Bacteria surround us, all day, every day. Fighting billions of tiny battles for and against each other and us. But in the epic struggle between good and evil, who will come out on top?
Words Lucy Jolin
Photograph of the original culture plate of the fungus Penicillium notatum, made by the Scottish bacteriologist Sir Alexander Fleming in 1928. One of Alexander Fleming’s petri dishes containing a sample of the mould Penicillium notatum sold for £11,163 at Christie’s. © Science Photo Library
In his busy laboratory, somewhere in the maze of corridors within the Eastman Dental Institute on Gray’s Inn Road, Dr Adam Roberts is analysing a petri dish full of bacteria that were, until a few weeks ago, lurking under someone’s fridge.
On the bench next to him are piled more dishes, bursting with a dizzying range of cultures. “That’s nice, that yellow one. And that tall one and the gloopy one – those are off the bottom of my shoe,” he observes. He produces a dish full of what looks like tiny white towers. It’s both fascinating and deeply creepy, as he cheerfully reveals: “Those are off the rim of a 10-year-old’s water bottle.”
This is Roberts’ Swab and Send project, now in its second phase. It’s a simple idea: email Roberts, pledge a small amount of cash and he’ll send you a swab. You rub it on anything in your environment – from banknotes, reptile vivaria, the terrifying world in the dark recesses of your home – and send the swab back to Roberts, Senior Lecturer in Microbial Diseases at the Eastman.
He grows the bacteria from that swab on an agar plate in his lab, then tries to identify it. A light ring around one kind of bacteria – a yellow stain, a splattering of white dots, a greenish tint – shows that it has managed to gain the upper hand over its neighbours as they all fight for a share of the nutrient-rich media on which they’re growing.
This might not sound like cutting-edge science – indeed, it’s more or less the same method that led Alexander Fleming to discover penicillin – but the project is actually on the front line in the global war against antibiotic resistance. One of those samples might, just might, contain an as-yet-unidentified bacteriam that could produce an antibiotic and save countless lives.
Bacteria surround us, all day, every day, fighting billions of tiny battles against each other and us. They’re in our guts, in our food, and they teem on everything we use – our phones, our computer keyboards, our fridges. Much of the time, we don’t even know they are there. Sometimes those bacteria have names – E.coli, C.difficile, MRSA – and they can make us very ill indeed. So we treat them with antibiotics, which are naturally produced by bacteria themselves.
And because we’re using antibiotics more and more to fight infections, they’re becoming less effective. Fleming was one of the first to point out this danger. “It is not difficult to make microbes resistant to penicillin in the laboratory by exposing them to concentrations not sufficient to kill them, and the same thing has occasionally happened in the body,” he said in his 1945 Nobel lecture. “The time may come when penicillin can be bought by anyone in the shops. Then there is the danger that the ignorant man may easily underdose himself and by exposing his microbes to non-lethal quantities of the drug make them resistant.”
The consequences of increased antibiotic resistance are frightening. “No antibiotics means that patients will die of trivial infections,” says Dr Paul Stapleton, Senior Teaching Fellow at the UCL School of Pharmacy. “And some people – those who undergo transplants, cancer patients, our ageing population, diabetics and so on – will succumb to infections relating to those conditions.
“Unfortunately, resistance is unavoidable, because many antibiotics are from bacteria and these organisms need a means to protect themselves from the agents they produce. Furthermore, they can also become antibiotic resistant through mutation, and resistance can be transferred from one bacterium to another. When you use an antibiotic, the susceptible bacteria population is wiped out. The resistant population then predominates, and is then able to take over that particular environment – in this case, within the patient, sometimes with devastating consequences.” This is because antibiotics harness what bacteria do best: they fight. They work by binding to a particular protein target in the bacteriam, which prevents that bacteriam from defending itself by, for example, making its cell wall strong. Consequently, the cell wall weakens and the bacteriam dies.
But then the bacteria fights back, explains Dr Jess Healy, Excellence Fellow in Pharmaceutical Chemical Biology. “It evolves a related enzyme that binds to the antibiotic and breaks it down. So penicillin, for example, is broken down before it gets a chance to work, giving the bacteria the chance to proliferate and make you more sick.”
