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Association between clinical-biological characteristics of Klebsiella pneumoniae and 28-day mortality in patients with bloodstream infection

BMC Microbiology volume 24, Article number: 552 (2024) Cite this article

Abstract

Background

Klebsiella pneumoniae bloodstream infection (KP BSI) is a severe clinical condition characterized by high mortality rates. Despite the clinical significance, accurate predictors of mortality in KP BSI have yet to be fully identified.

Methods

A retrospective analysis was conducted on the clinical data of 90 cases of KP BSI. The clinical data was extracted from electronic medical records. Antimicrobial susceptibility testing, string testing, and whole-genome sequencing (WGS) were performed on all isolates. Additionally, relevant bioinformatics analyses, such as phylogenetic analysis and assessment of resistance and virulence genes, were carried out. Logistic regression modeling was employed to evaluate the risk factors associated with 28-day mortality in patients with KP BSI, considering both host characteristics and the characteristics of the causative Klebsiella pneumoniae (KP) isolates.

Results

Among the 90 patients included in this study, the 28-day mortality rate for those with KP BSI was 30.00% (27/90). Multivariate analysis revealed several host-related factors associated with an increased risk of 28-day mortality. These factors included an elevated qSOFA score (odds ratio [OR] 2.98, 95% confidence interval [CI] 1.21–7.31, p = 0.017), presence of septic shock (OR 8.21, 95% CI 1.63–41.93, p = 0.008), and nosocomial infection (OR 7.72, 95% CI 1.71–34.74, p = 0.002). Regarding bacterial factors, the presence of the virulence genes rfbA/B/D (OR 8.53, 95% CI 1.41–51.57, p = 0.020) was identified as an independent risk factor, particularly for nosocomial infection patients. However, hypermucoviscosity phenotype, ST type, serotype, and resistance genes were not associated with an increased risk of 28-day mortality.

Conclusion

The carriage of virulence genes rfbA/B/D, which is responsible for the synthesis of O-antigen, was associated with poor prognosis of KP BSI. It may facilitate the clinical management of patients with bloodstream infection (BSI) caused by hypervirulent KP strains, especially those with rfbA/B/D genes.

Clinical trial number

Not applicable

Peer Review reports

Introduction

Klebsiella pneumoniae is a prevalent gram-negative pathogen responsible for community-acquired and nosocomial infections. It can cause infections in various anatomical sites, including the lungs, urinary tract, gastrointestinal tract, and bloodstream [1, 2]. Among these, KP BSI is a critical clinical presentation associated with high mortality rates. Previous studies have reported mortality rates ranging from approximately 11–40% for KP BSI patients [3,4,5], with an even higher incidence of 67.6% observed among Intensive Care Unit (ICU) patients [6]. Therefore, identifying predictors associated with mortality in KP BSI is crucial in clinical practice.

Numerous studies have investigated risk factors associated with fatal outcomes in patients with KP BSI. These factors include an increased Sequential Organ Failure Assessment (SOFA) score, septic shock, inappropriate empirical antibiotic treatment, and leucopenia [7,8,9]. Regarding bacterial pathogenic traits, it has been consistently reported that patients infected with carbapenem-resistant Klebsiella pneumoniae (CRKP) BSI have significantly higher mortality rates compared to those infected with carbapenem-sensitive Klebsiella pneumoniae (CSKP) BSI [7, 8, 10]. Moreover, the carriage of the carbapenem-resistant gene KPC is associated with significantly higher 30-day mortality in KP BSI patients [11]. Additionally, infections caused by hypervirulent Klebsiella pneumoniae (hvKP) have been recognized as another significant factor contributing to unfavorable clinical outcomes in BSI patients [3, 8]. Certain virulence genes such as pks cluster, iutA, and Kvar_1549 have been identified as independent risk factors associated with KP BSI [3, 9, 12]. However, the risk factors for fatal outcomes associated with these virulence genes were not consistently reported.

