Comparative analysis of the antimicrobial resistance and virulence traits in ESBL-producing-Klebsiella pneumoniae ST307 strains colonizing the gastrointestinal tract and causing a fatal bloodstream infection in a leukemia patient

生物 毒力 微生物学 肺炎克雷伯菌 质粒 病菌 殖民地化 抗生素耐药性 病毒学 基因 抗生素 遗传学 大肠杆菌
作者
Luana Boff,Humberlânia de Sousa Duarte,Gabriela Bergiante Kraychete,Gabriel Taddeucci-Rocha,Bianca Diniz Oliveira,Rodolpho Mattos Albano,Ana Paula D’Alincourt Carvalho-Assef,Silvana Vargas Superti,Ianick Souto Martins,Renata Cristina Picão
出处
期刊:Infection, Genetics and Evolution [Elsevier]
卷期号:121: 105598-105598
标识
DOI:10.1016/j.meegid.2024.105598
摘要

Klebsiella pneumoniae is an opportunistic pathogen that can colonize the gastrointestinal tract (GIT) of humans. The mechanisms underlying the successful translocation of this pathogen to cause extra-intestinal infections remain unknown, although virulence and antimicrobial resistance traits likely play significant roles in the establishment of infections. We investigated K. pneumoniae strains isolated from GIT colonization (strains Kp_FZcol-1, Kp_FZcol-2 and Kp_FZcro-1) and from a fatal bloodstream infection (strain Kp_HM-1) in a leukemia patient. All strains belonged to ST307, carried a transferable IncF plasmid containing the blaCTX-M-15 gene (pKPN3–307 TypeA-like plasmid) and showed a multidrug-resistance phenotype. Phylogenetic analysis demonstrated that Kp_HM-1 was more closely related to Kp_FZcro-1 than to the other colonizing strains. The Kp_FZcol-2 genome showed an 81 % coverage with the Kp_HM-1 246,730 bp plasmid (pKp_HM-1), lacking most of the plasmid's putative virulence genes. Searching public genomes with similar coverage, we observed the occurrence of this deletion in K. pneumoniae ST307 strains recovered from human colonization and infection in different countries. Our findings suggest that strains lacking the putative virulence genes found in the pKPN3–307 TypeA plasmid are still able to colonize and infect humans, highlighting the need to further investigate the role of these genes for the adaptation of K. pneumoniae ST307 in distinct human body sites.

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