Abstract
Background
Infections caused by Klebsiella pneumoniae carbapenemase-producing K. pneumoniae (KPC-Kp) are increasingly contributing to mortality in ICU patients. The study aimed to evaluate outcomes, identify mortality predictors, and assess antibiotic strategies for treating KPC-Kp bloodstream infections (BSIs) in critically ill ICU patients.
Materials and methods
This retrospective study at Chang Gung Memorial Hospital, Taiwan, from January 2017 to December 2021, analyzed 168 adult ICU patients with KPC-Kp BSIs. All patients experienced respiratory failure and were on mechanical ventilation.
Results
The 30-day mortality rate was 61.9%. Patients who died had higher Pitt bacteremia (7.0 ± 2.6 vs. 4.2 ± 2.9, P < 0.001) and SOFA scores (12.0 ± 4.1 vs. 6.2 ± 3.8, P < 0.001), greater need for renal replacement therapy (27.9% vs. 9.4%, P < 0.002), and higher intra-abdominal infection prevalence (9.6% vs. 0%, P < 0.001). Lower platelet counts (93.7 ± 84.7 vs. 171.1 ± 120.2, P < 0.001) and higher CRP levels (131.3 ± 92.3 vs. 88.7 ± 81.0, P < 0.003) were observed in deceased patients. Multivariate analysis identified CRP levels and SOFA scores as independent mortality predictors, while ceftazidime-avibactam treatment and appropriate antibiotic therapy within 48 h post-BSI onset correlated with better outcomes.
Conclusions
Early appropriate antibiotic treatments and ceftazidime-avibactam use are crucial for reducing mortality in critically ill ICU patients.
Clinical trial number
Not applicable.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12879-025-12401-4.
Keywords: Blood-stream infections, Klebsiella pneumoniae carbapenemase, Carbapenem-resistant, Mortality rate, Appropriate antibiotic treatments, Critically ill patients
Introduction
Klebsiella pneumoniae is a Gram-negative bacillus, that is associated with high rates of mortality and morbidity in community acquired or health care acquired infections, particularly among patients with multiple comorbidities [1–3]. The widespread use of carbapenems for the empirical treatment of critical or severe infections had led to an increase in the numbers of multi-drug resistant and carbapenem-resistant strains [4]. The detection rate of carbapenemase in carbapenem-resistant K. pneumoniae (CRKP) in Taiwan ranges from 5% to 41.2%, whereas that in other countries is high as 45.4%-80% [5]. Compared with carbapenemase-susceptible K. pneumoniae infections, CRKP infections associated with a higher risk of fatal outcomes in immunosuppressed and critically ill patients [1, 6–9].
According to the Taiwan Centers for Disease Control [www.cdc.gov.tw], K. pneumoniae has been the leading cause of infections in the intensive care units (ICUs) of medical centers in Taiwan since 2018. The prevalence of CRKP infections in Taiwan’s ICUs increased from 14.4% in 2014 to 45.5% in 2023 [10]. CRKP predominantly caused blood stream infections (BSIs) and pneumonia.
CRKP can be classified into 2 major subgroups on the basis of phenotypic resistance: carbapenemase-producing and non-carbapenemase-producing CRKP. Carbapenemase-producing CRKP can hydrolyze penicillins, cephalosporins, monobactams, and carbapenems [11]. Carbapenemases can be divided into the following classes by using the Ambler classification method: Classes A, B, and D. K. pneumoniae carbapenemase (KPC) belongs to Class A, which includes serine β-lactamases that are challenging to be inhibited with traditional β-lactam inhibitors [12–14]. KPC is the most commonly acquired carbapenemases produced by K. pneumoniae and has gained importance globally over the past 2 decades [15]. In East Asia and Taiwan, KPC is the most predominant carbapenemase, followed by NDM and OXA-48 [1, 8, 16, 17]. In response to the emergence of KPC-producing K. pneumoniae (KPC-Kp), several novel antimicrobial agents (β-lactam/β-lactamase inhibitor combination) have been developed. These agents exhibit high efficacy for the management of KPC-Kp infections, but larger-scale studies are warranted to evaluate their effects on the survival of patients with KPC-Kp infections [11, 18].