Many studies have explored risk factors associated with increased mortality in KP BSI, but most have focused solely on clinical characteristics [8, 10, 13, 14]. Moreover, most researchers have utilized polymerase chain reaction (PCR) as a method to identify virulence and resistance genes in KP isolates [2, 15, 16], which may not fully capture the clinically relevant genes influencing mortality in KP BSI. In this study, we employ deep WGS to comprehensively describe the molecular characteristics of strains, in conjunction with clinical characteristics, to identify risk factors associated with mortality in KP BSI.

Methods

Study design and clinical data collection

We conducted a retrospective cohort study at Zibo Municipal Hospital in Shandong Province, China, focusing on cases of KP BSI. We included the cases that started in January 2017 and ended in December 2021, and all patients diagnosed with KP BSI during this period at the hospital were included. For each patient, only the first isolate of KP BSI was selected for analysis. The inclusion criteria were as follows: (a) patients aged 18 years or older, (b) hospitalization with complete clinical data available, (c) a positive blood culture for KP with the samples preserved in our laboratory, and (d) clinical manifestations indicative of infection. Patients who were outpatients, those with incomplete data, and those lacking KP isolates were excluded from the study. The Ethics Committee of Zibo Municipal Hospital approved this study.

Various clinical features of the enrolled patients were collected, including sex, age, underlying diseases, empirical use of corticosteroids and antibiotics prior to or after the KP BSI diagnosis. The severity of the initial disease was assessed using the Quick Sequential Organ Failure Assessment (qSOFA) score at the time of recognizing the BSI [17]. Nosocomial infection was defined as an infection that occurred more than 48 h after the admission of the patient to the hospital [18]; appropriate antimicrobial treatment was determined to be the empirical administration of one or more antimicrobials after KP BSI, and the isolates were susceptible in vitro [19]. The outcomes of patients infected with KP BSI were evaluated based on the 28-day mortality rate.

Strain isolation and antimicrobial susceptibility testing

For this study, all intentionally collected isolates were cultured on blood agar plates at 37 °C in an incubator for 18–24 h. The isolates were then identified using matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry (BioMerieux, France). The minimum inhibitory concentrations (MICs) of various antibiotics, including ampicillin-sulbactam, aztreonam, cefazolin, cefepime, ceftazidime, ceftriaxone, piperacillin-tazobactam, tobramycin, sulfamethoxazole, ciprofloxacin, levofloxacin, ertapenem, imipenem, amikacin, and cefotetan, against the KP isolates were determined using Biomerieux Vitek 2 Compact ID/AST Microbial Analyzer (BioMerieux, France). The susceptibility of cefoperazone-sulbactam was detected using the Kirby-Bauer (K-B) method (Thermo, USA). The interpretation of drug sensitivity results was based on the guidelines outlined in the Clinical and Laboratory Standards Institute M100 document. All procedures were performed following the manufacturer’s instructions.

String test

The hypermucoviscosity phenotype was determined using the string test, following the previously described method [20]. KP isolates were subcultured on blood agar plates and incubated overnight at 37 °C. A standard bacteriology inoculation loop was used for the string test to sample single colonies of KP isolates. The loop was then slowly drawn away to observe whether a string of viscous material was formed. A positive string test was defined as the presence of a viscous string measuring more than 5 mm in length.

