Discussion

This study provides the most comprehensive report of CLABSI burden and pathogen susceptibility in Australia to date, with an analysis of time trends over the last decade. The data set is representative of adult ICU in Victoria, which comprises approximately 20% of ICU beds in Australia. ^{Reference Litton, Huckson and Chavan11} This report provides new insights into previously reported data from 2009 to 2013. ^{Reference Worth, Spelman, Bull, Brett and Richards8} We demonstrate a decreasing incidence of CLABSI in adult ICU settings, which plateaued in 2015. Although overall incidence has decreased, the burden of infections due to CNS has proportionally increased. Notably, we did not identify any significant time trend increases in antimicrobial-resistant organisms, including MRSA, vancomycin-resistant E. faecium, and extended-spectrum beta-lactamase (ESBL)-producing Enterobacterales. These findings are relevant for identifying priorities and suitable approaches to CLABSI prevention in Victorian adult ICU.

The trend we observed of decreasing central-line infections in adult ICU is consistent with trends reported internationally. ^{Reference Novosad, Fike and Dudeck7,12} This observed reduction in CLABSI rates corresponded to the introduction of CLABSI surveillance in Victorian hospitals in 2002, ^{Reference Worth, Spelman, Bull, Brett and Richards8} the inclusion of CLABSI as a key performance indicator for Victorian hospitals in 2008, ¹³ and the promotion and implementation of bundles of care for prevention by local hospital-level initiatives and release of guidelines on management of central lines by Australia New Zealand Intensive Care Society in 2012. ^{Reference Entesari-Tatafi, Orford, Bailey, Chonghaile, Lamb-Jenkins and Athan14,15} Reported rates are much lower than other countries with less developed programs of surveillance and infection prevention. ^{Reference Mathur, Malpiedi and Walia16,Reference Zeng, Wu, Li and Jia17}

Other studies have reported changes in patterns of pathogens in non-Australian ICU over time. US ICU participating in Centers for Disease Control and Prevention’s National Healthcare Safety Network surveillance reported a significant reduction in S. aureus incidence rates from 2006 to 2010 ^{Reference Fagan, Edwards, Park, Fridkin and Magill18} and a significant reduction in CNS and S. aureus with an increase in Candida spp./yeast CLABSIs in adult ICU from 2011 to 2017. ^{Reference Cronin, Poy Lorenzo and Olenski5} In US adult ICU in 2017, the most frequently reported pathogens were Candida spp./yeast (25.1%), followed by Enterococcus spp. (16.9%), CNS (13.8%), and S. aureus (9.1%) ^{Reference Weiner-Lastinger, Abner and Edwards19} . We previously reported significant reductions in Enterococcus spp., S. aureus, and CNS in the VICNISS adult ICU cohort from 2009 to 2013, with the most frequently identified pathogens being Enterococcus spp. (26.3%), Candida spp. (15.4%), S. aureus (13.3%), and CNS (10.4%). ^{Reference Worth, Spelman, Bull, Brett and Richards8}

From 2011 to 2022, we observed a reduction in the total number of pathogens in adult ICU corresponding to a decrease in CLABSI rates. However, we report significant increases in the proportion of CNS with over 1 in 5 CLABSI events attributed to CNS pathogens since 2014. These events were identified using internationally accepted surveillance criteria specifically developed to distinguish CLABSI events from potential contaminants (ie, requirement for 2 or more positive blood cultures to confirm infection). The contribution of CNS pathogens to CLABSI events is comparable to, or higher than, those reported by others using comparable surveillance methodology (the United States 14%, Scotland 19%, Belgium 19%). ^{Reference Novosad, Fike and Dudeck7,20} Potentially contributing factors include lapses in infection prevention measures such as hand hygiene, aseptic technique, and transmission-based precautions, which are amenable to targeted interventions.

