Abstract
Purpose
Acinetobacter baumannii is emerging as a pathogen that is a focus of global concern due to the frequent occurrence of the strains those are extensively resistant to antibiotics. This study was aimed to analyze the clinical and microbiological characteristics of a cohort of patients with A. baumannii bloodstream infections (BSIs) in western China.
Methods
A retrospective study of the patients at West China Hospital of Sichuan University with A. baumannii BSIs between Jan, 2018 and May, 2023 was conducted. Antimicrobial susceptibility of A. baumannii isolates was tested by microdilution broth method. Whole-genome sequencing and genetic analysis were also performed for these isolates.
Results
Among the 117 patients included, longer intensive care unit stay, higher mortality, and more frequent invasive procedures and use of more than 3 classes of antibiotics were observed among the carbapenem-resistant A. baumannii (CRAB)-infected group (n = 76), compared to the carbapenem-susceptible A. baumannii (CSAB)-infected group (n = 41, all P ≤ 0.001). Twenty-four sequence types (STs) were determined for the 117 isolates, and 98.7% (75/76) of CRAB were identified as ST2. Compared to non-ST2 isolates, ST2 isolates exhibited higher antibiotic resistance, and carried more resistance and virulence genes (P < 0.05). In addition, 80 (68.4%) isolates were CRISPR-positive, showed higher antibiotic susceptibility, and harbored less resistance and virulence genes, in comparison to CRISPR-negative ones (P < 0.05). Phylogenetic clustering based on coregenome SNPs indicated a sporadic occurrence of clonal transmission.
Conclusion
Our findings demonstrate a high frequency of ST2 among A. baumannii causing BSIs, and high antibiotic susceptibility of non-ST2 and CRISPR-positive isolates. It is necessary to strengthen the surveillance of this pathogen.
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Introduction
Acinetobacter baumannii has emerged as an important pathogen that causes infectious diseases such as pneumonia, bloodstream infections (BSIs), meningitis, and skin or soft tissue infections [1]. In recent years, there has been a sharp decline in the in vitro susceptibility to antibiotics among worldwide isolates of A. baumannii [2]. Critically, carbapenem-resistant A. baumannii (CRAB) is only susceptible to a small number of antimicrobial agents, which raises a worldwide health concern about the effective treatment of this pathogen [3, 4].
The molecular mechanisms of antimicrobial resistance and virulence of A. baumannii continue to be fully understood. The production of carbapenem hydrolases (e.g., OXA-23) is a key mechanism in the development of carbapenem resistance [5]. The pmrA, pmrB and mcr genes are related to colistin resistance [6]. Acquisition of the tetX gene and over-expression of resistance-nodulation-cell division efflux pumps have been observed in tigecycline-resistant strains [7, 8]. Virulence factors have also been identified, including outer membrane proteins [9], capsular polysaccharides [10], phospholipases [11] and acinetobactin-mediated iron acquisition system [12].
The occurrence of antimicrobial resistance and virulence genes or genetic elements, such as blaOXA−23 and blaOXA−72 [13], lipooligosaccharide genes in the outer core locus 1 (OCL1) [14], and genes involved in type VI secretory system (T6SS) [15], differed among A. baumannii strains causing BSIs. Also, various sequence types (STs) were identified among these isolates, and their relationship with the prognosis was variable. For example, the 30-day mortality was high in ST191, but rather low in ST451 [16]. ST191/195/208 strains prevailed in the patients with severe infections, demonstrated increased multidrug antimicrobial resistance, and caused excessive mortality, compared to the other stains [17]. Further research is needed to fully elucidate the clinical features of A. baumannii BSIs and to determine the antimicrobial susceptibility patterns and genotypes of the isolates, in order to guide optimal management of the patients. Therefore, the present study was aimed to identify the clinical and microbiological characteristics of a cohort of patients with A. baumannii BSIs.
Materials and methods
Patient inclusion and data collection
A retrospective study was conducted in the West China Hospital of Sichuan University, in Chengdu, China, according to the STROBE guidelines (Strengthening the Reporting of Observational Studies in Epidemiology) [18]. Medical data from patients suffering from A. baumannii BSIs between Jan 1st, 2018, and May 31st 2023 were retrieved from the hospital information system. A. baumannii BSI was defined as isolation of the bacterium from blood culture during the study period. Each case was ensured by the clinicians that the primary infection sites met the National Healthcare Safety Network (NHSN) definitions [19]. At last, 117 cases were included for further analysis. According to the in vitro susceptibility of A. baumannii isolates to carbapenem, the included cases were divided into a CRAB-infected group (n = 76) and a carbapenem-susceptible A. baumannii (CSAB)-infected group (n = 41). The flowchart for the patient inclusion and exclusion is summarized in Supplementary material Figure S1.