Whole genome sequencing and bioinformatics analysis

To comprehensively analyze the genetic features of KP isolates, WGS was performed using the Illumina Novaseq6000 PE150 platform (Illumina, USA) [21, 22]. The genomic DNA of the KP strains was extracted with Master PureTM Complete DNA and RNA Purification Kit (Lucigen, Cat No.: MC85200). The quantity and quality of DNA were assessed by Qubit 3.0 (Thermo Fisher Scientific, United States) and Nano-300 (ALLSHENG, China). The short-read libraries of DNA that passed the concentration and quality requirements were constructed using an optimized protocol for TruePrep® DNA Library Prep Kit V2 for Illumina (Vazyme, Cat. No.:TD501-01) and TruePrep® Index Kit V3 for Illumina (Vazyme, Cat. No.: TD203). After agarose gel electrophoresis and cutting the target bands to recycle with the E.Z.N.A. ® Gel Extraction Kit (Omega Bio-tek, Cat, No.: D2500-02), The libraries with insert sizes of about 300 bp were obtained. Then, PE150 sequencing was performed using an Illumina NovaSeq6000 sequencer at Berry Genomics, Beijing. For the Illumina sequencing data, the 2 × 150 bp paired-end reads were first trimmed by Fastp (v-0.20) [23]to remove adapters and low-quality reads. After trimming, the obtained sequencing data were assembled using Unicycler v 0.4.8. Multilocus sequence typing (MLST) was conducted using the MLST 2.0 tool to assign sequence types to the isolates [24]. Antimicrobial resistance genes and Virulence genes were identified using Abricate software [25, 26] through the Comprehensive Antibiotic Research Database (CARD) [27] and Virulence Factors Database (VFDB) respectively [28]. To construct a phylogenetic tree based on nucleotide sequence alignments, the PhyloPhlAn 3.0 [29] was employed. The resulting tree was visualized and annotated using the online tool Tree Visualization By One Table (tvBOT) (https://chiplot.online/tvbot.html) [30].

Statistical analysis

Statistical analyses were conducted using SPSS version 23.0. Group comparisons were performed using univariate analysis, employing χ2 tests for categorical variables and nonparametric tests (log-rank and Wilcoxon tests) for non-normally distributed data. Variables that showed significance (p < 0.05) in the univariate analysis, including clinically important variables, antimicrobial resistance, and virulence determinants, were selected for inclusion in a logistic regression model to evaluate their association with 28-day mortality. Prior to logistic regression, potential multicollinearity among these variables was assessed using the variance inflation factor (VIF) and the eigenmatrix method. Statistical significance was defined as p-values less than 0.05 for all analyses. Kaplan-Meier curves were constructed to visualize the survival probabilities, and the log-rank test was performed to compare the mortality rates between different groups. Statistical significance was defined as p-values less than 0.05 for all analyses.

Results

Clinical characteristics of KP BSI

A total of 121 cases diagnosed with KP BSI were identified during the four-year study period. Thirty patients were excluded due to missing KP isolates, and one case was excluded due to an unclear outcome. Ultimately, 90 KP BSI patients (52 male and 38 female) were included in this study. The clinical characteristics of KP BSI patients who survived and those who died are summarized in Table 1. The 28-day mortality rate among patients infected with KP BSI was 30.00%. The median age of all patients was 72 years (interquartile range, 62.75–81.00). Hypertension (38.89%) was the most prevalent underlying disease, followed by diabetes (31.11%) and coronary heart disease (13.33%). Among the KP BSI cases, 29 patients (32.53%) were classified as nosocomial infections, and 18 patients (10.28%) experienced septic shock. The median qSOFA score at the time of initial blood culture was 1 (interquartile range, 0–1). Approximately 20.00% of patients had been admitted to the intensive care unit. Corticosteroid treatment was administered to 16.67% of patients, and empirical antimicrobial treatment was initiated in 97.78% of patients following blood infection. The most frequently used antimicrobial agents were beta-lactam-beta-lactamase inhibitors (BLBLI, 70%) after BSI, followed by levofloxacin (26.67%) and carbapenems (15.56%).

Antibiotic resistance genes, MLST, and virulence factors of KP strains causing BSI

The antimicrobial resistance genes, hypermucoviscosity phenotype, and virulence genes are summarized in Table 2 and Supplementary Table S1. One hundred resistance genes were detected in the KP isolates, including genes associated with beta-lactams, aminoglycosides, quinolones, tetracycline, sulfonamides, and chloramphenicol. The most commonly observed beta-lactam-related gene was blaSHV (85.56%), followed by blaTEM (28.89%) and blaCTXM (22.22%). drfA (28.89%) was the most common sulfonamide related gene, fowllowed by sul1 (18.89%) and sul2 (18.89%), with sul2 being more prevalent in the group of patients who died. Quinolone-related genes, specifically OqxA and OqxB, were present in all isolates. No carbapenem resistance genes were detected in the KP isolates.

