Universal versus targeted chlorhexidine and mupirocin decolonisation and clinical and molecular epidemiology of Staphylococcus epidermidis bloodstream infections in patients in intensive care in Scotland, UK: a controlled time-series and longitudinal genotypic study.

Summary

In two ICUs with divergent policies, de-escalating from universal to targeted decolonisation did not increase overall bloodstream infections but significantly reduced MRSE-BSI incidence and the proportion of multidrug-resistant sequence types. MRSE-BSI incidence was positively associated with chlorhexidine use, suggesting selection pressure from universal biocide exposure.

Key Findings

• De-escalation at ICU1 reduced MRSE-BSI incidence from 10.4 to 4.3 per 1000 occupied bed days with no rise in overall BSI; no parallel changes occurred at the control ICU.
• The probability that SE-BSI were MRSE fell from 89.2% to 56.7% after de-escalation.
• MRSE-BSI incidence density correlated positively with chlorhexidine use but not with mupirocin.
• Genotyping (MLST and WGS) showed fewer multidrug-resistant sequence types and mobile genetic elements after de-escalation.

Clinical Implications

ICUs with low MRSA prevalence should consider shifting from universal to targeted decolonisation, monitor MRSE epidemiology, and rationalise chlorhexidine exposure to reduce selection of resistant S. epidermidis without increasing overall BSI.

Limitations

• Retrospective observational design susceptible to confounding
• Generalizability limited to two adjacent health boards and low-MRSA settings

Future Directions

Prospective multicentre or cluster-randomised evaluations of decolonisation strategies, dose-response of chlorhexidine exposure, and routine genomic surveillance to track resistance evolution.