Antibiotic resistance has been a self-perpetuating issue, in that as doctors attempt to treat bacterial infections with antibiotics, these bacteria become resistant and can no longer be killed. New, more powerful forms of bacteria such as MRSA have made headlines, and doctors and the human body is all but defenseless against these so-called “superbugs”. But how did this problem come up in the first place?
The first antibiotic was penicillin, invented by Alexander Fleming in 1928. Reportedly, he discovered this drug when he observed that bacteria were not growing in an area with this liquid. As mentioned in our Drug Discovery post, “stumbling” upon a treatment is rare, but this trip-up helped spark a revolution in the treatment of diseases.
Penicillin became a worldwide phenomenon, as more and more doctors became aware of the power of such a drug. However, as they say, with great power comes great responsibility. And people abused this power.
Nowadays, antibiotics are very prominent in drugs around the world. Antibiotics have been used to treat the biggest diseases and bacterial infections of our century, such as ear infections. However, antibiotics cannot treat viral infections, such as the common cold, because since viruses insert their genetic material into a human cell's DNA in order to reproduce, bacteria and viruses have different mechanisms and machinery to survive and replicate. The antibiotic has no “target” to attack in a virus. Doctors began to prescribe antibiotics for many diseases, sometimes excessively, contributing to the global issue of antibiotic resistance. The bacteria that survives the treatment is mutated to be able to do so, and pumping the body with the same medicine no longer has an effect.
However, there exists a different form of bacterial treatment: bacteriophage. Bacteriophage (phage) are microscopic virions that infect bacteria as a host. While phage therapy has existed in Russia, Western countries have been slow to adopt the novel-to-them idea, having placed strict regulations on phage therapy in humans. Phage may actually be more effective than Western antibiotics because they can mutate and kill bacteria despite some temporary resistance, as phage and host are locked in an evolutionary arms race. Since evolution forms the core of the global problem of antibiotic resistance, phage are able to attack the issue at its heart, continually evolving alongside their host.
Phage follow one of two infection pathways, more commonly through the lytic cycle. As soon as a lytic phage enters the bacteria, it uses the host’s organelles to produce more virions. Eventually, too many virions cause an increase in pressure within the bacterial cell, causing it to pop (lyse), releasing the phage that go on to infect new hosts.
Lysogenic phage, on the other hand, may transition between a lytic virion-production stage, and a dormant stage. In normal conditions, the phage inserts its genetic information into the bacteria, but is not translated into more virions. This info gets copied as the bacterium replicates, essentially placing land mines in the bacterial genome, waiting for the right time to go off. When the phage detects that conditions are deteriorating, its genes will “switch on”, transitioning to the lytic cycle and killing the host. While the mechanism for this detection is still unknown, lysogenic phage may still be useful in human treatment.
There still needs to be further research done on phage therapy to determine its safety and efficacy. However, they may hold promise of a future void of antibacterial resistance.