Approximately half of the isolates (45.56%) exhibited hypermucoviscosity phenotype. A total of 135 virulence genes were identified in the KP isolates, including genes associated with lipopolysaccharide (LPS), capsular polysaccharide (CPS), fimbriae, siderophore system, allantoin utilization and secretion system, etc. Almost all isolates possessed fimbriae and secretion system-related genes. 81.48% of strains isolated from the dead group patients carried the virulence gene rfbA. Notably, the strains carried by rfbA were also co-harbored with rfbB and rfbD. These three genes coexisted in the same strains. That is, the rfbA/B/D genes were more prevalent in deceased patients. In addition, Multilocus sequence typing (MLST) and serotype analysis revealed that the 90 clinical strains belonged to 54 MLST types and 35 serotypes. The serotypes K1 and K2 were frequently detected (17.78% and 16.67% respectively). The most commonly identified MLST type was ST23 (12.22%), followed by ST65 (6.67%) and ST700 (6.67%) (Supplementary Table S1).

Distribution of antibiotic resistance of KP isolates caused BSI

The antimicrobial resistance rates of KP isolates causing BSI are presented in Fig. 1. None of the isolates were resistant to ertapenem, imipenem, amikacin, and cefotetan. The highest resistance rate was observed for sulfamethoxazole (24.44%), followed closely by ciprofloxacin (23.33%) and ampicillin-sulbactam (17.78%). The resistance rates for Cefazolin, Cefuroxime, Ceftriaxone, ceftazidime, and Cefepime were 15.56%, 13.33%, 13.33%, 5.56%, and 3.33%. 12.22% of strains produced Extended-Spectrum β-Lactamases (ESBL). Ciprofloxacin resistance was more frequently observed in the group of patients who died (52.38%). 68.18% of strains resistant to sulfonamide have resistance genes sul1 and sul2. Notably, Among the 27 deceased patients, 13 (48.15%) were infected with KP strains that were sensitive to all tested antibiotics.

Risk factors for 28-day mortality in patients with KP-BSI

Of the 90 patients included in this study, 63 (70.00%) were classified as survivors and 27 (30.00%) as deceased. In the univariate analysis, several factors significantly associated with increased 28-day mortality, including host factors, ICU stay, increased qSOFA score at the onset of BSI, nosocomial infection, corticosteroid use before BSI, and septic shock. Conversely, corticosteroid use and appropriate antimicrobial treatment after BSI were associated with decreased 28-day mortality. Regarding the analysis of antibiotic resistance and virulence factors, the presence of resistant gene sul2 and LPS-related virulence genes rfbA/B/D were associated with increased 28-day mortality. However, String test positivity and capsule serotype were not associated with increased 28-day mortality in KP BSI patients.

Baseline variables that were considered clinically relevant or showed a univariate relationship with the outcome were included in a multivariate logistic regression model. Variables were carefully selected, given the number of events available, to ensure a parsimonious final model [31]. Candidate variables with a p-value < 0.05 in the univariate analysis were included in the multivariable model. The eigenmatrix method and VIF were conducted before the variables were selected for logistic modeling. As shown in Table 3, the increased qSOFA score(OR 2.98, 95% CI 1.21–7.31, p = 0.017), nosocomial infection (OR 8.57, 95% CI 2.27–32.31, p = 0.002), septic shock (OR 8.21, 95% CI 1.63–41.93, p =0.011) and carriage of virulence genes rfbA/B/D (OR 7.72, 95% CI 1.71–34.74, p = 0.008) were identified as independent predictors of 28-day mortality in KP BSI. To further assess the impact of the strains carrying rfbA/B/D genes infection on patients with KP BSI, survival curves were constructed using the Kaplan-Meier method (Fig. 2). The curves showed different impacts of the rfbA/B/D genes positive isolates infection between the nosocomial infection patients and non-nosocomial infection patients, with statistical significance (log-rank test, p = 0.048 in the nosocomial infection group and p = 0.317 in non-nosocomial infection group).