Several studies have investigated risk factors for KPC-Kp BSIs; nevertheless, such studies have provided inconsistent and controversial conclusions, particularly in critically ill ICU patients. To address this issue, the aim of the present study was to analyze clinical outcomes, determine mortality predictive factors and assess therapeutic strategies involving currently available antibiotic regimens for treating KPC-Kp BSIs in critically ill ICU patients.
Materials and methods
Study design and patient selection
This study was conducted at Chang Gung Memorial Hospital, a tertiary medical center in northern Taiwan and having a capacity of 3700 beds. We retrospectively analyzed the data of ICU patients with KPC-Kp BSIs during the period from January 2017 to December 2021. Patients who met the following criteria were included in the study: being an adult (aged 18 years or over), having respiratory failure necessitating mechanical ventilation, and being admitted to the ICU. The study protocol was adhered to the tenets of the declaration of Helsinki and was approved by the Institutional Review Board at Chang Gung Memorial Hospital (Approval number: 201801433B0). All methods in this study were conducted in accordance with relevant guidelines and regulations.
Ethics approval and consent to participate
This study was reviewed and approved by the Institutional Review Board of Chang Gung Memorial Hospital (Approval number: 201801433B0). A waiver for written consent was obtained due to the retrospective nature of this study and the lack of modifications in patient management, so written informed consent for participation was not required in accordance with national legislation and institutional requirements.
Definitions and outcomes
We retrieved the patient’s information from their medical records, the hospital’s computerized databases, and clinical charts. We retrospectively recorded the patients’ demographic information, laboratory data, underlying conditions, ICU hospitalization duration, and antibiotic regimens. Moreover, comorbidities were evaluated and summarized using the Charlson comorbidity index (CCI), and severity of the BSIs was assessed using the Pitt bacteremia score and the sequential organ failure assessment (SOFA) score [19].
We established the following definitions before conducting our data collection and analysis processes. A KPC-Kp BSI was defined as the occurrence of a positive blood culture result for a KPC-Kp strain and the presence of clinical signs of systemic inflammatory response syndrome [20]. In the event of repeated episodes of KPC-Kp BSIs during the study period, only the data from the first episode were analyzed. Moreover, infection sites (lung, skin and soft tissue, central venous catheter, urinary tract, and abdomen) were defined as sites from which the collected cultures exhibited evidence of the same pathogen found in the blood cultures. The date of BSI onset was defined as the date on which a positive blood culture for a KPC-Kp strain was collected and clinical signs of systemic inflammatory response syndrome were identified. In addition, a primary BSI was defined as a BSI occurring in patients without an identifiable source of infection, determined at the time of culture collection. The length if ICU hospitalization was defined as the period from the date of ICU admission to the date of discharge from the ICU or death. The length of days from culture day to mortality day was also defined as the interval from the date of BSI onset to the date of death. Furthermore, appropriate antibiotic treatment within 24–48 h after BSI onset was defined as the administration of one or more antibiotics to which the KPC-Kp strain exhibited in vitro susceptibility within 24–48 h after BSI onset. Finally, antibiotic treatment within the previous 30 days was defined as the intravenous administration of antibiotics for at least 5 days within the 30 days preceding BSI onset.
The dosage of tigecycline was 100 mg loading and 50 mg twice daily. Colistin dosages were administered at the dosages of 360 mg of colistin base activity (CBA) daily in patients with normal renal function. The dosage of ceftazidime-avibactam was 2.5 g every 8 h. According to Taiwan Food and Drug Administration, colistin and ceftazidime-avibactam required dose adjustment for patients based on renal impairment.
The primary outcome of the study was the identification of predictive factors for mortality within 30 days after KPC-Kp BSI onset. The secondary outcomes analyzed the in-ICU and in-hospital mortality of these critically ill patients.
