scholarly journals Building reusable phage and antibiotic treatments via exploitation of bacteria-phage coevolutionary dynamics.

2021 ◽  
Author(s):  
James Gurney ◽  
Sam P Brown

People with chronic (long-lasting) infections face the problem that treatment options diminish in time as the pathogen evolves increasing resistance. To address this challenge, we exploit phage and bacterial co-evolution, producing dynamic selection pressures that can return the pathogen to a state of susceptibility to the initial (regulator-approved) therapy. We show that phage OMKO1 alone triggers Arms Race Dynamic (ARD) co-evolution with the pathogen Pseudomonas aeruginosa, leading to generalized phage resistance and crucially - failure at reuse. In contrast, co-administration of the phage with antibiotics triggers Fluctuating Selection Dynamics (FSD) co-evolution, allowing for effective reuse after 20 days of treatment. We pursue medical relevance in our experiments with the use of clinically important pathogens, antibiotics, phage, and a benchmarked synthetic sputum medium. Phenotypic and genomic characterization of evolved isolates demonstrates that efflux-targeting phage OMKO1 exerts continued selection for antibiotic susceptibility regardless of co-evolutionary dynamic or antibiotic co-treatment, opening the door for evolutionary robust phage therapy.

Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1411
Author(s):  
Ying Li ◽  
Yichuan Qiu ◽  
Junping She ◽  
Xu Wang ◽  
Xiaoyi Dai ◽  
...  

The emergence of carbapenem-resistant Proteus represents a serious threat to global public health due to limited antibiotic treatment options. Here, we characterize a Proteus isolate NMG38-2 of swine origin that exhibits extensive drug resistance, including carbapenems. Whole-genome sequencing based on Illumina and MinION platforms showed that NMG38-2 contains 24 acquired antibiotic resistance genes and three plasmids, among which, pNDM_NMG38-2, a pPvSC3-like plasmid, is transferable and co-carries blaNDM-1 and lnu(G). Sequence analysis of pPvSC3-like plasmids showed that they share a conserved backbone but have a diverse accessory module with complex chimera structures bearing abundant resistance genes, which are facilitated by transposons and/or homologous recombination. The acquisition of blaNDM-1 in pNDM_NMG38-2 was due to the ISCR1-mediated integration event. Comprehensive analysis of the lnu(G)-bearing cassettes carried by bacterial plasmids or chromosomes revealed a diversification of its genetic contexts, with Tn6260 and ISPst2 elements being the leading contributors to the dissemination of lnu(G) in Enterococcus and Enterobacteriaceae, respectively. In conclusion, this study provides a better understanding of the genetic features of pPvSC3-like plasmids, which represent a novel plasmid group as a vehicle mediating the dissemination of blaNDM-1 among bacteria species. Moreover, our results highlight the central roles of Tn6260 and ISPst2 in the spread of lnu(G).


2021 ◽  
Author(s):  
Boris Estrada Bonilla ◽  
Ana Rita Costa ◽  
Teunke van Rossum ◽  
Stefan Hagedoorn ◽  
Hielke Walinga ◽  
...  

AbstractBacteriophages are an invaluable source of novel genetic diversity. Sequencing of phage genomes can reveal new proteins with potential uses as biotechnological and medical tools, and help unravel the diversity of biological mechanisms employed by phages to take over the host during viral infection. Aiming to expand the available collection of phage genomes, we have isolated, sequenced, and assembled the genome sequences of four phages that infect the clinical pathogen Klebsiella pneumoniae: vB_KpnP_FBKp16, vB_KpnP_FBKp27, vB_KpnM_FBKp34, and Jumbo phage vB_KpnM_FBKp24. The four phages show very low (0-13%) identity to genomic phage sequences deposited in the Genbank database. Three of the four phages encode tRNAs and have a GC content very dissimilar to that of the host. Importantly, the genome sequences of the phages reveal potentially novel DNA packaging mechanisms as well as distinct clades of tubulin spindle and nucleus shell proteins that some phages use to compartmentalize viral replication. Overall, this study contributes to uncovering previously unknown virus diversity, and provides novel candidates for phage therapy applications against antibiotic-resistant K. pneumoniae infections.


Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
AS Lima ◽  
B Lukas ◽  
J Novak ◽  
AC Figueiredo ◽  
LG Pedro ◽  
...  

2020 ◽  
Vol 20 (7) ◽  
pp. 490-500 ◽  
Author(s):  
Justin S. Becker ◽  
Amir T. Fathi

The genomic characterization of acute myeloid leukemia (AML) by DNA sequencing has illuminated subclasses of the disease, with distinct driver mutations, that might be responsive to targeted therapies. Approximately 15-23% of AML genomes harbor mutations in one of two isoforms of isocitrate dehydrogenase (IDH1 or IDH2). These enzymes are constitutive mediators of basic cellular metabolism, but their mutated forms in cancer synthesize an abnormal metabolite, 2- hydroxyglutarate, that in turn acts as a competitive inhibitor of multiple gene regulatory enzymes. As a result, leukemic IDH mutations cause changes in genome structure and gene activity, culminating in an arrest of normal myeloid differentiation. These discoveries have motivated the development of a new class of selective small molecules with the ability to inhibit the mutant IDH enzymes while sparing normal cellular metabolism. These agents have shown promising anti-leukemic activity in animal models and early clinical trials, and are now entering Phase 3 study. This review will focus on the growing preclinical and clinical data evaluating IDH inhibitors for the treatment of IDH-mutated AML. These data suggest that inducing cellular differentiation is central to the mechanism of clinical efficacy for IDH inhibitors, while also mediating toxicity for patients who experience IDH Differentiation Syndrome. Ongoing trials are studying the efficacy of IDH inhibitors in combination with other AML therapies, both to evaluate potential synergistic combinations as well as to identify the appropriate place for IDH inhibitors within existing standard-of-care regimens.


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