Journal of Pharmacogenomics & Pharmacoproteomics

Heterogeneous Clinical Isolates of Pseudomonas aeruginosa using Genomic Characterization of Lytic Bacteriophages

Doi Casey^* Department of Microbial Pathogenesis, University of Maryland School of Dentistry, Baltimore, Maryland, United States of America
^*Correspondence: Doi Casey, Department of Microbial Pathogenesis, University of Maryland School of Dentistry, Baltimore, Maryland, United States of America, Email:

Received: 01-Nov-2022, Manuscript No. JPP-22-19031; Editor assigned: 04-Nov-2022, Pre QC No. JPP-22-19031 (PQ); Reviewed: 18-Nov-2022, QC No. JPP-22-19031; Revised: 25-Nov-2022, Manuscript No. JPP-22-19031 (R); Published: 01-Dec-2022, DOI: 10.35248/2153-0645.22.13.029

Description

Pseudomonas aeruginosa infections can be challenging to treat bacteriophage therapy is a substitute for conventional antibiotics however there are enough isolated and well-characterized phases obtainable. We collected 23 different Pseudomonas aeruginosa isolates from patients with Cystic Fibrosis (CF) and clinical illnesses, and we then utilized those isolates to screen hospital wastewater and isolate over a dozen Pseudomonas aeruginosa- targeting phases. A severe threat to public health is created by the fact that multidrug-resistant bacteria are continuing to evolve at a faster rate than new antimicrobials are being created. Although efforts to stop the spread of antibiotic-resistant infections, rates of infection and mortality caused by these organisms are rising in both the United States and globally.

Genome sequencing, comparative genomics, and lytic activity testing against all 23 bacterial host isolates were used to characterise phases. We created four different phage-resistant bacterial mutants. Additionally, we examined the capacity of phases to eradicate Pseudomonas aeruginosa produced in biofilms further use airway epithelial cells. Overall, this study shows how precise antibiotic bacteriophages may be created through thorough genomic and phenotypic characterisation.

Seudomonas aeruginosa is a Gram-negative bacterium that can cause pneumonia and bacteraemia among other illnesses. Cystic fibrosis (CF) patients' airways become persistently colonised with Pseudomonas aeruginosa, which is linked to higher morbidity and death in this population. The genetic and phenotypic variety of the Pseudomonas aeruginosa species is quite broad, and strains that are multidrug resistant frequently develop as a result of protracted antibiotic therapy. Development of novel and more potent medicines to treat Pseudomonas aeruginosa infections is imperative due to Pseudomonas aeruginosa success as an opportunistic pathogen, tendency to develop drug resistance, and significant harm it poses to people with Cystic Fibrosis (CF).

Genomic and phenotypic differences of phage-resistant mutant bacteriophages and their prey co-evolve with their hosts and other members of host-associated microbial ecosystems. Strong selection pressure from phage predation on bacterial hosts frequently results in changes in the bacterial genome that confer resistance. We identified individual colonies of phage-resistant mutants for the four phases PSA09, PSA11, PSA20, and PSA34 during phage propagation. After being evaluated for phage resistance, whole-genome sequencing was performed on mutant isolates that had shown resistance. The hybrid assembled genome of the relevant phage-susceptible parent isolate and each resistant mutant were found by mapping sequencing reads to their respective genomes. One or two protein-altering mutations were encoded by each genome of a phage-resistant mutant. We were able to locate suspected phage resistance-granting mutations in the genome of each mutant isolate based on the annotation of each altered gene. Mutation was discovered in a phage-resistant mutant in the 639 isolate backgrounds that was resistant to the phage PSA20.

Mutants with phage resistance and phenotyping Phage-resistant mutants were kept for further characterisation when they were discovered when making high-dilution phage lysates. On BHI agar, isolated bacterial colonies were restricted. By dilution the same lysate of the phage on both the parent and resistant mutant isolates and confirming a high dilution on the parent isolate but no phage activity against the resistant mutant, phage resistance was established. To be sure they weren't glycogens resistant mutants were also discovered on the parent bacterial isolate's lawn.