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Background The emergence and transmission of tigecycline‐ and carbapenem‐resistant Klebsiella pneumoniae (TCRKP) have become a major concern to public health globally. Here, we investigated the molecular epidemiology and mechanisms of tigecycline resistance in carbapenem‐resistant K pneumoniae (CRKP) isolates. Methods Forty‐five non‐duplicate CRKP isolates were collected from January 2017 to June 2019. We performed antimicrobial susceptibility tests, multilocus sequence typing (MLST), and pulsed‐field gel electrophoresis (PFGE). PCR and DNA sequencing were performed for the detection and mutation analysis of acrR, oqxR, ramR, rpsJ, tet(A), and tet(X) genes, which are related to tigecycline resistance. The expression levels of efflux pump genes acrB and oqxB and their regulator genes rarA, ramA, soxS, and marA were assessed by quantitative real‐time PCR. Results The resistance rate to tigecycline in CRKP isolates was 37.8% (17/45). K pneumoniae ST307 was a predominant clone type (70.6%, 12/17) among the TCRKP isolates. The expression levels of acrB (P < .001) and marA (P = .009) were significantly higher in the tigecycline‐resistant group than in the tigecycline‐intermediate and tigecycline‐susceptible groups. Increased expression of acrB was associated with marA expression (r = 0.59, P = .013). Conclusions We found that the activated MarA‐induced overexpression of AcrAB efflux pump plays an important role in the emergence of tigecycline resistance in CRKP isolates. We introduce the mechanisms of tigecycline resistance in carbapenem‐resistant K pneumoniae (CRKP) isolates. The transcriptional activator MarA‐mediated overexpression of AcrAB efflux pump plays an important role in the emergence of tigecycline resistance in CRKP isolates.

Asymptomatic rectal carriers are recognized as reservoirs of carbapenem‐resistant Klebsiella pneumoniae (CRKp), which can spread epidemic high‐risk clones [e.g., sequence types (ST)‐307] and plasmids [incompatibility group (Inc)‐X3] in hospitals, with possible transmission into the community. This study investigated the epidemiology and characteristics of CRKp high‐risk clones ST307 among rectal carriage isolates from community hospitals. A carbapenemase positivity rate of 24% was observed for all rectal screening performed during hospital admission (February to August 2021) in Gauteng, South Africa; 252 CRKp isolates were characterized. Antimicrobial susceptibility was performed using the VITEK 2 automated system, and polymerase chain reaction assays were used to detect K. pneumoniae ST307, carbapenemase genes, and associated mobile genetic elements (MGEs e.g., IncX3, IS3000). Of the 252 isolates, 25% (64/252) were ST307 positive and 75% (188/252) were non‐ST307. Among the 64 ST307, 45% (29/64) harbored blaOXA‐181 on IncX3 plasmids. Occurrence of blaOXA‐181 among ST307 (69%; 44/64) when compared to non‐ST307 (48%; 91/188) was statistically significant (p‐value = 0.002). Fourteen isolates, including two ST307, harbored double carbapenemase genes. Carbapenemase gene combinations include six blaNDM+blaOXA‐48‐like, four blaNDM +blaOXA‐181, three blaKPC+blaOXA‐181, and one blaOXA‐181+blaVIM. One ST307 isolate harbored three carbapenemase genes (blaNDM+blaOXA‐48+blaOXA‐181). Level of antimicrobial resistance was significantly (p‐value < 0.001) associated with the occurrence of ST307, comprising 73% (47/64) extensively drug resistant. This study highlights the need for rectal screening of XDR clones and plasmids using simple and cost‐effective genomic methodologies suitable for low‐ and middle‐income countries for local risk management and control of infectious diseases in hospitals. Graphical presentation of rectal carriage of carbapenem‐resistant Klebsiella pneumoniae, highlighting ST307 high‐risk clone and IncX3 plasmid‐associated blaOXA‐181. This study highlights the threat linked to horizontal gene transfer of AMR genes by epidemic plasmids from Klebsiella pneumoniae high‐risk clones to other bacterial species.

