, Bacterial; D006801:Humans; D007723:Korea; D008826:Microbial Sensitivity Tests; D017720:Molecular Epidemiology; D009154:Mutation; D009268:Nalidixic Acid / Q000494:pharmacology*; D009930:Organic Chemicals / Q000494:pharmacology; D019105:Random Amplified Polymorphic DNA Technique; D012480:Salmonella Infections / Q000382:microbiology*; D019779:Salmonella enterica / Q000145:classification / Q000187:drug effects* / Q000302:isolation & purification; D012703:Serotyping; D012997:Solvents / Q000494:pharmacology
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D009930:Organic Chemicals; D012997:Solvents; D009268:Nalidixic Acid; D002939:Ciprofloxacin; D026942:DNA Topoisomerases