The resistance to resistance: 3 strikes, you’re out!

CHANCES ARE YOU have heard about antibiotic resistance. It is one of the biggest biological issues of our time, first discovered in 1945 where Staphylococcus species were found resistant to the landmark antibiotic, penicillin. In the US, two million people contract antibiotic resistant infections that result in 23 000 deaths every year.

The modern era of antibiotics started with penicillin in 1928. Image: PEXELS

Imagine a world where diseases such as tuberculosis, cholera and bacterial pneumonia are as common as the cold, yet incurable. Imagine a world where the threat of diseases characteristic of an ageing population become a thing of the past due to the impounding threat of diseases that are currently practically eliminated. This is the threat of antibiotic resistance.

Antibiotic resistance has arisen through overuse of antibiotics in the medical world and disease prevention in cattle. This has led to bacteria being under intense selection pressure to mutate and become resistant to that drug. It only takes one bacterium to become resistant for a whole population to become resistant; the non-resistant die allowing the resistant bacterium to survive and reproduce, this is called vertical gene transmission.

Once resistance has arisen in one species, the mutated gene can then be transferred to other species via a structure that extends from the bacterium to form a connection with another species. The resistance gene is then replicated and transfers into the connected neighbour, conferring antibiotic resistance in the recipient species.

The challenge of eliminating antibiotic resistance, or finding alternative treatments, has been a struggle for the scientific community. Identifying new antibiotics, rearranging genes in antibiotic producing species in order to obtain new variants of existing ones, using viruses to manipulate bacterial genomes.

However, progress is slow, and the bugs are evolving quickly. One key break through last month was the chemical alteration of the existing antibiotic, vancomycin. Traditionally, vancomycin was used as a ‘last resort’ to treat enterococci but the species became resistant to it and is now called: Vancomycin Resistant Enterococci (VRE).

This disease is often found in hospitals and can cause fatal infections in the blood. The WHO proclaim that VRE poses a significant risk to human health. Some drugs work against VRE but vancomycin, first discovered 60 years ago, is now useless against it.

Scientists hypothesise this new version of the drug is 1000 times more potent than the existing version, so it could be a key weapon in our fight against antibiotic resistance. Not only does it fulfill the original role of the drug but other modifications have given vancomycin new mechanisms of action.

The drug has been altered so it can attack bacterial cell walls causing cell lysis. Laboratory experiments demonstrated that the drug was very effective, retaining full effectiveness after 50 rounds of treatment to the bacterial cultures of VRE. The lead scientist, Dr Dale Boger, puts this down to a ‘multiple attack’ approach whereby no species can evolve to avoid three distinct mechanisms of action of a drug, meaning vancomycin can be used “without the fear of resistance emerging”.

The drug still needs to be tested on animals and humans but there is hope it will be available within five years. This research suggests that manipulating antibiotics to have more than one mechanism of attack is highly successful in killing bacteria. This approach could therefore be used on other drugs to avoid the prospect of a ‘post-antibiotic era’.

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