Coloured transmission electron micrograph of a deadly cluster of MRSA Staphylococcus aureus bacteria, resistant to most antibiotic drug agents. © Science Photo Library
A strain of the bacteria Mycobacterium tuberculosis, the cause of TB in humans. The bacteria is spread by coughing or sneezing and inhaled into the lungs where they proliferate to form lesions called tubercles. © Science Photo Library
Bacteria will always adapt. When we are long gone as a species, they will still be here
Then there are the bacteria that have evolved their own anti-antibiotic “pumps”. The drug goes into the bacteriam, which pumps it right back out again. Substances called porins in a bacteriam’s outer membrane can also provide a handy doorway for antibiotics to get in, but the bacteriam can then change its tactics and adapt to stop that happening – to do this it will simply reduce the number of porins, making the cells less porous, so antibiotics can’t get in. Time is on the bacteria’s side, too: while our abilities take generations to evolve, bacteria can whip through a hundred generations in 24 hours or so. “They’re tricky little buggers,” Dr Healy sums up.
Fighting them on the surfaces
Luckily, so are humans. Swab and Send is just one of the projects at UCL searching for the solution to the resistance problem. Dr Healy and her team, for example, are currently researching how bacteria protect themselves from enemies such as antibiotics and the human immune system. The bacteria use special enzymes to fight these stresses. Finding out more about how these enzymes work could, one day, help us find new drugs that could disarm a bacterial pathogen’s defences.
However, this search is hugely costly and time-consuming. A drug discovered tomorrow is likely to take at least another decade and billions of pounds before it reaches a single patient. So Ivan Parkin, Professor of Materials and Inorganic Chemistry, and his team are opening up a new front in the war against bacteria: fighting them on the surfaces.
His project originated in the work of Professor Mike Wilson of the Eastman Dental Institute, who invented a procedure to treat gum disease (incidentally, humanity’s most common disease) using an antimicrobial dye mouthwash which is activated by a hand-held laser. It’s now in use worldwide and 100,000 people have benefited from treatment. Wilson and Parkin met and discussed coating everyday surfaces in a similar antimicrobial material. This led to a long-term collaboration over 10 years. Recently Parkin and his team – Sacha Noimark and Dr Elaine Allan – have developed the world’s first light-activated antimicrobial surface that also works well in the dark.
Again, it’s a simple idea – surfaces are covered in a silicone coating with a thin layer of dye. When that coating is exposed to light, the dye creates chemicals that are very toxic to bacteria, but significantly less toxic to human and animal cells. Tests found that even when a surface was coated with a billion or more bacteria per square centimetre – in a contaminated hospital, you’d expect 1,000 bacteria per square centimetre – they were all dead within a few hours. The surface continued to kill bacteria, albeit at a slower rate, when the light was turned off. And it was even effective against hardy bacteria like C.difficile, which can live for thousands of years if undisturbed, and is estimated to affect 50 per cent of patients with hospital stays longer than four weeks.
Living in a microbial world
Parkin, honoured by the Royal Society with the prestigious Armourers and Brasiers’ Prize in 2014, hopes that the technology will be used to coat surfaces in healthcare environments – one of the main sources of infection. “Every person who goes into hospital has a 10 per cent chance of picking up a hospital-acquired infection,” he explains. “Bacteria are mainly transferred within the healthcare environment through touch. A contaminated person touches a surface; someone else will then come along and touch that surface again. So that surface is a reservoir for transmitting bacteria from one patient to another. Those surfaces include buttons in lifts, computer keyboards, bed rails, telephone, computer keyboards – any surface where multiple people are touching the same thing. Our treatment augments the cleaning regime – our surfaces will actually eliminate any contaminating bacteria on the surface, quickly.”
Back in the lab, Roberts admits that sometimes it feels like a losing battle. “Bacteria will always adapt,” he says. “When we are long gone as a species, they will still be here. It’s a microbial world – we’re just passing through. But something could be out there. At the moment, we only have about 50 antibiotics and there’s resistance to all of them.
“Imagine if, in 10 years time, a clinician could choose from 1,000 antibiotics. You never know what we could achieve if we make a concerted, global effort.”
Visit https://ucl.hubbub.net/p/swab-and-send-II to find out more about the Swab and Send project.
One of the first scientists to observe that mould could have germ-killing properties was French doctor Ernest Duchesne in the 1890s. The first recorded cure using penicillin was by Sheffield pathologist Cecil George Paine on 25 November 1930, who used it to treat a child with an eye infection. © grebcha/Shutterstock.com
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