Phylogenetic analysis

A phylogenetic analysis was conducted to investigate the relationship between KP strains further. Comparative genomic analysis revealed that strains with the same sequence type (ST) clustered in the phylogenetic tree, as shown in Fig. 3. K1-ST23 strains had the highest detection rate, and almost all these isolates contained Fimbriae, LPS, CPS, Siderophore system, Secretion, and Colibaction-related genes. But these strains were not associated with mortality of KP BSI. While strains isolated from patients who died exhibited sporadic primary distribution in the phylogenetic tree, ST25-K2 and ST375-K2 strains showed high affinity and 80% of patients infected with these strains died. All K1 and K2 serotype isolates had rfbA and rfbB genes simultaneously. In addition, Among the nosocomial infection patients, 19 cases were infected with KP strains carrying rfbA /B/D genes, and 13 cases (68.42%) died.

Table 1 Analysis of risk factors for 28-day mortality in patients with KP BSI
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Table 2 Bacterial characteristics of the survived and died patients with KP BSI
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Fig. 1
figure 1

The MIC distribution of all antibiotics against KP isolates from BSI. The tree on the left side was reconstructed by hierarchical clustering of MIC results using the TB tools. Black indicates resistance, grey indicates mediation, and white indicates sensitivity. ESBL, Extended-Spectrum β-Lactamases. Mortality, 28-day mortality. The orange blocks on the right represent the presence of resistant genes, and the white blocks represent the absence. SXT, Sulfamethoxazole; CIP, Ciprofloxacin, CXM, Cefuroxime; CRO, Ceftriaxone; SAM, Ampicillin sulbactam; ATM, Aztreonam; CZO, Cefazolin; FEP, Cefepime; CSL, Cefoperazone-sulbactam; CAZ, Ceftazidime; GEN, Gentamicin; LVX, Levofloxacin; TOB, Tobramycin; TZP, Piperacillin-tazobactam; CTT, Cefotetan; ETP, Ertapenem; AMK, amikacin

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Table 3 Multivariate analysis of predictors associated with the 28-day mortality of KP BSI
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Fig. 2
figure 2

Survival analysis according to the carriage of the rfbA/B/D genes positive isolates in nosocomial and non-nosocomial infection patients. Statistical significance was determined by the log-rank test. (A) rfbA/B/D genes positive isolates infection in all patients. (B) rfbA/B/D genes positive isolates infection in nosocomial infection patients. (C) rfbA/B/D genes positive isolates in non-nosocomial patients. IN, nosocomial infection, non-NI, non-nosocomial infection

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Fig. 3
figure 3

Evolutionary relationships and virulence gene distribution of KP strains. Evolutionary relationships and virulence genes are shown on the left and right. Each row of the heatmap indicates information about a strain, and each column functional cluster names on a colored background on the top represent the corresponding virulence genes. ST25-K2 and ST375-K2 strains are marked with an orange box on the tree. Grey blocks represent the presence of genes, and white blocks represent the absence

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Discussion

This study aimed to assess the risk factors associated with 28-day mortality in patients with KP BSI in terms of bacterial and clinical characteristics. All KP isolates included in this study were CSKP, and the 28-day mortality rate among patients with KP BSI was 30.00%. The presence of the hypermucoviscous phenotype and resistance genes did not affect mortality, whereas increased qSOFA score, nosocomial infection, septic shock, and carriage of the LPS-related genes rfbA/B/D by causative strains were identified as independent risk factors for mortality in KP BSI patients.

