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Klebsiella Infections / DNA Replication / Phage Therapy · Journal article
Virulence · August 24, 2026
Encouraging direction, but not yet definitive.
This study isolated a broad-host-range lytic phage (vB_KP_P4) capable of infecting 109 diverse K. pneumoniae strains, including multidrug-resistant and carbapenem-resistant isolates, and identified three phage-encoded genes (nadM, comEB, rfcS) whose deletion severely restricted the host spectrum. Targeted deletion of these genes reduced the host range to 5–9 strains and compromised infectivity, and wild-type phage improved survival in a mouse bacteremia model, suggesting these genes are functionally important for broad-spectrum lytic activity.
Phage isolation, genomic characterization, targeted mutagenesis (plasmid-assisted homologous recombination and CRISPR-based selection), plaque assays, and mouse bacteremia model. K. pneumoniae isolate panel (composition not detailed); multidrug-resistant, carbapenem-resistant, and ESBL-producing strains included. Mouse model (strain, numbers, and specific infection conditions not stated).. Intervention: Wild-type phage vB_KP_P4 and targeted deletion mutants (ΔnadM, ΔcomEB, ΔrfcS).. Compared with: Wild-type phage versus deletion mutants in host range assays; wild-type phage versus untreated or control group in mouse bacteremia model (details not provided).. Not explicitly stated; authors affiliated with institutions in Xinjiang, China..
Wild-type phage vB_KP_P4 lysed 109 diverse K. pneumoniae strains, including 58.8% of carbapenem-resistant, 40.0% of ESBL-producing, and 59.6% of multidrug-resistant isolates. Deletion of nadM reduced host range to 5 strains versus 109 for wild type. Deletion of comEB reduced host range to 9 strains versus 109 for wild type.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
These findings identify candidate genetic determinants of phage host range and suggest that rational engineering of anti-defense genes may expand the therapeutic window of phage therapy for drug-resistant K. pneumoniae. However, this work is preclinical and requires further validation in relevant infection models and safety assessment before clinical translation.
A sound single-centre phage isolation and characterization study with genetic validation in vitro and a single in vivo model, identifying candidate anti-defense genes associated with broad host range; results are real but require confirmation in clinical settings.
As stated by the source record.
Quoted from the source exactly as published.
These findings identify candidate genetic determinants of phage host range and suggest that rational engineering of anti-defense genes may expand the therapeutic window of phage therapy for drug-resistant K. pneumoniae. However, this work is preclinical and requires further validation in relevant infection models and safety assessment before clinical translation.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Phage therapy for drug-resistant Klebsiella pneumoniae (K. pneumoniae) is limited by narrow host ranges. We isolated a broad-host-range phage, vB_KP_P4, that lyses 109 diverse K. pneumoniae strains, including multidrug-resistant (MDR) and carbapenem-resistant isolates. We suggest that its broad lytic spectrum is likely linked to its capacity to overcome host intracellular defenses. We provide genetic and comparative genomic insights indicating that three phage-encoded genes, deoxycytidylate deaminase (comEB), nicotinamide-nucleotide adenylyltransferase (nadM), and a DNA polymerase clamp loader (rfcS), are correlated with the ability of vB_KP_P4 to infect diverse K. pneumoniae. Deletion of these genes collapsed the host spectrum from 109 strains to fewer than 10, significantly compromising antibacterial efficacy. The wild-type phage substantially improves survival in a mouse bacteremia model. Our study identifies candidate genetic factors associated with the broad host range phenotype, specifically targeting host immunity, and provides a new strategy for engineering therapeutic phages.
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