Objective This study aimed to establish a highly sensitive and rapid single‐tube, two‐stage, multiplex recombinase‐aided qPCR (mRAP) assay to specifically detect the khe, blaKPC‐2, and blaNDM‐1 genes in Klebsiella pneumoniae. Methods mRAP was carried out in a qPCR instrument within 1 h. The analytical sensitivities of mRAP for khe, blaKPC‐2, and blaNDM‐1 genes were tested using recombinant plasmids and dilutions of reference strains. A total of 137 clinical isolates and 86 sputum samples were used to validate the clinical performance of mRAP. Results mRAP achieved the sensitivities of 10, 8, and 14 copies/reaction for khe, blaKPC‐2, and blaNDM‐1 genes, respectively, superior to qPCR. The Kappa value of qPCR and mRAP for detecting khe, blaKPC‐2, and blaNDM‐1 genes was 1, 0.855, and 1, respectively (p < 0.05). Conclusion mRAP is a rapid and highly sensitive assay for potential clinical identification of khe, blaKPC‐2, and blaNDM‐1 genes in K. pneumoniae. We establish a highly sensitive and rapid single‐tube, two‐stage, multiplex recombinase‐aided qPCR (mRAP) assay to specifically detect the khe, blaKPC‐2, and blaNDM‐1 genes in Klebsiella pneumoniae (KP). mRAP was carried out in a qPCR instrument within 1 h. mRAP achieved the sensitivities of 10, 8, and 14 copies/reaction for khe, blaKPC‐2, and blaNDM‐1 genes, respectively, superior to qPCR.

Background Infections remain a major cause of morbidity and mortality in kidney transplant (KT) recipients. This study aimed to investigate the preservation fluid (PF) samples from deceased donors and report the impacts of possible donor-derived carbapenem-resistant Klebsiella pneumoniae (pdd-CRKP) infections on KT recipients. Methods A retrospective study was performed that included all recipients who received kidney transplantation from deceased donors in our hospital between December 2018 and December 2020. A total of 212 patients received kidney transplantation from deceased donors, a total of 206 PF samples were collected, and 20 recipients had a CRKP-positive culture. Both donors and recipients with CRKP-positive PF cultures were divided into two groups, and continuous variables between the two groups were compared using independent-sample t tests and Mann-Whitney tests. Categorical variables were compared using the chi-square test or Fisher’s exact test. The significance level of p values was set at 0.05. Results A total of 337 recipients underwent kidney transplantation, including 212 recipients of organs from deceased donors and 110 corresponding deceased donors. A total of 206 PF samples were collected, and 20 recipients had CRKP-positive PF cultures. The donors’ length of ICU stay was a potential risk factor for CRKP positivity in the PF culture ( P  < 0.05). Fifteen recipients were infected with pdd-CRKP, and the incidence of pdd-CRKP infection was 7.3% (15/206). The use of antibiotics, including ceftazidime-avibactam (CAZ-AVI), was a potential protective factor against death and graft loss in recipients with a CRKP-positive PF culture ( P  < 0.05). Conclusions This study shows that the incidence of pdd-CRKP is high in our centre, recipients with pdd-CRKP infection can still achieve a good prognosis with the use of antimicrobial agents including CAZ-AVI.

Background & objectives: To determine the effect of Wen Run Fei Ning formula (WRFNF) intervention in class I integron-mediated carbapenem-resistant Klebsiella pneumoniae. Methods: A drug-susceptibility test and PCR amplification were used to screen for carbapenem-resistant K. pneumoniae containing class I integrons. Following nasal drip and tail vein injection to infect healthy male rats with carbapenem-resistant K. pneumoniae, three models were created: control (group A); model (group B, tail vein injection); and model-WRFNF treatment group (group C, by tail vein injection). Rats in Group C were gavaged with pre-warmed WRFNF extract. On the third, fifth, and seventh days after the experiment, the rats in groups A and B were gavaged with an equal quantity of saline and killed in batches. Results: Group C showed considerably higher serum IL-6 and TNF- levels on days 3, 5, and 7 compared to group A, as well as a significant increase in peripheral blood leukocyte count and a histopathologic inflammatory cell infiltration of the lungs. As the WRFNF delivery duration was prolonged, group C's histopathologic inflammatory cell infiltration gradually improved in contrast to group B, with the biggest improvement occurring on day 7. Compared to group B, group C's serum IL-6 and TNF- levels were lower. When the trial's duration was increased to 7 days, the levels of IL-6 and TNF- in group C decreased on day 7 compared to on day 5. Interpretation & conclusion: WRFNF decreased inflammatory cell infiltration as well as IL-6 and TNF expression in the lung of the rats infected with carbapenem-resistant K. pneumoniae.

