ST1193 is an emerging new virulent and resistant clone among Escherichia coli with a tendency to spread rapidly across the globe. However, the prevalence of intracranial infection-causing E. coli ST1193 is rarely reported. This study aimed at determining the prevalence of E. coli ST1193 isolates, causing intracranial infections in Changsha, central China. A total of 28 E. coli isolates were collected from the cerebrospinal fluid of patients with intracranial infection over a four-year period. All isolates were differentiated using multilocus sequence typing (MLST), and phylogenetic grouping, and tested for antibiotic resistance. MLST analysis showed 11 sequence types (ST) among the 28 E. coli isolates. The most prevalent ST was B2-ST1193 (28.6%, 8/28), followed by B2-ST131 (21.4%, 6/28) and F-ST648 (10.7%, 3/28). Of the eight ST1193 isolates, three carried CTX-M-55, and one carried CTX-M-27. All eight ST1193 isolates were resistant to Ciprofloxacin, showing gyrA1AB/parC4A mutations. Two ST1193 isolates carried the aac(6′)-Ib-cr gene. All ST1193 isolates were recovered from infants with meningitis, with a fatal outcome for one three-month-old infant. ST1193 has emerged as the predominant type of E. coli strain causing intracranial infections in Changsha, China. This study highlights the importance of implementing appropriate surveillance measures to prevent the spread of this emerging public health threat.

Klebsiella variicola is an opportunistic pathogen often misidentified as Klebsiella pneumoniae, leading to misdiagnoses and inappropriate treatment in clinical settings. The genetic and molecular characteristics of clinically isolated K. variicola remain largely unexplored. We aim to fill this knowledge gap by examining the genomic properties of and evolutionary relationships between clinical isolates of K. variicola. The genomic data of 70 K. variicola strains were analyzed using whole-genome sequencing. A phylogenetic tree was generated based on the gene sequences from these K. variicola strains and public databases. Among the K. variicola strains, the drug resistance genes with the highest carrying rates were beta-lactamase and aminoglycoside. Locally isolated strains had a higher detection rate for virulence genes than those in public databases, with yersiniabactin genes being the most prevalent. The K locus types and MLST subtypes of the strains exhibited a dispersed distribution, with O3/O3a being the predominant subtype within the O category. In total, 28 isolates carried both IncFIB(K)_Kpn3 and IncFII_pKP91 replicons. This study underscores the importance of developing more effective diagnostic tools and therapeutic strategies for K. variicola infections. The continued surveillance and monitoring of K. variicola strains is essential for understanding the epidemiology of infections and informing public health strategies.

Hypervirulent Klebsiella pneumoniae (hvKP) causes invasive infections, including bloodstream infections and liver abscesses, and dysregulated host inflammation may exacerbate liver injury. We investigated whether pretreatment with Humanin, a mitochondria-derived anti-inflammatory peptide, could attenuate hvKP-associated liver injury. We measured serum Humanin in 20 patients with hvKP-associated bloodstream infection and liver abscess and 20 matched healthy controls. C57BL/6 mice received intraperitoneal Humanin (2.5 or 5 mg/kg/day) for five days before intravenous hvKP challenge. We assessed liver injury, inflammatory responses, hepatic transcriptomes, NF-κB activation, and survival. Serum Humanin was higher in patients than in the controls (p < 0.001). In infected mice, Humanin pretreatment was associated with less prominent histopathological liver injury and lower serum ALT, AST, and PCT, hepatic myeloperoxidase activity, F4/80 immunoreactivity, CD86 fluorescence, and pro-inflammatory gene expression. The effects were generally greater at 5 mg/kg than at 2.5 mg/kg. Transcriptomic analysis showed attenuation of inflammatory pathways, including NF-κB signaling (NES = −1.86, p = 0.002, FDR = 0.012). Humanin also reduced p-p65/p65 and p-IκBα/IκBα ratios in liver tissue and hvKP-stimulated bone-marrow-derived macrophages; 5 mg/kg prolonged survival (p < 0.05). Humanin pretreatment may therefore limit inflammatory liver injury during systemic hvKP infection. This effect was associated with reduced macrophage-associated inflammation and NF-κB activation, although its molecular targets remain unknown.