Clinical characteristics and molecular mechanisms of thrombocytopenia in patients with community-acquired Klebsiella pneumoniae and Escherichia coli bloodstream infections

Background: To explore clinical characteristics, risk factors, and potential molecular mechanisms of thrombocytopenia in patients with community-acquired Enterobac-terales bloodstream infections (CA-EBSI). Methods: The dynamic changes of platelets were analyzed in CA-EBSI patients in a tertiary teaching hospital. The LASSO regression model was established to screen the risk factors of severe thrombocytopenia during hospitalization and a nomogram model constructed to predict thrombocytopenia. Mouse models of bloodstream infections with Klebsiella pneumoniae (K. pneumoniae) and Escherichia coli (E. coli) were established to dynamically monitor changes in platelet counts. Scanning electron microscopy was used to observe platelet morphological changes and bacterial adhesion characteristics. Transcriptome sequencing technology was employed to analyze the platelet gene expression profile and signal pathway enrichment patterns. Results: A total of 164 patients (Klebsiella pneumoniae n = 53 and Escherichia coli n = 111) were included, among whom 80.5% developed thrombocytopenia during hospitalization. The incidence of severe thrombocytopenia (PLT <50 × 109/L) was numerically higher in the K. pneumoniae group than in the E. coli group (22.6% vs. 14.4%, p = 0.24). Age (OR = 1.15, p = 0.049) and mechanical ventilation (OR = 5.28, p = 0.037) were independent risk factors for severe thrombocytopenia, and the nomogram model presented excellent predictive performance (AUC = 0.975). In the animal infection model, the platelet counts of mice decreased to 44%–56% of the baseline 48 hours after infection. Scanning electron microscopy showed that platelets in mice with bloodstream infections exhibited aggregation, pseudopod extension, and bacterial adhesion. Transcriptome analysis revealed that processes such as adhesion disruption, enhanced pro-inflammatory signaling, and apoptosis induction collectively drive platelet consumption. Conclusions: Thrombocytopenia in CA-EBSI patients is characterized by early and rapid progression, and the baseline platelet level significantly affects the progression of the disease. Advanced age and mechanical ventilation are independent risk factors for severe reduction, and thrombocytopenia may be driven by multiple factors.

Thrombocytopenia; Community-acquired infection; Enterobacterales; Bloodstream infection; Platelets

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