The relatively higher mortality rate of 30.00% observed in this study, compared to previous studies, especially for CSKP-caused bloodstream infections (14.6% and 13.9% of 28-day mortality rate for CSKP BSI were reported) [8, 10], may be attributed to two factors. First, most previous studies have reported that compared with community-acquired infections, nosocomial infections caused by KP were associated with a higher mortality [18, 32]. In this study, nosocomial infection was identified as an independent risk factor for mortality, with 55.56% of patients with nosocomial KP BSI succumbing to the infection, a higher rate than in previous studies [3, 12]. This higher rate may contribute to the elevated mortality observed in the present study. On the other hand, consistent with previous studies, administering appropriate empirical antibiotic therapy after BSI was associated with decreased mortality in KP BSI patients [9]. 83.33% of patients who did not receive proper antibiotic treatment died, a higher percentage than that in previous studies [12]. These findings support the notion that the 28-day mortality in the present study was higher than that reported in previous studies. In addition, We observed that more virulent genes were exhibited in KP strains isolated from dead cases of nosocomial infection, and irrational application of antibiotics was more likely to occur in nosocomial infection patients (13.79% vs. 3.28%). The higher mortality of nosocomial patients was likely associated with these factors. Moreover, 6 cases did not receive appropriate therapy. Among them, 2 cases were not given any antibiotics, 4 cases were irrationally treated with ceftriaxone or levofloxacin after KP BSI, and 3 Klebsiella pneumoniae strains isolated from these patients produced ESBL. Therefore, clinical characteristics, the resistance spectrum of KP strains, and pharmacokinetics should be considered comprehensively to choose rational antibiotics. For ESBL-producing Klebsiella pneumoniae infection, Carbapenem is a better choice [33].

Several studies have suggested that the hypermucoviscous phenotype is not associated with increased mortality in KP BSI patients, which is consistent with the results of our research. However, Xu et al. reported that a few strains with both the hypermucoviscous phenotype and carriage of the carbapenem resistance gene blaKPC exhibited 100% mortality within 14 days [15]. Additionally, the virulence gene pks cluster (allS, allantoin metabolism) has been reported as a risk factor for KP BSI only when accompanied by multidrug resistance (MDR) [12]. Another virulence gene, iutA, has also been reported as an independent risk factor for patients with KP BSI [3, 9], with higher mortality observed when iutA carriage by causative strains was accompanied by MDR [9]. However, in our research, neither iutA nor the pks cluster affected the 28-day mortality of patients with KP BSI. The absence of carbapenem-resistant isolates in this study may explain this discrepancy.

In our study, we observed an increased mortality rate among patients infected with rfbA/B/D genes positive strains, The rfbA/B/D genes belong to members of the rfb cluster, which encode the enzymes for the synthesis of O-antigens [34]. As the first two genes of the cluster, rfbA and rfbB encode an ATP-binding cassette (ABC-2) transport system required for the export of O-polysaccharide across the cytoplasmic membrane [35]. RfbD encodes UDP-galactopyranose mutase (UGM), which is required for LPS biosynthesis in pathogens [36]. The presence and length of O-antigen in LPS play an essential role in bacterial pathogenesis. The O-antigen of KP prevents complement components from binding to bacteria and then contributes to resistance against complement-mediated killing [37]. Previous studies showed that deletion of rfbA, rfbB or rfbD, KP produced rough LPS (R-LPS), and the virulence of strains decreased [34, 38]. Deletion of the genes rfbD, Salmonella Enteritidis also showed an absence of O-polysaccharide and displayed R-LPS [39], and enhances bacterial colonization and virulence through inhibiting autophagy [40]. Additionally, Macrophages and microglial cells activated by the Toll-like receptor 4 agonist LPS switch their metabolism from oxidative phosphorylation to glycolysis, which is required for these cells to respond to infection or tissue injury during inflammation. Inhibition of the glycolytic pathway can suppress immune-mediated inflammation and damage [41, 42]. Furthermore, patients with diabetes mellitus are more susceptible to HvKP because of their impaired immunity, and leading to severe infections [43, 44]. Therefore, the mechanism underlying mortality caused by rfbA/B/D -carrying KP strains may be associated with enhanced virulence of isolates and abnormal immune response.