We have not observed increasing rates of antimicrobial-resistant MRSA or E. coli; however, we report persistently high rates of vancomycin-resistant E. faecium in the Victorian ICU. The proportion of vancomycin-resistant E. faecium isolated from our CLABSI cohort between 2017 and 2022 (61.5%–62.5%) is much higher than national data in 2020–2021 (12.5%–15.2%) but similar to data from their Victorian laboratories (61.6%–64.2%), where two-thirds are vanB type ²¹ . The proportion of E. coli resistance to ceftriaxone isolated from our CLABSI cohort between 2017 and 2022 (20.0%–22.2%) is higher than that reported in the Victorian cohort from national surveillance data in 2020–2021 (13.0%–17.0%) ²¹ . The proportion of MRSA isolated from our CLABSI cohort between 2017 and 2022 (15.8%–20.0%) is similar to that reported in the Victorian cohort from national surveillance data in 2020–2021 (approximately 12%–15%) ²¹ . Our reports of higher rates of resistance in E. faecium and E. coli than national surveillance reporting reflect different patient cohorts; although our data are derived from clinical infections attributed to healthcare intervention, national surveillance data are derived from sentinel pathology services around Australia and include hospital or community isolates and clinical or surveillance isolates. As community MRSA rates in Victoria are similar to hospitals, although ESBL E. coli and VRE rates are more common in hospitals, the differences in patient population are likely to partially account for our higher rates of resistance compared with national surveillance.

Our findings support the use of targeted approaches to further reduce CLABSI rates in Victorian ICU. CLABSI prevention approaches have involved the use of multimodal intervention bundles focused on CVC insertion and maintenance practices. ^{Reference Blot, Bergs, Vogelaers, Blot and Vandijck4,Reference Entesari-Tatafi, Orford, Bailey, Chonghaile, Lamb-Jenkins and Athan14} Not all bundles incorporate equivalent components, and these may need to be reviewed to determine if they are effective and optimal for addressing current-era pathogens and antimicrobial resistance. The risk of CLABSI caused by skin organisms such as CNS and S. aureus can potentially be mitigated by improvements in hand hygiene, aseptic technique, and chlorhexidine bathing. CLABSI caused by Enterobacterales may warrant novel approaches to active surveillance and isolation policies, environmental cleaning, and antimicrobial stewardship to further mitigate risk. The use of antiseptic or antimicrobial-impregnated devices is currently recommended as an additional strategy reserved for adult ICU settings with high CLABSI rates. ^{Reference Buetti, Marschall and Drees1} New interventions introduced into ICU settings to reduce the risk of HAI require careful consideration of their potential impact on environmental antimicrobial resistance against individual patient benefit. An example of this would be selective decontamination of the digestive tract in the treatment of critically ill patients. A meta-analysis ^{Reference Hammond, Myburgh and Seppelt22} showed that selective decontamination of the digestive tract with intravenous antibiotics reduced the risk for in-hospital mortality, ventilator-associated pneumonia, and ICU-acquired bacteremia.

Our evaluation of antimicrobial resistance in CLABSI pathogens can be used to assist local CLABSI treatment approaches. International guidelines support the use of empirical vancomycin for suspected device-related bloodstream infections, which is underpinned by our data where vancomycin would adequately cover many gram-positive organisms including MRSA and CNS but not VRE. We propose that the use of antibiotic agent/s to empirically cover antimicrobial-resistant organisms such as VRE and ESBL Enterobacterales should be based on local antimicrobial susceptibility data. Our findings highlight the need for healthcare facilities in our region to review local epidemiology and antibiotic susceptibility of infections to support appropriate prescribing practices.

A limitation of our study is the use of phenotypic antimicrobial resistance reports, rather than genotyping, to define antimicrobial-resistant pathogens responsible for CLABSI. Furthermore, we were not able to report on resistance trends in intrinsically sensitive Candida spp. such as C. albicans, due to missing data on fluconazole susceptibility. Although the evaluation of the relationship between CVC insertion and maintenance practices and infection burden was beyond the scope of the current study, we acknowledge this as a priority for future research to identify the impact of clinical practice on infection burden and pathogens.

Optimal infection prevention and control practices and implementing antimicrobial stewardship are essential measures to prevent HAI and the emergence of antimicrobial resistance in ICU. Further understanding of the burden and incidence of CLABSI, and changes in pathogen and resistance patterns, contributes to inform targets for future CLABSI prevention approaches. Although CLABSI rates in our region have continued to decline over recent years, the proportion attributable to CNS has increased, and novel approaches are required to specifically reduce risks for CNS infection.