The increasing prevalence of Carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a serious threat to global health. Phages and phage-derived enzymes gained increasing attention for controling CRKP infections. In this study, a lytic phage P510 infecting KL64 type K. pneumoniae was isolated and characterized. Whole genome analysis and electron microscopy analysis showed that phage P510 belonged to genus Przondovirus, family Autographiviridae, the order Caudovirales. The tail fiber protein of the phage was predicted to encode capsule depolymerase. Further analysis demonstrated that recombinant depolymerase P510dep had polysaccharide-degrading activity against KL64-types capsule of K. pneumoniae, and its lysis spectrum matched to host range of phage P510. We also demonstrated that the recombinant depolymerase was able to significantly inhibit biofilm formation. The discovery of the phage-derived depolymerase lays the foundation for controlling the spread of CRKPs.

耐碳青霉烯类肺炎克雷伯菌(CRKP)的日益流行对全球健康构成严重威胁。噬菌体和噬菌体衍生酶在控制 CRKP 感染方面受到越来越多的关注。在这项研究中，分离并表征了感染 KL64 型肺炎克雷伯菌的裂解噬菌体 P510 。全基因组分析和电子显微镜分析表明，噬菌体P510属于Przondovirus属，Autographiviridae，Caudovirales目。预测噬菌体的尾纤维蛋白编码荚膜解聚酶。进一步分析表明重组解聚酶P510dep对肺炎克雷伯菌KL64型荚膜具有多糖降解活性，其裂解谱与噬菌体 P510 的宿主范围相匹配。我们还证明重组解聚酶能够显着抑制生物膜形成。噬菌体衍生解聚酶的发现为控制CRKPs的传播奠定了基础。