Our study has several limitations that should be acknowledged. Firstly, it was a retrospective study with a relatively small sample size, and missing patient data may have introduced bias into the analysis. Secondly, the data were collected from a single hospital, which may limit the generalizability of the findings to other geographical areas or healthcare settings. Multicenter studies were needed to explore the risk factors associated with mortality in patients with KP BSI by deep WGS in conjunction with clinical characteristics in the future. Lastly, although we evaluated the presence of various virulence and resistance genes in the tested strains, we did not investigate the expression of these genes through in vitro or in vivo experiments. Assessing the functional activity of these genes could provide further insights into their role in the pathogenesis and clinical outcomes of KP BSI. Future studies should address these limitations to strengthen the validity and applicability of the findings.

In conclusion, our study revealed a relatively higher 28-day mortality rate of 30.00% among patients with CSKP BSI. Hypermucoviscous phenotype, resistance phenotype, and resistance genes were not risk factors for mortality of KP BSI, while strains carriage of virulence gene rfbA/B/D infection were associated with poor prognosis, especially for nosocomial patients. These findings emphasize the importance of careful management by clinicians when treating BSI caused by strains carrying the rfbA/B/D genes. Further studies are needed to elucidate the pathogenic mechanisms of hvKP with rfbA/B/D genes.

Data availability

The raw sequence data reported in this paper have been deposited in the Genome Sequence Archive in National Genomics Data Center, with the accession number CRA014424. The data can be obtained from the website ( https://ngdc.cncb.ac.cn/gsa ).

Abbreviations

KP BSI:

Klebsiella pneumoniae bloodstream infection

KP:

Klebsiella pneumoniae

BSI:

Bloodstream infection

ESBL:

Extended-spectrum β-lactamase

CRKP:

Carbapenem-resistant Klebsiella pneumoniae

CSKP:

Carbapenem-sensitive Klebsiella pneumoniae

HvKP:

Hypervirulent Klebsiella pneumoniae

MDR:

Multidrug resistance

ICU:

Intensive care units

WGS:

Whole genome sequencing

MIC:

Minimum inhibitory concentration

MLST:

Multilocus sequence typing

ST:

Sequence type

BLBLI:

Beta-lactam-beta-lactamase inhibitors

LPS:

Lipopolysaccharide

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Acknowledgements

Not applicable.

Funding

This study was supported by the Taishan Scholars Program of Shandong Province (tsqn202103196), Shandong Medical and Health Technology Development Project (202011000732), the Key Research and Development Project of ZiBo City (2020ZC060026), and the Beijing Reward Gene Association (YXJL-2019-0688-0036).

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Author notes

  1. Xiaofeng Yu and Yi Zhao contributed equally to this work and share first authorship.

Authors and Affiliations

  1. Department of Clinical Microbiology, Zibo City Key Laboratory of Respiratory Infection and Clinical Microbiology, Zibo Municipal Hospital, Zibo, 255400, China

    Xiaofeng Yu, Yi Zhao, Jiahui Luan, Haiyan Wang, Tianyu Sun, Bo Liu & Hongyun Cao

  2. Science and Education Department, Zibo Municipal Hospital, Zibo, 255400, China

    Xiao Sun

  3. Institute of Evolution and Marine Biodiversity, Ocean University of China, Qingdao, 266000, China

    Tongtong Lin, Xia Zhou, Wei Yang & Ziguang Deng

Authors
  1. Xiaofeng Yu
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  11. Bo Liu
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  12. Hongyun Cao
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Contributions

XY and YZ analyzed clinical data and drafted the manuscript; XS performed statistical analysis; JL, HW and TS conducted data collection; T L and WY conducted bioinformatics analysis; XZ and ZD performed whole-genome sequencing. HC and BL conceived and designed the study; All authors contributed to the article and approved the submitted version.

Corresponding authors

Correspondence to Bo Liu or Hongyun Cao.

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The studies involving patients were reviewed and approved by the Ethics Committee of Zibo Municipal Hospital ( no. 20190419 ).

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Yu, X., Zhao, Y., Sun, X. et al. Association between clinical-biological characteristics of Klebsiella pneumoniae and 28-day mortality in patients with bloodstream infection. BMC Microbiol 24, 552 (2024). https://doi.org/10.1186/s12866-024-03714-6

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BMC Microbiology

ISSN: 1471-2180

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