To our knowledge this is the first study to show a significantly higher prevalence of HCW colonization during EMRSA-15 outbreaks compared to Aus2/3-EMRSA outbreaks. Few prior studies provide details of the EMRSA strain type and a comparison of the prevalence of both patient and HCW colonization. Our study suggests MRSA strains vary in their ability to colonize HCWs and contribute to outbreaks. EMRSA-15 has become the predominant HA-MRSA in Australia and many other countries, so our results have implications for daily practice. We therefore believe MRSA typing should be determined during outbreaks to influence decisions on HCW screening and decolonisation and should be reported in infection control publications, to better determine the influence of MRSA type on outbreak characteristics and control.
A German study comparing MRSA carriage between staff and residents at a nursing home found more carriage of a PVL-positive strain (7.6% of 197 residents and 5.8% of 104 staff) compared with a multidrug resistant MRSA strain (3.0% of 197 residents and 1% of 104 staff). Although this study was not specifically designed to compare patient and HCW MRSA carriage rates based on ST type, it also suggests that HCW carriage rates vary between EMRSA ST types. We could not find any other studies specifically designed to address the question of variable HCW MRSA carriage rates by sequence type.
The prevalence of HCW colonization (3.4% EMRSA-15 and 0.81% Aus2/3-EMRSA) in our study was lower than other published Australia and New Zealand studies. This is probably attributable to our longstanding state-wide, “search and destroy” MRSA management policy that includes screening of high risk patients, aggressive outbreak management policies and strict isolation and contact precautions for patients with epidemic HA-MRSA colonization. The decrease in proportion of patients colonized over the study period suggests measures introduced to control MRSA transmission have been successful at RPH. However the proportion of HCWs colonized remained stable over the same period, suggesting control measures other than those designed to limit transmission via HCWs are responsible for the reduced proportion of colonized patients. This implies hand hygiene and methods to prevent transmission to HCWs should remain an ongoing focus of outbreak management. At RPH hand hygiene compliance rates were poor when a formal hand hygiene auditing program was first introduced in February 2008 – 40% across all HCW groups (personal communication, Rosie Lee).
The majority of colonized HCWs in this study were nursing staff, followed by PCAs. These two groups should remain a focus for education in outbreak management plans. A MRSA HCW prevalence study performed at RPH also showed highest levels of colonization in HCWs most in contact with patients – 6.8% of patient care assistants and 5.2% of nursing staff, compared with 0.7% of doctors. No agency nursing staff in our study were colonized despite representing a large proportion of nursing staff, possibly as a result of the low numbers who were available or agreed to be screened (results not presented). This finding may have introduced bias and suggests that strategies need to be developed to enable a larger proportion of agency staff to be screened to determine if they are an unidentified reservoir of MRSA transmission, particularly as they more commonly work at multiple hospitals and residential care facilities. All HCWs from outside of WA undergo pre-employment MRSA screening and decolonization, so any increase in HCWs transferring from EMRSA-15 endemic hospitals is unlikely to explain the increased HCW EMRSA-15 colonization rates.
Potential limitations of this study are the retrospective design and the small numbers of outbreaks and low colonization rates, but despite this our findings were statistically significant. Microbiology methods changed over the study period, which may have increased MRSA detection rates in the latter years of the study when EMRSA-15 predominated. Aus2/3-EMRSA has been noted anecdotally at RPH to preferentially colonize the perineum. The perineum was not screened in HCWs, so if this association is true then Aus2/3-EMRSA colonisation of HCWs may have been underestimated. A significant number of HCWs were not contactable or declined MRSA screening during each outbreak, which may have introduced bias, although the percentage of HCWs not screened was similar during EMRSA-15 and Aus2/3-EMRSA outbreaks. S. aureus carriage can be transient and HCWs in our institution are given decolonization therapy prior to any repeat screening, so this could have created biases within our dataset. Transient MRSA colonization rates in HCWs (32%) are known from a prior prevalence study at RPH. Changes to outbreak investigation policy in 2004 meant non-EMRSA-15 outbreaks were investigated only when a fourth patient was found colonized which may have caused a delay in HCW screening and less instigation of HCW screening during Aus2/3-EMRSA outbreaks. However, only one Aus2/3-EMRSA outbreak involved HCW screening after this guideline change, consequently this is unlikely to have affected the results. Increased awareness of MRSA amongst HCWs and improved infection control team EMRSA outbreak management over the decade should have reduced HCW colonization in the later stages of the study when EMRSA-15 became the predominant outbreak strain, nonetheless our HCW colonization rates remained higher during EMRSA-15 outbreaks.
The reasons for increased EMRSA-15 colonization of HCWs are largely unknown. Biologically plausible explanations include that EMRSA-15 carries fewer resistant traits, a smaller SCCmec element and “core” genome, together with the acquisition of additional accessory genomic elements may have conferred to this particular clone higher epidemicity and growth rate, greater biofilm formation, enhanced capacity for dissemination and invasion and ability to persist that might explain its greater success and fitness. Therefore, potential factors promoting colonization of HCWs by EMRSA-15 includes its preferential colonization of sites on patients likely to contaminate HCWs (e.g. skin or wounds, in preference to perineum), increased transmission into the environment, ability to adhere to skin and environmental surfaces and replication ability. The mechanisms by which EMRSA-15 leads to higher HCW colonization rates should be of foremost importance in future research studies.