Microbiological studied, carbapenemase gene detection, and capsular typing
We used matrix-assisted lase desorption-time of flight mass spectrometry (MALDI-TOF-MS) for the identification and molecular analysis of K. pneumoniae in blood culture. We screened for carbapenemase genes (blaKPC, blaOXA− 48, blaNDM, blaVIM, and blaIMP) through a multiplex polymerase chain reaction (PCR) conducted using a DreamTaq system (Thermo Fisher Scientific, Vilnius, Lithuania). Moreover, we determined the minimum inhibitory concentration (MIC) of the tested antibiotics by a BD Phoenix ™ M50 automatic detection machine. MIC was classified according to breakpoints established by the Clinical and Laboratory Standards Institute (CLSI). Specifically, the MIC of either imipenem or meropenem for CRKP was determined to be ≥ 4 µg/mL and that of ertapenem for CRKP was determined to be ≥ 2 µg/mL.
Statistical analysis
We compared continuous variables by using the Student t test for normally distributed variables and the Mann-Whitney u test for non-normally distributed variables. Categorical variables were evaluated using a two-tailed Fisher exact test. Results are presented as median ± standard deviation or as percentages of the group from which that were derived (for categorical variables). We calculated odds ratios (OR) and 95% confidence intervals (CI) for all observed associations. We used two-tailed tests to determine statistical significance, with a p value of < 0.05 being considered statistical significance. Variables with p value of < 0.1 in our univariate analysis were included in our multivariate Cox regression model to identify independent predictors of mortality. We conducted a Kaplan-Meier survival analysis to analyze the difference in 30-day mortality. All statistical analyses were performed using the Statistical Package for the Social Sciences (Version 26.0; IBM Corp., Armonk, NY, USA).
Results
We identified a total of 560 patients with CRKP induced BSIs during the period from January 2017 to December 2021. We removed patients aged < 18 years, those without ICU admissions, and those without KPC-producing K. pneumoniae infections. Thus, 168 patients remained and were included for analysis (Fig. 1). All patients experienced respiratory failure and were on mechanical ventilation. Most of these patients (144, 85.7%) were admitted to the medical ICU, with the remaining 24 hospitalized in the surgical ICU. The median CCI, Pitt bacteremia score and SOFA score were 6.2 ± 3.1, 5.9 ± 3.0, and 9.8 ± 4.9, respectively. Acute kidney injury after BSI onset was observed in more than half of the patients (106, 63.9%), with one-third of these patients (35 patients) requiring continuous renal replacement therapy. Moreover, 134 (79.8%) patients had received intravenous antibiotics for at least 5 days within 30 days before KPC-Kp BSI onset. Table 1 presents the baseline characteristics of patients who did and did not survive within 30 days after BSI onset.
Fig. 1.
Study flow chart
Table 1.
