关键词: Acinetobacter baumannii CirA Italy KPC-154 KPC-3 KPC-31 Klebsiella pneumoniae Providencia stuartii ST512 VIM-1 antimicrobial resistance avibactam bacteria carbapenemase carbapenemase co-production cefiderocol ceftazidime colistin resistance fosfomycin resistance inhibitor-resistant variants meropenem outer membrane porin disruption respiratory infections sequence type 512 siderophore disruption vaborbactam

Mesh : Humans Ceftazidime / pharmacology therapeutic use Meropenem / therapeutic use Anti-Bacterial Agents / pharmacology therapeutic use Klebsiella pneumoniae / genetics Bacterial Proteins / genetics beta-Lactamases / genetics Italy / epidemiology Klebsiella Infections / drug therapy epidemiology microbiology Microbial Sensitivity Tests Cefiderocol

来  源:   DOI:10.3201/eid2911.230921   PDF(Pubmed)

Abstract:
In February 2022, a critically ill patient colonized with a carbapenem-resistant K. pneumoniae producing KPC-3 and VIM-1 carbapenemases was hospitalized for SARS-CoV-2 in the intensive care unit of Policlinico Umberto I hospital in Rome, Italy. During 95 days of hospitalization, ceftazidime/avibactam, meropenem/vaborbactam, and cefiderocol were administered consecutively to treat 3 respiratory tract infections sustained by different bacterial agents. Those therapies altered the resistome of K. pneumoniae sequence type 512 colonizing or infecting the patient during the hospitalization period. In vivo evolution of the K. pneumoniae sequence type 512 resistome occurred through plasmid loss, outer membrane porin alteration, and a nonsense mutation in the cirA siderophore gene, resulting in high levels of cefiderocol resistance. Cross-selection can occur between K. pneumoniae and treatments prescribed for other infective agents. K. pneumoniae can stably colonize a patient, and antimicrobial-selective pressure can promote progressive K. pneumoniae resistome evolution, indicating a substantial public health threat.
摘要:
2022年2月,在罗马PoliclinicoUmbertoI医院的重症监护病房,一名患有耐碳青霉烯类肺炎克雷伯菌的重症患者因SARS-CoV-2而住院。意大利。在住院95天期间,头孢他啶/阿维巴坦,美罗培南/vaborbactam,连续给予头孢地洛治疗3种不同细菌制剂引起的呼吸道感染。这些疗法改变了在住院期间定植或感染患者的肺炎克雷伯菌序列类型512的抗性组。肺炎克雷伯氏菌序列512型耐药组的体内进化是通过质粒丢失发生的,外膜孔蛋白改变,和cirA铁载体基因的无义突变,导致高水平的头孢地洛抗性。交叉选择可以发生在肺炎克雷伯氏菌和其他感染因子的治疗之间。肺炎克雷伯菌可以稳定定植于患者,和抗微生物选择性压力可以促进进行性肺炎克雷伯菌耐药性进化,这表明了对公众健康的巨大威胁。
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