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高毒力肺炎克雷伯菌引发主动脉炎时,会保留其荚膜和黏液黏稠度,并且随着时间推移在基因型和表型上保持稳定。

Hypervirulent Klebsiella pneumoniae causing aortitis retains its capsule and mucoviscosity and remains genotypically and phenotypically stable over time.

作者信息

Russo Thomas A, Carlino-MacDonald Ulrike, Drayer Zachary J, Davies Connor J, Hutson Alan, Luo Ting L, Martin Melissa J, McGann Patrick T, Lebreton Francois, Sanders Alan

机构信息

University at Buffalo, State University of New York.

Roswell Park Comprehensive Cancer Center.

出版信息

Res Sq. 2025 Aug 5:rs.3.rs-6740913. doi: 10.21203/rs.3.rs-6740913/v1.

Abstract

Aortitis due to hypervirulent (hvKp) in a Belarusian male from central New York is described. Isolates at the time of diagnosis (Kp031824-1, Kp031824-2) and after 12 weeks of antimicrobial therapy (Kp070124) were characterized. Kp070124 was genomically and phenotypically unchanged retaining its capsular polysaccharide and mucoviscosity. studies established that capsule minus derivatives of Kp031824-1 and Kp031824-2 can occur due to mutations in . But this genotype/phenotype was not selected for in Kp070124 after ≥15 weeks in the systemic compartment. Compared to capsule minus derivatives, the capsule positive phenotype demonstrated resistance to phagocytosis, but not to complement mediated bactericidal activity, suggesting resistance to phagocytosis is a more important defense mechanism at this site of infection. These data also support that a capsule positive, mucoviscous phenotype is selected for during infections in the systemic compartment. The surprising result that capsule positive strains have increased sensitivity to complement mediated bactericidal activity compared to capsule minus strains requires further investigation. The duration of therapy for this syndrome remains unclear but should be prolonged; adjunctive therapies (e.g. phage therapy, passive immunization, augmentation of cell mediated bactericidal activity) may be needed to overcome the protection endowed by the mucoviscous capsule of hvKp.

摘要

本文描述了一名来自纽约中部的白俄罗斯男性因高毒力肺炎克雷伯菌(hvKp)引起的主动脉炎。对诊断时(Kp031824 - 1、Kp031824 - 2)和抗菌治疗12周后(Kp070124)分离出的菌株进行了特征分析。Kp070124在基因组和表型上均未发生变化,保留了其荚膜多糖和黏液性。研究表明,Kp031824 - 1和Kp031824 - 2的无荚膜衍生物可能是由于……中的突变而产生的。但在全身腔室中≥15周后,Kp070124并未选择这种基因型/表型。与无荚膜衍生物相比,有荚膜的表型表现出对吞噬作用的抗性,但对补体介导的杀菌活性不具有抗性,这表明对吞噬作用的抗性是该感染部位更重要的防御机制。这些数据还支持在全身腔室感染期间选择有荚膜、黏液性的表型。与无荚膜菌株相比,有荚膜菌株对补体介导的杀菌活性敏感性增加这一惊人结果需要进一步研究。该综合征的治疗持续时间仍不清楚,但应延长;可能需要辅助治疗(如噬菌体治疗、被动免疫、增强细胞介导的杀菌活性)来克服hvKp黏液性荚膜所赋予的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c8c/12340923/a1afe4d5b84e/nihpp-rs6740913v1-f0001.jpg

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