Baseline characteristics and comorbidities of critically ill patients with Klebsiella pneumoniae Carbapenemase-producing K. pneumoniae induced blood-stream infections
| Total (N = 168) |
30-day survival (N = 64) |
30-day non-survival (N = 104) |
p-value | |
|---|---|---|---|---|
| Age, years, median | 68.4 ± 13.8 | 66.7 ± 12.8 | 69.5 ± 14.4 | 0.214 |
| Male, n (%) | 108(64.3%) | 41(64.1%) | 67(64.4%) | 0.963 |
| Patient source, MICU, n (%) | 144(85.7%) | 57(89.1%) | 87(83.7%) | 0.315 |
| Charlson comorbidity index, median | 6.2 ± 3.1 | 6.4 ± 3.5 | 6.1 ± 2.8 | 0.613 |
| Pitt bacteremia score, median | 5.9 ± 3.0 | 4.2 ± 2.9 | 7.0 ± 2.6 | < 0.001 |
| SOFA score, median | 9.8 ± 4.9 | 6.2 ± 3.8 | 12.0 ± 4.1 | < 0.001 |
| Acute kidney injury, n (%) | 106(63.9%) | 35(54.7%) | 71(68.3%) | 0.083 |
| Continuous renal replacement therapy, n (%) | 35(20.8%) | 6(9.4%) | 29(27.9%) | 0.002 |
| Previous 30-days antibiotic treated, n (%) | 134(79.8%) | 51(79.7%) | 83(79.8%) | 0.985 |
| Appropriate antibiotic treatment within 24 h, n (%) | 41(24.4%) | 17(26.6%) | 24(23.1%) | 0.612 |
| Appropriate antibiotic treatment within 48 h, n (%) | 89(53%) | 39(61.0%) | 50(48.1%) | 0.100 |
| Comorbidity | ||||
| Coronary artery disease, n (%) | 26(15.5%) | 14(21.9%) | 12(11.5%) | 0.092 |
| Heart failure, n (%) | 26(15.5%) | 11(17.2%) | 15(14.4%) | 0.633 |
| Chronic obstructive pulmonary disease, n (%) | 17(10.1%) | 6(9.4%) | 11(10.6%) | 0.803 |
| Autoimmune disease, n (%) | 13(7.7%) | 4(6.3%) | 9(8.7%) | 0.574 |
| Liver cirrhosis, n (%) | 34(20.2%) | 14(21.9%) | 20(19.2%) | 0.681 |
| Diabetes mellitus, n (%) | 70(41.7%) | 29(45.3%) | 41(39.4%) | 0.455 |
| Hypertension, n (%) | 99(58.9%) | 40(62.5%) | 59(56.7%) | 0.463 |
| Chronic kidney disease, n (%) | 61(36.3%) | 25(39.1%) | 36(34.6%) | 0.563 |
| End stage renal disease, n (%) | 26(15.5%) | 8(12.5%) | 18(17.3%) | 0.406 |
| Solid malignancies, n (%) | 42(25.0%) | 15(23.4%) | 27(26.0%) | 0.716 |
| Leukemia and lymphoma, n (%) | 9(5.4%) | 2(3.1%) | 7(6.7%) | 0.276 |
| Infection sites | ||||
| Primary blood stream infection, n (%) | 25(14.9%) | 10(15.6%) | 15(14.4%) | 0.833 |
| Pneumonia, n (%) | 112(66.7%) | 41(64.1%) | 71(68.3%) | 0.577 |
| Intra-abdominal infection, n (%) | 10(6%) | 0 | 10(9.6%) | 0.001 |
| Catheter related blood stream infection, n (%) | 44(26.2%) | 25(39.1%) | 19(18.3%) | 0.005 |
| Urinary tract infection, n (%) | 32(19%) | 14(21.9%) | 18(17.3%) | 0.467 |
| Surgical site infection, n (%) | 3(1.8%) | 2(3.1%) | 1(1.0%) | 0.369 |
| Wound infection, n (%) | 12(7.1%) | 5(7.8%) | 7(6.7%) | 0.793 |
| Laboratory data | ||||
| WBC (109/L), median | 13.7 ± 10.2 | 13.0 ± 7.2 | 14.2 ± 11.7 | 0.429 |
| Hb (g/dL), median | 9.0 ± 1.3 | 9.2 ± 1.3 | 8.8 ± 1.4 | 0.051 |
| Platelet (109/L), median | 123.1 ± 106.2 | 171.1 ± 120.2 | 93.7 ± 84.7 | < 0.001 |
| CRP (mg/L), median | 114.6 ± 90.3 | 88.7 ± 81.0 | 131.3 ± 92.3 | 0.003 |
| Outcome | ||||
| In-ICU mortality, n (%) | 113(67.3%) | 19(29.7%) | 94(90.4%) | < 0.001 |
| In-hospital mortality, n (%) | 126(75%) | 23(35.9%) | 103(99.0%) | < 0.001 |
| Days from culture days to mortality days, day, median (IQR) | 17.8(4–60) | 58.1(37-66.5) | 9.8(1–16) | < 0.001 |
| ICU hospitalization, day, median (IQR) | 39.1(15–59) | 49.3(15.3–69.5) | 32.7(14.3–45.8) | 0.002 |
