Characterization and pathogenic mechanisms of a Klebsiella aerogenes strain isolated from a deceased ground thrush

Klebsiella aerogenes is a significant opportunistic pathogen, yet the virulence and resistance mechanisms of wildlife-originating strains remain poorly understood. This study aimed to investigate the biological characteristics of K. aerogenes strain S_KLB, isolated from the lung of a deceased ground thrush, and to elucidate its pathogenic mechanisms in murine pneumonia. The isolated strain was assessed for cultural characteristics, antibiotic susceptibility, and the presence of virulence genes via PCR. An acute pneumonia model was established in mice through intranasal infection. Clinical symptoms and histopathological alterations in lung tissues were evaluated using Hematoxylin and Eosin (H&E) and TUNEL staining. Quantitative PCR (qPCR) and Western blotting were employed to measure the expression of relevant genes and the activation of signaling pathway proteins in lung tissues. Strain S_KLB exhibited robust growth on both MacConkey and SS agar media. It demonstrated resistance to a majority of tested antibiotics, including imipenem and oxacillin, and harbored a diverse virulence gene profile encompassing siderophores, fimbriae, efflux pumps, and metabolic factors. Animal challenge revealed that S_KLB infection induced severe pneumonia, characterized by significant weight loss, pulmonary edema, extensive neutrophil infiltration, and increased cellular apoptosis. At the molecular level, infected lung tissues showed marked upregulation of pro-inflammatory cytokines ( TNF-α, IL-6, IL-1β ) and the chemokine CXCL1. Concurrently, the NF-κB, STAT3, and p38 MAPK signaling pathways were activated, accompanied by elevated expression of the apoptotic protein Cleaved Caspase-3. The ground thrush-derived K. aerogenes strain S_KLB is a multidrug-resistant isolate possessing a broad range of virulence associated genes. It induces severe pneumonic injury by activating the NF-κB/STAT3/p38 MAPK signaling cascades, which drive excessive inflammatory responses and cellular apoptosis. This study provides experimental evidence for assessing the pathogenic potential of a wildlife-originating bacterial strain in a murine pneumonia model.