Bacterial identification and whole-genome sequencing
A. baumannii strains isolated from the patients included were recovered on Luria-Bertani agar and incubated overnight at 37℃. The isolates were identified by a matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) Biotyper® Sirius System (Bruker Daltonics GmbH, Bremen, Germany), and confirmed via whole genome-sequencing using an Illumina NovaSeq 6000 platform (Illumina, San Diego, CA, USA). Escherichia coli ATCC25922 and A. baumannii ATCC19606 were used as control strains.
Antimicrobial susceptibility testing (AST) of the isolates
The in vitro susceptibility of the isolates to antibiotics was determined using a Vitek 2 compact system (bioMérieux, Lyon, France) according to the manufacturer’s recommendations. The results of minimum inhibitory concentration (MIC) were interpreted by the Clinical and Laboratory Standards Institute supplement M100-Ed33 [20]. E. coli ATCC25922 and Pseudomonas aeruginosa ATCC27853 acted as control strains.
Genomic analysis of the isolates
Raw data from the whole-genome sequencing were subjected to quality control check using FastQC v0.12 (https://www.bioinformatics.babraham.ac.uk/projects/fastqc/), and the trimmed reads were assembled by SPAdes v3.15.5 [21]. Genome sequences were annotated by Prokka v1.1 [22]. Acquired resistance genes were identified by ResFinder v4.0 [23] using the CARD database (https://card.mcmaster.ca/). Virulence genes were identified by ABRicate v0.9.8 (https://github.com/tseemann/abricate) using the VFDB database (http://www.mgc.ac.cn/VFs/). The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) arrays were searched by the CRISPRCasFinder v4.3.2 [24], CRISPRDetect v2.2 [25], and CRISPROne (https://omics.informatics.indiana.edu/CRISPRone/index.php). In this study, the strains were classified into CRISPR-positive or CRISPR-negative group according to the presence or absence of CRISPR array. The presence of cas genes was determined with NCBI RefSeq and TIGRFAM databases. And then, the type of CRISPR-Cas system was assigned [26].
Phylogenetic analysis of the isolates
Multi-locus sequence typing (MLST) was performed on the PubMLST (https://pubmlst.org/organisms). A sequence type (ST) code for each isolate was generated based on the Pasteur scheme, according to the detection results of the allelic genes cpn60, fusA, gltA, pyrG, recA, rplB, and rpoB. A total of 1871 core genes was identified from the pan-genome analysis by Roary [27]. To determine phylogenetic relationships among the isolates, the genomic sequences were aligned to a complete reference genome A. baumannii ATCC 17978 (accession no. GCA_000015425.1), then the single nucleotide polymorphisms (SNPs) variant types (snp, ins, del, complex) were determined using Snippy v4.6.0 [28]. The recombination events were filtered using Gubbins v2.4.1 (https://github.com/nickjcroucher/gubbins) under the GTRGAMMA model (https://github.com/tseemann/snippy). SNP-sites [29] were used to extract SNPs from the recombination-free multi-FASTA alignment, resulting 176,740 core SNPs. A pairwise SNP distance matrix was generated by SNP-dists v0.8.2 (https://github.com/tseemann/snp-dists). The phylogenetic tree based on maximum-likelihood method was built with RAxML [30] and visualized using the iTOL online server (https://itol.embl.de/). Clonal transmission occurred when single nucleotide variations (SNVs) ≤ 10 between the isolates [31]. To identify the main genetic branches and trace the relationship of ST2 versus non-ST2 isolates, and CRISPR-positive versus CRISPR-negative ones, the phylogenetic trees were constructed, respectively.
Statistical analysis
Continuous variables (e.g. ages, days) were expressed as the median with interquartile range (IQR), and categorical variables as frequency and percentage. The association between patients and bacterial characteristics was assessed with chi-squared tests for categorical variables and t-tests or Wilcoxon tests for continuous variables. Adjusted odds ratios (aOR) and 95% confidence intervals (CIs) were obtained from a multivariable logistic regression model. Data were analyzed using SPSS 26.0 software (SPSS Inc, USA) and a two-side P < 0.05 was considered statistically significant.