The overall 30-day mortality rate was 61.9%. The median (IQR) number of days from culture day to mortality day was 17.8 (4–60) days. The median (IQR) length of ICU hospitalization was 39.1 (15–59) days. Compared with surviving patients, those who died had a higher Pitt bacteremia score (7.0 ± 2.6 vs. 4.2 ± 2.9, p < 0.001), higher SOFA score (12.0 ± 4.1 vs. 6.2 ± 3.8, p < 0.001), a greater need for continuous renal replacement therapy in the ICU (27.9% vs. 9.4%, p < 0.002), and a higher prevalence of intra-abdominal infection (9.6% vs. 0%, p < 0.001). In addition, patients who died within 30 days had lower platelet counts (93.7 ± 84.7 vs. 171.1 ± 120.2, p < 0.001) and higher CRP levels (131.3 ± 92.3 vs. 88.7 ± 81.0, p < 0.003) compared with surviving patients. The ICU mortality rate and overall hospital mortality rate were 67.3% and 75%, respectively.
The antibiotic susceptibility test indicated that the resistance rates for colistin was 31.6% (53/168 patients), that for tigecycline was 17.3% (29/168), that for meropenem was 97.6% (164/168), and that for amikacin was 76.2% (128/168). Pneumonia was the most common infection source of BSI (112, 66.7%), followed by catheter-related BSI (44/26.2%) and urinary tract infections (32, 19%). However, we could not identify the source of infection for 25 (14.9%) patients. Intra-abdominal infection was observed in 10 (6%) patients, all of whom died.
Table 2 presents the main antibiotic regimens used in treating the critically ill ICU patients with KPC-Kp BSIs. The most common regimens for KPC-Kp BSI treatment in these patients were colistin based (51 patients, 30.4%) and those involving a combination of colistin and tigecycline (50, 29.8%). The colistin-containing regimens accounted for 60.2% of the treatments in all 168 patients. A ceftazidime-avibactam regimen was administered to 24 patients and this regimen seemed to be associated with a higher survival rate than did the other regimens (21.9% vs. 9.6%; p < 0.042). A total of 89 patients (53%) received appropriate antibiotic treatments within 48 h after BSI onset. In addition, 28 patients were treated with 2 or more in vitro susceptible antibiotics, but 24 (85.7%) of these patients died.
Table 2.
Antibiotic regimens for critically ill patients with Klebsiella pneumoniae Carbapenemase-producing K. pneumoniae induced blood-stream infections
| Total (N = 168) |
30-day survival (N = 64) |
30-day non-survival (N = 104) |
p-value | |
|---|---|---|---|---|
| Ceftazidime-Avibactam based, n (%) | 24(14.3%) | 14(21.9%) | 10(9.6%) | 0.042 |
| Colistin based, n (%) | 51(30.4%) | 23(35.9%) | 28(26.9%) | 0.229 |
| Tigecycline based, n (%) | 11(6.5%) | 2(3.1%) | 9(8.7%) | 0.119 |
| Tigecycline + Colistin based, n (%) | 50(29.8%) | 18(28.1%) | 32(30.8%) | 0.718 |
| Another antibiotic regimen, n (%) | 32(19%) | 7(10.9%) | 25(24.0%) | 0.024 |
| No in vitro susceptible antibiotic use within 48 h, n (%) | 79(47%) | 25(39.1%) | 54(51.9%) | 0.105 |
| Only one in vitro susceptible antibiotic treated within 48 h, n (%) | 61(36.3%) | 29(45.3%) | 32(30.8%) | 0.063 |
| 2 or more in vitro susceptible antibiotic treated within 48 h, n (%) | 28(16.7%) | 10(15.6%) | 18(17.3%) | 0.778 |
The results of our multivariate analysis are presented in Table 3, indicating that CRP levels and SOFA scores were independently associated with mortality. However, the ceftazidime-avibactam regimen and appropriate antibiotic treatment within 48 h after BSI onset were independently associated with favorable outcomes. We used Kaplan-Meier survival curves (Fig. 2) compare patient survival rates between patients who were treated with or without the ceftazidime-avibactam regimen; we also compared survival rates between patients who received appropriate antibiotic treatment within 48 h after BSI onset and those who did not.
