A total of 116 clinical isolates collected from a tertiary pediatric hospital and a primary pediatric department in Chicago were evaluated for resistance to fluoroquinolone antibiotics in 2003. Since October 2003, a subset of 11 resistant strains was examined to determine the mechanism of fluoroquinolone resistance. Point mutations were detected the in parC and gyrA genes. All isolates had a mutation in the parC gene that translates to a switch from serine 79 to alanine except one isolate that had no mutation in the parC gene but had a mutation in gyrA indicating a switch from methionine 99 to serine. All 5 isolates with moxifloxacin MIC 0.5 mg/ml had a mutation that represents a replacement of methionine 99 with serine in gyrA in addition to the mutation in parC. A significant increase in MIC appears to require mutations in both parC and gyrA that result in replacement of an amino acid residue. These residue replacements are similar to those described in S. pneumoniae. The dual mutations affect levofloxacin more than moxifloxacin. Moxifloxacin remains susceptible in those isolates in which levofloxacin becomes intermediate resistant. We are currently searching for point mutations in the par E and gyrB genes. To finish this study we will have the M type determined for each isolate and we will determine the relatedness of the isolates using Rep-PCR and Pulsed Field Gel Electrophoresis analysis. Results from this study were presented at the 104th American Society for Microbiology General Meeting, 2004, New Orleans, LA.
