New weapon in superbug war may be right under our no...

"Antibiotic resistance: 'snot wars' study yields new class of drugs," BBC News reports.

Researchers studying a type of bacteria found in many people's nostrils have used this knowledge to develop a possible new antibiotic called lugdunin.

While it has not yet been tested in humans, this is a development not to be sniffed at.

Lugdunin was found to eradicate Staphylococcal aureus bacteria, which is carried naturally on the human body, including inside the nostrils.

Staph. aureus wasn't always a concern in most cases, as it usually only caused mild skin infections such as boils. But in recent decades some strains of the bacteria have developed resistance to commonly used antibiotics.

These types of strains are known as methicillin-resistant Staphylococcus aureus (MRSA) and can be challenging to treat. They can also pose a significant threat to people with weakened immune systems.

Researchers found another bacterial strain called Staph. lugdunensis, which lives alongside Staph. aureus and so competes for resources, produces antibacterial enzymes to kill off its competitor – the so-called "snot wars" described by the BBC.

They identified the genetic mechanisms behind this, and from there developed a purified compound called lugdunin that had the same antibacterial activity.

First in human blood samples, and then in rodents and human nasal swabs, they demonstrated that lugdunin can reduce Staph. aureus colonisation.

These are undoubtedly promising findings, but this is early-stage research. There are many testing stages to go.

And Staph. aureus isn't the only resistant microbe out there, so it wouldn't provide the whole answer to antimicrobial resistance – but this research does provide a new avenue for exploration.

Where did the story come from?

The study was carried out by researchers from the University of Tübingen in Germany, and was funded by the German Research Council and the German Center for Infection Research.

It was published in the peer-reviewed journal, Nature.

The UK media's reporting is generally accurate, though headlines talking about a "new class of drugs" may suggest these drugs are already available when they're actually still in the very early stages of development and have not yet been tested in humans.

What kind of research was this?

This laboratory study aimed to develop a new type of antibiotic that prevents Staph. aureus bacterial colonisation.

Antibiotic resistance is a global health problem. A well-known example is methicillin-resistant Staph. aureus (MRSA) – so called because it doesn't respond to methicillin, an old type of penicillin antibiotic.

As the number of infections that do not respond to antibiotics continues to rise, increasingly stronger antibiotics have to be used to treat them.

But this puts us at risk of coming to a point where infections can't be treated, as our strongest antibiotics no longer work.

This means there is an urgent need to develop new antibiotics that can tackle resistant infections – but there is a limit on how quickly they can be developed.

The vast majority of severe infections in people who have weak immune systems or have had major surgery or trauma, for example, are caused by bacteria that are normally carried on the body by healthy people.

Staph. aureus is present in the nose of around a third of the population.

Bacteria that are naturally present in the body are in constant competition with other types of bacteria.

It has been found some actually produce antibacterial-type substances to kill off the competing bacteria. This is what this research aimed to build on.

What did the research involve?

The researchers first screened multiple types of Staphylococcal bacteria to see which had antibacterial activity against Staph. aureus.

They found one particular bacterial strain, Staph lugdunensis, was able to prevent growth of Staph aureus.

They investigated the way it did this and identified a cluster of genes called lug, which were responsible for producing a group of antibacterial enzymes.

They then used genetic engineering techniques to amplify the activity of these antibacterial genes to produce a purified compound, which they called lugdunin.

This compound was analysed in the laboratory to confirm its chemical structure and that it had the same antibacterial activity as the original bacteria.

The researchers then moved on to laboratory, animal and human experiments to test how effective it actually was.

What were the basic results?

When tested in human blood samples in the lab, the researchers found lugdunin had strong antibacterial activity against several resistant bacteria, including MRSA – and this was without causing damage to the human blood cells.

Further analysis showed it seemed to be breaking down the bacteria's energy resources.

Staph. aureus didn't develop resistance to lugdunin, even when repeatedly exposed to low levels of the compound (not enough to kill the bacteria) over the course of 30 days.

They then tested mouse skin infected with Staph. aureus. Mice were treated with lugdunin one to two days after infection. This showed that lugdunin was able to reduce or completely eradicate the bacteria.

They then moved into tests in cotton rats, which are said to be an established animal model for investigating Staph. aureus nasal colonisation.

These animals were infected with both Staph. aureus and the original bacteria, Staph. lugdunensis. This confirmed that production of the antibiotic compound can reduce Staph. aureus colonisation.

This was repeated by testing nasal swabs from 187 hospitalised patients. The researchers found about a third of samples carried Staph. aureus, while 10% carried its opponent, Staph. lugdunensis.

The number of Staph. aureus bacteria present was about six times lower in the swabs also carrying Staph. lugdunensis.

Further tests showed all Staph. aureus were also susceptible to the new compound lugdunin.

How did the researchers interpret the results?

The researchers concluded that, "Lugdunin or lugdunin-producing commensal bacteria could be valuable for preventing staphylococcal infections."

They further say the bacteria naturally carried by humans "should be considered as a source for new antibiotics".

Conclusion

This valuable research has found a possible new avenue in the battle against antibiotic resistance – by harnessing the mechanisms that our own natural bacteria use to compete against other bacteria.

Multi-resistant Staph. aureus bacteria are responsible for many severe infections in hospitalised and immunosuppressed people.

This research found Staph. lugdunensis bacteria produce antibacterial substances, and from this researchers managed to develop a new purified compound that carries these antibacterial properties: lugdunin.

These are undoubtedly promising findings, but it's important not to jump too far ahead. This is currently only an experimental compound in the early stages of development.

Many more stages of testing would be needed before it is better known whether this antibiotic could be effective in humans and how it could be used.

For example, we need to find out whether the antibiotic would be used for just reducing Staph. aureus colonisation on the skin or in the nose, or whether it could actually be given to treat severe infections that have infected the body.

We would also need to know it is safe.

The study has only demonstrated the effects of this compound against Staph. Aureus, not against confirmed MRSA strains, so we don't know if it would definitely combat the well-known superbug.

Staph. aureus aren't the only resistant microbes out there, nor are they responsible for all infections.

This means this single discovery doesn't provide the whole answer to antimicrobial resistance. What it does provide is a new avenue for exploration.

While the possible developments from this research are as yet unknown, there are things you can do to fight antibacterial resistance.

This includes recognising that many simple coughs, colds and tummy upsets are viral and self-limiting. They will likely get better on their own and neither need, nor respond to, antibiotics.

If you are prescribed antibiotics – or any other antimicrobial, for any reason – it is important that you take the full course, even when you start to feel better.

Not taking the full course will expose bacteria to the antibiotic but not kill them off, allowing them to build resistance to it.