Table 3.
Multivariate analysis for identifying factors associated with mortality in critically ill patients with Klebsiella pneumoniae Carbapenemase-producing K. pneumoniae induced Blood-stream infections
| Multivariate analysis | ||
|---|---|---|
| P value | HR (95% CI) | |
| CRP | 0.043 | 1.002(1.000-1.005) |
| SOFA score | < 0.001 | 1.208(1.126–1.298) |
| Appropriate antibiotic treatment within 48 h | 0.028 | 0.623(0.408–0.950) |
| Ceftazidime-Avibactam based | 0.002 | 0.312(0.151–0.648) |
Fig. 2.
Kaplan-meier survival curves comparing survival outcomes in critically Ill patients with Klebsiella pneumoniae carbapenemase-producing K. pneumoniae induced blood-stream infections: (A) patients treated with or without ceftazidime-avibactam regimen; (B) patients with or without appropriate antibiotic treatment within 48 h after blood-stream infections onset
Discussion and conclusion
According to our review of the literature, this is possibly the largest study in Taiwan to investigate predictive factors for mortality and outcomes in critically ill patients with KPC-Kp BSIs. We found that administering appropriate antibiotic treatments within 48 h after BSI onset can reduce the mortality rate in critically ill ICU patients. Moreover, treatment with a ceftazidime-avibactam regimen was also possible associated with more favorable outcomes.
Studies conducted over the past 2 decades have reported that the 30-day overall mortality rate of CRKP induced BSIs ranged from 26% to 53% [1–3, 21–23]. By contrast, we observed a 30-day mortality rate of 61.9%, which is higher than the previously reported rates. A possible explanation for the increased mortality rate in our study is that all our patient cohort were respiratory failure treated in the ICU, who had multiple comorbidities and high disease severity at the onset of KPC-Kp BSIs, as indicated by our CCI, Pitt bacteremia scores, and SOFA scores. Another possible explanation is the infection source. The most common infection source in our patients was pneumonia (66.7%). This differs from the findings of relevant studies in which pneumonia was not the most common source of infection and did not account for a high proportion of case [3, 22–24]. Several studies have corroborated that the mortality rate associated with pneumonia was higher than those associated with intra-abdominal and urinary tract infections [25, 26]. Accordingly, the high proportion of pneumonia cases, multiple comorbidities, and higher disease severity could be potential factors contributing to the high mortality rate observed in our study.
The administration of appropriate antibiotics within 48 h after BSI onset is crucial factor for reducing mortality, as documented by several relevant studies [2, 3, 21]. Specifically, our study demonstrated that administering appropriate antibiotics within 48 h after BSI onset can improve mortality rates. However, achieving this goal remains challenging with traditional microbiological techniques because the period from blood culture collection to the detection of CRKP often exceeds 48 h [6, 13, 27]. This necessitates the implementation of novel rapid molecular tests for early detection and diagnosis [13]. Studies have indicated that patients tested with rapid molecular diagnostics demonstrated superior clinical outcomes [27, 28]. For example, Satlin et al. reported that in patients who received rapid molecular testing, the median time from blood culture collection to active therapy was 24 h, whereas that in patients who did not receive rapid molecular testing was 50 h [29]. Mortality rates were also lower among patients who received rapid molecular testing. Another major finding of our study is the superior outcomes associated with the new antibiotics of our hospital - ceftazidime-avibactam regimen compared with other regimens. The ceftazidime-avibactam regimen has been increasingly used as a frontline treatment for carbapenem-resistant Enterobacterales infections. Various clinical studies have indicated lower mortality and nephrotoxicity rates in patients treated with the ceftazidime-avibactam [22, 29–31]. Our multivariate analysis also revealed the ceftazidime-avibactam regimen was associated with a superior survival rate compared with other antibiotic regimens, corroborating findings from other studies in different regions.