Ethics declarations
Ethical permission was obtained by approval of the institutional review board of the West China Hospital of Sichuan University Clinical Trial center (No.2020 -954), in accordance with the International Guideline for Ethical Review of Epidemiological Studies and Declaration of Helsinki. The informed consent was waived because this study was a retrospective study with review of related data through the electronic medical records.
Results
Characteristics of A. baumannii BSIs
The demographics, clinical and microbiological features of the cases in the CRAB-infected (n = 76) and CSAB-infected (n = 41) groups are summarized in Table 1. A high 7-day mortality (43.6%) was observed among the 117 patients, and the mortality of the CRAB-infected group was much higher than that of the CSAB-infected group (57.9% versus 17.1%, P< 0.001). Stay in intensive care unit (ICU), invasive procedures, and the usage of more than 3 classes of antibiotics were more common in the CRAB-infected group, compared to the CSAB-infected group (all P< 0.05). Multivariate logistic regression analysis found that stay in ICU (aOR: 5.95; 95% CI 1.84-20.04; P = 0.003), nasogastric tube placement (aOR: 6.50; 95% CI 1.44-33.78; P = 0.018), mechanical ventilation (aOR: 13.50; 95% CI 5.34-49.5; P < 0.001), and usage of more than 3 classes of antibiotics (aOR: 3.40; 95% CI 1.19-10.10; P = 0.023) were the independent risk factors for the patients with CRAB BSIs.
Antimicrobial resistance phenotype and genomic features of CRISPR-positive and CRISPR-negative A. baumannii isolates
As demonstrated in Figs. 1 and 2, 68.4% (n = 80) of the 117 isolates carried CRISPR arrays. The CRISPR-negative isolates were more resistant to the antibiotics tested, compared to CRISPR-positive ones (Table 2, all P ≤ 0.001). Also, there were larger number of genes related to antimicrobial resistance and virulence among CRISPR-negative isolates, compared to CRISPR-positive ones (Fig. 3A; Tables 3 and 4).
Antimicrobial resistance phenotype and genomic features of ST2 and non-ST2 A. baumannii isolates
In total, 24 STs, namely ST2, ST25, ST40, ST46, ST93, ST106, ST203, ST216, ST217, ST331, ST374, ST410, ST452, ST516, ST584, ST768, ST1153, ST1264, ST1336, ST1399, ST1512, ST1641, ST2034, ST2114, were determined via the Pasteur scheme. ST2 isolates accounted for 64.1% (75/117) of all the isolates and 98.7% (75/76) of CRAB isolates. The in vitro susceptibility of ST2 isolates to antibiotics was lower than that of non-ST2 isolates (Table 2, P< 0.001). ST2 isolates carried more resistance and virulence genes, compared to non-ST2 ones (Fig. 3B; Tables 3 and 4).
Phylogenetic analysis of A. baumannii isolates
The core-genome SNPs analysis of 117 A. baumannii isolates revealed an extensive genetic diversity, identifying 2 to 176,740 SNPs, 1,871 core genes that are common across all the strains, alongside a vast number of accessory (139,665) and unique (1,996) genes. Two clades, labeled as A and B in Fig. 1, were identified. The clade A included 75 ST2 (matrix distance: 2 ~ 720 SNPs), and the clade B had 42 non-ST2 ones (matrix distance: 3400 ~ 5474 SNPs). The closest genetic relationship was found among 10 ST2 CRAB and 2 non-ST2 CSAB isolates (Figs. 1 and 4), indicating clonal transmissions might occur.
Among the 75 ST2 isolates, a broad spectrum of genetic variation was characterized, including 3,355,802 variants (variant-SNPs 2,769,376, variant-insertions 30,120, variant-deletions 26,192, and variant-complex 530,114), which highlighted the prominence of ST2. The main genetic branches of ST2 versus non-ST2 isolates, and CRISPR-positive versus CRISPR-negative ones were shown in Figure S2-S5, respectively.
Discussion
BSIs caused by multidrug-resistant bacteria are usually associated with the poor prognosis of the patients. In present study, a high 7-day mortality (43.6%) was observed among the patients with A. baumannii BSIs. Moreover, the mortality of CRAB-infected group was much higher than that of the CSAB-infected group (57.9% versus 17.1%). The high mortality (69.4%, 75/108) of CRAB BSIs was also observed previously [32]. All of our cases in the CRAB-infected group received invasive procedures, and 92.1% of these cases were administered with more than 3 classes of antimicrobial agents. Interestingly, we observed that A. baumannii was also isolated from respiratory tract in 43.4% (33/76) of cases in the CRAB-infected group and 26.8% (11/41) of cases in the CSAB-infected group. These data may be due to the colonization of A. baumannii in the respiratory tract as a crucial step that precedes the development of BSIs [33].
