title: Selection for qacA carriage in CC22, but not CC30, methicillin-resistant Staphylococcus aureus bloodstream infection isolates during a successful institutional infection control programme.
abstract: OBJECTIVE
  The increasing use of chlorhexidine for methicillin-resistant Staphylococcus aureus (MRSA) decolonization raises concerns about reduced susceptibility. We evaluated the carriage of chlorhexidine resistance genes and chlorhexidine susceptibility in MRSA before and after introduction of an institutional MRSA control programme incorporating chlorhexidine-based decolonization in 2004.
  
  
  METHODS
  MRSA bloodstream infection (BSI) isolates identified between 2001 and 2009 were tested for spa and staphylococcal cassette chromosome mec type and carriage of qacA, qacB and smr. Selected isolates were tested for chlorhexidine susceptibility. Logistic regression was used to evaluate associations between clone type, carriage of resistance genes and chlorhexidine susceptibility. Temporal trends in qacA or smr carriage were analysed using separate binomial generalized linear models.
  
  
  RESULTS
  Typing identified two dominant clones: CC22 (n = 224) and CC30 (n = 197). Annual MRSA BSI rates declined from 2004, although the rate of decline for CC22 was slower than for CC30. Carriage of qacA and smr and having a chlorhexidine MIC ≥2 mg/L did not increase overall amongst MRSA BSI isolates; however, qacA carriage increased in CC22 compared with in CC30 (OR, 7.21; 95% CI, 1.32-39.17). Furthermore, qacA+ CC22 isolates were more likely to have a chlorhexidine MIC ≥2 mg/L than qacA+ CC30 isolates (OR, 21.67; CI, 2.54-185.20).
  
  
  CONCLUSIONS
  A successful infection control programme was associated with the selection of qacA linked with a higher chlorhexidine MIC in one dominant endemic MRSA clone (CC22), but not another (CC30). The slower reduction in the CC22 MRSA BSI rate suggests that carriage of qacA confers a selective advantage, with implications for the sustainability of decolonization practice.
authors.affiliation: Centre for Clinical Infection and Diagnostics Research (CIDR), Department of Infectious Diseases, King's College London & Guy's and St Thomas' NHS Foundation Trust, London, UK. jonathan.edgeworth@gstt.nhs.uk
authors.forename: Jonathan A
authors.initials: JA
authors.lastname: Otter
authors.forename: Amita
authors.initials: A
authors.lastname: Patel
authors.forename: Penelope R
authors.initials: PR
authors.lastname: Cliff
authors.forename: Eugene P
authors.initials: EP
authors.lastname: Halligan
authors.forename: Olga
authors.initials: O
authors.lastname: Tosas
authors.forename: Jonathan D
authors.initials: JD
authors.lastname: Edgeworth
mesh_terms: D016470:Bacteremia / Q000382:microbiology; D001426:Bacterial Proteins / Q000235:genetics*; D002710:Chlorhexidine / Q000494:pharmacology*; D004202:Disinfectants / Q000494:pharmacology*; D024881:Drug Resistance, Bacterial; D005838:Genotype; D006801:Humans; D017053:Infection Control / Q000379:methods*; D026901:Membrane Transport Proteins / Q000235:genetics*; D055624:Methicillin-Resistant Staphylococcus aureus / Q000145:classification / Q000187:drug effects* / Q000235:genetics / Q000302:isolation & purification; D008826:Microbial Sensitivity Tests; D017720:Molecular Epidemiology; D058889:Molecular Typing; D012641:Selection, Genetic; D013203:Staphylococcal Infections / Q000382:microbiology*
chemical_list: D001426:Bacterial Proteins; D004202:Disinfectants; D026901:Membrane Transport Proteins; C068498:qacA protein, Staphylococcus aureus; D002710:Chlorhexidine