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Bacteriophages come in different sizes and shapes but most of them have the same basic features: a head or capsid and a tail. A bacteriophage’s head structure, regardless of its size or shape, is made up of one or more proteins which protectively coats the nucleic acid. Though there are some phages that don’t have a tail, most of them do have one attached to its head structure.

How Bacteriophages Work

n oder to infect a host cell, the bacteriophage attaches itself to the bacteria’s cell wall, specifically on a receptor found on the bacteria’s surface. Once it becomes tightly bound to the cell, the bacterial virus injects its genetic material (its nucleic acid) into the host cell. Depending on the type of phage, one of two cycles will occur – the lytic or the lysogenic cycle. During a lytic cycle, the phage will make use of the host cell’s chemical energy as well as its biosynthetic machinery in order to produce phage nucleic acids (phage DNA and phage mRNA) and phage proteins. Once the production phase is finished, the phage nucleic acids and structural proteins are then assembled. After a while, certain proteins produced within the cell will cause the cell wall to lyse, allowing the assembled phages within to be released and to infect other bacterial cells.

Viral reproduction can also occur through the lysogenic cycle. The main difference between the two types of cycles is that during lysogeny, the host cell is not destroyed or does not undergo lysis. Once the host cell is infected, the phage DNA integrates or combines with the bacterial chromosome, creating the prophage. When the bacterium reproduces, the prophage is replicated along with the host chromosomes. Thus, the daughter cells also contain the prophage which carries the potential of producing phages. The lysogenic cycle can continue indefinitely (daughter cells with prophage present within continuing to replicate) unless exposed to adverse conditions which can trigger the termination of the lysogenic state and cause the expression of the phage DNA and the start of the lytic cycle. These adverse conditions include exposure to UV or mutagenic chemicals and desiccation.

http://phages.org/bacteriophage/

Patients in hospitals, especially those on breathing machines, those with devices such as catheters, and patients with wounds from surgery or from burns are potentially at risk for serious, life-threatening infections.

n hospitals, where the most serious infections occur, Pseudomonas can be spread on the hands of healthcare workers or by equipment that gets contaminated and is not properly cleaned.

https://www.cdc.gov/hai/organisms/pseudomonas.html

 P. aeruginosa can develop resistance to antibacterials either through the acquisition of resistance genes on mobile genetic elements (i.e., plasmids) or through mutational processes that alter the expression and/or function of chromosomally encoded mechanisms. Both strategies for developing drug resistance can severely limit the therapeutic options for treatment of serious infections. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772362/

Multidrug-resistant Pseudomonas can be deadly for patients in critical care.  An estimated 51,000 healthcare-associated P. aeruginosa infections occur in the United States each year. More than 6,000 (13%) of these are multidrug-resistant, with roughly 400 deaths per year attributed to these infections.   Multidrug-resistant Pseudomonas was given a threat level of serious threat in the  CDC AR Threat report .

https://www.cdc.gov/hai/organisms/pseudomonas.html

Antibacterial Resistance Trends

Presented in Table ​Table11 are rates of P. aeruginosa resistance to several antipseudomonal drugs (54, 95, 99, 100, 178, 211, 212). This summary is not meant to be inclusive of all of the published literature, but rather highlights data reported for isolates from several U.S. surveillance studies since January 2000. If multiple years were included in a study, the resistance rates for the most recent year are presented in Table ​Table11.

Rates of antibacterial resistance among P. aeruginosa isolates from hospitals and ICUs

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772362/

Each set must be modified twice a year to retain its ability to lyse a large proportion of the target species [5], [11]. P. aeruginosa bacteriophages are numerous, and current knowledge of their diversity shows that they are distributed in at least 7 genera of purely lytic phages (T7-like, ΦKMV-like, LUZ24-like, N4-like, PB1-like, ΦKZ-like, JG004-like) in addition to a similar number of temperate genera [12], [13]. Within each genus, phages with a variety of different host spectra are observed, in part at least reflecting differences in their tail-associated adhesins 

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0060575

In- vitro and In- vivo Phage Trials