Recently, the increasing resistance of A. baumannii to antimicrobial agents has emerged as a global health concern. According to the China Antimicrobial Surveillance Network report (http://www.chinets.com), the resistance of A. baumannii to imipenem increased from 32.9% in 2005 to 71.2% in 2022. In our study, all of the CRAB isolates were resistant to multiple classes of antibiotics. The infections in other sites (e.g. respiratory tract) and variable comorbidities (as described in Table 1) might contribute to the high mortality among our CRAB-infected group, despite 68.4% of them were administrated with last-line antibiotics such as tigecycline and colistin. Similarly, the previous studies found that although tigecycline and colistin had not significantly reduced the death of patients with CRAB associated infections for prominent toxicity (both nephrotoxicity and neurotoxicity) and low plasma concentrations of the colistin contributing to failed treatments [34, 35]. Therefore, the prevention of CRAB BSIs may be critically important under such circumstances.
Furthermore, we identified the resistance phenotypes and associated genes of the isolates in this study. We found that 96.1% (73/76) of the CRAB isolates carried blaOXA−23, a gene that encodes a class D carbapenemase and contributes to a higher level of carbapenem resistance in A. baumannii [36]. The 3 isolates of blaOXA−23-negative CRAB carried blaOXA−66, which is another kind of carbapenemase gene. The virulence factors identified in A. baumannii were mainly involved in immune modulation, biofilm formation, nutrition, metabolism, and regulation [37]. The ompA gene, encoding outer membrane protein A (OmpA) [38], was detected in all the CRAB isolates. The gene bap, contributing to biofilm production, cell adhesion, and invasion [39, 40], was identified in 97.4% (74/76) of CRAB isolates. The quorum sensing system abaI/abaR, as a signal transduction factor and acyl-homoserine lactone (AHL) synthase receptor [41], was detected in 93.4% (71/76) of CRAB isolates.
The CRISPR-Cas system is a form of bacterial immune protection against the invasion of mobile genetic elements [42]. CRISPR-positive isolates of Klebsiella pneumoniae have been shown to be more susceptible to antibiotics compared to CRISPR-negative ones [43]. In present study, CRISPR-positive A. baumannii isolates showed higher in vitro susceptiblity to antibiotics, and carried fewer resistance and virulence genes, compared to CRISPR-negative ones. This finding suggests that the CRISPR array may be a barrier to antimicrobial resistance in CSAB isolates, which might provide a new insight into the prevention and control of infections caused by this pathogen.
In our study, ST2 was identified in 64.1% of 117 A. baumannii isolates and 98.7% of 76 CRAB isolates. Other studies about A. baumannii BSIs reported that 52.0% of the isolates were identified as ST2 [44], and all the multidrug-resistant isolates as ST2 [32]. The dissemination of A. baumannii ST2 has attracted significant attention due to high resistance of the isolates and high mortality of the patients [44]. ST2 isolates showed multidrug resistance and harbored important virulence factors [45, 46]. Similarily, in our study, ST2 isolates carried more resistance and virulence genes, compared to non-ST2 ones. Furthermore, 12 isolates (with ≤ 10 SNVs) were found to be closely related genetically, which indicated that clonal transmission might occur.
There were some limitations in our study. It was a retrospective study conducted in a single center, and the sample size was small. Further research is needed to enlarge the sample size to find more genetic relationship among the A. baumannii isolates causing BSIs.
In conclusion, stay in ICU, nasogastric tube placement, mechanical ventilation, and usage of more than 3 classes of antibiotics were found to be the risk factors for CRAB BSIs. ST2 isolates exhibited higher antibiotic resistance, and carried more resistance and virulence genes, in comparison to non-ST2 ones. CRISPR-negative isolates were more resistant to antibiotics, and harbored more resistance and virulence genes, compared to CRISPR-positive ones. Phylogenetic clustering based on core-genome SNPs indicated a sporadic occurrence of clonal transmission. It is necessary to strengthen the surveillance of this pathogen.
Data availability
The data from this whole genome shotgun project have been deposited at the NCBI databases (Bio Project ID: PRJNA1014798 and PRJNA951345).
