Control of infections caused by carbapenem-resistant Klebsiella pneumoniae continues to be challenging. The success of this pathogen is favored by its ability to acquire antimicrobial resistance and to spread and persist in both the environment and in humans. The emergence of clinically important clones, such as sequence types 11, 15, 101, and 258, has been reported worldwide. However, the mechanisms promoting the dissemination of such high-risk clones are unknown. Unraveling the factors that play a role in the pathobiology and epidemicity of K. pneumoniae is therefore important for managing infections. To address this issue, we studied a carbapenem-resistant ST-15 K. pneumoniae isolate (Kp3380) that displayed a remarkable adherent phenotype with abundant pilus-like structures. Genome sequencing enabled us to identify a chaperone-usher pili system (Kpi) in Kp3380. Analysis of a large K. pneumoniae population from 32 European countries showed that the Kpi system is associated with the ST-15 clone. Phylogenetic analysis of the operon revealed that Kpi belongs to the little-characterized γ₂-fimbrial clade. We demonstrate that Kpi contributes positively to the ability of K. pneumoniae to form biofilms and adhere to different host tissues. Moreover, the in vivo intestinal colonizing capacity of the Kpi-defective mutant was significantly reduced, as was its ability to infect Galleria mellonella. The findings provide information about the pathobiology and epidemicity of Kpi⁺ K. pneumoniae and indicate that the presence of Kpi may explain the success of the ST-15 clone. Disrupting bacterial adherence to the intestinal surface could potentially target gastrointestinal colonization.

由耐碳青霉烯类的肺炎克雷伯菌引起的感染的控制仍然具有挑战性。该病原体的成功在于其获得抗菌素耐药性以及在环境和人类中扩散和持久的能力。临床上重要的克隆的出现，例如序列类型11、15、101和258，已在世界范围内报道。但是，促进这种高风险克隆传播的机制尚不清楚。因此，揭示在肺炎克雷伯菌的病理生物学和流行中起作用的因素对于控制感染很重要。为了解决这个问题，我们研究了耐碳青霉烯的ST-15肺炎克雷伯菌分离株（Kp3380），表现出显着的粘附表型，具有丰富的菌毛状结构。基因组测序使我们能够鉴定Kp3380中的伴侣-指肠菌毛系统（Kpi）。对来自32个欧洲国家的大量肺炎克雷伯菌的分析表明，Kpi系统与ST-15克隆有关。该操纵子的系统发育分析表明，KPI属于小表征的γ ₂ -fimbrial进化枝。我们证明Kpi有助于肺炎克雷伯菌形成生物膜并粘附于不同宿主组织的能力。此外，Kpi缺陷型突变体在体内的肠道定植能力显着降低，并且它感染了马勒菌廊。该发现提供了有关Kpi ⁺ 肺炎克雷伯菌的病理生物学和流行性的信息，并表明Kpi的存在可能解释了ST-15克隆的成功。破坏细菌对肠表面的粘附可能会靶向胃肠定植。