title: Fluoroquinolone resistance in Neisseria gonorrhoeae after cessation of ciprofloxacin usage in San Francisco: using molecular typing to investigate strain turnover.
abstract: BACKGROUND
  Ciprofloxacin resistance (CipR) among gonococcal strains in San Francisco (SF) increased between 2001 and 2006 and decreased between 2007 and 2009. Molecular typing of isolates obtained from 2005 to 2009 was performed to elucidate changes in CipR prevalence.
  
  
  METHODS
  A total of 2526 samples were collected at the SF City Clinic between 2001 and 2009. Minimum inhibitory concentrations to ciprofloxacin were obtained by agar dilution. Prevalences of CipR strains were determined, with corresponding confidence intervals (CIs). Between 2005 and 2009, 460 isolates were selected for molecular typing using Neisseria gonorrhoeae multiantigen sequence typing.
  
  
  RESULTS
  Between 2001 and 2006, the prevalence of CipR increased from 3.4% (95% CI, 1.3%-5.4%) to 44% (95% CI, 39%-50%). However, in 2007 prevalence began to decrease, reaching 9.6% (95% CI, 6.0%-13%) by 2009. Of the 203 strain types identified between 2005 and 2009, 126 genogroups of closely related strain types were formed (varying by ≤1% at both target loci). Levels of CipR within the data set correlate with the prevalence of 3 major genogroups (G): G437, G1407, and G3112.
  
  
  CONCLUSIONS
  Molecular typing reveals that CipR within the tested population is maintained by strain turnover between resistant genogroups. Despite early recommendation in 2002 to stop ciprofloxacin use in California, CipR in SF increased through 2006. The subsequent decrease in CipR corresponds with the 2007 national recommendation to cease ciprofloxacin treatment of gonorrhea, which suggests that national recommendations are potentially more effective at reducing CipR than regional recommendations in areas with high strain turnover.
authors.affiliation: From the *Department of Biology, Santa Clara University, Santa Clara, California; †Harvard School of Public Health, Boston, MA; ‡San Francisco Department of Public Health Labs, San Francisco, CA; §Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA.
authors.forename: Kiana
authors.initials: K
authors.lastname: Espinosa
authors.forename: Jason A
authors.initials: JA
authors.lastname: Park
authors.forename: Jillian J
authors.initials: JJ
authors.lastname: Gerrity
authors.forename: Sean
authors.initials: S
authors.lastname: Buono
authors.forename: Alexandria
authors.initials: A
authors.lastname: Shearer
authors.forename: Cindy
authors.initials: C
authors.lastname: Dick
authors.forename: Mae Ling
authors.initials: ML
authors.lastname: Mak
authors.forename: Kyla
authors.initials: K
authors.lastname: Teramoto
authors.forename: Jeffrey D
authors.initials: JD
authors.lastname: Klausner
authors.forename: Mark
authors.initials: M
authors.lastname: Pandori
authors.forename: David
authors.initials: D
authors.lastname: Hess
mesh_terms: D000328:Adult; D002939:Ciprofloxacin / Q000494:pharmacology*; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics*; D024841:Fluoroquinolones / Q000494:pharmacology*; D006069:Gonorrhea / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D017720:Molecular Epidemiology; D058889:Molecular Typing / Q000379:methods*; D009344:Neisseria gonorrhoeae / Q000187:drug effects* / Q000302:isolation & purification; D010641:Phenotype; D011159:Population Surveillance; D015995:Prevalence; D011634:Public Health; D012495:San Francisco / Q000453:epidemiology; D016896:Treatment Outcome
chemical_list: D024841:Fluoroquinolones; D002939:Ciprofloxacin