References
Wong D et al (2017) Clinical and pathophysiological overview of Acinetobacter infections: a Century of challenges. Clin Microbiol Rev 30(1):409–447
Hamidian M, Nigro SJ (2019) Emergence, molecular mechanisms and global spread of carbapenem-resistant Acinetobacter baumannii. Microb Genom 5(10):e000306
Wang Y et al (2024) Comparison of in vitro synergy between polymyxin B or colistin in combination with 16 antimicrobial agents against multidrug-resistant Acinetobacter baumannii isolates. J Microbiol Immunol Infect 57(2):300-308
De Oliveira DMP et al (2020) Antimicrobial Resistance in ESKAPE pathogens. Clin Microbiol Rev 33(3):e00181-19
Colquhoun JM et al (2021) OXA-23 β-Lactamase overexpression in Acinetobacter baumannii drives physiological changes resulting in New Genetic vulnerabilities. mBio 12(6):e0313721
Nang SC et al (2021) Rescuing the last-line polymyxins: achievements and challenges. Pharmacol Rev 73(2):679–728
Wang L et al (2019) Novel plasmid-mediated tet(X5) gene conferring resistance to Tigecycline, Eravacycline, and Omadacycline in a clinical Acinetobacter baumannii isolate. Antimicrob Agents Chemother 64(1):e01326-19
Lucaßen K et al (2021) Prevalence of RND efflux pump regulator variants associated with tigecycline resistance in carbapenem-resistant Acinetobacter baumannii from a worldwide survey. J Antimicrob Chemother 76(7):1724–1730
Sánchez-Encinales V et al (2017) Overproduction of outer membrane protein A by Acinetobacter baumannii as a risk factor for nosocomial pneumonia, Bacteremia, and mortality rate increase. J Infect Dis 215(6):966–974
Russo TA et al (2010) The K1 capsular polysaccharide of Acinetobacter baumannii strain 307–0294 is a major virulence factor. Infect Immun 78(9):3993–4000
Jacobs AC et al (2010) Inactivation of phospholipase D diminishes Acinetobacter baumannii pathogenesis. Infect Immun 78(5):1952–1962
Sheldon JR, Skaar EP (2020) Acinetobacter baumannii can use multiple siderophores for iron acquisition, but only acinetobactin is required for virulence. PLoS Pathog 16(10):e1008995
Gu Y et al (2022) Molecular epidemiology and carbapenem resistance characteristics of Acinetobacter baumannii causing bloodstream infection from 2009 to 2018 in northwest China. Front Microbiol 13:983963
Lowe M et al (2022) Molecular characterisation of Acinetobacter baumannii isolates from bloodstream infections in a tertiary-level hospital in South Africa. Front Microbiol 13:863129
Bai B et al (2022) Clinical and genomic analysis of virulence-related genes in bloodstream infections caused by Acinetobacter baumannii. Virulence 13(1):1920–1927
Yoon EJ et al (2019) Counter clinical prognoses of patients with bloodstream infections between causative Acinetobacter baumannii clones ST191 and ST451 belonging to the International Clonal Lineage II. Front Public Health 7:233
Niu T et al (2023) Prevalent Dominant Acinetobacter baumannii ST191/195/208 strains in bloodstream infections have high Drug Resistance and Mortality. Infect Drug Resist 16:2417–2427
Vandenbroucke JP et al (2007) Strengthening the reporting of Observational studies in Epidemiology (STROBE): explanation and elaboration. PLoS Med 4(10):e297
NHSN Bloodstream Infection Event (Central Line-Associated Bloodstream Infection and Non-Central Line-Associated Bloodstream Infection) Centers for Disease Control and Prevention, https://www.cdc.gov/nhsn/pdfs/validation/2023/pcsmanual_2023.pdf
CLSI (2023) Performance standards for antimicrobial susceptibility testing. 33rd ed. CLSI supplement M100. Clinical and laboratory standards institute
Bankevich A et al (2012) SPAdes: a new genome assembly algorithm and its applications to single-cell sequencing. J Comput Biol 19(5):455–477
Seemann T (2014) Prokka: rapid prokaryotic genome annotation. Bioinformatics 30(14):2068–2069
Bortolaia V et al (2020) ResFinder 4.0 for predictions of phenotypes from genotypes. J Antimicrob Chemother 75(12):3491–3500
Couvin D et al (2018) CRISPRCasFinder, an update of CRISRFinder, includes a portable version, enhanced performance and integrates search for Cas proteins. Nucleic Acids Res 46(W1):W246–W251
Biswas A et al (2016) CRISPRDetect: a flexible algorithm to define CRISPR arrays. BMC Genomics 17:356
