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Body & Mind

Achilles' heel to lower defenses of antibiotic-resistant bacteria found

By Darren Quick
June 20, 2014
Achilles' heel to lower defenses of antibiotic-resistant bacteria found
Researchers have discovered a way to lower the defenses of antibiotic-resistant bacteria, paving the way for a new class of drugs that could target superbugs, such as MSRA (Image: Shutterstock)
Researchers have discovered a way to lower the defenses of antibiotic-resistant bacteria, paving the way for a new class of drugs that could target superbugs, such as MSRA (Image: Shutterstock)
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Researchers have discovered a way to lower the defenses of antibiotic-resistant bacteria, paving the way for a new class of drugs that could target superbugs, such as MSRA (Image: Shutterstock)
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Researchers have discovered a way to lower the defenses of antibiotic-resistant bacteria, paving the way for a new class of drugs that could target superbugs, such as MSRA (Image: Shutterstock)

The discovery of antibiotics is one of the most important breakthroughs of the 20th century. But their effectiveness and low cost has led to their overuse, resulting in the worrying rise of antibiotic-resistant bacteria, or so-called superbugs. Researchers at the University of East Anglia (UAE) in England have now uncovered an Achille's heel in the bacterial cell defenses that could mean that bacteria wouldn't develop drug-resistance in the first place.

The World Health Organization's (WHO's) first global report on antibiotic resistance released earlier this year calls antibiotic resistance a serious threat that is "no longer a prediction for the future, it is happening right now in every region of the world and has the potential to affect anyone, of any age, in any country."

While we've seen other efforts to develop new ways to fight these superbugs, including antibiotic drug "smart bombs" that target specific strains of bacteria, "ninja polymers" based on semiconductor technology, and cold plasma therapy, UAE researchers have discovered a weakness that opens up the possibility of developing drugs that don't attack the bacteria itself, but target the defensive barrier that surrounds its cells.

Up until now, very little was known about how the outer membrane, which surrounds the drug-resistant bacterial cells and protects against attacks from the human immune system and antibiotic drugs, is built. But by examining a class of bacteria called "Gram-negative bacteria," which has an impermeable lipid-based outer membrane that makes it particularly resistant to antibiotics, the researchers found how lipopolysaccharides – the building blocks of this defensive barrier – are transported to the outer surface.

"We have identified the path and gate used by the bacteria to transport the barrier building blocks to the outer surface," said Professor Changjiang Dong, from UEA’s Norwich Medical School and leader of the research group. "Importantly, we have demonstrated that the bacteria would die if the gate is locked."

"The really exciting thing about this research is that new drugs will specifically target the protective barrier around the bacteria, rather than the bacteria itself," added PhD student Haohao Dong, who was the lead author of the study. "Because new drugs will not need to enter the bacteria itself, we hope that the bacteria will not be able to develop drug resistance in future."

If the research does indeed lead to the development of a new class of drugs that could effectively kill drug-resistant bacteria, it could be as groundbreaking and prove as important to human health as the development of antibiotics.

The UAE team's research is published in the journal Nature.

Source: University of East Anglia

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Body & MindCellsBacteriaAntibioticUniversity of East Anglia
9 comments
Darren Quick
Darren Quick
Darren's love of technology started in primary school with a Nintendo Game & Watch Donkey Kong (still functioning) and a Commodore VIC 20 computer (not still functioning). In high school he upgraded to a 286 PC, and he's been following Moore's law ever since. This love of technology continues as Managing Editor of New Atlas.

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9 comments
usugo
The nose is growing! It is admirable how many "scientists" exploit the ignorance of the media, funding agencies and public to look good and ensure fundings.
Penicillin doesn't enter the bacteria either and yet they have been very good at evolving resistance against it
Mel Tisdale
I am neither a chemist, nor a biologist, as I am about to prove.
Perhaps, when they have perfected the mechanism, it might be possible to include the necessary chemicals etc. as a component of other medicines, including headache pills and the like. That way drug resistant cells would be subject to attack almost universally, considering the amount we take today. Economies of scale would kick in and bring the costs down to the point where it might be possible to supply it for free or 'at cost' to poorer nations.
Just a thought.
I guess it is 30 - 40 on Old Mother Nature's serve. The question is: Is it match point, or are there many more sets to come? One thing we do know is that this game has no tie-breaks.
Haresh Metharam
What you need most is a healthy Immune system. There is over use of many antibiotics over the last 100 years which has led to resistance and bugs like MRSA . Tackle the cause and not the symptom. Wake up. No matter what you invent the only way a person gets better is with a strong Immune system.
windykites
The question is: how does the human immune system provide protection against bacterial infection? When do we need antibiotics? Is it just a matter of getting a strong immune system? How can this be achieved?
Skipjack
Obviously having a strong immune system is not enough to fight a strong infection. The assumption that modern medicine has done anything to weaken our immune systems is ridiculous. In fact, one could argue that our immune systems are too good resulting in allergies and autoimmune diseases. 100 years ago, pneumonia was almost certainly deadly. 45 years ago, thanks to antibiotics pneumonia was so rare, that the chief physician would call all the students in to get a chance to listen to a pneumonia when they finally had a case. Today pneumonia is making a return. In part it is because people do not take their antibiotics are prescribed, but stop them early. This then leads to relapses with resistant strains that are then passed on to others.
Synchro
One way to strengthen the immune system that isn't about to go away is vaccination. And it's probably going to be more important to emphasise prevention over post-infection treatment where possible given that antibiotics are going away, that is if the anti-vaccine camp doesn't succeed in its mission to kill everyone first.
ClassicPlastic
The key to a robust immune system is the ability to live a balanced and stress-free life. Otherwise, we're in a constant "Alert" mode that takes down the immune system.
If you can figure out a practical way for 7 billion people to live balanced and stress-free lives, please let the rest of us know.
Blazemonger
It's great that they are finding a new target to develop a new class of antibiotics. However if I were on Haohao Dong's committee I would hammer him for thinking it makes a difference if the drug in question enters the cell or not. As soon as you start widely distributing this stuff, you will select for bacteria that are less susceptible to it, until you finally have resistant strains. Evolution baby!
PaulW
This article includes a strange statement:
PhD student Haohao Dong, who was the lead author of the study, reportedly said, "Because new drugs will not need to enter the bacteria itself, we hope that the bacteria will not be able to develop drug resistance in future.”
Either Mr Dong was misquoted or he misunderstands how natural selection and evolution occurs.
If the drug doesn't enter the cell, then that limits some modes of drug resistance, but there is no hope that it will "not be able to develop drug resistance."
Whether drug resistance develops is not conditional upon where the drug acts. As the bacterial cells copy their DNA, mutations in the DNA are introduced randomly. Those random mutations result in a random set of phenotypic differences. Some of those differences will be harmful. Some will be beneficial. And, after billions of such mutations have occurred, one of them will produce a phenotype which evades or blocks the effect of the drug.
Admittedly, this proposed drug evades one of the most common methods of resistance: active export of the drug by the bacterium. However, there are many other pathways to drug resistance.
Also, if the active site of the drug is located outside of the cell, then direct attack on the drug can occur only by proteins expressed extracellularly. So, that might render it more difficult for the bacterium to directly attack the drug. But there are abundant ways to indirectly attack the effect of the drug.
This proposed drug may be promising. And it constitutes a new class of antibiotic. But it is unjustifiably optimistic to "hope that the bacteria will not be able to develop drug resistance in future.”