INTRODUCTION
Bacteriophages, also known as phages, are viruses that were first described in 1915 by an English bacteriologist, Frederick Twort, when he published findings of an agent capable of destroying bacteria.1,2 This has since led to the development of “phage therapy”, a process of utilizing these viruses to infect and lyse bacteria at a site of infection.3,4 In the past, naturally-occurring bacteriophages were used as treatment, however, recent advancements in bioengineering and molecular biology enabled for specific pathogen targeting through a multitude of modalities.4 One of the major advancements entails the utilization of phage lytic enzymes to lyse the bacteria via three major avenues including phage-derived lysins, bioengineered chimeric lysins, and the combination of lysins and antibiotics together.4 To date, these various advancements have successfully treated infections such as dysentery, sepsis, and meningitis.4-7
More recently, the treatment of acne, skin infections, and burn grafting have been explored as other potential avenues of bacteriophage usage. This sparked considerable interest in the dermatology community and inquisition as to whether or not bacteriophages can squelch difficult to treat infections and the growing concerns of antibiotic resistance. We highlight Cutibacterium acnes (C. acnes), Staphylococcus aureus (S. aureus), Pseudomonas aeruginosa (P. aeruginosa), and Klebsiella pneumoniae (K. pneumoniae) to endorse that bacteriophage therapy can, in fact, fight antibiotic resistance and offers an innovative solution to the field of dermatology.
Life Cycles
Bacteriophages contain genetic material in the form of either DNA or RNA that is enclosed within a protein coat.8 To spread this genetic material to a host, the bacteriophage must first bind specific receptors on the bacterial cell surface. Once bound, the “tail” of the bacteriophage creates a hole and injects viral genetic material into the host cell. Upon injection of their genetic material, phages are capable of entering one of two different life cycles: the lytic cycle or lysogenic cycle.
The lytic cycle, also referred to as a virulent infection, occurs when phages immediately hijack the host cell’s cellular processes for self-replication. The phage replaces the host DNA with its own and synthesizes additional proteins needed to construct new phage molecules. Eventually, the host loses its integrity and lyses to release hundreds of new phage progeny.9
In addition to the lytic cycle, bacteriophages are also able to enter the lysogenic cycle, also known as a non-virulent infection. In this particular cycle, phages do not rapidly divide and kill the host cell. Rather, they lay dormant and integrate themselves into the host genome using special proteins known as integrases. This integrated form of the bacteriophage is known as a prophage, and its genome is replicated along with the host's genome without negatively affecting the host. When the host comes across stressors such as UV light or low nutrient levels, the prophage may spontaneously enter the lytic cycle by removing themselves from the host genome in a process known as induction.
More recently, the treatment of acne, skin infections, and burn grafting have been explored as other potential avenues of bacteriophage usage. This sparked considerable interest in the dermatology community and inquisition as to whether or not bacteriophages can squelch difficult to treat infections and the growing concerns of antibiotic resistance. We highlight Cutibacterium acnes (C. acnes), Staphylococcus aureus (S. aureus), Pseudomonas aeruginosa (P. aeruginosa), and Klebsiella pneumoniae (K. pneumoniae) to endorse that bacteriophage therapy can, in fact, fight antibiotic resistance and offers an innovative solution to the field of dermatology.
Life Cycles
Bacteriophages contain genetic material in the form of either DNA or RNA that is enclosed within a protein coat.8 To spread this genetic material to a host, the bacteriophage must first bind specific receptors on the bacterial cell surface. Once bound, the “tail” of the bacteriophage creates a hole and injects viral genetic material into the host cell. Upon injection of their genetic material, phages are capable of entering one of two different life cycles: the lytic cycle or lysogenic cycle.
The lytic cycle, also referred to as a virulent infection, occurs when phages immediately hijack the host cell’s cellular processes for self-replication. The phage replaces the host DNA with its own and synthesizes additional proteins needed to construct new phage molecules. Eventually, the host loses its integrity and lyses to release hundreds of new phage progeny.9
In addition to the lytic cycle, bacteriophages are also able to enter the lysogenic cycle, also known as a non-virulent infection. In this particular cycle, phages do not rapidly divide and kill the host cell. Rather, they lay dormant and integrate themselves into the host genome using special proteins known as integrases. This integrated form of the bacteriophage is known as a prophage, and its genome is replicated along with the host's genome without negatively affecting the host. When the host comes across stressors such as UV light or low nutrient levels, the prophage may spontaneously enter the lytic cycle by removing themselves from the host genome in a process known as induction.