The emergence of hypervirulent carbapenem‐resistant Klebsiella pneumoniae (hvCRKP) represents an alarming convergence of enhanced virulence and extensive drug resistance. Here, we present a comprehensive genomic analysis of 2563 clonal complex 23 (CC23) isolates from 62 countries spanning 1932–2024. Our findings reveal that CC23‐K1, the dominant hypervirulent sublineage, emerged approximately 170 years ago and diversified into seven major clades with distinct regional dominance. We observe that carbapenem resistance in CC23‐K1 exhibits notable instability, with at least 130 independent acquisitions and 20 losses of resistance genes, suggesting an evolutionary trade‐off between hypervirulence and antimicrobial resistance. Experimental validation demonstrates that capsule production physically impedes plasmid conjugation, while isolates carrying blaKPC‐2, blaNDM‐1, or blaNDM‐5 frequently exhibit substantial deletion of virulence determinants. Conversely, blaOXA‐48‐carrying isolates maintain virulence gene integrity, potentially due to their lower hydrolytic activity and reduced fitness costs. The geographic distribution of these resistance mechanisms correlates with regional antimicrobial usage patterns, with European countries with moderate carbapenem use favoring blaOXA‐48 in CC23, while Asian countries with higher consumption show patterns favoring high‐efficiency carbapenemases incompatible with complete virulence determinants. We also identified core genomic regions with significantly higher mutation rates in resistant isolates, particularly affecting pathways involved in oxidative phosphorylation and reactive oxygen species production. These findings provide additional insights into CC23 evolution and geographical spread, complementing existing knowledge of carbapenemase distribution patterns observed across K. pneumoniae lineages. The global emergence of hypervirulent, carbapenem‐resistant Klebsiella pneumoniae (hvCRKP) poses a paradox: why do such dangerous clones remain geographically confined? By analyzing over 2500 CC23 genomes across 90 years, we uncover a core evolutionary constraint—virulence and resistance rarely coexist without trade‐offs. Potent carbapenemases (blaKPC, blaNDM) are frequently linked to large‐scale deletions in virulence loci, while capsule production physically hinders plasmid uptake. In contrast, low‐activity enzymes like blaOXA‐48 preserve full virulence. Experimental validation and mutational profiling reveal how metabolic adaptation and structural barriers limit convergence. Our findings reveal an evolutionary balancing act that restrains global dissemination of hvCRKP—and suggest new levers for containment and control. Highlights CC23‐K1 hypervirulent K. pneumoniae shows strong geographic compartmentalization with distance‐driven transmission patterns globally. Carbapenem resistance exhibits remarkable instability with >130 acquisitions and frequent losses. High‐efficiency carbapenemases (blaKPC/blaNDM), prevalent in Asia, are incompatible with hypervirulence, while low‐efficiency blaOXA‐48 in Europe preserves virulence determinants.

Objective: To investigate the epidemiology of carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-HvKP) and hypervirulent carbapenem-resistant Klebsiella pneumoniae (Hv-CRKP).Methods: Totally 436 K. pneumoniae strains were collected from 7 hospitals in mainland China between 2017.01 and 2018.02. Sequence types, serotypes, antimicrobial-resistance and virulence genes were analyzed. Additionally, string test, capsule stain, Periodic Acid Schiff stain, fitness analysis, quantitative real-time PCR and mouse lethality test were also performed. Molecular combinations were used to screen putative blaKPC(+)-HvKP and Hv-blaKPC(+)-KP, followed by the confirmation of mouse lethality test.Results: Diverse detection rates were found for the virulence genes, ranging from c-rmpA (0.0%) to entB (100.0%). According to the molecular criteria, 127, 186, 9 and 26 strains were putatively denoted as HvKP, blaKPC(+)-KP, blaKPC(+)-HvKP and Hv-blaKPC(+)-KP. Mouse lethality test confirmed 2 blaKPC(+)-HvKP strains (JS184 and TZ20) and no Hv-blaKPC(+)-KP. JS184 showed K2 serotype, thin capsule, positive exopolysaccharid and string test. TZ20 presented K20 serotype, thin capsule, negative exopolysaccharide and string test. Compared with the positive control NTUH-K2044, equal galF expression and growth curves were confirmed for JS184 and TZ20.Conclusions: Molecular determination of CR-HvKP and Hv-CRKP brings remarkable bias compared with mouse lethality test. The exact prevalence of CR-HvKP is less than 1.0%, which of Hv-CRKP is much lower.

