Mortality associated with healthcare-associated Staphylococcus aureus bacteraemia in Aotearoa New Zealand

Staphylococcus aureus is a common cause of both community-acquired and healthcare-associated bacteraemia.¹ The mortality associated with S. aureus bacteraemia (SAB) is high, with an all-cause 30-day mortality rate of approximately 20% reported by most studies.^2–9

Healthcare-associated SAB (HA-SAB) has been monitored in Aotearoa New Zealand for over 20 years. In 2017 the Health Quality & Safety Commission Te Tāhū Hauora (HQSC) Infection Prevention and Control (IPC) programme assessed the accuracy of reporting of the HA-SAB rate. Changes were made to improve the quality of the data: bed days were provided from the National Minimum Dataset (NMDS) and an implementation guide was developed to support the IPC teams in determining the source of the infection.¹⁰ From June 2012 the rate was recalculated using the bed days from the NMDS.¹¹

In 2021, because of increasing rates of HA-SAB (Figure 1), the source of HA-SAB events was investigated. IPC teams were asked to provide the source of HA-SAB events occurring in their hospital from 1 January 2017 until 30 June 2021. There were 1,575 HA-SAB events reported during the 54-month period and the source data were provided for 1,369 (73%) events. Invasive medical devices were the source for 65% of events.¹² Since July 2022 the source of HA-SAB events has been collected and reported.

View Figure 1–3, Table 1.

Mortality associated with SAB occurs across all ages, but rates are lower in children.^6,13 Studies looking at mortality tend to include all SAB events and do not distinguish between healthcare-associated and community-acquired infections. Risk factors associated with mortality include age, female sex, admission to intensive care, high Charlson Comorbidity Index at presentation, prior antibiotic exposure and unknown source of infection.^2,3,5,8

We report the 30-day and 90-day all-cause mortality associated with HA-SAB events reported from all publicly funded hospitals in New Zealand over a 2-year period. The aim was to identify risk factors for HA-SAB associated with healthcare-related interventions and determine those associated with increased mortality at 30 and 90 days to inform prioritisation of quality improvement (QI) initiatives to reduce harm caused by HA-SAB.

Methods

Data from the national surveillance programme for HA-SAB, involving patients of all ages, with HA-SAB events between July 2022 and June 2024, were provided by the HQSC.

The de-identified HA-SAB events were reported quarterly to the HQSC by the IPC teams at each Health New Zealand – Te Whatu Ora district hospital. The case definition for HA-SAB and attribution of the source data is standardised.¹⁰ The IPC teams were asked to retrospectively provide the National Health Index (NHI) number for each patient. This allowed matching with the NMDS.

Age, sex, ethnicity, source of HA-SAB and methicillin susceptibility were recorded, and 30- and 90-day all-cause mortality was determined. The rate of HA-SAB was calculated per 1,000 bed days. The bed days were provided by the Ministry of Health – Manatū Hauora’s NMDS using the monthly inpatient admission and discharge data. The number of HA-SAB events associated with each variable was reported as a percentage of all HA-SAB events.

Ethical review was not required as this work is part of a national quality improvement initiative.

Statistical analysis was performed using R statistical software (version 4.5.0, R Core Team, Vienna, Austria).

Results

Over the 24-month period there were 966 HA-SAB events reported to the HQSC, but only 961 HA-SAB events were matched with the NMDS. The five excluded events were either duplicate cases due to patients moving between districts or events where the wrong NHI number was provided. The date of extraction was 22 April 2025.

The national rate of HA-SAB events over this 2-year period was 0.15 HA-SAB per 1,000 patient bed days. The age range was less than 1 year to greater than 85 years. HA-SAB events were more common in males: 608 (63.5%). The 30- and 90-day all-cause mortality were 13.8% and 20.7%, respectively (Table 1).

Both the 30- and 90-day mortality rate increased with age (Figure 2 and Figure 3). Using the 15–24-year-group as the reference, at 30 and 90 days this increase was significant for patients ≥75 years of age; odds ratio (OR) 12.1 (95% confidence intervals [CI] 1.6–90.3, P<0.005) and OR 20.3 (95% CI 2.7–150.0, P<0.001), respectively.

The ethnicity of patients with HA-SAB and the 30- and 90-day all-cause mortality are shown in Table 1. There was no difference in mortality by ethnicity.

Seventy percent (n=673) of HA-SAB events were associated with the use of invasive medical devices, of which 324 (48.2%) were associated with peripheral intravascular catheters (PIVC), 290 (43.1%) were due to central vascular catheters (CVC) and 59 (8.7%) were due to other devices. The other sources for HA-SAB events were: organ source, 115 (12%); surgical site infection, 79 (8%); unknown, 57 (6%); associated with neutropaenic sepsis, 14 (1.5%); and another source, or not recorded, 23 (2.5%) (Table 1). Overall, 614 (64%) of HA-SAB were due to intravascular catheters. The 30- and 90-day mortality are reported in Table 1.

There were 199 deaths (Table 1). Two-thirds of the deaths occurred early, within 30 days of the event (133 [67%]), and the highest mortality rate at 30 days (32%) was seen when the source of the HA-SAB was unknown. There is no difference in mortality between PIVC and CVC (Table 1).

Almost 90% of S. aureus isolates, 842 (87.2%), were susceptible to methicillin. The rate of HA-SAB caused by methicillin-resistant S. aureus (MRSA) was lower in the Te Ikaroa (Central) and Te Waiponamu (South Island) health regions, compared to the rate in the Te Tai Tokerau (Northern) health region, OR (95% CI) 0.52 (0.31–0.89) P=0.023, and 0.23 (0.11–0.49) P<0.001, respectively. HA-SAB caused by MRSA were not associated with increased mortality (Table 1).

