Journal
FOODBORNE PATHOGENS AND DISEASE
Volume 11, Issue 9, Pages 698-705Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/fpd.2014.1736
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Funding
- National Natural Science Foundation of China [31171682]
- Outstanding Doctoral Dissertation of Shaanxi Province, China
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Four hundred sixty-two nalidixic acid-and/or ciprofloxacin-resistant Salmonella isolates were examined for presence of quinolone-resistance mechanisms. A total of 339 amino acid substitutions were identified in GyrA (204) and ParC (135). Ser83Phe/Asp87Gly (29.4%) were most commonly detected in GyrA in 136 isolates, and to a lesser extent of Asp87Asn (22.8%), Asp87Gly (19.1%), Ser83Phe/Asp87Asn (19.1%), and Ser83Tyr (5.1%). Ser80Arg (97.0%) was detected in ParC in 132 isolates. Simultaneous mutations in GyrA and ParC (n = 109) were commonly detected to be Ser83Phe/Asp87Gly(GyrA)-Ser80Arg(ParC) (35.8%), Asp87Asn (GyrA)-Ser80Arg(ParC) (22.9%), and Ser83Phe/Asp87Asn(GyrA)-Ser80Arg(ParC) (21.1%). qnrA, qnrB, qnrS, aac(6)-Ib, qepA, and oqxAB were detected in 52 (11.3%), 64 (13.9%), 11(2.4%), 107 (23.2%), 6 (1.3%), and 194 (42.0%) of 462 isolates, respectively. Isolates carried more qnr, aac(6')-Ib, qepA, and oqxAB genes, and amino acid substitution in GyrA and ParC was more resistant to nalidixic acid and fluoroquinolones.
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