As microorganisms mutate and procreate, each mutation makes them more resistant to drugs that once killed them. A time will eventually come when we cannot keep up with the pace of these mutations. A UK research revealed that presently about 700000 people die yearly due to infection by a drug-resistant microbe. This figure is expected to rise to 10 million by 2050. This by extension will cut off 2.5% from the world’s GDP. Also, it will impoverish about 24 million by the next 10 years.
Not to sound like a ‘prophet of doom’, but a time will come when it will be better to have cancer than to contract a multidrug-resistant pathogen. In that time basic surgeries will be banned because they could expose you to these rogue strains. In response, the UN says that the development of new drugs will go on a long way to ease things. But what then? The cycle of drug invention and drug-resistant continues. Research from Rockefeller may be the light of the world at the end of this tunnel. Perhaps a way to outmaneuver any drug resistances.
An answer to multidrug resistance
Ask any physician, one thing they dread the most is a pathogen that is resistant to strong antibiotics like penicillin, fluoroquinolones, Gentamycin, and tetracycline. It is truly a nightmare when a pathogen can also resist colistin because no stronger antibiotic can do the job. Researchers from Rockefeller University discovered a novel substance that could solve the problem.
In animal experiments, this prospective antibiotic was highly potent against dangerous opportunistic pathogens it proved this effectiveness against Acinetobacter baumannii, the major culprit of infections acquired in healthcare facilities.
At the core of colistin resistance, is a new gene, MCR-1, which it acquired in an evolutionary attempt to evade colistin toxicity. This resistance is driven by improper use or overuse of antibiotics. Because this gene is attached to a plasmid, it can spread quite fast. Zhongqing Wang, a postdoctoral associate commented, ”It jumps from one bacterial strain to another, or one patient’s infection to another’s”.
The breakthrough came based on a theory on bacterial survival. The theory explains that even pathogens compete among themselves for survival, they devise means to diminish other pathogen chances while maximizing theirs. As such, one of the most effective antibiotics, are products of bacteria that can kill its competing bacteria. By extension, if new strains of bacteria can evolve by acquiring MCR-1 genes, then their competitors will have to evolve by developing substances that can kill MCR-1 resistance.
If you can find such a substance, then you can end the resistance.
As such Brady, one of Rockefeller Evnin’s professors, and his team commenced a search for natural compounds from other bacteria that can combat colistin resistance.
To optimize results, they had to ditch the traditional culturing of bacteria in the lab for innovative techniques like searching the DNA of the bacteria for corresponding genes.
After checking about 10,000 bacterial genes, they discovered 35 groups of genes that produce colistin structure, just as they predicted. Interestingly, one group had genomes for a somewhat ‘modified colistin structure’, that can hopefully eliminate colistin resistance.
After they further probed these new genes, the team predicted the structure of these molecules and called them Macolacin. Then they synthesized this drug.
Unsurprisingly, Macolacin showed potency against multiple types of colistin-resistant bacteria even the intrinsically resistant Neisseria gonorrhea rated the highest threat level. On the foundation of this success, drugs have been developed to fight off the different resistant strains.
This discovery means that humans have a surefire recipe for developing drugs that can fight the most dangerous multidrug-resistant superbugs. Wang believes that we could apply our knowledge on evolution-based genome mining to address other areas of drug resistance.
Macolacin is truly a revelation to the science world. Finally, we can end the cycle of drug invention and drug resistance.
Multi-Drug Resistant Bacteria.