The Journal of infection · 2026
A nationwide genomic surveillance study of Gram-negative bacteria causing community- and hospital-acquired bloodstream infections in China.
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Xi Jingyuan, Jia Xinmiao, Li Song, Li Xuming, Hu Long, Xia Han, Xu Tao, Xu Yingchun, Yu Yunsong, Hu Fupin, Kang Mei, Sun Ziyong, Ma Lijuan, Shan Bin, Ma Xiaoling, Zou Mingxiang, Li Jihong, Hasi Chaolu, Liu Yong, Guo Dawen, Hu Xinlan, Liu Yang, Jin Yan, Ji Ping, Zhang Lixia, Li Yi, Xia Yun, Liao Kang, Yang Qiwen
Аннотация
OBJECTIVES: Community-acquired and hospital-acquired bloodstream infections (CA-BSI and HA-BSI) caused by Gram-negative bacteria (GNB) pose major clinical risks, but differences in their molecular epidemiology and prognostic etiologic factors remain unclear.
METHODS: A genomic epidemiology study analyzed 933 CA-BSI and 1001 HA-BSI isolates from 21 major Chinese teaching hospitals. We collected comprehensive clinical data and conducted molecular characterization, including sequence types, antibiotic resistance genes, virulence factors, and plasmid types, as well as clinical phenotypes of major pathogens. Multivariable Cox models were used to identify mortality predictors.
RESULTS: Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Acinetobacter baumannii, and Enterobacter cloacae complex were the predominant species in both CA-BSI and HA-BSI groups but exhibited distinct clinical and molecular characteristics between CA-BSI and HA-BSI. CA-BSI patients showed significantly higher inflammatory markers (CRP, PCT, WBC, and Neu%), while HA-BSI patients had significantly poorer prognosis including prolonged hospitalization, higher ICU admission rates and clinical deterioration or mortality. Genomic surveillance revealed a critical divergence: HA isolates were dominated by high-risk clones such as ST11 K. pneumoniae and ST2 A. baumannii, which were enriched in antimicrobial resistance genes, directly linking to worse outcomes. CA isolates, while more diverse, were characterized by specific lineages including ST131 E. coli (enriched with specific virulence genes: yersiniabactin, K1 capsule, and P fimbriae) and ST23 K. pneumoniae, which carried a significantly greater number of virulence genes. Multivariable analysis confirmed that mortality risk profiles are setting-specific, influenced by distinct combinations of patient comorbidities (including age, gender, agranulocytosis, and infection source) and bacterial genetic determinants (such as lacI or aadA2 for K. pneumoniae and aph(3')-Ia for A. baumannii).
CONCLUSIONS: This first genomic epidemiological investigation of GNB-BSIs stratified by acquisition setting reveals a fundamental clinical and epidemiological divergence between CA- and HA-cases. The study underscores that tracking mortality-associated strains and genes is essential for improving clinical outcomes and advancing etiological knowledge.
METHODS: A genomic epidemiology study analyzed 933 CA-BSI and 1001 HA-BSI isolates from 21 major Chinese teaching hospitals. We collected comprehensive clinical data and conducted molecular characterization, including sequence types, antibiotic resistance genes, virulence factors, and plasmid types, as well as clinical phenotypes of major pathogens. Multivariable Cox models were used to identify mortality predictors.
RESULTS: Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Acinetobacter baumannii, and Enterobacter cloacae complex were the predominant species in both CA-BSI and HA-BSI groups but exhibited distinct clinical and molecular characteristics between CA-BSI and HA-BSI. CA-BSI patients showed significantly higher inflammatory markers (CRP, PCT, WBC, and Neu%), while HA-BSI patients had significantly poorer prognosis including prolonged hospitalization, higher ICU admission rates and clinical deterioration or mortality. Genomic surveillance revealed a critical divergence: HA isolates were dominated by high-risk clones such as ST11 K. pneumoniae and ST2 A. baumannii, which were enriched in antimicrobial resistance genes, directly linking to worse outcomes. CA isolates, while more diverse, were characterized by specific lineages including ST131 E. coli (enriched with specific virulence genes: yersiniabactin, K1 capsule, and P fimbriae) and ST23 K. pneumoniae, which carried a significantly greater number of virulence genes. Multivariable analysis confirmed that mortality risk profiles are setting-specific, influenced by distinct combinations of patient comorbidities (including age, gender, agranulocytosis, and infection source) and bacterial genetic determinants (such as lacI or aadA2 for K. pneumoniae and aph(3')-Ia for A. baumannii).
CONCLUSIONS: This first genomic epidemiological investigation of GNB-BSIs stratified by acquisition setting reveals a fundamental clinical and epidemiological divergence between CA- and HA-cases. The study underscores that tracking mortality-associated strains and genes is essential for improving clinical outcomes and advancing etiological knowledge.