What can be done about antibiotic resistance? An easy answer would be to keep discovering or creating new antibiotics to which bacteria have not (yet) developed resistance. Although this is becoming increasingly hard to achieve, scientists around the world are still making valiant efforts to win this microscopic arms race against bacteria: One of the most recent is the discovery of an antibacterial compound named ‘Gladiolin’ (which, ironically, is produced by a bacterium). Researchers from Cardiff University and from the University of Warwick who managed to isolate this compound, believe that it may prove very potent in treating strains of tuberculosis that are resistant to multiple antibiotics.
Even though the discovery of ‘Gladiolin’ is an encouraging example of what can be done to combat antibiotic resistance, it is only a temporary fix, since it is only a matter of time before the tuberculosis bacterium develops resistance to it as well.
Healthcare practitioners are often pressured by their patients into prescribing antibiotics for diseases on which they will have no effect whatsoever.
Perhaps a more effective strategy would involve re-evaluating and redefining the point at which an antibiotic should be prescribed. Studies conducted in U.S. hospitals have shown that in nearly one out of every two cases, healthcare practitioners (HCPs) prescribe an antibiotic that is either incorrect or unnecessary, mostly because they neglect ordering laboratory tests to confirm that the patient’s symptoms are caused by a bacterium.
Even when these symptoms are indeed caused by a bacterium, HCPs usually prescribe multiple antibiotics at the same time so that the treatment will be effective against a broader range of pathogens, which, however, increases the probability for the development of antibiotic resistance.
Therefore, an efficient solution to the above problem would be to develop very accurate, fast and reliable diagnostic procedures, that would allow HCPs to identify the exact disease-causing organism and thus administer a more targeted, pathogen-specific treatment.
Additionally, HCPs are often pressured by their patients into prescribing antibiotics for diseases on which they will have no effect whatsoever, such as the common cold, thus unnecessarily subjecting the patient’s commensal (i.e. beneficial) bacteria to antibiotics to which they may also eventually develop resistance.
There are scientists that have given up on antibiotics altogether and have found a new ally at the face of bacteria-eating viruses.
In an effort to rectify this problem of ‘patient demand’, a review of multiple publications conducted by the Cochrane organisation in 2005 proposed the implementation of a policy called ‘delayed prescription’. Where applicable, the policy dictates that if HCPs prescribe antibiotics to patients, they should instruct them to fill their prescription only if the symptoms have not subsided on their own after a couple of days have passed. This way, the patient’s demands are satisfied while the unwarranted use of antibiotics is avoided, since most mild respiratory infections caused by viruses will have improved by then.
On the other hand, there are scientists that have given up on antibiotics altogether and have found a new ally at the face of bacteria-eating viruses, more scientifically known as bacteriophages. Ever since its establishment in 1923, the George Eliava Institute in Tbilisi, Georgia, has been at the forefront of bacteriophage research and its scientists have made tremendous progress at using bacteriophages to treat diseases caused by antibiotic-resistant bacteria. Simply put, bacteriophages are small viruses that infect bacteria, replicate within them and finally cause the bacterial cell to burst and release multiple copies of the bacteriophage. Besides being harmful solely against bacterial cells (and thus leaving human, animal and plant cells unharmed), each type of bacteriophage can only infect one type of bacterium, hence allowing for a very targeted and precise treatment.
Anyone familiar with the concept of evolution will probably ask: Won’t the bacteria evolve to develop resistance to the bacteriophages, just like they did with antibiotics? And the answer is yes. But, unlike antibiotics, bacteriophages also constantly evolve in order to bypass the bacteria’s defences and succeed in infecting them and reproducing within them.
It would therefore seem that there is actually plenty to be done about antibiotic resistance. Whether it is using our current antibiotics wisely and strategically or enlisting tiny bacteria-eating viruses to help us in our battles, is trivial. All that matters is that the disaster of antibiotic resistance must be averted.