Carbapenem-resistant (CRKP) represents a significant threat to public health and has already drawn worldwide attention. Hence, we aim to comprehensively analyze the case condition, as well as molecular epidemiology, resistance and virulence of three CRKP isolates with new sequence types (STs). Three CRKP were collected from November 2019 to April 2021. The three patients' clinical characteristics were analyzed through His system. In order to screen phenotype of metallo-carbapenemase, the modified Carbapenem Inactivation Method (mCIM) and EDTA-modified Carbapenem Inactivation Method (eCIM) were conducted. Three isolates were subjected to antimicrobial susceptibility testing (AST) using the agar dilution method or minimal broth dilution method. The string test, the sedimentation assay, biofilm formation and the serum resistance assay were performed as phenotypic experiments to assist in evaluating virulence. The presence of resistance and virulence genes were detected by Whole-Genome Sequencing (WGS). Serotypes and new STs were compared and determined by multi-locus sequence typing (MLST). Overall, all isolates were multi-resistant, but sensitive to tigecycline and colistin. Among them, all formed biofilms, strain 1 and strain 2 were classified as moderate-producers, while strain 3 as weak-producer. The results of the serum resistance assay indicated that only strain 2 was resistant. From WGS analysis, it showed that all isolates co-harbored multiple resistance genes, such as carbapenemase genes, sulfonamides, fluoroquinolones, aminoglycosides, and tetracyclines. Meanwhile, several virulence genes were also contained, including siderophores, fimbriae, capsule and lipopolysaccharides-associated genes. The serotypes of strain 1 and strain 2 manifested K35 and KL47, respectively. Three novel ST5365, ST5587, ST5647 were first discovered in North China. Our study suggested that we should pay more attention to their resistance. And the results will help treat CRKP infections caused by these novel STs.

Background The emergence of carbapenem-resistant Klebsiella pneumoniae (CR-KP) has become a significant problem worldwide and also being a major threat to children and newborns. Here we report an outbreak of NDM-1-producing K. pneumoniae in a neonatal unit. Results Six CR-KP strains, isolated from neonates with symptoms of infection, were identified using a VITEK-2 compact system, and the clinical data were retrieved from the electronic case records. In vitro susceptibility testing with broth dilution method showed that all six K. pneumoniae isolates were resistant to carbapenems and susceptible to colistin, aminoglycosides, fluoroquinolones and tigecycline. Based on the polymerase chain reaction results, each isolate was found to be bla NDM-1 gene positive. Clonal relationships were analysed using pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) and showed that two different PFGE patterns were formed, which belonged to sequence types ST234 and ST1412. Plasmids carrying bla NDM-1 were successfully transferred from four of the six isolates to an Escherichia coli recipient through conjugative assays. S1-PFGE and Southern blot hybridization showed that four NDM-1-producing K. pneumoniae were clonal and carried bla NDM-1 on the same plasmid. The outbreak was effectively controlled by reducing the potential infection sources. All the patients were successfully treated and recovered after receiving an increased dose of carbapenems. Although the source of this outbreak was not clear, comprehensive measures were carried out and the outbreak was effectively controlled. Conclusions ST234 and ST1412 of NDM-1-producing Klebsiella pneumoniae are the resistant clone spread in the neonatal unit, comprehensive infection control measures and optimized carbapenem therapy played an important role in controlling this NDM-1-producing K. pneumoniae outbreak.

Purpose Carbapenem-resistant Klebsiella pneumoniae (CRKP) represents a significant global threat due to its high prevalence rates and limited therapeutic options. The primary objective of this study was to investigate the clinical distribution and molecular epidemiology of CRKP collected between 2016 and 2023 from a tertiary care hospital in northern China. Methods Polymerase chain reaction (PCR) assays were used to identify resistance and virulence genes, while various assessments, including the string test and biofilm formation analysis, assessed CRKP’s virulence. Multilocus sequence typing (MLST) and whole-genome sequencing were employed to elucidate strain classification and plasmid characteristics. Results The study identified 100 unique CRKP strains, primarily isolated from neurosurgery and ICU, with sputum as the most common specimen type. The majority of strains harbored bla KPC−2 as the primary resistance mechanism. All CRKP strains harbored a minimum of four virulence genes, with entB , mrkD , fimH , and ybtS being most commonly detected across the isolates. Notably, 66 of 100 strains were classified as carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-hvKP). The prevailing sequence type (ST) observed was ST11, with serotype KL47 being most prevalent initially, subsequently supplanted by ST11-KL64. Specific strains harbored bla KPC−2 on IncFII-type plasmids, along with other resistance genes, such as bla TEM−1 . KP635_PlasmidB harbors multiple antibiotic resistance genes, and the sequence identity and coverage between KP635_PlasmidA and the NTUH-K2044 virulence plasmid are 99%, which contributes to the formation of a highly virulent and multidrug-resistant strain in KP635. Conclusion The emergence of high resistance and hypervirulence in CRKP requires vigilance, enhanced surveillance, and stringent infection control measures to limit its spread.