Issue: February 2010
February 01, 2010
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Chlorhexadine-based antiseptic may interrupt transmission of certain MRSA strains

Issue: February 2010
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Treatment with a chlorhexadine-based antiseptic may have reduced transmission of endemic strains of methicillin-resistant Staphylococcus aureus in intensive care by 70%, according to results of a recent study.

Results of this study also indicated that strains of MRSA carrying qacA/B genes may either be unaffected or spread more rapidly as a result of antiseptic treatment.

Researchers from several institutions in Thailand and the United Kingdom analyzed interrupted time-series data on MRSA acquisitions in two 15-bed ICUs. The aim was to determine the estimated impact of sequential introduction of an educational campaign, cohorting and a chlorhexadine-based antiseptic protocol on transmission rates of endemic MRSA and an outbreak strain of MRSA with sequence type 239. The researchers assessed isolates for carriage of qacA/B genes and susceptibility to the antiseptic.

The antiseptic protocol was associated with a highly significant, immediate 70% reduction in acquisition of endemic MRSA strains, according to the results. The estimated model-averaged incidence rate ratio for that association was 0.3 (95% CI, 0.19-0.47).

Use of the antiseptic protocol also was as associated with an increase in the acquisition of sequence-type 239 MRSA. That association had an estimated model-average incidence rate ratio of 3.85 (95% CI, 0.80-18.59).

Weak evidence of associations between the other study interventions and MRSA transmission was observed.

There were 21 MRSA isolates with the 239 sequence, all of which carried the chlorhexadine resistance loci qacA/B. Among 21 endemic MRSA isolates, <5% (1 of 21) carried the gene.

Results of an in vitro analysis indicated that the minimum bactericidal concentrations of sequence-type 239 strains were threefold higher than other strains. In vivo analysis indicated that only patients with the sequence-type 239 strains demonstrated a reduction in the number of colonization sites in response to treatment with chlorhexadine.

Batra R et al. Clin Infect Dis. 2010;50:210-217.