Makarova KS et al (2020) Evolutionary classification of CRISPR-Cas systems: a burst of class 2 and derived variants. Nat Rev Microbiol 18(2):67–83
Page AJ et al (2015) Roary: rapid large-scale prokaryote pan genome analysis. Bioinformatics 31(22):3691–3693
Seemann T (2015) Snippy: rapid haploid variant calling and core genome alignment, https://github.com/tseemann/snippy
Page AJ et al (2016) SNP-sites: rapid efficient extraction of SNPs from multi-FASTA alignments. Microb Genom 2(4):e000056
Togkousidis A et al (2023) Adaptive RAxML-NG: accelerating phylogenetic inference under Maximum Likelihood using dataset Difficulty. Mol Biol Evol, 40(10):msad227
Mao P et al (2021) Whole-genome sequencing elucidates the epidemiology of Multidrug-Resistant Acinetobacter baumannii in an Intensive Care Unit. Front Microbiol 12:715568
Yu K et al (2021) Bloodstream infections caused by ST2 Acinetobacter baumannii: risk factors, antibiotic regimens, and virulence over 6 years period in China. Antimicrob Resist Infect Control 10(1):16
Hafiz TA et al (2023) A two-year retrospective study of multidrug-resistant Acinetobacter baumannii respiratory infections in critically ill patients: clinical and microbiological findings. J Infect Public Health 16(3):313–319
Doi Y (2019) Treatment options for Carbapenem-resistant Gram-negative bacterial infections. Clin Infect Dis 69(Suppl 7):S565–S575
Zalts R et al (2016) Treatment of Carbapenem-Resistant Acinetobacter baumannii Ventilator-Associated Pneumonia: Retrospective Comparison between Intravenous Colistin and Intravenous Ampicillin-Sulbactam. Am J Ther 23(1):e78–85
Findlay J et al (2023) Dissemination of ArmA- and OXA-23-co-producing Acinetobacter baumannii Global clone 2 in Switzerland, 2020–2021. Eur J Clin Microbiol Infect Dis
Shan W et al (2022) Insights into mucoid Acinetobacter baumannii: a review of microbiological characteristics, virulence, and pathogenic mechanisms in a threatening nosocomial pathogen. Microbiol Res 261:127057
Nie D et al (2020) Outer membrane protein A (OmpA) as a potential therapeutic target for Acinetobacter baumannii infection. J Biomed Sci 27(1):26
De Gregorio E et al (2015) Biofilm-associated proteins: news from Acinetobacter. BMC Genomics 16:933
Khalil MAF et al (2021) Virulence characteristics of Biofilm-Forming Acinetobacter baumannii in Clinical isolates using a Galleria mellonella model. Microorganisms 9(11):2365
Sun X et al (2021) The abaI/abaR Quorum Sensing System effects on pathogenicity in Acinetobacter baumannii. Front Microbiol 12:679241
Faure G et al (2019) CRISPR-Cas in mobile genetic elements: counter-defence and beyond. Nat Rev Microbiol 17(8):513–525
Li HY et al (2018) Characterization of CRISPR-Cas systems in clinical Klebsiella pneumoniae isolates uncovers its potential Association with Antibiotic susceptibility. Front Microbiol 9:1595
Chuang YC et al (2019) Microbiological and clinical characteristics of Acinetobacter baumannii bacteremia: implications of sequence type for prognosis. J Infect 78(2):106–112
Baleivanualala SC et al (2023) Molecular and clinical epidemiology of carbapenem resistant Acinetobacter baumannii ST2 in Oceania: a multicountry cohort study. Lancet Reg Health West Pac 40:100896
Cherubini S et al (2022) Whole-Genome Sequencing of ST2 A. baumannii Causing Bloodstream Infections in COVID-19 Patients Antibiotics (Basel), 11(7):955
Funding
This work was supported by the National Natural Science Foundation of China (No.81201342) and funding of Science and Technology Department of Sichuan Province (No. 2021YFS0183).
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Y. Y., S. S.T. and C. L., collected clinical data and performed the tests. C.Y.W analyzed the data and prepared the manuscript. C.H. supervised the study design, data analysis and paper writing.
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Wu, C., Yuan, Y., Tang, S. et al. Clinical and microbiological features of a cohort of patients with Acinetobacter baumannii bloodstream infections. Eur J Clin Microbiol Infect Dis 43, 1721–1730 (2024). https://doi.org/10.1007/s10096-024-04881-0
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DOI: https://doi.org/10.1007/s10096-024-04881-0