Antibiotics and Superbugs, what happens next?

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In 1928, a group led by Scottish scientist Alexander Fleming accidentally discovered the antimicrobial properties of a strain of mold called Penicillium notatum. Although Fleming’s group could not isolate the specific causative agent, they named the active substance penicillin. Fleming’s interest in combating bacterial disease stemmed partly from his time as a doctor during World War I, where he saw many soldiers suffer profusely from bacterial infection. Nearly twenty years would pass before penicillin became a widely used drug during the battles of World War II. Antibiotics were largely seen as the magic bullet to microbial infection, giving doctors the ability to treat something as simple as strep throat and as dire as gangrene.

Today, medical professionals have an arsenal of antibiotic families at their disposal. These include penicillins, cephalosporins, carbapenems, macrolides, and others. Each family has been constructed to interfere with a specific essential property in bacteria survival, providing chemical warfare against a vast array of bacterial pathogens.

Unfortunately for us, the war is not one sided. And our bullets, although very good, have turned out to be less than magic.

In February of last year, the World Health Organization (WHO) released a report of 12 microbial species identified as priority pathogens in regards to human infection. These include a handful of culprits that can cause diseases most people are commonly aware of, such as Staph infection (s. aureus), stomach ulcers (h. pylori), Salmonella (multiple species), Gonorrhea (N. gonorrhoeae), and Pneumonia (P. aeruginosa and S. pneumonia). (Not included in this report was Tuberculosis, which is mostly treated as its own separate nightmare.) The bacterial members that comprised the list were noted because they have become resistant to some of the most potent antibiotics we have.

The resistance has come to fruition partly because of our own doing. In the last 70 years or so, antibiotics have been prescribed to the point that bacteria have simply adjusted. It’s difficult to blame doctors for trying to help people rid themselves of disease, but the truth is that many of the pathogens of antibiotic concern have simply become accustomed to seeing the same method of attack against them. This remains an issue today, as a collaborative 2016 study led by the CDC estimated that 1 in 3 antibiotic prescriptions are unnecessary.

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Perhaps the most serious resistant phenotype is propagated when a treatment is not entirely successful. To elaborate: say an antibiotic like ceftriaxone, a cephalosporin, kills 95% of a contagious infection like Gonorrhea (lovely, I know) and the infected individual believes all symptoms have passed. Unknown to them, the remaining 5% of the N. gonorrhoeae has a freshly mutated mechanism to escape death from ceftriaxone. Feeling back to normal and symptom free, he or she has sexual contact with a previously uninfected partner. Once this occurs, it’s possible that the newly contacted person has contracted Gonorrhea. To make matters worse, that strain might not succumb to treatment with ceftriaxone, or any cephalosporin for that matter. All of a sudden, there is a resistant strain of Gonorrhea and a new avenue of antibiotic treatment must be explored. Cases like this are why physicians adamantly instruct patients to take a prescription in its entirety, even if he or she feels better before the completion.

A somewhat separate but related issue that has arisen from antibiotic prescriptions has to do with off-target effects of treatment. This is most relevantly seen in C.Diff. Colitis, a rapidly emerging affliction that more than 20,000 Americans die from each year. When a person undergoes antibiotic treatment, the drug is often not only killing the pathogen present inside. Additionally, the drug will kill members of an individual’s microbiota. The microbiota is the full complement of bacteria housed naturally inside us. This vast community varies from person to person, and is essentially an organ that we are still in the infancy of understanding. Unintended depletion of natural microbial company (often called commensal species) we keep can have rather morbid consequences. Antibiotic elimination of these commensals can leave us vulnerable to infection from a secondary pathogen. Commensal bacteria have been shown to aid our immune system in keeping out foreign intruders that can harm us as humans. If an antibiotic happens to target a commensal that helps protect us from a particular form of secondary pathogen, it is easy to see how we become more susceptible to another infection. This is the case with Clostridium difficile, a species that is typically present in soil and can wreak serious havoc when introduced to individuals undergoing antibiotic treatment.

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In totality, it’s important to understand that antibiotic are not a bad thing. They’ve certainly saved thousands of lives in the past, and will continue to do the same. Certain bacteria though, with their short lifespans and tremendously efficient usage of metabolic resources, are evolutionarily equipped to overcome our methods of antibiotic treatment at a quicker pace than we can currently handle. The way forward for our fight against them is through successful drug development at research facilities worldwide. A hotbed of research emerging today is looking inside the aforementioned microbiota for helpful small molecules to deter pathogenic colonization. The development must also be followed by the proper level of prescriptions handed out by medical professionals. Additionally, it is critical that individuals prescribed antibiotic treatment use the medication appropriately by taking the supplement in full and not dispersing their pills to other people. As organisms who live much longer than bacteria who colonize us, we can not compete with them in evolutionary speed. Instead, we must collectively outsmart them by using our much larger brain.

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