Relevant studies have suggested that treatment with 2 or more antibiotics to which the KPC-Kp strain exhibited in vitro susceptibility could reduce mortality in KPC-Kp BSIs [24, 31, 32]. However, our study did not observe similar results, which may be attributed to the multiple comorbidities and higher severity of BSIs in our patients. Only 16.7% of our patients received 2 or more antibiotics, to which the KPC-Kp strain exhibited in vitro susceptibility, within 48 h, reflecting the ongoing challenge of reduced antibiotic susceptibility in KPC-Kp and the limited availability of effective options for combination therapy. Similarly, subsequent studies have demonstrated that the clinical outcomes of monotherapy are not inferior to those of combination therapy [33]. In addition, a high proportion of patients were treated with a combination of colistin and tigecycline in our study. Both antibiotics are known for their suboptimal clinical efficacy and unfavorable pharmacokinetic-pharmacodynamic profiles in BSI [3]. Therefore, even combined antibiotic therapy could not lead to reduced mortality rates in our study.
Several limitations in our study must be acknowledged. First, the clinical data were collected from a single center which may limit the generalizability of our findings to other institutions. Second, the study applied a retrospective design. The clinical data were derived from medicals records, which are inevitably subject to potential confounders and biases. Third, the number of patients treated with the ceftazidime-avibactam regimen in our study was relatively small; this is because this antibiotic regimen was introduced in our hospital in June 2020. Although these limitations, the extensive patient data provided can offer valuable therapeutic recommendations and clinical experience for clinicians managing KPC-Kp BSIs.
In conclusion, appropriate antibiotic treatments within 48 h after KPC-Kp BSIs onset and treatment with a novel new regimen were identified as crucial factors in improving mortality among critically ill ICU patients with respiratory failure. Limitations in traditional molecular techniques engender challenges in diagnosing and treating infections within this 48-hour window. Therefore, the utilization of novel rapid molecular tests in patients at high risk of hospital-acquired KPC-Kp infections is warrant and, subsequently, timely treatment with effective antibiotics is possible for these critically ill patients. Integrating these efforts into a robust antimicrobial stewardship framework can further optimize antibiotic use, reduce the emergence of resistance, and improve outcomes in this vulnerable population.
Supplementary Information
Below is the link to the electronic supplementary material.
Acknowledgements
We are grateful everyone who contributed towards the article and the editors and reviewer.
Abbreviations
- BSIs
Blood-stream infections
- CCI
Charlson comorbidity index
- CI
Confidence intervals
- CRKP
Carbapenem-resistant Klebsiella pneumoniae
- CRP
C-reactive protein
- ICU
Intensive care unit
- KPC-Kp
Klebsiella pneumoniae carbapenemase-producing K. pneumoniae
- MIC
Minimum inhibitory concentration
- OR
Odds ratios
- PCR
Polymerase chain reaction
- SOFA
Sequential organ failure assessment
Author contributions
MYT, BCW, and HCH planned and designed the study. MYT and BCW collected data. SWL and KWC performed microbiological analysis. LCC performed the statistical analysis. MYT, BCW, and HCH drafted the manuscript and designed tables and figures. LPC, SWL, MJH, HPW, and KCK reviewed the final version of the manuscript for intellectual content. All authors read and approved the final manuscript.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Data availability
The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.
Declarations
Ethics approval and consent to participate
This study was reviewed and approved by the Institutional Review Board of Chang Gung Memorial Hospital (Approval number: 201801433B0). Written informed consent for participation was not required for this study in accordance with national legislation and the institutional requirements.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.