Research Group for Host-Microbe Interactions, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway; Norwegian National Advisory Unit on Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway.
Research Group for Host-Microbe Interactions, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway.
J Glob Antimicrob Resist. 2024 Mar;36:116-122. doi: 10.1016/j.jgar.2023.12.010. Epub 2023 Dec 19.
Enterococci are opportunistic pathogens with plastic genomes that evolve, acquire, and transmit antimicrobial-resistant determinants such as vancomycin resistance clusters. While vancomycin-resistant enterococci (VRE) have emerged as successful nosocomial pathogens, the mechanism by which vancomycin-susceptible enterococci (VSE) transform to VRE in hospitalized patients remains understudied.
Genomes of Enterococcus faecium from two critically ill hospitalized patients subjected to multiple antibiotic therapies, including broad-spectrum antibiotics, were investigated. To identify mechanisms of resistance evolution, genomes of vancomycin-susceptible and -resistant isolates were compared.
While VSE isolates were initially identified, VRE strains emerged post-vancomycin therapy. Comparative genomics revealed horizontal transmission of mobile genetic elements containing the Tn1549 transposon, which harbours the vanB-type vancomycin resistance gene cluster. This suggests that broad-spectrum antibiotic stress promoted the transfer of resistance-conferring elements, presumably from another gut inhabitant.
This is one of the first studies investigating VSE and VRE isolates from the same patient. The mechanism of transmission and the within-patient evolution of vancomycin resistance via mobile genetic elements under antibiotic stress is illustrated. Our findings serve as a foundation for future studies building on this knowledge which can further elucidate the dynamics of antibiotic stress, resistance determinant transmission, and interactions within the gut microbiota.
肠球菌是具有可塑性基因组的机会性病原体,能够进化、获得和传播抗菌药物耐药决定因素,如万古霉素耐药簇。虽然万古霉素耐药肠球菌(VRE)已经成为成功的医院获得性病原体,但在住院患者中,万古霉素敏感肠球菌(VSE)向 VRE 转化的机制仍研究不足。
对两名接受多种抗生素治疗(包括广谱抗生素)的重症住院患者的屎肠球菌基因组进行了研究。为了确定耐药进化的机制,比较了万古霉素敏感和耐药分离株的基因组。
尽管最初鉴定出 VSE 分离株,但在万古霉素治疗后出现了 VRE 菌株。比较基因组学揭示了含有 Tn1549 转座子的移动遗传元件的水平传播,该转座子携带有 vanB 型万古霉素耐药基因簇。这表明广谱抗生素应激促进了耐药基因赋予因子的转移,可能来自另一个肠道居民。
这是首次对来自同一患者的 VSE 和 VRE 分离株进行的研究之一。本文阐述了在抗生素应激下通过移动遗传元件传播和患者体内万古霉素耐药性的进化机制。我们的发现为未来的研究提供了基础,这些研究可以进一步阐明抗生素应激、耐药决定因素传播以及肠道微生物群内相互作用的动态。