In this study, we evaluated the demographic characteristics, laboratory parameters, clinical outcomes, and mortality-related factors of 356 patients with SAB over eight years. The frequency of hospital-acquired SAB was 83.5% indicated an important clinical concern for nosocomial infections. This percentage is significantly higher than previously reported in large multicenter studies. For instance, Austin et al. reported a hospital-acquired SAB rate of 30% among 2,139 patients, while Le Moing et al. found a rate of 54% among 2,091 patients17,18. The higher rate of hospital-acquired SAB in our study may be related to the differences in patient characteristics, the frequent use of invasive procedures, antimicrobial stewardship policies, or high clinical workload among healthcare staff. The mortality rates were similar between community-acquired and hospital-acquired SAB in our study, consistent with previous studies19.
Our study’s methicillin resistance rate was 29.5% which aligns closely with the World Health Organization’s 2021 surveillance data for Turkey, reporting a rate of 31%20. The studies of Yılmaz et al. and Basetti et al. revealed that the rates of MRSA bacteremia were 39.2% and 54%, respectively21,22. These variations could be attributed to differences in healthcare settings, infection control measures, and patient populations.
Our findings showed that severe comorbid conditions, particularly hematologic malignancies such as leukemia, may significantly contribute to poor outcomes, even outside the ICU setting. Pneumonia as a primary focus of infection was also strongly associated with increased mortality. This may be related to delayed diagnosis, respiratory complications, and suboptimal treatment response. These findings highlight the importance of early identification of high-risk patients and prompt, targeted management, even outside the ICU setting. Most studies on SAB have been conducted in patients hospitalised in the intensive care unit (ICU) and non-ICU hospital wards3,21. However, we intentionally excluded patients in intensive care units from our analysis to focus on the other risk factors, thereby providing a comprehensive understanding of SAB.
According to some studies, males are more likely to develop SAB than females, but females may have a higher mortality rate6,21,22. However, in a large study by Kang et al. involving 1,974 patients, SAB-related mortality was similar between males (21.2%) and females (21.9%), with no statistically significant difference (p = 0.786)23. In our cohort, 58% of the patients were male, and the 30-day mortality rates were 7.69% in men and 6.75% in women. Consistent with previous findings, we observed no significant difference in outcomes based on sex.
The 30-day mortality rates have been reported to range from 15.3 to 21.5% in different series19,21,22,24. In our study, the 30-day all-cause mortality was 7.3%, suggesting a possible decline in SAB-related mortality. Some of these differences may be explained by variations in study design and patient characteristics, including differences in standards of care, underlying comorbidities, and advanced age.
We found the 30-day and in-hospital mortality rates similar in the MSSA and the MRSA bacteremia, consistent with some other studies19,25. Cosgrove et al. and Blot et al. showed that mortality rates were significantly higher for the MRSA group than the MSSA group (OR,1.93; 95% CI,1.54–2.42; p < 0.001), [OR,1.93; 95% CI,1.18 to 3.18; p = 0.009]7,26. A possible explanation for the similar mortality rates is the growing awareness of MRSA infection management through education of healthcare workers and continuous surveillance of SAB for effective treatment, and measuring effectiveness in our hospital. We cannot rule out that in some patients, the final cause of death was not an uncontrolled infection but the deterioration of the patient’s underlying comorbidities as a result of the infection.
Previous research has shown that the mortality rates in SAB rise with increased age, comorbidity load, and comorbid disorders22,27,28. In our study, the median CCI score was significantly higher in non-survivors compared to survivors (p < 0.001). Similarly, studies by Sharma et al. and la Vega et al. have found no association between comorbidity assessed by the CCI (p = 0.157, p = 0.144 )29,30. In contrast, Lesens et al. and Kim et al. reported a significant link between higher CCI scores and increased 30-day mortality in patients with SAB3,25.
Improving SAB-related outcomes requires a better understanding of risk factors and optimization of timely diagnosis and appropriate treatment strategies31. Differences in comorbidities profiles may partly explain the differences in reported mortality rates. SAB-related mortality differs according to the primary focus of infection, with the highest rates observed in patients with bacteraemic pulmonary infections19,32. In our study, patients with pneumonia demonstrated a mortality rate of 42.3%. Pneumonia significantly increased the risk of 30-day mortality, with a hazard ratio of approximately 15. (Table 1). These findings are consistent with some other studies showing high staphylococcal pneumonia mortality rates33,34,35,36. The proportion of patients presenting with sepsis was significantly higher among non-survivors compared to survivors (30.8% vs. 8.8%, p = 0.003) in our study like in previous studies10,31. Our findings emphasise the importance of detecting and managing deep foci of infection as soon as SAB is identified.
Furthermore, the site of SAB and source control are crucial for clinical outcomes.
Our findings, particularly identifying NLR, CRP, and albumin as independent predictors of 30-day mortality, have practical implications for patient care. These findings suggest that CRP and albumin may serve as useful biomarkers in predicting short-term mortality in patients with SAB. This is consistent with previous literature reporting the prognostic value of inflammatory markers in bloodstream infections37.
In addition to the infection focus, inflammatory biomarkers may help identify patients at increased risk of mortality. High NLR values are associated with a worsening prognosis regarding morbidity or mortality38. In the study of Greenberg et al., the NLR was associated with increased mortality in SAB (OR, 1.93; 95% CI 1.17–3.17, p = 0.01)39. In our study, NLR, CRP, and albumin were all found to be independent predictors of 30-day mortality. Similarly, Jacobsson et al. found CRP and albumin predictors of SAB mortality (p = 0.015, p = 0.023)36. These findings underscore the importance of identifying patients with SAB who are at high risk for mortality to provide timely and effective therapies.
This study had several limitations. First, because it was designed retrospectively, it was not possible to avoid selection and evaluation biases. Second, the data were collected from a single center, which may reduce the generalizability of the results. Furthermore, due to the retrospective design and the limited availability of detailed medical records, we were unable to obtain vital signs or other clinical information needed to assess the severity of sepsis. Despite these limitations, the study had several strengths. It focuses on patients with SAB who were treated in non-ICU wards, a category that is not frequently investigated. Furthermore, additional laboratory parameters were included in the multivariate analysis, which strengthens the findings. While this study offers valuable insights into the clinical course and outcomes of patients with SAB, the findings should be interpreted with caution and validated by future prospective, multicenter studies.
