Institute for Infectious Diseases, University of Bern, Bern, Switzerland; Department of Infectious Diseases, Bern University Hospital, University of Bern, Bern, Switzerland.
Institute for Infectious Diseases, University of Bern, Bern, Switzerland.
J Glob Antimicrob Resist. 2017 Sep;10:165-170. doi: 10.1016/j.jgar.2017.04.006. Epub 2017 Jul 17.
We describe the first two multifocal invasive infections due to Klebsiella pneumoniae recently observed in Switzerland.
Phenotypic (MIC assays and string test) and molecular analyses (PCR/Sequencing for bla, virulence factor genes and whole genome sequencing for one strain) were performed to characterize the causative K. pneumoniae isolates.
Both K. pneumoniae isolates (Kp1 and Kp2) were pan-susceptible to antibiotics and produced narrow-spectrum SHV β-lactamases. However, only Kp1 was string test positive. Kp1 was of ST380 and caused liver abscess as well as pneumonia and orbital phlegmon in an Eritrean patient. It belonged to the hypervirulent capsular serotype K2 and harboured the classic virulence-associated rmpA and aerobactin genes, fulfilling both the clinical and microbiological definitions for an invasive K. pneumoniae syndrome. Kp2 was of ST1043 and caused both liver abscess and endocarditis in a Swiss patient. Moreover, it did not possess the classic virulence-associated genes. Whole genome sequencing identified less well-known virulence factors in Kp2 that might have contributed to its virulence. Among these there were genes important for intestinal colonization and/or invasion, such as genes involved in adhesion (e.g., fimABCD and mrkABCD), regulation of capsule polysaccharide biosynthesis (e.g., evgS-evgA), as well as iron uptake (iroN), energy conversion, and metabolism.
This report confirms the continuous dissemination of hypervirulent K. pneumoniae strains among patients of non-Asian descent in Europe. Moreover, it highlights the genetic background of an atypical hypervirulent K. pneumoniae causing a severe invasive infection despite not possessing the classical virulence characteristics of hypermucoviscous strains.
我们描述了最近在瑞士观察到的首例两例由肺炎克雷伯菌引起的多灶性侵袭性感染。
对致病的肺炎克雷伯菌分离株进行表型（药敏试验和串珠试验）和分子分析（PCR/测序bla 基因、毒力因子基因和一株全基因组测序）。
两株肺炎克雷伯菌（Kp1 和 Kp2）对所有抗生素均敏感，产生窄谱 SHV β-内酰胺酶。然而，只有 Kp1 串珠试验阳性。Kp1 为 ST380 型，引起肝脓肿以及一名厄立特里亚患者的肺炎和眼眶蜂窝织炎。它属于高毒力荚膜血清型 K2，携带经典的与毒力相关的 rmpA 和 aerobactin 基因，符合侵袭性肺炎克雷伯菌综合征的临床和微生物学定义。Kp2 为 ST1043 型，引起一名瑞士患者的肝脓肿和心内膜炎。此外，它不具有经典的与毒力相关的基因。全基因组测序确定了 Kp2 中较少为人知的毒力因子，这些因子可能与其毒力有关。其中包括与肠道定植和/或侵袭有关的基因，如参与黏附的基因（如 fimABCD 和 mrkABCD）、调节荚膜多糖生物合成的基因（如 evgS-evgA），以及铁摄取（iroN）、能量转换和代谢的基因。
本报告证实了高毒力肺炎克雷伯菌在欧洲非亚洲血统的患者中不断传播。此外，它强调了一种非典型高毒力肺炎克雷伯菌的遗传背景，尽管它不具有高黏液性菌株的典型毒力特征，但仍能引起严重的侵袭性感染。
