Table 2

Fluoroquinolone resistance mechanismsa

Resistance mechanismNo. (%) of isolates
ST131-O25bST131-O16ST405OST
CIPr NALr (n = 37)CIPr NALr (n = 5)CIPs NALr (n = 13)CIPr NALr (n = 41)CIPr NALr (n = 22)CIPs NALr (n = 10)
QRDRs with >2 mutations37 (100)5 (100)0 (0)40 (98)22 (100)0 (0)
acrAB-associated mutations in marOR or acrR4 (11)0 (0)2 (15)15 (37)11 (50)2 (20)
    Mutation in MarA activator binding site of marO0 (0)0 (0)0 (0)5b (12)1 (5)0 (0)
    Loss of RNA binding site in marO0 (0)0 (0)0 (0)2 (5)0 (0)0 (0)
    Deletion and frameshift in marR0 (0)0 (0)1 (8)0 (0)0 (0)
    IS1 insertion in acrR3 (8)0 (0)1 (8)1 (2)0 (0)0 (0)
    Insertion and frameshift in acrR0 (0)0 (0)0 (0)1 (2)0 (0)0 (0)
    Deletion and frameshift in acrR0 (0)0 (0)0 (0)8b (20)5 (23)0 (0)
    Point mutation (stop codon) in acrR1 (3)0 (0)0 (0)1 (2)0 (0)0 (0)
    Point mutation (amino acid change) in acrR0 (0)0 (0)1 (13)2 (5)5 (23)2 (20)
PMQR determinants
    aac(6′)-Ib-cr3 (8)0 (0)0 (0)4 (10)0 (0)3 (30)
    oqxAB0 (0)0 (0)0 (0)0 (0)1 (5)0 (0)
  • a OST, other sequence types; CIP, ciprofloxacin; NAL, nalidixic acid; r, resistant; s, sensitive; QRDRs, quinolone resistance-determining regions, including GyrA and ParC; PMQR, plasmid-mediated quinolone resistance. One nalidixic acid-susceptible B2-ST131-O16 isolate had a point mutation (amino acid change) in acrR. The qepA gene was not found in this study. Only one nalidixic acid-susceptible OST isolate was positive for qnrB4. No other fluoroquinolone resistance mechanism was detected among nalidixic acid-susceptible isolates.

  • b Five isolates with mutation in the MarA activator binding site also had a deletion and frameshift in acrR.