title: The molecular epidemiology of Streptococcus pneumoniae with quinolone resistance mutations.
abstract: BACKGROUND
  The purpose of this study was to determine the prevalence of fluoroquinolone resistance and quinolone resistance-determining region (QRDR) mutations among Streptococcus pneumoniae isolates in the United States during the period of 2001-2002. A second objective was to examine the genetic relatedness of pneumococcal isolates with parC and/or gyrA mutations during the period of 1994-2002.
  
  
  METHODS
  Susceptibility testing was performed for 1902 S. pneumoniae isolates collected in the United States during the period of 2001-2002. On the basis of the minimum inhibitory concentration (MIC) of ciprofloxacin, 146 isolates were selected from the 2001-2002 study for QRDR analysis of parC, parE, gyrA, and gyrB genes. The genetic relatedness of isolates with parC and/or gyrA mutations from 2001-2002 (n=55) and from 3 US surveillance studies conducted during 1994-2000 (n=56) was determined by pulsed-field gel electrophoresis (PFGE).
  
  
  RESULTS
  Between 1999-2000 and 2001-2002, there was a 2-fold increase in the rate of ciprofloxacin resistance (MIC, >or=4 micro g/mL), from 1.2% to 2.7%, and in the rate of levofloxacin nonsusceptibility (MIC, >or=4 micro g/mL), from 0.6% to 1.3%. The 111 isolates with parC and/or gyrA mutations were assigned to 48 different PFGE types. Forty-four isolates (40%) belonged to 8 PFGE types that were closely related to widespread clones. Fifteen of the 43 levofloxacin-nonsusceptible pneumococci (LNSP) belonged to 4 PFGE types that were closely related to major clones (Spain(23F)-1 [n=6]; Spain(6B)-2 [n=5], Taiwan(19F)-14 [n=2], and Tennessee(23F)-4 [n=2]).
  
  
  CONCLUSIONS
  The population of fluoroquinolone-resistant S. pneumoniae in the United States has increased but remains genetically diverse. However, 35% of LNSP were related to widespread pneumococcal clones, increasing the potential for the rapid spread of quinolone resistance in this species.
authors.affiliation: Department of Pathology, University of Iowa Carver College of Medicine, Iowa City 52242-1009, USA. sandra-richter@uiowa.edu
authors.forename: S S
authors.initials: SS
authors.lastname: Richter
authors.forename: K P
authors.initials: KP
authors.lastname: Heilmann
authors.forename: S E
authors.initials: SE
authors.lastname: Beekmann
authors.forename: N J
authors.initials: NJ
authors.lastname: Miller
authors.forename: C L
authors.initials: CL
authors.lastname: Rice
authors.forename: G V
authors.initials: GV
authors.lastname: Doern
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002939:Ciprofloxacin / Q000494:pharmacology*; D027081:DNA Gyrase / Q000235:genetics; D027101:DNA Topoisomerase IV / Q000235:genetics; D024881:Drug Resistance, Bacterial; D006801:Humans; D064704:Levofloxacin; D008826:Microbial Sensitivity Tests; D009154:Mutation; D015242:Ofloxacin / Q000494:pharmacology*; D011008:Pneumococcal Infections / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*; D011159:Population Surveillance; D012703:Serotyping; D013296:Streptococcus pneumoniae / Q000187:drug effects* / Q000235:genetics; D013997:Time Factors; D014481:United States
chemical_list: D000900:Anti-Bacterial Agents; D002939:Ciprofloxacin; D064704:Levofloxacin; D015242:Ofloxacin; D027101:DNA Topoisomerase IV; D027081:DNA Gyrase