Discussion

The 30- and 90-day all-cause mortality for patients with HA-SAB in New Zealand is 13.8% and 20.7%, respectively. This rate is consistent with that reported for both community-acquired and healthcare-associated SAB in other countries and previously reported in national and Australasian data.^{3–7,14–19}

A review of predictors of mortality associated with SAB identified multiple factors that influence mortality.² Age is one of the strongest predictors, and this was seen in our study with a significantly higher 30- and 90-day mortality rate in those patients aged ≥75 years (Figure 2 and Figure 3). Increased mortality is also seen in those with a high Charlson Comorbidity Index, infection with MRSA, admission to intensive care and prior antimicrobial use.^3,8 We did not assess these clinical variables as the aim of this study was to focus on HA-SAB events occurring while receiving healthcare and the all-cause mortality associated with such events regardless of other contributing factors.

The incidence of staphylococcal infections, skin and soft tissue infections (SSTI), sepsis and pneumonia is higher in males than females in New Zealand, and the difference is most marked for staphylococcal sepsis (relative risk 1.9; 95% CI 1.8–2.0).²⁰ Other studies also report that SAB events are more commonly seen in males. However, the mortality rate has been reported to be higher in females.^2,21 Two-thirds (64%) of HA-SAB events occurred in males in our study; however, there was no difference in the 30- and 90-day mortality between males and females (Table 1).

There was no difference in the mortality rate by ethnicity (Table 1). A previous study looking at the longitudinal trends over an 11-year period for S. aureus disease across New Zealand showed marked ethnic and socio-economic differences for staphylococcal SSTI, staphylococcal pneumonia and staphylococcal sepsis, with the incidence of all disease types highest among Māori and Pacific peoples. Māori were three times more likely and Pacific people were almost five times more likely to have S. aureus SSTI than Europeans.²⁰ Whether Māori and Pacific people across all ages admitted to hospital have higher rates of colonisation with S. aureus, and therefore are at a greater risk of healthcare-associated infections including HA-SAB, is not known.

Invasive medical devices were the source for 70% of the events, with a 12.5% mortality rate at 30 days. Importantly, the 30-day mortality for PIVC and CVC were 14.5% and 10.0%, respectively. This rate is similar to a previous local study where approximately 10% of patients with HA-SAB associated with the use of PIVC died.²²

Up to 50% of HA-SAB may be preventable.^11,23 There are recently-updated evidence-informed guidelines on best practice for the prevention of bloodstream infections and other infections associated with peripherally inserted vascular catheters.²⁴

The highest mortality rate was seen in patients where the source for the HA-SAB was unknown. This may have been because the patient died before any investigations to determine the source could be performed, the patient had significant comorbidities and treatment was withdrawn avoiding unnecessary investigations, or the likely source was poorly recorded in the medical notes. We did not investigate this further, but the programme actively encouraged discussion of such cases with the clinical team to best determine a likely source for the HA-SAB.

The number of events caused by MRSA was 12.4%, with rates higher in the northern regions of New Zealand. The reported rates of SAB caused by MRSA vary between countries, with the rate being less than five percent in the Netherlands,⁷ five percent in the United Kingdom,²⁵ less than one percent to greater than 50 percent in European countries,²⁶ 16.8% in Canada²⁷ and approximately 50% in centres in the United States of America (USA).^8,28 A recent systematic review of mortality associated with HA-SAB reported a higher 1-month mortality associated with MRSA, adjusted OR 1.04 (95% CI 1.02–1.06) per 10% increase in MRSA proportion.⁶ A large retrospective study looking at administrative readmission data capturing 49.3% of all US hospital admissions in 2014, reported a higher mortality rate with MRSA bacteraemia. The adjusted odds of in-hospital death were 15% greater with MRSA bacteraemia than methicillin-susceptible SAB (OR 1.15, 95% CI 1.07–1.23).²⁸ There was no difference in mortality rates for cases of MRSA in our study, and this is likely due to local MRSA strains being resistant to beta-lactam antibiotics and one or two other classes of antibiotic only—the so called “community MRSA phenotype”.

The strength of this study is that it included all inpatients with HA-SAB cared for in the 20 Health New Zealand – Te Whatu Ora district hospitals over a 2-year period. Other studies have been single-centred, ^5,9,13 USA state–wide,⁸ or multi-centred but with a maximum of eight hospitals,^3,4,7 and may have been subject to selection bias.

Our study included almost 1,000 HA-SAB events. This number may have been too small to show statistical difference as the CIs for the mortality related to the source of the HA-SAB were wide. It may also have been underpowered to determine if there was a difference in mortality associated with ethnicity. This programme is ongoing and future analysis may provide a more accurate assessment. We also chose to only look at a limited number of variables and there may have been other confounders such as pre-existing comorbidities, type of recent surgical or medical interventions and severity of illness at diagnosis, all contributing to the mortality rate.

In summary, we once again draw attention to the increasing number of HA-SAB events occurring in our population and the high mortality rate associated with HA-SAB, including those events associated with PIVC and CVC use. HA-SAB events are largely preventable, and implementation of nationally led quality improvement initiatives, guided by evidence-informed guidelines where available, are required to reduce this level of harm.²⁴ As over half of adult inpatients have a PIVC and 10% have a CVC, preventing vascular device-related HA-SAB should be a national priority.²⁹ We also need to support local participation in multinational or global clinical trials and networks, to address some of the challenging unanswered clinical questions associated with this devastating infection.³⁰