Table 2.

Comparison between phage therapy and antibiotics (Kortright 2019)

Sr. No.	Parameters	Phage therapy	Antibiotics
1.	Bactericidal agent	Virulent phages cause cell lysis, which is bactericidal while bioengineered phages are bacteriostatic and prevent the growth of phages	Antibiotics cause cell death also known as bactericidal or can prevent the growth of bacteria known as bacteriostatic
2.	Discovery	Phage discovery is easy and rapid	Antibiotic discovery is time-consuming, expensive which requires drug design and development processes along with toxic potential testing
3.	Specificity	Bacteriophages are known to be highly specific and have a narrow spectrum of activity	Antibiotics have a broad spectrum of activity
4.	Microbiota disruption	Host specificity of phages leads to no disruption of the normal microbiota	Antibiotics with a broad-spectrum mode of action lead to disruption of the normal microbiota
5.	Side effects	Unlike antibiotics, phage therapy does not cause anaphylaxis in humans	Many include allergies and anaphylactic disorders
6.	Toxicity	Phages are nontoxic but lysed cell remnants may cause allergies in some cases	Toxicity levels can vary depending on the dosage and conditions of the patient
7.	Versatility	Phages are versatile, i.e., they display genetic diversity and abundance Phages can be delivered by various delivery systems and approaches Phages can be customized, i.e., phage cocktails can be administered depending on the bacteria that is being targeted	Antibiotics are not as versatile as compared to phages; to make them more effective, they can be used in combination with phages
8.	Resistance	The narrow range of activity of phages makes it specific; if resistance emerges then only a selected few bacterial species populations will be affected To reduce the chances of the development of resistance cocktail formulations can be used to treat antibiotic-resistant pathogens	A broad range of activity means that a large population of bacteria can be exposed to the antibiotic and there are greater chances of development of resistance against the bacteria and the potential for widespread resistance to emerge is greater
9.	Dosage	Dose concentration increases due to the process of host-dependent replication that increases the number of bacteriophages	The dose is dependent on the adsorption, distribution, metabolism, and excretion of the antibiotic
10.	Self-limitation	Once the target bacteria are killed, the bacteriophages stop functioning	No self-limitation occurs in antibiotics
11.	Availability of clinical evidence	Fewer clinical trials and studies are available; information about clinical relevance is still limited	Enough clinical studies and information about clinical relevance are available
12.	Development costs	Rapid and low-cost	Time-consuming and expensive
13.	Kinetics	Single hit or self-amplifying	Single hit
14.	Formulation	Fixed or variable	Fixed
15.	Immunogenicity	Low/yet to be established	Variable
16.	Regulation	Underway	Well-established