Fluoroquinolone resistance in clinical isolates of Streptococcus pneumoniae: Contributions of type II topoisomerase mutations and efflux to levels ofresistance
Dj. Bast et al., Fluoroquinolone resistance in clinical isolates of Streptococcus pneumoniae: Contributions of type II topoisomerase mutations and efflux to levels ofresistance, ANTIM AG CH, 44(11), 2000, pp. 3049-3054
We report on amino acid substitutions in the quinolone resistance-determini
ng region of type II topisomerases and the prevalence of reserpine-inhibite
d efflux for 70 clinical isolates of S. pneumoniae for which the ciprofloxa
cin MIC is greater than or equal to4 mug/ml and 28 isolates for which the c
iprofloxacin MIC is less than or equal to2 pg/ml. The amino acid substituti
ons in ParC conferring low-level resistance (MICs, 4 to 8 mug/ml) included
Phe, Tyr, and Ala for Ser-79; Asn, Ala, Gly, Tyr, and Val for Asp-83; Asn f
or Asp-78; and Pro for Ala-115, Isolates with intermediate-level (MICs, 16
to 32 mug/ml) and high-level (MICs, 64 mug/ml) resistance harbored substitu
tions of Phe and Tyr for Ser-79 or Asn and Ala for Asp-83 in ParC and an ad
ditional substitution in GyrA which included either Glu-85-Lys (Gly) or Ser
-ll-Phe (Tyr). Glu-15-Lys was found exclusively in isolates with high-level
resistance. Efflux contributed primarily to low-level resistance in isolat
es with or without an amino acid substitution in ParC. The impact of amino
acid substitutions in ParE was minimal, and no substitutions in GyrB were i
dentified.