Culture independent detection of chlorhexidine resistance genes qacA/B and smr in bacterial DNA recovered from body sites treated with chlorhexidine containing dressings

Md Abu Choudhury 1,2,3,4, Hanna Sidjabat 4, Irani Rathnayake 5, Nicole Gavin 1,2,6, Raymond Chan 1,2,5,6, Shahera Banu 5, Flavia Huygens 5, David Paterson 4, Claire Rickard 1,2,6,
David McMillan 2,3

NHMRC Centre of Research Excellence in Nursing (NCREN), Menzies Health Institute Queensland, Griffith University, Brisbane, QLD, Australia

Alliance for Vascular Access Teaching and Research, Griffith University, Brisbane, QLD, Australia

Inflammation and Healing Research Cluster, School of Health and Sports Sciences, University of the Sunshine Coast, Sippy Downs, Brisbane, QLD, Australia

University of Queensland Centre for Clinical Research, Royal Brisbane and Women’s Hospital Campus, Brisbane, QLD, Australia

Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia

Royal Brisbane and Women’s Hospital, Brisbane, QLD, Australia


Chlorhexidine gluconate (CHG) containing dressings are increasingly used in clinical environments for prevention of infection at central venous catheter insertion sites. Increased tolerance to this biocide in Staphylococci is primarily associated with the presence of qacA/B and smr genes.  Here we used a culture independent method to assess the prevalence of these genes in 78 DNA specimens recovered from the skin of 43 patients at catheter insertion sites in the arm that were covered with CHG-dressings. Of the 78 DNA specimens analysed, 52 (67%) possessed qacA/B and 14 (18%) contained smr; all sample positive for smr were also positive for qacA/B.  These prevalence rates was not statistically greater than that observed in a subsample of specimens taken from non-CHG treated arms. A statistically greater proportion of specimens with greater than 72 hours exposure to CHG dressings were qac-positive (p= 0.04), suggesting the patients were contaminated with bacteria or DNA containing qacA/B during their hospital stay. The presence of qacA/B was also positively associated with the presence of DNA specific for S epidermidis and S. aureus in these specimens. Our results show that CHG-genes are highly prevalent on hospital patients’ skin, even in the absence of viable bacteria.

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