The global spread of hypervirulent Klebsiella pneumoniae (hvKp) poses a serious public health threat. In this study, we conducted genomic epidemiology analysis on 2097 global hvKp isolates, including our 900 isolates sequenced through the Illumina platform (177 of them fully sequenced through PacBio platform), representing the most comprehensive genomic analysis of hvKp to date. Our results identified six dominant clonal groups (CGs), particularly including CG23 and CG258, and 17 major virulence determinant combinations (VDCs) comprising 10 virulence gene profiles (VGPs), four types of virulence plasmids, four ICEKp variants, Tn7399, and all_island. Each CG harbored distinct advantageous VDCs, indicating strong genomic correlation and co-evolution. Additionally, the phylogeny and evolutionary history of CG23 and CG258 were characterized in depth. Notably, 41.58% of the 2097 isolates were multidrug-resistant and 33.29% were carbapenem-resistant, indicating serious antimicrobial resistance. Overall, our study provides a global genomic landscape of hvKp, emphasizing the genetic basis for their global dissemination and the need for precise prevention and control.
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Original Research
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Uncontrollable bleeding and bacterial infections are the major reasons for the high mortality of post-traumatic. In this study, a composite hemostatic chitosan sponge CaO2@SiO2/CS was prepared by combining a novel core–shell inorganic nano hemostatic CaO2@SiO2 nanoparticles with carboxylated chitosan, which presents a multi-layered structure with a rough and hydrophilic surface for rapid absorption of blood. When the CaO2@SiO2 nanoparticles in the CaO2@SiO2/CS come into contact with blood, the silanol group on its surface and the released H2O2 and Ca2+ can recruit and activate platelets, while generating fibrin clots and activating the endo-exogenous coagulation cascade reaction to achieve rapid clotting. The H2O2 released from CaO2@SiO2 shows the antimicrobial capacity and stimulates the production of tissue factors by endothelial cells. Meanwhile, the silica coating reduces the cytotoxicity of bare CaO2, thus reducing the risk of secondary bleeding at the site of vascular injury. CaO2@SiO2/CS (48 s) showed a 1.83- and 2.52-fold reduction in hemostasis time compared to commercial gelfoam and CS in a femoral artery hemorrhage model. This study illustrates the hemostatic mechanism of CaO2@SiO2 and provides a reference for the development of clinical biomedical inorganic hemostatic materials.
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